Clinics in Developmental Medicine No.

r6z
PRECHTL,S METHOD ON THE qUALITATIVE
ASSESSMENT OF GENERAL MOVE}ENTS II,i
PRETERM, TERM AND YOUNG INFANTS

O 2004 Mc Keith

Press

3o Furnival Street, London

Editor: Hiluy M.

ec4.l

rq

Hut

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ll

fr,/;/1,0,,',D3
Clinics in Developmental Medicine No. r7

Prechl's Method on he
Q ua litatir;e Assessment of
Genera/ Morsements in Preterm,
Term and Young Infanrs
CHRISTA EINSPIELER

Medical University o{ Craz, Austria

HEINZ F.R. PRECHTL

University of Croningen, the Netherlands and
Medical University of Craz, Austria
AREND F, BOS
University of Groningen, the Netherlands
FABRIZIO FERRARI

University of Modena and Reggio Emilia, Italy

CIOVANNI CIONI

University of Pisa and Steila Maris Foundation, Italy

20o4

Mac Keith Press

D is trib

u te

d _,

(?rff[

LEY-

QC2sLncKwELl-

Il moto

causa

d'ogn vita.

LEONARDO DA VINCI
Ein Kind, sich bewegend, erzcihlt mit Berhrung sein Leben der Zeit.

GRAZ

2OO3

]],|'ITFNTS

AUTHORS' APPOINTMENTS

vii

ACKNOWLEDGEMENTS
INTRODUCTTON: HOW

viii
tT

ALL CAME ABOUT

1.

BASIC CONCEPTS OF DEVELOPMENTAL NEUROLOGY

2.

WHAT ARE SPONTANEOUS MOVEMENTS?

3. HOW TO RECORD AND ASSESS GENERAL MOVEMENTS

4. WHAT COULD INTERFERE WITH THE SUALITY OF GENERAL
MOVEMENTS?

5.

HOW OBJECTIVE, RELIABLE AND VALID

MOVEMENT ASSESSMENT?

I9
29

IS THE GENERAL

35

6.

THE CLINICAL APPLICATION OF THE METHOD

46

7.

QUANTITATIVE ASSESSMENT IS AN INSENSITIVE INDICATOR

OF IMPAIRED INTEGRITY OF THE NERVOUS SYSTEM

BRAIN ULTRASOUND AND GENERAL MOVEMENT ASSESSMENT

8.

NEUROLOGICAL EXAMINATION AND GENERAL MOVEMENT

ASSESSMENT

ix

O.

67

WHAT OTHER METHODS OF GENERAL MOVEMENT ASSESSMENT

EXIST?
EPILOGUE
REFERENCES
INDEX

72

IS
zo
B

- - --]Ot?S' APPOINTMEI\TS

Christo Einspieler

Professor of physiology, Medicol University

of Groz,

Austrio
Heinz F.R. Prechil

Arend

F. Bos

Fobrizio Ferrori

GiovqnniCioni

Professor Emeritus of Developmentol

Neurology.
University of Groningen, the Netherlonds
ono
Honorory Professor, Medicol University of
Groz,Austrio
Professor of Neonoiofogy, University of

Groningen,
the Netherlonds
Professor of poedioirics, University of
Modeno ond
Reggio Emitio, ttoly
Professor of Child Neurology ond psychiotry,
University of piso ond Stelto Moris Fondotion,ltolv

vll

ACKI\OWLEDGEIVEI\TS

Christa Einspieler lvould like to express her sincere gratitude to her cousin Dr Uli Todoroff
for creating a unique atmosphere in a medieval stone house in Vinci, Tuscany. This book
could not have been written lvithout her continuous supply of cooled lvater, fresh salads, and
dried apricots, and her battle against aggressive mosquitoes during three hot summer lveeks

in 2003.

,\]-IRODUCTION:

"OW

lT

ALL CAME ABOUT

Hein: F.R. Prechtl

The key to understanding and fully appreciating a newly introduced assessment technique
is to trace its history. One question frequently raised during the training courses on GM
assessment is: 'How did you hit on the idea of a qualitative assessment of general movements
as a specific predictor for neurological impairment?' Below I will outline the historical background of the 'whys' and 'lvherefores' that finally led to the rationale for this new method.
As is invariably the case with the anslver to a seemingly simple question, the approach
that led to the final solution lvas far from direct. Indeed, I have travelled dolvn a long
and winding path to reach the final goal. From my initial attempts to design a reliable and
standaidised method for a neurological examination of the fullterm neonare in the late 1950s
and early 1960s, my interest lvas focused on the early assessment of brain dysfunction
(Prechtl and Beintema 1964, Prechtl 1977). Atthe time, adult neurologists considered such
a neurological technique illusory because of the inconsistencies of reflex and response
pattems in nervborn infants. What was as yet unknolvn lvas the high dependency of these
patterns on the infant's behavioural state. As soon as this problem rvas solved (see Prechtl
1974), normal infants did respond consistently to the eliciting stimuli. So now, if they did
not respond despite being in the right behavioural state, it meant thar something must be
rvrong and it r.vas then an abnormal neurological sign.
Classic neurological assessment has trvo shortcomings, although it is still an indispensable tool even today. The first problem is twofold: a shortened version is unreliable
and to carry out a reliable (and therefore detailed and longer) version is perceived as too
time-consuming. Holvever, it should be remembered that the nervous system is the most
complex and complicated organ of any organism- This aspect is all too often not appreciated
sufficiently. The second shortcoming is that the classic neurological examination can
reveal the acute condition of the infant's nervous system but it lacks the polver to make a
specific prognosis of neurological outcome. From detailed follow-up studies and group
comparisons lve knelv the chance rate of normal outcome, minor abnormalities and severe
impairment. At the level of the individual infant and its parents, this approach lvas rather
much of a gamble and more of a burden than a help- Hence, there lvas felt to be a great need
for a technique of early neurological assessment that rvas at once cost-effective, easv to
leam, quick, and had a high individual predictive porver.
The path that led to the method that met these requirements'rvas long and rather
complicated as it first carried us to completely u-nrelated problems. In the 1970s, after already

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having rvorked for some 25 -vears in the field of infant neurology, I started lvondering about
the prenatal development of the many' spontaneous motor patterns seen in the nelvborn.

Birth could not be the starting point; these motor patterns must have a longer. prenatal
history. Because, until then, only'reflex studies had been carried out on aborted foetuses
(iv{inkorvski 1928, Hooker 1952), the advent of advanced real time ultrasound heralded the
beginning of non-invasil'e, intra-uterine observation of the foetus. It lvould enable us to
study the undisturbed foetus in its natural environment. Horvever, at the time, ultrasound
equipment had not y'et improved sufficientil' to allolv the observation of foetal movements.
I decided to carry out a preparatory study r.vith the unaided eye of unstimulated preterm
infants, just to observe what they' do if left alone, and perhaps to enable me later io recognise
certain movement patterns in the foetus (Prechtl et al 1979) . This was an unusual approach
then and unfortunately it still is.
A group of very lorv-risk preterm infants lvas painstakingly selected. These infants
sholved a large varie[,'' of spontaneous movement patterns, lvhich could be easily' recognised
each time they occurred. It lvas amazing holv many specific motor patterns lvere endogenously generated rvithout any external stimulation (Prechtl ef"al 1979). These observations
contrasted dramaticall-v- lvith the concept of a passive nervous system but for the grace

of

many sensor)' inputs. Our observations lvere an eye-opener and, armed r,vith this knowledge,
the foetal studies couid commence in 198 i - with technically more advanced ultrasound
equipment (de Vries JIP et al 1982, 1984, i985, 1987, 1988). Again, our focus of interest

lvas the complex repertoire of spontaneous moyements and our findin-ss conf,rmed that
postnatal behaviour has indeed a long prenatal histor). But, there lvas another important
discovery: the continuity from prenatal to postnatal life of many neural functions (Prechtl
198zla). Onl,'at 3 months does the nervous system become adapted to the requirements of
erta-uterine life. Of course, this holds true for non-vital functions only'(Prechtl 198;+b,
1986).

All of this lvould not

have given a ciue to a nerv assessment technique had rve not also

collected similar observations on high-risk preterm infants. Our original expectation of a

significant difference in the incidence of the various specic movement patterns betlveen
the lorv-risk and the high-risk infants rvas not conf,rmed (Prechtl and Nolte 1984). Horvever,
rve suspected that the hi,eh-isk infant moves differently from the normal infant. This marked
the be-einning of a nerv approach to assessing the young nerv'ous system, even if it lvas not
yet sufficiently specified. Significant heip came from nervl' developed video-recording
equipment. In contrast to previously used cine-filmin-e, video allolved us to vierv the
recording immediately after the session, and lve could even replay' it at different speeds.
Another crucial technical developmennvas the method of ultrasound brain examination.
We combined both techniques - the nerv video technologl and brain ultrasound - and
replicated the previous observational studies on a selection of cases lvith or rvithout brain
ultrasound abnormalities and video-recorded their spontaneous movement pattems (Ferrari
et al 1990, Prechtl 1990). The main focus lvas on the so-called general movements lvhich
had first been described in the observational study of normal preterm infants (Prechtl et al
I979). The studl by' Ferrari et al ( 1990) on preterm and term infants was the convincing first
indication that rve rvere on the right path: the qualitative assessment of general movements,

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hose mostfrequently occurring, long-lasting and complex spontaneous movement patterns.

is rvhat realll counts and not the quantitative differences.

The problem that nolv confronted us lvas that if you cannot count and reproduce
the
diffeences in numbers, might the technique not be too subjective? Therefore, a crucial
imponance for our nelv technique lvas the interscorer agreement, as the qualitative assessment of general movements is based on visual Gestalt perception. Indeed, an interscorer
a-*reement of 90 per cent is sufficiently high (see Chapter 5). It should be realised that visual
Gestalt perception is an excellent scientific tool. The importance of visual observation in
daill' clinical routine and research rvas recently emphasised by Bax (2002) inhis editoial
'

Clinical assessment still matters'.

The attention shift from exclusively reflex to spontaneous movements in the early
neurological assessment again has a historical background. The change of paradigm from
a passive to an active and endogenously generating central nervous system must have
consequences for neurological assessment. I must admit that the realisation of the importance of spontaneous motor activity, and of general movements in particular, came after our
empirical findings.
Classic neurophysiologists studied neural functions on the basis of experimentally
impaired neural systems. The quantitative relationship betrveen the sensory input and the
reflex (motor) output lvas the focus oftheir attention (Sherrington 1906). Clear-cut, quan-

titative results could only be obtained by excluding the nuisance of the interfering
spontaneous activity. This led to historical distortions of the concept of neural functions,
distortions that have not yet been fully overcome to this day. Neurology has come a long
lvay to rediscover the importance of endogenously generated activity, particularly in the
young organism, and to place reflex activity there rvhere it is of biological significance.

I would like to conclude by saying: if reflexes are performed more consistently by

de-cerebrated animals, reflexes cannot be the best tvay to study the consequences of brain
impairment. On the other hand, the qualitative assessment of spontaneous activity is a
sensitive indicator of certain neurological impairments and, hence, opens up a lvindolv into
the brain.

This then is the rationale for the method described in this book and the rvav it came
about.

XI

r ASIE EONEEPTS OF
] -VE LOPM E NTAL I\ E U|?OLOGY

The assessment of general movements within the concept

of ontogenetic adaptation
During the past 40 years, research in developmental neurology has provided a number
of

signiflcant nelv paradigms on the functional development of the human nervous

system. One
of the most fundamental nerv insights is the concept of ontogenetic adaptation with
its farreaching consequences (oppenheim r9g4). This concept acknowledges that
during the
development ofthe individual the functional repertoire ofthe developing neural
structure
must meet the requirements of the organism and its environment (prechtl
2001a).

Horvever, in comparison to neonatal infra-human primates the human

neonate is

less adapted to the extra-uterine environment as far as non-vital functions

are concerned.

The human pregnancy is relatively short in respect to the allometric measurements

of
marernal body weight, brain weight, metabolic rate and maximal life span (prechtl
19g6,
2001a). The first tlvo months after term are in a certain lvay a continuation
of foetal
behaviour. At the third month a majo transformation of many neural functions
occurs,
and

only then is the young human infant much more adapted to the requirements
of exa-uterine
life (Prechtl l9Szta, 1984b). Such a delay seems specific for rhe human species (prechtl
2001 a).

At 3 months the infant's muscle polver increases; the body posture changes from

a body-oriented to a space-oriented postural control (Prechtl 1989a);

the sucking pattern
changes from tongue peristaltic movements to a nelv pattern of sucking
rvith open corners

of the mouth (hvayama and Eishima 1997); control of visual attention and
binocular

vision develop (Braddick and Atkinson 19g3, Atkinson l9g4a, l9g4b);

social smiling and
pleasure vocalisation while looking towards the caregiver occur (van
Wulfften palthe
and Hopkins 1984); and general movements change their form (Hopkins
and prechtl I 9g4,
Prechtl 1986, 2001a). This list is farfrom complete. These changes occur
during a relatively
short period of a felv lveeks. The increased strength of the muscles
makes movements

more effective; the slvitch-on of antigravity postures and orientation

of the infant in
space, as lvell as the onset of true social interaction with the caregiver,
are signs of a more
effective ontogenetic adaptation to the new environment. It must
be assumed that

this
obvious developmental delay in the human species can be compensated
by the effectiveness
of the larger brain rvith higher 'intelligence' of caregiving in the parenls (prechtl
1e86).

l9g4b,

with the exception of the above-mentioned delay, the developing organism

is during
each developmental stage adapted to the internal and external
,"qui."rn-"nts. Therefore.

eachdevelopmentalstagemustbestudiedinitsolvnrightandnotinrelationtolater
dealing rvith qualitatively different nervous
developmenral stages. aidifferent ages we are
lvell as the functional repertoire'
These differences comprise the structtue as
s).stems.

Aconsequenceoftheage-specificdifferenceofthedevelopingnervoussystemisthe
Hence' the clinical consequence is that ageage-specific vulnerabilitl:of tht nt'uou' tissue'

diagnostic procedures (Prechtl 2001a)'

specific signs and syndrmes require age-adequate
must meet this requirement'
of course, an-v neurological eminaiion and assessment
takes full account of the
prechtl,s method of quaf,tatiue assessment of general movements
(Fig' l'l)'
age-specificity and the ontogenetic adaptation

of spontaneous movements

From reflex and tonus testing to observation

Iflveconsiderthelvorkofclassicneurophysiology,whichisassociatedrviththenameof
and spinal

car that de-cerebrated animals

the eminent Sir charles Sherrington, ir becomes
o"tts o'r detailed studies on reflexes a: t:ti:li"^t
*t,n this ingenious trick it rvas possible to get rid of the anno-ving

t:":'::::i:::

nr.ililffir"**^*.
ffi;;;i;ii"*
i;;;il;;;;ng

,- 1Ql'prrinotnn
(tl::"i::"it
svstem
from the siontaneous acriviry of the nervous

1906).onliunderde_cerebrationdiditbecomepossibletostudyindetailastable,quanreflerive motor output' Having accepted

titative relationship betrveen sensory input and
general, refle.r.es are poor indicators of brain
this fact, lve should not be too surprised if, in
function and dvsfunction.

ontheotherhand,asaiogicalconsequenceofalltheexperimentsintherealmof
neurai

the expression of spontaneous

classic neurophysiology, spontaneous motilit-v'
lesions' Nevertheless' it may still be
brain
but be an excellent marker of
as

activit-v, cannot

surprisingthatthisfacthasbeenoverlookedforsuchalongtime.Theenormoussuccessof

Age-sPecific
Ontogenetic AdaPtation s
of the Devloping Nervous Sysiem
Age-sPecific
Pattems of GMs

Age-adequate
GM Assessment

Fie.l.lGeneralmovementassessmentasamethodofdevelopmentalneurologywithitsbasicconcept
of ontogenetic adaptation and its consequences'

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ihe classic stimulus-response investigations has created a tremendous bias in our thinking
abour rhe function of the nervous system (Prechtl 1997a,2001a). Hence, it took a long time
rlr chage paradigms. In part, this task lvas

left to the young field of developmental neurology

Curin-e the second half of the twentieth century.

The concept of tonus or tone rvas introduced into the neurology of the young infant by
rhe eminent adult neurologist Andre-Thomas. His outstanding book on cerebellar diseases

ith tonus changes as an important clinical sign. His later co-operation lvith S. Saint-\nne Dargassies brought his ideas of tonus testing to infant neurology (Thomas and
Saint-Anne Dargassies 1952). This tradition continued with Claudine Amiel-Tison (AmielTison and Grenier 1983) and the Dubowitzs (Duborvitz and Dubowitz 1981, Duborvitz
etal 1999). Regrettably, the definition and assessment oftonus are not standardised and vary
greatly. Clinical experience indicates the inconsistent character of tonus in young infants,
and the inter-observer agreement is lveak. Severe cases of hypotonia and hypertonia are
exceptions to the case in point and are clinically important. Holvever, during the first lveeks
of life hypotonia and hypertonia are not specific signs of later neurological deficits (Prechtl
1997a.2001a).
In the observation of infants the interest has changed from the analysis of the capacities
to respond to a manifold of sensory stimulations, to the observation of the un-stimulated
infant. Naturalistic observations led to the conclusion of the dominance of sDontaneous
behaviour, i.e. behaviour not generated by sensory stimulation.
Two investigations must be mentioned. The pioneer rvork by Amold Gesell ( 1945) was
based on a developmental concept, lvhich rvas interpreted as a genetically determined
maturation of neural functions. His interest lvas focused on a developmental test, lvhich
lvould enable the examiner to discriminate betlveen normal milestones and retarded
development. The description of the various motor patterns at different ages lvas based on
cine-film ofthe infants and children. Holvever, the database lvas relatively small, and therefore the Zunch study (Largo et al 1990, Largo 1993) made improvements and corrections
to the Gesell study.
The other rvork along similar lines lvas carried out by the psychologist Myrtle McGrarv
(1943). In a period dominated by behaviourism it was understandable that the rvord
'spontaneous' lvas in quotation marks. McGraw said about the neonate: 'Perhaps the most
striking aspect of nervborn behaviour is general motility. The so-called "spontaneous"
behaviour of the neonate has attracted the attention of many investigators. It is the
incoordination and lack of form which differentiates sDontaneous movements from other
(reflexive) neuromuscular activity' (1943: 18-19).
This view has changed dramatically since unstimulated foetuses, preterm and term
infants have been systematically and longitudinally observed (Prechtl et al 1979, Cioni
et al 1989, Prechtl 1989b, Cioni and Prechtl 1990). In fact, all foetal movement patterns,
lvhich are endogenously generated by the unstimulated nervous system, are distinctly
patterned right from the first onset at about 8 to 9 weeks postmenstrual age. There exists no
phase of uncoordinated and amorphic movements (Prechtl 1989b, 2001 b). A rich repertoire
develops lvithin a felv lveeks, lvhich continues after birth unchanged for the first trvo to
three months (Prechtl 1992).
dealr

The question of holv spontaneous movements are generated by the nervous system has
recently been anslvered. Results from developmental neurobiology are rapidly accumulating
convincing evidence that, under normal conditions, the young neryous system is to a large
extent an active organ (see Chapter 2). The spontaneous motility offoetuses, preterm and
term infants as well as infants during their first months of life has great clinical signif,cance
(e.g. Ferrari et al 1990, Prechtl and Einspieler 1997, Prechtl et al 1997b). It proves to be an
important functional indicator of brain dysfunction at a very early age and tells us more about
the young nervous system than any amount of reflex testing does (Prechtl l9V/a,2001a).

.,,IAT

ARE SPOI\TAI\ EOUS

."lOVEMENTS?

That the young human nervous system endogenously, i.e. without

being constantly triggered
b;- specific sensory input, generates a variety of motor patterns
rras b"een known for more
than a century' william preyer (lgg5) was fulry alvare

of this fact, but it was forgotten

rvhile, only to be rediscovered later in animars
by Erich von Horst (1939) and by the
founders of ethology, Konad Lorenz and Niko Tinbergen.
Modern neurobiology has pro_
vided extensive experimental evidence for the existence
of
fo

endogenously generated activify.

The eyidence of endogenously generated motility

As early as 1913, Graham-Brolvn, rvho rvorked in Sherrington,s
laboratory, found that
locomotor movements in kittens are not based on reflex
activity but on intraspinal generation
(Graham-Brorvn 1913)' Erich van Holst spent his
experimental life's rvork on what he called
'zentrale Automatie' (central automatism) and
rvhat is norv called the central pattern
generator (cPG; see review by Grilrner 1999).
well-knorvn examples of cpGs are the
cental mechanisms for breathing, sucking and chewing,
and for locomotion such as slvim_
ming, crarvling and lvalking. It is only during the last
decade that rve have reached a better
understanding of the cellurar and molecular mechanism
responsible for endogenously
generated motor activity.
Lor'ver vertebrates especially, such as fish
and amphibians, but also mammalian
foetuses,
have provided good experimental possibilities
for exploration of rhythmical

patterns.

These
rhythmical patterns can be generated continuousry(e.g.
breathingl or episodically (e.g.
locomotion), when short or long bouts of rhythmic
activity are interspersed with periods
of quiescence' The latter arises from active, maintained
inhibition of an otherwise rhythmical active netlvork (Staras et al 2003). In addition,
there are ,nuny non_.hythmical
movement patterns, particularly in the human foetus
and young infant, ivhich have all the
characteristics of being endogenously generated,
i.e. wiitrouiany recognisable external
stimulus' Prechtl (1997a) suggested that in these
cases the generating neural mechanisms

should also be caled CpGs, because the relevant

motor patterns (e.g. general movements,
startles, stretches' yarvns) are also clearly constant
in form and, trererorel easily recognisable
every time they occur (see also revierv by Forssberg
r999). Their periodicar or episodical
rate of occurrence, as documented in many actograms
of foetal -otlty (de vries JIp et al
1985' 1988), pleads for central generation. Even
ii the theorerical possiultiry mighr exist thar
influences outside the foetus could play a role in generating
foetal movements, the striking
similarity of actograms of unstimulated low-risk preterm
infants at the same postmenstrual
age practically excludes such an explanation (prechtl
lgt|la).

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Directexperimentalevidenceforthecentraloriginofcomplerandco-ordinated
movementpatternscomes,ofcourse,onll,fromexperimentslvithdevelopinganimals,in
invitro' Not only do they
and spinal cord preparations are studied

rvhich isolated brainstem

various neurons of the cPG netrvork but
or lntracellula recordings from
extradirect
allo$.
and the use of receptor blockers' [n combination
the stuy of transmitters
permit
also
thev
of the neural
such an approach led to detailed knowledge
morphological
rvith
uslivitY' Most cPGs
""i"''
and provided an explanation of spontaneout

mechanism of

cp6s

consist,inpart,ofbrstaolen.u.on,lvhichgenerateself-sustainingoscillationsofmembrane
locomotor
structures. Isolated cPGs generate fictive

as pacemaker-like
ootentials and act
that the fundamental pattern
in the absence of movements), indicating
,rruttms (recorded
properties of these
on the intrinsic connectivity and electrical
of motor output depends

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alternating

is

.:^^-^itetion(BuchananandGrillnerlg8T)coupledlvithcrossedgl,vcinergic
excitator.v s)napses
Atford and williams 1989). Gluramatergic
rG^'*"

ctliL"t:igi:.1"t*"1',nrr,
inhtbttton \D uL

activateAlvlPAandNMDAreceptolsknolvntobenecessar-vforthemaintenanceofthe
and Alford 2002)' Intracellular Ca2+' acetylcholine'
lvell as
locomotor rh.vthm iiakahashi
L-DOPA' NMDA and AMPA receptors' as
monoarnine precursor
serotonin, the

Sadreyev
metabotropicglutamate....p,o,,playanimportantrole(RobertsandPerrinsl995,Spitzer
j
Fok and Stein 2002, Navarrete eta]-2002'
2007,Chen et al 2002,
antidromic
1995, Antri eta|
and
inhibition
Presynaptic
Alford 2002).
panchin 2002, f akaha]i,i un

and

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Gossard2003).Inratfoetuses,spontaneouslygeneratedactivit,vrecordedfromventlairoots
act as inhibitory
rs generated b'v gl1'cine and gABtlll:l-^"::t^t:itt
of lumbar segments
generating netlvorkfor hindlimb
et al 1996). In the neonaral rat, the
(Nishimart]
transmitters

4
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even
locomotionislocateointhefirstandsecondlttmbarsegments,lvhichdrivesthemotoneurons
(cazalets et a1.1995). This highl.v patterned locomotion
,.f-.nr,
lumbar
lorver
(Bracci et al 1996)'
of rhe
are pharmacologically blocked

dischargemayhaveanimportantroleinthecontrolofspontaneouslocomotion(Coteand

continues if ttre

inniuiirv

rransmifiers

the
Adifferentiaidistributionofphase-specificinterneuronsisinagreementlvithobservatlons
and extensor centres for lvalking in
distinct but overlapping flexor

that revealed

*uipunpo (Cheng

et al 2002)'

Alongthesameiinesaretheextensivestudiesontheisolatedbrainstem-spinalcord
preparationsoftheneonatalratforrecordingrespirator.v-likerh,,..thmgenelation(Suzue
pharmacological manipulations clarified
1995). Single unit recordingsnd
oni*uru
igg+,
The extent to rvhich genetic
f the"respirator- CPG in the medulla.
the compler n"rur.
cPG rvas sun'e1'ed b.v
respirator,v
for the production of the

,.rp"Jole
mechanisms ur.
Fortin (199"7)'
and
nurnoutnut

Therichmovementrepertoire:thecontinuityfromSrelltalto^postnatallife
lvith tactile
Earl.vstudiesonhumanfoetalmovementslverecarriedoutonexteriorisedfoetuses.The
during rvhich the foetus lvas stimulated
to a felv minutes
suwival rvas limrted

stimuli(lvfinkolvskl1928,Hooker1952).Thesestudiesremainedstrictlyinthetraditionof

a
J
{

a
4
{
{
*
{

d
*
)

-=
a

reflerorog) and behaviorism and it is not surprising that the endogenousry.generated

and
thus sponlaneous activity rvas totallv overlooked or lvrongly interpeted. To
be fair it should

it would hardly have been possible to see spontaneous

movements during
he short survil'al time' Today, lve knorv from non-invasive ultasound
observations that
hese earlier studies described rather abnormal movement pattems
of d;ing foetuses.
're mentioned that

\foreoler. the foetus responded to artificial tactile stimuli, never present

in the natural

,<iuation (Prechtl 1989b, 2001b).

In the 1980s the beakthrough in foetal movement studies came

from the introduction
of advanced ultrasound equipment. Prolonged and repeated direct
observations became
possible' Prechtl and co-lvorkers follolved 12 foetuses of carefully
selected lorv-risk
pregnancies in rveekly intervals fromT to 8 rveeks onlvards
until 20 weeks and than undl
rerm in three- to four-rveek inrervals (de vries JIp et ar r9gz, rgg1,

r9g5, r9g7, 19gg,

Prechtl 1989b' 1997b, 1999,2001b). Another nine foetuses were

followed from 2g rveeks
until term in four-lveek intervals (Roodenburg et al 1991). Continuous
one-hour recordings
lvee made and stored on videotape for off_line analysis.
The fist movement to occur is sidelvard bending of
the head. It is first seen af 7% fo
8 r'veeks postmenstrual age (counted from the first day of the
last menstruation befoe the
amenorrhoea). These first movements can clearly be seen
by transvaginal transducers (Fig.
2' 1) but are poorly detected by transabdominal ultrasound.
Time and movemenr pattern are
actually the same as in Hooker's (i952) observation after periorai
stimulation lvith a Frey,s
hair' Hooker's trigeminal stimulation elicited lateral bending
of the head as the fist foetal
movement due to the nervly formed connection of the
cervical motor neurons lvith neck

muscles.

At 9 to 10 lveeks postmenstrual age, complex and generalised

movements occur (de
vries JIP et al 1982, prechtr 19g9b). These are the so-calred general
movements (prechtl
et al 1979) and the startres. Both include the rvhole
body, buithe generar movemenm are
.3ig.i.z!,while
slorver and have a comprex sequence of invorved
a

body
quick, phasic movement of all limbs, trunk and
neck.

parts

the startle is

Fig' 2'1 video prints of first foetal movements observed

by transva-einal transducer: sidelvard bending
of the head at7%weeks postmenstrual age.

--]

Local and isolated movements of one arm or le-e emerge onh'

one lveek later (at 10 to 1 1 lveeks) than the generalised movements.

Itmal.besurmisedthatisolatedmovementsaremofedif|icu]t
to produce by the very .voung nervous svstem than global motor
is
activit.v. There rvas another unerpected finding. Traditionali,v, it
to
cranial
from
goes
accepted that tire eariv ontogenetic process
caudal. Although this lvas primariiy based on the sensory s,vstem
(Hooker 1952), the motor system does not follolv this rule' Isolated
arm and isolated leg movements emerge at the same time, at i0
rveeks. Holvever. it is true that isolated arm movements occur more

frequentl.v than isolated leg movements' and this might previousll

have been overlooked in short-lasting recordings (de Vries JiP

et al 1982, Prechtl 1989b,2001b).
Prechtl's obsewations led to changes of paradigms' In the traditional literature it rvas assumed that in ontogen,v jerk,v movements
precede slorv and tonic movements' This is not the case' Tonic
to l0
and phasic movements emerge at the same age' namely at.9

weekspostmenstrualage.Itmay-hal'ebeenthatthetraditionalll'
jerk-v- movements
short recordings overestimated the more frequent
lines, it is not
same
and thus led to the lvrong conclusion. Along the

truethatearlymovementsarerandomandamorphicfollorvedonll.

laterbyspecificanddistinctmovements.Infact.allearl,vandlater
foetal movement patterns are differentiated, right from their very
first appearance onrvards (Prechtl 1989b, 2001b)'
Table 2.1 illustrates the foetal repertoire from 10 rveeks postmenstrual age onrvards. A striking phenomenon in foetal motor
Both
development is the early emer,gence of stretches and larvns'
is
their
are complex movements and the most interesting aspect

their form
maintenance throughout the lvhole life lvithout changing
and pattern (Prechtl 1989b).
A very important aspect of foetal movements is the change
and ma'v
of foetal position in rttero. Positional changes are frequent
(de
JiP
Vries
pregnancy
of
end
run up to 25 changes per hour at the

et al i985). Trunk rotations, general movements and alternating

the feet
leg movements, leading to a somersault if proper contact of
intracan be made lvith the uterine lvall, all produce changes in the
an
ontogenetic
obviousl-v-.
are
patterns
motor
These
uterine position.

adaptationandhaveaneffectivefunctionduringprenatallife.The
and
alternating leg movements outlive the duration of pregnancy
areknorvnafterbirthasthenelvbornstepping(Prechtl200ib).
Fig.2.2 Videoprintof afoetus (1-lweeks postmenstrual
movemenls.

age) during general

3
F

l
L

TABLE 2.I

Foetal motor repertoire (Birnholz 1981, Bots et al 19g1, de Vries

JIP et al 1982, Prechtl 1989b). Age is given in postmenstrual weeks

i
I g rreeks

l-...iare d arm ms

I-.claed leg ms

Hiccup

12 rveeks

14 weeks

20 weeks

Starde

Startle

Startle

Glvls
Isolated arm ms
Isolated leg ms
Hiccup
Breathing ms
Hand-face contact
Head retroflexion
Head anteflexion
Head rotation
Stretch
Yalvn

GMs

UlVIS

Isolated arm ms
Isolated leg ms

Isolated arm ms
Isolated leg ms

Hiccup

Hiccup

Breathing ms
Hand-face contact
Head retroflexion
Head anteflexion
Head rotation
Stretch

Breathing ms
Hand-face contact
Head retroflexion
Head anteflexion
Head rotation
Stretch

Yalvn

Yawn

Sucking and swallowing

Sucking and swallowing

Eye ms

Breathing movements and eye movements, as lvell as the sucking and slvallowing movements, are anticipating later functions, only becoming effective during postnatal life, and
are evidence for the primacy of the motor system. The latter already have a significant intrauterine function of regulating the amounr of amniotic fluid (prechtl 19g9b, 2001b).
There are hardly any changes in the form and pattem of the movements in the first
!veeks after birth, despite the profound changes in the environmental conditions. postnatally,
some ofthe endogenously generated motor patterns gradually come under sensory control.

Rooting is an outstanding example. In the foetus

it is a rhythmical side-to-side head

movement and later it becomes directed to\,vards the stimulated peri-oral area (prechtl 1958).
While the foetus drinks amniotic fluid rvhenever sucking movements occur, after birth
sucking behaviour needs to be triggered in the actual feeding situation. Hence, it is a matter
of vital biological adaptation that rooting and sucking are elicited in the proper nursing
situation initiated by the caregiver. Other examples are postnatal breathing movements and
smiling movements (Prechtl 2001b).
Nerv in the motor repertoire after birth are functions depending on the nervly installed
lung ventilation. Reflexes for protection of the airrvay such as sneezing and coughing,
as lvell as the communication signal of crying, are only seen after birth (Prechtl 2001b).
Prenatally it rvas not possible to elicit any vestibular responses in the foetus, lvhen the
mother had been adequately moved by the experimenter and the foetus simultaneously
observedbyultrasound(Prechtl 1997b).Horvever,afterbirth,vestibularresponsessuchas
vestibular-ocular response (von Bernuth and Prechtl 1969, cioni et al l9g4) and the Moro
response are clearly present.
By and large, there is an amazing continuation of the prenatal repertoire during the
first trvo months postterm age (Prechtl 1984b, Cioni et al 1989, Hadders-Algra and Prechtl
1992). Needless to say, in the healthy preterm infant this continuarion lasrs until the same

many
postmenstrualageasintheinfantbornatterm,i.e.thecorrectedageforpretermbirth
life a major transformation of

prechtl 1gg0). At around the third month of

meet
iCioni and
makes the infant more fit to
o"'urs (Prechtl 1984a)' This
motor and sensory pun"'n'

ii.

environment'
..qulr.*"nts of the extra-uterine

Hlfl| .;:11Tff:il:JJlTL|n",,non,une

the s o- ca'e d gene rar

ous mov ement patte rns

movements(GMs)arethemostfrequentlyoccuningandmostcomPlexPattern.Theyare
he failed to describe these
'mass *ou"-!n"' but
(1932)called
lrrvin
rvhat
probably
for this specific pattern lvas
t"t''general.movements'
movements -o'" n'""t'lirli*
motility in carefully
ir u".bseriational study on spontaneous
coined by hechtl et al til
emergence of the
the
on

studies
infants. The subsequent fetal
selected lorv-risk preterm
GMs at 9 lveeks postmenstrual
of
onset
an
reveale
different prenatal
whole prenatal period
to u" pr"r.nt auring the
i"ontinue
al
et
Jtp
Vries
(de
age
5 to 6 months
p'"tt'tr isssu' nooa"nlu'g et al 1991) until about
rxS'
al
et
JIP
(de Vries

*.";;;;erns
i;;;;.

* "Eiil1t;:T""J[T ;l:iJ"r'Ji ?'t? v ari able que nc e of arm,. g, ne ck and trunk

gradual
speed, and they have a
rvane in intensity, i"*" ""0
movements. They lva,x and
in the direction
along the a'ris ot ttre timut f 1:Tllinges
beginning and end. R";;;;'
se

ofmovementsmakethemfluentandelegantandcreatetheimpressionofcomplexityand
variability(Prechtl 1990)'
/-1\,{c at
orterrraseanduntilabout.to
term age
GMs'
foetal or preterm
While before t""n o call them

grveekspostterm"r",'**^*calledrvrithing*ou"*"no(T:pOit:andPrechtl1984)'
and large a similar appearance
ti**nces exist, GiIs have by
rveeks
Even if age-related i*,
pot t"rm (Fig' 2'3)' At 6 to 9
end of th. s""orr -orr,t
from early foetal lif-e until the
lntentional
and
AntigravitY

Movements

P6hlenstrual Age (w*i<s)

5 10 15 2A 25 30 35 *k
Fig.2.3 Developmental

course of general movements'

10

s 10 15 20 25
Age
PGtsm

30

tweeKsi

posrterrn age, GMs with a writhing character gradually disappear while fidgety GMs
graduailv emerge (Hopkins and Prechtl 1984, Prechtl etal 1997a). Fidgety movements are
pesent up to the end of the first half-year of life when intentional and antigraviry movemen6
e-ccur and start to dominate (Fig. 2.3).
PR,FIER\I GMS
\.. dilference can be observed betlveen foetal and preterm GMs, indicating that neither the
j ncrease of the force of gravity after birth
nor maturation has an influence on the appearance
of Glvls. The GMs of a preterm infant may occasionally have large amplitudes and ae
ofren of fast speed (Cioni and Prechtl 1990; see Fig.2.4 and Cases A and B on rhe DVD).

;l'q

:::

*s

GMs are commonly referred to as lvrithing movements

(Hopkins and Prechtl 1984, Prechtl and Hopkins 19g6,
Cioni et al 1989, Cioni and Prechtl 1990, prechtl et al
I997a). They are characterised by small to moderate
amplitude and by slorv to moderate speed. Typically,
thez are ellipsoid in form, rvhich creates the impression
!

ryq

,.:*

Fig. 2.4

WRrrmNG MovltgNts
At term age and during the first two months posttem,

of a writhing quality

(see Fig. 2.5 and, Case C on the

DVD).

* -t"g,i

Three-second sequence

(36:02 to 36:04) of GMs with large

amplitude in a preterm infant, aged
34 weeks (Case B on the DVD).

Fig.2.5 Fullterm neonate with rvrithing movements (Case C on

the DVD).

ll

WIITH{NG

PRETERM GM

GM

33 wk

-tl..+<l'"l#}-

-*-{9|-_-.+'r*

.i.

F]DGETY GM
53 wk

'

----t|**{+_.-LNF

ts*-*{t

RNE

i**Mff{tiltaiF

I2oo iv

(left); writhing GMs at 1 week

Fig,2.7 EMG pattem of normal GMs in a 33-rveek-old preteffn infant
age (right) (reproduced rvith
postterm
rveeks
at
13
movements
fidgety
(middle);
and
olin".r ug"
permission from Hadders-Algra et al 199f).

L=left,R=right,p\4=pectoralismajor,DE=deltoidmuscle,BB=bicepsbrachii'TB=tricepsbrachii,FC=flexor
TE = thoracic extensor
carpi, EC = extensor carpi, NF = neck flexor, RA = rectus abdominis'

The main kinematic aspects of the transformation from lvrithing to fidgety movements
ef al (2002) have studied the
can also be seen by means of 3-D-motion analysis' Coluccini
a group of healthy fullterm
in
GMs
of
amplitude
distribution of movement veiocity and
of movement velocity and
decrease
clear
A
infants recorded from 7 to 12 lveeks of age.
amplitude lvas observed (Fig. 2.8).
occur
The temporal organisation of fidgety movements varies lvith age. Initially, they
in
increase
gradually
isolated events (score: + or +/-, Fig. 2.8, middle graph); they
as

(score: + or +/-)
frequency (score: ++, Fig. 2.8 bottom graph) and then decrease once again
(Prechtl etal 1997a,lgg7b).This temporal organisation can be defined as follorvs (Dibiasi
and Einspieler 2002).

Continual fidgery nxovements (score: ++)

fidgety
Fidgety movements occur flequently but are interspersed lvith short pauses' As
particularly
body,
lvhole
the
movements are by definition GMs, the movements involve
body posture,
the neck, trunk, shouldefs, lvrists, hips and ankles. Depending on the actual
in
in particular the position of the head, fidgety movements may be expressed differently
the different bodY Parts.

[ntermittent idgety movements (score : + )

Although fidgery movements occur regularly in all body parts, the temporal organisation
are
differs from fidgety movements ++. In fact, the pauses between fidgety movements
of
the
half
for
only
prolonged, giving the impression that fidgety movements are present
observation time.
13

PRETERM GM
33 wk

RNF
LNF

FIOGETY GM
53 wk

WRITHING GM
41 wk

---ffi----1--+--*tr
***_*.rirr -{.+-+

RE
R P"{

ri

t*$*ih

f*1fafs+dl34"

I2oo pv

Fig.2.7 EMG pattem of normal GMs in a 33-week-old preterm infant (left); writhing GMs at 1 week
postterm age (middle); and fidgety movements at 13 weeks postterm age (right) (reproduced rvith
permission from Hadders-Algra etal 1997).
l=left,R=right,PM=pectoralismajor,DE=deltoidmuscle,BB=bicepsbrachii,TB=tricepsbrachii,FC=flexor
carpi, EC = extensor carpi, NF = neck flexor, RA = rectus abdominis, TE = thoracic extensor

The main kinematic aspects of the transformation from lvrithing to fidgety movements
can also be seen by means of 3-D-motion analysis. Coluccini ef al (2002) have studied the
distribution of movement velocity and amplitude of GMs in a group of healthy fullterm
infants recorded from 7 lo 12 lveeks of age. A clear decrease of movement velocity and
amplitude rvas observed (Fig. 2.8).
The temporal organisation of fidgety movements varies lvith age. Initially, they occur
as isolated events (score: + or +/-, Fig. 2.8, middle graph); they gradually increase in
frequency (score: ++, Fig. 2.8 bottom graph) and then decrease once again (score: + or +/-)
(Prechtl etal1997a,l997b).Thistemporalorganisationcanbedefinedasfollolvs(Dibiasi
and Einspieler 2002).

Contirutal fidgety movements ( score : + + )

Fidgety movements occur frequently but are interspersed lvith short pauses. As fidgety
movements are by definition GMs, the movements involve the whole body, particularly
the neck, trunk, shoulders, wrists, hips and ankles. Depending on the actual body posture,
in particular the position of the head, fidgety movements may be expressed differently in
the different body parts.
Intermittent fidgety movements (score: + )
Although fidgery movements occur regularly in all body parts, the temporal organisation
differs from fidgety movements ++. In fact, the pauses betlveen fidgety movements are
prolonged, giving the impression that fidgery movements are present for only half of the
observation time.
13

god ss

:j$
E&trr2!*
:

{:

r\:

ru*rrunL,*"tLlo
::dl

:a[

Sr

r:'S

were applied
R"n"tiu'
joz, stt
Fie.2.S3.DmotionanalysisofGMsinanormal.infantrecordedatT,l0and12weeksposttermageDy
iTu;"
Kinematic data
pubis'
and
mJans of an opto-etecrro",.'rriJr'iiiie
stemum
ur,tt" ,f,ooto''
li
at the level of dorsal .,rO"""
""Ji*1,

;;li"f

ii;i
""'"i"J;;icfg ::i:{T,';:',$rc.$'1f,il";;il"i::i$"T:l:
,Jpo*ng.l. u.':?Y^i1'i:lT#i""'.[ifJ.f,:fi,i;;;;;,ver distar'*.*"n-o, rrom rvrithing

have been synchronised

du,ing u 3o-."cond

-'i'i "i"n

period.or,T:^11'j:::;":j:ilffiHliiir""*ii"

:*iif';y,.ll:"'*'.1]"'::::Tfiiill'""J,?'"ffie*pir

l0weeks(middl"eupl) uld
'z*eeksoccasionarhighverocitv

movements re suPerimPosed'

t:##r:#;"?,T;:K:;t:if"#J"o*"vemenrs+butinterspersedrvithevenronger
pauses.

wrists and
Fidgetymovementsareusuallyequallypresentinthedistal(D)andproximal(P)bodypans
*tin *"t" nag"ty activity in the

i"tu*'
tn"" u'"
'ot"
""'"t"tr,
anklesthaninetrunkandproximaljoints.ThesefidgetymovementsarescoredD>P,If
and hips' lve score this
in tir" n"ct, uu".rn, trtourers
p."*rn"nt
fidgety movements "r. -"..
optimal neurological
trre jr"oi"tion of a less

(score: D = P).

p > D. This differentiati'on

*"r"fl:::T_::1il:-t"tl

,"'"-,

,*"n$

."l"uurr, ror

fidgetv
mav occur rogether rvith
various orher movements

l4

movements, such as lviggling-oscillating and saccadic arm movements, slvipes, mutual

manipulation of fin-sers, manipulation (fiddling) of clothing, reaching and touching, legs lift
ith or rvithout hand-knee contact, trunk rotation, and axial rolling (Fig. 2.9 and Table
2.2). Fidgery movements are superimposed on other movements, or other movements may
occur during the pauses betrveen fidgety movements, or both.

General movements are most probably generated supraspinally

To our knowledge, no studies exist, not even in animal experiments, which address the
seneration of startles or GMs. As both movement rypes include activity of all segments
from cervical to lumbar spinal cord, it is likely that the generating neuronal structure is

Ntovement patterns, which may

r""".,r$tn1l"*li'our"O -rvements (Hopkins

and prechtt

1984, Cioni and PrechU l990, Hadders-Algra and Prechtl L992, Einspieler 1994, Prechtt 2001b)

Nfovement pattern

Definition

Period of occurrence

Wiggling-oscillating

Irregular, oscillatory, waving-like movements ; most

noticeable in partially or fully extended arms, where they
have a frequency of 2 fo 3 Hz; small amplitude and
moderate speed; should be clearly distinguished from
tremulous movements, which are less smooth in appearance
and have a more regular rhythm

6 to 14 weeks postterm

arm movements

age

Saccadic arm
movements

Jerky, zigzag movements, which continually vary in

direction; most noticeable in partially or fully extended
arms; moderate to large amplitude and moderate speed

Swiping movements

Movements with a sudden but fluid onset and smooth offset

lvith a ballisticlike appearance; can go in dolvnward or
upward direction; most noticeable in extended arms, but
also in partially or fully extended legs; large amplitude
and high speed

6 to 20 weeks postterm

Mutual manipulation
of fingers

Both hands are brought togeher in the midline and the

fingers of both hands repetitively touch, stroke or grasp
each other

From 12 lveeks

Manipulation
(fiddling) of clothing

The fingers of one or both hands repetitively touch, stroke

or grasp some object or the clothing

From

Reaching and
touching

One or both arms extend to some object in the immediate

environment. The fingers contact the surface of the object

Legs

lift

Both legs lift vertically upward; partial or full extension at

the knees; hips are slightly tilted uprvard: one or both hands
touching or grasping the knees; sometimes with anteflexion

6 to 15 weeks postterm
age

age

postterm age onwards

12 weeks

postterm age onrvards

From 12 weeks
postterm age onwards

From 15 weeks
postterm age onlvards

of the head
Trunk rotation

As a result of the soles of the feet pushing down on the

lying surface, one side of the hips is lifted and rotated

From 12 weeks

Axial rolling

The whole body is tumed from supine to prone lying in

a movement started by the head. Sometimes the infant
retums to prone lying

From

15

postterm age onlvards

18 weeks

postterm age onlvards

*;ff" .. ."it

Fig.2.gFourteen-week-oldinfantlvithfidgetymovements,mutualhandcontactwithfiddling.and
mutual feet contact.

at 9
movements emerge in the human foetus
located supraspinally (Prechtl 1997a)' Both

tol0weekspostmenstrualage,whichmakesitunlikelythathigherStructulesthanthe
of
that GMs of writhing quality and those
brainstem are involved. It can-also be assumed
Their temporal overlap at the transformation
fidgety quality u." g"n",*d by different CPGs'

fromtheonetypeintotheothermakesthismostplausible(Prechtl|997a),Thatwrithing
ai6 months is indicative of the prolonged
movements do not disappear during sleep even
preservationoftheirCPGduringthefidgetymovementperiodandthereafter(Einspieler

etal

1994).

Alternatinglegmovementsinfoetuses,lvhichareinvolvedinthefrequentchanges

oftheintra-uterineposition,haveaCPGlvithlolvspinallocalisation.Theresearchon
lumbar spinal

lvhich only the lolv thoracic and

anencephalic foetuses included one case in
lacking
1985). The more cranial structures lvere
cord was normally organised (visser et al

orseverelyabnormal.Thisfoetusgeneratedexcessivealternatinglegmovements'nevel
have existed
rhythmical activity must, therefore'
seen in an intact foetus. The CpG of this
in this limited spinal structure (Prechtl 1997a)'

if the nervous system is impaired

General moYements change their quality
by more cranial structures (e'g' cortico-spinal'
The quality of GMs is proUlUty modulated
impairments of these structures. A disruption
reticulo_spinal) and hence can te affected by
lesions of the corona radiata or intelnal
of the cortico-spinal projections by periventricular

lesions (leukomalacia) leads to abnormal

capsule due to haemonhges or hyporic-ischaemic
scan data the sensori-motor corfex
pET
fositronl-ission tomography)
GMs. According to

isalreadyactivein.i,"n"onu,"(ChuganiandPhelpslg36,Chuganietall98T).onthe
t6

---t

other hand' behavioural evidence for functional activity ofthese

cortical areas in the form
movements and differentiated isolated finger movements
i, ru.Hng ur,ii, ug;.
'oluntary
This is el'en more evident at preterm age. Despite these facts rve
must consia., u,oaunti'n-n
influence of these coftico_spinal connections on the GM_CpGs (prechtl
1997a).Cortico_
spinal fibres lvere found in the human foetus at the cervical se-sments
as early as l6 rveeks
posrmenstrual age (okado and Kojima 19g4). Their synaptic
input on lorver segments can
be espected at preterm and term age.
If the nervous system is impaired, GMs lose their complex and
variable character and
have a poor repertoire, or are cramped-synchronised or
chaotic. This holds true for the
preterm, term and early postterm age (first tlvo months).
Fidgety movements can be either
abnormal or absent.
of

:-

Poon RrpenrorRE GMs

This abnormal GM pattern occurs during preterm, term

and earry postterm age. The

sequence of the successive movement components

is monotonous ano movements of
the different body parts do not occur in the comprex
lvay seen in normar GMs (Ferrari
et al 1990, Einspieler et at 1997; Cases G and
H on the DVD). poor repertoire GMs are
frequent in infants with brain ultrasound abnormalities
and can be followed by normal,
abnormal or absent fidgety movement. Hence, the predictive
value is rather lolv (prechtl

etal 1997b).

Cnelrpen-Sv r.icsRomseo GMs

This is an abnormar pattern from preterm age
onlvards. Movements appear ngid and lack
the normal smooth and fluent character;
all limb and trunk muscles cont;t and relar
almost

simultaneously(Ferrarietar 1990,Einspieleretarr997;CasesJandKontheDVD).

Ifrhis
abnormal pattern is observed consistently over
a number of lveeks it is of high predictive

valueforthedevelopmentofspasticcerebralpalsy(Fenarietallgg0,prechtl
Ferrari et al 2002: see also Chapter 5).

Crnouc

GMs

etarl997b,

Movements of all limbs are of large amplitude

and occur in a chaotic order lvithout any
fluency or smoothness. They consistently
appear to be abrupt (Bos et ar rggTb,Einspieler
etal 1997, Ferrari etal 1997; case L on ttre
ovo;. Chaotic GMs can be observed during
preterm' term and early postterm age
but are rather rae. Infants with chaotic GMs
often
develop cramped-synchronised GMs a felv
weeks later.
ABNOR_N,LA.L

Frocery Moveuei.-rs

These look like normal fidgety movements

but thei amplitude, sped and jerkiness are
moderately or greatly exaggerated (Prechtl
et at |99zb;Case M on the DVD). Abnormal

fidgety movements are rare. Their predictive

value is low (prech tr et ar r9g7b; see aiso
Chapter
5).

17

;;____-----.-

other hand' behavioural evidence for functional activity

of these corticar areas in the
form
of voluntary movements and differentiated isolated finger
movements is lacking at this
age.
This is even more evident at preterm age. Despite these
facts lve must consider a modulating
of
these
influence
cortico_spinal connections on

the GM_CpGs (prechti 1997a).Cortico_

spinal fibres were found in the human foetus at the cervical
segments as early as 16 lveeks
postmenstrual age (okado and Kojima r9g4).
Their synaptic ilput on tcr*"r segments
can
be expected at preterm and term age.
If the nervous system is impaired, GMs lose their
complex and variable character and
have a poor repertoire, or are cramped-synchronised
or chaotic. This holds true for the
pretefm, term and early postterm age (first
two months). Fidgety movements can
be either
abnormal or absent.

Poon RrpRron GMs

This abnormal GM pattern occurs during preterm,
term and early posrterm age. The
sequence of the successive movement
components is monotonous uno
movements of
the different body parts do not occur in
the complex rvay seen in normar
GMs (Ferrari
et al lgg0' Einspierer et ar rggT; cases
G and H on tne vn;. eoo. ,.p"*oire
GMs are
frequent in infants r,vith brain ultrasound
abnormalities and can be folrowed
by
normal,
abnormal or absent fidgety movement.
Hence, the predictive value is rather
(prechtl
lolv
etal 1997b).

Cnevps-SyivcnnoNrsso GMs
This is an abnormal pattern from preterm
age onrvards. Movements appear
ngid and lack
the normal smooth and fluent character;
all limb and trunk muscles contract and
relax almost
simultaneously(Ferrarietal

l990,Einspieleretal1997;CasesJandKontheDVD).

If this
abnormal pattern is observed consisten;ly
over a number of lveeks it is of high
predictive
value for the development of spastic
cerebral palsy (Fenari et al l99,prechtl
et al r997b,
Ferrari et aL2002; see also Chapter
5).

Cueouc

GMs

Movements of alr limbs-are of large

amplitude and occur in a chaotic order
without any
fluency or smoothnesr.
consistentti appear to be abrupt (Bos et
ar
rggTb,Einspieler
T^"I
etal.1997, Ferrari etar 1997; Case
L on rh; bvD). chaotic GMs can be observed
during
pretenn' term and early postterm
age but are rather rare. Infants lvith
chaotrc
GMs
often
develop cramped-synchronised
GMs a felv rveeks later.
ANoR,r.q_

Frocnry Movguei.-rs

These look rike normal fidgety

movements but their ampritude, sped
and jerkiness are
moderately or greatly exaggerared (prechrr
et ar !g97b;case M on the DVD).
Abnormal
fidgety movements are rare. Their predictive
varue is low (prech tr et ar r997b;
see arso

Chapter 5).

l7

Aeselice or FtcgrY MovEMEI'rus

Iffidgetymovementsut"n"n"'observedfromgto20lveeksposttermwecallthisabnorcan'
on e DVD)' Other movements
(Cases N and O
mality 'absence of fidgety movements'
of fidgety movements
(prechtl et al 1997b). The absence
be commonly oir"ru"

horvever,

ishighlypredictiveforlaterneurologicalimpairments'particularlyforcerebralpalsy'
also
forms (Einspieler et a|2002; see
1gg7b) and dyskinetic
both the spastic (prechtl er al

Chapter5).Ifthecramped-synchronisedcharacterisstillpresentat3to4months(oreven
DVD)'
absent (Case O on the
longer), fidgety movements are

t8

3
_-3'''V TO I?ECORD

Ai\D ASSESS
3=I\=RAt MOVEMFI\IS

The simplest lvay of assessing motor activitlt is by directly observing the movements tvih
the unaided eye. Horvever, considerable improvement in the reliabilify of the assessment
is achieved if the infant's GMs are observed by replaying avideo recording. There is the
advanta-ge of repeated playback,

including at different speeds, and of storing the recordings

for documentation and future reference.

Recording technique
In order to provide a reliable assessment of GMs the recording procedure has to be standardised and certain behavioural states, such as crying, are not suitable for an assessment.

Eeutpnerr
The video camera should be placed high
above the infant (Fig. 3. l). In order to keep
the older infant's attention to the camera
to a minimum a small camera is preferable.
A single-chip camera does not even have
a blinking light during recording. In our
experience, it is not necessary to use a
camera hidden above a purpose-built bed
surrounded by rvhite curtains, as mentioned

by Geerdink and Hopkins (1993a), as the

infant quickly habituates to the camera.
Very attractive objects may interfere lvith
the temporal organisation of fidgety move-

ments. but this will not last more than 20

to 30 seconds (Dibiasi and Einspieler 2002,

4). Digital cameras are preferable. For the selection of GMs from the
recording and the subsequent analysis, a
time code signal superimposed on the tape
is helpful.
Watching a monitor outside the observation room is a useful rvay of observing
the infant lvithout causins interference. In
see Chapter

Fig. 3,1 Video recording of a preterm infant in

the incubator; the camera is placed high above the
infant on a tripod.

t9

/ .-- _

thisway,parentscanbeaskedtosoothetheilbabyifitstartsclyingbecausethenthe
recording must be intenupted an)'lva)"
PROCEDURE

DependingonitsagetheinfantshouldlieinaSupinepositionintheincubator,bedorona
mattressonthefloor'Recordinginfantslyingonatableorbaby-dressingtableshouldbe
presence lvill not only attract the infant,s
avoided for the infant,s safery. The caregiver'S
able
Gestalt percepon. The observer must be
attention but also interfere rvi the observer's
is
movements are not due to crying' This
to see the infant's face to make sule that rigid
especiallyimportantaSthelaterassessmentisdonelvithoutacousticsignals.
In very young preterm infants we usually
A small and non-restrictive nappy is advisable.
the postterm
resiriction of leg movements (Fig' 3'2)' During
open the nappy in order to avoid

periodinfantsshouldbedressedlightlyandcomfortably,leavingarmsandlegsbare
and clothing'
fittingthe infant's age

(Fig. 3.3). The room temperature shoulld be comfortable,

too high it lvill affectthe infant's behavioural
If the ambient temperatue is either too lorv or
state and the movement qualitY'

quality is the correct behavioural state

Most important for ihe u"""tn"n' of GM
(Einspielereta||99.7).Holvever'behaviouralstatesarenotestablishedbeforeabout36

lveekspostmenstrualage(Nijhuisetal1982)Ininfantsolderthan36lveeksrecordings
is characterised

4 (Einspieler et al 1997), which

should preferabty u" p"lo.*ea a,rring state
wake.
movements' and absent crying (active
by open eyes, irregular respiration, present

fulness;Prechtl1974).Youngerpreterminfantsshouldberecordedlvhenboutsofactiviry

$q"
',

,q

9;.

,\

:-R

b'

b'l
":S-

i-i$=.

-i

', .;,i - -;

*Y

Fig. 3.2 For the GM assessment the preterm

closed
inant's nappy is partly opened and only
above the bellY.

Fig. 3.3 During the postterm period

the- infant

leaving
shEuld be dressed lightly and comfortably'
arms and legs bare.

20

occur, irrespecrive ofrvhether the infant is arva\e-or sleeping (Einspierer

er ar 1gg7). The
same holds true for infants older than 36 weeks with severe u.in

l.riin u, their behavioural

mav be profoundly disorganised (prechtl 1974).
The duration of the recording depends on the age of the infant.
In order to collect about
three GMs for a reliable assessment lve usually record preterm infants
for 30 to 60 minutes.
This does not require the observer's presence during the recording nor the
later assessment
of the lvhole recording. Preferably, the recording should be started by the
staff of the neonatal
unit, provided it does not interfere rvith nursing. such a long recording
srares

ensures sufficient
activiry bouts on tape. Later, this recording is vielved at fast speed und
ubou, thee GM
sequences are copied onto the assessment tape.

From the rvrithing movement period onlvards, five to ten minutes

of optimal recording
sufficient. It is helpful if the sequential recordings of the infant,
taken at different
ages, are stored on a separate assessment tape for the documentation
of the individual
developmental course.
is usually

WHAT SHour-o ee AvorEo?

As GMs are dependent on the behaviourar state (prechtl 1990, Hadders-Algra
et ar 1993,
Einspieler et al 1994,1997),the movements change during fussing,
crying and drowsiness.
Therefore' the recording should not be continued during prolongedepisodes
offussing
and crying or during drorvsiness. Nor is it possible to judge the quality
or cu, properly if
the infant is sucking on a dummy. soothing the infant rvith a
dummy results in the sucking
posture (Prechtl and Lenard l96g) lvith flexed arms,
fisting, and extended legs (Fig. 3.4).
In cases of prolonged fussing and crying the recording must
be stopped. only restart
th-e recording after the infant has been soothed.
This may take some tlme. tt may even be

necessary to repeat the recording session on another day.

Holvever, it should be mentioned

Wsq$$,

Fig. 3.4 Sucking on

a dummy
results in the sucking posture.
GM assessment is no longer

&

possible.

21

cry after they start moving' e'g'

that infants lvith severe brain dysfunction may frequently
infants lvith cramped-synchronised GMs'
They interfere with the GMs
Prolonged episodes of hiccuping should not be assessed'
as rvell as rvith the observer's Gesralt perception'
presence of toys in the immediate
Interference by an observer (pareni, examiner) and the
movements are quite stable
vicinity should be avoided. Although lve knolv that spontaneous
(Dibiasi and Einspielet 2002; see also
and robust and hardly interfered with by stimulation
be destroyed by too many distracting
might
Chapter 4), the observer,s Gestalt perception

objectsorpersons(Fig.3'5).Thesameappliesforamattresscoveredbyacolourful
patterned blanket (Fig. 3.6).

Wecertainlyadviseagainstputtingtheinfantinfrontofamirror'whichisSometimes

image, acting as a 'tlvin" destroys the

used in recording or treatment rooms. The minor
are attracted by their 'trvin" touching
observer's Gestalt perception. In addition, older infants
the minor and smiling tolvards it.
three days after birth. During
Finally, lve advise against recording GMs during the first

to fluctuate more than they do later'

these early days, many ihysiological variables tend
changing rapidly from quiet sleep
There is also an initiat lnsUility of rcnavioural states,

tocrying'lvhichcaninterferewithaproperobservationofGMs.Itisthereforeadvisabie
indicated'
to avoidthis period of instability if not otherwise
movement analysis
Visual Gestalt perception as a scientific tool for general

of complex phenomena' In his

Gestalt perception is a polverful instrument in the analysis
the Nobel prize laureate
.estait
knor,vledge'
pe.."ption as a soufce of scientific
paper
into account a greater
take
to
is able
Konrad Lorenzpointed out that'Gestalt perception
than in any rational
these
betlveen
number of individual details and more relationships
is used lvhenever dynamic or static
calculation' (Lorenz 1971). visual Gestalt perception
is employed in this procedure'
images are globally assessed. Patlern recognition
old-fashioned direct observaprocedures,
In a time of ever more technical diagnostic
method' As soon as a machine
as
a
subjective
tion is lost or is, at least, treated lvith disrespect
as 'objective" It tends to
considered
is
is betlveen the patient and the examiner, the method

beforgottenthatvisualanalysisofanX-raypicture'anEEGrecording'MRIpictures'etc''

more objective than straightforrvard

is also based on visual C"sit perception and is no
recordings of movement patterns
observation lvith the unaided eye, analysing video
(Accardo 1997, Prechtl 2001a).

TheaverageinterscoreragleementofthequalitativeassessmentofGMsinanumber
pef cent (Einspieler et al 1997 '
of studies on several hundred infants lvas more than 90
agreement are provided in
interscorer
valentin, personai communication). Details on
chapter 5'
of GMs' the first step is
In applying the visual Gestalt perceptlon to the assessment

todifferentiatebetlveennormalGMsandabnormalGMs.IfGMsareconsideredtobe

are classified as: poor repertoire GMs'

abnormal the dift'erent age-specific sub-categories
fidgety movements' absence of fidgety
chaotic GMs, crampeo-sinchronlsed GMs' abnormal
movements (for definitions, see Chapter 2)'

22

i.::.{

Fig.3.5 Video print ofa 2-week_old infan:

too many toys might interfere lvith the
observer's Gestalt perception during GM
assessment.

Video print of a 7-rveek_old infanr: a colourful

IiS. -3.0
blanket might impair the visual Gestalt p"r""ption
unJ
makes GM assessment difficult.

During the video analysis of the GM quality,

environmental interference must

be
avoided. This includes doing the urr.rr-"nt without
acoustic signars. In addition, other
caregivers, siblings or twins, mirror images of the
infant, a bed crowded with toys (Fig. 3.5),
or an irritating coloured blanket (Fig. 3.6) on the
video all impair the observer,s Gestalt

perception.

As tiredness interferes r.vith the visual Gestalt perception,

the observer should never
for longer periods than about 45 minutes without
taking a break.
If many recordings of abnormal GMs are seen in a
series it is advisable to lvatch a
criterion standard normal recording from time
to time. This is necessary for re-calibrating
the Gestalt perception. The erampres on the
enclosed DVD should be at hand for this
assess

purpose.

Individual

developmentar trajectories based on longitudinar

recordings
The results of most follow-up studies provide
only a statistical chance that an individual
lvill eventually develop a particular impairment,
relative to a lolv-risk reference group.
A somervhat different approach seemed advisable (prechtl
1990). when the quality of
GMs is repeatedly assessed during the preterm,
term and postterm period until about 20
rveeks' an individual developmental
trajectory can be obtained inditing the consistency
or inconsistency of normal or abnormal
ndinjs (Prechtl 1gg0). Individuals with similar
trajectories can be,erouped,-which
improves thelpecific prediction of e individual
outcome.
A snapshot assessment of a single recording
must be avoided. An individual developmental
trajectory should document the following
GM assessments:
trvo to three recordings of the preterm period
(three GM sequences each)
one recording at term or early postterm
age or both

E
=
.E

o
(!

>!
v.E

oo

.E

a
C)

o\e

o;
.-:t
@q
>E
v=

6
q)
c)

(t

o(

ru

99

o
E

2
.P
tr
o-

o
o

(,

s,6

.=F

x;

o
o

'E*
vo
oa

o
(,
o

6
a

>t
va

o
o

.q|!
\a
>=

=6

=E
>y

o
(,

7,

.UA

Ep

co
>:

Ee

=o
L

Yt
,=E
-1<
=!

#s=

o=

=
=
.Y

SY>

Y'- 5
=Y5
3t t

-,^

z=

i P *

6X:
z7l
E=tr
!i:>
0o
:tg)
Z O,=

:r
!l

at least one recording betlveen g and 15

weeks posttem. If
an absence of fidgety
movements is found the infant should
be recorded a second
t*ou.ing
the fidgety
motement period, e.g. at 12 and i5 lveeks
postterm age

Fry. 3.7 provides the proforma of the individual

deveropmental trajectory.
The design of
this proforma is elated to the findings on
the predictive value of
GM
Chapter 5). The more often and the eariier the
individuar
fom the bo*om rine the higher is the probability
for the d.";i;-;; of neurorogicar
deficits. In addition, the individuar deveropmentar
trajectory d"";;;;; dereriorarion
improvement of GMs at particular ages.
or

a.u.top*"ntliil:H:I;I,::::

age'specific

Tlvo
motor optimality scores for semi-quantitatiye
assessment
After the global judgement, it can be worthrvhile
to look at differen, urp""-
uno components
of GMs, particurarly if they are abnormal.
A semi-quantification
1,
quarity can be
achieved by applying prechtl's optimality
"iri"
concept (prechtl 1gg0).
For
every movemenr
criterion such as amplitude, speed,
movem.n,

orrset or GMs, a score ror.optimar

or
the total optimaliry score the befter

"hu,
oon-o0.,-J,uffi::::t'il1.*

ff::fn::ili

is ttre qua[iy of the GMs.

Because of the age-specific characte.
or cvr, (see Chapter 2), two
different optimarity
scoring lists are necessary. The fist
scoring rist (Fig. 3.g) is concern"outi,
preterm and
-

prechil's Method
on General Movement Assessment

^- Optimality List
GM
for pretermGMs and Writhing
Movements
(Ferrari et al 1990, modfied)
Name:
Ill"^-_,1 l,,i .
hecordrng

_-

date:
1. Qualjty

-------:_r6uur

2. Sequence

Gesrationat
rdr age at
aI otnh:
birth.

Recordig

ug,'

weeks

normat, variable, complex ..........4

poorfepertore
..........2
-*""r.
chaotc.
.........1
cramped-synchronised .. .....
., ...1
variable.
.......2
monotonous

withn GM . . . . . . . . . . . .1
smtarfromGMtoGM ............1

orsorganised ............i
variabfe,fuilrange ........2
predomnanflysmall range
... . .. ...1
predominanfly

3. Amptitude

arge

varable.

..,.....

. 1

components

/. Unset and

.......2

monotonously slow . . . . . . .
. . . . . . . .i
monotonously fast . . . . . . . . . .
. . . . . .t
matnty one speed, not variable
. . . . . ..1
from horizonta to vertical plane
. . . . .2

5
s. Snao
vpoLc
o. Fioratory

range

marniyone range, notvariable

. . . . . .l

4. Speed

otfset

s.rremurousmovements

notthefullspaceused

............1

present, fluent anJaf"g"nt

.'. . . . . . . .2
no or Just a few rotations . . . .
. . . . . . .1
smootn . . . .

#:*i't1'","1'"":":"0:r:l i

present.......
GM Optimality Score

........l

Maximum: 16; Minimum: g

25

Fig. 3.8 Proforma for rhe GM

optimaliry score (preterm and
writhing GNIs).

-&".-l

*#x
Posfinerstrual Age:
Recording Dte: .

......-.....

Birth rveight:

PosttermAge:

Numberofmovementpattems observed:

I I lnormat(N) | I I anormal (A)

N A legs lifr' flexion at kees

contact
N A legs liff ertension at knees
contact
N hand-kneecontaci
hand-handcontacr.

NAwiggling'oscillatlngmovem'
"'
N A arching
hand-handmaniputation
N
N A szccadicarm*ou"*tno
N A trunkrotation
i'lfilgltiotttti'ttnLtt
i'
N Akicking
N a'rialrolling
reaehing

NAe:(citementbrr$s
N A v-isualscannhg
fnot'tbotcontact
A

'A'cha-dra-chamovemeflts'
N handregard
ioor-totnanipulation

N .4 snltes
N hedantefleion
Ri'g'ntntaltlout*tnttttmt
N
N A moutrmovenen .q tiE*tnur *ou*ttnG itgt
ty *-"]:T1"I in circles
+
N A rongue movemenrs
A almo*nolegmovemeflts
selm:discrepancyarm-lig
A
- l-lJnorml0$ Lu
N A headrotation
"olr:tT19].--^,..Numberofposturalpatternrs obsanleci:
A lt}?":*Ti:: of tle neck
finger postures
N
" variablc
N A head in midlire {20 ")
A h'vperexteuion of trunk
pieoominari,frstlng
a
N A ;,lmmetrical
A :dendcd sms1 on J above
spr*ding
hnger
i
or
absrnl
ii A spontaneous AT\8.
surf'acearapredominani
fcfurgerpr'*ures
A
couldbovelcoe
extanded legs 1on I abore
A
and
;;;"lit:
;
'A bo{ anrt limbs 'flar orr
"iening
surfhceatepredo$rinal
tiotingortrtttinsel;
srrfacs

N A fi@ety movemenrs N
N A sviping mr)vements N

hnd'fate

hand-mouth

lvlovement character lglobl score i:

snortlt

A jerky

andfluelrt

stiff

A cramPed
A q'nchrottous .
A cramped'synchronised

A monotonous

A temulous

A
A

flrgdoinartl-v tlos' Eeed

predomin. snall amPiitlde

.{

edoninantl-v fa-st speed

bredomin. large amPlituile

NIotor Clptimalitv L ist

i+#PD
?.

RePeftoir-e

of

co-existent othe'r

QualitY of other

mo1

elets

abnormal
abenl

age-adequate

n:
[1

reduced
absent

movements

B1

N>A

\T=A

trl

N<A
l\ /

Posture

.u

.tr

2
O

cr'amped-syrchr' tr
tr

N<A
5.

L'Iovement chaacter

1n

norna1

Fidge{Movements

flrrent

smooth and
oUnottrrul, not

"runaert-s'nchroni*ed

*t".#*k'#ftt**T*,

f----_l

Fig.3.gProformafortheassessmentofthemotorrepertoireof3-to5-month-oldinfants

26

Fo the definitions of the specific movement

patterns see.chapter 2 (rabre
2.2).segmental
movements and am movements in cicles
are described in Chapter 5.
Score the following movement patterns

abnormal

.
.
.
.
.
.'

fidgety movements are absent or

of abnormal quality;
slvipes are predominant;

wiggling-oscillating movements are

predominant;
saccadic arm movements are predominant;
kicking is monotonous;
excltement bursts are monotonous
and predominant

.:1,#;:hff;;l:*.,
accelerarions

.
.

.
o
.

ii

i'

(the abureviation

,u di.;:;::T?i1;J,llf;.",1t

in rhe rvhore bodv and not rerared

ro facial
smiles are frozen:
mouth movements are i
ro ns u e pror rus i o

n,,,"

l,

without pleasue mimic;

no, relared ro rhe dancej ae abnormat

monotonou', i nor.ir'otvped;
limb
'jesant'
rhev are ongoing

"^0."rr,j1""?:]ljffiff.r"',ir""t'

;:ff 1.:";.',:'jtJ:*,:i.

and

c r os i n g ;

head rotation is repetitive:

fiddling is arvkward:

foot-foot contact is rvithout small movements

and mainly on tibial side;

I"TfrilT',T?:#'J|.,?T#;.Tffi::iinilrv..p"'"ntin'itt'"'uppJio.t*uerextremities;
. legs
lift with extension
. arching is prolon,qed; at knees i. prrOorinuniand ofstiffcharacter;
. trunk rotation en bloc;
. visual scanningis consists
of rorving
eye movements.

Score the following postural patterns

abnormal

if:

is only in lateral position (more

rhan 20. from rhe midline);
Tr9 is asymmetrical;
.: posture
r spontaneous ATNR cannot be

overcome by the flexion of the jalv

arm.

For the age-adequare repertoire (item

2) see Chapter 2 (Table 2.2).

calculations and comIn addition, a GM optimality score can be used for statistical

Einspieler (1994)- She reported a

parisons lvith other measurements, as has been done b,v
the p02-values obtained during
high conelation betrveen the GM optimality score and

overnightpolygraphiesin3-to20'lveek.oldinfants,indicatingthatdropsinp02resulted
in a less optimai GM Performance.

28

WI-]AT EOUTD INTETTFERE

WITI] TI-]E QUALITY OF GENE|?AL

I\IOVEMEI\TS?

Developmental care for preterm infants

Individualised developmental care in the neonatal intensive care unit (NICU) focuses on
postural care (mainly by putting preterm infants into a 'nest') and on minimising distressing
factors for the infant. It has positive effects on the stability of some physiological indexes,
on the number of days of ventilatory support, the duration of hospitalisation and the rate of
weight gain (Stevens et al 1996, Brown and Heermann 1997).

Recently, the GMs of two groups of high-risk preterm infants matched for clinical
characteristics lvere compared (Baldi 2002). One group lvas submitted to conventional care
and the second to an individualised developmental care programme. The frequency of

normal, poor repertoire, cramped-synchronised and chaotic GMs lvas the same in both
groups. A slight reduction on some indexes of neonatal distress (such as number of startles
durin-s lvakefulness, number and duration of crying episodes) lvas observed in the infants
submitted to developmental care. More controlled studies are necessary in this field.
Skin-to-skin holding, also knorvn as kangaroo care, has been sholvn to be beneficial for
the preterm infant. In order to investigate an eventual change of rest-activity cycles the
occurrence of GMs as a marker of activity level has been studied (Constantinou et al 1999).
Horvever, the percentage of GMs did not differ as a result of skin-to-skin holding.
These studies indicate that GMs, being endogenously generated and a robust output of
the young nervous system, are hardly influenced by environmental stimulation. For
the
recording and GM assessment session, holvever, it is better to take the infant out of the nest
because of possible mechanical restriction.

Is general movement assessment under intensive care conditions possible?

In contrast to a neurological examination, GM assessment can be carried out even under
intensive care conditions (Albers and Jorch 1994). It is a great advantage that GM
assessment is caried out lvithout any handling of the infant and the infant is not even touched
(Prechtl 1990). Artificial ventilation, infusion lines (Fig. 4. l) and electrodes
allorv GM
assessment as long as the infant can and does move.

During these very early days after birth the GM assessment might mainly be used to
determine acute neurological dysfunction and eventually to evaluate possible
effects of
medication and intervention. It is not primarily used to predict later neurological outcome.

29

Effect of drugs on general moYement quaty

BenenuRArrs
No systematic studies on the effect of barbiturates
on GMs are available. Ten years ago, Prechtl et al

i' 'r *
'
{

"

"
'""

(1993) described how fullterm neonates with hypoxicischaemic encephalopathy are hypokinetic during their
first days or even a felv rveeks after birth' All of them
lvere under barbiturate treatment' Holvever, four infants
rvith mild asphyxia had received a comparable dosis of

ANTICONVULSANT THERAPY DURING PREGNANCY

Antiepileptic drug therapy (valproic acid, phenobarbital'
carbamazepine, lamotrigine, primidone) may have an

impact on the course

*\
*
,

of

pregnancy and pregnancy

outcome, and may also induce effects on the developing

brain that only appear later in life (Scolnik et al 1994'
Omoy and Cohen 1996, Parisi et al 2003)' A recent study
on eleven cases demonstrated that the optimality scores
GMs (according to the score list: see Fig' 3'8) at 7

for

days and 4lveeks lvere markedly reduced' Furthermore'

the lorver the GM optimality score, the lolver the Brunet-

Lezine (1967) Developmental Quotient at 30 months

lParisi et al 2003).
INDOME*THACIN

Tt"
ti
..9

of
Indomethacin is lvidely used for non-invasive closure
patent ductus arteriosus in preterm infants (Clyman
ln aition, lorv-dose indomethacin is used for the
prevention of intracranial haemonhage (Ment et al 1994)'

SgO).

After the first dose of indomethacin translent

with

lvere
effects on the quantity of spontaneous movements
duration
and
described (Bos et al 2000). The incidence
of several movement patterns, such as GMs, isolated

a superimposed rotation (from Case

limb movements and twitches, lvere substantially

A onthe DVD).

reduced, and the incidence and duration of rest periods

rvere increased. The quality of GMs did not change
due to indomethacin' Horvever, applying the detailed
a
scoring of GMs as described in Chapter 3 (Fig' 3'8)'
(2000)
recomreduction in speed lvas found. Bos et al

Fig. 4.1 29-rveek-old preterm infant:

despite infusion lines the left arm
moves from flexion to extension

mend a cautious use of bolus indomethacin for the

treatment of patent ductus aneriosus'
30

F
F
P
P
F
F
H

DEX.\\IETH-\SO\E
Until recently'. dexamethasone lvas frequently' used in preterm infants at risk for chronic luns
disease. However, mortality rates do not decline markedly after postnatal corticosteroi
rlierapl and concern has been raised about its neurolo-eical sequelae (Do1'le and Davis 2000.
Shin* ell et al 2000).
In their first studr on the effect of dexamethasone therapy Bos and co-w orkers ( 1998b)
reponed on a transient reduction in motility and a reduction of speed and amplitude of GMs
;uring preterm age. In a second study on a much larger sample, particularlv lvirh initially
ncrmai GMs. the same authors reported changes in the GM quality (Bos et al 2002a). Nine
out of 13 infants lvho initiallv sholved normal GMs developed abnormal GMs immediatelr,
atrer deramethasone therap,'. Tlvo of these infants still had abnormal fidgef_v- movements
ar 3 months postterm; holvever it lvas less certain rvhether dexamethasone lvas also to blame
for rhe long-term effects. Chronic lung disease r,vith repeated episodes of hypoxia could also
have contributed to the later deficits (Bos et al2002a).

Pt
l

*1

F
F
E
H
pl
d
F

Systernic diseases do not mimic brain lesion

A serious concem rvas the question rvhether a svstemic disease, such as infection lvithout
brain invoivement (candida species, coagulase-negative staphy'lococcus. staphylococcus
aureus), might mimic impairment of GM qualitl' similar to that in brain d1'sfunction. Bos
et al (1997a) could demonstrate that septicaemia has a limited influence on the GlvI
quality. At first sight, GMs can be mistaken for poor repertoire. Horvever, the ichness
in compleritl' and variability, in particular of the sequence of the movin_e body parts.
including superimposed rotations. rvas strictly different from trul,' poor repertoire Glvls.
Glvls of preterm infants lvith severe infectionjust have a sluggish character rvith a slorv
speed. Hence, it is possible to discriminate betrveen abnormal GNIs due to brain lesion and
sluggish GMs due to severe systemic infection, rvhen the complexit,v of the Glv{s is
considered as the main characteristic for normal GMs (Bos 1993, Bos et al 1997a).

H
F
F
H
F
F
H
H
F

The slug-eishness might be erplained b1'changes in muscle function. During septicaemia

the resting membrane potential in muscle cells is increased (Cunningham et al 1971 . Shiono

al 1989), -glucose transport in muscle tissue is impaired (Westfall and Sayeed 1988) and
protein breakdorvn in muscle tissue is enhanced (Hasselgren et al 1988)"
et

Avoiding confusion between abnormal general movements and seizures

For the less experienced observer it might sometimes be difficult to distinguish betrveen
abnormal GNIs and seizures. GMs lvith a poor repertoire shorv a monotonous sequence of
the successive movement components that recalls stereotyped movements of subtle seizures.

Similarl.v. some cramped-s,nchronised GMs may resemble tonic posturing of focal or

generalised tonic seizures.
PooB RpeBrotBp GMs AND SUBTLE SrzunEs rN PREreBrvr,qruo Fur-lrgn;v,r

Iur.vrs
Subtle seizures encompass a varietl'of paroxysmal alterations in neonatal behaviour
and motor automatisms (i.e. ocular phenomena, oral-buccal-lingual movements, limb

(4

a1
JI

&

_*--

movements, autonomic phenomena, apnoeic spells). Volpe (1995,2000) described peculiar

extremity movements, resembling 'boxing', 'hooking', or 'pedalling'. Mizrahi and Kellalvay

(1987, 1998) described rorving or srvimming movements of the arms and pedalling or
bicycling movements of the legs as'progression movements'.
What is peculiar to seizure movements, but certainly not to poor repertoire GMs, is
the extreme stereotypy and the ictal character of the clinical phenomena. The sequence
of movements does not change during the single seizure or even in successive seizures.
Poor repertoire GMs are monotonous in the sequence but are never stereotyped to such a
degree as seizures are. Other ictal motor phenomena such as abnormal eye movements,
oral-buccallingual movements or autonomic phenomena during limb movements are never
seen during poor repertoire GMs.

CRrvlpeo-SvNCHRoNTsED GMs eNo ToNlc Sezunps IN PRETERM AND

Fuu-renv INpeNrs
Focal tonic and especially generalised tonic seizures can be confused with crampedsynchronised GMs. Focal tonic seizures consist of sustained posturing of a limb or
asymmetrical posturing of the trunk or neck, most often associated with EEG seizure
discharge. Generalised tonic seizures can be observed as tonic extension of both upper and
lolver extemities (a decerebrate posture is mimicked), as tonic flexion of upper extremities
with extension of lolver extremities (a decorticate posture is mimicked), as tonic flexion
of the four limbs, or asymmetrical posture of the limbs that mimic the asymmetrical tonic
neck posture. Again, the stereotypy in addition to other ictal phenomena (e.g. eye movements, oral automatisms, vegetative phenomena) and the loss of consciousness indicate
a tonic seizure and not an abnormality of GMs. Cramped-synchronised GMs, holvever,
are not stereotyped despite all limb and trunk muscles contracting and relaxing almost
simultaneously.
If clinical observation does not enable a differentiation betlveen seizure and abnormal
GMs, an EEG-recording can be helpful, despite the fact that not all motor automatisms,
particularly tonic generalised seizures, are consistently accompanied by epileptic discharges
in the EEG.

Cnupe-SvNCHRoNISED GMs eNo SsIzuRes Ar-ren rHE NEoNATAL PERIoD

Infants with severe brain damage, such as full-term infants affected by severe hypoxicischaemic encephalopathy and preterm infants affected by severe periventricular leukomalacia or periventricular haemorrha-qic infarction, are at high risk for epilepsy. The risk
for recurrence of seizure is higher after neonatal seizures and after abnormalities of the
neonatal interictal EEG (Volpe 2000). During the first 2 to 5 months postterm age, tonic
seizures and tonic spasms of West syndrome may be confused lvith cramped-synchronised
GMs.

It can be difficult to recognise epileptic spasms as they may be subtle in appearance

and brief in duration, extremely heterogeneous in appearance (tonic, myoclonic, in flexion,
in extension, in adduction), they occur most often in clusters but sometimes as isolated
phenomena, and they may be superimposed on an abnormal motility. The typical spasms.

JZ

lvirh adduction and semi-flexion of the four rimbs and lvith flexion
of the head and trunk.
ma look similar to cramped-synchronised GMs, but are *' *J J rrrurlr
Illore stereotyped and
"

faster in

alr"yr;;;;;;

speed.

Infants lvith west syndrome are usually irritable, sholv

a rorv threshord to the
Moro
response. have tremors and jitteriness, suffer from abnormalities
of ti" mur"r" tone and
have
addition
cramped-synchronised
ma in
GMs. In case or.linr.ui ,uspicion,
a video_
EEG-polygraphical recording should be performed. clinical spasms
.oin.i.nt rvith EEG
parorysmal features are a confirmation of West syndrome.
othe tonic epileptic seizures. such as those seen in ohtahara
syndrome or in earrv
m-r'oclonic encephalopathy, are easy to recognise and cannot
u..or"J*lrii*-.fr;svnchronised GMs.
Does sensory

stimulation interfere with fidgety moyements?

Fidgety movements are only present in the alvake infant.

They can be obseved in anv
position of the infanr bur they can be observed best
if the infant is ,"oi;;;^;*;'l
reraxing chair. As mentioned earlier, fidgety movements
can hardry be seen rvhen the infant
is crying orfussing since all movements then
become jerky, even rigid, and speeded
up (see
chapters 2 and 3)' A different question is to rvhat
extent focused attention to vanous
stimuli
could interfere with fidgety movements.
A series of experiments has been carried out to investigate
the effects of visual,
acoustic, social and proprioceptive stimuli on
the quality and temporal organisation
of
fidgety movements (Dibiasi and Einspiele r
2002,2004). None of the stimuli changed
the
quality of fidgety movements. Horvever,
the results differed fo temporal
organisation.
A red ring did not attract the attention of l2-week-old
infants sufficiently and thus
did not change the temporar organisation
of fidgety movements. By contrast, visuaily
highly interesting features, such as a red puppet
rvith bi-e eyes (Fig. 4.2), maycounteract

:
,

',
!

_t

::1

Fig' 4'2 Stimulation with

:-:-ll-:l-

.:,:::.-

a red puppet

(left) causes focused attention counteracting

the temporar organtsatron of fidgerv movemenrs (righr).
During the rvhole stimulation;;
were observed
(y2-axis, right-hand scare) rvhereas
the infant was continuously looking
twrd, ,rr" ,.0 pupp", (y1 _axis,
lefrhand scale). After the red puppet ou*
,.*ou.d iiJgery mov^"m"nrs reappeared in the remporal
organisation seen before stimulation (reproduced
*itr, fen ,isrion from Dibiasl ind Einspieler
2002).

;;;il;;;-_*rs

JJ

decrease or stop of fidgety movements

the temporal organisation of fidgety movements. A
by an increase'
lasted for about 20 seconds and rvas subsequently followed
movements, interference
fidgety
The practical consequence is that, for the assessment of
If this is not possible, assessment
stemmirrg from highly interesting toys must be avoided.
place and fidgety movements are once again
should be postponed until habituaiion has taken
occurring in the expected temporal organisation'
g8 dB did not influence the temporal organisation
Short and unfamiliaruound, up to

offidgetymovements.Itseemsunlit<ety,therefore,thatlonger.lastingsoundsofthesame
intensitylvoulddoso.Consequently'fortheapplicationoftheGMassessmentoneneed

(Dibiasi and Einspieler 2002)'

not necessarily assess the infant in a quiet room
1997b)' fidgery movements
In contrast to what has been stated previously (Prechtl et al
or experimenter's presence and
are not influenced by social interference. The mother's
may be
joyful talking with the infant do not interfere with fidgety movements. Infants
e caregiver is in close proximity
recorded for the assessment of fidgety movements while
remains is that the analyser's
that
problem
to the infant or even talking to the infant. A
present during the recording
are
persons
visual Gestalt p"r""puon *u:y be impaired if other
(see Chapter 3).

WeconsiderfidgetymovementsaSanage-Specificfine-tuningoftheproprioceptive

Hence, it lvas of interest to examine

System (Prechtl and Hopkins 1986, Prechtl 2001a)'

if

fidgetymovements"r'ung"duringorafterproprioceptivestimulation.Braceletswithlead

legs or both, bilaterally and unilaterally'

pearls rvere put on the 3-month-old infant's arms or

(Dibiasi and Einspieler 2004)' Fidgety

Surprisingly, fldgety movements did not change
if the infant lvas weighted on one side lvith up to 140

movements remained the same even

grams per arm and leg, respectively (Fig' 4'3)'
the quality nor the temporal
That various environmental inierferences changed neither
that the major function of the
organisation of fidgety movements once again underlines
spontaneous activity that is robust
young nervous system is to generate spontaneous activity:
Fidgety movements are a transient but
and relatively independent-of sensory stimulation.
system'
very stable and predominant feature of the young neryous

Fig. zl.3 One-sided weighting of the 3-month-old infant

rvith 140 grams on the left

arm and the left leg, resPectively (Dibiasi and EinsPieler
2004).
1
J+

HOW OBJECTIVF, I?ELIABLE AI\D

VALID IS TI-JF GFNET?AL MOVEMTI\T
ASSESSMEI\T?

Inter'observer agreement and test-retest reliabitity are very high

As the qualitative GM assessment is based on pattern recognition it is of utmost importance
that the inter-observer agreement is sufficiently high, and thus the method can
be considered
as objective. So far, 1 I studies on 358 infants assessed by 90 observes
have revealed
an agreement of betrveen gg and g3 per cent (Table 5.1). cohen's kappa
is used to assess
inter-rater agreement rvhen observing qualitative vaiables. Kappa is considered
to be an
improvement over using percentage agreement to evaluate this type of reliability (cohen
1960). The average kappa in another four studies on 108 infants assessed
by I I observers
rvas

0.88 (Table 5.1).

The effectiveness of training in GM assessment rvas investigated

in 700 particitraining courses. They reached g3 per cenr correct

pants at various three- to four_day basic

TABLE 5.1
rnter-observer agreernent for the assessment of GM quatilv in 15 studies
on a totar number
of466 infants. AII together 101 observers participated in these studies
Number of
observers

Number of
infants observed

Inter-observer
agreement (LA.) or

kappa (K)
Prechtl 1990
Van Kranen-Mastenbroek et al 1992
Geerdink and Hopkins 1993a
Albers and Jorch 1994
Bos e al 1997a
Bos et al i997b
Cioni et al 1997a
Cioni et al 1997c

Einspieler et al 1997
Bos et al 1998a
Bos et al 1998b
Cioni et al 2000
Bos et al 2000

Einspieler et aI 2002
Guzzetta et al 2003

10

20

4
2

30
35

22

IA = 90Vo
K = 0.84
lA = 87lo to 93Va
IA = 67Vo to 99Vo
IA = 96Va

19

K=

66

IA = 91Vo

lA = 87Vo
IA=MVo to88Va

0.92

5l

30

27

K = 0.84

l.l

IA =

JL

2to6

48
36

K = 0.91

22

Kappa > 0.75, excellent agrement

J-)

IA=

98Vo

94Va

IA = 927o to 9-7Vo
IA = 92Vo to 97Vo

?Eg

4'E ?=z 3
?a;
-i=
-

I eH : : g= ite ,
g sEE 3 ii * i 3

E ?,

66
IL
oq
E=

ol

d--?Ee
q
bi
E
e
E r!
6 E

R g'i

&

fi

ss

ql

6t'
:l
ol
>l
OI
ol

*.',

3
i
i
279
Z
'.
HE e a

"=
9
i

;rt

ql
o

0l
6l

r.69l

el

9E

nnE

.:

.:o

-vl
F

. 0l

<'

=e?d5

fi

o
OI
!

>9

Es
o==6

lo
I+

a
h

a
!

ss
OO

t>
lil
IE

'.2

arah

?2q|tr

i;?E:G?6 ia

t9

t:
l
lo

&

Il.

=to-?UOJ=

'-'E

tY r'r:

iz

*^E e

o lo

judgements. Additionar training of almost r00 participants significantly

increasec.r rhe correct
judgements to89 per cent' If only the global discrimination b.too..n
no.mat an ab'omrl
GMs was considered, 9zl per cent had correct judgements. Interestingly,
ir rrlu, ,..r.. clifficulr

to correctly judge infants,

if they rvere recorded

around t.rrn

J!.

(vur.ntin.

personal

communication).
An analysis of 20 GM recordings repeated after a time interval of trvo
years obrainecr a
100 per cent test-rerest reliability for global judgement. and an g5 per
cenr reliabirity for
detailed analysis using the GM optimality list, as described in Chapter
3

(Einspieler l99J).

The validity of the general movement assessment

When introducing an assessment technique the effectiveness must be considered
carefullv:
how accurate is the method when it comes to detecting disease positives,
i... tut", n.ur_
logical deficits; and how accurate is the method at excluding disease negatives,
i.e. those
r,vho do not have later neurological deficits. The conventional indices emplJyed
to determine

this are sensitivity and specif,city (Bland 1996).

Sensitivity is the number rvho are both disease positive and test positive
divided by the
number rvho are disease positive, in other rvords the percentage ofcases lvhich
are correctlv

identified as high-risk for later neurological impairmenr (Bland 1996). Table 5.2 provides
the details of several studies on GM assessment and the calculated sensitivity
values. An
overall sensitivity of 94 per cent indicates that only 6 per cent rvere false negatives. The oniy
exception is the study on GM assessment during preterm age by Geerdink and Hopkins
(1993a) lvith a sensitiviry of 60 per cent (Table 5.2). Holvever, this study is not
comparable
with the others because the outcome lvas measured at 1 year of age and 'disease positive'

lvas defined as 'poor outcome according to neurological examination'. In all other

studies
the outcome was measured at the end of the second year, or later, and cerebral palsy or
developmental retardation (developmental scores belolv tlvo standard deviations) or both
lvere taken as 'disease positives'.

Specificity is the number who are both disease negative and test negative divided by
the number lvho are disease negative, in other lvods the percentage of cases lvhich are
correctly identified as normal (Bland 1996). Table 5.3 provides the details of several studies
on GM assessment and the calculated specificity values. Specificity rvas lorver during the
pretem and writhing movement period (ut6 to 93 per cent). This rvas due to the number
of infants lvith abnormal GMs (mainly poor repertoire) at this early age lvho normalised
before or at the fidgety movement period and lvho had a normal outcome (Fi-e. 5.1). Thus,
lvith inceasing age, specificity increased, revealing values betlveen g2 and 100 per cent
during the third month lvhen normal fidgety movements predict a normal neurological
outcome.

The largest study so far, in lvhich 130 infants participated, clearly emphasised
the importance of the fidgety movements (Prechtl et al 1997b). According to brain ultrasound findings 60 infants lvere at low risk and 70 at high risk. Ninety-six per cent of the

infants lvith normal fidgety movements had a normal neurological outcome, rvhereas
abnormal quality or total absence of fidgety movements lvas foilorved by neurological
abnormalities in 95 per cent of the cases (cerebral palsy in 82 per cent and developmental
37

!!

a a
?
G' eE
;e:iE ee;
Ei EF $
ez*?"i f r Eir iu
i s* g gi; g*t gt s

6l

.9

6s
'
a.=

:l
al

o
,:P
h'
eG

; +i
-

el
-l
el
>t
hl

;9 .:
=
=. i;.::

R gA

ol
sl
"I
9l
'-e
lnE

-I 2
F E
b
9

;
=

o.

?
i

P
=

E
6

I:
:-

=
6+

00

io

i 1l
<'t
t-tl

:nr,St
-

=E
IL LO

'

$ $p

s
F

CA

N
N

Fig. 5.1 Individual developmental trajectory of case I born at 30 weeks postr

reperroire GMs during prererm and term age are fouorved by
^'-ov!J rrr

(J r ean):

;";;"i;i[ilT'"lilil?j

normal.

F-, absence of dgety movements; AF, abnormal fidgety movements;

CS, camped-synchromsed

.;\i;;l*lili"illlllIi;",tvpokinesis;

N,

ni

GMs; wk, week'.

rh.

e";.#;i,.,.

?ii;_,ll;f

GMs; Ch, chaotic

ndg.ty.ou.m.nB

lc!lualulr alru rIllu(JI' lrulUlugrgal stBlls ril rJ pct.ccu[.r.

Jgvcr.al uult.jruulss uurrllrltr(r
conelation betlveen fidgety movements and neurological
outcome (Bos et al 1997b,
1998b, Cioni er ar 2000, Einspierer et ar 2002,Ferrari et

the high

ar;002, Guzzetaet ar 2003).

The likelihood ratios (LR) are dependent on sensitivity
and specificity. They indicate
a figure by which a positive (LR+) or a negative
test result (LR-) changes the odds for really
having the disease. The higher the LR+ and the rorver
the LR-, the betr a test is. In general,
an LR+ > 1 0 and an LR- < 0. l characterises
a very good test (Sackett et al 2000).
Calculating the LRs from previous results (prechtl
et ar r997b) gives an LR+ for
cramped-synchonised GMs of zt5 (95 per cent confidence
inte wai: 64tJzzr), and an LR+
for poor repertoire GMs of only 0.61 (95 per cent confidence
interval: 0.40 to 0.93). For
normal preterm and rvrithing GMs the LR- is 0.04 (95
per cent confidence interval: 0.005
to 0.27). The LR+ for an absence of fidgety
movements is > 5r, and for abnormal fidgety
movements it is 5. l (95 per cent confidence intervar:
1.5 to 17), whereas the LR_ for normal
fidgety movements is 0.05 (g5 per cent confidence
interval: 0.02 to 0.r7). Thus, normal
GMs at any age as rvell as cramped-synchronised
GMs and the absence of fidgety
movements have excellent LRs.
Specific signs predicting cerebral palsy
The traditional approach to diagnosing
cerebral palsy is to detect the first signs of this
neurological condition at the age of g to 12
months postterm. At this age, the first signs of
spasticity, or pareses, or merely ofconsistent
hypertonia, o. any othe, s[ns specific for one
or other form of cerebrar palsy, may be
detected. perlman ( r 99g) stated th-at no early
markers
for the later development ofcerebrar palsy
are recognisable
lvas referring to the traditional neurological
examination.
The change in paradigm from the traditional
testing

in the neonatar period, but he

of refle.xes, responses and tonus to

nelv assessment technique, which focuses
on the quality of GMs, is indeed a diagnostic
breakthrough (see Chapter r). with the qualitative
assessment of GMs, it is now possible
to detect prenataily in the foetus, or postnatally
in the preterm or,..- infant, specific
neurological signs rvhich are highly predictive
for the later deveropment of cerebral parsy.
a

39

i:::l'::x:ffi ?Jffi :slH':''f

*^#:Fff.H":i*J:MpiY::

**ffi ':'::":t'Ir'*iiii!
if.m::ru:*1".t';'::iff
*i:i:*:*l;;ul*ll"'"n"15::"::i'ii'*l{*::i1k',:;il:H'::i'';
'*''ff
confirmed'tnetliii"tit""tJ
haemorrhages'
consistentlv crampediffi;';;tions*or

:ffi ,iHTff :t.':;tJin*u:ru:""':il'-'*"iil'xTru:si'"""n'r

et al 1997b)'

m,*"i::-':':l,Till]:::TJ:i-$::t,tJ'::ffitilt""tr'

84pretef
corw
that the earlier
reported
(2002)
r"", ,."*u ": *:.i^t;r.1,"":i:il::Jr:il;
r.rrJ .t al
impairment'
motor
fun.,iot
later
gru>o lroto,
rhe rvorse the
"^--classificattorl ot
of
system
a
with
,t
"a""'d"""e
(Palisano et al 1997)'
. ,s the consistent preseT.e of poor repertorre
palsy
;-b

rnarecentstudyof

Ilt

tt::ir**

;:*::ff :"'#:T"'#ilT!ii';id;ii"''""**i:i:*:l::'Jfi

:T::'ffii

;ffi it':T*:"i:il:';:ffi ;ffiT:*f,2k.,:::';l.,lJ:,""J"'i:i?xl;

lve have
Thus' rve h
So

far'

.rovided

tht" 'ut" ;;;;t

(Fig' 5'2)'

interval coplications'

',t.nu,iu" findings

100%
80%
60%
40%
20%

o%4.**Fig.5.2

Aroncitudinar;11ir"",",].il.$x5;!i:",'.i,1[T:]ilili:T":illlTi:'1i:T:l"l;$:x

*; ffi:it;ffi ;,j#*
CP, cerebral Palsy'

40

: :*#:i,:",r,'ft

::$';

?':ff :,'i;'rr',i ::H :'i

t1
d4

F)

Consistent findings refe to about bi-lveeklv recordings during the preterm period, one
period, and at least one additional recording during the first trvo
recordin_g during the term

F
F

months Postterm'
There is yet another early marker for later development of cerebral palsy. In the stud1,
menrioned above (Prechtl et al 1997b), only three out of 70 infants r,vith normal fid-setv

F
F
Pt

moyements had later cognitive or motor impairment or both, and 67 (96 per cent) rvere
normal at 2 .t'ears of age; none developed cerebral palsy (Fig. 5.2). On the other hand, 4-l
our of 1 30 infants never shorved fidgety movements and 43 ofthem (98 per cent) developed

F
H
F
F
F
e
,ffi

5ei.ere spastic cerebral palsy. The remaining

infant, lvho had a poor repertoire of GNIs in

his pre-fid-eet;" movement period, had severe cognitive and motor impairment. Less clear
are the prognoses of those infants lvho sholved the exaggerated type of abnomal fidgety'
movements (N =

l6

out of 130). Three cases turned out normal, seven became co-enitivell

motorically impaired, and six (37 per cent) developed cerebral palsy (Fig. 5.2;. Horvever,
al1 sir cases lvith cerebral palsy had consistently cramped-synchronised Glvls before
shorving abnormal fidgety movements. In addition, it is remarkable that of the seven cases
or

that had consistentl),' poor repertoire GMs during their first lveeks of

life but later developed

cerebral palsy, none had ever developed fidgety movements.

Thus, in addition to consistently cramped-synchonised GMs during preterm and early

FI
FI

postterm age, the absence of fidge6,- movements is a specific sign of later spastic cerebral palsy.

In conclusion, specific early signs of later spastic cerebral pals,' are consistently
cramped-svnchronised GMs (Fig. 5.3) or absence of fidgef,v" movements (Fig. 5.:l) or both
(Fig. 5.5). Both abnormal qualities of GMs can be seen at an age at which no clinical
evidence of cerebral palsv is yet present, namelv as early as from foetal life onlvards or from
peterm or term birth until the third month postterm (Prechtl et al 1997b).

f,
r)

J,

f,
FI
l
l

t
,4

f'Jt

Fig. 5.3 Individual developmental trajectory of case 2 born at 28 rveeks postmenstrual age. Consistent
cramped-s1'nchronised GN{s durin-e the preterm, term and early postterm period are follolved by abnormal
fidgetv movements. Outcome: spastic cerebral palsy. Abbreviations as in Fig. 5.1.

Fig. 5.;l Individual developmental trajectory of case 3 born at 29 rveeks postmenstrual age. Consistent
poor repertoire Glvls during the preterm. term and early postterm period are follorved by absence of
fidsen movements. Outcome: spastic cerebral palsy. Abbreviations as in Fig. 5. l.

r
;

l,

tl1

:
-=

:,g

Fis.5.5Individualdevelopmentaltrajectoryofcase4hornat30weekspostmenstrualage.Consistent
p*n"it p"lt-1q:- followed bv an
;;ine i'" p'"ttt'n' ltT
"utrJ
as in Fig 5'1'
cramped'synchronise ctus
spastic cerebral patsy. Atbreviations
absence of fidgetu

i;

.ou"m"ns.utiome:

and the absence of

movemnts on the one hand'
The validity of normal fidgety
we deal with an individual
is clearly demonstrated if

rh;;h*;uni,
fidgety movemenrs
GMs' Transient cramped""
iiii
traectorf
(Fis' 5'6)'
developmental
"'u*p"d-'yn"hronised
"*'i*t
ir ng"q' movements'are absent
the
synchronised crur'
movements'
fidgety
GMs are followld ty no'mal
If transient
"ru*p"o-'yn"toonised
normal (Fig' 5'7; Ferrari et'a12002)'
neurological outcome *uy U"

t^v1"Jilt";;;;ur'v

EenlvDIFFERENTIAIStcNsoFLATERSpesucDrplr'ctVERSUSTE-rpqpl/pctR
and tetraplegia. Cases
GMs predict both Spastic diplegia
Consistent cra-p.o-,yn.t,,onised
of cramped-synchronised
onset and shorteriuration
rvith later diplegia tun"-u ru*,
addition to the crampedin
If,
(Ferrari o i rowl'
GMs than cases rvith r"*, ,",r"pr"gia
the upper
are frequently present in
s"gmentat movements
synchronised GMs, solcallea
probably develop
Iimbs, the child rvill most
movements are

istlncilou.n'"nr,

ipf"*u (Cioni et'al 1997b)'

Segmental

toes' occurring either

of hand and'feJ, fingers and

GMs at 37 weeks;
Fig.5.6Individualdevelopmentaltrajectoryofcase5bomat30weekspostmenstrualage.Poorreper.
and arly postterm p"riit-tftd-synchronised
rerm
preterm,
Fig' 5'l'
during
in
as
toire GMs
tt'"b'ui putsv' bbreviations
absence of frdgetv

movemenls:'b;;;";;i"'tit

weeks;
Fie.5.Tlndividualdevelopmentaltrajectoryofcase6bornat3llveeks-postmenstrualage.Poor
p::lf,t;;ili"',mlil;Yffl[T:1GMs at 3e

reiertoire Grvrs ou.ing p,.t",lo,

"J"r^h*"ty

i",*

".i"*rv
(3 years) : nonar'

.outrnintt' outcome

^.1

In the latter case they are not part of iimb flexion or extension
isolated or as part of GMs.
et al1999, Cioni et al 2000).
der
Heide
van
(Cioni et al1997b,

Enr-v SicNs or HvrPLscte

of cerebral palsy in term infants, and

Often. congenital hemiplegia, the most frequent type
diagnosed after the first
rhe second most frequent in preterm infants after diplegia, is only
the clinical signs, or to
a
delayed
onset
of
is
due
to
diagnosis
this
late
Whether
life.
of
vear
initial neglect of neurological signs already present' remains unclear.
From neonatal age onlvards, neuroimaging techniques provide the possibility of identifling brainlesions, mainly cerebral infarctions, whichmay cause hemiplegia. Consequentiy,
it is nolv possible to perform prospective studies on the neurological development of these
infants. In order to investigate lvhether the assessment of GMs may help in the earlier

an

detection of hemiplegia, two different studies rvere carried out the first on 16 preterm infants

lvith unilateral intraparenchymal echodensity at brain ultrasound, most likely venous

infarctions (Cioni et al 2000); and the second on 11 term infants with cerebral infarction
on bain magnetic resonance imaging (Guzzetta et al 2003). All infants rvith subsequent
hemiplegia had an absence of fidgety movements follorving bilateral cramped-synchronised
or poor repertoire GMs. The observation of abnormal movements from birth onlvards refutes

of later hemiplegia.
The first asymmetric sign, independent of the head position, is segmental movements
(as described above), lvhich are reduced or absent contra-lateral to the side of the lesion

the hypothesis of a silent period

(Cioru et al 2000,Guzzetta et al 2003). This asymmetry occurs in preterm-born infants from

3 months postterm age onlvards (Cioni et al 2000). In term-born infants lvith neonatal
infarction the asymmetry of segmental movements is already present during the second
month (Guzzetta et al 2003).

EeRrv Stcws or LareR DvsrrNstrc CeBpeRAI- Pemv

Recently, it has also been possible to document early markers specifically predictive for
the development of dyskinetic cerebral palsy. A dyskinetic group of 12 cases (Einspieler
etal2O02) comprised syndromes of choreo-athethosis as rvell as dystonic forms (Hagberg
and Hagberg 1993).
Until the second month postterm, the infant who will later become dyskinetic displays
a poor repertoire of GMs, 'arm movements in circles' and finger spreading. Characteristically, these abnormal arm and finger movements remain until at least 5 months postterm.
The abnormal unilateral or bilateral 'arm movements in circles' should not be confused
lvith normal lvrithing or srvipin-e arrn movements. The normal writhing character of GMs
consists of ellipsoid arrn movements of variable speed, intensity and amplitude, lvhile
swiping arm movements are ballistic, fast, of large amplitude and high speed (see Chapter
2). In contrast to these normal movements, the abnormal 'arm movements in circles' are
monotonous. slolv, forlvard rotations from the shoulder. The monotony in speed and amplitude, in particular, is the most characteristic quality of 'arm movements in circles'. Usually
these abnormal arm movements are accompanied by finger spreading (Einspieler et al 2002).
A lack of movements torvards the midline, particularly foot-foot contact, is an additional
A2

;'"''iii,',i.;i,,j*,lifil**'rl
,nnli

u,, obrigatory

:""'Jffi

;:*;d;:J^;
i}ffi1ft::#,li:5;:',ffi;
^".-in"*

;1J'i':iln*l*:t',n:f

,vho deveroped either

Ht"^':,i;absenceorl9,T:ililil:T:

{it

ilTH:T'"HT*f *:x,ffi'T"i',#il*:il1";J','.;;:ll:#r,ilff

ixilH[fx;;i:;,;,n'::r'"

g:::utin:, *fffi::!F,':ll

kffi+if ,fJfr fiffi'I#Lllt"'?fi

;;#;t

;;necessarytogeneratenormalndgetv

(EinsPieler et al 2oo2)'

neurorogitarffl"l:""ffi :lTTl"lJ't jjll':r.,gaheneurorogical

movements(:::-:t::t:Xlnt, (pr".ttt et al leelD) but have been
o *n u' o.o.':'; ji
1"" *" in^*n; "o' "::; ;: :];:,.],,ffi :$ l.li J
1,5Xffi ::
"*;oi
"

Predictionof

Abnormat fidgetv

:';nli'$-][in'led'u"ha'la

iT*:;;*ir;i1J';iffi';:"::1'*3fl

-llilfi trjl*'ji]it""*""'Jli#Hil-***i:;,t'tti:jlix
:.';n'lfiiliJi"l'j:til1,':1fi J:i!:';::'il:
il:::ilnt':;il:::ff
this nnding did not
*.""*"i

il:::Tffi

have

iJot"r

'lt::,^fiTiJhJ;:*"fftn#;;;."Ho'"eue,,
la

tlvo to three lveeks

-fli:"'"Tlil:a'.:ililJi"*::':1,':llil;f:1"::i;:*'",Tifi ?"i1"1il!:

g:ry,ii;ffl;'ff il.lil:,:il*if

*fi :l','",:"#:!1''.i1,1

:1tr*T#,$:';m:;"ru"':";':l;T;'il"*'"':x'",iJ:li'l.ffi
';ffi r!i],';-s,i,,sh.,vs'me

lTi*il.;TrT,*fr;;':r-::ffi

xfiffi :[il:f

"^;;'-'J*1?'""1**onnolilr:"r=.:'.T:1i,".::liit{r"?ff
. ua,e *.'li :; TT JJ,',:i, :'I
"o'.
I 3;ii* T lT:i i: : lH; ; "," r,,. ",.,, "
il:ff *:::ll"#il;i;[t3.1i1i"H,::1i""T::";J#*o'lo'p"'ro'malce
IH' #' ; n n'
ev

ff J*i:

a,

THh*N*t
ffi'
;ffi
mid-puberty (Touwen
preand

1979) rvere

ou

*+l.",F"iIT.J::.ffi

Fidgety movements (between 12 and l6 lveeks postterm

age) rvith an inrermirrenr
temporal organisation (for a definition, see chapter 2) might u" *1o." oii*
,"tut" ro rarer
mild neurolo-eical dysfunction than continuous fidgety movements (Bos,
Einspieler and
Milioti, personal communication).
After Prechtl had discovered the existence of fidgety movements as an
age_specific
distinct form of GMs, he speculated about the possible biological function or tr,i
t.an.i.ni
movement pattern (Prechtl and Hopkins 19g6, prechtl r997a; see chapter 2).
A possible
ontogenetic adaptive function of these ongoing small movements could be conjectured
in
a re-calibration of the proprioceptive system. This is supported by the fact that
fidgety
movements occur at the three-month major transformation of many neual functions (prechil
1986) and precede visual hand regard and the onset of intentional reaching and visually
controlled manipulation of objects. As many aspects of the adaptation to the extra-uterine
condition are not reached before the third month ofpostterm age
-the proprioceptive system
is still tuned to the intra-uterine condition
a
re-calibration
of
this
sensory system could be
mandatory for providing the proper control of later fine motor activity. The findings in
blind
infants (see Chapter 6), as well as the fine motor disability in children with a historv of
abnormal fidgety movements, support this conjecture.

45

6
TF]E C! \IIEAL APPLIEATIOI\
OF TF]E METF-]OD

A heterogeneous series of clinical conditions such as periventricular leukomalacia' intracranial haemorrhages, hypoxic-ischaemic encephalopathy, chronic lung disease, infantile
grolvth
apnoeas, brain malformations and spina bifida aperta, Rett syndrome, intra-uterine
chapter
This
GMs.
quality
of
the
affects
blindness
early
and
retardation, maternal diabetes,
provides case histories including individual developmental trajectories and the child's
neurological outcome.

Periventricular leukomalacia (PVL) and flares

cystic
Lesions in the periventricular lvhite matter, especially if they evolve into extensive

lesions,arepredictiveof laterseveremotordeficits (Fazziefal1994).Theyaffectthequality

fidgery
of GMs. Poor repertoire or cramped-synchronised GMs if follorved by the absence of
outcome'
movements are clearly related to an unfavourable
Much more common are echodensities in the periventricular lvhite matter, also called
.flares', which do not lead to cysts or ventricular dilatation. MRI investigations have revealed
that up to 50 to 75 per cent of preterm infants, most lvith apparently normal outcomes'
may have diffuse lvhite matter lesions (Counsell et al 2003). Therefore, the significance
of periventricular echodensities on ultrasound is unclear. GM assessment could help
this problem as there is a clear relationship betlveen the presence, duration

in elucidating

course of
and localisation of transient periventricular echodensities and the developmental
the GM quality (Ferrari et al 1990, Bos et al 1998a).

white
Transient periventricular echodensities, particularly in the parieto-occipital
of
trajectories
matter, persisting beyond 14 days are related to individual developmental
abnormal GMs (Fig. 6.1; Bos et al 1998a).
(Fig' 6'2)
Echodensities lvith a duration of up to 14 days may result in either abnormal
can be
or normal individual developmental trajectories (Fig. 6.3, Bos et al 1998a). This
venous
as
sttch
echogenicity,
increased
the
explained by the diverse conditions causing
(de Vries LS et al 1988),
congestion (Baarsma et al 1987, de Vries LS et al 1992), oedema
and gliosis (Leviton
microclsts
(DiPietro et al 1986), necrosis,

microscopic haemorrhage
and Paneth 1990).
day of
Echodensities in the frontal lvhite matter lvhich resolve before the fourteenth
rvith
life do not have any impact on the GM quality (Bos et al 1998a). This is in accordance
favourable outcome after isolated frontal cerebral lesion (Fazzi et al 1994'

reports on
Rademakeretal 1994).

46

#-a

H
t
t4
t4
FI
t4
F'
F
Ft
Ft

p+s

Fig. 6.1 Individual developmental trajectory of case 7 born at 29 rveeks postmenstrual age. Brain

ultrasound: transient periventricular echodensity in the parieto-occipital lvhite matter (5 rveeksj.

Normal
repertoire GNIs and abnormal fidgety movements. Outcome (24 months):
fine
motor abilities impaired (Bos et al 1998a).
GNf s are follor'ved by poor

F-. absence of dget1, movements; AF, abnormal fidgety movements; CS, cramped_svnchronised
GNls; Ch, chaotic
Givls; PR, poor repertoire GMs; H. hypokinesis: N, normal GVIs; wk, wee ks. The age priod where
f,dgety movements
are obligatory is marked in grey.

F
t4

F)

Fr

F
?
F)

Fig. 6'2 Individual developmental trajector, of case 8 born at 30 weeks postmenstrual

age. Brain

ultrasound: transient periventricular echodensitv in the parieto-occipital r.vhite

matter until the sixth dav.
Poor repertoire GiVls and abnormal fidgety movements. Outcome (2zl months):
f1yp.rtoniu unJ p,
coordination (B os et al 1 998a). Abbreviarions as in Fi e. 6.1 .

ffi

Fig. 6.3 Individual developmental trajectory of case 9 born at 30 weeks postmenstrual

age. Brain
ulirasound: transient periventricular echodensity in the parieto-occipital lvhite
matter untrl the sixth dav.
GN,IH-IVH (germinal marrix inrravenrricular traemorrhaee) grade 1 (volpe
movements folloived

bl

Abbreviations as in Fig.

isssi

refr.

o;ail;;ffig

normal fidge$ movements. Ou'tcome (2:l months): normal (Bos et al 199ga).

6. 1.

Intracranial haemorrhage
Infants lvith moderate (-erade 2, Volpe 1989) and severe (_srade 3 and
3 plus, Volpe t9g9)
intacranial haemcnha-ees mav consistentl-v have GMs of abnormal
qualitl These quaiitative
abnormalities are related to an abnormal neurological outcome
1fig. 6.+; Fenari et al 1990).
Infants rvith GMH-IVH grade I (volpe l9g9) ma1 develop neurologically.abnormaily
or may have a normal oulcome. In such cases the qualitative assessment
of GMs is of great
help. Infants rvith consistentlr abnormal GMs will develop neurological
deficits (Fig. 6.5),
lvhereas a normalisation of GNIs. particularly normal fidgety
movements. predicts a normal
neurological outcome (Fig. 6.6).
4'1

rveeks postmenstrual age (twin

Fig. 6.4 Individual developmental trajectory of case 10 born at 33

grade I (Volpe 1989) and ventricular asymmetry

(left>
right)' diffuse periventricular increased echogenicity'
if"flt.ig,l;ut:4weeks: GMH-IVH grade 3
multiple cysts' ventricular

prJgnancy. Brain ultrasound a 33 rveeks:

GMH-M

bilaterat
ventricular dilatation (lett > righO; at 3"5 weeks: reduce-d haemonhage,
imaging) at 8 months postterm:
dilatation (left > righi;; at 3weeks: ditto. MRI (magnetic resonance
and T2, ventricular diffuse
densiry
protonic
at
signal
increased
and
subcortical
diffuse periventricular
GMs and absence
Cramped-synchr.onised
atrophy.
dilatation, dilatation of subarachnoidal space, cortical
disability, visual cortical deficit
learning
tetraplegia'
spastic
(22
months):
outcome
of fidgety movemenrs.
(Ferrari et al 1990). Abbreviations as in Fig' 6'1'

Fig. 6.5 Individual developmental trajectory of

cas,e

1 born at 32 weeks postmenstrual age'

Brain ultra-

prolonged periventricular increased echogenicity'

sound at 3l weeks: GMH-IVi grua" i iVotpe 1989);
movements'
poor repertoire followed by .oirt"nt..*ped-synchronised GMs and absence of fidgety
quotient) (Brunet and
(developmental
DQ
disability,
learning
no
outcome (18 months): spastJiflegia,
as in Fig. 6'1'
Lezine 196'\= 90, srrabrsmus (enari et al 1990). Abbreviations

age' Brain

.3 weeks postmenstrual
Fig.6.6 Individual developmental trajectory of case_12 bornat2':
weeks:.ditto and right GMH-IVH
29
echogenicity;
ultrasound at2.7.4 and2g weeks: fronLl increased

grade
frontul and occipital icr.as.d echogenicity, right GMH-IVH
grade 2 (Volpe 1989); 3l *".k.,
-yrt.
( 18
outcome
movements.
f,dgery
normal
and
roo, ,.pertoire GMs
2; 3g weeks: small right froniui
l'
6'
Fig'
as
in
DQ = 98 (Griffiths 1954' Fenari et al 1990)' Abbreviations
months): no abnormal

'lgn''

Unilateral lesions

preterm infants lvith a unilateral increased parenchymal echodensity, very likely as a result
helps to identify
of a venous infarction, have a high risk for hemiplegia. GM assessment
not (Fig' 6'8)'
rvill
who
those
and
(Fie.61D
those infants who will later develp hemiplegia
Cramped-synchronised
5.
Chapter
The early signs of hemiplegia are escribed in detail in
48

t=t

H
t4
J-,

n
F'

F'
Pt
F'
FI
P4

Fig.6.7 Individual developmental trajectory of case 13 born at 26 rveeks postmenstrual age.

Brain
left increased periventricular

ultrasound:
echodensity, frontal and parietal. eurologrcal examination:
(Duborvitz and Duborvitz 1981) normal findings during the prererm period; (prechtl
hyp"ri""i;.
hyperexcitability and asymmetry during term age; hypertonia and asymmetries during ill. tl.,ira
*onirr.
The movement asymmetry score (Cioni et al 2000) revealed no asymmetries during the prererm period,
more age-adequate movements on the left side from term age onwards and more r"g-.ntul movements
on the left side from the third month onlvards. Poor repertoire follorved bv cramped-sl,nchronis.O
Clir,
absence of fidgety movements. outcome (2il months): right hemiplegia (Cioni
2o0;. Abbreviations
as in Fie.6.1.

rgT

F)
Fr
Ft
ffi
H

eil

F
F
F
e
F
Fr

Fig. 6.8 Individual developmental trajectory of case 1zl born at 26 rveeks postmenstrual age. Brain
ultrasound: left increased periventricular echodensity, frontal. Neurological examination: (Dubowitz

and Duborvitz I 98 1) h,v.-potonia during the preterm period; (Prechtl 1977) hyporonia
and h),perexcirabilir],
during term age; normal findings at 3 months. The movement asymmetry score (Cioni et al 2000)
reveale
no asvmmetries. N{ore segmental movements on the left side from the third month onr.yards. poor

repertoire GMs and normal fidgety movements. Outcome (24 months): normal (Cioni et al 2000).
Abbreviations as in Fig. 6.1.

Ur'ls and an absence or ndgety movements (both abnormalltles are bllateral) as \.vell as a
eduction of segmental movements on the side contra-lateral to the lesion (from 3 months
onrvards) are highly predictive for hemiplegia (Cioni et al 2000).
Cerebral infarction in term infants is not allvays followed by later neuromotor sequelae

4
*4

a
da

(wulfeck et al 1991, de vries LS et al 1997, Estan and Hope 1997 Guzzetta et al 2003).
,
Whereas GM abnormalities during the early postterm period do not ahvays differentiate
beilveen later hemiplegia and normal outcome, the fidgety movements are hi-ehly predictive
(Guzzetta et al 2003). Figs 6.9 and 6.10 demonstrate trvo similar

case histories: abnormal

GMs predicting hemiple-eia (Fig. 6.9); and normal GMs predicting a normal motor outcome

(Fig.6.10).
In contrast to preterm infants lvith focai lesions rvho later develop hemiplegia, term
infants have an earlier onset of the asymmetry of segmental movements, at
3 to 6 lveeks.
This difference is probably due to the timing and tvpe of lesion. In preterm nelvborns
the
lesion occus at an earlier stage of brain development lvhen neurolo-eical
functions ae

.4

J'4

4
4

perhaps less clearly localised, and the pattern of lesion is different.

Even rvhen these preterm

infants shorv a predominantly unilateral lesion they also have contra-lateral

densities or

49

La-.

at term age. Brain ultrasound and MRI (at

Fig. 6.9 Individual developmental trajectory of case 15 bom
cerebral artery' The lesion involved the
the seventh day): infarction of a left coitical tranch of the medial
More segmental movements on the
capsule.
parietal and te;poral lobe, the basal ganglia and thejntemal
GMs and absence of fidgety
repertoire
Poor
weeks.
16
at
to
9
asymitetiy
but
no
weeks,
left side at 3 to 6
as in Fig' 6' 1'
Abbreviations
al
2003)'
(Guzzetta
et
movements. outcome tz+ *""itt' rightiemiplegia

(at
at term age' Brain ultrasound and MRI
Fig. 6.10 Individual developmental trajectory of case 16 bom
movements
segmental
More
cerebral artery'
,f.rnf,n Auy;, infarction of a ieft corticaibranch of the medial
lveek. Normal writhing movements and
on the left side at 3 to 6 weJs, but no asymmetry at 9 to 16
et al 2003)' Abbreviations as in
(Guzzetta
normal
(24
months):
outcome
normal fidgery movements.

Fig.6.1.
presence of transient bilateral
ventricular dilatation, which may explain the long-lasting
term infant is less frequently
the
in
infarction
neurological signs. ln contrast, artelialteritory
al 2003)'
et
(Guzzetta
accomp;nied by contralateral tissue involvement

Hypoxic ischaemic encephalopathy (IIIE) in fullterm infants

generalised reduction of motility

In the first days of life most asphyxiated infants shorv a
starts moving, GMs are
(hypokinesis - for a definition see chapter 3). As soon as the infant
ischaemic encephalopathy (HIE)
usually abnormal and tremulous. The degree of hypoxic
with the severity and duration
according to sarnat and Sarnat (1976) strongly correlates
In this respect, the results of
1993).
al
(Prechtl
et
of the abnormal changes of the GMs

neuroimagingcorrelatewithGMabnormalities(Fig'6.11).Holvever,thereareinfantswith
normal brain ultrasound findings
abnormal GMs, partrcularly in the first tlvo lveeks, and

(Fig.6.12).Moreover,thereareinfantslvithdocumentedmorphologicalchangesand
transient changes in GMs.

If GMs normalised,

the outcome lvas favourable (Fig' 6' 13)'

Chronic lung disease

also at risk for brain

very low birth lveight infants at risk for chronic lung disease are

and intracranial haemorrhage'

abnormalities such as increased echogenicify, leukomalacia,
(BPD) have a lvorse neuroTherefore, preterm infants rvith bronchopulmonary dysplasia
(Bregman and Farrell 1992)'
developmental outcome than preterms without BPD

50

Fie. 6.11 Individual developmental trajectory of case 17 born at 40 lveeks; late foetal heart rate decel-

,ritionr;outborn; Apgar2at5minutes,intubated; transfertoneonatalintensivecareunitat3hours;

hyperexcitability syndrome (Prechtl 1977), neonatal status epilepticus (until tenth day). Brain ultrasound
o2 duyt diffuse white matter and basal ganglia increased echogenicity; at 1 week: ditto and thalamic
echogenicity; at 2 weeks: ditto; at 3 weeks: ditto, subcortical cysts, enlarged subarachnoidal spaces,
moderate ventricular dilatation. MRI at 4 weeks: moderate ventricular dilatation, enlarged subarachnoidal
spaces, diffuse periventricular, subcortical, and basal ganglia increased signal at protonic density and T2
(iortical and subcortical atrophy). Hypokinesis followed by poor repertoire and cramped-synchonised
GMs; fast tremulous movements from 2 to 5 weeks; absence of fidgety movements. Outcome (24 months):
tetraplegia, epilepsy, severe leaming disability (untestable), head circumference < 3rd percentile (Prechtl
et al 1993). Abbreviations as in Fig. 6.1 .

Fig. 6.12 Individual developmental trajectory of case 18 born at 39 weeks; late foetal heart rate
decelerations, meconium aspiration, Apgar 3 at 5 minutes, intubated, tracheal suction, hyperexcitability
syndrome for three days (Prechtl 1977), moderate EEG abnormalities. Repeated brain ultrasound scans

were nornal. Hypokinesis follolved by poor repertoire and abnormal fidgety movements. Outcome
(24 months): motor and cognitive retardation, autistic behaviour, DQ (Griffiths 1954) <50 (Prechtl et al
1993). Abbreviations as in Fig. 6.1.

Fig.6.13 Individualdevelopmentaltrajectoryof

case

19bomat39weeks: latefoetal heartratedecelera-

tions, cord prolapse, stained and slimy amniotic fluid; outborn; Apgar 5 at 5 minutes, resuscitation bag
and mask, transferred to neonatal intensive care unit at 6 hours, neonatal status epilepticus until 4 days.
Brain ultrasound at 2 days: reduced ventricular size, diffuse periventricular increased echogenicity, mild
increased thalamic echogenicity; at 1 lveek: diffuse white matter increased echogenicity (left > right),
more pronounced in frontal and occipital lobes; at 3 rveeks: enlarged subarachnoidal spaces, dyshomogeneous increased rvhite matler echogenicity. MRI at 5 rveeks: diffuse increased signal (at protonic density
and T2) of hemispheric lvhite matter and basal ganglia. Nloderate ventricular dilatation, enlarged
subarachnoidal spaces (cortical and subcortical atrophy). Hypokinesis followed by poor repertoire and
normal fidgety movements. Outcome (17 months): no abnormal signs; DQ (Griffiths 1954) = 98 (Prechtl
et al 1993). Abbreviations as in Fig.6.1.

51

infant
case report on an

lvith

severe

BPD provided a detailed

description of a

spontaneousmou'-*tdi':';""'!1"11'""5t":hl::t-";f"1il|i"IT1t'.b"ffi
and EMG bursnc.tP;;;;i"

il;^;;.*"rt

:';

et al
\LrrvurqJ (Hadders-Algra

characteristics

the striato-tnalarruL "ir"oioy

a dysfunction of
The authors assumed

1994).ItmentisfrequentlyusedininfantswithBPDtofacilitatelveantng

Dexamethasone tret
i n, n r
(.
"i
rrom rhe v ent' ator
of respiquality rvill o:'u"ttlt^lllrone
on GMs' The improvement
,it" -"tt"ry andthe

J;;

il ;

" :*T,5:: :1""1ru*;ilqr"r11

i;:fl Ii
iuirll*:":::;i['::Tiliiil:".;'L:^#:il;i:"nilifi
lvtt
not
treatment' is
associated

dexamethasone

2002a).
In some infants

and
, r:+: ^- --"ci cr untffi;;fi
[ntil 3 months postterm
GM abnormalities Persist

*ount

*on"*""t

Tilil;;;;mal

;;l;;

p,"oi"tiu'io-'^ti"

or abnormal

o""o*' q'::il.'^f;',"?;*"" ,"::l::tii""1,nilI1",:l;

of GMs
scans' Those rr
Despite the impairment
on utr
found'"t-:t"l;"r."nd
rvas
damage
brain

in.rl#oi

inoullu
urtrasound rrun'

ubnormalities

riag'tv
':::llil:t"J'kly"ffil;;nJ*g''
quality - again

quesdon or wh"m"'o"lofi"'"t'u^'l*
episodes.of hypoxi:
remains open. Repeated
as rvett
their presence or absence

rnoua*an" -

even beyond' The

*"**'t' ""*::?;;;ry;tt

i11i:lJ"Hl]fiffi

fffi:

i;iil";}fi"n:T'T::J::#*-ti*T,***;n:;""::*ilL*':''*"T*
when adn
brain damage' but
noo.^t"-ttd"ced

,JJ;; A;;'
rnfantile

et al leee)'
et al 1ee3' rsubota

ininfants is maifv,refol:::]rti::ilH:t;
ringevent(ALTE)
t1*itill'?"r;rt;
becomtng
meir infant as suddenlv
ii",*tr;"0"0.

apnoeas

An apparentlo:

lHrFi::lT::*T:rt'il,:'ilffi
This is heterogeneous
corrt
but thev i"l:"*";n:;,rT,#jl:tili'}'fi',ff

possible diagnoses'
ilJ;;;;
development
2002)'
al9g'Farrell et al
' olic studies, the neurological
;;;;;,
t"'"in"uol,,tlto
*u-:"i::::;H;il;".*ou"*.r,,t
during sleep
polysomnographic
of movel*ln
The reported reduction
a Jetaite
tTtu
rvas th";;;;t;r"rest.
1992) rvas partially
of these infanrs
al
iss;. ictrecryl t
*on,n, after the
decreased a ter
(coons and G*i'.*"""i,
during sleep only

oic*n'

""0'''it '*
:l::311,,"lu,o:::,y:,T,,::1",t}i1ru;U:"JliliG'$

f+j",ffi
observational

in asphyxiated

r"l)?;;;r.;

"r"r"",i"",
ments !vere

^","

:;':,:t':ffi

lT:i,'.:'ffi

il;;

,ittP

nervborns.(lt:tlli:'ri;i""t"t
et al 1ee4), but also
(Einspitttt tt.J,o;n,r,
o.t,"o.l:.:,"*

sleep

sometimes

i'lrg;iT-fi
d'lftiJ;::5ftr*":,'.T:;,l:l*l;
*t'" ost'ved (EinsPieler et
a

<)

Ft

FC
FD
FD
FD
Fs
Fg
F'

PD

F
H
F
F
H
F
H
F
+a
P
F
#4
rt

G4

-a
;1

Fig. 6.14 Individual developmental trajectory of case 20 born at term: apparent life-threatenin-e event
clinical examination revealed no cause. Poor repertoire'but tremulous GMs,
abnormal
fldgety movements. Outcome (14 years): minor neurological dysfunction according to Touwen (1979),
fine manipulative disabilities. poor quality of movements. dyskinesia, poor co-ordition of extremities;
lorv score in the Bruininks oserersky Test (Bruininks 1 97g). Abbrevitions as in Fi e. 6. l.
at 5 rveeks. detailed

present in only one out of 21 infants rvith ALTE. This child developed severe cognitive
and
moderate moto retardation (outcome at 15 yeas of age). Abnormal fidgery movements
were rare but indicative for late fine motor disabilities. Fig. 6. 1:1 illustrates a case
histor1,.

In the conte.rt of research and prevention of sudden infant death the analysis of

respiratory patterns and apnoeas has receiled perhaps undue attention. Holvever. the
relationship betr'veen repeated hypoxic events during infancy and a possible impairment
of neural function is rvell documented (Devkin et al 19&1, Lscher et al 1990, Einspieler

1994, Einspieler er al 19921, Einspiele 1995, Kahn et al 1996). The largest srudy
so far
on this topic reported a high correlation betr.veen prolonged apnoeas and an impairment
of
the qualitl of spontaneous movements, including GMs, in I 14 infants, aged
betrveen 3 and
26 rveeks (Einspieler 1994).

Tem infants lvith repeated and prolonged apnoeas during sleep may have poor reper_
toire GNIs' even incidentally cramped GMs, but seldom temulous GMs during their
first

tlvo months. At 3 to 5 months, fidgety movements can be of abnormal e.xaggerated quality.

Together rvith a poor attention to the environment, some infants may have
a markedlv
reduced movement repertoire and even stereotypies.

Brain malformations
GMs are present but abnormal in infants lvith anencephalv (fronto-nasal encephalocele),

paneto-occipital encephalocele, hydrocephaly, hydranencephaly, polymicrogyria,

holoprosencephaly, hemime-ealoencephaly, macrocephaly and microcephaly (Fenari
etal1997).
Horvever, several other spontaneous movement patterns usuallv present in normal youn_e
infants ae lacking (for the normal repertoire see Chapter 2). Isolated arm
or leg movements
lvere not observed in the infants lvith anencephaly, hydranencephaly.
holoprosencephaly,

macrocephaly and microcephall'. The infant rvith poly'microgyria and the

infant lvith
microcephaly'did not have startles. The infannvith a parieto-occipital encephalocele
never
rotated the head. No relationship rvas obsen'ed betlveen the
defective movemenr patrems
and specific brain malformation (Ferrari et al 1997).

The temporal organisation of the GMs rvas clearly abnormal in the infant with
anencephaly and the infant rvith macrocephall'(pachygyria and
cerebellum hy,poplasia).
The GMs occuned in burst-pause patterns instead of being scattered
over the one-hour
53

recording. Similar findings rvere obseved in sir out of ei-sht anencephalic foetuses (Visser
et al 1985).

Unusual postures were described for the majority of infants with brain malformations
(Ferrari et al L997). None of these cases showed the variability of postures described for
the healthy infant (Cioni et al 1989).

As expected, all infants with distinct brain malformations exhibit abnormal movements.
The study by Fenari et al (1997) failed to demonstrate any connection betrveen the degree
of tissue loss and the degree of GM abnormality expressed by the GM optimality score
(Ferrari et al 1990; see Fig. 3.8). Anencephaly and hydranencephaly rvere the tlvo cases
lvith the most defective brain tissue, yet the GM optimality score lvas not lvorse than in
microcephaly, holoprosencephaly and other brain malformations rvith less defective brain
tissue (Ferrari et al 1997).

ANeNcepnelv, FRoNIo-NASAL ENcepncl-ocet-g

The GM assessment revealed a variety of distinct abnormal GMs during the same recording
(Fig. 6. 15). Myoclonic jerks rvere superimposed on GMs (Ferrari et al 1997).

PnRlsro-occrprrAI- ENCEpneLocrLs
The monotony of the movement sequence lvas rather marked during term age. Fidgety
movements lvere absent, but the motor repertoire consisted of cramped, repetitive, even
synchronised movements of all limbs (Fig. 6.16). There rvere no movements torvards the
midline (Ferrari et al 1997).

CsRor,rosorret- ABNoRMALITv [DEL(4XP

A

SY

5.

)] nNo CoNGENITAL

MME"TRICAL HYDRoCEPHALUS

The GMs of

patient, bornat42 rveeks, rvere of poor repertoire and floppy. At the 43-week

recording a monotonous repetition of exo-rotations of the arms and fragmented limb

AF
CS

H
N
38

3!

Fig.6.15 GMassessmentof case2l bornat33lveekspostmenstrual age.Extensionof braintissueand

cerebrospinal fluid through a defect in the skull base in the region of the cribriform plate and crista galli
(computer tomography at I month); hypoplasia of the parietal bones of the skull, marked cerebrum
hypoplasia, minimal shrinkage of the hemispheres, thinning of the cortex of the cerebellum, which lvas
of normal size. Chaotic, cramped-synchronised and poor repertoire GMs at 39 weeks. Outcome: died at
4 months (Fenari et al 1997). Abbreviations as in Fig. 6.1.

54

Fig' 6'16 Individual developmental trajectory of case 22 born

at 36 rveeks postmenstual
age. Vast
occipital meningo-encephalocele, h1'perintensity of
its nlenchryi p"ft
rmages qutRt
zl
at months)' Poor repertoire Glvls, absence
of figety mou"m"nts. ouicome: lost at tfre
age of i I months
(Ferrari et al 1 997). Abbreviarions as in Fi
s. 6. 1

i;ii;;igiteo

movements lvere obseved' In addition, the infant

had an unusual preference posture rvith
of the neck and retroflexion of the head. The patient
rea at 2 months (Fenari
et a\ 1997.
a scoliosis

HynIaNcEPHALY
Fig' 6' l7 demonstrates the longitudinal inconsistency
of abnormal writhing movements ln
a parient rvith
hydranencephaly.

PoLyMrcRocyRrA AND lvlulrrple X,L+r_ronuerroNs

In addition to pol,micro-eyria the parient (born
at 4r rveeks postmenstrual age) had
a left
eve coloboma and agenesis of the olfactory
bulbs. GMs rvere recorded at 5 lveeks posfterm
age and lvere scored as poor repertoie
GMs due to the repetition of the same sequence. .I-he
patient died at 2 months of age (Ferrar
i et al 1997 t.

Fig' 6.17 Individual

deveropmentar trajectory of case 23 born.at

25 weeks posrmenstrual age.
Hydranencephaly' cerebral hernisp.heres
n""rrf
replaced by cerebrospinal fluid; a
portton of the right fronto-temporal,
minimal
"omply
right andieft o..ipioi
and ceebeltum
are present (MRI at 33 rveeks
Postmenstrual age). Poor repertoire, chaotic and crampeo-synchronised
Glvls' outcome (3 years): macrocephall',
severeiearning disability, spastic tetraplegia.
blindness (Ferrari
et al 1997). Abbreviarions
us in fis. O.i.

l"ill; ;r;;;,;#;,

)-)

AF

ch
PR
H
N
3S

40

Corpus callosum' falx cerebri

Fig. .18 GlvI assessment of case 24 bom at 39 weeks postmenstrual age.
present, a crescent-shaped
not
ventricle
third
thalami
fused
agenesis,
fissure
and interhemispheric
hemispheric white matter
the
of
thinning
marked
holoventricle surrounds fused tialami, pachygyria,
fused by means
(MRI at 2 rveeks); microcephaly, bilateral agenesis of the olfactory bulbs' frontal lobes
hypoplasia of
bilateral
pachygyria,
detectable,
is
of meninges, a shrimp of separation of the hernispheres
(Fenari et al 199'7)'
months
at
8
poor.
died
o.":
Out
bM..
repertoire
tU".
occipital
and
the parieial
Abbreviations as in Fig. 6. I '

HOLOPROSENCEPILALY

lvrist Iotations lvere

Despite a marked monotony of the movement sequence, elegant

lveeks later the poor repertoire

observed in a tefm-age patient with holoprosencephaly. Three

(Fig. 6.18). In addition, frequent asynmetric tonic neck postules, stereofyped

to myoclonic jerks,
pedailing, shortJasting limb movements, small in amplitude and similar
and tremor occurred (Fenari et al 1997).

rvas marked

Hrr,ttrrgceLoENCEPHALY
poor repertoire' The patient
The lvrithing GMs of a patient born at term age lvere scored as
of the cortex' The
had a marked magnification of the right hemisphere rvith thickening
at 2 rveeks)' After a right
right frontal lobe lvas normal (on magnetic resonance imaging
and learning
hemispherectomy at 12 months, the patient developed a left hemiplegia
disability (Ferrari et al 1997).
I\LA,cRocepF{el-Y

repertoile of writhing
GM assessment of a patient lvith macrocephaly revealed a poor
The onset of the
GMs (at 3 lveeks postterm age) with additional tremulous movements.
brisk head rotations were
movements lvas bfisk and synchronised. From time to time

and still tremulous (Fig' 6' 19)'

observed. A rveek later the GMs lvere cramped-synchronised
(Fenari etal 1997)'
movements
limb
rvith
the
The opening of the mouth lvas synchronised

CoNcgNrral MtcnocePrtqlY
(born at 38 lveeks postThe rvrithing GMs of a patient rvith congenital microcephaly
menstrual age) lvere

,.or.d u, poor repertoire. In addition, repetitive rolving

and pedalling

movements,stereorypedadduction-abductionoftheforearms,andabruptandjerkyhead
pattern. The patient develrotations lvere observed. crying did not change the movement
1997)'
oped severe learning disability (Ferrari etal

fo

Fig' 6'19 GM assessment of case 25 bom at 40 rveeks postmenstrual age. occipital

horn of the lateral
ventricles dilatated, corpus callosumtrypoplasia (computer tomography at lv"e...);
4
macrocephaly and
pachygyria' corpus callosum and cerebellum hypoplasia, dilatatediareri
ventricles, elayed myelination.
Poor repertoire and cramped-synchronised GMs. outcome: died at 10
months (Feriari eial 1997).
Abbreviations as in Fig. 6.1.

No infant displayed GMs

similar to those of another infant. With the exception of the

anencephalic patient, the repetition of the same sequence lvithin a
GM or from GM to GM
is the common feature of the brain malformed infant. Hence, the putative
role of the forebrain
structures in modulating the GM quality seems to be confirmed
by the observation in these
infants.
Spina bifida aperta
Recently, the quality of GMs rvas investigated in 20 term nervborns
lvith spina bifida aperta

(Sival et al 2003). GMs rvere normal in eight infants and abnormal

in nine (poor repertoire
GMs in eight and cramped-synchronised GMs in one infant), lvhile
three infants rvere hypokinetic. There rvas a positive correlation betrveen higher thoraco-lumbar
myelomeningocoeles and abnormal GMs. In spina bifida aperta, the spinal
defect (myelomeningocoele)
often coexists lvith cerebral malformations such as Arnold-Chiari
malformation, hydrocephalus, and corpus callosum hypoplasia. No relationship,
holvever, betrveen these brain
malformations and the quality of GMs was found. The authors suggest
that the abnormal
qualitative characteristics of GMs in infants lvith higher thoraco-lumbar
myelomeningocoeles relate to a more functionally impaired condition of the
brain or brainstem.

Rett syndrome
Rett syndrome is due to an X-linked dominant disorder caused
by mutations in a gene
encoding merhyl-cpG-binding prorein 2 (Amir et al 1999).
This protein binds to methy_
lated DNA and may function as a transcriptional repressor
b-v- associating with the DNA
chromatin-remodelling complexes. The resulting syndrome
begins in selmingly normal
6- to lS-month-old infants and causes profound cognitive
impairment. The cognitive impairment occurs without significant neurodegeneration but rather
lvith a reductron in neuronal
stze (Bauman et al 1995), loss of dendritic development (Armstrong
1992, Armstrong et al
1995) and neuropile throughout grey matter areas in
conjunction with a decrease in lvhite

mafter (Akbarian2002).

)/

TABLE 6.1
Developmental course of fidgety movements in Rett syndrome (Einspieler et al 2004)

Quality of fidgetv movements

End of 2nd month

3 to 4 months

5 to 6 months

N=12

N=10

N=11
U

Normal

Jerky, fast and disorganised

Jerky and slow

Absent as an abnormal sign

Not yet or no longer present

An apparently nonnal prenatal and perinatal period followed by an apparently normal

psychomotor development during the first six months of life were considered as criteria for
classical Rett syndrome (Hagberg et al 1983, Trevarthen and Moser 1988, Kerr 1995).
Holvever, several investigators consider it to be a developmental disorder manifesting at or
very soon after birth (Witt-Engerstrm 1987, Naidu et al 1995, Percy 1995).
Recently, movements, posture and behaviour of 22 girls with Rett syndrome during
their first half-year of life rvere carefully assessed from family videos. As rvell as a
number of peculiar signs (e.g. abnormal finger movements. asymmetric eye opening and
closing, bizarre smiling, bursts of abnormal facial expressions), all cases had abnormal
GMs.
Writhing movements rvere of a poor repertoire. Some infants had predominant jerky
and fast movements; others moved in slorv motion and seemed to almost get stuck in their
movement sequence. None of the 12 infants lvho lvere recorded during the fidgety movement period shorved normal fidgety movements (Table 6. 1). In addition, five infants
already shorved their abnormal fidgety movements at the end of their second month. Fidgety
movements had disappeared unusually early - at 4 months - in six other infants.
The fact that none of the Rett cases had normal fidgety movements confirms the finding
that normal fidgety movements are highly predictive for normal development (Prechtl
et al 1997b). The absence of fidgety movements is clearly predictive for the spastic and
dyskinetic forms of cerebral palsy (see Chapter 5). Interestingly enou-9h, those infants with
Rett syndrome rvithout fidgety movements did not develop either hypertonicity or dystonic
features. The abnormal quality of fidgety movements in infants with Rett syndrome is
clearly different from the abnormal fidgety movements observed in infants with brain
lesions, lvhich are exaggerated with regard to their amplitude, speed and jerkiness (see
Chapter 2). The fidgety movements of infants rvith Rett syndrome are jerky and are exhibited
as eithe disorganised or in slorv motion (Einspieler et al 2004).

Intra-uterine growth retardation

Intra-uterine grorvth retardation (IUGR) due to placental dysfunction is a risk factor for
an impaired neurodevelopmental outcome (Allen 1984, Teberg et al 1988). This is the case
particularly in grolvth-retarded foetuses lvhose conditions in utero are so compromised that
they have to be delivered before term (Walther 1988, Sival et al 1992a).

)5

F'

Grorvth reradation is determined mosrl). on the basis *:1i1

*,eight, and so
ILrcR is
considered more or less equar to 'small for gestational a_ee' (scel.'Hc
crireria are used to define sGA. Some neonatologists define sGA as
t,'jl
"
5 (<P5) or 2'3 percentile (<P2'3) on a birth rveight versus
age
curve.
others
-eestational
all infants belorv the 1Oth percentile (<P10) as SGA. Especially if the broader regard
crirerion
is applied, many of theseifants rvould not qualify'as intra-uterine grolvth-retarded
at
all; they just happen to fall into the lorver ran,ee of the normal population

rl:];iiT:i:I

dirt.ib;;;;:

In addition, some infants ae born small because of an (undetected) chromosomal

abnor_
mality or dysmorphic syndrome' Finally, rvithin the group of infants grorvrh-restricted
due to placental dysfunction' the onset and severity of the grolvth retardatlon
add to the

heterogeneity ofthe SGA group (Bos et al 2001).

Generaliy speaking, there is an increased risk for mild neurodevelopmental
abnormalities lvith cognitive disabilities and behavioural problems, more
so than for motor
disturbances (Zubrick et al 2000)' The risk for major neurological
abnormalities in SGA
infants is less clear. Several studies reported a slightly increased incidence
of cerebral
palsy, especially in term
-grorvth-retarded infants (uvebrant and Ha_eberg r992, Topp et al
1996). but also in preterm infants (Hadders-Algra et ar 19gg,
Hagberg erar r996).
In grorvth-retarded foetuses, a reduction in the quantity of
GIVIs is a rather iate sign of
foetal deterioration (Bekedam et ar r995, r9g7, sival et ar r99za),since
a reduction belorv
the lolver limit of normal only occurs in pre-terminal or terminal
foetuses (Sivai et al 1992a,
Ribbert et al 1993). In SGA preterm infants, the rate of occurence
of varrous movemenr
patterns did not differ from that found in lorv-risk prererm infants
(Bos
et al 1997c), r.vith
the exception of the duration of GMs during the first lveek after birth,
lvhich lvas significantl;
shorter in the SGA infants.

Several studies have investigated the qualitl of GMs in IUGR tbetuses

and infants.
Movement qualitl'lvas found to be impaired in IUGR foetuses (Bekedam et
al 19g5. Sir,al
et al 1992b). Similar findings rvere reported in cross-sectional srudies in prelerm
SGA
infants (Geerdink and Hopkins 1993b) and fullterm SGA infants (van Kranen-Mastenbroek
er

al 1994).
The developmental course of the quality of GMs in preterm SGA infants has also

been investigated. A clear relationship exists betrveen specific developmental trajectories

of GM qualitl' and the neurolo-eical outcome at 2 years of age (Bos et al 1997b). Horvever,

the neurological outcome lvas not correlated to brain ultrasound findings. obstetrical
variables indicative of foetal distress, the clegree of grorvth etadation or the
extent of
brain sparin-e.It appears that most IUGR infants have an abnormal quality of GMs during
their preterm period, but the longitudinal approach reveals that the quality of GNIs
normalises in the majority of the infants, aibeit at or afrer term age (Bos et al i997b).
Fig.
6.20 demonstrates GM nomalisation around term age follolved by a normal neurological
outcome.

A large proportion of foetuses and infants have slorv motion GMs (Sival et al 1992b.
Bos et al 1997b).In addition to the poor repertoire the Glvls are predominantl,v
slorv rvith a
small amplitude. They can precede a normalisation of GMs and hence a normal
outcome
(Fi,s. 6.21) or a deterioration of GNls and an impaired ourcome (Fig.6.22),
59

Fig.6.20Individualdevelopmentaltrajectory-ofcase26bomat3l.4lveekspostmenstfualage,birth
rveight 16'7
for birth weight -1 '89; percentage ofbrain
lveighr: 1010 grurn.t ,,unourl "uiurlon ,"or"
the umbilical artery: absent
of
indei
(Cooke et al l9'77);pregnancy-induced hyp:rqT-i.o]!utt"utitity
weight < P3' Brain
placenta: ischaemra 15 pr.cent idltt-tl:l:
diastolic florv (Reuwer et al 1987);
1 (de vries Ls et al
grade
leukomalacia
lsj; p"rlu"nrricular
ultrasound: GMH-IVH gr"" i ryip'.,
1992);durationofflares:threeweeks.PoorrepertoireGMsduringthepretermperiod:normalisation
1997b).bbreviationsasinFig 6'1'
aroundtermage.outcome(lmontrrs):nor*ui 1Bo,etal

Fig.6.2|Individualdevelopmentaltrajectoryofcase2Tbornat32lveekspostmenstrualage,birth
brain lveight: 16'8
ior uirttr weigirtl -1'65; p"t"tntge of
\,veisht: I 1 15 grumr; ,tunourl;;;i"ti";i"*"
et al 1987);
(Reuwer
flow
art# absent distolic
(Coke et at 1977); putsatitii;;;;;';i,h"
< P3' Bratn
weight
"*U'rcar
infarctio'
cent
per
0
ir"nu"mr"
iate foetal heart rate deceleration; placenta:
grade 1 (de vries LS
(Volpe i989); p"riu"*ri"utur teukomalacia
ulrrasound: GMH-IVH grade 1 right
during the preterm
(SL)
GMs
motion
slorv
and
threJweeks. Poor repeftoife
as in
et al 1gg2); duration of flares:
Abbreviations
1997b)'
rnon*,ol n""u1 (Bos et al
period; normaliruuon ur," u!". rr""." tz
Fig.6.1.

Fig6.22lndividualdevelopmentaltrajectoryofcas23bomat2g.4weekspostmenstfualage,birth
brain weighu 16'2
Ulrtt' wi!ii't'-t.gZ,p":t:":+" :l
weight: 840 gru*r, ,,unouri'"uiuiioni"or"-for
enlarged' prenatal
homs
occipital
sruin i'l-t;o,rnd:
(cooke et al 1g7,7);pru."n*, .torio-amnionitis.
O"tt'no fidgety

cramped-synch:l:":

(SL) GMs foffon*JUV

(24 months):
onset. Poor repertoire un *o* *tion
fidgety movemen* ;t 16 rveeks' Outcome
abnormal
and
movements at 13 weeks postierm
Abbreviations as in Fig' 6'1'
ut
tggZ)'
(Bos
p"cl'
neurologically abnormal,

""tii*tion

"t

ChaoticGMsarefrequentlyobservedingrolvth-fetardedinfants(Figs6.23and6.24,
buthavenotbeenreportedingrolvth-retardedfoetuses(Bosetal2001).InfulltermSGA
infants,thequalitativeassessmentofmovementpatternsrevealedT^il:tt*"dincidence
In preterm SGA
Kranen-astenbroek et al 1994).
of jerky and tremulous movements ivan
infants,thepresenceofthisabnormalmovementpattemlvaslelatedtolatefoetalheart-rate
60

decelerations and ischaemic alterations of the placenta (Bos et al 1997b).

This indicates

rhat acute foetal deterioration, superimposed on chronic placental insuffiiency,

might be
responsible for the occurrence of this movement type. Chaotic GMs in SGA

infants are not

related to detectable brain lesions (Bos et al 2001).

It must be noted that cramped-synchronised GMs occur, if at all, postnatally
rather
late in grolvth-retarded infants (Fig.6.22; Bos et al 2001). As demonstrared in rigs
o.zt to
6.24, the quality of fidgety movements, in particular, is predictive for the final outcome.

Interestingly, a large proportion of grorvth-retarded infants who have abnormal

GMs
have normal flndings on brain ultasound scans. This suggests that the chronically reduced
foetal supply of oxygen and nutrients may lead to a longer-lasting but often transienr brain
dysfunction, rvhich is not necessarily caused by haemonhagic or hypoxic-ischaemic lesions
detectable on ultrasound scans (Bos etal 1997b).
A final point deserves mentioning. The qualitative assessment of GMs has proved
lvorth
mainly in relation to the prediction of motor disorders. Future studies will need
its
to elucidate rvhether the quality of GMs is also predictive for the cognitive disabilities and
behavioural problems which are found more often in IUGR infants (Bos et al 2001).

Fig. 6.23 Individual developmental trajectory of case 29 bom at 28.7 weeks postmenstrual aee. birth
weight: 640 grams; standard deviarion score for birth weighr:
-1.97; percenrage of brain weiiint ZZ.l
(Cooke et al 1977); pulsatility index of the umbilical artery: increase
6"utu"i et al 1987); late foetal
heart rate deceleration; placenta: severe ischaemia, retroplacental haematoma, no infarction, weieht
P3-P10. Brain ultrasound: GIvIH-IVH grade 2 right (Volpe 1989); periventricular leukomalacia grad"e I
(de Vries LS et al 1992); duration of flares: four rveeks. Poor repefoire GIVIs follorved
by chaotii GMs,

normalisation at term age. Outcome (24 months): normal (Bos

et

al 1997b). Abbreviations

as

in Fie. 6.1.

i
t

I
I

I
I

I
I
I

I
I

I
1
I

Fig. 6-24 Individual developmental trajectory of case 30 bom at 32.1 lveeks postmenstruat age, birth
rveight: 810 grams; standard deviation score for birth lveight:
-2.65; percentage of brain weight: 21.7
(Cooke et al I 977); pregnancy-induced hypertension; pulsatility index of th" u-ili.ul
artery: increased
(Reurver et al 1987); late foetal heart rate deceleration; placenta: not known.
Brain ultrasound: normal.

Poor repertoire and slorv motion GMs followed by chaotic GMs, abnormal fidgety movements.
Outcome
(2zl months): abnormal neurological findings, poor coordination, habitual
toe wajking (Bos et al 1997b).

Abbreviations as in Fie. 6.

l.
61
E

1
E

Maternal diabetes mellitus

Foetuses of lvomen lvith fype-I diabetes are at increased risk for malformation, macrosomia,

and impaired development of the central nervous system (Jovanovic et al 198i, Laurini
et al 1984, Mulder 1992,Rzzo etal 1994, Persson and Hanson 1996, Nelson et al 2000,
Penney et al 2003).
In a longitudinal study on tlvelve cases, foetal GMs were analysed at trvo-lveekly
intervals from l6 lveeks postmenstrual age onlvards and after birth during the first, second
and third to fourth month (Kainer et al 1997). Foetal hyperinsulinism might cause foetal
hypoxia (MacFarlane and Tsakalakos 1985, Petry etal1994), and correlates with abnormal
GMs, i.e. poor repertoire GMs or abrupt, jerky and fragmented GMs (Kainer et al 1997).
As foetal hyperinsulinism may develop despite satisfactory maternal metabolic control, the
latter is no guarantee against developmental disorders. Abnormal foetal GMs have ahvays
been associated with abnormal postnatal GMs (poor repertoire lvrithing movements and
abnormal fidgety movements) and a reduced Bayley (1969) score at 10 months. On the
other hand, normal foetal GMs may be follorved by abnormal postnatal GMs if difficulties
during delivery lead to neurological dysfunctions (Kainer etal1997).

Early blindness
For a better understanding of the contribution vision makes to the development of other
sensory systems and to movement and posture, lve studied the effects of early blindness
by examining lengthy and repeated video recordings of 14totally blind infants. The infants
lvere born either at term or preterm and sholved no evidence of brain damage (Prechtl et al
2001).

As in sighted infants, the early blind infant shorved complex, fluent and frequently
occurring GMs prior to the third month of age. No differences rvere observed for isolated
arm and leg movements, stretches, yalvns, tunk and head rotations, nor for short phasic
movements such as startles and trvitches (Prechtl et al 2001).
A very striking feature concerned a peculiar type of fidgety movement. In all blind
infants, observed during the relevant age range, fidgety movements lvere grossly disturbed
in a specific lvay. They lvere exaggerated in amplitude and jerky in character and their
presence lasted longer than in sighted infants. In fact, they lvere observed until 8 to 10 months
postterm age (Prechtl et al 2001). Moreover, these movements lvere distinctly different
from the abnormal fidgety movements seen in some brain-damaged infants (see Chapter 2).
In order to investigate if actual visual control is necessary for nornal fidgety movements,
six 3-month-old sighted, alvake infants lvere filmed in the dark with a special light-sensitive
camera. Their fidgety movements did not change in character and continued to look normal.
Experiments to blindfold these infants failed because they immediately protested by
crying, rvhich itself inhibits fidgety movements. Prechtl (1997a) conjectured thatthe period
of normal fidgety movements is necessary to re-calibrate the proprioceptive system (see
also Chapters 4 and 5). The observation of the early blind infants supports this hypothesis.
We speculate that exaggerated fidgety movements may be indicative of an attempt to
compensate for the lack of integration of proprioception and vision (Prechtl et al 2001).

62

QUAI\TITATIVF ASSESSM EI\T iS

AI\ INSF|\SITIVE II\ DIEATOI?
OF IMPAII?ED I|\TEG[?ITY OF TL_IE
I\EI?VOUS SYSTEM

There is a large range of intra-individual and inter-individual variability

in the rate of
movement pattems throughout pregnancy (de vries JIp et al 19g5,
19g7. Roodenburg et al
1991)' The same holds true for healthy preterm and fullterm infants (prechrl
et al 19j9,
Prechtl and Nolte 198r, cioni et ar 19g9, cioni and prechtl i990).
Perhaps biased by the keen interest of obstetricians in the quantity
of foetal movements
as an indicator of foetal lvell-being, it lvas originally erpecied
that a decrease (or even
an tncrease) in the quantity of postnatal motility might act
as a reliable indicator of brain
d1'sfunction. This expectation turned out to be ,vvron-s. The large
scatter in the quantitative

data of spontaneous motility in uncompromised foetuses and

in healthy inlants makes
quantitative assessment an insensitive indicator of compromisin-9
conditions of the newous

system.

Prechtl and Nolte (198'1) compared quantitative data of l:[ lolv-risk

preterm infants
lvith data of 13 infants ofa hi,eh-risk group and failed to find differences.
This rvas coroborated by Ferrai et al ( 1990) r'vho compared the rate of movement
patterns such as startles,
GNIs (Fig. 7.1), isolated arm and leg movements, tlvitches, cloni
and tremulous movements
in l2 matched pairs of preterm infants rvith and lvithout brain lesion. respectively.
An
interesting findin-e was that even the comparison of the occurrence
of tremulous movements
reached onll' borderline significance (p 0.06, Wilcoxon text
for matched pairs: Ferrari
=
et

al

1990..

other authors confirmed the lack of difference in the quantity (frequency

and duration)
of various movement patterns betrveen a high-risk group rvith
brain lesion and subsequent
disabilitl', and a lorv-risk group developing normalll'(Hines et al
19g0, Erkinjuntti lggg).

In grorvth-retarded

preterm infants, the rate of occurrence of various movement

patterns did not differ from that found in lorv-risk prererm
infants (Bos et al 1997c), rvith
the erception ofthe duration ofGNIs during the first lveek
after birth, lvhich rvas significantlv
shorter in the grolvth-retarded infants (see Chapter 6). Hardly
any correlations w,ere found
betlveen the quantity of movement patterns afte birth and obstetrical
variables indicative
of a compromised foetal condition. Only a reduction in foetal
heart ate variatron lvas found
to correlate sli-ehtly lvith an inceased incidence of startles
and t,i,vitches in the f,rst lveek afte
birth (Bos etal1997d.

63

f--'cH;rs

l-:

tO r-Ow RISK

:u:
u)

a
aj

I
I

c)

u
E

-i

t:2
5e
a.\ ai5

al
a

?E

22

I
a

8:,

o!

-O
nR
&B
3s
o
f)

loo

--i-*." ---r..----.

JU

.J

' 32 33 34 35 3O 37 3A 39
'/vee<S

of Conceptional

40

age

Fig' 7.1 Longitudinal comparison of the incidence of GMs (rate per l0 minutes) in
l2 matched pairs

of preterm infants with and without brain lesion, respectively (reprduced with
pe'rmission from Ferrari

etal 1990).

Even in severely brain-malformed foetuses (Visser et al 1985) and infants (Fenari

et al
1997), qualitative changes in spontaneous movements prevailed over quantitative
changes.
As for the quantitative abnormalities of spontaneous movements, in nine infants
with
various

brain malformations, they consisted of the lack of one or more movement pattems (see
Chapter 6)' Holvever, the defective movement pattern, or combination of patterns,
lvas not
related to specific brain abnormality or the severity of tissue loss (Ferrari e t
al 1997).
It is obvious that quantitative changes in motility are unsuitable markers of neurological
dysfunction in foetuses and young infants. This is in striking contrast to the qualitative
aspects of motility which change dramatically in the case of brain damage.

ffi

8
BI-IAII\

LTI_iASOU t\ D

A\] D GEI\

MOVEMENT ASSESSMEI\T

EI-?AL

Brain ultrasound is the most frequently used

imaging technique to detect structural changes
in the nelvborn's brain and has been considered
the best preictor of neurological outcome
(Levene 1990)' Studies on the relationship
betlveen ultrasound findings, developmental

trajectories and neurological outcome revealed

the GM assessment to be superior

to
ultrasound findings (Fenari et al 1990, cioni
et ar r99ia, r997c,prechtr r9g7b,Bos
199g,
Bos et al 1998a, Ferrari etar2002). case
hisrories provided in Chapter 6 (Figs 6.3, 6.5,6.6,

6'8' 6'10, 6'12,6'13,6.20' 6.2r,6.23,6.24) illusrrate

th" ,up"rio, predicrive porver of
longitudinal GM assessment as indicated by
individual developmental trajectories.
The largest longitudinal study so far on GM
assessment lvas carried out on 130 infants.
Their ultrasound findings, ranging from normal
to severelv abnormal. rvere classified into
trvo groups: 70 low-risk and 60 high-risk
cases. Examples of abnormar ultasound
findings
judged to be mild enough to allorv
classification into the lorv-risk group rvere
short-lasting
increased echogenicity or grade I intraventricular
haemorrhug"."uigi-.irk infants were
found to have definite abnormalities of their
brains on ultru.ouni"*amination (periventricular leukomalacia
2 to 4 according to de vries LS et al 1992,
andgrade 2 to
ryad,e
3 plus intra- and periventricurar
haemonhage lccording to volpe 19g9).
The sensitivity
of the GM assessment during the first weeks
of life (94 per cent) and of the assessment

of fidgety movements (95 per cent) rvas higher

than that of brain ultrasound imaging, rvhich
lvas 80 per cent. Specificity for GM assessment
during the fidgety movement period rvas
96 per cent rvhereas for brain ultrasound
it rvas g3 per cent qrrechir et a, r997b).
Similar results lvere reported for 66 preterm and 58
fullterm infants (Cioni et al lgg7a,
1997c)' A recent study on 34 infants with cystic
and 34 infants rvith non-cystic abnormalities of the white matter confirmed the high
predictive polver of GM assessment (Ferrari
et al 2002). The receiver operating characteristic
(Roc) curve analysis rvas used (Metz
1978) to compare the power of brain ultrasound (5
to 7.5 MHz headsiand GM assessment
to predict cerebral palsy (Fig. 8.1). This method
provides a porverful means of assessing
a
test's ability to discriminate betrveen tlvo groups
of pati"ntr, rith th" udvantage that analysis
does not depend on the threshold value
selected (Metz l97g).
The areas under the RoC curve analysis for GM
assessment and ultrasound

scans rvere
quite large (97.4 and 8g.3, respectively), lvhich
shorvs that they are both accurare tests.
A statistically significant difference rvas found, horvever,
betrveen the tlvo methods (p <
0'001)' indicating that the GM assessment is a
better index

to predict neurological outcome

in a group of infants lvho lvere selected
on the basis of abnormal ultrasound findings
(Ferrari

ef al2002).

65

.:
C

q@

0.4

0.4
'I

- 5pecificity

Fig. E.1 The area under the receiver operating characteristic (ROC) curve for quality of GMs and
ultrasound (USOUND) scans in high-risk preterm infants. The ROC curve is generated by plotting the
proportion of true positive results against the proportion of false positive results for each value of a test.
The curve for an arbitrary test (AT) that is expected to have no discriminatory value appears as a diagonal
line, whereas a useful test has an ROC curve that rises rapidly and reaches a plateau (reproduced with
permission from Fenari et al 2002).

In infants rvith

severe brain lesion, the longitudinal assessment of GMs (individual

developmental trajectory) helps to distinguish those infants lvho have a fair prognosis from
those lvho have not. For infants lvith minor ultrasound abnormaiities the GM assessment
is particularly helpful and helps to identify those infants rvho are at risk for developmental
problems and those lvho are not (Prechtl 1997a, Bos 1998). We have to bear in mind that
during the last felv years brain ultrasound equipment and assessment have improved
considerably.
Of course, GM assessment can never replace neuroima-sin-s techniques but it is a
worthwhile method to be used in combination lvith neuroimaging. This has also been illustrated by tlvo studies on GM assessment and neonatal magnetic resonance imaging (Cioni
et al 2000, Guzzetta et al 2003). Another recent study on term infants w,ith hr poxic ischaemic
encephalopathy demonstrated that the combined use of GM assessment and proton magnetic
resonance spectroscopy (1H MRS) increases the prognostic value (Rapisardi et al 2002).

66

I
144

4
4
4
4

4
l

14

14?

4
i

tq
FA
q
i

4
4

of sophisticated neuroimaging techniques has supplemented but

not replaced the neurological examination of the nervborn. The information provided by
this examination is still very important for a rapid diagnosis of a neurological disorder in
a newborn, for deciding on the need for and type of imaging, electrophysiological or other
eraminations to be carried out, for formulating a prognosis and for monitoring, by repeated
checks, the development of the disorder (Cioni et al 1997c).
Since the first description of concepts and criteia for the neuological examination of
nervborns by Andr Thomas and Saint-Anne Dargassies (1952), several protocols have
been published. Holvever, only tlvo comprehensive methods of neonatal neurolo,eical
examination have been standardised and validated, those of Prechtl (1977, Prechtl and
Beintema 1964) for term infants and of Dubolvitz and Duborvitz ( 1981. Duborv itz et al
1999) for both term and preterm infants.
A svstematic comparison of the qualitative assessment of GMs and the traditional
neurological examinatirn in selected groups of preterm and term infants revealed the
superior predictive polver of the assessment of GMs for all age groups, but particularlv at
the younger ages (Cioni et al 1997 a, I 997c, Ferrari et al 2002).
The introduction

)q

I\ E U t?O tOG ICAL EXAIV I\ATI O I\

AN D GEN ETIAL IVOVEM Et\T
ASSESSMENT

The preterm infant

Pretem infants are generally submitted to a neurological examination in the neonatal
period, r,vith the aim of assessing the functional consequences of brain lesion, which may'
have been found by neuroimaging, and to predict long-term neuroiogical outcome. It is
allvays preferable to use a comprehensive, structured and standardised neurological
e.tamination than a random selection of items. Standardised and validated protocols
permit testing the different subsystems of the neonatal nervous system. For the preterm
period the protocol by'Duborvitz and Duborvitz (198i; nerv edition: Dubolvitz et al 1999)
is available. It is difficult to apply' some of the Duborvitz items to fragile preterms (Cioni
et al 1997a) and the predictive values are rather lorv (Dubowitz et ai 1984, lvlolteno et al
1995).

In a comparative study on 66 preterm infants lvith various brain ultrasound findings

(from normal to grade 3 intraventricular haemonhage and periventricular leukomalacia)
the percentage of a-greement (normal versus abnormal) betlveen GM assessment and neuro-

logical examination during the preterm period lvas quite lor,v, namely 73 per cent. As these
67

ffi

s0

EF]

80
7A

ffi

ffi

,4{$.f,,

AN

ffi

50
40

,N

",l
:,v;1

F.,,,r.r-rfi',5 FEffil

W
prternase lermee

t"Hinr,:*'

"::i,yJ*'

t"::,u*T#n'

Fig. 9.1 Percentage of agreemenl between GM assessment and neurological examinatron at preterm age
according to Dubowitz and Duborvitz (1981), at term age according to Prechtl (1977), af tle postterm
periodaccordingtoAmiel-TisonandGrenier(1983)andTouwen(19'76),reportedbyCioni
etatqlgna).

infants lvere repeatedly examined, the percentage of agreement constantly increased,

reaching 92.6per cent at the 4- to s-month-examination (Fig. 9.1). overall agreemenr rvas
80 per cent (Cioni et al 1997a).
The sensitivity of the GM assessmenr is very high at all ages (Fig. 9.2), but the specificity

is low during the preterm, term and early postterm period (Fig. 9.3). This is due to
a consistent number of infants with abnormal GMs lvho normalise during the fidgety
movement period and have a normal outcome (see also Chapter 5). Thus, specificity only
becomes high at 3 to 4 months.
The sensitivity of the neurological examination is quite lolv at preterm and term age,
because of infants with apparently normal findings during their neurological examination

rvho develop cerebral palsy (Fig. 9.2). ln the first postnatal lveeks, physical conditions

100

i.t
,a-i

90
5U

;n*

ii:

ffi

ffi
ffi

70

E)

'f,#

ffi

;,:

:1,

tr

40
9rflgm

ege

teimge

iffi

and ?nnrhs 3 and 4

po5[em

mnths

pctilem

and 6 rcntis

posferm

tr GM Assessment tr Neurological Examination

Fig. 9.2 Sensitivity (in 7o) of GM assessment and neurological examination at pretenn age according to
Dubowitz and Dubowitz (1981), at term age according to Prechtl (1977), at the postterm period according
to Amiel-Tison and Grenier ( 1983) and Touwen ( 1976), rvith respect to an abnormal neurological ourcom

at 2 years (Cioni er

al

1997a1.

68

100

90
80
70
60
RN

40
praterm ag

term

age

'l and 2 mntns 3 and 4

pogIem

tl

GM

mnhs

5 and 5

Pstlerm

mtnlhs

DsEeam

Assessment tr Neurological Examination

Fig. 9.3 Specificity (in %) of GM assessment and neurological examination at preterm age according to
Dubowitz and Dubowitz (1981), atterm age according to Prechtl (1977),afthepostterm period according
to Amiel-Tison and Grenier (1983) and Touwen (1976), with respect to a normal neurological outcome
at 2 years (Cioni et al 1 997a).

(e.g. anaemia, jaundice, apnoeas, cardiac instability) might account for poor responses at
the neurological examination and its failure in terms of long-term prediction of disabilities.
At term, some infants lvho later develop spastic diplegia sholv a normal neurological
examination. As mentioned by Dubowitz ( 1988), this might be due to transient normalisation
of the muscle tonus lvhile changing from preterm hypotonia to postterm hypertonia. The
specificity for the neurological examination is low until 4 months (Fig. 9.3..
The very high sensitivity for the GM assessment right from preterm age onrvards is
mainly due to cramped-synchronised GMs and their high predictive value for cerebral palsy
(Ferrari et al 1990, 2002; see also Chapter 5). A recent comparison betlveen GM assessment
and neurological examination of 84 preterm infants replicated and confirmed the results
provided in Figs 9.2 and 9.3 (Fenari etal2002).
In addition, a four-centre study on preterm infants with unilateral intraparenchymal
echodensity replicated also the superior predictive porver oflongitudinal GM assessment.
Particularly at preterm and term age, neurological examination had a higher numbe of
false-negatives and false-positives for the neurological outcome than the GM assessment.
Moreover, the three cases rvith unilateral intraparenchymal echodensity who did not develop
hemiplegia had normal fidgety movements, although one of them had abnormal findings at
the neurological examination, i.e. hypertonia and asymmetry (Cioni et al 2000).
The authors of the above-mentioned studies recommended caution in the comparison
of GM assessment and neurological examination. The units involved in the studies used
different protocols for the neurological examination, namely those adopted in their daily
practice. The GM observation, holveve, had the advantage of being carried out subsequently
from video recordings and rvas certainlv more consistent.

69

The fullterm infant

in fullterm infants
A first comparison between GM assessment and neurological examination
value of
prognostic
higher
a
slightly
rvith hypoxic-ischaemic encephalopathy indicated
at about
examination
GM assessment in the first trvo lveeks postterm and of neurological
5 to 6 months (Prechtl et al 1993)'
(Cioni et al 1997c)
The first systematic comparison rvas carried out on 58 infants
hypoxic-ischaemic
representing unevenfful obstetrical and neonatal histories as well as

system (Levene et al
encephalopathy of various degrees according to a three-point grading
1976' Prechtl 1977,
(Touwen
ages
various
1982). The neurological examination at the
than did the GM
findings
abnormal
Amiel-Tison and Grenier 1983) resulted in more
similar to that
thus
and
per
cent
assessment. The overall percentage of agreement lvas 81

in preterm infants (Cioni et al 1997a; see Fig' 9'1)'

(Table 9'1)'
GM assessment and neurological examination had good sensitivity values
for both techniques at
slightly better for the former at all age periods. Specificity rvas lorv
neurological abnorterm age, because some subjects lvith poor repertoire GMs or mild
specificity for the
the
postterm
months
2
At
malities at that age lvere normal at} yeafs.
(Table 9' l)'
examination
the
neurological
GM assessment lvas good and already superior to
earlier by
assessed
be
might
According to these data, normalisation of transient disorders
GM observation (Fig. 9.4).
was reported
A lolver agreement between GM assessment and neurological examination
in that study lvas
by Hadders-Algra et al (lgg7). Horvever, the number of cases included
was made for
quite small (16 cases), no distinction betlveen term and preterm infants
lvas applied'
abnormalities
GM
of
the comparison, and a more eiaborate classification
10)'
distinguishing more different categories (see Chapter
in fullterm
According to these findings, the prognostic value of the GM assessment
limitations
are
there
infants also is superior to the neurological examination. Holvever,
encephto the application of GM assessment. In infants with severe hypoxic-ischaemic
techniques,
alopathy, in their first hours after birth neuroimaging, electrophysiological

TABLE 9.1

(Touwen 1976'
Predictive values of GM assessment and neurological exmination
prechtl 1977, Amiel-Tison and Grenier 1983) with respect to the neurological outcome
at 2 years in 58 term-born infants (Cioni et al 1997c)
SpecificitY

Sensitivity

examination

GNI assessment Neurological

examination

947a

88Vo

591o

59Vo

947o

88Vo

86Va

68Vo

94%

89Vo

83Vo

I J-/O

GMassessment Neurological

Writhing

Term age

movements land2months
Fidgety

3 and 4 months

movements

70

Fig 9.4 Individual developmental trajectory of

case 31 born at 39 weeks postmenstrual age. Glvl

assessment and neurological examination (Toulven 1976, Prechtl 1977, Amiel-Tison and Grenier 1983).
Brain ultrasound: periventricular leukomalacia grade2, bright thalami. GM assessment: poor repertoire

followed by normal fidgety movements. Neurological examination: abnormal findings until 12 weeks
postterm. Outcome (24 months): normal (Cioni et al 1997c).
F-, absence of fidgety movements; AF, abnormal fidgety movements; CS, cramped-synchronised GMs; Ch, chaotic
GMs; PR, poor repertoire GMs; H, hypokinesis; N, normal GMs; wk, weeks. The age period where fidgety movements
are obligatory is marked in grey.

and some subtests of traditional clinical assessment have a prominent role in detecting
the severity of brain impairment and indicating the prognosis (Eken et al 1995, Mercuri and
Dubolvitz 1996). Moreover, traditional neurological assessment provides a more comprehensive picture of the various neural subsystems, some of which (e.g. the oculo-motor
system or peripheral nerves) cannot be tested by GM observation.
GM assessment clearly should complement but not replace the neurological examination. Both have different properties and diagnostic tasks (Prechtl I997a).

'71

-1-iaaj-a---'-t--11.,--:=_z-_:;j_)_

. :=:::r=..

"

-^=-

IO
V/F]AT OTHET? IVETF-]ODS OF

GENE[?AL MOVEMENT
ASSESSMEI\T EXIST?

There are a number of reports lvhich are based on different criteria of qualitative assessment

of early spontaneous motility.

Touwen ( 1990) did not focus on

particular movement pattern but classified the quality

'of movements' according to three paired categories: patterned versus unpatterned

and

isolated; smooth versusjerky; and variable versus stereotyped or monotonous.

With his classification scheme Tourven observed 47 preterm infants betrveen 33 and 36
lveeks postmenstrual age. Motility is classified as 'patterned' lvhen the movement patterns
are consistently composite and recognisable. The movements involve either the whole
body or only sin-ele parts, such as an affn or a leg. They must consist of more than one
component; a single flexion of the arm is not considered to be a pattern but a flexionextension movement is. 'Isolated movements' are limited to single joints and consist of,
for example, just an extension of the arm not follolved by a flexion. If no consistent pattern
can be recognised, motility is termed'chaotic'or'erratic'; this, horvever, occurs rarely
(Tourven 1990).
Movements are termed 'smooth' when they are uninterrupted, continuous and fluent

'lvith gradual accelerations and decelerations' similar to holv Prechtl and co-lvorkers
described normal GMs (Prechtl 1990). Movements termed 'jerky' are abrupt, oscillating or

tremulous, lvith an interrupted, broken course and sudden accelerations and decelerations

(Touwen 1990).

'Variable' movements denote changes in speed, amplitude and direction, as lvell as

the presence of various patterns and postures. It implies a repertoire of movements, but
also variations in the repertoire. 'Monotonous' motility is characterised by invariability
in type, direction, speed and often amplitude of movements. There is a lack of variation in
patterns and infants may persist in one - often rather poor - pattern for long periods.
Persistent asymmetries or preferences in motility or posture are also considered to be
stereotyped (Touwen 1990).
These three paired categories are summarised in a variable/stereotyped ratio, lvhich
could vary from 3/0 to 0/3. A high ratio correlates lvith a normal outcome lvhereas a lolv
ratio is not predictive for the outcome (Toulven 1990). Data on interscorer agreement are
not available.

Van Kranen-Mastenbroek and co-rvorkers used general movements for their qualitative
assessment but employed a different categorisation of normal and abnormal quality. The

main difference lies in the attention to too

many details instead of focr
global Gestalt judgement. The latter is
only used as the rast irem
pltjlJop"l'Ii*t T":
lrems are: onset of movement, variability
"rr.
in speed,.overan ,p".a,
,f"Jo
of arms compared
to legs, force against gravity, variabiliry
in amptituoe, ou..uti u.nptiiu-de, amplitude
of anrs
compared to legs, fluency, variability
in movement pattern, variability in
am patterns,
variability in leg patterns, fine distal
movements, and end of movement (van
Kranen_
Mastenbroek et aI 1992,1994). The agreement
rates of four observers scoring
50
neonates
ranged from kappa 0'36 to 0.84, and
r'vere best for the global judgernent
=
(see aiso chapter

5) and below 0.40 for 'amplitude', .variabirity

in movementsi and .variability in
movements' (van Kranen_Mastenbroek
et

at

1992).

reg

GM quality rypes I to v are distinguished.

Type I GMs are similar to the normal
GMs
described by prechtl (1990). Type II -GM,
u." fasr movements with an abrupr and jerky
appearance. They are variable in speed
and amplitude. Type III GMs ur"
uu.upt and jerky,
have lost their variability and complexity
and give a stereotyped impression.
The speed is
high and the amplitude is large. Type
IVGMs are fluent wi'slow ,i""0, uo, stereoryped.
Type v GMs are tremurous, sometimes
flapping, with a stereotyped character (van
Kranen_
Mastenbroek et al 1994).
Predictive values are based on 30 neonates
and on an outcome measurement

at 9
months indicating relationships betlveen
the GM assessment and the 9-month
investigation
(van Kranen-Mastenbroek et al
1994).
Hadders-Argra and co-rvorkers introduced

a nelv terminorogy and a considerably

enlarged caregorisation of the existing
types of GM abnormalities, baJd on
EMG recordings
of six term-born and ten preterm-born infants.
As weil as normal GMs, which are defined
prechtl's
according

to

definition (prechtr 1990, prechtl et al 1997a),adders-Algra

et al
(1997) distinguish berween 'mildly
abnormar GMs, and .definitely aunormat
cl.ls,.
Mildlyabnormal GMs are spritinto'fragmented,and.tense'GMs. .Fragmented
GMs,
are moderately complex and moderately
variable with ajerky and broken appearance.
They
may give the impression of a reduced
capacity to modulate movement speed
and
force.
From 3 months onlvads a fragmented
io.--of fidgety movements can be observed.
Fragmented fidgety movements lack
the elegance of normal fidgety movements
and
are usually accompanied by a large
amount of very rapid arm movements,
so_ca'ed .slvats,
(Hadders-Algra and prechtr rggz),
and kicking leg movements. .Tense
GMs, are also
moderately complex and moderately variable
GMs rvith a rather strrupp.*un"e. The
onset
can be abrupt, but the ensuing movemenrs
are slow. The tense charu"i", i, more
strikingly
present in the rolver harf than in the
upper harf of the body. A common
observation is
stifflegs sticking up in extension (Haddeis_Algraetal
I9g7).
Definitely abnormar GMs are split into foui
categories. ,Torpid GMs, consist of slorv_
motion movements, which in generar have
a small ampritude. The movements give
the
impression that the drive to move is depressed.
During torpid GMs rotations superimposed
on flexion and extension movements can
occasionally be observed. These movements
are
only present until 2 months postterm age. 'Monotonous-abrupt
GMs, are predominated by
abrupt and fast movements. In generar,
the movements of the rimbs have a large
amplitude.
There is a characteristic repetition of
similar abrupt and fast movements. They
often elicit
/J

crying. 'Monotonous-cramped GMs' are monotonously stiff, rigid and very tense. They
have an abrupt and synchronous onset of movement activity in all limbs and are obviously

synonymous lvith the cramped-synchronised GMs of Prechtl's method. 'Monotonous GMs'

are characterised by a complete lack of complexity and total absence of variation, but do
not have an abrupt or cramped character (Hadders-Algra et al 1997)"
By and large, the category of poor repertoire GMs of Prechtl's method is divided into
four categories, namely fragmented, tense, torpid and monotonous GMs' With the exception
of 'torpid GMs' all abnormal patterns can be observed from preterm age onlvards including
the fidgety movement period. Thus, Hadders-Algra and co-lvorkers do not use any more the
categorisation into abnormal fidgety movements or the highly predictive absence of fidgety
movements. In addition, the terminology is interpretative (e.g. 'mildly abnormal', 'definitely

abnormal') instead of descriptive.

Interscorer agreement ranged from kappa values of 0.53 up to 1.00. Validity data are
provided for 16 children, tlvo of lvhom lvere classified as normal at around 19 months.
Kakebeeke and co-lvorkers used a ten-point scale based on the assessment of fluency,
spatio-temporal variability and sequencing of GMs. Fluency and variabiliry are separately
assessed

in arms and legs. The scoring system lvas applied in 39 preterm infants

and

20 fullterm infants during their preterm and term period. Interscorer agreement was betlveen
56 per cent, for sequencin g, and 76 per cent, for leg variabiiity (Kakebeeke et aI 1997 '
1998). No data on the predictive values are given.
The scoring of the qualiry of spontaneous movements is also included in the neurological
assessment of the preterm and fullterm nelvbom infant by Duborvitz et al (1999). Fluent
and alternating movements of arms and legs with a good variability are classed as optimal.

Stretches alternating tvith fluent and smooth movements are classed as borderline, lvhereas
only stretches, monotonous movements and cramped-synchronised movements afe
classed as suboptimal.

'74

EPILOGUE

This book is an introduction to Prechtl's method on GM assessment. Training is needed

for a proper application of this objective, reliable and valid method. In order to provide
standardised training courses the General Movement Trust rvas founded in 1997. Heinz
prechtl (president of the Trust), Arend Bos, Christa Einspieler, Giovanni Cioni, Fabrizio
Ferrari, Paola Paolicelli and Federica Roversi are licensed tutors for GM Trust training
courses. These courses last four to five days and are aimed at physicians, physiotherapists
and other professionals working in the field of infant neurology. They are regularly provided
in English, German and Italian at a basic and advanced level. More than one thousand
doctors and therapists have been trained around the world. The GM assessment is nolv
widely employed in clinical routine. The high efficacy ofthese training courses is described

in Chapter 6.
In addition to the DVD attached to this book, there is

demonstration video available

(prechtl 1997a).Thevideo is published in English (contact: Dr ChristaEinspieler, Fax: +43
316 380 9630; e-mail: christa.einspieler@meduni-graz.at),Italian (contact Editrice Speciale
a

Riabilitazione s.r.l.. Fax: +39 02 541162T/:e-mail: edspriab@tin.it), and Japanese (contact:

Igakueizou Company, Fax: +81 3 3303 1434 http:/hvrvrv.igakueizou.co jp; for a Japanese
revierv see Yuge et al 2001 and Tsubokura2}}2).

/)

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*it p'""tnoiJ'ir*

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' p"""*n

'

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3
P e d iat ic s
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"

78

*t4
l)
F)
J4

J)
F)
J4)

t4

la

n
r)
n
lE)

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84

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and its sate dependency
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_Neuropcidiatrie r,1lq.

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ar routrne medical examination
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BMc,
subsequent mental healrh

proble.. i"

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studv on potenriar earry predi*ive

cognitive and ringuistic reatures

orinranrs arter earry

M, suzuki J. (200r) Assessment of general

movement

itti*u.

o To Hattatsu 33: 246_252.

silbum sn, o""i.,
Fetal growth and
+ to t: y"u.r. Dev Mea ch,ii
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II\DEX

Note: page numbers in ifallcs refer to figures and

tables. General movments are referred to as GMs

prognosis 35-45, 66
quantitative abnormalities in spontaneous
movements 63-64

in subentries

unilateral 43,18-50
venous infaction 43, 48-50
brain dysfunction, crying 22
brain malformations 53-57

3-D-motion analysis 13, 14

airway protection reflexes 9
amniotic fluid regulation 9
anencephaly 16, 53-51, 57
anticonvulsants in pregnancy 30
antidromic discharge 6
antigravity movements 1 1
absence in cerebral palsy prediction 44
apnoea, infantile 44, 52-53
apparent life-threatening event (ALTE) 52
arm
abnormal movements 43
circular movement 43
fluent altemating movements 74
isolated foetal movement 8
saccadic movements 15
symmetrical movements 52
rviggling-oscillating movements 1 5

brain ultrasound examination x, 6l-66

brainstem preparations 6
breathing movements 9
bronchopulmonary dysplasia 50, 52
Bruininks Oseretsky Test scores 44,5J
Brunet-Lezine Developmental Quotient 30,
48
central pattern generator (CPG)

cerebral palsy
cramped-synchronised GM predictive value i7,

40,4142,4849,51,69
diplegia 4243,48
dyskinetic 43-44
fi dgety movement abnormality/absence I 8, 37,
39,40-43, 48-5 I
hemiplegia early signs 43,49-50
intra-uterine grolvth retardation 59
neurological examination sensitivity 68-69
prediction 38-44, 66

assessment tape 2 I

attention deficit hyperactivity disorder (ADHD) 44

automatism, central sd central pattern generator
(CPG)
axial rolling 15
barbiturates 30
Bayley score 62
behavioural instability period in neonates 22
behavioural problems, intra-uterine grolvth
retardation 59,61
behavioural state, general movements 20-22
blindness, early 45,62
brain damage/lesions
behavioural states for general movement
recording 2 I
GIV assessment 16, 46-52. 6U6 I, 67 49, 7 V7
neurological examination 67-69, 70-:7 1

l-6

GMs 16-17
cerebral infarction 43, E-50,

spastic 40-42
tetraplegia 42, 48,
choreo-athetosis 43

chromosomal abnormalities 54-55

chronic lung disease 50-52
cognitive impairment
intra-uterine grorvth retardation 59, 61
Rett syndrome 57
Cohen's kappa 35
continuity, prenatal to postnatal x, 6-1 1
co-ordination problems 44, 47, 53,6(Ml
corpus callosum hypoplasia 57

86

cortico-spinal fibres
disruption l6-17
foetal occurrence l7
coughing 9
cramped-synchronised GMs l7, 18, 22
cerebral palsy prediction 40, 4142,43,

assessment sensitiviry 65
biological function 45
blindness 62
caregiver presence 34

concurrent movement patterns 1 i-16

continual 13,45
distal 1,{
fragmented 73
generation 16
importance 36,37 , 38,39
interference avoidance 3z{
intermittent 13,45
inha-uterine grorvth retardation 0, 61
matemal diabetes mellitus 62
minor neurological deficit prediction 44,45
neurological outcome 37, 39
normal 12-16
intraparenchymal echodensity 69
likelihood ratios 39
predictive for normal developmenf 38,40, J
v^lidity 42, 47-5 I , 6U6I
normalisation before 37 , 39
occurrence l2
phasic bursts 12
proprioceptive stimulation 34, 62

4849,5I
fidgety movement absence 41-42
hemiplegia prediction 48-49

infantile apnoea 52-53

intra-uterine growfh retardation 61
likelihood ratios 39
macrocephaly 56
predictive value 69
segmental movements 42-43
seizue distinction 32-33
spastic diplegia prediction 42-43
tetraplegia predi ction 42
crying 9
brain dysfunction 22
recording discontinuation 2 1
de-cerebrated animal studies 2
developmental neurology 1-4
developmental retardation I
fi dgety movement abnormality/absence 37,

proximal 14

39,40

recording 25
sensory stimulation effects 33-34
sound lack of effect 3zl
sporadic 14
temporal organisation 13-14
fingers
abnormal movements t3
isolated movements l7
mutual manipulation l5

dexamethasone 3 1, 52
diabetes mellitus, maternal 62
diagnostic procedures, age-adequate 2
digital camera 19

disobedient behaviour 44
drolvsiness, recording discontinuation 2 1
drugs, general movement quality effects 30-3 1
Dubowitz neurological examination 3, 49, 67-69
ductus arteriosus, closure of patent 30
dummy 21

spreadi ng -13

flares 46,47
foetal movement 6-10
early 8

EMG 12, 1J
epilepsy 32
eye coloboma 55
eye movements, foetal 9

nrsr /
head bending 7
late 8

fiddling15,16,44

local isolated
pattems 3, 9

fidgety movements 11, 12-15, 16, 24, 26, 27,

phasic 8

position changes in utero 8

repertoire 9
tonic 8

abnormal 17,22,37, 47, 5I, 53, 6U6I

blind infants 62
fine motor disability prediction 53
likelihood ratios 39
Rett syndrome 58
absence 18, 22, 25, 3'7, 48-51, 55, 58
cerebral palsy prediction 40-42, 44
hemiple gia prediction 49, 50
likelihood ratios 39

foetus

adaptation 1-2
deterioration 59, 6 1
GMs 7, 9-10, 11
maternal diabetes mellirus 62
occurrence 7, 8
grolvth retarded 59
ontogenic process direction 8

validity 42

87

interference rvith qualiry 29-3zl

interscorer agreemer xi, 22, 35, 3'7
monotonous 17,74
monotonous-abruPt 73
monotonous-cramPed 74
nervous system impairment l6-18
optimaliry scores, age-specifrc 25' 26'

rat ventral root activity 6

ultrasound observations x, 7, 8
foot-foot contact, lack 43-44
forebrain, quality modulation of GMs 57
fronto-nasal encePhal ocele 53, 54
fussing, recording discontinuation 21

assessment

ons

semi-quantifi cation 25, 26'

recording
duration 2 1
during sleep 21,52
procedure 20-21
sequential 21
technique 19-22
sequence 25
slorv motion 59, 0-.f
suboptimal T4

46-62

Duborvitz terminologY 74
equipment 19-20
Hadders-Al gra terminolo gy 4;1., 73-1 4
hypoxic-ischaemic encephalopathy 66' 7 0-'7 I
Kakebeeke terminologY 74
neurological outcome prediction 65
periventricular leukomalacia 16, 67 -69
predictive porver 67
sensitivity 3, 3'7 , 65,66,68,70
specificity 37, 38, 65-66,69-70
Touwen terminologY 72
training 35, 37,75
validity 37, 38, 39
Van Kanen-Mastenbroek terminology

fluent 10,74
foetal 9, 10, I

matemal diabetes mellitus 62

occurrence 7, 8
fragmented 73
generation 15-16
individual developmental trajectories
intensive care conditions 29
interference avoidance 22

23

'

27

-28

tense 73
torpid 73

tremulous 52
s ee als o cramped-synchronised GMs;
poor repertoire GMs; visual Gestalt
percePtion
Gestalt perception se visual Gestalt Perception
Griffiths scores 4'1,48, 5-1
growth retardation see intra-uterine growth
retardation
head

banging 52
foetal movements 9
retroflexion in hYdrocePhalus 55

IL-IJ

behavioural state 20-2 I

blindness 62
borderline 74
brain malformations 53-57
central pattem generator 16
cnaottc t /, .a
intra-uterine growth retardation 60
correctjudgement 37
drug effects on quality 30-3 I
duration in growth-retarded preterm infants 63
environmental interference avoidance 23

-28'

qualiry/qualitative assessment x-xi

1-2,19-28

clinical applicati

27

30
preterm 10, l1
likelihood ratios 39
quality types I to V 73

general movements (GMs) x, 10-18

abnormal 16-18,22,27
assessment sPecifrcitY 37, 3 9, 7 0
defrr.\te 73-:74
hemiplegia prediction 49, 50
hypoxic-ischaemic encephalopathy 50, 51
intracranial haemonhage 47, 48
maternal diabetes mellitus 62
mildly 44,73
prognostic signifi cance 37-45
seizure distinction 3 1-33
amplitude 25

rotation 9,56
sidelvard bending in foetus 7
53, 56

hemimegaloencePhalY

hemiplegia
early signs 43
unilateral lesions 48-50
hccup 9,22
holoprosencephalY 53, 54' 56
hydranencephalY 53. 5-1. 55
hydrocephalus
congenital asYmmetrical 53, 54-55
spina bifida coexistence 57
hyperinsulinism, foetal 62
hypenonia 3. 47.45.69.7 |
hypokinesis 24, 50, 5 I
hypotonia 3, 69,71

hypoxia

24' 25

corticosteroid theraPY before 52

foetal 62

88

hypoxic-ischaemic encephalopathy 32
prognosis 66

movement patterns
abnormal in brain malformation 53_57
central origin 5_6
changes ar third month of life l,
l0
continuity from prenatal to postnatal
life 6_10
foerus 3, 6-10
grotvth-retarded preterm infants

terminfants 50,Si,iO
individual developmental rrajectory
4

t42,

47_5

I,

53, 5 5,

indomethacin 30

23, 24,

g,

6U6l

infantile chorea 52

monotonous 72
pregnancy 63
rhythmical 5

seizures 32-33

small-for-gestational_age (SGA) 5g_6 1

see also neonates; preterm infants; term
infants
.
infections, severe 3 I
intensive care conditions 29
intentional movements 10
interobserver/interscorer agreem ent xi,
ZZ, 3 5, 37
intracranial haemonhage 16, 47, 4g
intraparenchymal echodensiry 69
intra-uterine grorvth retardarion (IUGR) 5&61,
63
intraventricular h aemonhage 67 _69

lamprey, ventral root activitv 6

l"g

fluent alternating movements 74

foetal movements
central pattem generator 16
isolated 8, 9
kicking movements 73
IIIT IJ
stiff in extension 73
likelihood ratios (LR) 39

lung
chronic disease 50, 52
ventilation 9

5s_56,66

sponfaneous in prenatal development

x
sponraneous in preterm infants x

muscle power development

myelomeningocoele 57

myoclonic encephalopathy 33
neck
asymmetric tonic response 44
scoliosis 55
tonic postures 56
neonaral intensive care unit (MCU) 29
nonates

adaptation 1
behavioural instability period 22
hindlimb locomotion in rat 6
resprratoryJike rhythm generation in at
6
neural function maturation 3
neural transformation, major 1, lZ_I3, 45
neurodevelopmental abnormalities in IUGR
5g, 59
neuroimaging techniques 65_66
neurological defi cits, mild
fidgefy movement abnormality/absence 44,
45
prediction 44
neurological dysfunction
delivery diffi culties 62
fidgery movement abnormality/absence 37,
39
general movement assessment 29
neurological examination ix, 67_7 I

kangaroo care 29
kappa, Cohen's 35

macrocephaly 53, 56,57

macrosomia 62
magnetic resonance imaging

63

jerky 7,57-58

infants
adaptarion 1
clothing for recording procedure 20
cramped-synchronised GMs 32_33

classic

ix

preterm infants 67_69

sensitiviry 68-69
standardised method ix
term infants 70-71
neurological outcome predicti on 44, 65
neurons, bistable 6

MRI) 43,4S, j1,

malformarions, brain 53-57

manipulation 15,44
maternal diabetes mellitus 62
membrane potential oscillations 6
microcephaly, congenital 53, 54, 56
midline movement, lack 43-44
minor neurological dysfunction 44
minor 22-23
Nforo response 9
West syndrome 33
motility, endogenously generated 5_6

Obtahara syndrome 33

olfactory bulb agenesis 55

ontogenic adaptation l_2

optimality score 25-26, 2g

parieto-occipital encephalocele 53, 54,
55
panerning, foetal movement 3. 9
periventricular haemorrhagic infarction 32
ultrasound examination 65

89

63-64
quantity, movement xi, 59'

16'32' 46' 47
Deriventricular leukomalacia
6'7-69
assessment
GM
i'eurol o gical examination -67-69
ultrasound examination b5
echodensities 46'
p.riu.noi"utu' nuhite matter

rat studies 6
reaching 15

."."i".i "p.*,i"g characteristic

anatYsis 65' 6

47
PET

reflexes xi

studies 2

phasic movement 8

oolvmicrogYria 53,55

42'
17' 22' 31-32 ' 3q'

il.i';;;;;:;;cMs

47-st'

53,60-61

40

cerebral PalsY Prediction

coqnitive imPairment 41
43-4-l
dvikinetic cerebral PalsY

seizures 3 l-33

GNfs
distinction from cramped-synchronised
32-33
neonatal
after
Period

growth retardation 59

likelihood ratios 39

recurrence risk 32

62

maternal diabetes mellitus

motor imPairment 4l
postnatal movement 9-10
posture 1

stereotYPY 32,33
subtle J r-J

tonic 32

70
sensitivity 36,3'7' 65-66' 68'

hYdrocePhalus 55

sensory stimulation 2
33-34
nAgerY movements effects
skin{o-skin holding 29

54
-r'rt brain malformation

"'^"t""ioptimaliry

concePt 25

Prechtl's

Dregnancy

sleeP
aPnoea during 53
general movements 52
fo, gestational age (SGA) 59
movements' Postnatal 9

inticonvulsants 30
diabetes 62

movement quantity 63

,.ill

presYnaptic inhibition 6

ir.i*'gtnttut

smiling

movement 1o' / /

Preterm infants

u"togr"ms of unstimulated

sneezing 9

42-43
,purti" iPt"gi", earlY signs
69' 70
specincitY :2, :A ,65-66'

asseisment sensitivity 37' -i8

i.on"ttoputrnonury

soina bifida aPerta : I

2' 6
soinal cord PreParations

dysplasia-5^0

GMs 32

+u
"ru.Pta-tYn"tt'onised
early consistent

iniviA"ati'ea evelopmental

u"iuitY' fidgery movements34

5-18
.io.trun"out movements xi' 3'

;;;;il

care 3zl

oualirative assessment
infants 64

startles 7, 9,29'63
stePPing, newbom 8
gations' classic 3
stimulus-response lnvesti

Poor

iecording Procedure 20
skin-to-skin holding 29
31
,fuggittt general morements
59
age
gestational
sm for
x
sPontaneous movement Patterns
subtle seizures 3 1-32
tonic seizurss 32
unilateral brain lesions 49-50

""l,li;J"il*

stretches 8,

protonmagnetic

9,74

sucking movements 9
sudden infant death 53
9
slvallolving movements' foetal
slvats 73

swiPing movements 15
sYstemic disease 31

system

:'*';-'"ffi #:n"

Kl

in brain-damaged
"""ii*ti"t i^ormalities

kangaroo care 29
67-69
neuiological examination
2'7
25'
scores
oDtimality
rePertoire GMs 3l-32

orimate I
oroprioceptive

scoliosis 55
49' 50
segmental movements 42-43'

56
hemime galoencePhatY

i*u-u,Jtin"

retiabilitY 35,37
respiratory CPG 6
Ren sYndrome 57-58

rooting

aonoea during sleeP 53

'

(ROC) curve

o*"'

term infants

4;
,2.

".

"

?ll*.:.'JJ:$L;

"^
resonance'nJJ'1"''lioio^'l
:L:ffi:ilX'fftl"lion70-71

66

90

optimaliry scores 25, 26, 27

poor repertoire general movements
subtle seizures 3 1-32
tonic seizures 32
unilateral brain lesions 49_50
test-retest eliability 3 5, 37
tetraplegia, early signs 42_43
tonic movement 8

video analysis, environmental interference

3 1_32

avoidance 23

video camea 19
video-recording x
visual Gestalt perception xi, 20, 73
envronmental interfeence avoidance
,,2,

general movement analysis ZZ_23

loss in semi-quantitative assessment

tonus

abnormalities 44

re-calibration 23

testing 3

touching 15
training 75
effectiveness 35,37
trunk rotation l5

27

West syndrome 32,33

wiggling-oscillating movement I 5
writhing movements 10, 1 t_12
generation l6
hemimegaloencephaty 56
hydranencephaly 55

ultrasound
advanced equipment 7
real time x

likelihood ratios 39
macrocephaly 56
maternal diabetes mellirus 62
microcephaly 56
Rett syndrome 5g
transformation to fidgety movements
l3
tremulous 52

see also brain ultrasound examination

validiry 37-45
ventilator, weaning from 52
vestibular responses, postnatal 9
vestibular-ocular response 9
video, demonstration 75

yawns 8,9

9I