773

J7ournal of Neurology, Neurosurgery, and Psychiatry 1994;57:773-777

Journal

of

NEUROLOGY
NEUROSURGERY
& PSYCHIATRY
Editorial

Pathophysiology of spasticity
Spasticity is a frequent and often disabling feature of
neurological disease. It may result in loss of mobility and
pain from spasms. The core feature of the spastic state is
the exaggeration of stretch reflexes, manifest as hypertonus. The stretch reflex threshold is reduced,' and its
gain may be increased.2 The result is the velocity-dependent increase in resistance of a passively stretched muscle
or muscle group detected clinically. Often, this is associated with a sudden melting of resistance during stretch,
the clasp-knife phenomenon. In addition, there may be
other related signs, such as weakness, impairment of fine
movements of the digits, hyperreflexia, loss of cutaneous
reflexes, Babinski's sign, clonus, spasms and changes in
posture. Spasticity is traditionally ascribed to damage to
the pyramidal tract. Work, however, particularly in animals, clearly implicates additional motor tracts in the
pathophysiology of the spastic syndrome. The present
editorial draws together old and new observations to provide a working hypothesis explaining the pathophysiology
of spastic hypertonus, and some of the related elements
of the human spastic syndrome. Possible changes in
spinal neuronal circuitry have been the focus of several
recent reviews34 and will not be discussed.
Inhibitory supraspinal influences
Some instances of lesions of the pyramidal system causing hypertonus and hyperreflexia have been reported in
animals, but these signs were not striking5 6 and may have
resulted from coincidental damage to non-pyramidal
motor pathways.78 More remarkable is the fact that pyramidal tract lesions have not led to spasticity in the hands
of many experimenters. Destruction of the primary
motor cortex in area 4,9-11 section of the medullary pyramids," '14 or lateral corticospinal tract'5 16 have lead to
weakness (particularly involving fine movements of the
digits), hypotonia and hyporeflexia in monkeys and apes
observed for up to several months following lesioning.
The findings in humans have been rather more difficult to interpret. Attention must be paid to the exact
extent of pathological or iatrogenic lesions, and sufficient
time must be allowed for spasticity to develop. Flaccid
weakness may be present for up to six weeks before spasticity develops after cerebral and spinal lesions.
It is often argued that the lesions of the pyramidal tract
in man can cause spasticity on the basis that hypertonia
may follow surgical excision of the precentral gyrus and
therefore of the primary motor cortex in area 4.17-20 Such

operations, however, may entail damage to areas other

than area 4, and to the cortical origins of motor systems
separate from the pyramidal tract. Excision of the ventral
precentral gyrus (arm area) involves removal of part of
area 4 and, in addition, the ventral portion of area 6 (the
premotor area), which occupies the anterior border of the
precentral gyrus.21 Removal of the superior part of the
precentral gyrus (leg area) risks damage to the supplementary motor area, and fibres leaving it.8 "1 More important therefore may be those cases in whom hemiparesis of
cortical origin is not accompanied by spasticity.22 One
such case was recently reported in whom MRI demonstrated a lesion confined to the precentral gyrus.23
Spasticity does not follow the unilateral section of the
corticospinal tract in the human cerebral peduncle.2425
Flaccid hemiparesis has been reported after infarcts
involving the basis pontis26 and medullary pyramid2728
but tone was examined just days after the stroke. Other
cases have been reported in whom spasticity has
supervened, but infarction extended beyond the pyramids.272930 Brown and Fang describe a case of sharply
localised infarction of the corticospinal tract at the pontomedullary junction in which an initially flaccid hemiparesis may have become spastic, but clinical details are
scanty.3' Hypertonus is conspicuously absent in limited
cordotomies involving the lateral pyramidal tracts.32
In summary, it is unlikely that damage to the pyramidal tract alone plays a major role in the production of
spasticity. This is in contrast to weakness and loss of
superficial reflexes, such as the abdominal reflexes, which
are common accompaniments of isolated lesions of the
pyramidal tract.'6 31 The association between corticospinal tract damage, and tendon hyperreflexia and the
Babinski response is less clear cut.'62032-34
This does not mean, however, that the motor cortex
cannot influence tone. Perhaps the most tangible proof of
this is the common clinical observation that capsular
lesions often lead to more striking spasticity than cortical
lesions. The implication must be that such lesions interrupt fibres originating in cortical areas other than the primary motor cortex (area 4), and that these fibres form
part of a motor system influencing tone separate from the
corticospinal tract. Extensive cortical lesions, involving
premotor and supplementary motor areas, add spasticity
to the paralysis seen with focal lesions of area 4 in monkeys.891' 1314 Forester reported an epileptic patient with a
mild hemiparesis due to traumatic injury of the precentral gyrus who developed a spastic hemiplegia following

774

excision of the premotor cortex.35 In animal experiments,

spasticity is more marked if such lesions are bilateral,"
suggesting that these non-pyramidal projections can have
bilateral effects. The fibres influencing spasticity run with
the corticospinal tract as far as the cerebral peduncles.3637
In the cat they lie in the medial portion of the peduncle
and in the area just dorsal to this, before ending in the
bulbar reticular formation dorsal to the medullary pyramids.38 Within the internal capsule there may be some
separation of the pathways, with axons from the primary
motor cortex, premotor cortex, and supplementary area
passing through the posterior limb, genu, and anterior
limb of the internal capsule respectively.39 This may
explain why small capsular lesions in the anterior limb
tend to be associated with spastic hypertonus, whereas
those involving the posterior limb are not.39 Large infarctions in the middle cerebral artery territory and subcortical infarcts undercutting most of the descending fibres in
the corona radiata lead, in time, to a spastic hemiplegia
as they involve both corticospinal and corticoreticular

projections.
Although the available evidence suggests that isolated
lesions of the pyramidal tract do not cause spasticity,
this, of course, need not mean that the pyramidal tract
has no influence over tone under normal circumstances.
This point is admirably illustrated by Bucy's analogy that
removal of one kidney has little effect on homeostasis.'4
This does not mean that the excised kidney was without
effect, only that the remaining kidney has assumed the
entire load. Similarly, ipsilateral supplementary motor
and premotor areas, or contralateral motor cortex may
assume some of the functions of the destroyed corticospinal fibres from the precentral gyrus. This has been
increasingly recognised as underlying the return of power
following pyramidal lesions; but its role in tone has not
been addressed.
The influence of cortical motor areas over tone is principally mediated by a powerful inhibitory mechanism in
the bulbar reticular formation. Electrical stimulation of
the ventromedial reticular formation dorsal to the pyramids inhibits the patellar reflex40 and gastrocnemiussoleus tonic vibration reflex4' in intact cats, and abolishes
extensor tone in decerebrate preparations40 and in cats
rendered spastic by chronic cerebral lesions.4' The
inhibitory effects in intact animals are potentiated by
simultaneous stimulation of the premotor cortex or internal capsule.4' The anterior and paramedian cerebellar
cortex and fastigial nucleus may also modulate the
inhibitory actions of the reticular formation, at least in
the cat.4'
Inhibitory influences survive section of the pyramidal
tract in the medulla37 and are conducted in the cord by
the dorsal reticulospinal tract in the dorsal half of the lateral funiculus.44 The available evidence suggests that the
tract occupies a similar position in humans in close relationship with the lateral corticospinal tract.45 It is the loss
of the cortical drive to the bulbar inhibitory centre which
is principally responsible for the spastic hypertonus following lesions of the frontal cortex or internal capsule. In
contrast, spasticity is not often a striking feature of
human bulbar lesions, perhaps because lesions in the
region of the inhibitory centre also involve respiratory
and vasomotor centres and are usually incompatible with
life.
The inhibitory centre in the caudal brainstem and the
dorsal reticulospinal pathway tonically inhibit flexor
reflex afferents as well as spinal stretch reflexes. Thus
damage to this system in the lateral funiculus releases
flexor reflexes in animals.4446 Shahani and Young47 have

Editonial

pointed out that flexor spasms are qualitatively no different to the flexor reflexes recorded in patients with spinal
transections and normal subjects, raising the possibility
that flexor spasms are a release phenomenon consequent
to damage to the dorsal reticulospinal pathway. In addition, it is now believed that the clasp-knife phenomenon
is caused by the inhibitory effects of flexor reflex afferents,48 and lesions involving different levels of the dorsal
reticulospinal system release the clasp-knife phenomenon
in cats.49
Excitatory supraspinal influences
Vestibulospinal activity is important in maintaining
decerebrate rigidity, but may have a lesser role in
supporting tone in spasticity. Injury to the vestibular
nuclei alone has little effect on spasticity in the spastic
cat.50 In contrast, transection of the bulbopontine
tegmentum leads to a marked reduction in spasticity.50
Electrical stimulation of the reticular formation of the
dorsal brainstem facilitates the patellar reflex in the intact
animal, and increases hyperreflexia, hypertonus, and
clonus in the cat made chronically spastic by previous
extirpation of the motor cortex.4' The facilitatory effects,
unlike the inhibitory effects of the reticular formation, are
not affected by stimulation of the motor cortex or internal capsule.41 Thus the reticular formation gives rise to
both inhibitory and excitatory systems influencing spasticity. The latter originates in a diffuse area extending
from the basal diencephalon, central grey and tegmentum of the midbrain, the pontine tegmentum, and the
lateral bulbar reticular formation, outside of the
inhibitory field.40 The spinal projections of this system
involve the ventral half of the cord.505' This facilitatory
reticulospinal system is central to the state of spasticity,
although vestibulospinal influences may make some contribution as lesions of the vestibular nuclei and bulbopontine tegmentum have a greater effect on spasticity in
the cat than tegmental lesions alone.50 Damage to
vestibulospinal and facilitatory reticulospinal pathways in
the anterior funiculus of the cord may also contribute to
the release of flexor reflexes and spasms.46

Descending spinal pathways

The lesions of the spinal cord affecting tone have been
carefully documented in the monkey.'6 Lesions of the
ventral funiculus lead to hyperreflexia in the setting of
essentially normal tone, while those confined to the lateral corticospinal tract in the lateral funiculus lead to
hypotonia, hyporeflexia and loss of cutaneous reflexes. In
contrast, extensive lesions of the lateral funiculus (that
include the dorsal reticulospinal tract) are followed by
spasticity and hyperreflexia, as is severing of the lateral
funiculus in animals with a previously disrupted corticospinal tract. Spasticity is less marked if the vestibulospinal tracts are also cut. The distribution of hypertonia
following the disruption of the dorsal reticulospinal fibres
in the lateral funiculus is identical to that following
frontal lobe lesions.
Information about the distribution of pathways influencing stretch reflexes and tone in humans comes from
cordotomies. Putnam52 performing this operation for
parkinsonism, observed that unilateral section of the dorsal half of the lateral funiculus was followed by a severe
initially flaccid paralysis. As power returned spasticity,
hyperreflexia, and clonus appeared. Hyndman," treating
intractable pain, cut the intermediate portion of the lateral funiculus bilaterally at the thoracic level, and found

7775

Editorial

that hyperactive knee and ankle jerks, ankle clonus and

Babinski's sign appeared immediately, but spastic hypertonus only developed in one out of six patients, and then
was only mild. Histological confirmation of the extent of
the lesions, however, was absent in these cases. Spasticity
did not develop after bilateral anterolateral cordotomies,
in some cases extending posteriorly to involve the lateral
corticospinal tracts.'25'54
Cordotomies have also been used in the treatment of
spasticity. Bucy observed that unilateral or bilateral section of the vestibulospinal tract in the anterior funiculus
of patients with congenital spastic paraplegia or quadriplegia only caused a transient reduction in extensor tone
in the lower limbs." He concluded that the vestibulospinal tract contributes to the maintenance of human
spasticity, but other descending pathways are capable of
maintaining spasticity at its full intensity in the absence
of vestibulospinal influences. The cordotomies performed
by Bucy were said to spare the deeper sulcal regions of
the anterior funiculi, but there was no histological confirmation of this. In contrast, extensive unilateral or bilateral anterior cordotomy (which included the deeper
sulcal areas) was followed, after a transient period of flaccidity, by the loss or considerable reduction of extensor
tone in the legs, despite the reappearance of hyperreflexia, adductor spasm, and clonus.56
On the strength of these findings it seems that lesions
must involve the dorsal half of the lateral funiculus to
produce spastic hypertonus in man. Presumably lesions
here interrupt the inhibitory dorsal reticulospinal tract to
cause spasticity.45 In patients already spastic, extensive
anterior cordotomy, but not partial anterior cordotomy,
abolishes extensor tone. This, like the results of animal
experiments,50 suggests that the medial reticulospinal
tract originating in the excitatory areas of the brainstem
reticular formation5' is more important than the vestibulospinal tract in maintaining spastic extensor tone. The
human medial reticulospinal tract runs in the sulcomarginal territory, in association with the median longitudinal bundles,45 and is likely to have been spared by Bucy's
limited incisions.55
In summary, two major balancing descending systems
exist controlling tone in humans: on the one hand, the
inhibitory dorsal reticulospinal tract; and, on the other,
the facilitatory medial reticulospinal and vestibulospinal
tracts.

Propriospinal and segmental influences

The striking feature of the hypertonicity and hyperreflexia that develops following complete transection of
the spinal cord is the variable period of spinal shock that
precedes the tone changes. During this period, which
may last several weeks, muscles are toneless and areflexic
below the level of transection, as might be expected following the simultaneous loss of inhibitory and excitatory
supraspinal influences on segmental and propriospinal
reflexes. The delayed appearance of tone and reflexes has
lead to the suggestion that plasticity within the spinal
cord, namely receptor hypersensitivity and sprouting of
axon terminals, is responsible for hypertonicity in complete spinal cord lesions.5758 This hypertonicity, may differ from the velocity dependent spasticity seen in partial
cord lesions, and result from virtually continuous flexor
spasms.59 Loss or reduction of knee and ankle jerks, paraplegia in flexion, and mass reflexes (exaggerated flexor
spasms which also involve bowel and bladder contraction) are common in this situation.60

Peripheral effects
Recent studies have challenged the classic view that exaggerated stretch reflexes are the major cause of established
spasticity. In the swing phase of gait, the tibialis anterior
shows abnormally high levels of activity, despite the lack
of any EMG activity in its antagonist, the triceps surae
muscle.61 This suggests that mechanical changes in the
extensor apparatus of the ankle, rather than muscle activity in the triceps surae itself, lead to increased resistance
to dorsiflexion movements. Direct measurement of the
resistance of the relaxed ankle to slow displacement in
hemiparetic subjects has confirmed the importance of
mechanical factors.2 Factors that might contribute to the
increased mechanical resistance to movement are alterations in tendon compliance2 and physiological, morphometric, and histochemical changes in muscle fibres.'
Given the velocity dependence of the stretch reflex,62
these mechanical factors may be particularly important
during functional movements of the leg, which occur at
low angular velocities.6'
How the influence of central and mechanical factors
on tone and function change with time is, as yet, unclear.
There is limited evidence to suggest that stretch reflex
gain reduces over the months to years following the initial lesion.2 Conversely, if we are to assume that contractures represent the extreme end of the mechanical factors
resisting limb movement, then there is reason to believe
that their development is delayed. The issue of the natural history of central and mechanical factors is an
important one, as early treatment of hypertonia may
avert mechanical changes. This has been the finding in
an animal model of spasticity, and has prompted an
investigation of the disease modifying effects of botulinum toxin in spastic cerebral palsy.6'
Conclusion
Normal tone consists of a balance between inhibitory
effects on stretch reflexes mediated by the dorsal reticulospinal tract and facilitatory effects on extensor tone,
mediated by the medial reticulospinal tract, and, to a
lesser extent in humans, by the vestibulospinal tract. In
cortical and capsular lesions some of the drive on the
inhibitory centre in the caudal brainstem is lost resulting
in a spastic hemiplegia, in which antigravity posture predominates, but flexor spasms are unusual. In practice
partial spinal lesions usually involve the lateral corticospinal and dorsal reticulospinal tract, as most commonly seen in multiple sclerosis where demyelinating
lesions have a predeliction for the lateral funiculi.64
Damage to the corticospinal tract leads to paresis, while
loss of inhibitory influences from the dorsal reticulospinal
tract, leaves the effects of the medial reticulospinal and
vestibulospinal tracts unopposed. In this situation there is
often severe spasticity with tone being greatest in the
antigravity muscles, so that paraplegia in extension may
be seen. Extensor and flexor spasms are common,
although the former tend to predominate.59 This is the
clinical picture of multiple sclerosis relatively early in its
course.

The present hypothesis may also explain the marked

spasticity in the legs in the presence of spasms, but little
or no weakness in many patients with hereditary spastic
paraparesis. Here, there is involvement of the dorsal
reticulospinal tract in the thoracolumbar cord with a
degree of sparing of the corticospinal tracts. Support for
this comes from pathological reports65 and from the relative normality of electromyographic responses in leg

Editorial

776

muscles to electrical stimulation of the motor cortex in

patients with this condition.66
In severe or complete cord lesions there is loss of all
supraspinal influence on the cord. Hypertonicity is not as
marked as in some cases of incomplete cord lesions, as
the descending excitatory systems are no longer acting
unopposed. Flexion spasms are very prominent, however,
as flexor reflexes are released from the inhibitory influences of the dorsal reticulospinal, vestibulospinal and
medial reticulospinal tracts. Paraplegia in flexion may
then supervene. This is often the clinical picture of
advanced multiple sclerosis, when lesions have also interrupted function in the descending tracts of the anterior
funniculus.
Of course the pattern of spasticity is not fixed and
solely determined by the degree of damage to different
descending pathways. Stimulation of flexor reflex
afferents-for example, by pressure sores, can transform
paraplegia in extension into paraplegia in flexion.
Conversely, standing reduces flexor tone and favours
extensor tone, a phenomenon that is readily used to
advantage in physiotherapy. An additional factor in complete transection is the delayed reorganisation within the
isolated cord, which may underline the change in balance
from flexor to extensor spasms sometimes seen a year or
more after division of the cord.67
I have expanded on old hypotheses to provide a
schema explaining the pathophysiology of human spastic
hypertonus. The hypothesis is largely based on animal
work, as relevant clinical observations are few and imperfect. Opportunities to study spasticity in patients are
common and it is hoped that this editorial will encourage
careful clinical observation, supported, where necessary,
by lesion localisation with MRI, to refute or develop this
schema in the future. Acquired pathology rarely respects
neuroanatomical boundaries and it may be that further
investigation in humans requires the technique of lesion
superimposition that has proven so useful in other contexts.

P BROWN
MRC Human Movement and Balance Unit,
Institute ofNeurology, National Hospitalfor Neurology and
Neurosurgery, Queen Square, London WCIN 3BG, and
Department ofNeurology, Guy's Hospital, London SEI 9RT, UK

I thank Dr P W Nathan and Dr J C Rothwell for their helpful comments and

discussion.

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Ser 1992;20:3-8.

NEUROLOGICAL STAMP
Jan Evangelista Purkinje (1787-1869)
Purkinje was born in Libochovice, Bohemia (now
----Czechoslovakia) and educated by Piarist monks. He
studied philosophy at the University of Prague, was
ordained a priest and became Father Salverius. In 1819,
,
-- ,aged 32, he graduated in medicine. Purkinje, who had
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already made significant contributions to physiology,
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applied unsuccessfully for several University appointments within the Austro-Hungarian Empire. Through1:
friendship with Goethe he was appointed Professor of
Physiology at Breslau University in 1823 against the
opposition of the Faculty. In 1850 he was invited to the
/43
Chair of Physiology in Prague which he held until his K

deathi.
His early work included the influence of the head

position on the directional component of vertigo, and the

4Fi
maintenance of posture and equilibrium, culminating in
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Purkinje's Law of Vertigo. Purkinje explored aspects of i
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vision and discovered in 1825 a phenomenon known as
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the Purkinje effect (as light intensity decreases, red
objects are perceived to fade faster than blue objects).
W
While examining birds' eggs he discovered the
germinal follicle, sometimes called the Purkinje vesicle. L_____
,.
In 1837 he located the Purkinje cells in the cerebellar
cortex, and two years later the Purkinje fibres lying
beneath the endocardium.
Purkinje also introduced the term protoplasm to
describe the living embryonic material of the egg. He
made original contributions to the histology of sweat
glands, skin, bone, dental structures and was the first to
discover the uniqueness of the human fingerprint. He
noted that pancreatic extracts digested protein and he
made comparative studies of cellular structures of plants
and animals. Purkinje was among the first to use a
microtome and one of the first to teach microscopy as
part of a university course. He also studied digitalis toxicity (on himself) and the effects of belladonna and opium.
Purkinje translated poetry from German, Russian, and
Polish and wrote some of his own. At age 80, he learned
Hungarian so that he could translate a libretto.
He was honoured by Czechoslovakia in 1937 (Stanley
Gibbons 371 and 372, Scott 232 and 233) on the 150th
anniversary of his birth.
L F HAAS