Handbook of Clinical Neurology, Vol.

103 (3rd series)

Ataxic Disorders
S.H. Subramony and A. Dürr, Editors
# 2012 Elsevier B.V. All rights reserved

Chapter 45

Balance and gait problems in the elderly

ANAND VISWANATHAN 1 * AND LEWIS SUDARSKY 2
1
Stroke Service and Neurology Clinical Trials Unit, Department of Neurology, Massachusetts
General Hospital, Boston, MA, USA
2
Department of Neurology, Brigham and Women’s Hospital, and
Harvard Medical School, Boston, MA, USA

INTRODUCTION
Gait and balance problems are common with advancing
age. Balance difficulties are reported by 13% of
patients at age 65, 35% at age 75, and 46% at age
85 (Sixt and Landahl, 1987; Gerson et al., 1989).
Gait impairment has been estimated to occur in 8% to
19% of elderly individuals living in the community
(Newman et al., 1960; Dawson et al., 1987; Sudarsky,
1990). In East Boston, a degree of shuffling or
difficulty with turns was noted in 15% of the population
aged 67–74, 29% of those 75–84, and 49% of the
population 85 and above (Odenheimer et al., 1994).
Disorders of balance and gait are particularly impor-
tant in the elderly because they compromise indepen-
dence and contribute to the risk of falls and injury
(Rubenstein and Josephson, 1997). Falls were attributed
to impaired balance and gait in 32% of subjects over 75
in a community-based study (Tinetti et al., 1988).
Falls are associated with increased morbidity and mortal-
ity (Tinetti, 1986; Lipsitz et al., 1991). Hip fractures and
other fall-related injuries often result in hospitalization
and nursing home admission, and carry with them large
healthcare expenditures (Cummings et al., 1990; Tinetti
and Williams, 1997).
Although they are considered as separate
clinical entities, balance and gait disturbance are often
intertwined (Mori, 1987; Nutt and Horak, 2004). This
chapter considers some of the relevant mechanisms
and common patterns of gait and balance disturbance.
ANATOMYAND PHYSIOLOGY
Balance and postural control
Postural control requires the maintenance of an indivi-
dual’s center of mass over his base of support (in
humans, the stance as a function of the lower extremi-
ties) (Horak, 1987; Lee, 1989; McCollum and Leen,
1989). More generally, this demands the center of mass
be maintained within the limits of stability (area in which
the center of mass can be moved without changing the
base of support). Stability limits are a function of three
major components: the biomechanics (body morphology
and configuration, joint torque strength, speed at which
the torque strengths can be developed, and joint range
of motion), body support and task requirements, and
the nature of the support surface (e.g., angle, compli-
ance, friction) (McCollum and Leen, 1989; Shumway-
Cook and Horak, 1990; Alexander, 1994). Postural
control responses vary with the task and challenge
(Alexander et al., 1992; Alexander, 1994). For example,
in elderly individuals, unipedal stance is considerably
more difficult than bipedal stance (Bohannon et al.,
1984). Standing on a slowly moving reduced-support
surface is more challenging than standing on a slowly
moving full-support surface (Alexander et al., 1992).
Balance and postural control are crucial to carry out
most daily activities. Examples include the ability to
maintain various positions, automatically respond to
voluntary body and extremity movements, and react

*Correspondence to: Anand Viswanathan, MD, PhD, Stroke Service and Memory Disorders Unit, Associate Director, Telestroke
Services , Massachusetts General Hospital Hemorrhagic Stroke Research Program, 175 Cambridge Street, Suite 300, Boston,
MA 02114, USA. Tel: 617.643.3876, Fax: 617.726.5346. E-mail: aviswanathan1@partners.org
624 A. VISWANATHAN AND L. SUDARSKY
to external disturbances (Berg et al., 1992). It thus is
reasonable to assume that any disruption of postural
control could result in increased risk of falls and injury.
The neuroanatomical basis for postural control has
been explored in quadrupedal animals. The hind limbs
of cats with spinal transection have muscle tone for
weight support, however, they do not adequately
respond to postural perturbations to prevent falls
(Macpherson and Fung, 1999). These animals require
support to maintain upright stance (Grillner and
Wallen, 1985; Macpherson and Fung, 1999). Stimulation
of the dorsal and ventral tegmental areas of the pons
can elicit coordinated postural responses in animals
(Mori, 1987; Mori et al., 1989). These data suggest that
postural control depends on supraspinal mechanisms.
These higher centers are thought to adapt postural
responses to both environment and circumstance. Pos-
tural adjustments surrounding voluntary movements
are constantly being made in order to maintain postural
stability (Massion, 1994). The vestibular system and cer-
ebellum have been thought to serve as the primary med-
iators of control in integrative models of postural control
(Keshner and Cohen, 1989; Nutt and Horak, 2004). The
cerebellum may modify limb and trunk movements
initiated by the vestibulospinal tract (Keshner and Cohen,
1989; Llinas and Walton, 1979). Without cerebellar input,
there is lack of balance of opposing muscle forces, and
the postural response is not graded over the appropriate
time to optimize muscle co-activation to the task
demands (Keshner and Allum, 1986; Diener et al., 1992).
Muscle and joint proprioceptors provide the somato-
sensory information for balance and gait used for trigger-
ing rapid postural responses. Romberg observed the
importance of dorsal column afferents from the lower
limbs in maintenance of standing balance (Romberg,
1853). Cutaneous sensory information is used to
distinguish the contour and characteristics of support sur-
faces and to measure pressure under the feet in contact
with these surfaces. Graviceptors in the trunk help to
define postural verticality (Mittelstaedt, 1999). Vestibular
inputs control head and trunk orientation in space and
stabilize gait. Vision also contributes to postural stability
and is used to avoid obstacles and plan trajectories during
gait (Paulus et al., 1984; Rondot et al., 1992). Finally,
postural responses are modified and adapted by context,
previous experience, and expectation.
In older individuals, peripheral sensory information
(touch sensitivity and proprioception) is the most
important contributor to postural stability, followed
by visual and vestibular input (Lord et al., 1991). The
variance between individuals is not well explained by
this model, and may be due to central integrative fac-
tors such as problem-solving ability, motivation, and
attention (Tinetti, 1986).
Gait
NEURAL NETWORKS FOR LOCOMOTION
In quadrupedal animals, locomotion depends on the
activity of a spinal pattern generator. Cats and dogs
with high spinal transection achieve a crude pattern of
walking on the treadmill, provided their balance is
supported. This “fictive locomotion” can be stimulated
with levodopa or clonidine, and occurs independent of
sensory feedback (Grillner and Wallen, 1985). While it
is difficult to produce sustained spinal locomotion in
primates (Eidelberg et al., 1981), efforts have been
made to harness spinal stepping in the rehabilitation
of spinal injury patients (Dietz et al., 1995).
Primate bipedal locomotion depends on higher com-
mand and control centers in the brainstem, cerebellum,
and forebrain (Orlovsky, 1972). There are four areas
where stepping and postural response can be evoked by
electrical stimulation in animals: a subthalamic and a
mesencephalic locomotor region, and a dorsal and
ventral tegmental field in the caudal pons. Eidelberg
and colleagues (1981) evoked a form of “controlled loco-
motion”, more natural than spinal stepping, by stimula-
tion of the mesencephalic locomotor region (MLR) in
primates. The MLR is of particular interest as it includes
the cholinergic neurons of the pedunculopontine nucleus
(PPN). In the cat, stimulation of the PPN produces step-
ping, and inhibition slows walking (Garcia-Rill, 1991).
A complex pattern of activity is recorded from cells
in the PPN during locomotor activity (Pahapill and
Lozano, 2000).
Locomotor commands from the brainstem are
passed through descending pathways in the spinal cord,
including the reticulospinal and vestibulospinal tracts
(Lawrence and Kuypers, 1968). Eidelberg et al. (1981)
observed that primates with partial spinal transection
can recover the capacity for locomotion, provided that
one ventral quadrant of the spinal cord is preserved.
CEREBRAL CONTROL
Although apparently natural locomotion can be exe-
cuted by pathways in the brainstem, cerebellum, and
spinal cord, many of the gait disorders seen in the
elderly result from pathology in the forebrain: the basal
ganglia, motor cortex, and frontal subcortical circuits
(Garcia-Rill, 1986; Armstrong, 1988; Mori, 1997).
Humans suffer significant impairment after injury to
motor cortical areas. The forebrain provides a goal
and purpose for walking. It specifies when to start,
when to stop, where to change direction, and it anima-
tes the performance. The cerebral control provides an
element of skill and finesse. For example, cats with pyr-
amidotomy recover an ability to walk on flat ground,
 BALANCE AND GAIT PROBLEMS IN THE ELDERLY
but fail to walk on a narrow beam or across a ladder.
Cerebral control is also involved in context-dependent
adaptation, and avoidance of obstacles (Drew, 1993).
The importance of cerebral control of gait and bal-
ance has been emphasized in recent studies of dual-task
walking. There is evidence to suggest that postural con-
trol in the elderly deteriorates when older adults per-
form a secondary dual task whilst walking (Beauchet
et al., 2009). The deterioration is even more pro-
nounced in older individuals who have previously fallen
(Chen et al., 1996; Lajoie et al., 1996a; Woollacott and
Shumway-Cook, 2002). A recent study examined the
relationship of dual-task walking to cognition in two
groups of elderly individuals (those who have fallen
and those who have not) compared to healthy young
adults. The performance of dual tasks decreased gait
speed in all groups. However, swing time variability (a
measure of dynamic balance) was increased in the
elderly falling group. Furthermore, executive function
(as measured by the Stroop and Go-NoGo tests) was
more impaired in the falling group (Springer et al.,
2006). This may suggest that loss of frontal subcortical
pathways, important in executive function, may also
impact gait and postural control.
CLASSIFICATION
Introduction
With a large network of neural systems involved in pos-
tural control and locomotion, impairment can occur at
various different levels. Indeed, balance and gait disor-
ders encountered in older people are heterogeneous and
sometimes multifactorial. Neurologic disorders overlap
with arthritic and antalgic gaits. Failing gaits may
appear fundamentally similar even when they are mech-
anistically different. The disorder of balance and gait
that is observed clinically is the product of a physiolog-
ical abnormality modified by a compensatory response.
Some features such as widened stance are non-specific,
and represent biomechanical adaptations to improve
stability and efficiency. Classification of these disor-
ders based on clinical history, physical examination,
and gait observation is a difficult challenge. Nutt
and Horak (2004) have proposed a classification of
common patterns of falls and gait disorders which
provides a helpful starting point.
Fall patterns
Information on falls is generally ascertained by clinical
history obtained from the patient or caregivers. Falls
due to loss of postural tone (termed collapsing falls)
should be distinguished from falls with retained tone.
These falls are not always associated with loss of
625
consciousness and confusion. The patient is described
by others as “collapsing in a heap”. The differential diag-
nosis includes disorders such as syncope, orthostatic
hypotension, akinetic seizures, and asterixis.
By contrast, in falls with retained muscle tone, the
patient falls in a particular direction. In these falls, the
patient is often described as “toppling like a falling
tree”. When eliciting the history, it should be distin-
guished whether the patient experiences “near-falls”
(falling with a late or inadequate compensatory postural
response) or consistently falls to the ground. The latter
would suggest that the patient has inadequate postural
defense. Some toppling falls occur as the patient seems
to lose equilibrium standing still. This type of fall most
commonly occurs in progressive supranuclear palsy
(PSP) or thalamic and putaminal astasia (Masdeu and
Gorelick, 1988; Labadie et al., 1989). Falls that occur
with change of momentum (gait initiation, stopping,
or turning) are more characteristic of parkinsonism. In
these types of falls there may be little or no evidence
of effort to resist the fall. This is unlike patients with
cerebellar disease who, although lacking equilibrium,
tend to make protective efforts to arrest falls.
Tripping falls occur due to the failure to clear the
support surface, the foot catching on irregularities or
obstructions on the surface. Most commonly forward
falls, they result from foot drop, spasticity, or parkin-
sonism. Tripping and slipping falls are common,
and are sometimes referred to as mechanical falls.
Falls due to “freezing” occur when the patient’s feet
apparently stick to the floor while the center of mass
continues to move forward. Along similar lines, the
steps of a festinating gait are too short to keep the
patient’s feet under the moving center of mass. Both
types of falls result in the patient falling forward.
Falls due to peripheral or central vestibular deficits
may result from patients experiencing vertigo, or walking
in a challenging sensory environment. Falls that occur as a
result of walking on uneven surfaces suggest inadequate
sensory input for balance. This may be seen in peripheral
neuropathies and disease affecting the dorsal columns.
In sensory falls, patients tend to recognize their lack of
equilibrium and attempt to compensate before falling.
Finally, it has been suggested that non-patterned falls
may represent failure of attention and insight. This type
of fall may occur in dementing illnesses (Nutt and
Horak, 2004). Fall patterns are summarized in Table 45.1.
Gait patterns
Neurologic disorders of gait can be classified based on:
1) common clinical syndromes, 2) underlying physiologic
mechanisms, or 3) etiologic factors. Each classification
has its proponents and its limitations. Nutt (1998, 2001)
626 A. VISWANATHAN AND L. SUDARSKY
Table 45.1 The major difficulty with this approach is that the
Fall patterns criteria for the five highest-level gait disorders are
somewhat arbitrary and are not always uniformly
Fall pattern Common causes applied. The categories do not correlate well with etio-
logic diagnosis, and may change in the same patient
1. Collapsing falls (loss of Syncope, orthostatic over time.
muscle tone) hypotension, akinetic Classification of gait disorders based on etiology is
seizures, negative practical (Sudarsky, 2001). Indeed, etiologic diagnosis is
myoclonus the first step in therapeutic intervention. Neurologic eval-
2. Toppling falls uation of 50 patients over 65 with an undiagnosed neuro-
(maintained muscle Progressive supranuclear
logic disorder of gait was successful at identifying the
tone) palsy (PSP)
Falling while standing Parkinsonism
principal etiologic factor in 85% of cases. Treatable
Falling with change Cerebellar disease disorders were identified in 25% (Sudarsky and Ronthal,
of position 1983). However, this system is not easily applied to older
Weaving from side to patients with higher-level gait disorders, or patients with
side until fall more advanced disability. Sometimes an etiology is not
3. Tripping Foot drop known and cannot be established, or the disorder is
Parkinsonism clearly multifactorial.
Spasticity Efforts have been made to incorporate the strengths
4. Freezing Parkinsonism of each system into a single framework, or to develop a
Normal pressure hybrid system to be of practical use for the clinician
hydrocephalus
(Jankovic et al., 2001; Sudarsky, 2004). Some of the
Frontal lobe disease
Multi-infarct state
common patterns of failing gait in the elderly are
5. Sensory falls (falling in Vestibular disorders described below and summarized in Table 45.2.
specific environments Peripheral neuropathy
or with concurrent Table 45.2
sensory symptoms)
6. Non-patterned Attentional or insight Gait patterns
failure (dementia)
Gait pattern Differential diagnosis
Adapted from Nutt JG, Horak FB (2004). Classification of balance
and gait disorders. In: AM Bronstein, T Brandt, M Woollacott, et al. 1. Cautious gait Common in the elderly, non-specific,
(Eds), Clinical Disorders of Balance, Posture and Gait. Hodder & multifactorial
Stoughton, London, pp. 63–73. Subcortical white matter
hyperintensities
2. Stiff-legged Parkinsonism
has proposed a classification of gait disorders into eight gait Dystonia
groups based on clinical characteristics: cautious, weak, Stroke, multi-infarct state
stiff, ataxic, veering, freezing, marche à petits pas, and 3. Freezing gait Parkinsonism
bizarre. The advantage of this syndrome-based approach Normal pressure hydrocephalus
is that it lends itself to observational analysis, and is Frontal lobe disease
Multi-infarct state
easily understood and applied. It tends to cluster together
4. Frontal gait Multi-infarct state
cases that share a similar physiologic mechanism, though 5. Dystonic gait Focal or generalized dystonia
many complex cases are not easily handled. 6. Cerebellar gait Cerebellar lesions
A physiologic, systems-based approach has also 7. Sensory ataxia Peripheral neuropathies of various
been proposed (Nutt et al., 1993). In this model, gait causes
disorders are categorized into three levels. The lowest- 8. Psychogenic ‘Fear of falling’ gait (seen in the
level gait disorders include those due to arthritis, neuro- gait elderly; demonstrate abnormal gait
muscular disease, and sensory loss. Middle-level gait with an exaggerated compensatory
disorders include hemiplegic gait, cerebellar gait, and response)
the extrapyramidal syndromes. The highest-level gait Psychogenic disorders
disorders (common in the elderly) are subdivided
Adapted from Nutt JG, Horak FB (2004). Classification of balance
further into five categories: cautious gait, subcortical and gait disorders. In: AM Bronstein, T Brandt, M Woollacott, et al.
disequilibrium, frontal disequilibrium, isolated gait igni- (Eds), Clinical Disorders of Balance, Posture and Gait. Hodder &
tion failure (i.e., pure freezing gait), and frontal gait. Stoughton, London, pp. 63–73.
 BALANCE AND GAIT PROBLEMS IN THE ELDERLY
CAUTIOUS GAIT
In their landmark paper on higher-level gait disorders,
Nutt and colleagues (1993) introduced the concept
of the “cautious gait”. The pattern of reduced stride,
wider base, and shorter swing phase with preservation
of rhythmic stepping is an adaptation to perceived
imbalance. Older people commonly adopt a guarded
or cautious pattern of locomotion in order to achieve
better stability (Murray et al., 1969). While this pattern
of gait is non-specific, more characteristic features of
an underlying neurologic deficit may emerge over time.
The cautious gait may be the most common higher-level
gait disorder.
This term is sometimes used to describe the appre-
hensive elderly patient with recent falls, who walks
with the arms abducted, clutching at walls and furni-
ture, as if walking on a slippery surface (Murphy and
Isaacs, 1982). A better description for this phenomenon
is the pathologically cautious or phobic gait. It is
particularly amenable to rehabilitation therapies.
STIFF-LEGGED (SPASTIC) GAIT
A variety of stiff-legged gaits are observed among
patients with strokes, demyelinating disease, spinal dis-
orders, and cerebral palsy. However, spastic gait is not
a unitary disorder. Although there is an element of
spasticity in all these conditions, there are distinct pat-
terns of abnormal locomotion (Mayer et al., 2001).
There may be inappropriate flexion at the hip or knee.
Some patients have adductor spasm, with circumduc-
tion and scissoring. Equinovarus is another common
pattern. With progressed disease, toe-walking may be
seen. The shoes of a patient often reflect uneven wear.
Intervention with botulinum toxin, nerve block, or sur-
gery may be successful if the intervention is appropri-
ately targeted (O’Brien, 2001).
FREEZING GAIT
Freezing of gait was first described by Charcot (1877) in
patients with Parkinson’s disease. It is a distinctive
phenomenon with arrests of movement (motor blocks),
usually brief, often occurring with gait initiation or
when the patient turns to change direction. Motor
blocks during gait initiation are sometimes termed start
hesitation or “gait ignition failure”. There may be a
series of quick, ineffective stepping movements with
side-to-side shifting of weight, without forward
engagement (“slipping clutch syndrome”). Locomotor
movements are then normal or near normal once the
patient is in motion, but freezing may return as the
patient turns or attempts to navigate the door threshold.
There is variability, in that the same doorway may be a
627
problem on one occasion but not the next. Freezing is
often overcome with the aid of sensory cues; visual
cues may be particularly effective.
Freezing of gait is particularly common in Parkinson’s
disease; the frequency increases with disease duration,
motor disability, and duration of levodopa treatment
(Giladi et al., 2001). Freezing of gait was reported in
26% of Parkinson’s patients at the 14-month endpoint
of the DATATOP study (Giladi et al., 2001), and in
25% of patients at 3–4 years in the ropinirole 056 study
(Rascol et al., 2000). In patients with motor fluctuations,
gait freezing is most often observed during off time.
“Off period” gait freezing may respond to an upward
adjustment or redistribution of anti-parkinsonian medi-
cation. “On period” gait freezing is more difficult to
treat with medication, and responds best to rehabilita-
tion-based interventions. Falls due to freezing occur
when the patient’s center of mass continues to move
forward while the feet remain in place. Cueing to
lengthen stride seems to be the most productive strategy
(Rubinstein et al., 2002).
Gait freezing also occurs in patients with other neu-
rodegenerative parkinsonian disorders. In one study,
freezing of gait was present in 24% of patients with
atypical Parkinson’s at the time of presentation (Muller
et al., 2002). A syndrome of primary progressive freez-
ing gait (“pure gait ignition failure”) has been
described. (Achiron et al., 1993; Atchison et al., 1993).
Factor and coworkers reported on the natural history
of 30 patients with primary progressive freezing gait
who were not levodopa-responsive. Most developed
falls within 3 years and lost independent ambulation
in 5 years (Factor et al., 2002). Subsequent long-term
follow-up suggests that patients with this presentation
ultimately evolve into a recognizable neurodegenerative
disorder, and that primary progressive freezing gait is
not a distinct morbid entity (Factor et al., 2006).
FRONTAL GAIT (MARCHE À PETIT PAS)
The frontal gait is a combination of impaired stepping
(shuffling, freezing gait) and some degree of disequi-
librium. A major cause of this phenomenon is cerebro-
vascular disease, and it is commonly seen in older
patients. Small-vessel disease involving the basal gang-
lia and periventricular white matter is the most frequent
underlying abnormality. The anatomic basis for the
phenomenon is presumed to involve the disconnection
of the cortical motor areas from the basal ganglia and
brainstem locomotor centers. White matter lesions
within this network produce a gait disorder in patients
with hypertensive cerebrovascular disease and patients
with hydrocephalus. Other somewhat imprecise terms
such as lower body Parkinsonism (FitzGerald and
628 A. VISWANATHAN AND L. SUDARSKY
Jankovic, 1989) and gait apraxia (Meyer and Barron,
1960) have been used to describe the phenomenon in
the literature.
Thompson and Marsden (1987) characterized the
gait disorder in 12 patients with subcortical arterioscle-
rotic encephalopathy (Binswanger’s disease), based on
observational analysis of the patients’ chair rise and
gait (Thompson and Marsden, 1987). Elble and collea-
gues (1996) studied the physiology of gait initiation
in five patients with vascular disease (lower body
Parkinsonism). The basic architecture of the first step
was preserved in these patients, though steps were
irregular and sometimes aborted. Postural shifts neces-
sary to initiate forward movement were not effectively
generated (Elble et al., 1996; Ebersbach et al., 1999).
The major avenue of treatment for the frontal gait
disorder of subcortical arteriosclerotic encephalopathy
is physical therapy. Iansek and colleagues (2001) trained
patients with frontal gait using a paradigm of balance
training, attentional cues, and stride lengthening.
DYSTONIC GAIT
Dystonia has a variety of causes, and can produce
unusual and sometimes bizarre disorders of gait. Walking
and running may be differentially affected; dystonia may
disappear when walking backwards. In younger patients
with generalized dystonia, there may be torsion of the
trunk, and the twisted posture of the lower body may
make walking difficult altogether.
The most common focal disorder is dystonic inversion
at the ankle, sometimes associated with extension of the
great toe. Dystonic toe flexion also occurs, as do more
complex proximal lower limb dystonias. Focal dystonia
is sometimes amenable to botulinum toxin injection,
provided that the active muscles can be successfully iden-
tified and targeted (O’Brien, 2001). Dystonic flexion of
the thoracolumbar spine (camptocormia) has been identi-
fied in patients with Parkinson’s disease. It is activated as
the patient stands to walk, and remits when lying supine,
which helps distinguish the disorder from contracture
(Nieves et al., 2001).
CEREBELLAR GAIT
Gordon Holmes characterized the gait ataxia in studies
of patients with penetrating head injury (Holmes, 1922).
Cerebellar disease produces imbalance (disequilibrium)
and a distinct locomotor disorder. The gait is often slow
and halting, with a widened base of support. Stepping is
irregular, which results in a lurching quality as the
upper body segments struggle to maintain alignment.
The patient may stumble or veer off to the side. Truncal
instability is more pronounced when attempting to walk
on a narrow base, or tandem, heel to toe. Patients also
exhibit imbalance when they turn or change direction.
Control of gait and balance is localized within the
cerebellum to the midline structures, including the
efferent pathways of the interposed and fastigial nuclei
(Thach et al., 1992; Thach and Bastian, 2004; Schoch
et al., 2006).
Kinematic studies in cerebellar patients confirm the
features described above. The essential physiologic abnor-
mality is irregular stepping – increased variability of
timing, direction, and amplitude (Ebersbach et al., 1999).
Palliyath and coworkers (1998) have noted a reduced veloc-
ity and stride length in 10 patients with cerebellar degener-
ation. Analysis of movements about the knee and ankle
joints revealed poor intra-limb coordination, indicating a
decomposition of multi-joint movement. Other character-
istic features included reduced dorsiflexion of the ankle
at the onset of the swing phase, which might predispose
to tripping (Palliyath et al., 1998). Studies by Horak and
Diener (1994) show that postural responses in cerebellar
patients have a normal latency, but are hypermetric in
force, contributing to truncal titubation. Patients often fall
in a direction opposite to the force by which they were
perturbed (Horak and Diener, 1994).
Patients with alcoholic cerebellar degeneration,
which affects primarily the midline vermis, often have
a gait ataxia out of proportion to findings in the
oculomotor system and limbs. Although there are no
neuropathological data to support the concept of age-
related cerebellar degeneration, it is clear that healthy
older subjects have more difficulty performing tasks
such as one-limb stance and tandem gait.
SENSORY ATAXIA
Locomotor ataxia was described in the nineteenth cen-
tury in patients with tabetic neurosyphilis. Such patients
are visually dependent in their walking, and do poorly in
the dark. Features that distinguish sensory ataxia from
cerebellar are summarized in Table 45.3. Although there
is redundancy of sensory information about the position
of the body in space during locomotion, humans are
particularly dependent on proprioception. Patients with
peripheral neuropathy affecting large fibers are at a
substantially increased risk for falls (Richardson et al.,
1992). Causes of a predominantly ataxic neuropathy in
clinical practice include vincristine and cisplatin chemo-
therapy, cobalamin deficiency, paraproteinemia, and
subacute sensory neuropathy, which may be autoim-
mune or paraneoplastic (Sabin, 1997).
Several studies have examined the impact of propri-
oceptive deficits on postural control and gait. Horak
(2001) has demonstrated increased body sway during
stance, and displacement of the center of mass while
walking in patients with diabetic neuropathy. In order
 BALANCE AND GAIT PROBLEMS IN THE ELDERLY
Table 45.3
Clinical distinction of ataxic and unsteady gaits
Cerebellar ataxia
Stance Wide-based
Velocity Variable
Stride Irregular, lurching
Romberg þ/
Heel!shin Abnormal
Initiation Normal
Turns Veers away
Postural instability þ þþþ
Falls Uncommon
to compensate for excess motion of the center of mass,
patients alter lateral step placement. Somatosensory
information derived from fingertip contact with a sta-
ble object (haptic information) can help with balance
compensation (Horak, 2001). Lajoie and colleagues
(1996b) have reported kinematic studies in a patient
with advanced sensory neuropathy, who had absent
proprioception in the limbs by clinical measures.
Compensatory strategies that enabled locomotion to
proceed in the absence of somatosensory feedback
were examined. A forward tilt was observed, with flex-
ion of the neck such that the patient could monitor the
performance visually. EMG demonstrated co-activation
of the vastus lateralis and medial hamstring during
weight acceptance, effectively bracing the leg during
the stance phase (Lajoie et al., 1996b).
Vestibular deficits can also impair control of the
head and center of mass during locomotion (Horak,
2001). Fife and Baloh (1993) found bilateral vestibular
deficits in 7 of 26 patients over 75 with disequilibrium
of uncertain cause. This syndrome is most often asso-
ciated with a cautious gait and a feeling of unsteadiness
in the elderly, as opposed to a gross sensory ataxia
(Kerber et al., 1998).
PSYCHOGENIC GAIT DISORDERS
Psychogenic disorders of gait occur at all ages, though
caution should be used in making this diagnosis in the
elderly (Hayes et al., 1999). Older people often exhibit
a combination of physical disability and an exaggerated
compensatory response, particularly if there is appre-
hension and fear of falling.
Lempert and colleagues (1991) have characterized
the recognition features which help identify psycho-
genic disorders of gait, from a review of video in 37
cases. The abnormalities are often distinctive. Extreme
629
Sensory ataxia Frontal gait
Looks down Wide-based
Slow Very slow
High-stepping Short, shuffling
Unsteady, falls þ/
þ/ Normal
Normal Hesitant
þ/ Hesitant, fragmented
þþþþ
Poor postural synergies
Frequent Frequent
slow motion may occur, as if the patient were walking
through a viscous substance. Uneconomical postures
with wastage of muscular effort are another classic
example. Dramatic fluctuations may occur over min-
utes, which is unusual for patients with neurologic
disease. Observation and distraction may activate or
suppress the findings. A video atlas has been published
by Hayes and colleagues (1999), which elaborates on
these criteria and notes some diagnostic pitfalls. Prog-
nosis is often good for those patients in whom the his-
tory is recent and the decompensation of walking is
acute. Dramatic cures are often possible in this setting
(Keane, 1989). When psychogenic disorders of gait per-
sist for 6 months or longer and become part of an
established pattern of dependence and disability, it is
often difficult to restore function (Bhatia, 2001).
GAIT AND BALANCE AS A MARKER
Introduction
As described above, higher-level gait disorders are
common in the elderly. With the increasing use of
neuroimaging in recent years, an effort has been made
to better understand these gait disorders using radio-
graphic markers. Specifically, there has been consider-
able research on the relationship between balance and
gait abnormalities in the elderly and changes in CT or
MRI (Baloh and Vinters, 1995; Baloh et al., 1995, 2003;
Tell et al., 1998; Guttmann et al., 2000; Starr et al.,
2003). Even more recently, there has been developing
interest in the relationship between balance and gait
impairment and cognitive dysfunction and dementia in
older individuals, in the hope of defining disease predic-
tors as well as prognostic markers. Efforts have been
focused on both vascular dementia and Alzheimer’s
disease (Verghese et al., 2002; Scarmeas et al., 2005).
630 A. VISWANATHAN AND L. SUDARSKY
White matter disease
White matter hyperintensities (WMH) have been shown to
be associated with impaired gait and balance in both cross-
sectional and prospective studies of healthy older indivi-
duals (Baloh and Vinters, 1995; Baloh et al., 1995, 2003;
Tell et al., 1998; Guttmann et al., 2000; Starr et al., 2003;
Baezner et al., 2008; Silbert et al., 2008). This is presum-
ably due to lesions of higher cortical tracts which interrupt
pathways critical for gait and balance, although the precise
mechanism has not been defined. Baloh and colleagues
(2003) prospectively followed 59 healthy subjects older
than 75 years with serial gait and balance examinations
in order to determine variables that predicted change in
gait and balance. Both severity and volume of white mat-
ter lesions were significantly correlated with functional
measures of gait and balance. WMH volume was shown
to be a predictor of yearly change in Tinetti score in mul-
tivariable stepwise regression analysis (Baloh et al., 2003).
In the population-based Cardiovascular Health
Study, investigators found an association between slo-
wed gait speed and WMH (Rosano et al., 2005). They
found that in 321 elderly individuals (mean age 78.3
years), those with gait speed < 1.02 m/s were more likely
to have severe grade of WMH (as evaluated by a semi-
quantitative scale). Furthermore, in another recent
report from this study, worsening white matter lesions
in 1919 participants undergoing two MRI scans sepa-
rated by 5 years predicted decreased gait speed on fol-
low-up examination (p<0.036) (Longstreth et al., 2005).
White matter lesions in the brainstem have also
recently been shown to impact balance function in older
individuals. Starr and coworkers (2003) analyzed gait
speed and balance and their relationship to clinical vari-
ables and WMH in 97 healthy elderly. In multivariable
analysis, only brainstem WMHs were associated with
impaired balance in their population (Starr et al., 2003).
More recently, in a cross-sectional analysis 639 older
individuals in the Leukoaraiosis and Disability (LADIS)
study, severity of white matter lesions was also found to
significantly impact gait speed and balance (p<0.001
for both comparisons) (Baezner et al., 2008).
This finding is consistent with physiologic studies
that have shown that interruption of brainstem tracts
can affect postural control and gait.
Predictor of vascular dementia
Disorders of gait are a well-known presenting feature of
vascular dementias (Rosen et al., 1980; Roman, 1987; Chui
et al., 1992). As gait abnormalities are often present at the
onset of these dementias, Verghese and colleagues (2002)
examined whether they may be a predictor of vascular
dementia. In this community-based study, 422 subjects
aged over 75 years and free of dementia were evaluated.
Subjects’ gait was characterized as one of seven distinct
types (unsteady, hemiparetic, parkinsonian, ataxic,
frontal, spastic, neuropathic). During follow-up (median
follow-up 6.6 years), there were 125 newly diagnosed
cases of dementia (70 Alzheimer’s dementia, 47 vascular
dementia, 8 other). Subjects with gait abnormalities had
an increased risk of developing vascular dementia (hazard
ratio [HR], 3.46; 95% confidence interval [CI], 1.86–6.42)
but not Alzheimer’s dementia (HR, 1.07; 95% CI, 0.57–
2.02). The types of abnormal gait which predicted vascular
dementia were unsteady gait (HR, 2.61), frontal gait (HR,
4.32) and hemiparetic gait (HR, 13.13).
Poor outcome in Alzheimer’s disease
In recent years, there has been a growing interest in the
relation between gait abnormalities and Alzheimer’s
dementia. A recent study has examined the impact of
motor deficits on outcome of patients with early Alzhei-
mer’s disease (AD) (Scarmeas et al., 2005). These inves-
tigators evaluated and then followed 533 patients with
early AD (score of  16 on Folstein Mini-Mental State
Examination [MMSE]) every 6 months (mean follow-up
3 years). Using a standardized portion of the Unified Par-
kinson’s Disease Rating Scale, the presence of motor
signs (including posture and gait abnormalities) were
assessed. The outcomes assessed were in four domains:
a cognitive endpoint (MMSE  10/30), a functional end-
point (Blessed Dementia Rating Scale  10), an institu-
tionalization equivalent index, and death. Those
individuals with posture and gait abnormalities were
found to be at increased risk for institutionalization
(RR, 1.70; 95% CI, 1.16–2.49) and death (RR, 1.56; 95%
CI, 1.17–2.06) after adjustment for covariates including
initial functional and cognitive impairment, age, and edu-
cation. Interestingly, posture and gait abnormalities in
these AD patients were not associated with an increased
risk of poor cognitive or functional outcome.
CONCLUSIONS
Age- and disease-related changes in the central and
peripheral nervous system result in balance and gait
impairment in elderly individuals. Over time, this
impairment can result in falls and injury, with signifi-
cant associated morbidity and mortality.
A systematic approach should be employed in the
evaluation of balance and gait problems in older indivi-
duals. This should include methodical testing of both
patient posture and gait. Fall and disequilibrium pat-
terns should be recorded. Similarly, characterization
of patient gait pattern should be made. Imaging and
laboratory testing may be of benefit in certain cases.
 BALANCE AND GAIT PROBLEMS IN THE ELDERLY
Intervention should be focused on an effort to iden-
tify treatable disorders. Programs to improve postural
control and muscle strength, and reduce the risk of fall
injury have been used with some success, even in frail
seniors (Fiatarone et al., 1994; Tinetti et al., 1994). A
rehabilitation-based intervention or a Tai Chi exercise
program can be recommended when a more specific
treatment is unavailable (Whipple, 1997).
Quantitative measures and imaging techniques may
be useful in future studies to better characterize impair-
ments and to further elucidate mechanisms of gait and
balance dysfunction. Integrative models of balance and
gait dysfunction may lead to better understanding of
different balance and gait phenotypes in the elderly.
In particular, the influence of cognitive and behavioral
domains needs to be better characterized.
REFERENCES
Achiron A, Ziv I, Goren M et al. (1993). Primary progressive
freezing gait. Mov Disord 8: 293–297.
Alexander NB (1994). Postural control in older adults. J Am
Geriatr Soc 42: 93–108.
Alexander NB, Shepard N, Gu MJ et al. (1992). Postural
control in young and elderly adults when stance is per-
turbed: kinematics. J Gerontol 47: M79–M87.
Armstrong DM (1988). The supraspinal control of mamma-
lian locomotion. J Physiol 405: 1–37.
Atchison PR, Thompson PD, Frackowiak RS et al. (1993).
The syndrome of gait ignition failure: a report of six cases.
Mov Disord 8: 285–292.
Baezner H, Blahak C, Poggesi A et al. (2008). Association of
gait and balance disorders with age-related white matter
changes: the LADIS study. Neurology 70: 935–942.
Baloh RW, Vinters HV (1995). White matter lesions and dis-
equilibrium in older people. II. Clinicopathologic correla-
tion. Arch Neurol 52: 975–981.
Baloh RW, Yue Q, Socotch TM et al. (1995). White matter
lesions and disequilibrium in older people. I. Case-control
comparison. Arch Neurol 52: 970–974.
Baloh RW, Ying SH, Jacobson KM (2003). A longitudinal
study of gait and balance dysfunction in normal older peo-
ple. Arch Neurol 60: 835–839.
Beauchet O, Annweiler C, Dubost V et al. (2009). Stops
walking when talking: a predictor of falls in older adults?
Eur J Neurol 16: 786–795.
Berg KO, Wood-Dauphinee SL, Williams JI et al. (1992).
Measuring balance in the elderly: validation of an instru-
ment. Can J Public Health 83: S7–S11.
Bhatia KP (2001). Psychogenic gait disorders. Adv Neurol
87: 251–254.
Bohannon RW, Larkin PA, Cook AC et al. (1984). Decrease in
timed balance test scores with aging. Phys Ther 64: 1067–1070.
Charcot J (1877).Clinical Lectures on Disease of the Nervous
System. Vol. 1. New Sydenham Society, London.
Chen HC, Schultz AB, Ashton-Miller JA et al. (1996). Step-
ping over obstacles: dividing attention impairs performance
631
of old more than young adults. J Gerontol A Biol Sci Med
Sci 51: M116–M1122.
Chui HC, Victoroff JI, Margolin D et al. (1992). Criteria for
the diagnosis of ischemic vascular dementia proposed by
the State of California Alzheimer’s Disease Diagnostic
and Treatment Centers. Neurology 42: 473–480.
Cummings SR, Rubin SM, Black D (1990). The future of hip
fractures in the United States. Numbers, costs, and poten-
tial effects of postmenopausal estrogen. Clin Orthop Relat
Res 163–166.
Dawson D, Hendershot G, Fulton J (1987). Aging in the
eighties: functional limitations of individuals age 65 and
over, Advance Data from Vital and Health Statistics. No.
133. National Center for Health Statistics, Hyattsville,
MD, pp. 1–11.
Diener HC, Dichgans J, Guschlbauer B et al. (1992). The coor-
dination of posture and voluntary movement in patients
with cerebellar dysfunction. Mov Disord 7: 14–22.
Dietz V, Colombo G, Jensen L et al. (1995). Locomotor
capacity of spinal cord in paraplegic patients. Ann Neurol
37: 574–582.
Drew T (1993). Motor cortical activity during voluntary gait
modifications in the cat. I. Cells related to the forelimbs.
J Neurophysiol 70: 179–199.
Ebersbach G, Sojer M, Valldeoriola F et al. (1999). Compar-
ative analysis of gait in Parkinson’s disease, cerebellar
ataxia and subcortical arteriosclerotic encephalopathy.
Brain 122: 1349–1355.
Eidelberg E, Walden JG, Nguyen LH (1981). Locomotor con-
trol in macaque monkeys. Brain 104: 647–663.
Elble RJ, Cousins R, Leffler K et al. (1996). Gait initiation
by patients with lower-half parkinsonism. Brain 119:
1705–1716.
Factor SA, Jennings DL, Molho ES et al. (2002). The natural
history of the syndrome of primary progressive freezing
gait. Arch Neurol 59: 1778–1783.
Factor SA, Higgins DS, Qian J (2006). Primary progressive
freezing gait: a syndrome with many causes. Neurology
66: 411–414.
Fiatarone MA, O’Neill EF, Ryan ND et al. (1994). Exercise
training and nutritional supplementation for physical frailty
in very elderly people. N Engl J Med 330: 1769–1775.
Fife TD, Baloh RW (1993). Disequilibrium of unknown
cause in older people. Ann Neurol 34: 694–702.
FitzGerald PM, Jankovic J (1989). Lower body parkinsonism:
evidence for vascular etiology. Mov Disord 4: 249–260.
Garcia-Rill E (1986). The basal ganglia and the locomotor
regions. Brain Res 396: 47–63.
Garcia-Rill E (1991). The pedunculopontine nucleus. Prog
Neurobiol 36: 363–389.
Gerson LW, Jarjoura D, McCord G (1989). Risk of imbalance
in elderly people with impaired hearing or vision. Age
Ageing 18: 31–34.
Giladi N, McDermott MP, Fahn S et al. (2001). Freezing of
gait in PD: prospective assessment in the DATATOP
cohort. Neurology 56: 1712–1721.
Grillner S, Wallen P (1985). Central pattern generators for
locomotion, with special reference to vertebrates. Annu
Rev Neurosci 8: 233–261.
632 A. VISWANATHAN AND L. SUDARSKY
Guttmann CR, Benson R, Warfield SK et al. (2000). White
matter abnormalities in mobility-impaired older persons.
Neurology 54: 1277–1283.
Hayes MW, Graham S, Heldorf P et al. (1999). A video
review of the diagnosis of psychogenic gait: appendix
and commentary. Mov Disord 14: 914–921.
Holmes G (1922). Clinical symptoms of cerebellar disease
and their interpretation, the Croonian Lectures. Lancet 2:
59–65.
Horak FB (1987). Clinical measurement of postural control in
adults. Phys Ther 67: 1881–1885.
Horak FB (2001). Postural ataxia related to somatosensory
loss. Adv Neurol 87: 173–182.
Horak FB, Diener HC (1994). Cerebellar control of postural
scaling and central set in stance. J Neurophysiol 72: 479–493.
Iansek R, Ismail NH, Bruce M et al. (2001). Frontal gait
apraxia. Pathophysiological mechanisms and rehabilita-
tion. Adv Neurol 87: 363–374.
Jankovic J, Nutt JG, Sudarsky L (2001). Classification, diag-
nosis, and etiology of gait disorders. Adv Neurol 87:
119–133.
Keane JR (1989). Hysterical gait disorders: 60 cases. Neurol-
ogy 39: 586–589.
Kerber KA, Enrietto JA, Jacobson KM et al. (1998). Disequi-
librium in older people: a prospective study. Neurology
51: 574–580.
Keshner EA, Allum JHJ (1986). Plasticity in pitch sway sta-
blization: normal habituation and compensation for
peripheral vestibular deficits. In: W Bles, T Brandt
(Eds.), Disorders of Posture and Gait. Elsevier, New York,
pp. 289–314.
Keshner EA, Cohen H (1989). Current concepts of the vestib-
ular system reviewed. 1. The role of the vestibulospinal
system in postural control. Am J Occup Ther 43: 320–330.
Labadie EL, Awerbuch GI, Hamilton RH et al. (1989). Fall-
ing and postural deficits due to acute unilateral basal
ganglia lesions. Arch Neurol 46: 492–496.
Lajoie Y, Teasdale N, Bard C et al. (1996a). Upright standing
and gait: are there changes in attentional requirements
related to normal aging? Exp Aging Res 22: 185–198.
Lajoie Y, Teasdale N, Cole JD et al. (1996b). Gait of a deaf-
ferented subject without large myelinated sensory fibers
below the neck. Neurology 47: 109–115.
Lawrence DG, Kuypers HG (1968). The functional organiza-
tion of the motor system in the monkey. II. The effects of
lesions of the descending brain-stem pathways. Brain 91:
15–36.
Lee WA (1989). A control systems framework for under-
standing normal and abnormal posture. Am J Occup Ther
43: 291–301.
Lempert T, Brandt T, Dieterich M et al. (1991). How to identify
psychogenic disorders of stance and gait. A video study in
37 patients. J Neurol 238: 140–146.
Lipsitz LA, Jonsson PV, Kelley MM et al. (1991). Causes and
correlates of recurrent falls in ambulatory frail elderly.
J Gerontol 46: M114–M122.
Llinas R, Walton K (1979). Vestibular compensation: a
distributed property of the central nervous system. In:
H Asanyma, VT Wilson (Eds.), Integration in the Nervous
System. Igaku-Shion, Tokyo, pp. 145–166.
Longstreth WT Jr., Arnold AM, Beauchamp NJ Jr. et al.
(2005). Incidence, manifestations, and predictors of wors-
ening white matter on serial cranial magnetic resonance
imaging in the elderly: the Cardiovascular Health Study.
Stroke 36: 56–61.
Lord SR, Clark RD, Webster IW (1991). Postural stability
and associated physiological factors in a population of
aged persons. J Gerontol 46: M69–M76.
Macpherson JM, Fung J (1999). Weight support and balance
during perturbed stance in the chronic spinal cat. J Neuro-
physiol 82: 3066–3081.
Masdeu JC, Gorelick PB (1988). Thalamic astasia: inability
to stand after unilateral thalamic lesions. Ann Neurol 23:
596–603.
Massion J (1994). Postural control system. Curr Opin Neuro-
biol 4: 877–887.
Mayer NH, Esquenazi A, Keenan MA (2001). Patterns of
upper motoneuron dysfunction in the lower limb.
Adv Neurol 87: 311–319.
McCollum G, Leen TK (1989). Form and exploration of
mechanical stability limits in erect stance. J Mot Behav
21: 225–244.
Meyer JS, Barron DW (1960). Apraxia of gait: a clinico-
physiologic study. Brain 83: 261–284.
Mittelstaedt H (1999). The role of the otoliths in perception
of the vertical and in path integration. Ann N Y Acad
Sci 871: 334–344.
Mori S (1987). Integration of posture and locomotion in acute
decerebrate cats and in awake, freely moving cats. Prog
Neurobiol 28: 161–195.
Mori S (1997). Neurophysiology of locomotion: recent advances
in the study of locomotion. In: JC Masdeu, L Sudarsky,
L Wolfson (Eds.), Gait Disorders of Aging: Falls and Thera-
peutic Strategies. Lippincott-Raven, Philadelphia.
Mori S, Sakamoto T, Ohta Y et al. (1989). Site-specific pos-
tural and locomotor changes evoked in awake, freely
moving intact cats by stimulating the brainstem. Brain
Res 505: 66–74.
Muller J, Seppi K, Stefanova N et al. (2002). Freezing of
gait in postmortem-confirmed atypical parkinsonism.
Mov Disord 17: 1041–1045.
Murphy J, Isaacs B (1982). The post-fall syndrome. A study
of 36 elderly patients. Gerontology 28: 265–270.
Murray MP, Kory RC, Clarkson BH (1969). Walking patterns
in healthy old men. J Gerontol 24: 169–178.
Newman G, Dovermuehle RH, Busse EW (1960). Alterations
in neurologic status with age. J Am Geriatr Soc 8: 915–917.
Nieves AV, Miyasaki JM, Lang AE (2001). Acute onset dys-
tonic camptocormia caused by lenticular lesions. Mov
Disord 16: 177–180.
Nutt JG (1998). Gait and balance disorders, a syndrome
approach. In: J Jankovic, E Tolosa (Eds.), Parkinson’s
Disease and Movement Disorders. Williams and Wilkins,
Baltimore.
Nutt JG (2001). Classification of gait and balance disorders.
Adv Neurol 87: 135–141.
 BALANCE AND GAIT PROBLEMS IN THE ELDERLY
Nutt JG, Horak FB (2004). Classification of balance and gait
disorders. In: AM Bronstein, T Brandt, M Woollacott
et al. (Eds.), Clinical Disorders of Balance. Posture and
Gait. Hodder & Stoughton, London, pp. 63–73.
Nutt JG, Marsden CD, Thompson PD (1993). Human walk-
ing and higher-level gait disorders, particularly in the
elderly. Neurology 43: 268–279.
O’Brien CF (2001). Chemodenervation with botulinum toxin
for spasticity and dystonia. The effects on gait. Adv
Neurol 87: 265–269.
Odenheimer G, Funkenstein HH, Beckett L et al. (1994).
Comparison of neurologic changes in ’successfully aging’
persons vs the total aging population. Arch Neurol 51:
573–580.
Orlovsky GN (1972). The effect of different descending sys-
tems on flexor and extensor activity during locomotion.
Brain Res 40: 359–371.
Pahapill PA, Lozano AM (2000). The pedunculopontine
nucleus and Parkinson’s disease. Brain 123: 1767–1783.
Palliyath S, Hallett M, Thomas SL et al. (1998). Gait in
patients with cerebellar ataxia. Mov Disord 13: 958–964.
Paulus WM, Straube A, Brandt T (1984). Visual stabilization
of posture. Physiological stimulus characteristics and clin-
ical aspects. Brain 107: 1143–1163.
Rascol O, Brooks DJ, Korczyn AD et al. (2000). A five-year
study of the incidence of dyskinesia in patients with early
Parkinson’s disease who were treated with ropinirole or
levodopa. 056 Study Group. N Engl J Med 342: 1484–1491.
Richardson JK, Ching C, Hurvitz EA (1992). The relationship
between electromyographically documented peripheral
neuropathy and falls. J Am Geriatr Soc 40: 1008–1012.
Roman GC (1987). Senile dementia of the Binswanger type.
A vascular form of dementia in the elderly. JAMA 258:
1782–1788.
Romberg MH (1853). Manual of the Nervous System of Man.
Vol. 2. Sydenham Society, London.
Rondot P, Odier F, Valade D (1992). Postural disturbances
due to homonymous hemianopic visual ataxia. Brain 115:
179–188.
Rosano C, Brach J, Longstreth Jr WT et al. (2005). Quantita-
tive measures of gait characteristics indicate prevalence of
underlying subclinical structural brain abnormalities in
high-functioning older adults. Neuroepidemiology 26:
52–60.
Rosen WG, Terry RD, Fuld PA et al. (1980). Pathological
verification of ischemic score in differentiation of demen-
tias. Ann Neurol 7: 486–488.
Rubenstein L, Josephson KR (1997). Interventions to reduce
the multifactorial risks for falling. In: JC Masdeu,
L Sudarsky, L Wolfson (Eds.), Gait Disorders of Aging:
Falls and Therapeutic Strategies. Lippincott-Raven,
Philadelphia, pp. 13–36.
Rubinstein TC, Giladi N, Hausdorff JM (2002). The power of
cueing to circumvent dopamine deficits: a review of phys-
ical therapy treatment of gait disturbances in Parkinson’s
disease. Mov Disord 17: 1148–1160.
Sabin TD (1997). Peripheral neuropathy: disorders of propri-
oception. In: J Masdeu, L Sudarsky, L Wolfson (Eds.),
633
Gait Disorders of Aging: Falls and Therapeutic Strategies.
Lippincott-Raven, Philadelphia.
Scarmeas N, Albert M, Brandt J et al. (2005). Motor signs
predict poor outcomes in Alzheimer disease. Neurology
64: 1696–1703.
Schoch B, Dimitrova A, Gizewski ER et al. (2006). Func-
tional localization in the human cerebellum based on vox-
elwise statistical analysis: a study of 90 patients.
Neuroimage 30: 36–51.
Shumway-Cook A, Horak FB (1990). Rehabilitation strate-
gies for patients with vestibular deficits. Neurol Clin 8:
441–457.
Silbert LC, Nelson C, Howieson DB et al. (2008). Impact of
white matter hyperintensity volume progression on rate
of cognitive and motor decline. Neurology 71: 108–113.
Sixt E, Landahl S (1987). Postural disturbances in a 75-year-
old population: I. Prevalence and functional conse-
quences. Age Ageing 16: 393–398.
Springer S, Giladi N, Peretz C et al. (2006). Dual-tasking
effects on gait variability: the role of aging, falls, and
executive function. Mov Disord 21: 950–957.
Starr JM, Leaper SA, Murray AD et al. (2003). Brain white
matter lesions detected by magnetic resonance imaging
are associated with balance and gait speed. J Neurol
Neurosurg Psychiatry 74: 94–98.
Sudarsky L (1990). Geriatrics: gait disorders in the elderly.
N Engl J Med 322: 1441–1446.
Sudarsky L (2001). Gait disorders: prevalence, morbidity,
and etiology. Adv Neurol 87: 111–117.
Sudarsky L (2004). Gait disorders. In: RL Watts, WC Koller
(Eds.), Movement Disorders: Neurologic Principles and
Practice. McGraw-Hill, Columbus, pp. 813–824.
Sudarsky L, Ronthal M (1983). Gait disorders among elderly
patients. A survey study of 50 patients. Arch Neurol 40:
740–743.
Tell GS, Lefkowitz DS, Diehr P et al. (1998). Relationship
between balance and abnormalities in cerebral magnetic
resonance imaging in older adults. Arch Neurol 55:
73–79.
Thach WT, Bastian AJ (2004). Role of the cerebellum in the
control and adaptation of gait in health and disease.
Prog Brain Res 143: 353–366.
Thach WT, Kane SA, Goodkin M (1992). Cerebellar output:
multiple maps and models of control in movement coordi-
nation. In: RSC Llinas (Ed.), The Cerebellum Revisited.
Springer Verlag, New York.
Thompson PD, Marsden CD (1987). Gait disorder of sub-
cortical arteriosclerotic encephalopathy: Binswanger’s
disease. Mov Disord 2: 1–8.
Tinetti ME (1986). Performance-oriented assessment of
mobility problems in elderly patients. J Am Geriatr Soc
34: 119–126.
Tinetti ME, Williams CS (1997). Falls, injuries due to falls,
and the risk of admission to a nursing home. N Engl
J Med 337: 1279–1284.
Tinetti ME, Speechley M, Ginter SF (1988). Risk factors for
falls among elderly persons living in the community.
N Engl J Med 319: 1701–1707.
634 A. VISWANATHAN AND L. SUDARSKY
Tinetti ME, Baker DI, McAvay G et al. (1994). A multifacto-
rial intervention to reduce the risk of falling among
elderly people living in the community. N Engl J Med
331: 821–827.
Verghese J, Lipton RB, Hall CB et al. (2002). Abnormality of
gait as a predictor of non-Alzheimer’s dementia. N Engl J
Med 347: 1761–1768.
Whipple RH (1997). Improving balance in older adults: iden-
tifying the significant training stimuli. In: J Masdeu,
L Sudarsky, L Wolfson (Eds.), Gait Disorders of Aging:
Falls and Therapeutic Strategies. Lippincott - Raven,
Philadelphia.
Woollacott M, Shumway-Cook A (2002). Attention and the
control of posture and gait: a review of an emerging area
of research. Gait Posture 16: 1–14.