A history of falling into the sink or imbalance when splashing water on the face (wash-basin sign),

passing a towel over the face or pulling a shirt over the head should also be sought.

Pseudoathetosis–”piano-playing” movements—when the patient has his arms outstretched and eyes

closed, the affected arm will wander from its original position.

Vibration and position sense are usually lost together.

Positive Romberg’s test is a hallmark of sensory ataxia.

Vestibular ataxia is due to lesion of vestibular pathways resulting in impairment and imbalance of

vestibular inputs, e.g. vestibular, neuronitis, and streptomycin toxicity.

Vertigo and associated tinnitus and hearing loss.

Direction of the nystagmus is away from the lesion.

Optic ataxia was first described in a man with lesions of the posterior parietal lobe on both sides of the

brain, later known as Balint syndrome.

Among the symptoms that characterize the syndrome are a restriction of visual attention to single

objects and a paucity of spontaneous eye movements.

Patients have difficulty in completing visually guided reaching tasks in the absence of other sensory

cues.

Frontal lobe ataxia (Brun’s ataxia) is due to involvement of subcortical small vessels, Binswanger’s

disease, multi infarct state or normal pressure hydrocephalus (NPH).

The gait may appear to be a combination of awkward, magnetic (stuck to the floor), cautious, slow,

and shuffling. This is also known as a frontal gait disorder, referring to the frontal lobe conditions

which often cause gait apraxia.

CEREBELLAR ATAXIA

Fig. 6D(vii).11: Anatomical and functional areas of cerebellum.

Zone [Fig.

6D(vii).11]

Corresponding

anatomical site

Function Loss of function

Midline zone Anterior and posterior

parts of the vermis,

fastigial nucleus

Posture, locomotion, position of head

relative to trunk, control of extraocular movements

Disorders of stance/gait, truncal postural

disturbances, rotated postures of the head,

disturbances of eye movements

Intermediate

zone

Paravermal region of

cerebellum and

interposed nuclei

(emboliform, globose)

Control of velocity, force and pattern of muscle activity

—

Lateral zone Cerebellar hemisphere

and dentate nucleus

Planning of fined and skilled movement (in connection with neurons

in the Rolandic region of the cerebral

cortex).

Hypotonia, dysarthria, dysmetria,

dysdiadochokinesia, excessive rebound,

impaired check, kinetic and static tremors,

past pointing

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CAUSES OF CEREBELLAR ATAXIA

Symmetrical Cerebellar Ataxias

Acute Subacute Chronic

Drugs: Phenytoin, phenobarbitone, lithium, Chemotherapeutic

agents

Alcohol

Infectious: Acute viral cerebellitis, post-infectious

Toxins: Toluene, glue, gasoline, methyl mercury

Alcohol, or Nutritional (B1

, B12

)

Paraneoplastic

Antigliadin or anti-GAD antibody

Prion diseases

MSA-C

Hypothyroidism

Phenytoin toxicity

(GAD: glutamic acid decarboxylase; MSA-C: multiple system atrophy with cerebellar ataxia)

Asymmetrical Cerebellar Ataxias

Acute Subacute Chronic

Vascular: Cerebellar infarction or

hemorrhage, subdural hematoma

Infectious: Abscess

Neoplastic: Glioma, metastases,

lymphoma

Demyelination: MS

HIV related: Progressive multifocal leukoencephalopathy

Congenital lesions: Arnold Chiari malformation, Dandy Walker syndrome

Treatable Causes of Ataxia

Hypothyroidism

Ataxia with vitamin E deficiency (AVED)

Vitamin B12 deficiency

Wilson’s disease

Ataxia with antigliadin antibodies and gluten sensitive enteropathy

Ataxia due to malabsorption syndromes

Lyme’s disease

Mitochondrial encephalomyopathies, aminoacidopathies, leukodystrophies and urea cycle abnormalities Wernicke’s encephalopathy

Cerebellar Syndromes

Rostral vermis syndrome

(anterior lobe)

For example, alcoholics

Wide-based stance and gait.

Ataxia of gait; proportionally less ataxia is seen on

performing Heel-shin test while the patient is lying down.

Normal or slightly impaired arm coordination.

Infrequent hypotonia, nystagmus and/or dysarthria.

Caudal vermis syndrome

(flocculonodular, posterior lobe)

For example, tumors (medulloblastoma)

Axial disequilibrium; staggering gait.

Little or no limb ataxia.

Spontaneous nystagmus might be seen.

Rotated postures of head.

Hemispheric syndrome

(Posterior lobe, anterior variants also possible)

For example, infarcts, neoplasms, abscesses.

Incoordination of ipsilateral limb movements.

More noticeable with fine motor skills.

Incoordination affects most noticeably muscles involved in

speech and finger movements.

Pancerebellar syndrome

For example, infectious/parainfectious processes, hypoglycemia,

paraneoplastic disorders, toxic-metabolic disorders

Combination of all the other syndromes.

Bilateral signs of cerebellar dysfunction involving trunk,

limbs, cranial musculature.

LOCALIZATION OF CEREBELLAR LESIONS

Signs and symptoms Most probable region of involvement

Higher cognitive changes Lateral hemispheres

Action tremor Dentate and interposed nuclei OR cerebellar outflow to ventral thalamus

Palatal tremor Dentate nucleus, Guillain Mollaret triangle

Titubation Any zone; especially anterior vermis and associated deep nuclei

Dysarthria Posterior left hemisphere and vermis

Gait ataxia Anterior vermis

Limb ataxia Lateral hemispheres

Saccadic dysmetria Dorsal vermis

Square wave jerks Cerebellar outflow

Gaze evoked nystagmus Flocculus and paraflocculus

Mnemonics for cerebellar signs

Danish pen Vanishd

Dysdiadochokinesia

Ataxic gait

Nystagmus

Intention tremor

Scaning/Staccato speech

Hypotonia/Heel-shin test

Pendular knee jerk

Vertigo

Ataxia

Nystagmus

Intentional tremor

Scanning speech

Hypotonia

Dysdiadochokinesia

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D(viii). GAIT

NORMAL GAIT CYCLE [FIGS. 6D(VIII).1A TO G]

The gait cycle is the time interval or sequence of motions occurring between two consecutive initial

contacts of the same foot, i.e. cycle of stance and swing by one foot.

Figs. 6D(viii).1A to G: Normal gait cycle.

Observation to be noted while the patient walks:

Posture of the body while walking

The regularity of the movement

The position and movement of the arms

The relative ease and smoothness of the movement of the legs

The distance between the feet both in forward and lateral directions

The ability to maintain a straight course

The ease of turning

Stopping

Position of feet and posture just before initiation of gait.

ABNORMALITIES OF GAIT

Neurogenic gait disorders should be differentiated from those due to skeletal abnormalities

(characterized by pain producing an antalgic gait, or limp).

Gait abnormalities incompatible with any anatomical or physiological deficit may be due to functional

disorders.

Pyramidal (Circumduction/Hemiplegic) Gait [Fig. 6D(viii).2]

Lesions of the upper motor neuron lesions produce characteristic extension of the affected leg. There

is tendency for the toes to strike the ground on walking and outward throwing/swing of lower limbs.

This movement occurring at the hip joint is called circumduction. There is leaning towards the

opposite normal side. The arm of the affected side is adducted at the shoulder and flexed at the

elbow, wrist, and fingers.

In hemiplegia/hemiparesis, there is a clear asymmetry between affected and normal sides on walking,

but in paraparesis both lower legs swing slowly from the hips in extension and are stiffly dragged over

the ground (walking in mud).

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Fig. 6D(viii).2: Circumduction gait.

Foot Drop (High Stepping/Slapping Gait) [Fig. 6D(viii).3]

In normal walking, the heel is the first part of the foot to hit the ground. A lower motor neuron lesion

affecting the leg will cause weakness of ankle dorsiflexion, resulting in a less controlled descent of the

foot, which makes slapping noise as it hits the ground. In severe cases, the foot will have to be lifted

higher at the knee to allow room for the inadequately dorsiflexed foot to swing through, resulting in a

high-stepping gait. Cause, e.g. common peroneal nerve palsy.

Fig. 6D(viii).3: High stepping gait.

Myopathic Gait/Waddling Gait [Fig. 6D(viii).4]

During walking, alternating transfer of the body’s weight through each leg, needs adequate hip

abduction.

Causes: Weakness of proximal lower limb muscles (e.g. polymyositis and muscular dystrophy)

causes difficulty rising from sitting. The hips are not properly fixed by these muscles and trunk

movements are exaggerated, and walking becomes a waddle or rolling. The pelvis is poorly supported

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by each leg. This may be seen with bilateral congenital dislocation of hip (Trendelenburg gait). The

patient walks on a broad base with exaggerated lumbar lordosis.

Gluteus Medius Gait or Abductor Lurch

Lurch of body towards affected side in every stance phase (abductor lurch). Seen with congenital coxa

vara, gluteus medius paralysis, polio, and Perthes disease.

Fig. 6D(viii).4: Waddling gait.

Ataxic Gait (Cerebellar Ataxia: Broad-based Gait) [Fig. 6D(viii).5]

In this type of gait, the patient, unstable, tremulous and reels in any direction (including backwards)

and walks on a broad base. Ataxia describes this incoordination. The patient finds difficulty in

executing tandem walking.

Causes: Lesions of the cerebellum, vestibular apparatus or peripheral nerves. When walking, the

patient tends to veer to the side of the affected cerebellar lobe. When the disease involves cerebellar

vermis, the trunk becomes unsteady without limb ataxia, with a tendency to fall backwards or

sideways and is termed truncal ataxia.

Fig. 6D(viii).5: Cerebellar/ataxic gait.

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Apraxic Gait

In an apraxic gait, the acquired walking skills become disorganized. On examination of the legs, the

power, cerebellar function, and proprioception are normal. Leg movement is normal when sitting or

lying and the patient can carry out complex motor tasks (e.g. bicycling motion). But patient cannot

initiate and organize the motor act of walking. The feet appear stuck to the floor and the patient

cannot walk.

Causes: Diffuse bilateral hemisphere disease or diffuse frontal lobe disease (e.g. tumor,

hydrocephalus, and infarction).

Marche à petits pas

It is characterized by small, slow steps, and marked instability. In contrast to the festination found in

Parkinson’s disease, it lacks increasing pace and freezing.

Cause: Small-vessel cerebrovascular disease and accompanying bilateral upper motor neuron signs.

Extrapyramydal/Shuffling/Festinant Gait [Fig. 6D(viii).6]

It is characterized by stooped posture and gait difficulties with problems initiating walking and

controlling the pace of the gait. Patients make a series of small, flat footed shuffles, and become stuck

while trying to start walking or when walking through doorways (freezing). The center of gravity will be

moved forwards to aid propulsion and difficulty in stopping. It is characterized by muscular rigidity

throughout extensors and flexors. Power is preserved, pace is shortened and slows to a shuffle, and

its base remains narrow. There is a stoop and diminished arm swinging and gait becomes festinant

(hurried) with short rapid steps. Patient will be having difficulty in turning quickly and initiating

movement. Retropulsion, i.e. small backward steps are taken involuntarily when a patient halts.

Cause: Parkinsonism.

[Kinesia paradoxa—presented in Parkinson’s disease patients, who generally cannot move but under

certain circumstances of need exhibit a sudden, brief period of mobility (walking or even running)]

Scissoring Gait [Figs. 6D(viii).7A and B]

Seen classically with cerebral palsy due to bilateral spasticity.

Sensory Ataxia: Stamping Gait [Fig. 6D(viii).8]

It is characterized by broad based, high stepping, stamping gait, and ataxia due to loss of

proprioception (position sense). This type of ataxia becomes more prominent by removal of sensory

input (e.g. walks with eyes closed) and becomes worse in the dark. Romberg’s test is positive.

Cause: Peripheral sensory (large fiber) lesions (e.g. polyneuropathy), posterior column lesion (vitamin

B12 deficiency or tabes dorsalis).

Fig. 6D(viii).6: Stages of Parkinson’s gait.

Figs. 6D(viii).7A and B: Scissoring gait.

Fig. 6D(viii).8: Sensory ataxia.

Choreiform Gait (Hyperkinetic Gait)

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The patient will display irregular, jerky, and involuntary movements in all extremities. Walking may

accentuate their baseline movement disorder.

Cause: Sydenham’s chorea, Huntington’s disease, and other forms of chorea, athetosis or dystonia.

Antalgic or Painful Gait

Decreased duration of stance phase as the painful limb is unable to bear full weight. It is seen in any

painful lesion of the lower extremity, i.e. foot, knee, and hip.

Coxalgic Gait [Figs. 6D(viii).9A and B]

In patients with hip pain, the upper trunk is typically shifted towards the affected side during the stance

phase on the affected leg. This is an unconscious adaptive maneuver which reduces the force exerted

on the affected hip during the stance phase.

Figs. 6D(viii).9A and B: Trendelenburg gait versus coxalgic gait.

Toe-walking or Equinus Gait

Heel strike is avoided. It is seen in patients with heel pain, clubfoot, congenital short Achilles tendon,

and cerebral palsy.

Quadriceps Weakness Gait

Inability to maintain knee extension at heel-strike and patient may push on thigh to extend the knee and

lock. It is seen in quadriceps paralysis.

Astasia-Abasia

It is a psychogenic pattern of walking in which the patient seems to alternate between a broad base for

stability and a narrow, tightrope-like stance, with contortions of the trunk, and limbs that give the

appearance of an imminent fall.

Alderman’s Gait

Patient walks with chest and head thrown backwards with protuberant abdomen and legs thrown wide

apart. It is seen in tuberculosis of lower thoracic and upper lumbar vertebra.

GAIT ABNORMALITIES ANALYSIS

Gait initiation, maintenance, and

termination

Difficulty starting PD, atypical parkinsonism

Freezing of gait PD, atypical parkinsonism

Inability to stop (festination) PD, atypical parkinsonism

Stance width

Narrowed base of support PD, spastic paraparesis

Widened base of support Cerebellar ataxia, sensory ataxia, vestibular

ataxia

Scissoring of the legs Spastic paraparesis

Unable to walk in a straight line, sideways deviation

(veering) of gait

Unilateral vestibular ataxia, unilateral

cerebellar ataxia

Step length,

height, and

cadence

Reduced step height PD, parkinsonism; foot drop

Small steps PD, atypical parkinsonism, normal pressure

hydrocephalus

Irregular step size Cerebellar ataxia, vestibular ataxia, chorea

Reduced stance phase on the affected side (limping) Pain (antalgic gait)

Arm swing

Unilaterally reduced Hemiparesis, dystonia, PD

Bilaterally reduced PD, parkinsonism, dystonia

Excessive Chorea, levodopa‑induced dyskinesias, NPH

Tremor appearing in hand during walking PD, parkinsonism

Movement fluidity

Dropped foot, lifting the leg higher than normal (steppage

gait)

Neuropathy of common fibular nerve or

sciatic nerve, L5 radiculopathy, Charcot– Marie–Tooth disease

Knees giving way (buckling of the knees) Quadriceps weakness (for example,

limb‑girdle myopathy, IBM)

Locking of the knees Cerebellar ataxia

Pelvis drop at side of the swing leg, resulting in alternating

lateral trunk movements (waddling gait and bilateral

Trendelenburg gait)

Bilateral proximal muscle weakness in the leg

and hip girdle

Bizarre gait pattern Chorea

Gait speed

Slow PD

Fast Vestibular disease, Alzheimer’s disease

(PD: Parkinson’s disease; NPH: normal pressure hydrocephalus; IBM: inclusion body myositis)

BEDSIDE TESTS TO DIAGNOSE PES CAVUS AND PES PLANUS

Wet Test [Fig. 6D(viii).10]

There are three basic foot types, each based on the height of the arches. The quickest and easiest way

to determine your foot type is by taking the “wet test,” below. (1) Pour a thin layer of water into a shallow

pan. (2) Wet the sole of your foot. (3) Step onto a shopping bag or a blank piece of heavy paper. (4)

Step off and look down. Observe the shape of your foot

Fig. 6D(viii).10: Wet test and appearance.

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