Practical approach to the assessment
of gait:
watch the patient walk along a stretch of
corridor and observe the characteristics of the
gait.Note the following:
-Whether the patient walks unaided:if not,does the
patient walk with a stick or crutches?.
-Whether the patient walks in a straight
line:patients who are ataxic are unsteady and may
be unable to tandem walk i.e.heel-to-toe walking.
-Normal arm swing: arm swing may be reduced in
patients who have an extra-pyramidal
syndrome.This may be more marked on one side
than the other,especially in idiopathic Parkinson’s
disease.
-Turning around:patients who have an extrapyramidal syndrome or ataxia perform this with
difficulty.
-Standing and walking on the toes(S1)and then
heels(L5):patients with a common peroneal nerve
palsy and L5 or S1 radiculopathy will find this
difficult,as will patients with a hemiparesis.
-Perform Romberg’s test:ask the patient to stand
with feet together and eyes closed.The test is
positive if the patient is more unsteady with eyes
closed than with eyes open.This occurs in patients
with a sensory ataxia who have impaired
proprioception.It cannot be tested reliably in
patients with a cerebellar disorder or moderate to
severe weakness from any cause as the patient will
be unsteady irrespective of whether there is
sensory ataxia.
Differential diagnosis of disorders of gait
Gait of cerebellar ataxia:
Patients with cerebellar ataxia stand and walk unsteadily,as
if drunk.They soon begin to compensate for this by
adopting a broad base with feet further apart(fig).The gait
is unsteady ,with irregularity of stride.
The trunk sways and the patient may veer towards one side.In
mild cases,the only manifestation of gait disturbance may
be difficulty walking heel-to-toe in a straight line(i.e.
tandem walking).
On neurological exam there may also be
nystagmus,dysarthria and cerebellar signs in the
limbs.Ataxia may be confined to the gait when the
cerebellar lesion is in the midline.
Cerebellar ataxia(cont’d)
Causes include:
-Multiple sclerosis
-Vascular disease (ischemic,hemorrhagic, AVMs)
-Alcoholic cerebellar degeneration
-Anticonvulsant therapy : carbamazepine,
phenytoin
-Posterior fossa tumours
-Cerebellar paraneoplastic syndrome
-The hereditary cerebellar ataxias.
Hemiparetic gait
Patients with a hemiparetic gait have a
characteristic posture on one side,of flexion and
internal rotation of the upper limb and extension
of the lower limb(fig).The leg moves stiffly and is
swung around in a semicircle to avoid scraping the
foot across the floor.However such scraping does
occur to some extent and the toe and outer sole of
the shoe become worn.
Causes include:cortical or internal capsule
strokes,cerebral hemispheric tumour and
traumatic lesions.
Spastic gait
A spastic gait is seen in patients who have a spastic
paraparesis or bilateral hemiparesis.The legs move
slowly and stiffly and the thighs are strongly adducted
such that the legs may cross as the patient walks or
“scissor gait”.
Causes of spastic gait:
-Spinal cord compression.
-Trauma/spinal surgery.
-Birth injuries or congenital deformities:
cerebral palsy,spina bifida.
-Multiple sclerosis.
-Motor neuron disease.
-Parasagittal meningioma.
-Subacute combined degeneration of the cord.
Parkinsonian gait
The patient often has a stooped and flexed posture
with loss of arm swing,which is almost always
more marked on one side in idiopathic Parkinson’s
disease(figs).The steps are short and the patient
shuffles.
There may be difficulty starting and
stopping.Turning may occur “en bloc”(i.e. not
smoothly but in stiff stuttering
movements).Having started to walk,the patient
leans forward and the pace quickens,as though the
patient is attempting to catch up on himself or
herself(festinant gait).
Gait of sensory ataxia
Sensory ataxia arises from impaired proprioception
caused by a lesion of the peripheral nerves,posterior
roots,dorsal columns in the spinal cord or rarely the
ascending fibres to the parietal lobes.The gait is
unsteady and wide-based and often stamping
(fig).Romberg’s test is positive and there is impaired
perception of joint position on examination of the
lower limbs.
Causes of sensory ataxia:
*Posterior spinal cord lesions:
-Multiple sclerosis
- Cervical spondylosis
- Tumours
- Vitamin B12 deficiency
- Tabes dorsalis
*Sensory peripheral neuropathies include:
-hereditary:Charcot-Marie-Tooth disease
-metabolic:diabetes
-inflammatory:Guillain-Barre syndrome
-malignancy:myeloma,paraneoplastic syndrome
-toxic:alcohol,drugs(e,g. isoniazide)
Steppage gait
Steppage gait arises from weakness of the pretibial and
peroneal muscles of lower motor neuron type.The
patient has footdrop and is unable to dorsiflex and
evert the foot(fig).The leg is lifted high on walking so
that the toes clear the ground.On striking the floor
again,there is a slapping noise.Shoe soles are worn on
the anterior and lateral aspects.
Causes of steppage gait:
-Charcot-Marie-Tooth disease(bilateral footdrop)
- -Common peroneal nerve palsy e.g.from a fibular
fracture(unilateral footdrop)
- Anterior horn cell disease e.g. polio,motor neuron
disease (often asymmetrical footdrop)
Myopathic gait
Myopathic gait ic the so-called waddling gait caused by
weakness of the proximal muscles of the lower limb
girdle.The weight is alternately placed on each leg,with
the opposite hip and side of the trunk tilting up
towards the weight-bearing hip,which sways
outward,with the opposite pelvis dropping as does the
trunk on that side.
Causes of waddling gait:
Muscular dystrophies:Duchenne’s,Becker’s,
limb-girdle,facio-scapulo-humeral.
- -Metabolic myopathies:periodic paralysis,hypo- and
hyperkalemia.
- -Endocrine myopathies:Cushing’s disease
Addison’s disease,hypo- and hyperthyroidism.
-Inflammatory myopathies:polymyositis and
dermatomyositis.
Apraxic gait
Diseases of the frontal lobes gives rise to an apraxic
gait.The patient walks with feet placed apart and
with small hesitant steps,which may be described
as ‘walking on ice’ or ‘marche a petit pas’.There is
difficulty with initiation of walking and,in
advanced cases,it may seem as though the patient’s
feet are stuck to the floor .
There are no abnormalities of power,sensation or
coordination.There may be other signs of frontal
cortical dysfunction(e.g. grasp or rooting
reflex);the tendon reflexes may be brisk and the
plantar responses extensor.
Causes of apraxic gait include:
- Bilateral subcortical cerebrovascular disease
- Normal-pressure hydrocephalus
- Frontal lobe tumours e.g. meningioma
-Frontal subdural hematomas(rare;
bilateral usually)
-Advanced Alzheimer’s disease.
Antalgic gait
Antalgic gait arises from pain(e.g.a painful hip or knee
due to arthritis).The patient tends to bear weight
mainly on the unaffected side,only briefly putting
weight onto the affected side.
Functional gait
A functional ,hysterical or non-organic gait arises from
psychological or behavioural disturbance.It does not
conform to any descriptions given above.It can take a
number of forms and is variable in character.There are
no objective abnormal neurological signs on formal
examination.
Functional gait(cont’d)
There are often other positive features of an underlying
psychiatric disturbance.
However,the only manifestation of a midline
cerebellar lesion may be severe ataxia of gait and
stance,with normal limb signs on formal examination
and this can sometimes be mistaken for a non-organic
illness.
The character of a patient’s gait will provide clues to the clinical
signs that might be expected on further neurological exam.
The abnormal types of gait are:
*Ataxic:broad-based and unsteady.
*Hemiplegic:unilateral flexed posture of the upper limb and
extended posture of the lower limb.
*Spastic:’scissoring’ posture of the legs.
*Parkinsonian:stooped posture,shuffling small stepped gait
with loss of arm swing.
*Sensory ataxia:high stepped ‘stamping’ gait.
*Steppage:footdrop.
*Myopathic:’waddling’gait.
*Apraxic:hesitant ‘walking on ice’ gait.
*Non-organic:bizarre and variable.