Gait Assessment

1. Instruct the patient to walk as normal.  Observe for:
   1. Posture
   2. Stride length
   3. Reduced arm swing and/or tremor
   4. Circumduction of leg/hemiplegic gait
   5. High steppage gait
   6. Waddling gait
2. Ask the patient to walk heel-toe to assess for balance and ataxia
3. Ask the patient to walk on heels/toes. If patient is unable to walk on heels this indicates a subtle foot dorsiflexion weakness and if unable to walk on toes this indicates subtle foot plantar flexion weakness.
4. Rombergs sign- establish balance is normal with eyes open and then instruct patient to close eyes and see if balance is maintained.
5. Pull test to assess for retropulsion.

 

Different Gait Patterns:

 

Spastic gait:

1. What does it look like?
Stiff shuffling gait. The patient walks slowly, dragging both legs and not lifting them properly off the ground. When severe the knees may cross with each other because of increased tightness of the hip adductors. If it is caused by a stroke the gait will be what is referred to as “circumducting” where the hemiplegic leg will be swung out because of a combination of spasticity in the leg and also weakness of the distal leg muscles.

2. What is the mechanism?
A spastic gait is caused by dysfunction of the upper motor neurons or the pyramidal tract. The reason for the pattern is that when there is damage to the pyramidal tract there is interruption of all stimuli of voluntary movement from the motor cortex to the anterior horn cell. As a result, the feedback mechanisms controlling the length of muscles is interrupted and this is especially for the flexors of the upper extremities and extensors of the lower extremities because each of these muscle groups have greater cortical representation. The patient can no longer voluntarily inhibit the overactivated flexors (upper extremity) and extensors (lower extremity) and this leads to the characteristic spastic gait pattern. Another reason for the disproportionate effect on flexors in the upper extremity and extensors in the lower extremity is due to the arrangement of activating and inhibiting fibres around the pyramidal cells. Inhibiting fibres are more involved than activating fibres based on anatomical reasons and this produces this pattern of weakness.

3. Where is the lesion?
Subcortical- tumour, stroke, plaque

Internal capsule- most commonly MCA stroke- here a small lesion can have a dramatic impact as there are so many fibres that gather here on their way to the brainstem.

Brainstem

Cervical lesion- Lateral pyramidal tract from illnesses such as ALS or MS. In older people consider a myelopathy as a cause of a spastic gait.

Thoracic lesion- Again conditions such as ALS or MS may be responsible for a lesion here.

Anterior horn cell- this may lead to a combination of both upper and lower motor neuron signs so there may be a spastic gait with wasting of muscles in the arm for example.

 

Parkinsonian gait:

1. What does it look like?
There will be a delayed initiation and when the patient does start walking there will be a stooped posture with short shuffling steps. There will be reduced arm swing and if there is a tremor present it may become more apparent. On turning around there will be many small steps taken and this is referred to as clock-face turning. There may be freezing of gait- this is usually present on gait initiation or when turning. This freezing might improve with some forms of a visual input. There may also be retropulsion demonstrated by the pull test.

2. What is the mechanism?
Parkinson disease is hypokinetic movement disorder that is characterised by slowness of movement and the gait abnormality that occurs is one of the manifestations of this. The basal ganglia is the part of the brain that produces dopamine which through both inhibitory and excitatory pathways allows smooth controlled movement. Dopamine has a net excitatory effect on the thalamus. In Parkinson disease there is loss of dopamine leading to a net inhibitory effect on the thalamus and this clinically leads to slowness of movement and the characteristic gait pattern.

3. Where is the lesion?
For the purposes here the lesion in relation to Parkinson disease is in the basal ganglia.

 

Ataxic gait:

1. What does it look like?
An ataxic gait will have a wide base. When ataxia is mild regular walking may be normal but assessment of tandem gait will reveal the ataxia. When the ataxic gait is due to loss of proprioception function there will be a high stepping and stamping quality to the gait. The stamping may increase sensory feedback. One of the important distinguishing features between a cerebellar and sensory ataxia is that the latter becomes worse in the dark or with the eyes closed.

2. What is the mechanism?
Cerebellar ataxia- The cerebellum receives huge sensory and motor inputs from various regions of the brain. This information is used in smoothly coordinating movements and in motor planning. Cerebellar outflow contributes to the adjustment and timing of limb movements.  Ultimately the cerebellum can be regarded as an information processing centre for learned and programmed movement. When there is a dysfunction here there will be disordered contractions of agonist and antagonist muscles and lack of normal coordination between movements at different joints and this clinically translates in to an unbalanced unsteady gait.

Sensory ataxia- Here the mechanism is loss of proprioception and therefore no concept of where your hands or feet are in space. This type of ataxia is helped by visual feedback and therefore is worse with the eyes closed.

3. Where is the lesion?
Cerebellum- here gait or truncal ataxia is caused by lesions of the vermis or medial portions of the cerebellum. When the lateral cerebellar hemispheres are damaged there may not be an appreciable gait or truncal ataxia.

Cerebellar peduncles or pons.

Prefrontal cortex- lesions here can produce an ataxic gait that may look like a cerebellar ataxia- see frontal gait below.

Posterior columns- damage here produces a sensory ataxia.

Dorsal root ganglia

 

Frontal gait:

1. What does it look like?
Slow, shuffling, narrow or wide-based, “walking on ice”- looks like they are barely raising feet off the floor. The gait is cautious. There may be difficulty initiating the movement. Can resemble a parkinsonian gait. Patients can often perform cycling movements while lying on their backs much better than they can walk.

2. What is the mechanism?
There is a gait centre in the frontal lobe. A frontal gait is thought to be generated by failure of motor programming. The primary motor cortex, premotor area and the supplementary motor area are involved in the initiation, guidance and internal cueing of gait. Damage to these regions interrupts any or all of these functions leading to what is referred to as a frontal gait pattern.

3. Where is the lesion?
Frontal lobes: Cerebrovascular disease- especially subcortical white matter disease interrupting anterior projection fibres and adjacent association fibres connecting the frontal gait regions to the thalamus and basal ganglia etc.Normal pressure hydrocephalus. Frontal lobe tumours.

 

Waddling and steppage gait:

1. What does it look like?
Waddling has the appearance of just that. A high-steppage gait has the appearance of someone lifting their leg high and then almost slapping their foot on to the ground.

2. What is the mechanism?
For a waddling gait the most likely pathology is in the pelvic girdle muscles. They are weak which is what gives the waddling appearance. For a high steppage gait the mechanism is weakness of the foot dorsiflexors which means the patient cannot lift their foot adequately to clear the ground and so they compensate by lifting the foot much higher and then the foot almost slaps on to the ground.

3. Where is the lesion?
For the waddling gait the weakness usually lies in the pelvic girdle muscles. The cause may be a limb girdle muscular dystrophy or some other form of a myopathy.

For the high steppage gait the lesion may be at the nerve root level (L4-5) or at the fibular neck where the common peroneal nerve may become compressed. A distinguishing feature is whether or not tibial innervated muscles are involved. If it is root then foot inversion (tibialis posterior) will be involved. If it is common peroneal nerve then just dorsiflexion (tibialis anterior) and eversion (peroneus longus) will be involved. There is also a possibility of the pathology localising to the lumbosacral plexus, however, distinguishing between these and deciding which is more likely is often based on the history as well as the clinical examination.

Once the location is established tests can be done to look for aetiology. For example, patients with inherited neuropathies such as Charcot Marie Tooth may have a foot drop. There are also many acquired neuropathies that can also cause foot drop such as Guillain Barre syndrome.

 

Remember to consider non-neurologic causes of gait dysfunction:

1. Orthopaedic problems such as arthritis
2. Pain- usually causes what is referred to an antalgic gait where the posture is adjusted to a position where pain is minimised.
3. Rheumatologic disorders
4. Visual loss
5. Side effects of drugs