What is gait?
It is the posture of the patient during walking. Decubitus is the same while patient is in bed.
The ability to stand and walk normally is dependent upon input from multiple systems, including: visual, vestibular, cerebellar, motor, and sensory.
The precise cause(s) of gait dysfunction can be determined by identifying which aspects are abnormal and then incorporating this information with that obtained during the rest of the exam to paint the best picture for example; difficulty getting out a chair and initiating movement, could be consistent with Parkinson’s Disease. On the other hand, lack of balance and a wide based gait might suggest a cerebellar disorder.
In each case, historical features and investigatory findings help point you in the right direction.For the screening exam, simply observing as the patient walks into your office and gets up and down from the exam table should provide you with the relevant information.
If there is suspicion of neurological disease (based on history, other exam findings, observation of gait) then more detailed testing should be performed.
Proceed as follows:
- Ask the patient to stand from a seated position. Weakness, in particular of proximal muscles, can make this difficult. Alternatively, problems initiating movement (e.g. Parkinsons), musculoskeletal disease (e.g. arthritis), or other processes can also have a negative impact.
- Romberg test– Have the patient stand in one place. Make sure that you are capable/in position to catch and support them if they fall. This is a test of balance, incorporating input from the visual, cerebellar, proprioceptive, and vestibular systems. If they are able to do this, have them close their eyes, removing visual input. Loss of balance suggests impaired proprioception, as it is this pathway which should provide input that allows the patient to remain stably upright.
- Ask the patient to walk across the room, turn, and come back towards you. Observe patient for:
- Balance: Do they veer off to one side or the other as might occur with cerebellar dysfunction. Disorders affecting the left cerebellar hemisphere (as might occur with a stroke or tumor) will cause the patient to fall to the left.Right sided lesions will cause the patient to fall to the right. Diffuse disease affecting both cerebellar hemispheres will cause a generalized loss of balance.
- Rate of walking: Do they start off slow and then accelerate, perhaps losing control of their balance or speed (e.g. as might occur with Parkinson’s Disease)?Are they simply slow moving secondary to pain/limited range of motion in their joints, as might occur with degenerative joint disease? etc.
- Attitude of Arms and Legs: How do they hold their arms and legs? Is there loss of movement, evidence of contractures (e.g. as might occur after a stroke), or any other obvious abnormal feature?
- Heel to Toe Walking: Ask the patient to walk in a straight line, putting the heel of one foot directly in front of the toe of the other. This is referred to as tandem gait and is a test of balance. Realize that this may be difficult for older patients (due to the frequent coexistence of other medical conditions) even in the absence of neurological disease.
A few common pathological gait disorders and their causes are described below-
Notable for patients walking with their arm abducted, elbow flexed, hand closed, and hip circumducted in order to move their leg due to weakness of distal muscles (foot drop) and extensor hypertonia in lower limb . Exam will be remarkable for unilateral weakness, increased tone and hyper-reflexia of limbs on the affected side of the body. This is most commonly seen in motor cortex stroke with mild hemiparesis or other structural brain disease affecting that area of the brain
Patients have involvement on both sides with spasticity in lower extremities worse than upper extremities.
The patient walks with an abnormally narrow base, dragging both legs and scraping the toes. This gait is seen in bilateral periventricular lesions, such as those seen in cerebral palsy. There is also characteristic extreme tightness of hip adductors which can cause legs to cross the midline referred to as a scissors gait. In countries with adequate medical care, patients with cerebral palsy may have hip adductor release surgery to minimize scissoring.
Neuropathic Gait (Steppage Gait, Equine Gait)
From foot drop- Seen in patients with foot drop (weakness of foot dorsiflexion), the cause of this gait is due to an attempt to lift affected leg high to keep foot from dragging.The shoe on the affected side is often scuffed at the toe. Exam is remarkable for weakness in dorsiflexion on the affected side.
If unilateral, causes include peroneal nerve palsy and L5 radiculopathy. If bilateral, causes include amyotrophic lateral sclerosis, Charcot-Marie-Tooth disease and other peripheral neuropathies including those associated with uncontrolled diabetes. From sensory neuropathy- Notable for raising the leg high and striking it firmly on the ground with each step, done in order to help identify the precise location of the feet. On exam, sensation will be impaired (e.g. light touch, pin prick, vibratory, proprioception). Etiology can be from toxic effects (e.g. ETOH), metabolic disorders (e.g. diabetes), deficiency states (e.g. B12), autoimmune and other diseases affecting the sensory system.
If you have weakness on one sidein hip girdle muscles, this will lead to a drop in the pelvis on the contralateral side of the pelvis while walking (Trendelenburg sign).
With bilateral weakness, you will have dropping of the pelvis on both sides during walking leading to waddling. Seen in patient with myopathies, such as muscular dystrophy.
Choreiform Gait (Hyperkinetic Gait)
The patient will display irregular, jerky, involuntary movements in all extremities.
Walking may accentuate their baseline movement disorder. This gait is seen with certain basal ganglia disorders including Sydenham’s chorea, Huntington’s Disease and other forms of chorea, athetosis or dystonia.
Ataxic Gait (Cerebellar)
Most commonly seen in cerebellar disease, this is described as unbalanced, uncoordinated, clumsy, staggering movements with a wide-based gait. While standing still, the patient’s body may swagger back and forth and from side to side, known as titubation.
Patients will not be able to walk from heel to toe or in a straight line i.e. impaired tandem walking. The gait of acute alcohol intoxication will resemble the gait of cerebellar disease(e.g. stroke, degenerative disease, multiple sclerosis, metabolic deficienciesthiamine, tumor, toxic effect etc), vestibular system, and other motor or sensory disorders. The patient may also have difficult-to-understand speech (dysarthria), problems with fine movements like picking up small objects, buttoning clothes, or drawing, difficulty with finger to nose movement and impaired rapid alternating movements. Nystagmus and tremor may also be present. Patients with more truncal instability are more likely to have midline cerebellar disease at the vermis. Note- A common reversible cause for ataxia is acute alcohol intoxication. In fact, sobriety testing done by police officers is designed to identify the acute cerebellar dysfunction caused by this toxin.
In this gait, the patient will have rigidity and bradykinesia.
He or she will be stooped with the head and neck forward, with flexion at the knees. The whole upper extremity is also in flexion with the fingers usually extended. The patient walks with slow little steps known at marche a petits pas (walk of little steps). Patient may also have difficulty initiating movement, impaired ability to stop and turn, balance problems, and limited arm movement. The patient may show an involuntary inclination to take accelerating steps, known as festination. Other findings can include masked/inexpressive facies and resting tremor of hand or head. This gait is seen in Parkinson’s disease or any other condition causing parkinsonism, such as side effects from drugs.
As our feet touch the ground, we receive propioreceptive information to tell us their location.
The sensory ataxic gait occurs when there is loss of this propioreceptive input. In an effort to know when the feet land and their location, the patient will slam the foot hard onto the ground in order to sense it. A key to this gait involves its exacerbation when patients cannot see their feet (i.e. in the dark). This gait is also sometimes referred to as a stomping gait since patients may lift their legs very high to hit the ground hard. This gait can be seen in disorders of the dorsal columns (B12 deficiency or tabes dorsalis) or in diseases affecting the peripheral nerves (uncontrolled diabetes). In its severe form, this gait can cause an ataxia that resembles the cerebellar ataxic gait.