Gait Disorders



Gait Disorders


Michael Ronthal



▪ INTRODUCTION

Walking is easy—we do it all the time in an unconscious sort of way. Yet, if the gait mechanism breaks down, the consequences may be disastrous.

Of people over the age of 60, 15% have some degree of gait difficulty. Approximately 25% of people over the age of 80 use a mechanical aid for walking. Along with a gait disorder goes the risk for a fall. According to the National Safety Council, the leading cause of death in patients 65 and older is a fall. Accidents are the fifth leading cause of death in people in this age-group; of these, falls account for two thirds of accidental deaths.

Walking is hard-wired in the nervous system. Animals can walk immediately after birth. Humans walk during the first year of life as part of normal development. Newborn infants will produce automatic stepping and placing movements if the sole of the foot is stimulated. Even anencephalic infants will demonstrate automatic walking. Experimentally, decapitated animals can be made to walk on a treadmill. All of this is evidence for the presence of a central spinal pattern generator for walking operating in the absence of higher centers. This central pattern generator can produce a basic locomotor rhythm, but higher centers are required to activate and regulate the rhythm of walking.

There are scattered centers in the brainstem that are activated during walking; by definition, if a region contains neurons that when activated chemically or electrically cause locomotion, that area is called a brainstem locomotor region. These locomotor areas are in turn connected with the cerebellum, basal ganglia, and frontal regions of the brain. The basal ganglia play a role in exploratory behavior and the lateral hypothalamic region in appetitive walking. The medial hypothalamus and central gray matter are recruited in defensive behavior. Such goals are interactive with the motor cortex, and frontal cortical function ranges from a subtle control modification of gait to complete control of locomotor activity. Proprioceptive feedback from the limbs to gait centers regulates their responses.

It is therefore evident that the gait mechanism is complex and scattered over multiple regions of the brain and malfunction at any particular level will result in its own relatively specific gait disorder.


▪ CLINICAL EVALUATION OF GAIT DISORDERS IN THE ELDERLY

The complaint “I can’t walk” requires meticulous physical examination to pinpoint the functional deficit with a view to further investigation to elucidate the pathology. The history is very rarely sufficient to make the diagnosis, which comes from the clinical examination.


▪ GAIT DISORDERS

The causes of gait disorders can be divided into those caused by neurological deficits and those secondary to nonneurological problems.


In the latter category, one should consider a defect of vision, pain, and arthritis, as well as medical problems such as cardiorespiratory failure, angina, postural hypotension, and side effects of drugs. A discussion of these is beyond the scope of this chapter.


Neurological Causes of Gait Disorders


Weakness

The diagnosis of weakness has been discussed in Chapter 2.

Lower Motor Neuron Weakness: In distal lower motor neuron weakness the most prominent sign is foot drop. Because the more proximal muscles, the hip flexors, are intact, the gait is high-stepping, often with an audible slap as of the foot hits the ground.

With predominantly proximal weakness, because the gluteus medius is involved, the gait becomes waddling, with an abnormal pelvic tilt with each step.

Upper Motor Neuron Weakness: Weakness secondary to central disease results in a circumduction gait. Hip flexion is weak, so the often spastic foot drop cannot be compensated for by raising the leg higher. The quadriceps, on the other hand, is relatively spared, which facilitates knee locking, and the patient can bear weight. Often, in association with the circumduction gait there is flexion of the upper limb across the chest.


Deafferentation

Proprioception is tested as described in Chapter 3. Lack of proprioceptive feedback may have a profound effect on gait and when severe can render the patient completely unable to walk. In patients with milder deficits, with each step there is a normal heel strike and then a more pronounced or forcible slap of the sole to the ground. Textbooks often refer to a so-called stamping gait, an attempt to increase sensory feedback, but classic stamping is seldom present.

The Romberg sign is positive. To test for this, the patient is asked to stand with the feet together and the eyes closed. Marked body sway indicates a positive Romberg sign.


Cerebellar Ataxia

Cerebellar signs on examination are described in Chapter 13. Common adjectives used to describe a cerebellar gait include “staggering, reeling, or drunken.” Characteristically, there is a wide-based stance with wide-spread legs, and the patient may stagger from side-to-side. Stride length is slightly shortened. Staggering may be brought out by sudden turning. Cerebellar hemisphere dysfunction produces appendicular clumsiness and ataxia. Vermis dysfunction causes trunk ataxia, and patients with superior vermis lesions, as in alcoholic degeneration, present particularly with gait ataxia.


Vestibular Dysfunction

A mismatch in afferent visual, proprioceptive, and vestibular information leads to the complaint of dizziness or loss of balance. A subjective sensation of rotation or spinning is characteristic of vestibular dysfunction, whereas nonvestibular dizziness may be described as light-headedness, floating, or loss of balance.

The gait of vestibular dysfunction progresses from an occasional stumble, to veering, to frank ataxia. With unilateral vestibular dysfunction the patient veers toward the pathological side.


Extrapyramidal Disorders

Extrapyramidal disorders may present with hypokinetic or hyperkinetic movement disorders (see Chapter 13).


Parkinson’s Disease: In Parkinson’s disease there is paucity of movement, and gait abnormalities are the presenting complaint in approximately 15% of these patients. The gait is narrowbased, and stride length is reduced, leading to a shuffle (marche a petit pas). Speed may be increased, leading to the descriptive term “festinating” or hurrying. There is reduced arm swing and a tendency to thoracic kyphosis. The patient is easily displaced backward and may spontaneously take backward steps or even fall (retropulsion). When asked to turn on a dime or about-face, the patient takes many small steps to complete the maneuver. As the disease progresses there is difficulty initiating gait, and the patient may take many small steps on the spot before forward movement ensues (start hesitation). A similar phenomenon may occur when stepping through the portal of a door or attempting to make a sudden turn, when frequent small steps in place without propulsion are seen. When asked to rise from a soft chair, the patient may fall back two or three times before attaining the erect posture.

Varying degrees of Parkinsonian gait are seen in patients with multiple system atrophy in which parkinsonism plays a varying role. In progressive supranuclear palsy, Parkinsonian features and disturbances of ocular motility are seen. Early falling with failure of down gaze is a clue to the diagnosis.

Lower Half Parkinsonism: In lower half parkinsonism, leg movements when walking look to be severely Parkinsonian, but the upper limbs are furiously in movement as if coaxing the patient to walk. This gait is usually caused by subcortical arteriosclerotic dementia (Binswanger’s disease).

Hyperkinetic Movement Disorders: In hyperkinetic disorders the extra movements may interfere with gait, leading to scattered and various intrusions that cause the patient to stagger.


Frontal Gait Disorders

The highest centers for the control of gait are in the frontal lobes, and dysfunction there leads to difficulty with initiation and occasional freezing, with or without multiple steps in place. The patient walks on a narrow base with a markedly shortened stride length. There is hesitation on turning. There is disequilibrium and impaired ongoing locomotion.

At times the prime deficit is one of initiation (ignition failure), when the patient hesitates and may take three or four steps on the spot, with the feet barely clearing the floor. Once underway, however, the stride lengthens and foot clearance is normal.

Rarely, profound breakdown in the control of gait results in an ataxic-like gait. The feet may cross or move in a direction inappropriate to the center of gravity, resulting in a bizarre, uncoordinated gait.

When the cause of frontal gait dysfunction is apparent on investigation, for example, hydrocephalus, the dysfunction is regarded as symptomatic, but in approximately 8% to 10% of patients no obvious cause is found and the label “degenerative” or “idiopathic” is appropriate.


Psychogenic Gait Disorder

The Cautious Gait: Murray et al (1969) described the cautious gait as follows: “The walking performance of older men gave the impression of a guarded or restrained type of walking in an attempt to obtain maximum stability and security. The walking of older men resembled that of someone walking on a slippery surface. This is regarded as a compensatory adaptation with an appropriate response to real or perceived disequilibrium.”

Fear of Falling: Fear of falling may be exaggerated, but it usually has a rational basis because of prior experience such as a previous fall. The anxiety may be so severe that it could be called a phobia. Such patients, in open spaces, may resort to crawling on hands and knees, and this may
culminate in a wheelchair existence. Fear of falling is associated with increased mortality and may be more frequent in women.

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Sep 7, 2016 | Posted by in PSYCHIATRY | Comments Off on Gait Disorders

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