3.

Pathological Gait

Aaron Glockenberg DPM

The ability to analyze the different pathological gaits has to be correlated to having the basic understanding of normal gait patterns. The normal gait patterns will differ based on individuals age groups, thus relating to neuromuscular and skeletal systems development as the individual matures. The precise complex interplay between the above systems allows the creation of an efficient synchronized gait pattern with maturation. The two major factors essential for walking include equilibrium and locomotion. Basic overview of the normal gait patterns based on age will be as follows: At one year of age, equilibrium and locomotion are problematic, thus necessitating wide base of gait, prolonged knee and hip flexion, short-step length, low velocity, high cadence and arm abduction. Between one-to-two years of age, there is narrowing of the base of gait, in addition, appearance of reciprocal arm swing, increased step length and velocity, and mild foot drop is also noticed. At three years of age, gait pattern is becoming similar to that of an adult, including low velocity, increasing stride length, and single support phase. Exception is high cadence, which around seven years of age is decreasing. In adulthood a full mature gait develops, which includes the following main characteristics of increased ratio of the pelvic width to ankle spread, increased velocity stride length, single support phase, and decreased cadence. Normal changes of gait pattern develop in individuals at around 60 years of age, which include decreased velocity, shorter stride length, and step length. In addition, there is a reduction in the joint angle amplitude and increased gait variability. The above finding should be differentiated from a pathological state of gait, due to the fact that older adults might have an alternation of balance ability, sensory feedback and leg muscle strength, which diminish with age. In order to achieve a normal gait, intact bone and joints, adequate muscle strength, normal muscle tone, reciprocal innervation of muscles are necessary. Normal vision, vestibular auditory, and sensory motor systems are necessary to achieve and equilibrium and locomotion. Evaluation of the gait necessitates knowledge of the different phases of the gait cycle based on the following flow chart (see Figure 1 Gait Cycle).

Figure 1. Gait Cycle Knowing the normal pattern of gait enables us to better understand and evaluate the abnormal gait patterns that are categorized into two types, general and specific.

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The general type is associated with pain resulting in an antalgic gait. A good subjective and objective evaluation will pinpoint the cause of the above. The following condition could be associated with an antalgic gait: Foot Problems Fractures Hemophilia Immunization Infection Limb Length Discrepancy Myositis Shin Splints Chondromalecia Potellae Tendinitis Improper Shoe Gear Diabetic Foot Trauma Arthritis The antalgic gait is characterized by avoiding the involved site, resulting in a limp with decreased single support time of the affected side, shortened stride length of the uninvolved limb, and increased double support time. Effective walking is also compromised by the following factors, that avoiding pain is enabled by deformity at the joints associated with loosening of the capsule and ligaments in addition to muscle weakness resulting in reduced activity followed by disuse atrophy. Specific type of abnormal gait is associated with unique characteristics. The above might occur due to pathology at different anatomical sites of the central nervous system. Involvement could include the cerebellum, vestibular system, pyramidal and extrapyramidal tracts. In general terms, before evaluating gait disorders, knowledge of the different neurological pathways and their associate symptoms and signs is of major importance: Pyramidal tract carries impulses for voluntary movement Extrapyramidal tract is basically associated with balance coordination and fluidity of movement Weakness could be associated with pathology to corticospinal tract (CST) and lateral corticospinal tract (LCST), ventral horn, peripheral nerves, and muscles Spasticity could be related to CST and LCST lesions Rigidity will occur with pathology to basal ganglia (extrapyramidal tract) Hypotonia is due to lesions in the cerebellum Clinical examination as to the posture and walking is of major importance. Posture should be evaluated as to truncal posture, stance, and postural reflexes. Truncal posture in a normal walking individual is in an upright position. In case of extrapyramidal pathology, the trunk is stooped and flexed as in the Parkinsons disease, while extension of the neck is present with progressive supranuclear palsy, which is a degenerative disease involving the basal ganglia, brain stem, and cerebellar nuclei. Evaluation of stance as to width, ability to balance, and body sway could be informative as to the primary cause. Wide base gait might be indicative of cerebellar and sensory ataxia, cerebral vascular disease, and frontal lobe pathology.

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The body sway could be anterior, posterior, or lateral. Ability to balance could utilize the Rombergs test, which will differentiate sensory ataxia from the cerebellar one. Postural reflexes evaluation is important as to the equilibrium status upright posture; their absence is a characteristic of the early stages of secondary Parkinsonism. Walking should be evaluated as to initiation, stepping, associated movements sensory and motor examination. Initiation requires proper postural adjustments before the gait can start. Hesitation with shuffling in place of inability to lift the foot prevents proper initiation of the gait as is seen in extrapyramidal gait syndrome and on occasion in the frontal lobe lesions. Stepping is evaluated as to rhythm, speed of walking, and stride length. In case of extrapyramidal disease, steps are short, slow, and regular in rhythm. In ataxic disorders, step length is variable and irregular in rhythm. Some step characteristics are peculiar as in sensory ataxia. In the above, the steps are deliberate and under visual control, due to proprioceptive loss, presenting as a slopping gait. In case of foot drop, steppage gait will be the presentation. In upper motoneuron disorders, spastic paresis is associated with slight flexion at the hip; legs are extended and foot plantarflexed. Circumduction is bilateral with slowing down of gait. There is tendency toward a scissor gait type. Noticing an excessive hip mobility and abnormal lumbar posture is a result of weak upper leg and hip muscles, which could result in a lumbar lordosis, flexion of the hips, instability of the pelvis during steppingresulting in its excessive rotation and a waddling gait. Slowness of steps is present with a kinetic-rigid ataxic or spastic syndromes. Slowness of the above will be caused by hesitation, shuffle, and episodic freezing. At the extreme, there are conditions with bizarre abnormalities. Dystonia is associated with sustained plantarflexion and inversion of the foot usually while running, hip and knee flexion, and tonic extension of the hallux. Huntingtons disease presents with chorea, which includes increase in body sway, wide base, variable step length and rhythm, spontaneous knee flexion and leg raising. In chorea, there is a continuous random flow of muscle activity from one muscle group to another. Associated synergistic movements are of importance for normal gait that of the head, trunk, and arms. Unilateral loss of arm swing upon ambulation could be indicative of early clinical finding of Parkinsons disease. A loss of truncal mobility is mostly associated with hemiparesis, acute cerebellar lesions, and akinetic-rigid syndromes. Motor and sensory evaluation should be performed in addition to gait to enable better understanding of the gait disorders. Asymmetry in limb diameter and length might be associated with congenital deformity of the spinal cord, brain or leg, resulting in a limping gait. Examination of the muscle power could localize muscle weakness. In case of footdrop, weakness of the ankle dorsiflexors could be pinpointed. Waddling gait will indicate proximal muscle weakness. Presence of myopathic weakness is usually symmetrical. Muscle tone examination will indicate the following: Spasticityupper motor neuron pathology Rigiditybasal ganglia problems Gegenhaltenfrontal lobe disease, in which there is an increase in muscle tone upon passive manipulation The following presentation will discuss the different types of gait specifically.

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Ataxic Gait
Ataxic gait is associated with two types of presentation: The cerebellar and sensory types. When discussing the cerebellar type of ataxic gait, it is important to review some of the basics of anatomy and function of the cerebellum. It is proposed that cerebellar hemispheres are involved in planning of the extremity movements rather then execution of movement; thus it is preprogrammed. Pars intermedia is responsible for coordination and control of movement. Cerebellar vermis is involved in controlling segmental reflexes important in posture and gait. The above areas are involved in fine tunning related to excitatory function of mossy fibers and inhibitory activity of the Purkinje cell fibers. Gait abnormalities due to cerebellar lesions will relate to anatomical site pathology. Anterior lobe involvement due to alcoholism and malnutrition affecting the upper vermis and par intermedia will result in a wide base, unsteady, staggering type of gait and ataxia. The characteristic type of swaying is in the anterior posterior direction. The above resulting from improper coordination of agonist-antagonist muscle activity and lack of modulation of the tendon reflexes. The individual has a tendency to rely on their visual sensation to improve the ataxia. Lower Vermisportion of flocculonodular lobe with lesions, due to hemorrhage or medulloblastomas, will result in ataxias effecting the head and trunk and to lesser extend the extremities. The truncal ataxia is not improved with visual input. The swaying here is omnidirectional. Cerebellar hemisphere lesion will result in a ipsilateral limb ataxic with a tendency to lean toward the involved cerebellar hemisphere. The severity of the above increases with additional involvement of the dentate nucleus. Hypotonia and intentional tremor will also be present. Afferent cerebellar lesions progress from spinocerebellar tract and posterior column to the cerebellum resulting in ataxic gait with a lateral sway in addition to being stiff-legged due to increased tone. It is a spastic-ataxic gait (Frederich-Ataxia). The overall presentation of cerebellar ataxia as to gait will include an alternating wide and narrow base during a double limb stance. Simple support decreases with increased double support. During the swing phase, swaying could be wide, crossing the midline or outside the persons normal base of gait. Throughout the gait, lurching, staggering, and attempting to control constantly the equilibrium are other characteristics. Objective confirming signs will include difficulty walking tandem performing finger-to-nose and heel-to-shin tests. Rombergs sign will mostly be positive. The sensory ataxia could be due to multiple sclerosis, tabes dorsalis-syphylitic, chronic polyneuropathy, and diabetic neuropathy. The posture is stooped-upright. The gait will be associated with high stepping and common falls.

Parkinsons Gait (Propulsive or Festinating Gait)

Basal ganglia pathology will result in Parkinsons gait. The above ganglia are important in communicating information from cerebral cortex and the thalamus. If the information from the cerebral cortex is related to the caudate and putamen it will inhibit the globus pallidus pars interna; thus preventing the latters inhibition of the thalamus, which will in return enable this inhibition of the excitatory thalamocortical pathway. If on the other hand, the cerebral cortex information is related to the caudate and putamen to the globus pallidus pars externa and to the subthalamus nucleus, then to globus pallidus pars interna, inhibition of the thalamocortical pathway will occur. The latter pathway has a slowing effect on ongoing motor activities of the cerebral cortex. Pathology of basal ganglia will interfere with posture and balance maintenance, initiation of gait, and turning. The ability to adapt to changes in the walking surface and environment is also lost. The onset of gait disorder with Parkinsons disease could be insidious and unilateral, associated with diminished arm swing and stride length. As the disease progresses the following occurs: The posture is stiffening, arm swing

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decreases considerably, velocity decreases and stride length shortens. Initiation of gait is difficult which might require a few short steps in place or progression. Festination giving the appearance of a propulsive gait, with difficulty to stop could be a major visual observation by the examiner. Due to postural reflex impairment, turns are difficult and so is the balance. With any forward push, patient may try to regain balance by retropulsive steps. But with severely advanced state of Parkinsons falling down becomes frequent, and in the final stages, the patient is wheelchair bound. The gait phases are affected. The stance and double support increase, while the swing phase decreases. The stride length decreases, but its duration increases. Arm swing is abnormal as to amplitude and timing. There is no heel strike but rather toe and/or mid-stance strike. There is no push-off at terminal stance and preswing; thus resulting in trunk falling forward. The above gives the appearance of a propulsive gait but the propulsive force during the end of stance phase is really minimal. Parkinsonian gait can be improved by sensory input as to gait initiation, velocity, and stride length, but there is no improvement relating to abnormal foot strike and propulsive force.

Other Parkinsons Type Disorders

The propulsive supranuclear palsy is a rapid progression disorder that could be associated with a broad-base ataxic gait, and after an average of eight years results in a wheelchair-bound state. The multiple system atrophies, which are associated with degeneration of the central nervous system, result in a variety of presentations. The Shy-Drager Syndrome, which is an automatic nervous system failure, might be associated with Parkinsons gait features of ataxia and peripheral neuropathy. Orthostatic hypertension presence will prevent the ability to stand and walk. The olivopontocerebellar atrophy will be associated with Parkinsonian gait, wide base of gait and cerebellar ataxia. The striatonigral degeneration is associated with Parkinsonian gait with absence of tremor. Other extrapyramidal disorders are associated with chorea, which is a random irregular nonrepetitive, purposeless type of movement. In Huntingtons disease, which is a hereditary disease, the gait presentation includes involuntary choreic and dystonic movements and Parkinsonism resulting in decreased velocity, stride length, and cadence. The posture of the above condition is that lordosis or scoliosis. Tardive dyskinesia has a similar gait as Huntingtons disease, but the stride length is increased. Dystonia could be present in extrapyramidal disorders that manifest itself with sustained muscle contracture with twisting and repetitive movement. The gait presentation will depend on the distribution of dystonia from a focal to a generalized form. Localized dystonia could involve the foot involuntary supination at the terminal swing before heel contact. Generalized type of dystonia will present with severe lordosis and twisting movement of the shoulders, trunk, and pelvis with reduced velocity and variability in step length throughout the gait.

Spastic Gait
Conditions resulting in spastic gait include cerebral palsy, brain tumor, brain abscess, cerebral vascular accident, head trauma, and multiple sclerosis. General appearance will include a stiff and foot-dragging walk. Due to the upper motor neuron involvement, there is an imbalance in muscle activities as to timing and intensity relating to the upper and lower extremities. The outcome could manifest itself as a prolonged or out of phase muscle activity, simultaneous activity of several muscles, and concurrent agonistic/antagonistic muscle activity. The spasticity could be that of diplegia, paraplegia, hemiplegia, and quadriplegia. In the above, total paralysis or weakness of muscles is present. The most common type is hemiplegia. Hemiplegia alters the gait cycle phases, resulting in a stance phase instability on the affected side associated with knee hyperextension, and during swing phase, improper limb clearance. Compensation on the hemiplegic side will precede with circumduction at the hip, enabling foot clearance. Difficulty with the foot clearance arises from the knee being hyperextended. The ankle is usually in an equinovarus position, resulting in a forefoot contact first during stance phase. There is an internal rotation and adduction of the entire involved leg.

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Variation in hemiplegia could include absence in spasticity. The compensation to ensure foot clearance will include excessive hip and knee flexion during the mid-swing with tiptoe walk due to premature relaxation of the tibialis anterior and premature activation of the soleus muscle. In summary, spastic gait with hemiplegia results in decreased velocity, stance phase, and weight bearing. There is an increase in swing phase on the affected side, as well as an increase in the stance phase and decreased step phase on the unaffected side.

Steppage Gait (Drop Foot Gait)

Steppage gait could be associated with the following conditions: Guillan Barre Syndrome, multiple sclerosis, herniated lumbar disc, peroneal muscle atrophy, poliomyelitis, peroneal nerve trauma, polyneuropathy, and spinal cord trauma. The foot drop presentation is associated with tibialis anterior weakness, which could be unilateral or bilateral, and results in the following gait patterns: A slap-foot gait from heel strike to foot-flat. A toe drag or compensatory increased knee inflection. Last gait pattern will include a compensatory use of the extensor longus muscles.

Scissor Gait
Scissor gait could be associated with cervical spondylosis, cerebral vascular accident, liver failure, multiple sclerosis, spinal cord trauma and tumors, syringomyelia and pernicious anemia. Scissor gait is really a spastic gait resulting from a spastic paralysis of the hip adductor muscles, seen in spastic paraplegia, in which the legs are drawn toward the midline of the body. Individual will take short steps in addition to giving the appearance of crouching due to some flexion of the hips and knees.

Waddling Gait
Waddling gait could be associated with congenital hip dysplasia, muscular dystrophy, and spinal muscle atrophy. The gait pattern is due to the gluteus medius weakness bilaterally, resulting in a positive Trendelenburgs sign. Upon ambulation, there will be a pelvic instability that could lead to a lumbar lordosis and a wide base of gait. Gower sign will be present in case of muscular dystrophy or spinal atrophy.

Apraxic and Senile Gaits

Aging is usually associated with changes in gait pattern. Two types of gait are described in literature, that of gait aparxia and senile gait. Their precise existence is controversial. In both gaits, the basic neurologic examination is normal. Gait apraxia for the most part is believed to be associated with frontal lobe pathology, resulting in a gait with decreased velocity and stride length, increased double support time and sway. Normal phasic activity is affected with continuous activity of antigravity muscles. Senile gait is described as a gradual appearance of broad-based gait with diminished arm swing and small step, and appearance of a stoop posture and flexed hips and knees. There is a problem with gait initiation and turning and there is a tendency to fall. The overall belief is that the cause for above presentation is related to diffuse neurodegenerative and cerebrovascular lesions.

Drug Induced Gait Disorders

Drug induced gait Disorders are common in the elderly. Doctors should be aware of the above and be knowledgeable as to the different drug side effects. There are basically five physiological systems that might be compromised by different medications: orthostatic blood pressure control, cerebellar and vestibular systems, extrapyramidal systems, muscles and peripheral nerves. Medication contributing to postural hypertension include tricyclic antidepressants, levodopa, bromocryptine, antipsychotics, antihypertensive diuretics and nitrates. Drug induced Parkinsonism could be due to drugs contributing to the blockage of dopamine receptors such as antipsychotics, inhibit dopamine synthesis such as alpha methyldopa, and inhibit dopamine storage such as reserpine. Medications contributing to myopathies are multiple, but the most common are due to glucocorticoids and

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lovastatin. Drug-induced peripheral neuropathies contributing to gait disorder include methromidazole, isoniazid, phenytoin, etc. In summary, familiarity with gait disorders depends on the knowledge as it relates to the neuromuscular and skeletal systems. Familiarity with physiology of the above systems and communicative interplay between the systems enables us to understand the different abnormalities of gait. It is recommended to refer to a few of the many references available such as: Clinical Disorders of Balance, Posture and Gait. Edited by Adolfo M. Bronstein, Thomas Brandt, and Marjorie Woollacott. Published by Arnold, 1996. Evaluation and management of Gait Disorders. Edited by Barney Spivack. Published by Marcel Dekker, Inc., 1995.

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