Gait Disorders

JOSEPH C. D’AMICO

Gait is the momentary loss and regaining of balance that takes place with each step. Of course most people never think about this complex, rhythmic process that takes place thousands of times each day which is dependent upon a myriad of three systems working interdependently to allow for a smooth-in-form bipedal gait. The visual, vestibular, and proprioceptive senses comprise the afferent sensory system. Nerves, muscles, bones, joints, and tendons comprise the locomotor efferent system, and all are monitored and under the control of the central nervous system (CNS).¹ It is only when one of these systems begins to falter either as a result of systemic disease or as a result of the inevitable aging process that the individual and those closest to them begin to notice these changes.

Most children take their first steps at approximately 1 year of age; however, complete adultlike coordination is not achieved until 6 years of age. It is at this time that the lower extremity nervous system receives its full myelin coating making it easier for the neuromotor system to orchestrate a mature gait pattern.² The act of adult walking begins with a confidence inherent in the human organism that instills in the individual the belief that if he or she thinks they can walk from point A to point B they automatically will be able to do so. They think they can because they have done it before and therefore should be able to do it again until one day that process is interrupted and their feet do not respond in the same coordinated manner as they once did. They begin to notice their gait is not as graceful, smooth, or spry as it once was. There may be an irregularity in arm-leg coordination and symmetry, increased sway, shorter steps, slower speed, trips, slips and falls, rigidity with motion, and an overall loss of confidence in being able to accomplish basic locomotor tasks. Compensatory adjustments made by the individual in an attempt to improve stability may result in further disassociation from a normal-appearing gait pattern. It is at this point that professional consultation is usually sought to determine whether or not this alteration in function is due to systemic disease, the manifestation of idiopathic gait changes associated with the aging process or as simple as an improperly fitting shoe.

Locomotion is the act of getting from one place to another and involves not only the lower extremity but the arm/hand complex as well. Gait is the means of achieving this action. Balance and gait are intimately connected. Walking is a form of gait with a particular pattern of footfalls and specific requirements (Table 10-1). It is a complex process involving the musculoskeletal and nervous systems, which represents the sum total of all the functional and structural capabilities of the individual. Walking is the response of the individual who is actively solving a specific motor problem. It is dictated by individual constraints and task environment, that is, walking on a wet, sloped cobblestone street is a much more difficult task than walking on a dry, flat, level sidewalk. Gait solutions to locomotor challenges emerge, which are task and individual neuromotor capability appropriate.

Speed is a key indicator of the functional status of the locomotor system. In fact, observation of the unprompted speed at which an individual walks is a cost-effective determinant used to predict the overall health of the individual—the speedier live longer.³,⁴ Walking speed inversely correlates with the ability of the individual to live independently, perform various activities of daily living such as being able to cross an intersection before the light changes, and the risk of falling.⁵ An inevitable result of living a longer life is that at some point, usually somewhere in the sixth decade, people start slowing down.⁶ This process can to some extent be delayed through exercise and proper nutrition; however, no one in their later years walks as spritely, runs as fast, or balances as well as they did in their youth.

Central pattern generators (CPGs) are groupings of neurons or neural circuits that can generate and control coordinated movements. It is an innate neuromotor and spinal reflexive neural network.⁷ CPGs are modified by sensory input. Changes in neural output are dependent upon joint angle, interjoint relationships, center of gravity (COG), and the weightbearing status of the limb and are recognized by multisensorial afferent input or by peripheral receptors.⁷ Activation patterns for the leg musculature and stance to swing phase transitions during ambulation are determined by local information received through mechanical receptors in the plantar aspect of the feet and from proprioceptive inputs in the extensor foot musculature.⁸ Locomotor control is distributed across neural networks organized at higher and lower levels with parallel ascending and descending pathways for integration among different subsystems. Age-resistant neurospinal circuits control limb movements and modulate antigravity muscle tone and active propulsion. However, active propulsive power deteriorates with advancing age. The
challenge for the aging individual is the precise regulation of their musculoskeletal system function while maintaining balance and propelling the body forward. The maintenance of dynamic neuromuscular equilibrium providing external stability essential for safe locomotion is adversely affected by age and systemic disease.

It has been stated that gait and balance are intimately connected, and when stepping is impaired there is an increased risk for falls. This may be due to the displaced COG, impaired CNS regions, an inability to correct perturbations or due to the manifestation of a gait disorder affecting postural stability.¹

There are a number of factors that influence gait (Table 10-1). Most individuals experience an increasing difficulty in ambulation with increasing age.⁹ Gait abnormalities increase with age even in otherwise healthy individuals. In 75% of the cases the etiology is multifactorial, but if solitary it is probably musculoskeletal in nature.⁹

Spielberg in his landmark study investigating the walking patterns of older people classified gait changes with advancing age into three stages (Table 10-2).¹⁰ The challenge for health practitioners is to be able to ascertain whether or not alterations in gait can be ascribed to the expected changes accompanying the aging process, resulting in an idiopathic geriatric gait due to or aggravated by an underlying systemic disorder. Systemic disorders affecting gait may be divided into the following etiologic categories: neurosensory, metabolic, cardiovascular, musculoskeletal, and idiopathic.

Table 10-1. Walking Requisites

Upright posture

Ability to alternately swing from double limb support to single limb support

Single limb support

Lateral stability

Alternately generate and resist self-produced forward momentum

Intact central pattern generators

Table 10-2. Geriatric Gait Stage (by Age)

Stage 1: 60-72 y

Decreased velocity (>63 y = 1.6%/y)

Decrease cadence

Decrease vertical excursion (COG)

Decreased step length

Disturbed coordination of upper and lower extremities

Stage 2: 72-86 y

Arm-leg synergy is lost

Increased unwanted movements

Stage 3: 86-104 y

Rapid disintegration of gait patterns

Arrhythmic stepping patterns

Observational Gait Analysis

Human gait should be effortless and efficient with minimal energy expenditure and minimal shift in the COG from its protected, balanced position anterior to the second sacral vertebrae as it moves forward to its intended destination.¹¹ The greater the number of contact points in the locomotor apparatus the simpler the effort. In the case of a wheel the number of contact points is infinite; however, in humans there are only two.¹¹

Gait is virtually impossible to measure through observational gait analysis (OGA), and although it is an unreliable indicator of the body in motion, significant deviations from the norm should be relatively easy to discern even to the untrained clinician. The correlation of the biomechanical examination findings as well as knowledge of musculoskeletal constraints is critical in the evaluation of gait observations. When observing gait begin by obtaining a gross review of the organism in motion, that will provide a sense of flow to the action taking place. Begin from the foot upward and compare each segment with normal and with the contralateral side, paying particular attention to lower extremity articulations.¹² Note head tilt; shoulder, spinal, or pelvic deviations; arm swing; or limp. The eyes should be level to the horizon and the mouth parallel to the eyes. Shoulders should be level. The knee should be straight ahead at heel contact without excessive adduction or abduction of the femur. There should be neutral to inverted calcaneus at heel contact without undue impact and normal sequencing of the gait cycle. The heel should not be seen to “bounce” up prematurely during propulsion, and all observations should be symmetrical and expected. The gait angle and base of gait should be within normal ranges and symmetrical. During swing phase, the foot should clear the ground efficiently without excessive activity of the extensor group (Table 10-3).

Table 10-3. Gait Influences

Advancing age

Vision disorders

Inactivity

Chronic disease

Frailty

Medications

Alcohol

Balance disturbances

Musculoskeletal disease

Foot discomfort

Foot dysfunction

Foot deformity

Footwear

Idiopathic gait disturbances

Pathologic Gait Observations

During heel contact phase of the gait cycle, the heel should contact the ground before any other part of the foot. A toeheel gait would be an indicator of anterior leg musculature weakness and/or posterior group contracture with or without spasm. This may be observed in any disorder resulting in an imbalance between dorsiflexors and plantarflexors with secondary paralysis or weakness of the common peroneal nerve with triceps surae contracture resulting in a dropfoot (pes equinus) deformity such as post cerebrovascular accident. There may or may not be an accompanying or prodromal forefoot slap or forefoot scuff early in the disease evolution. A steppage gait, where the entire foot contacts the ground at heel strike, is seen in lower motor neuron disease such as common peroneal or popliteal nerve disease. In common peroneal nerve pathology gait, there is an accompanying foot slap with the steppage gait, and in popliteal involvement it is a more flaccid, exaggerated steppage gait that is observed. Steppage gait is a prominent distinguishing feature seen in Charcot-Marie-Tooth disease (CMT). During the midstance phase of gait, an early heel lift off may be observed and may be due to equinus influences on the lower extremity especially affecting the triceps surae. This may be seen in congenital spasticity as observed in cerebral palsy (CP), congenital contracture of the gastrocnemius-soleus musculature or bony block at the ankle. A scissor, ataxic, or Trendelenburg gait is seen in upper motor neuron (UMN) disease disorders such as CP. Propulsive phase of gait disorders may be due to cerebellar pathology, lower motor neuron lesion such as diabetic neuropathy, or an antalgic gait due to increased forefoot pressure due to hallux valgus or hammertoe deformities. A calcaneus gait due to gastroc/soleus paralysis may be seen in lower motor neuron lesion diseases such as diabetes mellitus, Guillain-Barré, porphyria, and others. Patients with diabetic neuropathy exhibit reduced active propulsion due to a deficit of gastroc/soleus function.

Antalgic gait is a compensatory gait in which the gait alteration is an alteration in gait designed to relieve pain. It ceases when the pain is absent. This is frequently seen in musculoskeletal disorders affecting the lower extremity such as inflammatory of degenerative disease disorders affecting the spine, hip, knee, ankle, or foot. Disorders affecting posture or balance may result in either a cautious or reckless gait. Cautious gait is caused by an overresponsiveness to gait instability and features slower shorter steps with increased double support. Patients walk with arms outstretched as if on ice and is linked to “fear of falling” syndrome or “fall phobia.”¹ Reckless or careless gait is seen in individuals with poor assessment of their own falling risk. Ataxic gait from the Greek for “without order” is an example of reckless gait with wide base of support to neutralize medial to lateral instability commonly seen in CNS disorders.

Neurosensory Disorders Affecting Gait

Normal function of the foot and its ability to support a normal locomotor pattern is dependent on intact neural pathways. Neurosensory gait disorders include myopathy, neuromuscular junction disease, and upper or lower motor neuron lesions. Myopathic gait disorders are caused by impairment of the conduction of muscle impulses such as seen in Duchenne muscular dystrophy or alcoholic myopathy. The gait is described as dystrophic or atrophic with exaggerated lateral trunk movements resulting in a penguin- or duck-like gait. Commonly observed gait deviations include Trendelenburg, toe-walking, hyperlumbar lordosis, knee instability, recurvatum, and balance disorders.¹³ Gowers sign, named by the renowned British neurologist Sir William Richard Gowers in the late 19th century, is an inability to stand from a kneeling position due to lower limb muscular weakness. The patient is forced to “walk” over his own body to achieve the upright position. Although classically a classic sign of Duchenne muscular dystrophy, it is also seen in centronuclear myopathy and myotonic dystrophy. Individuals with myopathic disease require arm assistance to rise from a chair.

Myasthenia gravis is an example of a neuromuscular junction disease in which the gait is labored as a result of their ability to easily fatigue. There is difficulty maintaining the upright posture as well as in climbing stairs. The accompanying double vision disorder magnifies these deficits.

UMN Gait Disturbances

UMN lesion pathology is associated with muscle paresis, overactivity-spasticity, and stiffness. CPGs may be intact in these individuals; however, due to dysfunctional spinal reflexes and supraspinal inputs motor control and gait patterns are pathologically affected.⁷ UMN-induced gait disturbances are seen in cerebellar dysfunction secondary to tumor, abscess, cardiovascular accident, CP, multiple sclerosis (MS), or Parkinson disease (PD). There is axial instability with few focal neurologic signs. A wide base, slow and small steps, shuffling, unsteadiness, and lurching toward the affected side (vestibular ataxia) characterize the typical ataxic gait seen in these conditions. The patient has difficulty turning with severe truncal instability. At times, the individual may appear “frozen” with an inability to initiate a step. Sensory ataxia is due to proprioceptive sensory deficits and is exemplified by a staggering gait, which may include stomping, slapping, or heavy heel strike to increase sensory feedback as an aide to ambulation.⁷ Patients with sensory ataxia exhibit a positive Romberg sign. UMN lesion patients may be unable to accomplish unsupported stance.

Cerebellar ataxia is caused by cerebellar dysfunction involved in limb movement and dynamic balance control. Cerebellar gait has been described as a “drunken” gait that is unstable, veering, and irregular. Studies have demonstrated
that the main feature of ataxic gait is increased intrasubject performance variability.¹⁴,¹⁵ Tandem walking, the act of placing one foot directly in front of the other while walking, is a sensitive clinical test for cerebellar dysfunction.¹⁶

Cerebrovascular Accident

In an average year, 0.2% of the population will suffer a stroke.¹³ It is the most common neurologic deficit and leading cause of gait impairment in rehabilitation facilities.¹³ Stroke results in a hemiparetic gait with marked asymmetry and increased stance time on the unaffected limb, decreased stance and decreased swing on the affected side, and increased double support time,⁷ all in essence increasing stability by decreasing demands placed on the affected limb. Speed of ambulation in stroke patients is also negatively affected.¹⁷ This has been shown to be due to weak ankle plantarflexors, hip flexors, and knee extensors.¹⁸ Arm swing may be absent or diminished on the affected side. Initially, the arm may be flaccid or held in adduction and flexion.⁷ The affected limb is held stiff-legged in extension, internal rotation, and equinovarus of the foot and ankle. This creates difficulty in achieving forefoot clearance during swing phase with compensatory adjustments including hip elevation, increased trunk sway, circumduction, and occasionally contralateral vaulting.⁷ Swing phase initiation is difficult, delayed, and prolonged. Electromyogram (EMG) studies have revealed prolonged tibialis anterior function in an attempt to dorsiflex the forefoot to clear the ground.¹⁹

In patients with transient brain ischemia (TBI), the zone of neurologic insult is not as well circumscribed. Therefore, the range of neurologic deficits is wider. TBI patients generate increased step length and normal stance time on affected limb compared with stroke patients in spite of increased stance time on the unaffected extremity.⁷

Parkinson Disease

PD is a progressive asymmetrical disorder caused by a basal ganglia dopamine deficiency and is responsible for 10% of gait disturbances in adults.²⁰ Due to neurotransmitter imbalances, PD patients progressively lose flexibility and adaptability in locomotor responses and walk with a stereotypical shortened-step, narrow-base, shuffling gait. The ability to respond to gait challenges including cognitive demands made during ambulation and gait perturbations are significantly compromised in the PD patient.²¹

Although initially asymmetrical, the contralateral limb eventually becomes affected in 80% of cases though not as severely as the side of inception.²⁰ Approximately 1% of those over 50 years of age have PD.¹³ In a community dwelling, 15% of those 65 to 74 years of age exhibit gait abnormality and one or more signs of PD. This number rises to 30% for the 75-to-84-year group and 50% in those over 85 years of age.²² There has been reported a 35% incidence in gait disorders in community dwellers over 70 years of age.²³

Like other UMN disease disorders, parkinsonian gait is ataxic in nature with distinctly different and distinguishing “hallmark of the disease” characteristics. These include pill rolling, tremor, festination, rigidity, postural instability, and an overall slowness of gait known as hypo- or bradykinesia (Table 10-4). In some severe cases, there may be akinesia or complete loss of mobility. Unlike pyramidal disorders, strength is preserved with the lower extremity that is rigid in nature. Festination is the inability of the parkinsonian patient to slow down once gait has been initiated. This is due to muscular hypertonicity manifested by ankle and knee stiffness along with pelvis and trunk flexion.²⁴

Asymmetric arm swing and accompanying tremor as well as staggering and en-bloc turning are suggestive of early PD.²⁵ As the disease progresses, there is pronounced tendency to drag the ipsilateral leg and decreased foot clearance and reduced step length may be more clearly evident.²⁵ Patients with PD typically increase cadence in an attempt to compensate for the shorter step length and reduced velocity.¹ In addition to the above-mentioned deficits, it is significant to note that balance control is asymmetrical in about 75% of patients with PD.²⁰

Parkinsonian gait is characterized by a foot flat strike placing the entire foot on the ground at the same time.²⁶ In advanced stages, a toe-heel gait may be observed. Patients have reduced foot lift during swing phase of gait with resultant reduced toe clearance between the foot and the ground.²⁷ There is reduced impact at heel strike in parkinsonian patients with additional decreases as the disease progresses.²⁸ The load on the forefoot is increased with a tendency toward medial displacement. The interpatient gait variability in foot strike pattern is less than in the normal population.²⁸ The vertical ground reaction force (GRF) has two peaks in the normal individual: one at heel contact and one at propulsion. In
early stages of PD, there are reduced forces in the heel and forefoot resembling those seen in the geriatric population.²⁹,³⁰ As the disease progresses with a shuffling type gait, only one narrow peak in the vertical GRF is shown.

Table 10-4. Parkinsonian Gait Characteristics

Increase muscle tone and tremor

Stiff arms held closely to body

Absent arm swing

Impaired postural reflexes

Stiffly stooped

Arms close to sides

Reduced stride length

Increased double limb support

Increased cadence

Slow, shuffling steps

Difficult to initiate steps or turns (“freezing”)

Cog wheel rigidity

Pill rolling

Festination

Freezing of gait is a disabling, episodic affectation in which the feet appear to be “glued to the floor.” Falls and freezing of gait have been linked together since freezing in many instances may lead to falls. Both are more common in the latter stages of the disease process.³¹ Freezing of gait is a common and disabling feature of PD and is most commonly experienced during gait initiation, turning, and negotiating obstacles of other tasks.³² The pathophysiology of freezing of gait has been linked to asymmetries in leg coordination.³³,³⁴ Falls may result from attempting sudden movements or changes in postural positions. The risk of falls is increased in the PD patient who attempts to perform more than one activity at a time such as carrying a shopping bag while ambulating. Most of these falls are forward (45%) and 20% laterally.³¹

Postural sway is the ability to maintain balance during upright stance and locomotion. Postural sway characteristically increases in most UMN lesion disorders, creating balance disorders. However, in PD it is diminished. This fact, coupled with an inability to maintain the center of mass over the base of support, increases the risk of falls in the parkinsonian patient.²¹ EMG studies have demonstrated a significant reduction in tibialis anticus muscle activation in early stance and early and late swing phases of gait and a reduction in triceps surae action at propulsion.³⁵ The hamstrings and quadriceps show prolonged activation during stance.³⁵ The passive stiffness of ankle joints and co-contraction of leg muscles in stance result in abnormal postural sway in PD patients.³⁶

Subcortical arteriosclerotic encephalopathy (SAE) also referred to as lower-body parkinsonism and cerebral ataxia are gait disorders that resemble that of PD but have common underlying mechanisms different from that of parkinsonism.³⁷

Cerebral Palsy

CP is an idiopathic perinatal disorder with an incidence of 2 per 1,000 live births.¹³ The underlying neurologic pathology is nonprogressive; however, the secondary effects including muscular contractures and abnormal bone growth continue and cause deterioration in function. Spasticity occurs in 80% of CP patients. Only 20% are quadriplegic, 30% hemiplegic, and 50% diplegic.³⁸ Seventy percent of those with CP are able to walk. The fundamental problems in this disorder include weakness, spasticity, and loss of selective motor control with retention of primitive reflexes and postural reactions. These neurologic deficiencies result in equinus function with knee and hip contractures, premature heel off, foot drop, and excessive limb flexion during swing. Foot deformities include hammer, claw, and mallet toe deformities; hallux flexus; equinus; varus; valgus; planovalgus; and the most commonly occurring equinovarus.³⁸ In weaker patients, excessive pronation, crouch gait with knee and hip flexion, and toe drag are observed. The crouch gait position deleteriously affects loading patterns of the knee and surrounding structures, leading to a load that is two and one half times greater than that of the normal pain-free individual.³⁹

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