Gait Disorders

Published on 12/04/2015 by admin

Filed under Neurology

Last modified 12/04/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 6013 times

Chapter 22 Gait Disorders

The maintenance of an upright posture and the act of walking are among the first, and ultimately the most complex, motor skills humans acquire. From an early age, walking skills are modified and refined. In later years, the interplay between voluntary and automatic control of posture and gait provides a rich and complex repertoire of motion that ranges from walking to running, hopping, dancing, and so on. The pattern of walking may be so distinctive that individuals can be recognized by the characteristics of their gait. Many diseases of the nervous system are identified by the disturbances of gait and posture they produce.

Physiological and Biomechanical Aspects of Gait

Humans assume a stable upright posture before beginning to walk. Mechanical stability when standing is based on musculoskeletal linkages between the trunk and legs. Dynamic equilibrium during walking is maintained by coordinated synergies of axial and proximal limb muscle contraction and a hierarchy of postural reflexes and responses. The latter include automatic righting reflexes keeping the head upright on the trunk, supporting reactions controlling antigravity muscle tone, anticipatory (feed-forward) postural reflexes occurring before limb movement, and reactive (feedback) postural adjustments counteracting body perturbations during movement. Postural responses are also modified by voluntary control according to the circumstances, such as rescue reactions to preserve the upright posture (a step or windmill arm movements), and protective reactions to prevent injury (an outstretched arm to break a fall). Postural reflexes and responses are generated by the integration of visual, vestibular, and proprioceptive inputs in the context of voluntary intent and ongoing changes in the environment in which the subject is moving. Once the trunk is upright and stable, locomotion can begin. The initiation of gait is heralded by a series of shifts in the center of pressure beneath the feet during the course of an anticipatory postural adjustment—first posteriorly, then laterally toward the stepping foot, and finally toward the stance foot to allow the stepping foot to swing forward. This sequence is then followed by the stereotyped stance, swing, and step phases of the gait cycle.

Anatomical Aspects of Gait

The neuroanatomical structures responsible for equilibrium and locomotion in humans are inferred from studies in lower species that suggest two basic systems. First, brainstem locomotor centers (Takakusaki, 2008) project through descending reticulospinal pathways into the ventromedial spinal cord. Stimulation of brainstem locomotor centers results in an increase in axial and limb muscle tone to assume an upright posture before stepping begins. Second, assemblies of spinal interneurons (central pattern generators or spinal locomotor centers) activate motoneurons of limb and trunk muscles in a patterned and repetitive manner to drive stepping movements and stimulate propriospinal networks that link the trunk and limbs to facilitate the synergistic coordinated limb and trunk movements of locomotion. In quadrupedal animals, spinal locomotor centers are capable of maintaining and coordinating rhythmic stepping movements after spinal transection. The cerebral cortex and corticospinal tract are not necessary for experimentally induced locomotion in quadrupeds but are required for precision stepping. The isolated spinal cord in humans can produce spontaneous movements, but it cannot generate rhythmic stepping or maintain truncal balance, indicating that brainstem and higher cortical connections are necessary for bipedal walking in humans. In monkeys, spinal stepping requires preservation of the descending ventromedial brainstem and ventrolateral spinal motor pathways. Lesions of the medial brainstem in monkeys interrupt descending reticulospinal, vestibulospinal, and tectospinal systems, resulting in dysequilibrium.

The control of posture and locomotion in humans may be mediated by similar networks, with an additional level of supraspinal control needed to maintain bipedal stance and the complex repertoire of gait. Frontal cortex, via corticospinal tract and the basal ganglia, provide the signals to brainstem locomotor centers such as the pedunculopontine and adjacent nuclei of the midbrain to increase postural tone and commence rhythmic stepping. The corticospinal tract also projects to spinal cord motoneurons, enabling precision foot movements for stepping or dancing. The parietal cortex integrates sensory inputs indicating where the individual is in space, the relationship to gravitational forces, the speed and direction of movement, and the characteristics of the terrain and environment. The cerebellum modulates the rate, rhythm, amplitude, and force of stepping and also contributes to the medial brainstem efferent system controlling equilibrium and truncal posture through projections from the flocculonodular and anterior lobes. Much of the automatic control of truncal posture and walking in humans must be derived from integration of these various functions at the highest levels of motor organization, but the precise details remain unknown.

History and Common Symptoms of Gait Disturbance

A detailed account of the patient’s walking difficulty and its evolution provide the first clues to the underlying diagnosis. When evaluating the history, it is helpful to note the particular circumstances in which the walking difficulty occurs, the leg movements most affected, and any associated symptoms. Because disorders at many levels of the peripheral and central nervous systems give rise to difficulty walking, it is necessary to consider whether the problem is caused by muscle weakness, a defect of higher motor control, or imbalance due to cerebellar disease or proprioceptive sensory loss. Walking over uneven ground exacerbates most walking difficulties, leading to tripping, stumbling, and falls. A ligamentous ankle strain or even a bony fracture may result from tripping, and falling may be the presenting symptom of a gait disorder. Fear of falling may lead to a variety of voluntary protective measures to minimize the risk of injury. In some patients, particularly the elderly, compensatory strategies and a fear of falling lead to a “cautious” gait that dominates the clinical picture. Often an individual is unaware of their gait abnormality, and family or friends note altered cadence, shuffling, veering, or slowness.

Slowness and Stiffness

Slowness of walking is encountered in the elderly and in most gait disorders. Recent pooled analysis from nine selected cohorts has provided evidence that the speed of gait may correlate with longer survival in older adults (Studenski et al., 2011). Walking slowly is a normal reaction to unstable or slippery surfaces that cause postural insecurity and threaten balance. Similarly, those who feel their balance is less secure because of any musculoskeletal or neurological disorders walk slower. In Parkinson disease (PD) and other basal ganglia diseases, slowness of walking is due to shuffling with short, shallow steps. Difficulty initiating stepping when starting to walk (start hesitation) and when encountering an obstacle or turning (freezing) are common in more advanced stages of parkinsonian syndromes.

Difficulty rising from a chair or turning in bed and a general decline in agility may be clues to loss of truncal mobility in diffuse cerebrovascular disease, hydrocephalus, and extrapyramidal diseases. Axial muscle weakness due to peripheral neuromuscular diseases may also interfere with truncal mobility. Fatigue during walking accompanies muscular weakness of any cause and is a frequent symptom of the extra effort required to walk in upper motor neuron syndromes and basal ganglia disease.

The circumstances in which leg stiffness occurs when walking may be revealing. It is important to recognize that leg muscle tone in some upper motor neuron syndromes and dystonia may be normal when the patient is examined in the supine position but is increased during walking. An action dystonia of the foot is a common initial symptom of primary torsion dystonia in childhood. Stiffness, inversion, and plantar flexion of the foot and a tendency to walk on the toes may only become evident after walking some distance or running. Patients with dopa-responsive dystonia and prominent diurnal fluctuation typically develop symptoms in the afternoon. Exercise-induced dystonia of the foot when running may be the presenting symptom of PD.

Examination of Posture and Walking

A scheme for the examination of posture and walking is summarized in Box 22.1. A convenient starting point is to observe the overall pattern of limb and body movement during walking. Normal walking progresses in a smooth and effortless manner. The truncal posture is upright, and the legs swing in a fluid motion with a regular stride length. Synergistic head, trunk, and upper-limb movement flow with each step. Observation of the pattern of body and limb movement during walking also helps the examiner decide whether the gait problem is caused by a focal abnormality (e.g., shortening, hip disease, muscle weakness) or a generalized disorder of movement, and whether the problem is unilateral or bilateral. After observing the overall walking pattern, the specific aspects of posture and gait should be examined (see Box 22.1).


The width of the stance base (the distance between the feet) during quiet arising from sitting, standing, and walking gives some indication of balance. Wide-based gaits are typical of cerebellar or sensory ataxia but also may be seen in diffuse cerebrovascular disease and frontal lobe lesions (Table 22.1). Widening the stance base is an efficient method of reducing body sway in the lateral and anteroposterior planes. Persons whose balance is insecure for any reason tend to adopt a wider stance and a posture of mild generalized flexion and to take shorter steps. Those who have attempted to walk on ice or other slippery surfaces will recognize this phenomenon. Eversion of the feet is another manner in which to increase stability and is particularly common in patients with diffuse cerebrovascular disease. Spontaneous sway, drift of the body in any direction, postural tremor, or ability to stay upright without touching furniture or assistance of another person are important clues.

Trunk Posture

The trunk is normally upright during standing and walking. Flexion of the trunk and a stooped posture are prominent features in PD. Slight flexion at the hips to lower the trunk and shift the center of gravity forward to minimize posterior body sway and reduce the risk of falling backward is common in many unsteady cautious gait syndromes. Neck and trunk extension is characteristic of progressive supranuclear palsy. Neck flexion occurs with weakness of the neck extensors in motor neuron disease and myasthenia and as a dystonic manifestation in multiple system atrophy and parkinsonism. An exaggerated lumbar lordosis, caused by hip-girdle weakness, is typical of proximal myopathies. Paraspinal muscle spasm and rigidity also produces an exaggerated lumbar lordosis in the stiff person syndrome. Tilt of the trunk to one side in dystonia is accompanied by axial muscle spasms, the most common being an exaggerated flexion movement of the trunk and hip with each step. Truncal tilt away from the affected side is observed in some acute vascular lesions of the thalamus and basal ganglia. Misperception of truncal posture and position results in inappropriate movements to correct the perceived tilt in the pusher syndrome, associated with posterolateral thalamic hemorrhages (Karnath et al., 2005). Acute vestibular imbalance in the lateral medullary syndrome leads to sway or tilt toward the side of the lesion (lateropulsion). Abnormal truncal postures occur in paraspinal myopathies that produce weakness of trunk extension and a posture of truncal flexion (camptocormia). Dystonia and parkinsonism also may alter truncal posture and lead to camptocormia or lateral truncal flexion (Pisa syndrome). Abnormal thoracolumbar postures also result from spinal ankylosis and spondylitis. A restricted range of spinal movement and persistence of the abnormal spinal posture when supine or during sleep are useful pointers toward a bony spinal deformity as the cause of an abnormal truncal posture. Truncal postures, particularly in the lumbar region, can be compensatory for shortening of one lower limb, lumbar or leg pain, or disease of the hip, knee, or ankle.

Postural Responses

Reactive postural responses are examined by sharply pulling the upper trunk backward or forward while the patient is standing. The pull should be sufficient to require the patient to step to regain their balance. This maneuver is referred to as the pull test (Hunt and Setni, 2006). The examiner must be prepared, generally by having a wall behind them, to prevent the patient from falling. A few short, shuffling steps backward (retropulsion) or a backwards fall after backward displacements, or forward (propulsion) after forward displacements, suggest impairment of postural righting (reactive postural) reactions. Falls after postural changes such as arising from a chair or turning while walking suggest impaired anticipatory postural responses. Falls without rescue arm movements or stepping movements to break the fall indicate loss of protective postural responses. Injuries sustained during falls provide a clue to the loss of these postural responses. A tendency to fall backward spontaneously is a sign of impaired postural reflexes in progressive supranuclear palsy and gait disorders associated with diseases of the frontal lobes.