Clinical Vignette

A 70-year-old woman presented with a 2-year history of gait slowness and unsteadiness. Over that time, she experienced several falls, usually falling backwards. She began using a cane 1 year ago. She has noticed difficulty getting out of chairs or out of the car. Her husband described her walking as if “her feet are glued to the floor.” In addition to her gait difficulties, she noted increased urinary urgency and had one episode of urinary incontinence. She also described being more forgetful.

Neurologic exam was notable for a slow, shuffled, broad-based gait with shortened stride length and heel strike, and en bloc turning. Arm swing was intact. When the patient was quickly pulled backward, she demonstrated marked postural instability and retropulsion. She could not arise from a chair without using her arms to push herself up. Cognitive testing was notable for limited object recall, one third objects at 5 minutes, as well as associated evidence of executive dysfunction.

The patient underwent testing, including a brain magnetic resonance imaging (MRI), which revealed an enlarged ventricular system out of proportion to the degree of brain atrophy. A large-volume lumbar puncture was performed, and the patient was noted to have marked improvement in her gait and balance afterwards. A ventriculoperitoneal shunt was placed, and the patient’s gait improved to normal. She also experienced mild improvement in her urinary function. Her cognitive functioning was relatively unchanged.

Anatomy and Pathophysiology

Normal gait requires the integration and coordination of the central and peripheral nervous systems and the musculoskeletal system. Gait consists of two key components: (1) locomotion, the generation and maintenance of rhythmic stepping, and (2) equilibrium, the ability to keep the body upright and maintain balance. In quadripedal animals, locomotion is mainly dependent on spinal pattern generators, which produce rhythmic stepping movements. In contrast, locomotion in primates can be elicited by electrical stimulation of brainstem areas, including the posterior subthalamus, dorsal and ventral portions of the caudal pons, and the mesencephalic tegmentum. The latter includes the pedunculopontine nucleus (PPN), a group of cholinergic neurons that receives input from the basal ganglia and motor cortex and projects to the spinal cord and reticular nuclei. Although the exact function of the PPN is not clear, it is uniquely situated to modulate the influence of the basal ganglia on locomotion and balance. Higher cortical centers are also important in the maintenance of gait and balance. The frontal cortex is implicated in the control, coordination, and planning of automatic and voluntary movements. In addition, the posterior parietal cortex is involved in the perception of body position and posture.

Etiology and Classification

Because gait is dependent on the proper functioning and integration of different aspects of the nervous system, a variety of lesions in the central and/or peripheral nervous systems can produce walking difficulties. In a recent series of 120 patients presenting to an outpatient neurology clinic with gait disorder in which patients with hemiparesis, known Parkinson disease (PD), neuroleptic exposure, and orthopedic deformity were excluded, the distribution of etiologies were as follows: myelopathy (17%), sensory deficits (17%), multiple infarcts (15%), parkinsonism (12%), hydrocephalus (7%), cerebellar dysfunction (7%), psychogenic (3%) and toxic/metabolic causes (3%).

Gait disorders can be classified in a number of ways: etiologically (Table 32-1), anatomically (Table 32-2), and clinically (Table 32-3; Fig. 32-1). Perhaps the most useful approach to understanding gait disorders is a clinicoanatomic one. According to this method, gait disorders can be divided into roughly three anatomic categories: cortical, subcortical, and peripheral. A variety of well-defined clinical gait syndromes can be described under each anatomic rubric.

Table 32-1 Gait Disorders—Etiological Classification

Table 32-2 Gait Disorders—Anatomic Classification

Table 32-3 Clinical Gait Syndromes: Specific Examples