Gait disorders in adults and the elderly : A clinical guide

Abstract

Human gait depends on a complex interplay of major parts of the nervous, musculoskeletal and cardiorespiratory systems. The individual gait pattern is influenced by age, personality, mood and sociocultural factors. The preferred walking speed in older adults is a sensitive marker of general health and survival. Safe walking requires intact cognition and executive control. Gait disorders lead to a loss of personal freedom, falls and injuries and result in a marked reduction in the quality of life. Acute onset of a gait disorder may indicate a cerebrovascular or other acute lesion in the nervous system but also systemic diseases or adverse effects of medication, in particular polypharmacy including sedatives. The prevalence of gait disorders increases from 10 % in people aged 60-69 years to more than 60 % in community dwelling subjects aged over 80 years. Sensory ataxia due to polyneuropathy, parkinsonism and frontal gait disorders due to subcortical vascular encephalopathy or disorders associated with dementia are among the most common neurological causes. Hip and knee osteoarthritis are common non-neurological causes of gait disorders. With advancing age the proportion of patients with multiple causes or combinations of neurological and non-neurological gait disorders increases. Thorough clinical observation of gait, taking a focused patient history and physical, neurological and orthopedic examinations are basic steps in the categorization of gait disorders and serve as a guide for ancillary investigations and therapeutic interventions. This clinically oriented review provides an overview on the phenotypic spectrum, work-up and treatment of gait disorders.

Keywords: Aging; Falls; Neurological gait disorders; Orthopaedic gait disorders; Parkinsonism.

Fig. 1

Phases of the normal gait cycle

Fig. 2

Basic terminology describing the gait cycle

Fig. 3

Graphic representation of the step sequence in classical gait disorders. a normal gait, b spastic paraparetic gait, c cerebellar ataxic gait, d parkinsonian gait and e frontal gait. Note narrow step width and inwards rotation in paraspastic gait, broadened base and marked irregularity in cerebellar gait, shortened and mildly irregular step length in parkinsonian gait and broad-based, short-stepped, irregular walking in frontal gait disorder

Fig. 4

Pathophysiology of cauda equina compression in lumbar spinal stenosis. Flexed lumbar spine (a) as in the normal sitting position. Extension of the spine (b) as during normal walking or during the hyperextension maneuver leads to thickening of the ligamentum flavum and a decrease in the gap between the posterior margin of the intervertebral disc and the facet joints, both resulting in a reduction of the diameter of the spinal canal and dural sac