Ataxia and gait disturbances may be symptoms of many disease processes and generally are not in themselves diagnoses. Ataxia is uncoordinated movement. A gait disorder is an abnormal pattern or style of walking. The presenting problem may be articulated by the patient or family as weakness, dizziness, stroke, falling, or another nonspecific chief complaint. Such symptoms must always be viewed in the context of the patient’s overall clinical picture. This chapter reviews the more common causes of acute ataxia and gait disorders (Table 169-1).
TABLE 169-1Common Etiologies of Acute Ataxia and Gait Disturbances |Favorite Table|Download (.pdf) TABLE 169-1 Common Etiologies of Acute Ataxia and Gait Disturbances
Intoxications with diminished alertness
Intoxications with relatively preserved alertness (diminished alertness at higher levels)
Other metabolic disorders
Disorders predominantly of the nervous system
Clinicians often erroneously think that ataxia and gait disorders result primarily from cerebellar lesions. However, such ataxia and gait problems may result from systemic conditions that affect different elements of the central or peripheral nervous systems. Cerebellar lesions may indeed cause ataxia, but isolated lesions of the cerebellum are not the most common cause of these complaints. Ataxias may be classified as either motor (cerebellar) or sensory.
Motor ataxias (also referred to as cerebellar ataxias) are usually caused by disorders of the cerebellum. The sensory receptors and afferent pathways are intact, but integration of proprioceptive information is faulty. Involvement of the lateral cerebellum (one of the cerebellar hemispheres) may lead to a motor ataxia of the ipsilateral limb. Lesions affecting primarily the midline portion of the cerebellum often cause problems with axial muscle coordination, which is reflected in difficulty maintaining a steady upright standing or sitting posture.
There are many reports of CNS lesions producing motor ataxia in what intuitively seem unlikely locations. Supratentorial infarctions, particularly small, deep infarctions, and lacunae of the posterior limb of the internal capsule have been reported to cause isolated hemiataxia. It is postulated that interruption of either ascending or descending cerebellar to cortical pathways are the cause of this motor-type ataxia.1 Small infarctions or hemorrhages in thalamic nuclei may produce a clinical picture of motor- or cerebellar-like ataxia with hemisensory loss. These effects are seen contralateral to the lesion.2 Lesions affecting the frontal lobe, such as tumors or cystic masses, may cause a motor ataxia of ...