Chapter 143. Ataxia and Gait Disturbances

Ataxia is the inability to produce smooth, intentional movements. Ataxia and gait disturbances are not disease entities themselves, but are manifestations of either systemic or nervous system conditions.

Key symptoms suggesting disease processes beyond the sensory and motor systems include headache, nausea, fever, and decreased level of alertness. The physical examination may also show abnormalities outside the nervous system. Orthostatic vital sign changes point to systemic illness.

Once the physician has determined that ataxia is the principal problem and not a manifestation of broader illness, the examination should attempt to differentiate between sensory and motor causes of ataxia. While cerebellar lesions may cause ataxia, isolated cerebellar lesions are not the most common cause. Dysmetria (undershoot or overshoot of movements) may be elicited by finger to nose testing. Dysdiadochokinesia (clumsy rapid alternating movements) may be seen when the patient alternately flips their palms and backs of their hands on their thighs. Both of these are suggestive of cerebellar causes. Having the patient slide one heel down the opposite shin is useful for distinguishing between cerebellar and sensory causes. Overshoot of the knee or ankle signifies cerebellar disease, while a wavering course down the shin suggests a deficit of proprioception.

Vibration and position sense in the toes test the posterior columns, which degenerate in tabes dorsalis (neurosyphilis) and vitamin B12 deficiency. Nystagmus suggests an intracranial cause. In the Romberg test, the patient is asked to stand with arms at sides. Significantly worsening instability with eye closure (a positive Romberg sign) suggests that the patient is relying on visual input for balance caused by a sensory ataxia including posterior column disease or vestibular dysfunction. Instability with the eyes still open suggests a cerebellar lesion.

Observing the patient rise from a chair and walk on heels and toes may expose subtle proximal or distal weakness. Tandem walking (heel to toe) may elicit subtle ataxia. A motor ataxic gait is characterized by broad-based, unsteady steps. Sensory ataxia with loss of proprioception may be notable for abrupt movements and slapping of the feet with each impact. A senile gait that is slow, broad based, and with a shortened stride may be seen with aging, but also with neurodegenerative disease such as Parkinson disease and normal pressure hydrocephalus. Parkinson disease may also show a festinating gait that is narrow-based, with small shuffling steps that become more rapid. Peroneal muscle weakness causes foot drop, known as an equine gait.

Table 143-1 shows common causes of acute ataxia and gait disturbances.

The extent of ED evaluation will depend on the acuity and severity of symptoms, with patients who have become unable to walk over hours to days requiring extensive evaluation. CT is less sensitive than MR for lesions of the posterior fossa, and is insensitive for acute ischemia. Perform a lumbar puncture if infection is suspected.

Consider vitamin B12 deficiency in patients with loss of position sense in the second toe and a positive Romberg test. A serum cyanocobalamin level and complete blood count are the initial steps in evaluation, although neurologic manifestations often precede macrocytic anemia. Neurosyphilis will cause similar symptoms of posterior column disease and can be screened for by the VDRL or RPR tests.

Suspect normal pressure hydrocephalus in an elderly patient with a broad-based, shuffling gait, urinary incontinence, and dementia. CT will show ventricular dilatation out of proportion to sulcal atrophy.

1. Administer thiamine 100 milligrams IV to alcoholics and other malnourished individuals who might have Wernicke disease, which is suggested by findings of ataxia, altered mental status, and ophthalmoplegia.

2. Admit patients with an acute inability to walk for further evaluation and diagnostic testing.