Ross J. Fleischman
PATHOPHYSIOLOGY
Ataxia is the failure to produce smooth, intentional movements.
Ataxia and gait disturbances are not diseases in themselves, but are symptoms of systemic or nervous system conditions.
CLINICAL FEATURES
Orthostatic vital sign changes and abnormalities beyond the neurologic examination point to systemic illness.
Key symptoms of serious problems beyond the sensory and motor systems include headache, nausea, fever, and decreased level of alertness.
Nystagmus suggests an intracranial cause.
Cerebellar lesions (motor ataxia) are suggested by dysmetria (undershoot or overshoot on finger-to-nose testing) and dysdiadochokinesia (clumsy rapid alternating movements when flipping palms on thighs). Overshoot when sliding one heel down the opposite shin is a sign of cerebellar disease while a wavering course 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.
Ask the patient to stand with arms at sides. Instability with the eyes open suggests a cerebellar lesion. 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.
Observing the patient rise from a chair and walk, including tandem walking (heel to toe), is critical, as this may expose subtle weakness and ataxia.
Motor ataxia is characterized by broad-based, unsteady steps.
Peroneal muscle weakness causes foot drop, known as an equine gait.
Sensory ataxia with loss of proprioception may be notable for abrupt movements and slapping of the feet with each impact.
A senile gait which is slow, broad based, and shortened may be seen with normal aging, neurodegenerative disease such as Parkinson’s, and normal pressure hydrocephalus. Parkinson’s disease may also manifest with a festinating gait, which is narrow based, with small shuffling steps that become more rapid.
DIAGNOSIS AND DIFFERENTIAL
Attempt to classify the problem as a systemic versus nervous system disorder (Table 145-1).
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.
An abrupt onset of gait disturbance and a severe headache may reflect intracranial hemorrhage and should be evaluated by non-contrast CT.
CT scan is less sensitive than MRI for lesions of the posterior fossa, and is insensitive for acute ischemia.
A lumbar puncture should be performed if central nervous system infection is suspected.
Vitamin B12 deficiency should be considered in patients with loss of position sense in the second toe or a positive Romberg test, caused by degeneration of the posterior columns. A serum cyanocobalamin level and complete blood count are the initial steps in evaluation, although neurologic manifestations often precede macrocytic anemia.
Tabes dorsalis (neurosyphilis) causes similar symptoms of posterior column disease and can be screened for by the VDRL or RPR tests.
Normal pressure hydrocephalus should be suspected in an elderly patient with a broad-based, shuffling gait, urinary incontinence, and dementia. Non-contrast CT scan will show ventricular dilatation out of proportion to sulcal atrophy.
TABLE 145-1 Common Etiologies of Acute Ataxia and Gait Disturbances
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Administer thiamine 100 milligrams IV to alcoholics and other malnourished individuals who might have Wernicke’s encephalopathy, which is suggested by findings of ataxia, altered mental status (confusion and impairment of short-term memory), and ophthal-moplegia.
Patients with an acute inability to walk or who cannot be cared for at home may require admission for further evaluation.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 163, “Ataxia and Gait Disturbances,” by J. Stephen Huff.