I recently saw a patient referred for the generic complaint of “Dizziness.” When he got up from the chair in the waiting room, he had an obvious gait disorder and used both a cane and a family member’s arm to make it back to the examining room. He did not complain of vertigo or lightheadedness, but reported that he had a history of frequent falls. He had fallen and hit his head a few months earlier, and the referring physician wondered if his “dizziness” might be related to that fall. The patient offered up little useful information. When the patient was in the hearing test booth, the family reported that he was unsteady long before the fall, and had a 20-year history of alcohol abuse. He had not had a drink in several months.
Chronic alcohol abuse can lead to a variety of neurologic disorders, and a full discussion is beyond the scope of this blog and beyond my scope of practice and knowledge. For more information on this topic, click here. I post this condensed case study because this patient had such a clear presentation of cerebellar dysfunction, it may be helpful for developing diagnosticians to see how the pieces of this puzzle fit together.
He had a symmetrical mild bilateral hearing loss and normal tympanograms. His rotational chair and calorics were perfectly normal. For someone who could not take a few steps without holding on to something or someone, his platform posturography was actually surprisingly good. He “fell” on conditions 5 and 6, but was normal in conditions 1 through 4. His oculo-motor tests were all grossly abnormal, consistent with or suggestive of cerebellar dysfunction. Informal cerebellar exam showed obvious deficits in rapid alternating hand movements, finger to nose pointing and heel to shin tests.
The auditory evoked potential test was interesting. Waves I and III were prominent, normal and easily identified. Wave V was present at normal latencies, but it took a lot of tweaking to find a repeatable peak. In other words, morphology fell apart after wave III. There has not been much published in recent years about ABR’s and alcoholic related cerebellar degeneration, but back in the 1980’s a study showed ABR abnormalities in the majority of chronic alcoholic patients.
What I find interesting is that his complaints (from the limited perspective of a balance clinic) appear to be strictly related to motor control. His Vestibular-Ocular Reflex (VOR) was perfectly normal, and his balance wasn’t all that bad either. His problem was that he could not generate efficient movement to take a step and rely on his feet landing where he wanted them to land, or to respond efficiently and quickly to any type of unexpected surface or movement. This is a case of pretty normal ascending pathway function, and severe deficit in the descending pathway.