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Show Journal of Clinical Neuro-ophthalm%gy 7(1): 23-25, 1987. © 1987 Raven Press, New York Reversible Downbeat Nystagmus Secondary to Excessive Alcohol Intake Michael L. Rosenberg, M.D. Three patients are reported who presented with primary position downbeat nystagmus without any other evidence of cerebellar dysfunction. After 2 weeks of abstinence from alcohol, the downbeat nystagmus resolved totally in two cases, and could be elicited only with head hanging in the third. Radiologic evaluation, including computed tomographic (CT) scan of the posterior fossa and craniocervical junction, were normal in each case. These are the first cases reported of reversible downbeat nystagmus secondary to alcohol intake. They suggest that a patient with downbeat nystagmus and a history of recent significant alcohol intoxication should be observed for resolution of this sign after a period of abstinence before extensive radiologic evaluation is undertaken. Key Words: Alcohol-Nystagmus. From the Neuro-ophthalmology Section, Department of Neurology, Uniformed Services University of the Health Sciences, F. Edward Hebert School of Medicine, Bethesda, Maryland. The opinions or assertions contained herein are the private ones of the author and are not to be construed as official or reflecting the views of the Department of Defense or the Uniformed Services University of the Health Sciences. Address correspondence and reprint requests to Dr. Michael Rosenberg, Neuro-ophthalmology Section, Department of Neurology, Uniformed Services University of the Health Sciences, F. Edward Hebert School of Medicine, Bethesda, Maryland. 23 Primary position downbeat nystagmus is typically associated with structural lesions in the area of the foramen magnum. Rarely, reversible downbeat nystagmus has been reported from toxic causes including phenytoin (1), carbamazepine (2), toluene (3), magnesium depletion (4) and lithium intoxication (5,6). It has also been caused by chronic cerebellar degenerations of either hereditary or acquired etiology (6,7). In 1968 in the first large review of patients with primary position downbeat nystagmus Cogan described two patients with downbeat nystagmus secondary to alcohol- induced chronic cerebellar degeneration (7). This association, however, was not widely acknowledged until it was emphasized by Costin et al. in 1980 (8). Three patients are reported who were found on initial examination to have primary position downbeat nystagmus as an incidental finding. All admitted to significant recent alcohol intake. In contrast to the patients reported by Costin et al. with alcohol-induced downbeat nystagmus (8), the nystagmus in the patients reported herein resolved after a period of abstinence. This implies that the alcohol had had a reversible toxic effect on the central nervous system in these patients. CASE REPORTS Case 1 A 54-year-old woman was evaluated for migraine headaches that had been present for many years. The pain was increased with alcohol intake, and as this had increased recently, so had the headache frequency. When first seen, the patient was mildly intoxicated. Examination was normal except for a leftsided Horner's syndrome and primary position downbeat nystagmus that increased on lateral gaze and in the head-hanging position. 24 M. L. ROSENBERG After one week of abstinence from alcohol, the patient had no nystagmus in the primary position, but did have minimal downbeat nystagmus on lateral gaze to either side. Two weeks later, the patient had downbeat nystagmus only in the headhanging position. A CT scan and visual, auditory, and somatosensory-evoked potentials were normal. Case 2 During the course of evaluation for a peripheral neuropathy that was presumed to be secondary to chronic alcohol use, a 63-year-old man was found to have primary position downbeat nystagmus. Although he admitted to significant alcohol intake, he was not intoxicated at the time of examination. He was taking no medications. The downbeat nystagmus increased in amplitude with lateral gaze and with head-hanging. He was told to abstain from alcohol. One week later, reevaluation showed a marked diminution of the nystagmus in the primary position but it still increased markedly with head-hanging. After two weeks of continued abstinence the patient had no oculomotor abnormalities on examination. CT scan of the posterior fossa was normal. Case 3 A 53-year-old woman complained of unsteadiness. She described herself as having been only a light social drinker for many years, but said she had recently increased her alcohol intake significantly as a response to family problems. She denied taking any type of medications or drugs other than alcohol. Examination findings were totally normal except for primary position downbeat nystagmus. There was no evidence of drug or alcohol intoxication. She was told to abstain from alcohol, and 2 weeks later there was no nystagmus in primary position or on lateral gaze. However she still had downbeat nystagmus in the head-hanging position. One month later she was re-evaluated and there was no change in the examination findings. Evaluation of the posterior fossa with CT scan was normal. DISCUSSION These three patients all showed primary position downbeat nystagmus with no other evidence on examination or CT scan evaluation of cerebellar degeneration or of a structural lesion in the area of I Clin Neuro-ophthalmol, Vol. 7, No.1, 1987 the foramen magnum. All gave a history of recent significant alcohol intake, but of no other drug or toxin exposure. After a period of abstinence, the primary position nystagmus resolved. These cases suggest that in addition to producing a chronic cerebellar degeneration with permanent downbeat nystagmus, alcohol can produce an isolated downbeat nystagmus as a reversible toxic effect. This is not due to an acute intoxication as the patients described here had no evidence of increased blood alcohol levels at the time of examination. Other toxins and abnormal metabolic states have also been reported to cause such a syndrome on rare occasions, although usually in the setting of an acute cerebellar syndrome (1-4). Although a posterior fossa CT scan does not rule out a craniocervical junction anomaly, this is extremely unlikely to be the etiologic factor in these cases. There were no other neurologic signs or symptoms suggestive of cranio-cervical junction anomaly and reversibility is not typically a feature of lesions in this area. Other patients with an alcohol-induced cerebellar syndrome who seemed to improve with abstinence have been reported. Most recently a study measuring postural instability objectively documented improvement in function with abstinence (9). The recovery in those patients was postulated to be due either to plasticity in the nervous system or to actual recovery of neurons that were damaged but not lethally so. CT scanning has documented improvement in cerebral atrophy after cessation of drinking. This may also be due to either plasticity and growth of new connections or to remyelinization of old previously injured tissue (10,11). Peripheral nerve function is another parameter that has also been shown by electrophysiologic parameters to improve after abstinence (12). Because of the relatively short response time in our patients (less than 1 month) it seems most likely that the dysfunction causing downbeat nystagmus was due to recovery from a nonlethal injury rather than to neuronal loss and myelin or glial regrowth. Neuronal loss followed by changes from neuronal plasticity is still possible. Certainly changes in examination secondary to neuronal plasticity can be seen over the course of several hours (13). Other possible etiologies in addition to direct alcohol effect in these patients include Wernicke's encephalopathy and magnesium depletion (4). Wernicke's consistently causes ocular motility disorders, but vertical nystagmus has never been reported without other associated eye movement abnormalities (14). None of the patients had any ALCOHOL-INDUCED DOWNBEAT NYSTAGMUS 25 mental status changes suggestive of this disorder, and none were given thiamine during their period of abstinence. Thus it seems extremely unlikely that thiamine deficiency was the cause of the nystagmus in these patients. These patients were not tested for magnesium depletion. This remains a possibility, but the absence of malnutrition by history or physical examination makes this diagnosis also unlikely. The persistence of downbeat nystagmus in the head-hanging position only is of uncertain significance. Although it may be the initial sign of a posterior fossa mass, it would not be expected to be reversible. To determine the frequency of downbeat nystagmus as an incidental finding in alcoholic patients, 175 consecutive patients admitted to an alcohol rehabilitation ward were evaluated (Kelly B, Rosenberg ML, unpublished observations). None had downbeat nystagmus in primary position, on lateral gaze, or in the head-hanging position. All of these patients had been abstinent for periods ranging from several weeks to several months, however. It may be that the incidence would be higher in alcoholics with a more recent history of increased intake. It is possible that patients with downbeat nystagmus in the head-hanging position may be prone to go on to develop the full picture of chronic cerebellar degeneration. REFERENCES 1. Berger JR, Kovacs AG. Downbeat nystagmus with phenytoin. I Gin Neuro-ophthalmol 1982;2:209-11. 2. Wheeler SO, Ramsay RE, Weiss J. Drug induced downbeat nystagmus. Ann NeuroI1982;12:227-8. 3. Maim G, Tunell UL. Cerebellar dysfunction related to toluene sniffing. Acta Neurol Scand 1980;62:188-90. 4. Saul RF, Selhorst JB. Downbeat nystagmus with magnesium depletion. Arch NeuroI1981;38:650-2. 5. Coppeto JR, Monteiro MLR, Lessel S, Bear L, MarinezMaldonado M. Downbeat nystagmus. Long-term therapy with moderate dose lithium carbonate. Arch Neurol 1983;40:754-5. 6. Halmagyi GM, Rudge P, Gresty MA, Sanders MD. Downbeating nystagmus. A review of 62 cases. Arch Neurol 1983;40:777-84. 7. Cogan DG. Down-beat nystagmus. Arch Ophthalmol 1968;80:757-68. 8. Costin JA, Smith JL, Emery S, Tomsak RL. Alcoholic downbeat nystagmus. Ann OphthalmoI1980;12:1127-31. 9. Diener HC, Dichgans J, Bacher M, Guschlbauer B. Improvement of ataxia in alcoholic cerebellar atrophy through alcohol abstinence. I NeuroI1984;231:258-62. 10. Carlen PL, Holgate RC, Wortzman G, Wilkinson DA, Rankin JG. Reversible cerebral atrophy in abstinent chronic alcoholics measured by computed tomography scans. Science 1978;200:1076-8. 11. Ron MA, Acker W, Shaw FK, Lichman WA. Computerized tomography of the brain in chronic alcoholism. A survey and follow-up study. Brain 1982;105:497-514. 12. Hawley RJ, Kurtzke JF, Armbrustmacher VW, Saini N, Manz H. Course of alcohol induced nutritional peripheral neuropathy. Acta Neurol Scand 1982;66:582. 13. Abel LA, Schmidt MD, Dellosso LF, Daroff RB. Saccadic system plasticity in humans. Ann NeuroI1978;4:313-8. 14. Victor M, Adams RD, Collins GH. The Wernicke-Korsakoff Syndrome. Philadelphia: F. A. Davis Co., 1971:27. J Clin Neuro-ophthalmol, Vol. 7, No.1, 1987 |
