Psychosomatics 43:335-336, August 2002
© 2002 The Academy of Psychosomatic Medicine
Phenytoin-Induced Visual Disturbances Misdiagnosed as Alcohol Withdrawal
Molly M. Shores, M.D., and
Kevin L. Sloan, M.D., University of Washington, Seattle, Washington
Key Words: TCAs • Alchohol Withdrawal
TO THE EDITOR: Visual disturbances are well-known side effects of anticonvulsant drugs.1 Phenytoin is associated with more visual abnormalities than other anticonvulsants and may cause diplopia, oscillopsia, vertical nystagmus, and impaired convergence. We report a case of visual disturbances initially attributed to alcohol withdrawal that appeared to be due to an adverse reaction to phenytoin.
Case Report
A 71-year-old man was admitted to the neurology service following a seizure. The patient had aortic stenosis, chronic obstructive pulmonary disease, gastroesophageal reflux, and a history of alcohol use, drinking approximately 2-3 beers a day. The psychiatry department was consulted for management of "hallucinations from alcohol withdrawal."
The patient denied any alcohol withdrawal symptoms. His last drink had been 4 days before the onset of visual changes. He reported no history of withdrawal symptoms except for mild tremulousness. The visual changes occurred after his first dose of phenytoin and initially consisted of double vision. Then, objects appeared to vibrate, shrink or increase in size, and had a reddish hue. He reported that he had not been experiencing depression, paranoia, headaches, or visual, auditory, olfactory, or tactile hallucinations. He was anxious about the visual changes and asked, "Have they given me that drug that makes you hallucinate... LSD?"
His medication regimen included phenytoin, 300 mg/day; cisapride, 10 mg q.i.d.; ranitidine, 300 mg b.i.d.; aspirin, 325 mg/day; one daily multivitamin with folate; oral thiamine, 100 mg/day; and oral lorazepam, 1 mg every 4-6 hours as need for treatment of agitation. Abnormal laboratory data included the following: mean corpuscular volume=101.5 fL; platelets= 113 x 103/µl and sodium=130 meq/liter. Results of his albumin, liver function, and thyroid function tests were within normal limits, and blood alcohol level at the time of admittance was undetectable. Trough phenytoin level drawn after two doses was 5.4 µg/ ml. An EEG performed at admittance revealed right frontotemporal epileptiform discharges; a second EEG showed no epileptiform discharges. A non-contrast computerized tomography (CT) scan of the head showed no mass lesion or intracranial hemorrhage.
He was alert and oriented during a physical examination. The neurologic examination was notable for a broad-based gait. The remainder of the neurologic exam was unremarkable (full extraocular movements, no nystagmus, pupils reactive and equal in size, intact visual fields, and normal funduscopic exam).
Following psychiatric consultation, phenytoin was discontinued, and carbamazepine was initiated. The day after phenytoin was discontinued, the visual disturbances resolved. The patient had no alcohol withdrawal symptoms and required no benzodiazepine treatment.
Discussion
Because of his history of alcohol use, the patient's visual changes were initially attributed to alcohol withdrawal. Alcohol withdrawal syndromes can be divided into four categories: tremulousness, hallucinations, seizures, and delirium tremens.2 Isolated hallucinations, without delirium tremens, commonly occur early in the course of alcohol withdrawal, 10-30 hours after the last drink. Delirium tremens occurs from the 3rd to 5th day after cessation of alcohol in patients who already have alcohol withdrawal symptoms.2 In addition to hallucinations, delirium tremens is characterized by confusion, autonomic hyperreactivity, and fever. Although the patient had hallucinations, he had a clear sensorium, no symptoms of alcohol withdrawal, and did not have any of the other cardinal signs of delirium tremens. Thus, the onset of visual hallucinations occurring 4 days after stopping alcohol was not consistent with either alcohol withdrawal hallucinations or delirium tremens.
Other diagnostic possibilities include a posterior cerebrovascular accident, occipital lobe seizure, or posterior transient ischemic attack. A cerebrovascular accident and occipital lobe seizure were ruled out by a CT scan and a second EEG. Although a posterior transient ischemic attack could not be definitively ruled out, the temporal relationship between initiation of phenytoin and onset of symptoms and resolution of symptoms with discontinuation of phenytoin strongly suggests that the visual disturbances were due to phenytoin. Other conditions that are characterized by hallucinations in a clear sensorium include chronic sedative hypnotic abuse and alcoholic hallucinosis. However, there was no history of chronic sedative use or abuse. In addition, the patient's symptoms were not typical of alcoholic hallucinosis, which is a rare condition that occurs after long-standing, excessive alcohol use and is characterized by primarily auditory hallucinations that may develop into a chronic psychotic disorder.3,4
Visual disturbances of diplopia and oscillation are more typical of an adverse medication effect3 than alcohol withdrawal, and changes in color intensity and diplopia are well-known side effects of anticonvulsant drugs.5 Since the patient's phenytoin level was low, the visual changes were not initially attributed to phenytoin treatment. However, elderly patients may have adverse effects from low doses of medication, and visual disturbances have been reported with low-therapeutic phenytoin levels in patients receiving multiple medications.6
This case illustrates the importance of taking a careful history, keeping a broad differential, and recognizing that medically ill, elderly patients being treated with multiple medications may have adverse side effects, even at subtherapeutic drug levels.
REFERENCES
- Paulus W, Schwarz G, Steinhoff BJ: The effect of anti-epileptic drugs on visual perception in patients with epilepsy. Brain 1996; 119:539-549[Abstract/Free Full Text]
- Erwin WE, Williams DB, Speir WA: Delirium tremens. Southern Med J 1998; 91:425-432[Medline]
- Asaad G, Shapiro B: Hallucinations: theoretical and clinical overview. Am J Psychiatry 1986; 143:1088-1097[Abstract/Free Full Text]
- Turner RC, Lichstein PR, Peden JG, Busher JT, Waivers LE: Alcohol withdrawal syndromes: a review of pathophysiology, clinical presentation, and treatment. J Gen Intern Medicine 1989; 4:432-444
- Remler BF, Leigh RJ, Osorio I, Tomsak RL: The characteristics and mechanisms of visual disturbance associated with anticonvulsant therapy. Neurology 1990; 40:791-796[Abstract/Free Full Text]
- Bayer AU, Thiel HJ, Zrenner E, Dichgans J, Kuehn M, Paulus W, Ried S, Schmidt D: Color vision tests for early detection of antiepileptic drug toxicity. Neurology 1997; 48:1394-1397[Abstract]
This article has been cited by other articles:
|
|
|
|
 
M. Levy
Delirium Likely Caused by Interaction Between Phenytoin and Temozolomide
Psychosomatics,
August 1, 2007;
48(4):
359 - 360.
[Full Text]
[PDF]
|
|
|
Get information about faster international access.
Privacy Policy
Copyright © 2002
Academy of Psychosomatic Medicine.
All rights reserved.
Home
| Search
| Current Issue
| Past Issues
| Subscribe
| All APPI Journals
| Help
| Contact Us
|
