pose that such rupture may be the consequence of local violent vasospasm following embolic occlusion.
While our list of potential causes of cerebral vasospasm was not meant to be exhaustive, we would emphasize that none of our patients had evidence of embolic arterial occlusion demonstrated by acute angiographic studies. Vazquez-Cruz has called our attention to his report of 11 patients with migraine who suffered intracerebral hemorrhage. Nine of those patients had hypertension or identified vascular malformations, one was an alcoholic, and one had no predisposing cause. We are unaware of an association between alcoholism and intracerebral hemorrhage except in the setting of coagulopathy or direct trauma. None the less, none of our patients were alcoholics. Migraine is a common disorder, and it is likely that a signif¬ icant number of patients who sustain intracerebral hemorrhage, from what¬ ever cause, also suffer from migraine. The point of our report was to empha¬ size that, in a number of patients without other identifiable cause for intracerebral hemorrhage, migraine itself may be causative. We suspect that Dr Vazquez's last case may fit into this group. Cole, MD Department of Neuroscience The Johns Hopkins Andrew J.
University School of Medicine
725 N Wolfe St Baltimore, MD 21205 Michel Aub\l=e'\,MD Montreal Neurological Institute 3801 University St Montreal, Quebec, Canada H3A 2B4
Isopropyl Alcohol Intoxication To the Editor.\p=m-\On reading the article "Isopropyl Alcohol Intoxication" by
Rich et al1 in the March issue of the Archives, I was struck by the fact that in all three of the cases presented there was
nothing neurologically unique
about these alcoholic subjects. In case 1, the sluggish pupils, prominent horizontal nystagmus, and appendicular and gait ataxia associated with peripheral neuropathy suggests Wernicke's encephalopathy.2 No mention is made of treatment with thiamine. In case 2, the patient had an alcohol-related seizure and subsequent delirium tremens. I am surprised that a computed tomographic scan of his brain was not performed, given his recent head trauma. In case 3, the coma is consistent with intoxication with isopropyl alcohol, which is well described.3 The conclusions about the presentation of isopropyl alcohol intoxication presenting in two distinct patterns
(stupor in a known alcoholic or encephalopathy in alcoholic subjects who hide their addiction) is not warranted. The only unique clinical points about iso¬ propyl alcohol are the reflections of its metabolic handling. Unlike ethanol, ethylene glycol, and methanol, isopro¬ pyl alcohol causes ketosis without a significant wide-gap metabolic
acidosis.3 The emergent care of pa¬ tients who may have ingested isopro¬ pyl alcohol involves support of the air¬ way and attention to ruling out meth¬ anol or ethylene glycol ingestion. Since all three cause a widened osmolar gap, specific levels of ethanol, methanol, and ethylene glycol are necessary in order to make a decision about treat¬ ing with an ethanol drip. This is not indicated for isopropyl ingestion, but is indicated for methanol and ethylene glycol. Finally, attention to replace¬ ment of both thiamine and niacin in any alcoholic with neurologic findings is paramount because the clinical di¬ agnosis of either Wernicke's encephal¬ opathy or alcoholic pellagra is very difficult.4·5 There is very little toxicity associated with replacement therapy. Keith Wrenn, MD 601 Elmwood Ave, Box 655 Rochester, NY 14642
1. Rich J, Scheife RT, Katz N, Caplan LR. Isoalcohol intoxication. Arch Neurol. 1990; 47:322-324. 2. Harper CG, Giles H, Finlay-Jones R. Clinical
propyl
signs in the Wernicke-Korsakoff complex.
J Neurol Neurosurg Psychiatry. 1986;49:341-345. 3. LaCouture PG, Wason S, Abrams A, Lovejoy FH. Acute isopropyl alcohol intoxication. Am J
Med. 1983;75:680-686. 4. Lindboe CF, Loberg EM. The frequency of brain lesions in alcoholism. J Neurol Sci. 1988; 88:107-113. 5. Serdaru M, Hausser-Hauw C, Laplane D, et al. The clinical spectrum of alcoholic pellagra encephalopathy. Brain. 1988;111:829-842.
are the only ones that are repeatedly and deliberately ingested for prolonged periods. The chronic effects of isopropyl alcohol are thus important. We are pleased to know that Wrenn's neurological experience in
anol
emergency medicine is extensive enough that he can chide us on the neurological uniqueness of our case 1, the only patient with chronic isopropyl alcohol use. Wrenn thinks the pa¬ tient's findings are not separable from Wernicke's encephalopathy. During the senior author's (L.R.C.) training at the Boston (Mass) City Hospital and since, he has seen well over 100 pa¬ tients with Wernicke's encephalopa¬ thy and is very familiar with the find¬ ings. In Wernicke's encephalopathy, the signs develop rapidly and are not due to a direct effect of ethanol or any other toxic agent on the nervous sys¬ tem and do not respond quickly to ab¬ stinence. The ocular findings may re¬ spond within hours to days to thia¬ mine, but the other signs resolve more slowly or not at all. Our patient had the gradual onset of a constellation of signs that indicated diffuse cerebral, pyramidal tract, and cerebellar dys¬ function that disappeared within 4 days of stopping isopropyl alcohol in¬ gestion. He had received thiamine at the Boston City Hospital 3 weeks be¬ fore and had been eating very well at his sister's house since then. His neu¬ rologic signs indicated subacute iso¬ propyl alcohol toxicity and not Wer¬ nicke's encephalopathy. No other ex¬ amples of subacute or chronic isopropyl alcohol intoxication have been reported to our knowledge, but we are confident that readers will now be able to identify such patients now that they are alerted to their presence and
the findings. In Reply.\p=m-\Weagree with Dr Wrenn that identification of the specific offending alcohol is important in managing patients with acute intoxications. One purpose of our report was to alert readers to the laboratory findings in patients with acute isopropyl alcohol intoxication, a disorder that we believe is common, yet little appreciated. Unfortunately, many breathalyzer tests as well as a newly introduced "saliva alcohol dipstick" method1 do not distinguish between alcohols. We agree with his comments about management of the acute intoxications, including generous administration of thiamine in these patients, many of whom also abuse ethanol and eat sparingly and poorly. Among the intoxicant alcohols (ethanol, methanol, isopropyl alcohol, ethylene glycol) isopropyl alcohol and eth-
Louis R. Caplan, MD Nathaniel Katz, MD Richard Scheife, DPharm Jaime Rich, MD Department of Neurology Tufts University 750 Washington St Boston, MA 02111
1. Rodenberg H, Bennet J, Watson WA. Clinical utility of a saliva alcohol dipstick estimate of serum ethanol concentrations in the emergency department. Ann Pharmacother. 1990:24:358-361.
Seizures After Stroke
To the Editor.\p=m-\Thestudy of epilepsy in stroke by Kilpatrick et al1 probably represents the largest study to date of a topic that has been largely neglected. However, we found the quality of data obtained rather disappointing. For instance, surely the authors should have strived to obtain complete
electroencephalographic documenta-
Downloaded From: http://archneur.jamanetwork.com/ by a Indiana University School of Medicine User on 05/11/2015
While our list of potential causes of cerebral vasospasm was not meant to be exhaustive, we would emphasize that none of our patients had evidence of embolic arterial occlusion demonstrated by acute angiographic studies. Vazquez-Cruz has called our attention to his report of 11 patients with migraine who suffered intracerebral hemorrhage. Nine of those patients had hypertension or identified vascular malformations, one was an alcoholic, and one had no predisposing cause. We are unaware of an association between alcoholism and intracerebral hemorrhage except in the setting of coagulopathy or direct trauma. None the less, none of our patients were alcoholics. Migraine is a common disorder, and it is likely that a signif¬ icant number of patients who sustain intracerebral hemorrhage, from what¬ ever cause, also suffer from migraine. The point of our report was to empha¬ size that, in a number of patients without other identifiable cause for intracerebral hemorrhage, migraine itself may be causative. We suspect that Dr Vazquez's last case may fit into this group. Cole, MD Department of Neuroscience The Johns Hopkins Andrew J.
University School of Medicine
725 N Wolfe St Baltimore, MD 21205 Michel Aub\l=e'\,MD Montreal Neurological Institute 3801 University St Montreal, Quebec, Canada H3A 2B4
Isopropyl Alcohol Intoxication To the Editor.\p=m-\On reading the article "Isopropyl Alcohol Intoxication" by
Rich et al1 in the March issue of the Archives, I was struck by the fact that in all three of the cases presented there was
nothing neurologically unique
about these alcoholic subjects. In case 1, the sluggish pupils, prominent horizontal nystagmus, and appendicular and gait ataxia associated with peripheral neuropathy suggests Wernicke's encephalopathy.2 No mention is made of treatment with thiamine. In case 2, the patient had an alcohol-related seizure and subsequent delirium tremens. I am surprised that a computed tomographic scan of his brain was not performed, given his recent head trauma. In case 3, the coma is consistent with intoxication with isopropyl alcohol, which is well described.3 The conclusions about the presentation of isopropyl alcohol intoxication presenting in two distinct patterns
(stupor in a known alcoholic or encephalopathy in alcoholic subjects who hide their addiction) is not warranted. The only unique clinical points about iso¬ propyl alcohol are the reflections of its metabolic handling. Unlike ethanol, ethylene glycol, and methanol, isopro¬ pyl alcohol causes ketosis without a significant wide-gap metabolic
acidosis.3 The emergent care of pa¬ tients who may have ingested isopro¬ pyl alcohol involves support of the air¬ way and attention to ruling out meth¬ anol or ethylene glycol ingestion. Since all three cause a widened osmolar gap, specific levels of ethanol, methanol, and ethylene glycol are necessary in order to make a decision about treat¬ ing with an ethanol drip. This is not indicated for isopropyl ingestion, but is indicated for methanol and ethylene glycol. Finally, attention to replace¬ ment of both thiamine and niacin in any alcoholic with neurologic findings is paramount because the clinical di¬ agnosis of either Wernicke's encephal¬ opathy or alcoholic pellagra is very difficult.4·5 There is very little toxicity associated with replacement therapy. Keith Wrenn, MD 601 Elmwood Ave, Box 655 Rochester, NY 14642
1. Rich J, Scheife RT, Katz N, Caplan LR. Isoalcohol intoxication. Arch Neurol. 1990; 47:322-324. 2. Harper CG, Giles H, Finlay-Jones R. Clinical
propyl
signs in the Wernicke-Korsakoff complex.
J Neurol Neurosurg Psychiatry. 1986;49:341-345. 3. LaCouture PG, Wason S, Abrams A, Lovejoy FH. Acute isopropyl alcohol intoxication. Am J
Med. 1983;75:680-686. 4. Lindboe CF, Loberg EM. The frequency of brain lesions in alcoholism. J Neurol Sci. 1988; 88:107-113. 5. Serdaru M, Hausser-Hauw C, Laplane D, et al. The clinical spectrum of alcoholic pellagra encephalopathy. Brain. 1988;111:829-842.
are the only ones that are repeatedly and deliberately ingested for prolonged periods. The chronic effects of isopropyl alcohol are thus important. We are pleased to know that Wrenn's neurological experience in
anol
emergency medicine is extensive enough that he can chide us on the neurological uniqueness of our case 1, the only patient with chronic isopropyl alcohol use. Wrenn thinks the pa¬ tient's findings are not separable from Wernicke's encephalopathy. During the senior author's (L.R.C.) training at the Boston (Mass) City Hospital and since, he has seen well over 100 pa¬ tients with Wernicke's encephalopa¬ thy and is very familiar with the find¬ ings. In Wernicke's encephalopathy, the signs develop rapidly and are not due to a direct effect of ethanol or any other toxic agent on the nervous sys¬ tem and do not respond quickly to ab¬ stinence. The ocular findings may re¬ spond within hours to days to thia¬ mine, but the other signs resolve more slowly or not at all. Our patient had the gradual onset of a constellation of signs that indicated diffuse cerebral, pyramidal tract, and cerebellar dys¬ function that disappeared within 4 days of stopping isopropyl alcohol in¬ gestion. He had received thiamine at the Boston City Hospital 3 weeks be¬ fore and had been eating very well at his sister's house since then. His neu¬ rologic signs indicated subacute iso¬ propyl alcohol toxicity and not Wer¬ nicke's encephalopathy. No other ex¬ amples of subacute or chronic isopropyl alcohol intoxication have been reported to our knowledge, but we are confident that readers will now be able to identify such patients now that they are alerted to their presence and
the findings. In Reply.\p=m-\Weagree with Dr Wrenn that identification of the specific offending alcohol is important in managing patients with acute intoxications. One purpose of our report was to alert readers to the laboratory findings in patients with acute isopropyl alcohol intoxication, a disorder that we believe is common, yet little appreciated. Unfortunately, many breathalyzer tests as well as a newly introduced "saliva alcohol dipstick" method1 do not distinguish between alcohols. We agree with his comments about management of the acute intoxications, including generous administration of thiamine in these patients, many of whom also abuse ethanol and eat sparingly and poorly. Among the intoxicant alcohols (ethanol, methanol, isopropyl alcohol, ethylene glycol) isopropyl alcohol and eth-
Louis R. Caplan, MD Nathaniel Katz, MD Richard Scheife, DPharm Jaime Rich, MD Department of Neurology Tufts University 750 Washington St Boston, MA 02111
1. Rodenberg H, Bennet J, Watson WA. Clinical utility of a saliva alcohol dipstick estimate of serum ethanol concentrations in the emergency department. Ann Pharmacother. 1990:24:358-361.
Seizures After Stroke
To the Editor.\p=m-\Thestudy of epilepsy in stroke by Kilpatrick et al1 probably represents the largest study to date of a topic that has been largely neglected. However, we found the quality of data obtained rather disappointing. For instance, surely the authors should have strived to obtain complete
electroencephalographic documenta-
Downloaded From: http://archneur.jamanetwork.com/ by a Indiana University School of Medicine User on 05/11/2015
