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Complex partial status epilepticus provoked by УcrackФ cocaine.

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Complex Partial Status
Epilepticus Provoked by
“Crack” Cocaine
Abayomi 0. Ogunyemi, MD, George E. Locke, MD,
Lynn D. h e r , MD, and Lowell Nelson, PhD, MD
A 53-year-old woman with a history of chronic abuse
of “crack’ cocaine developed isolated complex partial
status epilepticus after 3 days of frequent cocaine use.
The electroencephalogram demonstrated focal epileptiform activity. Follow-up for 1 year during which she
reported continuous abstinence from cocaine and anticonvulsants revealed n o recurrence of seizures.
Ogunyemi AO, Locke GE, Kramer LD,
Nelson L. Complex partial status epilepticus
provoked by “crack cocaine.
Ann Neurol 1989;26:785-786
There has been a resurgence in the recognition and
documentation of the neurological complications of
cocaine abuse, such as stroke {1-4}, subarachnoid
hemorrhage [Sl, and seizures t3, 6, 71. Although generalized tonic clonic seizures have been reported to
occur in up to 14% of cocaine users [7}, very little
information is available on the occurrence of partial
From the Department of Neuroscience and Epilepsy Center,
Charles R. Drew University of Medicine and Science and Martin
Lurher King Jr. General Hospital, Los Angeles, CA.
Received Feb 2, 1989, and in revised form May 12. Accepted for
publication May 15, 1989.
Address correspondence to Dr Locke, Department of Neuroscience
and Epilepsy Center, King/Drew Medical Center, 1621 E. 120th
Street, Los Angeles, CA 90059.
seizures in association with the use of the drug. We
report the case of a middle-aged woman who developed complex partial status epilepticus following the
abuse of “crack cocaine.
Case Report
A 53-year-old woman had used cocaine spordcally for almost 4 years without any medical complications. Six days
prior to hospital admission, she indulged in smoking “crack
cocaine for 3 consecutive days. After this tune, her relatives
noted that she developed bizarre behavior and confusion.
She was restless and aggressive and did not seem to recognize some of her close relatives. Two days later fluctuation of
sensorium was observed, during which alert, responsive behavior alternated with periods of lethargy and mutism or
with periods of restlessness and inappropriate speech. She
was incontinent of urine at times.
She had no history of seizures or mental illness and no
family history of convulsions. Mild hypertension had been
recently diagnosed and was being treated with a thiazide
diuretic.
Vital signs were normal with the exception of a heart rate
of 112 beats per minute. Findings on the general physical
examination were normal. Neurological examination demonstrated agitation, confusion, and disorientation to time, place,
and person, but no focal neurological deficits.
Urine toxic screen was positive for cocaine metabolites
but negative for amphetamine, phencyclidine, and opiates.
Routine hemogram and s e m biochemical measurements
were within normal limits. Cranial cerebral tomography (CT)
was normal. An emergency electroencephalogram (EEG)
(Figure) revealed recurrent, focally originating 12- to 20-Hz
rhythmic activities that emanated from the right anterior and
midtemporal regions and showed progressive increase in amplitude and decrease in frequency. Nystagmoid jerks of the
eyes with fast phase to the right were noted in association
with the onset of this EEG activity. The left arm was held in a
tonic flexed posture while the right hand fumbled around.
The abnormal EEG pattern was continuously recorded for
about 1 hour during which diazepam (total of 20 mg) and
phenytoin (1,000 mg) were administered intravenously. The
patient became fully alert approximately 9 hours after treatment with antiepileptic drugs commenced. However, she
had no memory for events for almost 2 weeks preceding
hospitalization. During 1 year of follow-up, she remained
free of illicit drugs and seizures despite lack of anticonvulsant therapy.
Discussion
As a result of the excessive use of “crack cocaine, our
patient exhibited abnormal neurological signs including fluctuations in sensorium, lethargy, confusion, disorientation, and incontinence of urine. EEG confirmed
the diagnosis of complex partial status epilepticus.
Many studies have demonstrated that cocaine can
cause seizures in experimental animals. Cocaine used
in animal models of epilepsy has been shown to alter
excitability of the limbic system and facilitate spread
of afterdischarges to the contralateral hemisphere @-
Copyright 0 1989 by the American Neurological Association
785
Electroencephalogram of a S3-year-oki umzun with complrx partial status epilepticus pmoked 64 “crack”cocaine. 1)uring complex partial status epilepticus the grdph showed recurrent spikes
with semirhythmic 2- to 3-Hz &ha slou: waves in the right
temporal region. FP = fmntopolar, F = fmntal. 7’ = temporal,
0 = occipital,MCV = micmzalts.
lo}. Presumably, therefore, a high concentration of
cocaine in the brain of abusers may result in generalized convulsions, whereas relatively smaller concentrations may be sufficient to exceed the seizure threshold
of the limbic structures and therefore cause complex
partial seizures. Despite these experimental observations, partial seizures have rarely been reported in patients who abuse cocaine. The association of cocaineprovoked complex partial status epilepticus has been
reported, although cocaine use in that patient was not
well documented Ill}.
Cocaine is available on the streets in various forms
and different grades of purity and concentration. However, street users smoke the potent alkaloidal derivative often called “free base” or “crack,” the inhalation
of which has been demonstrated to produce a rapid
rise in the plasma level of cocaine with the potential
for an increase in the risk of medical complications
[12, 13). Cerebrovascular complications including cerebral ischemia and infarctions have been reported
particularly in association with the use of “crack
cocaine 12, 41. The possibility exists, therefore, that
the complex partial status epilepticus in our patient
may have been triggered by focal ischemia involving
the temporal region. We believe that the medical community should be aware of the possibility that noncon-
vulsive status epilepticus may complicate the abuse of
cocaine.
We wish to thank Carol Parsons, Ellen Laurienti. and Leo Maestripieri for manuscript preparation.
References
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786 Annals of Neurology Vol 26 No 6 December 1989
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