LETTERS

Seizures Associated with a New Combination “Pick-Me-Up” Pill Shirley M. Mueller, MD, and Elizabeth B. Solow, MS

Recently, the news (Wall Street Journal 61 [2291, Sep- tember 8, 1981; Time 118 [12], September 21, 1981) and television media have drawn attention to the relationship between the ingestion of a new “pick-me-up” pill and fatal cerebral hemorrhage. “Pick-me-ups” consist of high doses of caffeine and lesser amounts of phenylpropenolamine plus an occasional third drug. The pills are commonly made to look like prescription medications and therefore are also called “look-alikes.” The buyer is often told they are am- phetamines. The reports of associated cerebral hemorrhage (Barry Diskant, MD, and Douglas Barrett, MD, personal communication, 1981) are believed to be due to am- phetamine-like qualities.

This communication reports an association between “pick-me-ups” and seizures in a normal 17-year-old white woman who was two weeks postpartum. The woman took a single “pick-me-up” pill which she believed to be an am- phetamine compound. Approximately 20 to 30 minutes later, she stated, she became tense and developed a severe, generalized, throbbing headache. The woman was noted to stiffen and rock backward, and her head and eyes deviated to the left. She choked and bit her lip. Tonic-clonic move- ments of both arms lasted 4 to 5 minutes. Approximately 10 minutes after the first seizure the woman had a second, similar attack. A neurological examination revealed no focal abnormalities or papilledema. The patient complained of a severe right temporal-occipital headache. Routine blood values were normal. Lumbar puncture and computed tomographic scan were normal. An electroencephalogram revealed slow and poorly organized background activity over the right posterior cerebral hemisphere. Focal, low- amplitude, irregular theta activity was present over the right middle posterior temporal region and was interpreted as being compatible with a focal structural lesion. No fur- ther seizures occurred, and the woman was discharged sev- eral days later on a regimen of phenobarbital, 30 mg three times a day. Two months later her EEG and CT scan were normal. Six months after the initial event, she had had no further seizures in spite of discontinuing phenobarbital.

The patient provided a tablet identical to that which she had taken. It resembled Histalet Forte. The pill contents were screened with a gas-liquid chromatography-mass spectrometry system with electron impact ionization. A large amount of caffeine was present with lesser amounts of phenylpropenolamine and pseudoephedrine. We conjec- ture that the vasoconstrictor properties of the last two components of the pill may have led to the acute hyperten- sion, headache, and seizures. Neurologists should be alert to the possibility that seizures in addition to fatal cerebral hemorrhage can be associated with “pick-me-ups” that are also known as “look-alikes.”

Departments of Neurology and Neurological Surgery Indiana University School of Medicine Indianapolis, IN 46202

Inappropriate Secretion of Antidiuretic Hormone Associated with Guillain-Bar& Syndrome M. Seth Hochman, MD,* Steven A. Kobetz, MD,” and John V. Handwerker, M D t

The association of Guillain-Barre syndrome (GBS) with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) has been reported in twelve patients since 1958 [2, 51. GBS is generally restricted clinically and pathologically to the peripheral nervous system [3], and most cases involving SIADH have demonstrated au- tonomic dysfunction [2, 51. Abnormalities of peripheral autonomic afferent fibers arising from vascular stretch re- ceptors have been thought to reduce vagal inhibitory ac- tion on the release of antidiuretic hormone from the neurohypophysis [5]. We have recently encountered a pa- tient who had SIADH and mild GBS without dysphagia, cardiac irregularities, or blood pressure instability.

A 62-year-old white man was admitted with fever, sore throat, myalgia, low back pain, and occipital headache. Physical examination revealed pharyngitis and symmetrical 2+ knee and I + biceps, triceps, and ankle jerks. Cranial nerve, motor, sensory, and mental status examinations were normal. Lumbar puncture was normal except for an opening pressure of 230 mm CSF. The following labora- tory tests were normal: white and red blood cells, hemo- globin, hematocrit, mean corpuscular volume, sedimenta- tion rate, prothrombin time, partial thromboplastin time, cholesterol, triglycerides, glucose, albumin, phosphorus, total bilirubin, alkaline and acid phosphatase, creatinine, creatine phosphokinase, aspartate aminotransferase, anti- streptolysin 0 titer, Australia antigen, mono test, antinu- clear antibody, fluorescent treponemal antibody-absorbed, and protein electrophoresis. The electrocardiogram re- vealed sinus rhythm.

On the sixth hospital day, the patient developed numb- ness in his lower extremities. Knee and ankle jerks were ab- sent, and mild weakness of both extensor hallucis muscles was noted. Iliopsoas muscle strength was reduced to 4/5 and left hamstrings and quadriceps muscles were 5 4 5 . Sensory examination was normal to pinprick. Tidal volume was 250 to 300 cc and forced vital capacity, 1,850 cc. The serum sodium dropped from 131 mEq/L on the second hospital day to 114 mEq/L on the seventh; the blood urea nitrogen fell from 15 mg/dl to 7. Serum potassium and car- bon dioxide remained unchanged at 4 and 27 mEq/L, re- spectively. Serum creatinine was 0.9 mg/dl and urine os- molality, 674 mOsm/kg. Urine sodium concentration was 56 mEq/L and potassium, 34 mEq/L.

The patient was started on a regimen of 3% saline and fluid restriction. Sixteen hours later, serum sodium was 129 mEq/L and serum osmolality, 260 mOsmikg. With further fluid restriction, serum sodium increased to normal by

Address reprint requests to Dr Hochman, 3661 S Miami Ave, Miami, FL 33133.

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