NOTES AND LETTERS Bilateral Asterixis in Frontal Tumor Shosaku Noda, MD, and Hirotoshi Umezaki, M D Bilateral asterixis is commonly regarded as a reliable sign of metabolic encephalopathy . W e describe a patient with bilateral asterixis resulting from a large frontal tumor. Our case emphasizes that the presence of bilateral asterixis does not always rule out a mass lesion. A 42-year-old woman was admitted to our clinic because of headache and drowsiness. A computed tomographic (CT) scan showed a ring-enchancing cystic mass in the left frontal lobe, and a diagnosis of brain abscess was made. Penicillin, glycerol, and betamethasone were administered. Two weeks later she became alert and her headache disappeared. However, five weeks later the headache recurred. She was oriented but obtunded. H e r blood pressure, pulse, respiration, and body temperature were unremarkable. H e r pupils were 2 mm in diameter and reacted to light. Ocular movements were intact. No muscle weakness was noted. Hyperreflexia was present in her four limbs. A striking finding was the presence of asterixis involving both hands and feet. The asterixis was asynchronous but symmetrical. Serum hepatic enzymes, blood ammonia, serum creatinine, blood urea nitrogen, serum electrolytes, and blood gas levels were normal, as was serum osmotic pressure. She was not taking any anticonvulsant agents. A C T scan showed a large cystic tumor in the left frontal lobe and marked midline shift with compression of the left ventricle. A left frontotemporal craniotomy was performed. An olfactory neuroblastoma with a large cyst in the left frontal lobe was confirmed. The cyst was filled with a yellowish transparent fluid and was totally removed. The next day she became alert but the asterixis in her right limbs persisted. Two days after operation the asterixis cleared. Our patient developed bilateral asterixis when the clinical signs and C T scan suggested bilateral hemispheral dysfunction or impaired function of the diencephalon. Metabolic and toxic factors were excluded. The asterixis resolved after the operation. These observations indicate that the bilateral asterixis was caused by the frontal tumor. Only three cases with bilateral asterixis and structural lesions have been reported previously 12-41, Weinreb and colleagues  reported a case of bilateral asterixis and hydrocephalus caused by midline frontal hemorrhage but the patient had received phenytoin, which accentuates asterixis. Bril and co-workers f l } described it in a patient with midbrain infarction. The ocular signs in their patient suggested bilateral perinuclear lesions in the rostral midbrain. Santamaria and colleagues [ 3 ] presented a patient with bilateral asterixis caused by a large left subdural hematoma. The C T scan of their patient showed marked midline shift as in our patient. Unilateral asterixis has been described with structural lesions involving the parietal lobe, thalamus, or midbrain . Although the pathophysiological nature of asterivis is not clear, dysfunction of these structures may be responsible. In our patient the bilateral asterixis seems to result from bilat- 366 eral hemispheral or diencephalic impairment caused by the large frontal tumor. Department of Neurology Kyushu-Kosei-Nenkin Hospital 2-1-1 Kishinoura, Yahata-Nishiku Kitakyushu, 806 Japan Rejereences 1. Bril V, Sharpe JA, Ashby P: Midbrain asterixis. Ann Neurol 6:362-364, 1979 2. Plum F, Posner JB: The Diagnosis of Stupor and Coma. Philadelphia, Davis, 1980, pp 191-192 3. Santamaria J, Graus F, Genis D: Bilateral asterixis in unilateral subdural hematoma. J Neurol 229:87-89, 1983 4. Weinreb WH, Perry RJ, Jenkyn LR:Rhythmic alternating asterixis. J Neurol Neurosurg Psychiatry 45:857-858, 1982 The Effects of TRH on F Waves Recorded from Antagonistic Muscles in Human Subjects Paul J. Delwaide, MD, and J. Schoenen, M D Thyrotropin releasing hormone (TRH) has been demonstrated in the ventral horn of the cervical and lumbar enlargement of the spinal cord by radioimmunoassay and immunohistochemical methods [ 5 ] . It can also be detected in the cerebrospinal fluid. Its functional role remains a matter of speculation. It has been claimed that TRH facilitates noradrenergic and serotoninergic transmission, but few neurophysiological studies have explored its mode of action at the spinal level. In animal experiments [l], TRH depolarizes motoneurons slightly but it is not yet known if this effect is direct (on motoneuronal membranes) or indirect (e.g., through interneurons or by facilitation of neurotransmitter activity). Motor effects of TRH are of great interest to neurologists because of its potential therapeutic benefit to patients with amyotrophic lateral sclerosis [ 3 ] and spinocerebellar degenerations . In an attempt to understand more about the possible functional role of this peptide, we were interested to see if TRH modifies the F wave in normal human subjects. The F wave is a muscle response produced by antidromic activation of motoneurons following peripheral nerve stimulation; F waves are thought to reflect excitability of the motoneuron pool . We have previously shown that TRH enhances the F wave in the musculus flexor hallucis brevis (FHB) and that 200 pg is the optimal dosage to modify it 121. The present study was conducted in parallel on two antagonistic muscles, the FHB and the extensor digitorum brevis (EDB) in order te explore mechanisms that underlie TRHinduced modifications of motoneuronal excitability. If T R H acts directly on motoneuronal membranes, one would expect similar effects on antagonistic motoneurons.