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To the Editor.— Painful muscle cramps may occur under a variety of conditions, such as during pregnancy, after dehydration and salt depletion, in hypothyroidism, thyrotoxic myopathy, uremia, and hypomagnesemia. 1 The mechanism of muscle cramps in these conditions may not be the same. In the past two years we have seen five patients who underwent gastrectomy with postoperative muscle cramps. Their ages ranged from 40 to 64 years. Four were men and one a woman. Painful exertional muscle cramps in them began mostly from four to six years after subtotal gastrectomy for a peptic ulcer. On neurological examination deep tendon reflexes of the extremities were mostly hyperactive, and two patients exhibited scattered fasciculations. Mild muscle atrophy was noted in two cases. In one subject muscle cramps were induced by repetitive tapping of the muscle tendon as well as by strong voluntary contractions. In another patient manual muscle testing during neurological

To the Editor.— In the past two years, we have seen four patients with muscle cramps after each patient underwent a subtotal gastrectomy. Our patients' ages ranged from 43 to 64 years. Painful exertional muscle cramps began from four to six years after each patient underwent a subtotal gastrectomy for a peptic ulcer. All of the patients were men. Cramps involved the upper and lower extremities in every case, as well as the abdominal wall in two cases. Cramps were sustained for several minutes with visible and palpable contraction of muscles (Figure, A). Electromyographically, irregular bursts of muscle action potentials were recorded from the affected muscle (Figure, B). Reflexes were hyperactive in three patients. Fasciculations and mild muscle atrophy were noted in two patients. In one patient, the cramps were induced by repetitive tapping of the muscle tendon, as well as by strong voluntary contractions. In another patient, manual muscle

• We measured several parameters of cortical potentials evoked by visual stimulation to produce a profile suggestive of retrochiasmatic lesions. Characteristic abnormal responses included (1) very low amplitude or absent transient visual evoked potentials (T-VEPs) after stimulation of the affected hemifield, (2) reversal of normal pattern amplitude of the T-VEP distribution after stimulation of the affected hemifield, (3) abnormal lateral occipital ratio, (4) absent or very low amplitude steady-state VEPs after stimulation of affected hemifield, and (5) abnormal midoccipital ratio.

• We performed electrophysiologic and neuroradiologic studies on a patient who had epilepsia partialis continua (EPC) to elucidate the pathophysiologic mechanism of repeated myoclonic jerks confined to the right toes. A computed tomographic scan revealed a small cortical lesion in the left parasagittal rolandic area corresponding to the sensorimotor cortex of the right toes. A pretrigger EEG analysis with a jerk-locked averaging technique revealed a positive spike 32 ms before the jerks. A similar positive spike was evoked at a latency of 48 ms after an electrical stimulation of the right posterior tibial nerve; it was followed by a myoclonic jerk with a 32-ms latency. We suppose that in our patient, an epileptogenic focus in the motor cortex and transcortical long-loop reflexes played an important role in generating EPC.

To the Editor.— We wish to describe the computed tomographic (CT) manifestations of a patient with idiopathic familial basal ganglia calcification. A detailed history of this patient and his family can be found in earlier reports. 1,2 Report of a Case.— A 45-year-old man was brought to the St Louis Veterans Administration Hospital in June 1976. Progressive slowing of mentation had started when he was 36 years old. For several years before admission, grand mal seizures had been frequent. He had become irritable and irrational. When he was 39 years old, bilateral basal ganglia calcification was found by skull roentgenography. His mother had similar symptoms and was also found to have basal ganglia calcification. His children and his sister's children also had roentgenographic evidence of basal ganglia calcification, but none of them had displayed neurologic deficits. On examination, the patient appeared dull and unkempt. His recent memory was markedly impaired.

To the Editor.— Alpha coma has been well described in postanoxic encephalopathy and brainstem stroke 1.2 and has generally been considered to have a serious prognostic implication. However, a striking exception is presented by the occurrence of alpha coma in acute drug intoxication. 3 The following patient recovered completely from drug-induced alpha coma. Report of a Case.— A 41-year-old man was brought to the emergency room at 3:15 PM of Oct 4, 1979. He had attempted suicide on the day of admission, swallowing an overdose of tranquilizers. On arrival at our hospital, he was in deep coma, as well as cyanotic in the absence of spontaneous respiration. Treatment consisted of immediate resuscitative measures for respiratory failure and support of blood pressure and ventilation. There was no response to painful stimulation. The pupils were extremely miotic and failed to react to light. The patient remained comatose for more than 20 hours. Then