The pat ient , t a 41-year-old right-handed school-teacher and housewife, had had a subarachnoid hemorrhage without localizing signs at the age of 16 years. She was well until 5 days before her admission, at which time, while a t home, she suddenly experienced severe headache, nausea and vomiting, and became comatose. Lumbar puncture revealed bloody spinal fluid. She was then hospitalized at a local hospital. Neurological examination disclosed a right hemiparesis and some difficulty with speech. She continued to improve until 4 days later when there was an increase in the severity of the symptoms and of the blood in the spinal fluid. She was then transferred to the Mount Sinai Hospital. Examination. She was a noncommunicative, aphasic patient with right-sided weakness, including the face. Right hyperreflexia and Babinski's sign were present. The fundi were normal. There was vertical nystagmus, with paralysis of upward gaze. An electroencephalogram showed severe diffuse slowing, accentuated in the left frontotemporal region. Her state of alertness improved but tile signs persisted. I t was now possible to ascertain that there was no apparent sensory disturbance within the limits of testing and tha t visual fields were full to confrontation. Thirteen days after admission, a left carotid angiogram was carried out. I t showed, in the anteroposterior projection (Fig. 1), a small vascular malformation lying lateral and slightly dorsal to the internal cerebral vein, to which it shunted. The lat ter structure was not shifted across the midline. The malformation seemed to derive most of its blood supply from ganglionic vessels arising inferiorly. The lateral angiogram (Figs. i and 3) also showed the malformation and its shunt to the dilated internal cerebral vein. The lat ter structure was dislocated upwards, indicating a mass in the thalamic region. The anomaly could be seen to project superiorly to the striatothalamic vein and it was judged that a t least part of it might be in proximity to the left lateral ventricle. For this reason a pneumoencephalogram was carried out. The anteroposterior erect films disclosed marked elevation of the thalamic shadow (Fig. 4), with some irregularity of its roof, possibly indicative of the malformation. The lateral view (Fig. 5) showed a marked general increase of the left thalamic outline with local accentuation anterodorsally, in the area under suspicion. There was no filling of the posterior part of the third ventricle. The impression was that this was an arteriovenous anomaly of the left thalamus which was superficial and had ruptured into the thalamus and the left lateral ventricle. I t was felt that the lesion might be safely approached through the hydrocephalic ventricle, and removed, because of its small size. Operation, Under hypothermia and hypotension, 6 weeks after admission, the left su-