SUMMARY A 44-year-old woman with prolonged coma and hypotension following drug overdosage developed bilateral hemorrhagic infarcts in the dorsolateral brainstem. The regional distribution of these paired lesions corresponds to the area of confluence of penetrating arteries in the brainstem. It is suggested that under exceptional circumstances brainstem arterial end-zones may be vulnerable to anoxic-ischemic insult. Stroke Vol 14, No 6, 1983THE STRUCTURAL ALTERATIONS of cerebrum and cerebellum following anoxia-ischemia have been studied extensively in man and in experimental ani mals. [1][2][3][4][5] Selective vulnerability of particular regions within the cerebrum and cerebellum has been attribut ed in part to vascular anatomic factors such as arterial boundary or end-zone distributions. In contrast, stud ies of the topography of anoxic-ischemic involvement in the brainstem suggest that lesions are topistic; i.e., selective for specific neuronal structures. 5^9This pat tern of selective vulnerability in brainstem has been attributed to metabolic factors such as the higher blood flow and metabolic requirements of these nuclei 10 and their high level of lactic acid content during anoxia." The influence of vascular anatomic factors in the distri bution of anoxic-ischemic lesions in brainstem has been given little attention.A patient with bilateral symmetric columnar necro sis of the brainstem associated with prolonged hypo tension is reported. Evidence implicating vascular ana tomic factors in the pathogenesis of these brainstem lesions is reviewed. Case ReportA 44-year-old woman was found unresponsive at her home. Her blood pressure was unobtainable and respirations were irregular and shallow. She had a past history of epilepsy and had been under treatment with phenytoin 300 mg and phenobarbital 45 mg daily for many years through her family physician. She had also taken chlorpromazine 75 mg daily for a chronic schi zophreniform illness. From the circumstances of her discovery, and the clinical observation of early gan grene in one upper extremity it was deduced that she had lain unresponsive for many hours, possibly several days in all. On arrival to a local Emergency Room, treatment for presumed drug overdose was instituted including endotracheal intubation and assisted ventila tion. Physical examination revealed a brachial blood pressure of 60/40 mm Hg, pulse rate 32 per minute, rectal temperature 29°C. She was unresponsive to sound, or painful stimulation. There was a superficial pressure sore on the left hip, and gangrene of the left hand. She had spontaneous, nonrhythmic eyelid blink ing, random and conjugate roving eye movements lat erally, and pupils which were equal, mid-position, round and unreactive bilaterally. Corneal stimulation elicited reflex blinking. The neck was supple. Extrem ities were flaccid to passive movements and all deep tendon reflexes were absent. Plantar responses were unelicitable. Toxicology studies demonstrated the presence of chlorpromazine and phenytoin in thera peutic levels, and...

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A Negro patient presented with diabetic ketoacidosis. Following usual therapy and an inchoate clinical response, the patient worsened, became comatose and died. Postmortem examination indicated diffuse intravascular sickling as a significant antemortem mechanism in this patient's death.