SUMMARY We report two patients with large subcortical hemispheric infarctions, located in areas prone to the development of lacunes, who had occlusion of the middle cerebral artery demonstrated by arteriography. The cortical vessels were perfused by leptomeningeal collaterals. We suggest that large vessel arterial disease should be considered as a possible etiology of large subcortical infarctions and propose that the term lacune should not be used in cases in which neither the size nor the pathophysiologic mechanism of the lesion conform to C. M. Fisher's description. Stroke Vol 14, No 6, 1983AS DESCRIBED BY C. M. Fisher, lacunar infarc tions are small vascular lesions 0.5-1.5 mm in diame ter encountered at autopsy in deep gray structures of the brain, adjacent white matter, or brainstem, in pa tients with a history of chronic hypertension.1 " 5All of the arterial beds in which lacunes can be found are distinguished by a pattern of terminal perfusion with out collaterals. These small infarctions are the result of small atherosclerotic plaques, fibrinoid necrosis or lipohyalinosis of small arterioles (e.g., lenticulostriate or thalamoperforating arteries, paramedian branches of the basilar artery), rather than a consequence of cerebral embolism, internal carotid artery disease or diabetes mellitus. 5-7As an example, Capsular lacunes are considered to result from blockage of penetrating deep branches of the middle cerebral artery, rather than from occlusion of the middle cerebral artery itself or of the internal carotid artery. 7In patients with presumed lacunar infarction com puted tomography (CT) may be normal or show a small deep lesion. [8][9][10][11][12][13] But recently, relatively large le sions of the basal ganglia, internal capsule and thala mus, in patients with unquestionable vascular disease have also been designated as "lacunar" infarctions, or distinguished by such terms as "super" lacunes or "giant" lacunes."-14 It appears to us that these large infarctions may be consequent to pathologic processes different from those described by C. M. Fisher for lacunes and that the use of the now classical term may be questionable. 7For instance, preexisting hyperten sion is no longer an invariable finding. 15In addition, large vessel arterial stenosis and occlusion or cardiac sources of arterial embolism, are being increasingly described in patients with these larger infarctions. [10][11][12] To underline the importance of major vessel arterial occlusion as a cause of such alleged "lacunar" infarc tions, we report two patients who sustained subcortical infarction involving the putamen, the anterior limb of the internal capsule and the caudate nucleus, as a result of middle cerebral artery occlusion at its stem. Case Reports Case 1A 24 year old right-handed woman was admitted with progressive left-sided weakness of 12 hours dura tion. She did not have a history of hypertension, heart disease or diabetes mellitus. For a two year period she had used oral contraceptive pills but had stopped the drug three months ...

Neurological signs are a frequent manifestation of left atrial myxoma, but the association of cardiac myxoma with multiple cerebral aneurysms is rare. A case of left atrial myxoma was detected in the course of a long-lasting psychiatric and neurological illness. Four-vessel study showed the presence of multiple saccular and fusiform aneurysms, regularly and almost symmetrically distributed. The intracardiac mass was removed, and the patient improved.

A 17 week, double-blind, randomized, parallel, multicenter study compared naproxen sodium 550 mg bid, propranolol hydrochloride 40 mg tid, and placebo in 129 patients with classical or common migraine. Daily efficacy data were collected during the 12 week full treatment phase. Characteristics measured included headache days, headache severity, nausea, vomiting and visual disturbances. Patients and investigators, separately, rated the overall response and tolerance to the medication at the end of the trial.Patients' daily records revealed a trend toward superiority in the reduction of headache frequency, headache severity, nausea and visual disturbances for naproxen sodium and propranolol hydrochloride when compared to the placebo. In the overall evaluation of therapeutic response, both patients and investigators favored naproxen sodium in comparison with placebo. In a similar paired comparison the patients, but not the investigators, judged the overall response to propranolol better than placebo. In the overall evaluation of tolerance, both the patients and investigators favored propranolol hydrochloride. The majority of patients reported a high incidence and severity of gastrointestinal complaints associated with naproxen sodium treatment than propranolol hydrochloride treatment. The incidence and severity of nongastrointestinal complaints related to naproxen and propranolol hydrochloride treatment were comparable.Headache activity occurring before and after the onset of menses was analyzed for a subset of 30 patients. Those treated with naproxen sodium experienced lesser headache frequency and severity during the week prior to menses, compared with the week after onset of menses. The difference in severity in the naproxen sodium treated patients was statistically significant when compared to the placebo treated patients and approached significance when compared to the propranolol hydrochloride treated patients.In this study naproxen sodium was shown to be an effective prophylactic medication for migraine. A long-term study, to confirm these findings, seems warranted. (Headache 25:320-324, 1985)

SUMMARY A dose-escalation study was performed in 27 patients to determine the highest safe and potentially optimal dose of naloxone for treatment of acute cerebral ischemia. All patients received a bolus of naloxone followed by a continuous 24 hour infusion at an hourly rate 50% of the bolus. Loading doses ranged from 2.5 to 200 mg/m 2 . Total patient doses ranged from 52.3 to 4978 mg. No major dose-related side effects occurred. This study was not designed to determine naloxone's efficacy in stroke, but transient or sustained improvement was observed in 13 patients. Three patients' neurological condition worsened within three hours after the naloxone was discontinued. Our experience suggests that further therapeutic trials of naloxone are worthwhile.