Lysosomotropic aminoesters act as H+(-)ATPase inhibitors in yeast.
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Biomedical subjects
Publications and source records attributed to J Nader.
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In a prospective study of 70 patients with infarcts in the posterior circulation admitted consecutively to a population-based primary-care center, we assessed infarct location and etiology using magnetic resonance imaging, three-dimensional time-of-flight magnetic resonance angiography, and noninvasive cardiac tests. The brainstem (mainly the paramedian pons) was the most commonly infarcted site (41/70, 59%), followed by the cerebellum (33/70, 47%). Combined supra- and infratentorial multiple vertebrobasilar infarcts occurred in 11 patients (16%). Overall, 27 patients (39%) had > or = 50% stenosis or occlusion of the basilar artery. There were other large-artery lesions in 19 patients (27%), including vertebral (V2-V4) stenosis or occlusion (in seven) and dolichoectatic vertebral/basilar arteries (in 12). Fifteen of the 70 patients had a potential cardiac source of embolism, which coexisted with large-artery disease in more than one-third of the cases. Cerebellar infarct without concomitant brainstem or occipital infarct was associated with cardioembolism (67%), while isolated paramedian pontine or midbrain infarct was associated with basilar artery stenosis (71%), suggesting in situ occlusion of the mouth of the perforators off the stenosed basilar artery. After exclusion of other potential causes of stroke, presumed small-artery disease associated with chronic hypertension remained the likely etiology in only 11 patients (16%), but these infarcts were not associated with any of the classical lacunar syndromes. Our findings emphasize the high frequency of severe intracranial large-artery disease in posterior circulation infarcts.
This review focuses on the recent advances in the management of acute ischemic stroke. We highlight the best current treatment, as proposed by different authors, as well as future lines of treatment.
Mortality and physical impairment in patients undergoing cardiac surgery are to a large extent due to cerebro-vascular complications that are second in frequency only to cardiopulmonary incidents. In spite of the extracorporeal circulatory support as well as progress in cardiac surgery that have improved the perioperative conditions, neurologic complications mainly of embolic nature are still common after extracorporeal circulatory assistance.
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Seventeen patients with hemiataxia as a manifestation of thalamic infarction were studied. Hemiataxia had the main clinical characteristics of a "cerebellar type" of ataxia, though it never occurred in isolation, being associated with ipsilateral sensory disturbance (hemiataxia-hypaesthesia) in 7 patients, with ipsilateral sensory disturbance and hemiparesis (hypaesthetic ataxic hemiparesis) in 8 patients, and with hemiparesis (ataxic hemiparesis) in 2 patients. Recovery was good, and in all patients the sensory and motor disturbances improved or cleared before the hemiataxia. All patients had an infarct involving the lateral part of the thalamus (thalamogeniculate territory in 16, tuberothalamic territory in 1), also affecting the posterior limb of the internal capsule (PLIC) in 7 patients. Hemiataxia seemed linked to involvement of the caudal part of the ventral lateral nucleus of the thalamus or the immediately adjacent medial part of the PLIC. These structures are near the corticospinal pathways and the ventral posterior nucleus of the thalamus, explaining why hemiataxia is associated with hemiparesis or hypaesthesia in this type of infarct.
A 64-year-old man developed unilateral third nerve palsy and somnolent mutism. Computed tomography (CT) revealed a small unilateral midbrain infarct. Previous reports of somnolent mutism placed the lesion in both sides of the midbrain tegmentum, usually extending into the thalamus. The unilateral third nerve palsy, and high-resolution 4-mm contiguous tomographic sections of the brainstem, helped localize the lesion. To our knowledge, this is the first CT clinical report of somnolent mutism induced by unilateral midbrain infarct.