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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The paper comprises 70 cases of extensive supratentorial infarctions. The topography and structure of secondary lesions occurring in the region of herniation and displacements caused by the coexisting brain edema were analysed. The extent of edema served as criterion in the division of the material into three groups in dependence on the occurrence of herniations and displacements. Most frequent was herniation of hippocampal uncus and most rare that of the cerebellar vermis. In group I showing no herniations selective necrosis was noted of neurons particularly sensitive to ischemia and anoxia, especially in Sommer's sector of the hippocampus. In group II secondary necrosis was visible in the regions of herniae, and in the group III also in the translocated deep brain structures in the hemisphere contralateral to the infarct and in the brain stem where, moreover, secondary hemorrhages were present. Supratentorial secondary hemorrhages were less frequent. They were noted in the thalamus both on the side of the infarct and in the contralateral hemisphere. Supratentorial necroses were more frequent. Their intensity varied from selective necrosis to Jacob's edematous necrosis. Severe displacement of deep structures and of the brain stem was associated with development of secondary internal hydrocephalus, especially in the hemisphere contralateral to the herniation. To the most important pathogenetic factors causing development of secondary morphological lesions belong disturbances of blood supply occurring as the result of pressure differences between the supra- and infratentorial space, resulting from pressure and displacement of arterial vessels, damage of their walls and distrubances of venous flow and also development of secondary internal hydrocephalus. Extensive necroses and hemorrhages increase the area of primary necrosis. Lesions resulting from herniation, displacement and compression of vessels were superposed on the picture of brain edema both present or passed. Secondary necroses damaging bilaterally structures belonging to the limbic system and reticular formation may be an additional factor in the development of edematous encephalopathy and the development of a psychoorganic syndrome after stroke.
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PMID:[Topography and structure of secondary brain damage in edema associated with supratentorial foci of encephalomalacia]. 262 77

Binswanger's encephalopathy is reviewed in respect to history, computed tomography, magnetic resonance imaging, epidemiology, pathology, clinical picture, laboratory findings, differential diagnosis, and treatment. The various viewpoints on the pathogenesis of the process are discussed, in particular the role of ischemia, vascular disease, high blood pressure, lacunar infarction, hypoxia, edema, and hydrocephalus. The white matter hypomyelination of congophilic angiopathy and Alzheimer's disease should provide clues. A unifying hypothesis has not been attained.
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PMID:Binswanger's encephalopathy: a review. 265 69

The authors report a case of brain abscess following cerebral infarction. A 73-year-old man was admitted to our clinic with symptoms of right hemiparesis and total aphasia. CT scan revealed abnormal low density area in the left fronto-temporo-parietal region. Cerebral angiography demonstrated occlusion of the left middle cerebral artery at the M1 portion. On the 16th hospital day, an episode of generalized seizure with high fever appeared, and intermittent high fever persisted thereafter. Two months after admission, CT scan revealed several cystic lesions with marked ring enhancement at the site of cerebral infarction, suggesting multiple abscesses. Aspirations of left frontal and parietal abscesses were accomplished and the cultures of the pus disclosed Proteus vulgaris. Due to progressive hydrocephalus, a ventriculoperitoneal shunt was constructed one month later. Repeated CT scans showed a gradual diminution of the abscesses. It is considered that the blood-brain barrier is broken and the local immunological system against bacteria may be weakened when the brain is damaged by ischemia. Brain abscess seems to be developed in such circumstances even under the influence of transient bacteremia which originates in other parts of the body. Therefore the possibility of cerebral abscess should be suspected if patients with cerebral infarction suffer from the symptoms such as fever, neck stiffness or disturbance of consciousness.
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PMID:[Brain abscess following cerebral infarction: a case report]. 267 75

Subcortical arteriosclerotic encephalopathy (SAE) is a common though infrequently recognized dementia of the elderly. The unique vascular anatomy of the subcortical white matter and central brain stem probably predisposes those regions to chronic ischemia and incomplete infarction in the presence of various cardiovascular and hemodynamic insults. Recent studies have begun to define the risk factors for SAE, and others have shown it to be a condition frequently comorbid with the dementias of Alzheimer's disease, the multi-infarct state, and normal pressure hydrocephalus. Recent research into the etiologies of these disorders suggest certain pathogenetic links between them, strongly implying that they are not neatly distinct disease entities, as is commonly believed, and accounting for some of the overlap between these dementing illnesses seen clinically.
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PMID:Binswanger's disease (Part II): Pathogenesis of subcortical arteriosclerotic encephalopathy and its relation to other dementing processes. 269 55

A case of a young man who was a victim of strangulation is presented. He arrived at the hospital in refractory status epilepticus, controlled only with intravenous pentobarbital. The initial CT scan showed mild cortical edema. Two days later, a CT scan showed diffuse cortical swelling and bilateral basal ganglia infarcts. Upon discontinuation of pentobarbital therapy, his neurological examination revealed spontaneous ventilation and a gag reflex. A CT scan 4 weeks after the insult demonstrated hypodensities in both cerebral hemispheres and hydrocephalus. EEG was isoelectric throughout his hospitalization. He survived nearly 5 months and succumbed to pneumonia. Neuropathological examination demonstrated severe encephalomalacia, multiple cystic infarcts and generalized compensatory ventriculomegaly. Microscopic examination was particularly remarkable for a pronounced gemistocytic astrocyte proliferation in the white matter. This case illustrates the long-term neuropathological consequences of severe, global hypoxia/ischemia and the paucity of intact brain required to maintain a persistent vegetative state.
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PMID:Late neuropathological consequences of strangulation. 282 56

70 fetuses (10 to 37 weeks) and 30 full term infants were examined by ultrasound (U.S.). Anatomic correlations were made with frontal, axial and sagittal sections of 43 fetal and 3 neonatal brains. At 12 weeks gestational age (w.g.a.) only the inter hemispheric fissure is seen by U.S. The sylvian fissure (21 w.g.a.), the callosal sulcus (21 w.g.a.), the parieto-occipital sulcus (25 w.g.a.), the calcarine fissure (25 w.g.a.), the cingulate sulcus (26 w.g.a.) and the collateral sulcus (25-27 w.g.a.) are visualized rather late with in-utero U.S. The other sulci are more difficult to see. The peripheral location of these sulci contributes to the difficulty encountered in their visualization. The morphology of the sylvian fissure is quite characteristic on U.S. imaging and can be used to estimate the gestational age of the fetus. Compared to the embryological development there is a 2-4 weeks delay between the first infolding of the brain and the visualization of a sulcus by U.S. Abnormal sulcal patterns can be recognized based on the normal appearance for each gestational age. Sulcal anomalies are quite specific in holoprosencephaly, lissencephaly, micropolygyry, schizencephaly, agenesis of the corpus callosum. Silhouetting of the sulci may occur if the parenchymal echogenicity is sufficiently increased that the sulci no longer stand out (ischemia, tumors, encephalitis). Thickening of the sulci occurs in subdural hematomas, external hydrocephalus, meningitis and toxoplasmosis.
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PMID:[Echographic aspects of cerebral sulci in the ante- and perinatal period]. 305 86

To better define the clinical significance of vertebrobasilar dolichoectasia, the clinical signs and symptoms and basilar artery parameters of diameter, height, and transverse position were evaluated in two groups of symptomatic patients. Ten patients had isolated involvement of the third, sixth, or seventh cranial nerves. The other 10 patients had multiple neurologic deficits including combinations of compressive cranial nerve deficits, both ischemic and compressive central nervous system deficits, and hydrocephalus. Although significant differences for mean basilar artery diameter and height exist between these two groups, the symptomatology and basilar artery parameters present as a spectrum. A symptomatic patient with a normal-caliber, but tortuous, basilar artery is more likely to have isolated cranial nerve involvement. Conversely, the patient with marked basilar artery dilatation (ectasia) is far more likely to present with multiple compressive or ischemic neurologic deficits. Conventional angiography in patients with dilated basilar arteries carries a significant risk for brainstem ischemia. Most authors agree that when vertebrobasilar dolichoectasia has been demonstrated by computed tomography, additional angiography, if required at all, should be performed by digital subtraction techniques.
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PMID:High-resolution computed tomography of the basilar artery: 2. Vertebrobasilar dolichoectasia: clinical-pathologic correlation and review. 308 45

The prevailing sentiment of North American neurosurgeons is that there is no significant difference in overall morbidity between patients who are treated with early aneurysm surgery and those who are treated with delayed aneurysm surgery. This concept is based primarily on the high incidence of ischemic events after early intervention. Recent experience, however, indicates that prophylactic hypervolemic hypertensive therapy may be beneficial in reducing delayed ischemia after early aneurysm surgery. During the preceding 21 months, we have performed 125 operations for intracranial aneurysms. Fifty-six patients in this group presented less than 7 days after subarachnoid hemorrhage (SAH) (47 within 3 days) and were treated by a prospective protocol of urgent aneurysm surgery performed within 24 hours after presentation. In all cases, the aneurysm was clipped with the use of mannitol and spinal drainage for brain relaxation. All patients were then treated with prophylactic volume expansion therapy and induced hypertension with a central venous pressure or a Swan-Ganz catheter until the 14th day after SAH. Preoperatively, 17 patients were Hunt and Hess Grade I, 9 were Grade II, 28 were Grade III, and 2 were Grade IV. In this group of 56 patients at risk for delayed ischemia from vasospasm, 5 patients had significant intraoperative complications. Ten patients (18%) had delayed cerebral ischemia, totally reversible in 6 cases, with small infarcts in 3 cases, and with 1 death (2% mortality from delayed ischemia), there were 5 cases of shunted hydrocephalus, and 3 deaths from other complications. Overall, 41 patients (73%) returned to their premorbid occupations without neurological deficit.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early aneurysm surgery and prophylactic hypervolemic hypertensive therapy for the treatment of aneurysmal subarachnoid hemorrhage. 321 66

The pathological changes in the brains of seven patients who had been clinically diagnosed as normal pressure hydrocephalus (NPH) are described and the possible etiological mechanisms are discussed. The pathological findings in all cases consisted of demyelination akin to Binswanger's type of encephalopathy, especially in the frontal lobes. Arteriosclerosis accompanied by occasional organized thrombi and scattered microinfarcts in the periventricular white matter were seen. Focal leptomeningeal fibrosis, diminution of arachnoidal granulations, and non-specific aging processes were noted. Among the above of particular interest, was the degeneration of both periventricular and deep white matters with microinfarcts, and moderate to severe arteriosclerosis. On the basis of these observations, we assume that the degeneration in the white matter is not merely a secondary change due to the result of enlargement of ventricle, but plays an important role in the development of NPH. The development of NPH requires not only the disturbance of cerebrospinal fluid, but also the pre- or coexisting vulnerability in the white matter caused by variables such as ischemia, hypoxia, and trauma.
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PMID:Normal pressure hydrocephalus. Neuropathological study. 357 65

Monitoring modalities unique to the neurologic intensive care unit include intracranial pressure monitors and neuroelectrophysiologic monitors. Each modality fullfills criteria for accuracy, responsivity during clinical change, and stability over time for trend analysis. Intracranial pressure monitoring may be accomplished by any of three approaches--ventricular catheter, subarachnoid bolt, or epidural pressure transducer. Intracranial pressure control has proved beneficial in at least three different illnesses--acute closed head injury, acute noncommunicating hydrocephalus, and Reye's syndrome. Other illnesses, such as cerebral hemorrhage, near drowning, meningitis, encephalitis, and cerebral mass lesions, are often associated with ICP elevations. Neuroelectrophysiologic monitoring encompassing electroencephalography (EEG), signal-processed EEG, and evoked potentials has proved to be most beneficial to the intensive care setting. Evoked potentials are most useful for monitoring patients in drug-induced coma or muscle paralysis in whom a clinical neurologic examination is unreliable. Focal neurologic deficits, incipient brainstem ischemia, and possibly brain death can be deduced from multimodality-evoked potentials (brainstem auditory and somatosensory). Evoked potential apparatus can be used to record sequential stimuli and trend changes. Signal-processed EEG apparatus (compressed spectral array and cerebral function monitor) are used to assess global or regional EEG activity for longer periods of time. Interpretation of signal-processed EEG recording requires some experience with this technique, but it is much easier to interpret than a standard 16-lead EEG. These monitors are useful in evaluating some forms of abnormal EEG activity and in monitoring gross changes in global or regional electrical activity. Currently available technology offers dynamic insight into the management of acute neurologic illnesses. The technology in evoked potential and signal processed EEG monitoring will eventually reduce the size and complexity of the instrumentation, making its application routine. Intracranial pressure monitoring is already routine in many intensive care units, although its use is occasionally sporadic. We believe that application of appropriate neurologic monitors improves therapy and outcome in neurologically injured and ill patients.
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PMID:Neurologic intensive care unit monitoring. 391 79


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