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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With 60 million Americans meeting criteria for either essential or secondary hypertension, elevated arterial pressures remain a major health problem. While efforts to find etiologies for essential hypertension continue, clinicians battle its effects on organ systems, including the nervous system. Hypertensive changes in the nervous system may be acute, chronic, or both. The intracerebral vasculature is commonly affected. Not infrequently, acute changes including hemorrhage, encephalopathy, and cerebral edema are superimposed on chronic changes of hyaline and fibrinoid arteriolosclerosis. Chronic vascular changes sacrifice vascular lumina. The resulting ischemia is responsible for cystic (lacunar) lesions and subcortical ischemic white matter lesions consistent with Binswanger's disease.
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PMID:The effects of hypertension on the nervous system. 206 1

The pathogenesis of perinatal hypoxic-ischemic encephalopathy is poorly understood. Most insults are thought to occur before or during birth. We have investigated the evolution of parasagittal EEG activity and distribution of neuronal damage after cerebral ischemia in chronically instrumented fetal sheep (119-126 d gestation). The vertebral-carotid anastomoses were ligated and cerebral ischemia was induced by inflating occluder cuffs around the carotid arteries for 30 min. Parietal cortical EEG activity was analyzed with real-time spectral analysis with reference to control fetuses. After ischemia, EEG activity was suppressed, then rapidly increased in intensity at 8 +/- 1 h to a peak at 9 +/- 1 h postischemia. There was increased intensity of the lower frequencies (1-7 Hz) apparent as epileptiform activity with convulsions. This low-frequency hyperactivity gradually resolved by 28 +/- 7 h postinsult. After 72 h, the loss of intensity at all frequencies and laminar necrosis of the underlying parasagittal cortex indicated irreversible brain injury. Ranking the structures in order of decreasing amounts of damage: parasagittal cortex greater than hippocampal CA1, 2, and 3 regions greater than lateral cortex, hippocampal CA4 region and striatum greater than amygdala, dentate gyrus, thalamus, and cerebellum. The evolution of EEG activity and the distribution of damage after cerebral ischemia closely resembles the time course and pathology of hypoxic-ischemic encephalopathy seen in some severely asphyxiated term neonates. The consistent electrophysiologic and histologic outcome should allow this experimental approach to be valuable in testing a number of current hypotheses relating to perinatal asphyxial encephalopathy.
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PMID:Delayed seizures occurring with hypoxic-ischemic encephalopathy in the fetal sheep. 235 99

Three cases of movement disorders secondary to hypoxic-ischemic encephalopathy are reported. Despite similarities among the clinical events, the neurological syndromes produced were dissimilar. Cerebral hypoxia-ischemia typically produces lesions of the globus pallidus that may result in an akinetic rigid syndrome. Due to its unique blood supply, vascular insufficiency is found to be a major factor. Lesions in the putamen also occur, and these tend to be associated with dystonia. Recent evidence supports a specific neuronal sensitivity in the striatum, possibly due to afferent excitatory amino acid connections. These two components and changes in the levels of neurotransmitters during hypoxia-ischemia may interact to produce varied clinical outcomes. These factors must also be considered when planning therapeutic interventions.
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PMID:Hypoxic-ischemic damage of the basal ganglia. Case reports and a review of the literature. 238 37

We reviewed the clinical histories and autopsy records of 35 pediatric patients (ranging in age from 9 months to 18 years) who underwent orthotopic liver transplantation using ciclosporin and corticosteroids for immunosuppression. At the time of death, 19 children (54%) had encephalopathy, 16 (46%) were lethargic or in coma, 10 (29%) had seizures, and 10 were normal. Neuropathological lesions were found on postmortem examination in all 35 patients. Vascular lesions such as infarction, ischemia, thrombosis, and hemorrhage were the most common neuropathological findings (86%) followed by infectious processes (29%). Candida albicans (2 patients) and Aspergillus fumigatus (3 patients) were the only offending organisms identified, both causing meningoencephalitis. Alzheimer type II astrocytes, a characteristic feature of chronic liver disease, were the single most common autopsy finding (69%). Central pontine myelinolysis was seen in 3 children and basilar artery thrombosis affected 1 child. Neurological complications and their subsequent neuropathology are a significant cause of morbidity and mortality after pediatric liver transplantation. Vascular insults, electrolyte abnormalities, and infections that involve the central nervous system are directly related to liver function and the immunosuppression necessary to maintain graft viability. Only with continued observation after surgery combined with rapid medical and surgical treatment can we hope to improve the prognosis following liver transplantation in the pediatric population.
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PMID:Neuropathology of pediatric liver transplantation. 248 84

Diffuse carcinomatous leptomeningeal metastases "carcinomatous meningitis") have the usual clinical course involving multifocal nerve root deficits and a variable diffuse encephalopathy. In contrast, we describe a patient with carcinomatous leptomeningeal metastases who presented with clinical signs of meningitis and focal cerebral infarction. Over an 8-month period, multiple cerebral infarctions and cranial neuropathies developed. Postmortem examination of the patient's brain revealed diffuse leptomeningeal infiltration by a signet-ring adenocarcinoma. The extensive involvement of the subarachnoid space with tumor was associated with dense neoplastic infiltration of the Virchow-Robin spaces. These perivascular tumor infiltrates were accompanied by multifocal mural invasion and, less frequently, by intravascular tumor cells obliterating the lumen. Focal hemorrhagic infarcts in the cerebral cortex corresponded to areas of microscopic vasculopathy. This case provides evidence that tumor-associated vasculopathy with resultant ischemia plays a role in the pathogenesis of focal cerebral infarctions in carcinomatous leptomeningeal metastases.
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PMID:Focal cerebral infarctions associated with perivascular tumor infiltrates in carcinomatous leptomeningeal metastases. 255 69

Computed tomography is often insensitive to such lesions as atrophic demyelination, enlarged perivascular spaces and infarction in the periventricular white matter. In attempt to better understand the discrepancy between the pathologic and X-CT findings, the author correlated areas that had focal, patchy on X-CT and brains with gross and microscopic findings. Patients with cerebral strokes had larger volume infarcts characterized centrally by necrosis, axonal loss, and demyelination. The progressive subcortical vascular encephalopathy (Binswanger's disease) is characterized by ischemic demyelinization of white matter provoked by hypertensive vascular changes in small vessels and is usually accompanied by multiple lacunar infarcts in a periventricular area and the basal ganglia. Small, deep hemispheric infarcts may be of no clinical significance unless a sufficient aggregate of these occurs. It should be pointed out that many small infarcts are clinically silent, and chronic multifocal ischemia may be responsible for observed senescent changes in cerebral tissue. The extension of the infarcted area might be most important in the development of cerebrovascular dementia. Mixed forms of degenerative dementia and any type of cerebral vascular disease are common and account for 10-20% of all dementias.
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PMID:[Cerebrovascular dementia; correlation of computed and histopathologic findings]. 260 Oct 93

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

Delayed nonhemorrhagic encephalopathy following mild head trauma is a rare condition with an unknown etiology. The few cases reported in the literature are in young adults, all of them in the era before computerized tomography (CT) became available, and all had a devastating clinical course with multifocal ischemia or necrotic lesions found at autopsy. A case is presented of a young man with this syndrome who survived the acute encephalopathic phase with severe residual neurological deficits. Repeat CT scans during and following the acute phase as well as magnetic resonance imaging showed diffuse multifocal lesions compatible with ischemic changes and demyelination in the "watershed" areas of the brain.
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PMID:Delayed nonhemorrhagic encephalopathy following mild head trauma. Case report. 279 80

The cAMP levels and adenylate cyclase activity have been studied in the grey brain substance and striatum system of dogs during circulation arrest due to electrotrauma of different duration (1-2, 15, 45 min) and in postresuscitation period in animals recovered after 15-min clinical death. Adenylate cyclase is strongly activated and cAMP levels are increased in the brain areas under study during complete brain ischemia. The cAMP levels in the grey substance and in striatum system are reduced considerably compared to the control, accounting for 12-20 on days 2-5 of postresuscitation period in animals with neurologic deficit. Adenylate cyclase and phosphodiesterase enzyme activity is twice higher in the striatum system and 50% lower in the grey brain substance than the baseline. The disturbances in cyclic nucleotide exchange, along with other factors seem to play an important role in the pathogenesis of postresuscitation encephalopathy.
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PMID:[Adenylate cyclase activity and cyclic AMP content in brain tissue of dogs during clinical death and in the post-resuscitation period]. 299 52

A number of CT head scans, covering a 2-year period and showing a variety of distinct curvilinear subinsular lucent lesions, were collected and reviewed. Variations in extent of involvement, tendency toward bilateral symmetry, and clinical background allowed the lesions to be grouped into four general patterns, most of which, to our knowledge, have not been specifically described in the radiologic literature. This project was undertaken first to bring to the attention of those involved in interpretation of cranial CT images several patterns of injury they may not heretofore have been aware of and second to attempt to derive a specific etiology for each of the patterns described. Pattern 1, which appears as a distinct curvilinear lesion (sometimes cystic) apparently limited to the lateral aspect of the putamen, is thought to represent the residua of previous lateral striatal hemorrhage. Pattern 2, occurring in a markedly younger age group appears as relatively symmetrical bilateral subinsular lucencies, which in one case completely resolved. A specific etiology for this pattern remains uncertain. Acute demyelination, either secondary to a variant of anoxic leukoencephalopathy or to a limited form of diffuse encephalomyelitis, is postulated. A third pattern, which extends from generalized deep frontal white-matter lucency across the anterior limb of the internal capsule and tapering posteriorly in the subinsular area is thought to be on the basis of chronic ischemia similar to subcortical arteriosclerotic encephalopathy. The fourth pattern, occurring as a broad band of lucency extending from the frontal horn of the lateral ventricle and also tapering posteriorly is due to relatively proximal occlusion of the lateral lenticulostriate arteries.
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PMID:CT of subinsular infarction and ischemia. 310 79


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