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

Hypertensive encephalopathy is a potentially fatal condition associated with cerebral edema and the breakdown of the blood-brain barrier (BBB). The molecular pathways leading to this condition, however, are unknown. We determined the role of deltaPKC, which is thought to regulate microvascular permeability, in the development of hypertensive encephalopathy using deltaV1-1 - a selective peptide inhibitor of deltaPKC. As a model of hypertensive encephalopathy, Dahl salt-sensitive rats were fed an 8% high-salt diet from 6 weeks of age and then were infused s.c. with saline, control TAT peptide, or deltaV1-1 using osmotic minipumps. The mortality rate and the behavioral symptoms of hypertensive encephalopathy decreased significantly in the deltaV1-1-treated group relative to the control-treated group, and BBB permeability was reduced by more than 60%. Treatment with deltaV1-1 was also associated with decreased deltaPKC accumulation in capillary endothelial cells and in the endfeet of capillary astrocytes, which suggests decreased microvasculature disruption. Treatment with deltaV1-1 prevented hypertension-induced tight junction disruption associated with BBB breakdown, which suggests that deltaPKC may specifically act to dysregulate tight junction components. Together, these results suggest that deltaPKC plays a role in the development of hypertension-induced encephalopathy and may be a therapeutic target for the prevention of BBB disruption.
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PMID:Sustained pharmacological inhibition of deltaPKC protects against hypertensive encephalopathy through prevention of blood-brain barrier breakdown in rats. 1809 80

Hypertensive encephalopathy is a life-threatening condition due to elevation of cerebral perfusion pressure beyond the limits of autoregulation. Breakdown of the blood-brain barrier (BBB) leads to cerebral edema and reduced blood flow. In this issue of the JCI, Mochly-Rosen and colleagues demonstrate a novel molecular strategy for preserving the BBB in a model of hypertension-induced encephalopathy (see the related article beginning on page 173). Using a rationally designed peptide inhibitor of deltaPKC, they stabilized the BBB and improved mortality in hypertensive rats. This study highlights the therapeutic potential of deltaPKC inhibitors in hypertensive encephalopathy and provides incentive to elucidate deltaPKC signaling pathways that mediate BBB dysfunction in other disease states.
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PMID:Hypertensive encephalopathy and the blood-brain barrier: is deltaPKC a gatekeeper? 1809 71

The posterior/potentially reversible encephalopathy syndrome is a unique syndrome encountered commonly in hypertensive encephalopathy. A 13-year-old boy presented with of intermittent high grade fever, throbbing headache and non-projective vomiting for 5 days. The patient had a blood pressure of 120/80 mmHg but fundoscopy documented grade 3 hypertensive retinopathy. The patient improved symptomatically following conservative management. However, on the 5(th) post-admission day headache reappeared, and blood pressure measured at that time was 240/120 mmHg. Neuroimaging suggested white matter abnormalities. Search for the etiology of secondary hypertension led to the diagnosis of pheochromocytoma. Repeated MRI after successful surgical excision of the tumor patient showed reversal of white matter abnormalities. Reversible leucoencephalopathy due to pheochromocytoma have not been documented in literature previously.
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PMID:The posterior reversible encephalopathy syndrome. 1881 Mar 59

Hypertensive encephalopathy is a medical emergency whose clinical manifestations are usually associated with bilateral parieto-occipital lesions. Predominant brainstem edema without accompanying occipital lesions is rare in hypertensive encephalopathy and usually occurs in patients with secondary hypertension. We describe the clinical and radiological features of two patients with reversible hypertensive brainstem encephalopathy. Both patients had chronic renal failure, but the extensive neuroimaging abnormalities revealed few clinical features of brainstem involvement. The clinical findings and neuroimaging abnormalities resolved once the hypertension was treated.
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PMID:Two cases of hypertensive encephalopathy involving the brainstem. 1951 43

Reversible posterior leukoencephalopathy (RPLS), also known as posterior reversible encephalopathy syndrome, is characterized by magnetic resonance imaging (MRI) findings of reversible vasogenic subcortical edema without infarction. The clinical presentation is usually nonspecific and typically involves global encephalopathy, seizures, headache, or visual symptoms. MRI of the brain is essential to the diagnosis of RPLS. Typical findings of RPLS include high-intensity signal on T2-weighted images predominantly in the posterior lobes of the brain that is caused by subcortical white matter vasogenic edema. Fluid-attenuated inversion recovery (FLAIR) sequences on MRI improve sensitivity and detect subtle peripheral lesions. This clinical radiographic syndrome has been described in a number of medical conditions, with hypertensive encephalopathy, eclampsia, and the use of immunosuppressant drugs (most notably calcineurin inhibitors) being the most common. It has occasionally been reported with cisplatin and rarely with carboplatin. Its occurrence with oxaliplatin is very unusual. An extensive literature search including PUBMED and direct contact with the drug manufacturer yielded only 2 known case reports. Herein, we describe a case that had classic clinical and radiologic features of RPLS. We also briefly describe 2 other patients who have been described to have RPLS with oxaliplatin in the literature.
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PMID:Delayed reversible posterior encephalopathy syndrome following chemotherapy with oxaliplatin. 1963 31

A 14-year-old female had repeated vomiting, headache, abdominal pain, visual field deficit and lethargy at the onset of hypertensive encephalopathy. Cerebrospinal fluid (CSF) test revealed a high level of IgG and protein. MRI demonstrated no supratentorial cerebral lesions but hyperintense lesions were observed from the lower pons to the Th8 level of spinal cord and cerebellar cortex on T2 weighted and FLAIR images without contrast enhancement. The two antihypertensive drugs stabilized to control her blood pressure and improved her clinical symptoms. Reexamination of MRI and cerebrospinal fluid test also revealed clear improvement of the above abnormalities. The abnormal findings on abdominal CT and renography led us to suspect renal infarction. Abdominal angiography demonstrated multifocal stenoses of renal interlobar arteries, which were supposed to supply the renal infarcted regions. These suggested that the renal infarctions due to fibromuscular dysplasia caused systemic hypertension. There have been only two reports that demonstrated spinal cord lesions in reversible posterior leukoencephalopathy syndrome (RPLES). We report extensive spinal lesions on MRI and a high level of IgG in CSF at the subacute phase in a young female with RPLES associated with hypertensive (brainstem) encephalopathy.
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PMID:A case of hypertensive encephalopathy with extensive spinal lesions on MRI. 1973 90

The pathology of posterior reversible encephalopathy syndrome (PRES) is undefined, since it is rarely fatal and is biopsied in only exceptional circumstances. We describe rapidly progressive PRES following stem cell transplant for acute lymphoblastic leukemia. After development of altered mental status, this 8-year-old girl had T2 prolongation of the white matter in a posterior-dominant distribution, eventually developing cerebellar edema, hemorrhage, hydrocephalus, and herniation. Despite surgical and medical management, she died 36 hours later. At autopsy, the occipital and cerebellar white matter and focal occipital cortical gray matter showed a spectrum of microvascular changes, including dilated perivascular spaces containing proteinaceous exudates and macrophages, as well as fibrinoid necrosis and acute hemorrhage, in a distribution corresponding to the neuroimaging abnormalities and reminiscent of those seen in patients with acute hypertensive encephalopathy. Of note, similar microvascular changes were not seen in the kidney or other systemic sites. Thus, the findings indicate a brain-specific microvascular compromise as the substrate of PRES, at least in the rare instance of cases progressing to fatal outcome.
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PMID:Neuropathology of a fatal case of posterior reversible encephalopathy syndrome. 2015 77

The relationship between headache and hypertension has been debated for many years. Although most studies have shown that chronic hypertension and headache are not associated, the myth of a hypertensive headache still exists. There are several reasons why the "hypertension headache" misperception persists: Hypertension is an epiphenomenon of pain. Headache is a common side effect of some antihypertensive drugs. Headache is the most common presenting symptom of hypertensive encephalopathy, followed by seizures, focal neurological deficits and loss of consciousness. This review summarizes the existing literature and highlights the relationship between headache, hypertension and disease with a focus on hypertensive encephalopathy and posterior reversible encephalopathy syndrome with acute endothelial damage.
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PMID:[Headache and hypertension. Myth and evidence]. 2041 65

Posterior reversible encephalopathy syndrome is a recently described clinicoradiological entity. Neuroimaging is very demonstrative and can be the first clue to the diagnosis. Common causes of posterior reversible encephalopathy syndrome are hypertensive encephalopathy, immunosuppressive treatment, renal failure and eclampsia. Its pathogenesis remains poorly understood. Clinical findings are not sufficiently specific; however, neuroimaging is often characteristic.
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PMID:Posterior reversible encephalopathy syndrome. 2058 57

Hypertensive encephalopathy (HE) is one of the acknowledged hypertensive emergencies. Isolated hypertensive brainstem encephalopathy (HBE) without concomitant typical parietooccipital lesion is unusual. Patients with HBE may or may not present with symptoms attributable to brainstem and the diagnosis is challenging in an emergency setting. The most important differential diagnosis in HBE is brainstem infarction, because the goals of blood pressure treatment are different. Evidence of vasogenic edema on magnetic resonance image, i.e. absence of high signal lesions on diffusion weighted images and increased value of apparent diffusion coefficient are diagnostic indicators of HBE, but not brainstem infarction. Prompt recognition of HBE and adequately lowering blood pressure offer the best outcomes.
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PMID:Isolated brainstem involvement in a patient with hypertensive encephalopathy. 2071 52


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