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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe the clinical course and outcome following decompressive craniectomy in six patients. Five patients suffered from severe intracranial hypertension due to middle cerebral artery infarction. In one patient the cause was bacterial meningoencephalitis. Acute clinical and neuroradiological signs of intracranial hypertension were seen in all cases. Following ineffective conventional brain edema therapy, decompressive craniectomy was undertaken. In five cases intracranial pressure was sufficiently lowered. One patient developed transtentorial herniation with subsequent brain death. Four patients with middle artery infarction showed moderate neurological disorders and one patient with bacterial meningoencephalitis recovered completely after treatment. Craniectomy in malignant middle artery infarction should be taken into consideration if conventional brain edema therapy does not sufficiently reduce critically raised intracranial pressure. Craniectomy provides development of brain herniation. This treatment may reduce high lethality rate and high frequency of severe neurological disorders.
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PMID:[Decompressive craniectomy for severe intracranial hypertension due to cerebral infarction or meningoencephalitis]. 1188 18

Advances in neurologic therapeutics and intensive care medicine have expanded the arsenal of treatments available for the critical care of ischemic stroke. Several agents are available for acute reperfusion of the ischemic brain. These include intravenous recombinant tissue-plasminogen activator (rtPA), which is effective in a 3-hour time window, and intra-arterial thrombolytics, which may be effective within 6 hours. In addition, newer agents such as Ancrod and abciximab may be effective within the acute time period. Efforts to prevent secondary brain injury in critically ill patients with stroke often include prevention and reduction of fever, induced hypertension, and mechanical ventilation. Finally, death due to severe brain edema after massive hemispheric infarction can often be prevented with surgical or medical intervention. Unfortunately, there is a critical lack of well-designed clinical studies to guide the clinician in the use of these interventions. In addition, there is concern that some of these interventions may preserve life at the cost of quality of life. This article reviews the evidence behind these approaches to the critical care of ischemic stroke.
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PMID:Critical care of acute ischemic stroke. 1189 73

Stimulation of the bradykinin (BK) B(2) receptor by kinins is associated with pathophysiological as well as pronounced beneficial effects. Consequently, interference with BK B(2) receptors by either antagonism or agonism offers promising therapeutic approaches for the development of drugs for the treatment of various human diseases. BK B(2) receptor antagonists may prove useful for the treatment of pathological situations caused by excessively increased local kinin concentrations, such as inflammation, tissue injury and pain. Beneficial effects of peptide BK B(2) receptor antagonists in perennial rhinitis, asthma and brain edema have already been demonstrated in clinical trials. On the other hand, kinins have also been identified as potent vasodilatory and organ-protective peptides. Therefore, BK B(2) receptor agonists may have the potential to become valuable therapeutics in the treatment of cardiovascular diseases such as hypertension, myocardial hypertrophy, myocardial infarction and arrhythmias as well as diabetic disorders. For both approaches, potent, selective and even orally active non-peptide compounds have been discovered recently. Prototypes of these novel third generation classes of compounds are the alkylphosphonium salt WIN-64338, the pseudopeptide NPC-18884, the thiosemicarbazide bradyzide and especially the imidazo[1,2-a]pyridine FR-167344 and the quinolines FR-173657 and LF-16.0687 as non-peptide BK B(2) receptor antagonists, whereas the 4-(2-pyridylmethoxy)-substituted quinoline FR-190997 and the 3-(2-pyridylmethyl)-substituted benzimidazole FR-191413 emerged as non-peptide BK B(2) receptor agonists. These antagonists and agonists of the BK B(2) receptor have already demonstrated efficacy a various animal models of human diseases, which offers promising therapeutic approaches for the development of drugs for the treatment or even prevention of a variety of severe human diseases either via stimulation or via blockade of BK B(2) receptors.
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PMID:Non-peptide antagonists and agonists of the bradykinin B(2) receptor. 1196 53

We report two cases of malignant hypertension with reversible diffuse leukoencephalopathy demonstrating a nocturnal blood pressure (BP) rising pattern ("riser" pattern). Case 1 was a 54-year-old man diagnosed with malignant hypertension who presented with diffuse leukoencephalopathy and nocturnal BP rise during the acute phase. These abnormal findings diminished after treatment of hypertension. Case 2 was a 50-year-old woman diagnosed with malignant hypertension in association with leukoencephalopathy, heart failure and acute renal failure. She also presented with a "riser" pattern during the acute phase. In contrast to case 1, the leukoencephalopathy and "riser" pattern in case 2 were not improved even after 1 month of treatment. Following intensive antihypertensive treatment, renal failure was improved in case 1, but renal failure was not improved after 1 month in case 2. In conclusion, a possible explanation of this phenomenon is that a causative volume overload due to renal dysfunction produced the temporal leukoencephalopathy-like brain edema and "riser" pattern in these cases.
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PMID:Two cases of malignant hypertension with reversible diffuse leukoencephalopathy exhibiting a reversible nocturnal blood pressure "riser" pattern. 1213 28

Brain oedema is defined as an abnormal accumulation of fluid in the brain tissue accompanied by an increased volume of the brain. It results in the intracranial hypertension directly endangering the patient's life. No causal treatment of the brain oedema is known at present. The brain oedema is not a disease, but it is a symptom of various clinical states. That is why experimental studies of its pathophysiology become the centre of attention. Though the classification of brain oedema according to the pathogenesis is still used (the vasogenic type--resulting from the increased permeability of blood-brain barrier; the cytotoxic type--caused by the cell metabolism impairment), recent papers has shown a definite retraction from such categorisation. It has been shown that neither type of brain oedema comes alone, but both can occur simultaneously during the development of the pathological state of the brain. The most important appears to be the primary insult. It affects the state of blood-brain barrier and brings about the vasogenic extracellular oedema or it can influence the cell metabolism with subsequent cytotoxic, cellular oedema. Categorisation of oedema into extracellular and cellular reflects more precisely the impairment of the homeostasis of the internal environment of the brain. Contemporary view on the classification and pathophysiological mechanisms of the brain oedema is discussed in our review.
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PMID:[Pathophysiology and clinical aspects of brain edema]. 1242 66

In patients with hypertensive encephalopathy, brain edema is frequently distributed in the parieto-occipital white matter. We report a patient with high arterial blood pressure of over 300/160 mmHg on admission, who had extensive MRI-documented reversible lesions throughout the whole brain, including the brainstem, thalami, basal ganglia, and cerebellum. Extraordinarily severe acceleration of hypertension may be essential for the breakdown of autoregulation in the deep structures, especially in the brainstem including medulla.
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PMID:Hypertensive encephalopathy extending into the whole brainstem and deep structures. 1245 35

DMSO is an amphipathic molecule with a highly polar domain and two apolar methyl groups, making it soluble in both aqueous and organic media. It is one of the most common solvents for the in vivo administration of several water-insoluble substances. Despite being frequently used as a solvent in biological studies and as a vehicle for drug therapy, the side-effects of DMSO (undesirable for these purposes) are apparent from its utilization in the laboratory (both in vivo and in vitro) and in clinical settings. DMSO is a hydrogen-bound disrupter, cell-differentiating agent, hydroxyl radical scavenger, intercellular electrical uncoupler, intracellular low-density lipoprotein-derived cholesterol mobilizing agent, cryoprotectant, solubilizing agent used in sample preparation for electron microscopy, antidote to the extravasation of vesicant anticancer agents, and topical analgesic. Additionally, it is used in the treatment of brain edema, amyloidosis, interstitial cystitis, and schizophrenia. Several systemic side-effects from the use of DMSO have been reported, namely nausea, vomiting, diarrhea, hemolysis, rashes, renal failure, hypertension, bradycardia, heart block, pulmonary edema, cardiac arrest, and bronchospasm. Looking at the multitude of effects of DMSO brought to light by these studies, it is easily understood how many researchers working with DMSO (or studying one of its specific effects) might not be fully aware of the experiences of other groups who are working with it but in a different context.
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PMID:Multidisciplinary utilization of dimethyl sulfoxide: pharmacological, cellular, and molecular aspects. 1266 39

The aim of this study was to compare nonsurgical versus stereotactic aspiration of intracerebral hematomas in relation to clinical aspects, computed tomographic imaging features of the brain, laboratory parameters and specific risk factors that may influence the outcome in southeast Asian Malay patients. Fifty-five of the patients with intracerebral hemorrhage (ICH) underwent stereotactic aspiration and 57 did not. Analysis was done on risk factors, locations and treatments of ICH, and the final outcomes measured by the Glasgow Outcome Scale. A total of 112 patients were evaluated. Mean age was 52 years with ages ranging from 12 to 80 years. Hypertension was seen in 60.7% of patients with ICH. The mortality rate was 25% by 3 months. 58.9% had a poor final outcome, while 41.1% had a good outcome. The selected variables were incorporated into models generated by multiple logistic regression method analysis to define the significant predictors of outcome. Significant predictors of outcome were the Glasgow Coma Scale score on admission, the duration of surgery and the total volume of the hematoma. Significant predictors of mortality were high total white blood cell differential count, low plasma protein, and high plasma lactate dehydrogenase and brain edema. The study suggests that stereotactic aspiration of patients with ICH does not offer any definite advantage over conservative treatment.
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PMID:Spontaneous intracerebral hemorrhage in northeast Malaysian patients: a four-year study. 1271 51

Brain edema is a reaction to any brain injury and can be the first stage in the beginning of intracranial hypertension. This paper puts forth a modern classification of brain edema types, based on a etiopathogenic interpretation. The hydroelectrolitic and/or proteinic buildup can occur within cells and/or in the extracellular space and differentiates three types of brain edema: cellular brain edema; extracellular brain edema and combined brain edema. Cellular brain edema (cytotoxic brain edema) occurs through intracellular hyperosmolarity or extracellular hypotonicity. Extracellular brain edema (interstitial) appears as a result of the buildup of edema fluid in the extracellular space of the brain parenchyma and can be: hydrostatic extracellular brain edema (through ultrafiltration), oncotical extracellular brain edema (vasogen brain edema) and hydrocephalic extracellular brain edema. Combined brain edema includes in variable ratios both types of brain edema, cellular and extracellular; they can be present together from the beginning or can appear successively.
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PMID:Brain edema -- a new classification. 1278 51

Brain oedema leading to intracranial hypertension occurs in a significant proportion of patients with acute liver failure in whom it is a leading cause of death. Although precise pathogenic mechanisms associated to this severe complication remain incompletely understood, increasing evidence points to gut-derived neurotoxins including ammonia as key mediators in cerebral osmotic and perfusion disturbances. The management of brain oedema and intracranial hypertension requires a multidisciplinar approach in a center where liver transplantation is available, as this option is the only treatment modality that provides improvement in outcome. This article reviews the most common causes of acute liver failure and the standard of supportive care management, and describes future potential therapeutic aspects of brain oedema and intracranial hypertension.
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PMID:[Brain oedema and acute liver failure]. 1281 25


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