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 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with renal failure may manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. After the institution of adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. These central nervous system disorders are referred to as uremic encephalopathy. The dialytic treatment of end-stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system; dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation, and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. There are at least three different forms of dialysis encephalopathy: sporadic, epidemic; and that associated with renal disease in children. In addition to the foregoing neurologic diseases which are specifically related to uremia and/or dialysis, a number of other neurologic disorders occur with increased frequency in patients with end-stage renal disease on chronic hemodialysis. These include subdural hematoma, electrolyte disorders, vitamin deficiencies, drug intoxication, hypertensive encephalopathy, and acute trace element intoxication. Renal transplantation is associated with a variety of central nervous system infections, reticulum cell sarcoma, and central pontine myelinosis. The present manuscript will review the clinical, structural, and biochemical components of those neurologic disorders which are peculiar to the uremic state and its treatment with dialysis.
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PMID:Uremic encephalopathies: clinical, biochemical, and experimental features. 675 30

Hypertension causes marked adaptive changes in the cerebral circulation. The excess risk of stroke associated with hypertension is eliminated in controlled trials of antihypertensive treatment. Such treatment may even prevent transient ischaemic attacks in the elderly. In rare cases, overzealous antihypertensive treatment may cause cerebral ischaemia, especially in the initial treatment of very severe hypertension. Headache may occasionally be caused by severe hypertension, which may also lead to the rare syndrome of acute hypertensive encephalopathy. Finally, the importance of white-matter lesions, or leukoaraiosis, in hypertension is not yet fully established.
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PMID:Cerebrovascular damage in hypertension. 760 37

A 13-year-old girl with a severe headache, blurred vision, altered mental status, seizures, high blood pressure, edema and hematuria is presented. With a previous history of upper respiratory tract infection, acute onset of edema, gross hematuria, high ASO and low C3 levels, she was diagnosed with acute poststreptococcal glomerulonephritis (APSGN) and hypertensive encephalopathy. Computed tomography (CT) revealed symmetric hypodense areas representing edema in the parieto-occipital regions. As noted in previous reports, these CT findings are of value in establishing the diagnosis of hypertensive encephalopathy. In this particular case the CT appearance and the subsequent clinical improvement without any neurological deficit supported the diagnosis of hypertensive encephalopathy due to APSGN. We emphasize that awareness of the CT findings of hypertensive encephalopathy may facilitate in making the correct diagnosis in symptomatic hypertensive patients, especially in cases with an unusual presentation or clinical course.
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PMID:Cranial computed tomographic findings in a patient with hypertensive encephalopathy in acute poststreptococcal glomerulonephritis. 782 39

The prevalence and clinical picture of hypertensive urgencies and emergencies in an emergency department are poorly known. The aim of the present study was to evaluate the prevalence of hypertensive crises (urgencies and emergencies) in an emergency department during 12 months of observation and the frequency of end-organ damage with related clinical pictures during the first 24 hours after presentation. Hypertensive crises (76% urgencies, 24% emergencies) represented more than one fourth of all medical urgencies-emergencies. The most frequent signs of presentation were headache (22%), epistaxis (17%), faintness, and psychomotor agitation (10%) in hypertensive urgencies and chest pain (27%), dyspnea (22%), and neurological deficit (21%) in hypertensive emergencies. Types of end-organ damage associated with hypertensive emergencies included cerebral infarction (24%), acute pulmonary edema (23%), and hypertensive encephalopathy (16%) as well as cerebral hemorrhage, which accounted for only 4.5%. Age (67 +/- 16 versus 60 +/- 14 years [mean +/- SD], P < .001) and diastolic blood pressure (130 +/- 15 versus 126 +/- 10 mm Hg, P < .002) were higher in hypertensive emergencies than urgencies. Hypertension that was unknown at presentation was present in 8% of hypertensive emergencies and 28% of hypertensive urgencies. In conclusion hypertensive urgencies and emergencies are common events in the emergency department and differ in their clinical patterns of presentation. Cerebral infarction and acute pulmonary edema are the most frequent types of end-organ damage in hypertensive emergencies.
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PMID:Hypertensive urgencies and emergencies. Prevalence and clinical presentation. 859 78

Hypertensive encephalopathy is an uncommon but recognized complication of malignant hypertension in children. We reviewed the clinical course, laboratory studies, and outcomes of 12 patients with hypertensive encephalopathy seen at the University of Iowa Hospitals and Clinics between 1979 and 1994. The most common presenting symptoms were seizures, headache, and vision changes. Laboratory studies were nonspecific and in some patients were normal. Hypertensive encephalopathy is a clinical diagnosis. Management consists of recognition of this syndrome and aggressive treatment of hypertension. The neurologic outcome in our series was good.
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PMID:Hypertensive encephalopathy in childhood. 873 20

A 36-year-old male presented with headache, vomiting, and gait disturbance. Examination found marked anemia, renal failure, markedly choked disks, and hypertensive encephalopathy. Magnetic resonance imaging demonstrated diffuse swelling of the brainstem and cerebellum, and obstructive hydrocephalus. Treatment with steroid, glycerol, and antihypertensive drugs resulted in a slow decrease in the brain swelling and cerebral edema. However, hydrocephalus and intracranial hypertension persisted, requiring a shunt operation. Hypertensive encephalopathy is usually improved by the treatment of hypertension, but shunt operation may be required to treat exacerbated intracranial pressure associated with obstructive hydrocephalus.
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PMID:Malignant hypertension associated with obstructive hydrocephalus--case report. 909 27

Human recombinant erythropoietin is used to treat chronic anemia in patients with end-stage renal failure. Erythropoietin causes hypertension, and hypertensive encephalopathy has been associated with its use. We describe six dialysis-dependent, chronic renal failure patients who developed hypertension, headache, and seizures while on erythropoietin. Four of the six patients had posterior white matter changes on neuroimaging. The encephalopathy was managed by prompt antihypertensive and anticonvulsant treatment and by discontinuation of erythropoietin. Hypertensive posterior leukoencephalopathy is associated with erythropoietin use.
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PMID:Erythropoietin-associated hypertensive posterior leukoencephalopathy. 971 75

OBJECTIVE AND IMPORTANCE: Brain stem and cerebellar edema rarely have been described as the principal manifestation of hypertensive encephalopathy. In addition, secondary hydrocephalus has been described in only a few cases in the literature. We present an unusual case of posterior fossa swelling and hydrocephalus resulting from hypertensive encephalopathy. CLINICAL PRESENTATION: A 53-year-old man presented with increased shortness of breath, headache, and visual changes, which had been worsening for several months. Blood pressure on presentation was 253/140 mm Hg. Neuroradiological studies revealed brain stem swelling predominantly affecting the pons, with compression of the adjacent cisterns and fourth ventricle and resultant hydrocephalus. The diagnosis of brain stem glioma was briefly entertained. INTERVENTION: The patient's blood pressure was brought under control with medical management, and he was treated with dexamethasone for 48 hours. Subsequent neuroradiological studies revealed decreased posterior fossa edema as well as marked improvement in the hydrocephalus. CONCLUSION: Hypertensive encephalopathy can present principally in the posterior fossa and can give rise to obstructive hydrocephalus. Invasive treatment of the hydrocephalus is not necessarily required in this clinical setting because reduction of the blood pressure may result in rapid improvement of the hydrocephalus.
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PMID:Posterior fossa swelling and hydrocephalus resulting from hypertensive encephalopathy: case report and review of the literature 1037 34

Cerebrovascular disease (CVD) is the third leading cause of death in United States and hypertension is a leading cause of both stroke and heart disease. It may cause headache, acute hypertensive encephalopathy, dementia and various types of strokes e.g., thrombotic, haemorrhagic, lacunar infarcts and transient ischaemic attacks. It remains the singlemost important treatable risk factor for stroke in all age groups and modern antihypertensive therapy has its documented prevention of stroke. Hypertension in acute phase of ischaemic stroke should not be treated. Hypertension in acute stroke should be treated. In advanced centres with specialised stroke units, the favoured drugs are short acting vasodilators e.g., sodium nitroprusside and labetalol. Nifedipine is the most popular drug followed by captopril, both sublingually and orally.
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PMID:Hypertension and cerebrovascular disease. 1064 96

Posterior leukoencephalopathy syndrome is a newly recognised brain disorder that predominantly affects the cerebral white matter. Oedematous lesions particularly involve the posterior parietal and occipital lobes, and may spread to basal ganglia, brain stem, and cerebellum. This rapidly evolving neurological condition is clinically characterised by headache, nausea and vomiting, seizures, visual disturbances, altered sensorium, and occasionally focal neurological deficit. Posterior leukoencephalopathy syndrome is often associated with an abrupt increase in blood pressure and is usually seen in patients with eclampsia, renal disease, and hypertensive encephalopathy. It is also seen in the patients treated with cytotoxic and immunosuppressive drugs such as cyclosporin, tacrolimus, and interferon alfa. The lesions of posterior leukoencephalopathy are best visualised with magnetic resonance (MR) imaging. T2 weighted MR images, at the height of symptoms, characteristically show diffuse hyperintensity selectively involving the parieto-occipital white matter. Occasionally the lesions also involve the grey matter. Computed tomography can also be used satisfactorily to detect hypodense lesions of posterior leukoencephalopathy. Early recognition of this condition is of paramount importance because prompt control of blood pressure or withdrawal of immunosuppressive agents will cause reversal of the syndrome. Delay in the diagnosis and treatment can result in permanent damage to affected brain tissues.
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PMID:Posterior leukoencephalopathy syndrome. 1150 3


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