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At least 19 recordsLinked to original sources
PubMed2002

Hyperperfusion encephalopathies: hypertensive encephalopathy and related conditions.

BACKGROUND: Hypertensive encephalopathy (HTE) is a syndrome typified by headache, seizures, and neurologic signs associated with increased systemic blood pressures; edema in the subcortical white matter is seen on imaging studies and is usually reversible, although infarction or hemorrhage may supervene. Based on previous work, we theorize that HTE is associated with increased perfusion to the brain. Syndromes related to HTE may also be encountered in clinical situations in which perfusion to the brain is acutely increased without systemic hypertension (i.e., after treatment of high-grade carotid stenoses or large intracranial arteriovenous malformations, or in high altitude mountain sickness). We therefore refer to these conditions more generally as hyperperfusion encephalopathies (HPE). REVIEW SUMMARY: The clinical and radiographic data of 110 patients (average age, 50.1 years) who presented at the Brigham and Women's Hospital with clinical and radiographic signs of HPE were reviewed; 104 had systemic hypertension and 6 had postcarotid endarterectomy hyperperfusion syndrome. Edema involved the subcortical white matter and occasionally the cortex in all patients. In patients with systemic hypertension, the edema was usually bilateral and located predominantly in the occipital lobes; other brain regions included the parietal lobes, posterior frontal lobes, cerebellum, and splenium of the corpus callosum. The six patients with postcarotid endarterectomy hyperperfusion syndrome had edema in the hemisphere ipsilateral to the operated side involving the anterior and middle cerebral artery territories. The edema in HPE was associated with: increased low attenuation on CT; decreased T(1) and increased T(2) signal on MR imaging; increased cerebral perfusion on single emission computed tomography (SPECT) and perfusion MR imaging;did not show restricted diffusion on MR imaging. The syndrome resolved completely in most cases after the administration of antihypertensive agents, although rarely small infarcts and hemorrhages occurred. Three patients with thrombocytopenia developed large fatal intracranial hemorrhages. CONCLUSION: The symptoms of HPE are usually nonspecific, but the radiographic findings are consistent. Treatment should be instituted rapidly and patients should be followed until the condition resolves either clinically or radiographically; hemorrhagic complications, although rare, can be serious.

Journal Article↗
PubMed1992

Oral nifedipine in the treatment of hypertensive crises in patients with hypertensive encephalopathy.

Hypertensive emergencies, including hypertensive encephalopathy represents an acute threat to vital organ functions and call for urgent treatment. The intravenous medications currently available for the management of hypertensive emergencies, have significant potential for serious side effects and acute lowering of blood pressure has often been the cause of considerable morbidity and mortality. Nifedipine is known to be effective as an antihypertensive agent and it is widely used in hypertensive emergencies. We studied the efficacy and effective dose of nifedipine in 22 patients (9 females and 13 males; mean age 51) with hypertensive encephalopathy. Nifedipine (20 mg by oral drop) caused a significant fall in diastolic an systolic blood pressure in all patients from 236/121 to 172/96 mmHg after 30 minutes (P less than 0.005, P less than 0.001). Continuous therapy with nifedipine (2-5 mg every 2-3 hours, mean total dose 52 mg/24 h) gave successful control of blood pressure. These data prove that nifedipine can be used as the first-line drug for the treatment of hypertensive crises in patients with hypertensive encephalopathy.

Administration, Oral↗
PubMed2007

Hyperperfusion syndromes: insight into the pathophysiology and treatment of hypertensive encephalopathy.

Hypertensive encephalopathy is one of the manifestations of a hypertensive crisis. It is not the absolute value of the blood pressure that causes the encephalopathy, rather the presence of an abrupt rise in pressure. In terms of clinical and radiographic findings, there are many similarities among a group of entities, including hypertensive encephalopathy, eclampsia, and immunosuppressant neurotoxicity. Hyperperfusion syndromes may represent these clinical disease states that may share the same pathophysiology. Magnetic resonance imaging fluid attenuated inversion recovery sequences have recognized the prominent cortical involvement of the disease that had been previously missed on computed tomography. Studies have found cortical involvement in 94% of their patients, particularly in mild cases. Animal models demonstrate endothelial damage and enhanced pinocytosis in the cortex as reasons why edema may begin in that region of the brain. Patients diagnosed with hypertensive encephalopathy should be diagnosed and treated promptly in order to avoid further neurological complications. The mean arterial pressure should be lowered by 20% to 25% within the first hour of patient presentation, followed by further gradual reduction in blood pressure over the following 24 hours. Hypertensive emergency in acute ischemic stroke should be managed with more caution. According to the 2003 American Stroke Association treatment guidelines, for patients with ischemic stroke not eligible for thrombolytic therapy, target blood pressures are a diastolic blood pressure <120 mmHg and systolic blood pressure <220 mmHg. The systolic pressure must be <185 mmHg and diastolic pressure <110 mmHg at all times if eligible for thrombolytic therapy.

Animals↗
PubMedDate not supplied

[Imaging findings in hypertensive encephalopathy].

Hypertensive encephalopathy is a neurologic syndrome caused by a marked and rapid rise of blood pressure above baseline levels. Efficacy of current anti-hypertensive drugs greatly diminished the frequency of this situation in which diagnosis is essentially based on clinical parameters. This can justify the few papers found in radiologic literature. Nevertheless it is sometimes important to exclude ischemic or hemorrhagic complications or establish a differential diagnosis with other neuropathologic conditions. Then a striking imagiologic picture of focal or diffuse reversible edema of cerebral white matter can be found. We present three clinical cases of hypertensive encephalopathy. Imagiologic findings are reviewed and correlated with the pathophysiologic basis of the disease.

Adolescent↗
PubMed1975

An electron microscope study on permeability in cerebral venules in the rats with hypertensive encephalopathy.

Hypertensive encephalopathy was induced in the rat by clipping one renal artery and contralateral nephrectomy. The possible changes of vascular permeability of the cerebral blood capillaries and venules were investigated by using ferritin as a tracer. The uninephrectomized rats served as controls. In controls, ferritin was never seen in the basement membranes, within plasmalemmal vesicles on the basal surface of the endothelium, or in endothelial cell junctions of cerebral capillaries and venules up to 180 min after the injection. In venules of the brain in rats with hypertensive encephalopathy, a number of ferritin particles appeared in the basement membrane in 60 min after the injection. Many plasmalemmal vesicles in the endothelial cells of venules were labeled with ferritin. However, ferritin particles were never found in the endothelial cell junctions. The results suggested that leakage of macromolecules, such as serum proteins, occurred in venules mainly by increased vesicular transport.

Animals↗
PubMed2002

CT and MRI findings of cyclosporine-related encephalopathy and hypertensive encephalopathy.

We present the MRI and CT findings of one child with cyclosporine-related encephalopathy, and one child with hypertensive encephalopathy following cyclosporine-related encephalopathy. The imaging findings were shown well on T2-weighted and fluid-attenuated inversion recovery (FLAIR) MR images. Cyclosporine-related encephalopathy was distributed predominantly in the posterior white matter. Hypertensive encephalopathy showed similar changes of CT attenuation, but with wider distribution. These two disorders seem to have the same pathogenesis.

Brain↗
PubMed1983

Hypertensive encephalopathy.

Hypertensive encephalopathy is examined in the context of an acute cerebral episode precipitated by sudden, severe hypertension. Since it is a medical emergency and responds to prompt and vigorous treatment, the author discusses its clinical manifestations, diagnosis, pathology, pathogenesis, and treatment.

Brain Diseases↗
PubMed1996

A case of Guillain-Barré syndrome accompanied by sympathetic overactivity and hypertensive encephalopathy.

Hypertension has often been observed in patients with Guillain-Barré syndrome, and various underlying mechanisms have been implicated. We report the case of a child with the Guillain-Barré syndrome whose hypertension was associated with increases in both renin activity and circulating catecholamines. This case also appeared to be complicated by hypertensive encephalopathy. Following administration of intravenous regitine, a blood pressure change was observed and cardiac performance was assessed by two-dimensional echocardiography. Results indicated that increased total peripheral resistance may have been responsible for the symptoms and the hypertension. The hypertension was effectively managed by nifedipine, captopril and prazosin without the need for beta-blockade.

Child, Preschool↗
PubMed2026

MRI-Negative Posterior Reversible Encephalopathy Syndrome: Comparison of Hypertensive Encephalopathy With and Without Vasogenic Edema.

OBJECTIVE: To explore whether posterior reversible encephalopathy syndrome (PRES) can present with negative magnetic resonance imaging (MRI) by comparing clinical features between cases of PRES with vasogenic edema and cases of hypertensive encephalopathy without MRI changes. PATIENTS AND METHODS: Patients diagnosed with hypertensive encephalopathy from August 1, 2008, to December 31, 2017, were identified retrospectively and matched by age (&#xb1;5 years) and sex in a 1:2 ratio to patients retrospectively identified as having PRES from January 1, 2002, to November 30, 2017. A review of MRI images and clinical information was performed. RESULTS: We identified 16 cases of hypertensive encephalopathy and 32 age- and sex-matched controls with PRES showing vasogenic edema on MRI. There were no statistically significant differences in the odds of presentation with headache (odds ratio [OR], 1.372; 95% CI, 0.458 to 4.106), encephalopathy (OR, 2.303; 95% CI, 0.433 to 12.236), visual disturbance (OR, 0.826; 95% CI, 0.185 to 3.697), or focal neurologic deficit (OR, 4.000; 95% CI, 0.767 to 20.872). Seizures were more common in patients with vasogenic edema (OR, 0.082; 95% CI, 0.010 to 0.664). There were no significant differences in odds of acute kidney injury (OR, 2.90; 95% CI, 0.679 to 12.449) or odds of having a history of malignancy (OR, 0.295; 95% CI, 0.076 to 1.152), transplantation (OR, 3.347; 95% CI, 0.594 to 18.880), or autoimmune disease (OR, 0.400; 95% CI, 0.104 to 1.532). Systolic blood pressure at presentation was higher in patients with hypertensive encephalopathy and negative MRI as compared with patients with PRES and vasogenic edema (OR, 1.03; 95% CI, 1.01 to 1.05). CONCLUSION: Most presenting symptoms and risk factors were not significantly different between cases of hypertensive encephalopathy with and without vasogenic edema, arguing that the diagnosis of PRES in the setting of acute severe hypertension may not depend on MRI confirmation.

Humans↗
PubMed1978

Management of hypertensive encephalopathy.

The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena. The syndrome may complicate acute glomerulonephritis, toxemia of pregnancy and essential or malignant hypertension. Two syndromes must be differentiated from true hypertensive encephalopathy: 1. acute anxiety state with labile hypertension and 2. acute pulmonary edema due to hypertensive heart disease. At least in patients with acute anxiety states, the use of antihypertensive agents is usually not indicated. Since encephalopathy is always accompanied by increased vascular resistance and since clinical experience has demonstrated clearing of the sensorium, cessation of convulsions and release of vasoconstriction following reduction of blood pressure, the primary aim of therapy should be prompt lowering of arterial pressure. The two agents of choice are diazoxide and sodium nitroprusside. Stroke is differentiated from encephalopathy by the persistence of lateralizing signs. The aggressiveness of antihypertensive therapy in this situation depends on the severity of the hypertensive process. Rapid reduction of blood pressure is indicated in patients found to have accelerated hypertension while a more gradual lowering of pressure appears warranted for patients with chronic arterial hypertension and evidence of generalized arteriosclerosis.

Brain Diseases↗
PubMed2005

Hypertensive encephalopathy of brain stem with minimal supratentorial involvement: a rare manifestation of hypertensive encephalopathy.

We report a case of a 38-year-old man with brain stem hypertensive encephalopathy. MR imaging revealed diffuse hyperintensities in the brain stem. Diffusion-weighted imaging (DWI) was normal, and apparent diffusion coefficient (ADC) values were increased in the brain stem. The supratentorial regions were largely spared, and only subtle high intensities were seen. The lesions completely resolved after stabilization of blood pressure. The findings of normal DWI and high ADC values were compatible with vasogenic edema due to hypertension.

Adult↗
PubMed2006

Posterior reversible encephalopathy syndrome caused by hypertensive encephalopathy and acute uremia.

INTRODUCTION: The posterior reversible encephalopathy syndrome (PRES) is a recently proposed cliniconeuroradiological entity. The most common causes of PRES are hypertensive encephalopathy, eclampsia, cyclosporin A neurotoxicity, and the uremic encephalopathy. On magnetic resonance imaging (MRI) studies, edema has been reported in a relatively symmetrical pattern, typically in the subcortical white matter and occasionally in the cortex of the posterior circulation area of the cerebrum. METHODS AND RESULTS: A 19-year-old woman undergoing chronic hemodialysis was admitted with encephalopathy. High signal intensity was seen bilaterally in the subcortical and deep white matter areas of the temporal, frontal, parietal, and occipital lobes on cranial MRI. CONCLUSION: Particular attention needs to be given to PRES because initiation of appropriate intervention can reverse the encephalopathic condition in most cases. Cerebral lesions may be more prominent in the anterior circulation area in some patients.

Acute Disease↗
PubMed1996

Hypertensive encephalopathy in childhood.

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.

Acute Disease↗
PubMed2006

Posterior reversible encephalopathy syndrome: a variant of hypertensive encephalopathy.

Posterior reversible encephalopathy syndrome (PRES) is a recently described variant of hypertensive encephalopathy characterized by headache, visual disturbances and altered mental function. Its causes are diverse and in contrast to hypertensive encephalopathy, it can develop without significant elevation of blood pressure. This syndrome is mostly reversible when correctly managed; however, failure to recognize it can lead to cerebral infarction and death.

Adult↗