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Richard B Schwartz - One of the best experts on this subject based on the ideXlab platform.

  • Hypertensive Encephalopathy as a complication of hyperdynamic therapy for vasospasm report of two cases
    Neurosurgery, 1999
    Co-Authors: Sepideh Aminhanjani, Richard B Schwartz, Sumeer Sathi, Philip E Stieg
    Abstract:

    OBJECTIVE AND IMPORTANCE: After developing subarachnoid hemorrhage, patients may deteriorate from a variety of well-known causes, including rebleeding, hydrocephalus, and vasospasm. Many patients now undergo empirical hyperdynamic vasospasm therapy with hypervolemia, induced hypertension, and nimodipine. CLINICAL PRESENTATION: We report two cases of iatrogenic Hypertensive Encephalopathy occurring during hyperdynamic therapy for cerebral vasospasm after subarachnoid hemorrhage. Hypertensive Encephalopathy is a syndrome of rapidly evolving generalized or focal cerebral symptoms occurring in the setting of severe hypertension, which is reversible with antiHypertensive therapy. INTERVENTION: The syndrome can be diagnosed in the appropriate clinical setting with computed tomographic or magnetic resonance imaging that demonstrates characteristic findings. In both cases, decreasing the blood pressure resulted in neurological improvement. CONCLUSION: In the setting of induced Hypertensive/hypervolemic therapy for vasospasm, Hypertensive Encephalopathy should be considered as a potentially reversible cause of delayed neurological decline.

  • diffusion weighted mr imaging in Hypertensive Encephalopathy clues to pathogenesis
    American Journal of Neuroradiology, 1998
    Co-Authors: Richard B Schwartz, Robert V Mulkern, Hakon Gudbjartsson, Ferenc A Jolesz
    Abstract:

    PURPOSE Hypertensive Encephalopathy, a complex of cerebral disorders, including headache, seizures, visual disturbances, and other neurologic manifestations, is associated with a variety of conditions in which blood pressure rises acutely. It has been ascribed to either exuberant vasospasm with ischemia/infarction or breakthrough of autoregulation with interstitial edema. Diffusion-weighted MR imaging may be used to determine whether the edema in Hypertensive Encephalopathy is cytotoxic or vasogenic in origin. METHODS Diffusion-weighted imaging was performed using the double line scan diffusion imaging technique on a 1.5-T MR system. Seven patients with Hypertensive Encephalopathy were imaged within 1 day of the onset of their symptoms. Apparent diffusion coefficient maps as well as low and high b-factor images were acquired. The two-tailed paired Student9s t-test was used to compare the apparent diffusion coefficients in edematous brain regions with those of normal white matter. RESULTS In all cases the apparent diffusion coefficient maps of the patients with Hypertensive Encephalopathy showed increased signal in regions corresponding to increased T2 signal on standard T2-weighted (low b-factor) images. Quantitative apparent diffusion coefficients in regions of abnormal T2 signal were 1.36 +/- 0.14 microm2/ms, compared with 0.80 +/- 0.05 microm2/ms in normal white matter. Diffusion-weighted (high b-factor) T2-weighted images did not show abnormal signal. CONCLUSION Diffusion-weighted MR imaging shows that the edema in Hypertensive Encephalopathy is of vasogenic origin and does not represent ischemia or infarction. This finding may have therapeutic implications.

  • Hypertensive Encephalopathy findings on ct mr imaging and spect imaging in 14 cases
    American Journal of Roentgenology, 1992
    Co-Authors: Richard B Schwartz, Kendall M Jones, P Kalina, R L Bajakian, M T Mantello, B Garada, B L Holman
    Abstract:

    Hypertensive Encephalopathy is a syndrome consisting of headache, seizures, visual changes, and other neurologic disturbances in patients with elevated systemic blood pressure. The purpose of this study was to analyze the imaging findings in 14 patients with Hypertensive Encephalopathy. CT (n = 13), MR (n = 12), and single-photon emission computed tomography (n = 2) examinations performed in these patients before and after resolution of symptoms were reviewed. Eight had the preeclampsia-eclampsia syndrome, and six had Hypertensive Encephalopathy due to other causes. CT and MR findings in all patients having these examinations were indicative of edema in the cortex and subcortical white matter in the occipital lobes. Two of the 14 patients also had similar findings in the cerebellum and frontal lobes. Single-photon emission computed tomography showed increased vascular perfusion adjacent to areas that appeared abnormal on CT and MR. The findings on the imaging studies resolved on follow-up examinations per...

Rajat Dhar - One of the best experts on this subject based on the ideXlab platform.

Craig J. Gardner - One of the best experts on this subject based on the ideXlab platform.

  • Hyperperfusion Syndromes: Insight into the Pathophysiology and Treatment of Hypertensive Encephalopathy
    Cns Spectrums, 2014
    Co-Authors: Craig J. Gardner
    Abstract:

    : 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

  • hyperperfusion syndromes insight into the pathophysiology and treatment of Hypertensive Encephalopathy
    Cns Spectrums, 2007
    Co-Authors: Craig J. Gardner
    Abstract:

    : 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.

Abhay Kumar - One of the best experts on this subject based on the ideXlab platform.

Robert E Breeze - One of the best experts on this subject based on the ideXlab platform.

  • posterior fossa swelling and hydrocephalus resulting from Hypertensive Encephalopathy case report and review of the literature
    Neurosurgery, 1999
    Co-Authors: Marjorie C Wang, Edward J Escott, Robert E Breeze
    Abstract:

    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.