| A 68-year-old woman presented with thunderclap headache, which led to a search for subarachnoid hemorrhage. Both computerized tomography of the head and cerebrospinal fluid examination were normal. magnetic resonance imaging revealed abnormalities in the white matter in the parieto-occipital regions. There was no aneurysm on magnetic resonance angiography. Treatment of hypertension led to resolution of the posterior leukoencephalopathy. hypertensive encephalopathy with reversible posterior leukoencephalopathy can present as a thunderclap headache. ( info) |
12/73. Reversible posterior leukoencephalopathy syndrome in a patient with hypertensive encephalopathy--case report. A 58-year-old male presented with reversible posterior leukoencephalopathy syndrome (RPLS) manifesting as headache, papilledema, and renal hypertension. T2-weighted magnetic resonance (MR) imaging showed hyperintensity lesions in the medulla, pons, bilateral thalami, and bilateral deep white matter of the parieto-occipital lobes. The pons was swollen. diffusion-weighted MR imaging did not show increased intensity in these lesions. The lesions disappeared with improvement of clinical symptoms after treatment for hypertension. These findings suggested the lesions were vasogenic edema and the diagnosis was RPLS. T2-weighted and diffusion-weighted MR imaging are useful modalities to differentiate RPLS from other central nervous system abnormalities such as infarction, multiple sclerosis, and central pontine myelinolysis. The clinical and neuroradiological findings of RPLS can be reversed by timely initiation of treatment for the causative factor. ( info) |
| Reversible posterior leukoencephalopathy syndrome (RPLE) is an increasingly recognised disorder, most commonly associated with malignant hypertension, toxaemia of pregnancy or the use of immunosuppressive agents. Two cases of RPLE syndrome occurring in the setting of accelerated hypertension and eclampsia are described. Both patients had seizures, altered sensorium and typical findings on neuroimaging. They had complete clinical and radiological recovery. The clinical course, pathophysiology and neuroimaging features of RPLE syndrome are discussed. ( info) |
| We describe two unrelated children with almost identical clinical illnesses comprising of severe, burning dysesthesia, allodynia, hypertensive encephalopathy, and laboratory evidence of both sympathetic and parasympathetic autonomic disturbance after a nonspecific viral illness. No underlying etiology was identified. Both patients displayed complete resolution of their clinical and radiologic findings after a number of months, and there was no recurrence over a follow-up period of 17 months to 4 years. Treatment of the patients' dysesthesias proved difficult, requiring multiple analgesics and intensive physiotherapy. We speculate that their illnesses may represent a pure autonomic variant of guillain-barre syndrome. ( info) |
15/73. Adverse neurologic events associated with rebound hypertension after using short-acting nifedipine in childhood hypertension. INTRODUCTION: Short-acting nifedipine (SA-NIF) is widely prescribed for acute hypertension (HTN) in children despite reports of ischemic complications in adults. We describe two children with neurologic events caused by rebound hypertension following SA-NIF use. CASES: Patient 1 is a 7-year-old with acute nephritis and blood pressure (BP) of 185/130. She received SA-NIF which decreased BP to 114/79. When BP rebounded to 160/103, she developed severe cortical visual impairment. Head CT demonstrated edema and petechial hemorrhages in the watershed region. Patient 2 is a 10-year-old renal transplant recipient who received SA-NIF for a BP of 155/98, which resulted in a prompt decrease to 114/74. Two hours later he developed aphasia and right-sided neglect. His BP increased to 168/88 and he developed partial complex seizures. Brain MRI showed high signal intensity in the watershed areas with early gadolinium enhancement. DISCUSSION: The temporal association of the neurologic events with the rebound increase in BP suggests a possible role for the SA-NIF, consistent with its pharmacokinetic profile. Although the adult literature has focused on the unpredictable decline in BP after SA-NIF treatment, these cases suggest that rapid increases in BP following the maximal SA-NIF effect may be associated with impaired cerebral autoregulation and encephalopathy in children. These cases underscore the need for frequent blood pressure determinations and therapy to prevent rebound hypertension. ( info) |
16/73. Hypertensive brain stem encephalopathy: clinically silent massive edema of the pons. hypertensive encephalopathy is a medical emergency whose clinical manifestations are associated with bilateral parieto-occipital lesions. We describe a case of hypertensive brainstem encephalopathy in which high blood pressure was accompanied only by nuchal headaches of violent onset. T2-weighted magnetic resonance images showed hyperintensity and edema of the pons without any parietooccipital lesions, but with hyperintense lesions at the level of the basal nuclei, insula and temporal lobes. The lesions rapidly regressed once the hypertension had been controlled. ( info) |
| We report a female, 10 years of age, with juvenile rheumatoid arthritis accompanied by hypertensive encephalopathy. The patient developed a cytotoxic brain lesion, as revealed by the high signal intensity on diffusion-weighted magnetic resonance imaging, which corresponded to the hypoperfusion area on single-photon emission computed tomography scan using (99m)Tc-ethylcysteinatedimer. cerebrospinal fluid interleukin-6 activity was elevated when the hypertensive encephalopathy revealed active central nervous system disease, and its activity decreased when the encephalopathy recovered from the central nervous system manifestations. We speculated that the cytotoxic edema and associated parenchymal damage in hypertensive encephalopathy were closely related to the intrathecal overproduction of interleukin-6. ( info) |
18/73. Selective renal embolisation for renovascular hypertension? An 11 year old girl developed hypertensive encephalopathy and renal failure from reflux nephropathy. Resection of her shrunken left kidney did not control her hypertension. Two selective arterial embolisations of the scarred right lower pole produced only transient benefit, but a heminephrectomy gave good control. Embolisation may delay definitive treatment. ( info) |
19/73. Serial investigation of perfusion disturbances and vasogenic oedema in hypertensive encephalopathy by diffusion and perfusion weighted imaging. Serial MRI including diffusion and perfusion imaging was performed in a patient with hypertensive encephalopathy. At admission, the patient was disorientated and presented with seizures and cortical blindness. perfusion imaging showed a marked reduction in blood volume and flow, with corresponding vasogenic oedema in the occipital, posterior temporal, and, to a lesser extent, frontal lobes. The clinical symptoms disappeared rapidly following treatment, whereas the disturbed circulation pattern and vasogenic oedema resolved more slowly. A complete normalisation was seen after 1 year. ( info) |
| 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. ( info) |