1/83. Decreases in blood pressure and sympathetic nerve activity by microvascular decompression of the rostral ventrolateral medulla in essential hypertension.BACKGROUND: Neurovascular compression of the rostral ventrolateral medulla, a major center regulating sympathetic nerve activity, may be causally related to essential hypertension. Microvascular decompression of the rostral ventrolateral medulla decreases elevated blood pressure. CASE DESCRIPTION: A 47-year-old male essential hypertension patient with hemifacial nerve spasms exhibited neurovascular compression of the rostral ventrolateral medulla and facial nerve. Microvascular decompression of the rostral ventrolateral medulla successfully reduced blood pressure and plasma and urine norepinephrine levels, low-frequency to high-frequency ratio obtained by power spectral analysis, and muscle sympathetic nerve activity. CONCLUSIONS: This case suggests not only that reduction in blood pressure by microvascular decompression of the rostral ventrolateral medulla may be mediated by a decrease in sympathetic nerve activity but also that neurovascular compression of this area may be a cause of blood pressure elevation via increased sympathetic nerve activity.- - - - - - - - - - ranking = 1keywords = muscle (Clic here for more details about this article) |
2/83. Cervical subarachnoid hematoma of unknown origin: case report.OBJECTIVE AND IMPORTANCE: Spontaneous spinal subarachnoid hematoma is rare, having been reported in the English literature in only seven other cases. We describe the first case of spontaneous subarachnoid hematoma located in the cervical spinal cord of a 43-year-old man. The pathologic examination showed no apparent source of bleeding, but there was evidence of cervical spondylotic myelopathy. CLINICAL PRESENTATION: The patient presented with a 10-day history of severe neck pain, followed by the onset of quadriparesis that was more evident on the left side, urinary retention, and sensory loss below C5. His medical history included hypertension. magnetic resonance imaging showed a massive hemorrhage in the cervical spinal canal. INTERVENTION: A C4-C5 subarachnoid hematoma was removed. The patient died due to respiratory distress and uncontrollable hypotension on day 6 after surgery. Surgical exploration, neuroradiologic examinations, and autopsy showed no evidence of vascular malformations, tumors, or other possible sources of bleeding. CONCLUSION: After excluding more common causes of spontaneous subarachnoid hematoma in this patient, we suggest that chronic spinal cord compression (spondylotic myelopathy) and arterial hypertension in this patient may have caused the pathogenesis of this rare clinical entity. Experimental data supporting this hypothesis are discussed.- - - - - - - - - - ranking = 18.686507852421keywords = paresis (Clic here for more details about this article) |
3/83. Simultaneous bilateral thalamic hemorrhage: case report.A 60-year-old man presented with an extremely rare case of simultaneous hypertensive bilateral thalamic hemorrhage manifesting as left hemiparesis with headache followed by deterioration in consciousness and tetraparesis. CT scan confirmed the bilateral thalamic hemorrhages 17 hours after onset. magnetic resonance imaging showed the bilateral thalamic lesions had similar signal intensities, consistent with the simultaneous onset, and had no evidence of hemorrhagic reason. Conservative treatment achieved some neurological improvement, but he died of pneumonia six months after onset. The prognosis of a patient with bilateral hemorrhages is worse than would be indicated by the size of the hemorrhages.- - - - - - - - - - ranking = 83.527016906983keywords = hemiparesis, paresis (Clic here for more details about this article) |
4/83. Mechanism in progressive lacunar infarction: a case report with magnetic resonance imaging.BACKGROUND: The mechanism of a progressive lacunar infarction is not well understood, and changes in ischemic tissue after onset have not yet been clarified clinically. OBJECTIVE: To investigate the pathophysiological characteristics of a case of progressive lacunar infarction using diffusion-weighted and conventional magnetic resonance imaging (MRI) scans. PATIENT: A 73-year-old woman was hospitalized 18 hours after stroke onset and was diagnosed as having a lacunar infarction in the perforating territory of the left middle cerebral artery. Despite treatment, the hemiparesis worsened, with the peak on the fourth day after onset. diffusion-weighted and conventional MRI scans provided clues to the pathogenesis. FINDINGS AND CONCLUSIONS: In the acute stage, gradual enlargement of the hyperintense lesion, reflecting fresh ischemic tissue, and neurological deterioration were observed by serial examination of diffusion-weighted MRI scans. A conventional coronal MRI scan revealed a 2-layered ischemic lesion, suggesting the involvement of perforating arteries. These findings indicated that hemodynamic impairment of the microcirculation in the perforators was the major cause of the lacunar infarction.- - - - - - - - - - ranking = 64.840509054562keywords = hemiparesis, paresis (Clic here for more details about this article) |
5/83. brain stem stroke causing baroreflex failure and paroxysmal hypertension.BACKGROUND: Paroxysmal neurogenic hypertension has been associated with a variety of diseases affecting the brain stem but has only rarely been reported after brain stem stroke. The mechanism is thought to involve increased sympathetic activity and baroreflex dysfunction. We undertook microneurographic recordings of muscle sympathetic nerve activity (MNSA) during beat-to-beat blood pressure (BP) monitoring to investigate this hypothesis. CASE DESCRIPTION: We investigated a 75-year-old woman who developed paroxysmal hypertension (BP 220/110 mm Hg) after a large left-sided medullary infarct. The paroxysms were triggered by changes in posture and were accompanied by tachycardia, diaphoresis, and headache. serum catecholamines were substantially increased (norepinephrine level, 23.9 nmol/L 9 days after stroke; normal level, <3.8 nmol/L), and heart rate variability, measured by spectral analysis, was decreased in both low- and high-frequency domains (0.04 and 0.06 ms(2), respectively; normal level, 0.14 /-0.02 ms(2)). MNSA was increased in frequency (61 bursts per minute; normal level, 34 /-18 bursts per minute), and the burst amplitude was not inversely related to diastolic BP. BP and MNSA responses to cold pressor and isometric handgrip stimuli were intact. CONCLUSIONS: Extensive unilateral infarction of the brain stem in the region of the nucleus tractus solitarius may result in partial baroreflex dysfunction, increased sympathetic activity, and neurogenic paroxysmal hypertension.- - - - - - - - - - ranking = 1keywords = muscle (Clic here for more details about this article) |
6/83. pathology of a dissecting intracranial aneurysm.The pathological findings of six autopsy cases of dissecting intracranial aneurysm are studied. Clinically, all cases exhibited systemic hypertension or left ventricular hypertrophy. Macroscopically, all cases exhibited rupture of the vertebral artery and subarachnoid hemorrhage. Two types of lesion were present. First, all cases showed the formation of a dilatated pseudoaneurysm with widespread disruption of the entire arterial wall, which was composed of thin adventitia. Second, a medial disruption of the arterial wall and subadventitial dissecting hemorrhage, which formed a false lumen and stenosis of the 'true' lumen of the artery, was also found. However, these lesions were found to be connected to the site of rupture. The autopsy cases within 1 day of onset of intracranial dissecting aneurysm showed the formation of fibrin thrombus, a marked degree of leukocyte infiltration and necrosis of the arterial wall at the site of the lesion. The cases that survived more than 1 week showed smooth muscle cell proliferation, macrophage accumulation and lymphocytic infiltration. No arteriosclerosis was found in any lesion studied. These data suggest that the disruption of the entire arterial wall might initially occur and cause medial disruption and subadventitial hemorrhage. hypertension and arteriosclerosis might function as causal and protective factors in the pathogenesis of dissecting intracranial aneurysms, respectively.- - - - - - - - - - ranking = 1keywords = muscle (Clic here for more details about this article) |
7/83. A case of renin-producing adrenocortical cancer.Here we report a case of a renin-producing adrenocortical carcinoma. A 57-year-old woman was referred to our hospital complaining of thirst and generalized muscle weakness. She was diagnosed as being hypertensive and diabetic with associated hypokalemia and she had a hard elastic mass with a diameter of 10 cm on the left side of her neck. An abdominal computed tomography scan revealed a suprarenal mass on the left side (8.5 x 8 x 6.5 cm). Endocrinological examination demonstrated a marked elevation in the patient's serum glucocorticoid and sex steroid hormones as well as plasma renin activity. Histological examination of a sample taken from the neck mass revealed a metastasis from an adrenal carcinoma, which was stained positively with antibodies against cytochrome P450 and renin, establishing the diagnosis of a renin-producing adrenocortical carcinoma. Trilostane was effective in reducing serum cortisol levels, but mitotane was ineffective.- - - - - - - - - - ranking = 1keywords = muscle (Clic here for more details about this article) |
8/83. Apical aneurysm and left ventricular hypertrophy.A 59-year-old woman presented with an embolic transient ischemic attack and a history of controlled hypertension for 16 years. Both echocardiogram and MRI showed severe biventricular hypertrophy and an apical aneurysm with a thrombus. The occurrence of an apical aneurysm in the presence of cardiac hypertrophy is a rare finding and has been described in patients with hypertrophic cardiomyopathy. However, it has not been reported in patients with systemic arterial hypertension. In this patient the lack of a relationship between the severity of the hypertrophy and the levels of blood pressure, together with the presence of histologic disorganization of myocardial cardiac muscle cells by endomyocardial biopsy suggested the diagnosis of hypertrophic cardiomyopathy.- - - - - - - - - - ranking = 1keywords = muscle (Clic here for more details about this article) |
9/83. hypertension, hyperekplexia, and pyramidal paresis due to vascular compression of the medulla.MRI showed impingement of the vertebral artery on the left lateral medulla in two patients with arterial hypertension, exaggerated startle reflexes (hyperekplexia), and progressive spastic paresis. One patient underwent microvascular decompression with normalization of arterial hypertension, disappearance of hyperekplexia, and improvement of spastic paresis. The combination of arterial hypertension, hyperekplexia, and progressive spastic paresis should arouse suspicion of neurovascular compression of the lateral medulla.- - - - - - - - - - ranking = 130.80555496695keywords = paresis (Clic here for more details about this article) |
10/83. Severe postpartum hypertension and reversible cerebral angiopathy associated with ergot derivative (methergoline) administration.A 36-year-old woman (gravida 2, para 2) delivered a healthy child by cesarean section at the 37th week of an unremarkable gestation. blood pressure remained within normal range throughout the pregnancy, surgery, and for the 9 following days. On day 10, about 36 hours after the initiation of oral methergoline to suppress lactation, the patient complained of severe posterior headache, flashing scotomata, hypertension, tonico-clonic seizures and then homonymous left hemianopsia and hemiparesis. blood pressure monitoring confirmed intermittent and severe hypertension. angiography demonstrated diffuse narrowing of the small and medium cerebral arteries. Transcranial Doppler ultrasound examination disclosed a bilateral increase in mean flow velocity. Progressive normalization of blood pressure, obtained with labetalol and oral clonidine, was accompanied by amelioration of the neurological deficits until a complete recovery and normalization of transcranial Doppler flow velocity occurred. This case provides further evidences that hypertension might play a major pathogenetic role in reversible cerebral angiopathy. Some ergot derivatives (including methergoline) might trigger the initial rise in blood pressure.- - - - - - - - - - ranking = 64.840509054562keywords = hemiparesis, paresis (Clic here for more details about this article) |
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