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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case histories of 125 children with hypertension and no apparent primary CNS disease were analyzed for neurological symptoms or complications. Eleven children had neurological symptoms of high blood pressure. In only one of these patients was the diagnosis of arterial hypertension made before the observation of the neurological findings. The symptoms were severe headache in eight children, convulsions and coma in four, hemiplegia in two, and impaired vision and apraxia in one child. Symptomatology was rapidly reversed by antihypertensive treatment in four children, while six had long-term stigmata and one child died in hypertensive crisis. Because elevated arterial pressure can cause severe neurological disease, routine blood pressure measurement in children--especially those with neurological symptomatology--is stressed.
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PMID:Central nervous system involvement in severe arterial hypertension of childhood. 51 Mar 17

A Developmental Gerstmann syndrome in a 7 years-old-boy with hyperactivity, short attention span, acalculia, agraphia, right-left confusion, finger agnosia and constructional apraxia is reported. An initial trial with methylphenidate was done with good improvement regarding hyperactivity, attention span and constructional apraxia. In the clinical course developed a cerebellar syndrome and intracranial hypertension. Surgical exploration of the cerebellum discovered a medulloblastoma. The author believes that this is the first described association of Developmental Gerstmann syndrome and cerebellar neoplasia. The clinical findings, the etiology and the topography of the Gerstmann syndrome are discussed.
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PMID:[Developmental Gerstmann syndrome associated with cerebellar neoplasm. Report of a case and review of the literature]. 116 10

We studied clinical characteristics and coexisting causes of stroke in 305 patients admitted to a population-based primary care center with an initial ischemic stroke and a potential cardiac source of embolism (PCSE). Using systematic standardized cardiac, arterial, and cerebral investigations and the logistics of the prospective Lausanne Stroke Registry, we found that nonprogressive onset, hemianopia without hemiparesis or hemisensory disturbances, Wernicke's aphasia, ideomotor apraxia, involvement of specific territories (posterior division of middle cerebral artery, anterior cerebral artery, cerebellum, multiple territories), and a hemorrhagic component were associated with the presence of a PCSE, as compared with 1,006 initial ischemic stroke patients without PCSE. Although age and sex did not differ, the frequency of hypertension, diabetes, cigarette smoking, elevated blood cholesterol, and deep hemispheric or brainstem infarcts was higher in the patients without a PCSE. Nearly one-fourth of the patients with a PCSE had a coexisting potential arterial cause of stroke (large artery greater than or equal to 50% stenosis or small-vessel disease). In the majority of patients with a PCSE (76.7%), cardioembolism was the most likely cause of stroke, although a direct source of embolism was uncommon (4.3%) and intracranial embolic occlusions were present in less than one-half of the patients who were angiographed.
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PMID:Cardiac sources of embolism and cerebral infarction--clinical consequences and vascular concomitants: the Lausanne Stroke Registry. 204 30

A case-control study was performed to verify the association between the risk factors for cerebrovascular disease and the syndrome of ventricular enlargement with gait apraxia (VEGAS). This syndrome was defined on the basis of clinical and CT criteria alone; however, it may be representative of patients with idiopathic normal pressure hydrocephalus in whom gait disturbance is the initial symptom. Seventeen patients were matched for age and sex with one hospitalised and two general population controls. Among the risk factors considered we found a significant statistical association between VEGAS and hypertension (odds ratio = 3.14; p = 0.032), ischaemic heart disease (odds ratio = 4.20; p = 0.013), ECG ischaemic changes (odds ratio = 3.67; p = 0.029), low HDL-cholesterol levels (odds ratio = 3.75; p = 0.028) and diabetes (odds ratio = 6.00; p = 0.018). Our findings indicate that risk factors for cerebrovascular disease may play a role in the development of VEGAS.
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PMID:Risk factors for the syndrome of ventricular enlargement with gait apraxia (idiopathic normal pressure hydrocephalus): a case-control study. 276 78

A 74-year-old right-handed man with multiple cerebral infarction who presented with dementia simulating dementia of Alzheimer type (DAT) is reported. He had been well until April 20, 1987 when he developed transient right hand palsy lasting overnight. Eleven days later, he became confused, disorientated, and amnestic. He was admitted to this hospital on June 8. Physical examination revealed hypertension (170/90mmHg). On neurological examination, his consciousness was clear but he was demented. He showed disorientation, amnesia, and urinary incontinence. His most prominent symptom was disturbance of speech, including fluent aphasia and alexia with agraphia. Additionally, he showed ideomotor apraxia, construction apraxia, right-left agnosia, finger agnosia, and acalculia. On July 9, he had a transient attack of right hemiplegia with confusion. The brain CT scan performed on admission was unremarkable except for cavum septi pellucidum and a small low density area in the right basal ganglia. However, single photon emission computed tomography (SPECT) by 123I-labeled N-isopropyl-p-iodoamphetamine disclosed hypoperfusion of the cerebral blood flow in the border zones of the temporoparietal and frontal lobes on the left. A follow-up brain CT scan taken one month later demonstrated low density in the new areas corresponding to hypoperfusion shown by SPECT. Although the clinical features of the present case resembled those of DAT, dementia in this case was regarded as the result of multiple cerebral infarction since it occurred acutely with mild motor deficits, and brain CT scans and SPECT showed lesions indicating focal cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Multi-infarct dementia clinically simulating dementia of Alzheimer type. A comparison with angular gyrus syndrome]. 278 20

A case of multiple cerebral hemorrhage in the bilateral parietal lobes related to cerebral amyloid angiopathy (CAA) is reported. A 66-year-old man was admitted to our hospital because of headache and vomiting on Feb. 21, 1983. He had no history of hypertension, diabetes mellitus, recent head injury, or dementia. Four days prior to admission, he had behaved as if he were blind, but, had denied any blindness. On examination, he was confused and disoriented. Blood pressure was 130/80 mmHg. Abnormal findings on neurological examination included memory disturbance, apraxia for dressing, right-left disorientation, finger agnosia and Balint's syndrome. A CT scan showed multiple subcortical hematomas in the bilateral parietal lobes. Intracerebral hemorrhage related to CAA was suspected. Confirmation of the presence of amyloid in the cerebral vessels was established by examination of brain biopsy specimens. The characteristics of cerebral hemorrhage related to CAA are as follow--occurrence in elderly, sometimes demented people; localization to the cortex and subcortical white matter, with direct extension into the subarachnoid space; frequent multiple occurrence in time and/or at several sites within the cerebral hemispheres; sometimes occurrence after operative procedures or head injuries. A specific diagnosis of CAA can only be made by histological examination, but the indication of brain biopsy should be carefully decided because of hemostatic difficulty and tendency to rebleed. In conclusion, CAA should be considered as a cause of hemorrhage in elderly patients who are often normotensive and demented.
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PMID:[A case of multiple cerebral hemorrhage related to cerebral amyloid angiopathy]. 339 10

Twenty-five patients with various types of gait disorders of multi-infarct dementia (MID) were reported. The types of gait disorders consisted of lower body parkinsonism (LBP) plus ataxia (6 patients), LBP plus apraxia (5 patients), and a combination of LBP plus ataxia and apraxia (14 patients). Hypertension occurred in 23 (92%) of the 25 patients. Nevertheless, individual stroke risk factors and the locations of infarcts were not significantly different between the subgroups. Ventriculomegaly and "leuko-araiosis" as demonstrated by computed tomography occurred in more than 80% of patients in each subgroup. Atrophy of the superior vermis was seen in 16 (80%) of 20 patients with ataxia as compared to 2 (40%) of the 5 patients without ataxia (p < 0.005). These data suggest that LBP and apraxia of MID were probably determined by the presence of ventriculomegaly or leuko-araiosis or both, and the presence of ataxic component of gait disorder most probably indicates the presence of vermian atrophy.
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PMID:Gait disorders of multi-infarct dementia. CT and clinical correlation. 847 97

Differential diagnosis of dementing diseases is very important to rule in the so-called treatable dementia. The new DSM-IV criteria for dementia include memory disturbances and one or more of aphasia, apraxia, or frontal lobe dysfunctions as essentials. Alzheimer disease requires, in addition, slowly progressive course and ruling out other brain or systemic diseases. Vascular dementia requires focal neurological or neuroimaging signs. Other diseases which cause dementia include chronic subdural hematoma, infection and brain tumor. CT or MRI can readily diagnose them if suspected and they may be treated. Systemic diseases associated with treatable dementia include electrolyte disturbances, hypothyroidism, vitamin deficiency, alcohol or drug intoxication, syphilis and HIV infection. Prevention of dementia seems to be the future problem as we could prevent cerebrovascular diseases by treating hypertension.
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PMID:[Clinical aspects of dementia]. 875 26

Medical treatment of stroke is dependent on a narrow therapeutic time window. We prospectively analyzed the influence of demographic, medical, and pathophysiologic factors on admission delay in 1,197 unselected, acute stroke patients. Twenty five percent were admitted within 3 1/2 hours, 35% within 6 hours, 50% within 14 hours, and 68% within 24 hours after stroke onset. Living alone (odds ratio [OR] 1.75, 95% CI 1.3 to 2.3) and retired working status (OR 1.61, 95% CI 1.01 to 2.54) delayed admission. A well-working social network thus seems important to early admission. The milder the stroke, the higher was the risk of delayed admission (OR 1.25 per 10 points decrease in stroke severity [Scandinavian Neurological Stroke Scale score on admission], 95% CI 1.14 to 1.36). A history of TIA increased the relative chance of early admission by odds 1.64 (95% CI 1.06 to 2.54). Other factors such as age, sex, diabetes, hypertension, ischemic heart disease, other comorbidity, previous stroke, headache, aphasia, apraxia, anosognosia, neglect, lowered consciousness, mental status (Mini-Mental State Examination) and type of stroke (hemorrhage/infarct) had no independent influence on admission time. Admission was markedly delayed in most patients. This represents a major barrier to medical treatment. Patients with the most severe strokes are admitted early, but patients with milder symptoms should also be encouraged to seek immediate admission. The observation that a history of TIA reduced admission time indicates that an increase in public awareness and knowledge may reduce delay and save precious time.
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PMID:Factors delaying hospital admission in acute stroke: the Copenhagen Stroke Study. 875 8

We report a 76-year-old man who developed blurred vision and dementia. He was apparently well until April 4, 1990 (70-year-old at that time) when he had a sudden onset of bilateral loss of vision. Corrected vision was 0.1 (right) and 0.09 (left). He was admitted to the ophthalmology service of our hospital on April 9, 1990, and neurological consultation was asked on April 11. Neurologic examination revealed alert and oriented man without dementia. Higher cerebral functions were intact. He had bilateral large visual field defects with loss of vision; he was only able to count the digit number with his right eye and to recognize hand movement with his left eye. Otherwise neurologic examination was unremarkable. General physical examination was also unremarkable; he had no hypertension. Cranial CT scan was normal on April 11; lumber spinal fluid contained 1 cell/microliter, 63 mg/dl of sugar, and 97 mg/dl of protein; myelin basic protein was detected, however, oligoclonal bands were absent. He was treated with methylprednisolone pulse therapy and oral steroid, however, no improvement was noted in his vision. He started to show gaze paresis to left, ideomotor apraxia, agnosia of the body, and dementia. Cranial CT scan on June 11 revealed a low density area in the deep left parietal white matter facing the trigonal area of the lateral ventricle. He was discharged on July 2, 1990. Hasegawa dementia scale was 2/32.5 upon discharge. In the subsequent course, he showed improvement in his mental capacity and Hasegawa dementia scale was 22.5/32.5 in 1991, however, no improvement was noted in his vision. In 1994, he started to show mental decline in that he became disoriented, and showed delusional ideation of self persecution and depersonalization with occasional confusional state. He also showed unsteady gait. Cranial MRI on February 13, 1996 revealed a T2-high signal intensity lesion on each side of the parietal deep white matter more on the left and another T2-high signal intensity lesion in the left pons as well as in the right thalamus. He complained of right hypochondrial pain and was admitted to another hospital on April 22, 1996. He was markedly confused and demented. He continued to show bilateral loss of vision, but no motor palsy was noted. Cranial CT scan on April 23, 1996 revealed diffuse cortical atrophy and ventricular dilatation in addition to the low density areas in both parietal deep white matter. He developed jaundice in the middle of May. Abdominal CT scan revealed multiple low-to iso-density areas in the liver and marked iso-to high-density swelling of the right kidney. The patient expired on June 9th, 1996. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had had a carcinomatous limbic encephalitis with optic neuropathy and a choleduct carcinoma. Other opinions entertained included acute disseminated encephalomyelitis with optic neuritis, and granulomatous angiitis of the central nervous system. Some participants thought the primary site of the carcinoma was the right kidney with metastasis to the liver. Post mortem examination revealed a mixed type carcinoma in the right kidney with liver metastases. Neuropathologic examination revealed an incomplete softening in the optic chiasm and the left optic nerve, and in the left parieto-occipital areas. (The right hemisphere was frozen for future biochemical assay.) One of the adjacent cortical arteries had an organized thrombus. Other arteries and arterioles also showed sclerotic changes. Some of the leptomeningeal arteries were positive for Congored staining as well as for beta-amyloid immunostaining. Many senile plaques were seen diffusely in the cerebral cortex and neurofibrillary tangles were seen in the CA1 area and the parahippocampal gylus. No cellular infiltrations or demyelinated foci were seen. The neuropathologic features were consistent with circulatory disturbance based on the amyloid angiopa
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PMID:[A 76-year-old man with loss of vision and dementia]. 928 74


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