Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Small, deep lesions of the internal capsule are an uncommon cause of infantile hemiplegia. We report the clinical and radiographic findings of three children with hemiplegia with capsular lesions. Although the etiology of capsular stroke in these children remains uncertain, neither hypertension, coagulopathy, nor vascular malformation was an important factor.
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PMID:Capsular stroke as a cause of hemiplegia in infancy. 668 99

A child with neurofibromatosis had hypertension and acute hemiplegia resulting from both renal and cerebral vascular occlusive disease. This case illustrates the importance of recognizing surgical antihypertensive therapy was attempted, and may have contributed to rapid neurologic deterioration. Children with neurofibromatosis and hypertension require a careful neurologic evaluation, including computed tomography, before therapy.
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PMID:Childhood hypertensive stroke with neurofibromatosis. 677 Feb 88

Pure motor hemiplegia (PMH) is a well defined syndrome usually caused by ischemic lesions of lacunar type located either in the internal capsule or in the pons. Angiography and isotope scanning are usually normal. CT scan reveals small deep infarcts and appears to be the most reliable investigative method. The CT scan findings are described of thirty patients with PMH of rapid onset (less than 36 hours). In 29 of the 30 cases a lesion was found which could explain the PMH. Small hemorrhages (2 cm in diameter) in the posterior limb of the internal capsule were noted in two cases. Ischemic lesions were found in 27 patients, 22 patients had a single lesion (20 capsular and 2 pontine), while 5 patients had 2 lesions (2 bi-capsular, 3 capsular and pontine). Three varieties of ischemic capsular lesions were observed. We found in 15 cases a capsulo-putamine-caudate infarct (type I); in 8 cases a capsulo-pallidal infarct (type II); and in 2 cases an anterior capsulo-caudate infarct (type III). Type I corresponded to the area of the lateral lenticulostriate branches of the middle cerebral artery. Type II involved the territory of the perforating branches of the anterior choroidal artery. We suggest that type III involves the territory of the internal lenticulostriate branches of the anterior cerebral artery. Lacunes are generally linked to arterial systemic hypertension. However, only 16 of 30 patients in this series were chronically hypertensive.
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PMID:Pure motor hemiplegia: CT study of 30 cases. 706 72

A clinicopathologic study was made of 45 elderly persons whose autopsied brains showed the pathologic changes of progressive subcortical vascular encephalopathy (Binswanger type). Progressive subcortical vascular encephalopathy (PSVE) was observed in 3.8 per cent of all autopsied brains of elderly persons and in 6.7 per cent of the brains of those with cerebrovascular diseases. White matter lesions were graded from I to III (slight to severe). Small infarcts in the basal ganglia, thalamus, and pons were common, but the cerebral cortex was usually preserved. Neuropsychiatric symptoms included dementia, urinary incontinence, hemiplegia, pseudobulbar palsy, psychosis, parkinsonism, and mutism. In thge Grade III group there was a high incidence of pseudobulbar palsy, parkinsonism, and mutism. Pathologic study showed marked cerebral arteriosclerosis in almost all cases. Angionecrosis was observed in 60 to 80 per cent. Fibrotic and stenotic changes of the blood vessels in the deep white matter were also noted, particularly in 90 per cent of the Grade III cases. A suggested explanation for the pathogenesis of PSVE is based on the effects of various complications such as hypertension, cardiac disease and malnutrition which may play an important role in PSVE when they occur in elderly persons with a history of long-standing hypertension, marked cerebral arteriosclerosis, and arteriolar changes in the cerebral white matter.
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PMID:Clinicopathologic study of progressive subcortical vascular encephalopathy (Binswanger type) in the elderly. 709 54

The case of a 26 year old woman who had been taking tranexamic acid to prevent uterine bleeding due to an IUD and who died from thrombosis of the left internal carotid artery is reported. The patient's father had died at age 54 of myocardial infarction. Otherwise the family history was entirely negative for thromboembolic disease. The patient was a mild smoker. She had been previously healthy and in particular, she was not affected with hypertension, diabetes, or dyslipidemia. She had carried to term 2 uncomplicated pregnancies. 40 days prior to hospital admission her gynecologist had inserted an IUD. The insertion of the IUD was followed by persistent uterine bleeding, and for this reason she began treatment with tranexamic acid (1.5 g/daily). Uterine bleeding persisted despite this treatment, and the IUD was removed. Because of persistence of a mild uterine bleeding, tranexamic acid was continued. 2 hours before admission the patient suddenly presented a left sided hemiparesis with disarthria and vomiting. On admission she was stuporous. The left side of her face drooped and the strength of the left arm and leg was markedly decreased. Both arm and leg reflexes were symmetrical. Her blood pressure was 110/70. An electroencephalogram on arrival confirmed a right sided cerebral lesion. Subsequently the patient's condition deteriorated rapidly. She developed a full left hemiplegia and became deeply comatose. A CAT scan performed 4 hours after admission showed no abnormalities. A CAT scan performed 3 days after admission showed a large cerebral infarction involving nearly the whole right cerebral hemisphere. The patient's condition remained essentially unchanged until she died 6 days after admission. Permission for autopsy was refused. Antifibrinolytic drugs competitively inhibit plasminogen activators and noncompetitively plasmin. Thromboembolic complications after the administration of antifibrinolytic drugs have long been recognized. The use of IUDs is often associated with troublesome uterine bleeding and particularly excessive menstrual bleeding. To avoid these complaints, antifibrinolytic drugs are increasingly used.
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PMID:Tranexamic acid, intrauterine contraceptive devices and fatal cerebral arterial thrombosis. Case report. 710 62

Hypertension intracerebral hemorrhages are caused by leakage from small penetrating branches of larger cerebral vessels. In the brainstem, these vessels penetrate in a median, paramedian, and more lateral orientation. As illustrated by three patients reported here, hemorrhage from the lateral vessels may be limited to the lateral tegmentum, or spread to the dorsal basis pontis. The syndrome is relatively consistent and includes (1) ipsilateral conjugate gaze palsy, (2) ipsilateral internuclear ophthalmoplegia, (3) small reactive pupils with a smaller pupil ipsilateral to the lesion, (4) limb ataxia of the cerebellar type (often greater ipsilaterally), (5) contralateral hemiplegia, and (6) contralateral severe hemisensory loss. Patients frequently survive after lateral tegmental hemorrhages, which can be diagnosed by CT.
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PMID:Lateral tegmental brainstem hemorrhages. 719 35

Forty-eight patients with intracranial hematomas are reviewed. In all cases diagnosis was established by CT scan. Volume was calculated with the Steiner method. Treatment was supportive for all patients. Mortality rate was 33%. Arterial hypertension was an associated factor in 58.33%. Clinical evolution was influenced by age of patient, volume and site of the hematoma. Mortality rate was highest in the cases with thalamic hematomas. Early coma or hemiplegia also carried a poor prognosis.
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PMID:[Intracerebral hematoma: clinical and prognostic correlations (author's transl)]. 727 26

The authors report clinical and scanographic findings in 26 cases of capsulo-thalamic hemorrhage. They stress the frequency of arterial hypertension as a pre-disposing factor. The clinical picture is represented by the association of disorders of consciousness (usually obnubilation), contralateral flaccid hemiplegia with hemianesthesia, oculomotor disorders (disturbance of vertical gaze, miosis) and disorders of linguistic and motor behaviour. The paraclinical examination of choice is scanography which enables the site, volume and extent of the hemorrhage to be estimated, together with the mass effect and intraventricular rupture. Clinical and scanographic follow-up indicates a favourable prognosis for capsulo-thalamic hemorrhage (77% survival). Follow-up findings point to several unfavourable prognostic factors: immediate coma, persistent and massive flaccid hemiplegia, hemorrhage size exceeding 3 cm, and severe intraventricular rupture. In the light of the data in the literature, the authors discuss the clinical and scanographic signs of capsulo-thalamic hemorrhage.
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PMID:[Capsulo-thalamic hemorrhage (author's transl)]. 730 26

Fifty-seven young stroke patients (aged 45 years and below) admitted to a rehabilitation centre were assessed for underlying risk factor/aetiology and functional outcome after rehabilitation. The mean age was 37.2 +/- 6.3 years and the mean length of stay in the rehabilitation ward 38.3 +/- 19.9 days. There were 37 (64.9%) haemorrhagic and 20 (35.1%) ischaemic strokes. Hypertension was the single most important risk factor accounting for 49.1% of all strokes. Vascular abnormalities (arteriovenous malformation, mycotic aneurysm, vasculitis and Moya-moya disease) and cardiogenic embolism secondary to rheumatic valvular heart disease were also significant causes. There was significant improvement in functional status--activities of daily living (ADL) and mobility--after rehabilitation, the mean Functional Status score improving from 9.76 +/- 2.2 on admission to 5.07 +/- 1.95 on discharge (P < 0.01). Higher ADL and mobility function and upper and lower limb motor power of grade 3 and above on admission, absence of dysphasia, left hemiplegia, age less than 40 years and rehabilitation stay of less than 28 days were associated with better functional outcome whilst sex, nature and site of stroke, and length of stay in the acute ward had no significant bearing.
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PMID:Functional outcome in young strokes. 760 88

A case of severe epistaxis with hypertension and arteriosclerosis was treated by embolizing the ipsilateral internal maxillary artery after routine methods of hemostasis had failed. Although epistaxis stopped after embolization, cerebral infarction, hemiplegia and deep coma developed, and the patient died on the ninth postoperative day. We conclude that superselective embolization of the branches of external carotid artery for treating severe epistaxis should be used with great caution or not be used in patients with arteriosclerosis.
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PMID:[Arterial embolization leading to fatal cerebral infarction (a case report)]. 780 19


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