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

A 15-year-old woman with a history of transient dysarthria two years before, suddenly developed weakness of right upper extremity, right facial palsy, and dysarthria. She was admitted to our hospital on the third day. She had no hypertension, heart murmur and oedema. On neurological examination, she had mild right hemiparesis including face muscles and mild dysarthria. The right knee jerk was brisk with no Babinski's sign. Ataxia and sensory disturbance were not present. T2-weighted MRI showed a hyperintensity at the posterior limb of the left internal capsule. Cerebral angiography was unremarkable. Ultracardiography and 24-hour electrocardiography were normal. Laboratory data revealed no inflammatory findings, liver dysfunction, hyperglycemia and hyperlipidemia. Antinuclear and anticardiolipin antibodies were negative. Prothrombin time was normal, but activated partial thromboplastin time was slightly prolonged (35.4 sec, normal 25.2-34.4). Protein C, protein S and antithrombin III were normal. Heparin cofactor II (HC II) activity was decreased (44%) with normal HC II antigen (79%) and so she was diagnosed as heparin cofactor II deficiency type II (heparin cofactor II abnormality). Her father manifesting thromboangitis obliterans also had low HC II activity with normal HC II antigen. However, on her genetic analysis, we didn't detect any mutations in the coding region of HC II gene. Until now she has no recurrence of cerebrovascular attacks. On the basis of these results, we suspect that HC II deficiency was a possible risk factor of cerebral infarction in this case because she was so young and had no general risk factors except for HC II. No stroke associated with HC II deficiency type II has been reported up to date. This case is worth considering etiologies of juvenile cerebral infarction.
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PMID:[Juvenile cerebral infarction associated with heparin cofactor II abnormality. A case report]. 1096 62

Lacunar infarcts represent a stroke subgroup with controversial risk factors. Lacunar syndromes may be divided into two groups: the classic group (pure motor hemiplegia, pure sensory stroke, ataxic hemiparesis, dysarthria-clumsy hand syndrome, sensorimotor stroke) and the miscellaneous group including all other lacunar syndromes. We studied risk factors of 200 consecutive patients with symptomatic lacunar infarcts diagnosed by magnetic resonance imaging. This study tested whether lacunar infarcts represent a homogeneous subgroup of strokes or not. Using descriptive and bivariate statistics, we found that the prevalences of arterial hypertension and cigarette smoking are lower in the miscellaneous group. Analysis of variance shows a significant difference in age between subgroups without interaction of sex. Nevertheless, using multivariate analysis, we did not find a difference between subgroups. Thus, lacunar infarcts seem to be a homogeneous subgroup of strokes, and the miscellaneous group of lacunar infarcts may be included into the lacunar infarct group and not into the vertebrobasilar large-artery infarct group.
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PMID:Risk factors for lacunar infarcts. 1097 Oct 25

Primary leptomeningeal lymphoma (PLML) is a rare disease. The most common presentation is symptoms of increased intracranial pressure. Confusion, dysarthria, hearing loss, paraparesis and lumbosacral spinal root symptoms have also been reported. Chemotherapy and radiotherapy have been tried, but its prognosis is usually poor. We experienced a case of PLML with a relatively benign course in an 18-year-old girl. Initial diagnosis was made as idiopathic intracranial hypertension. Lumbosacral shunt was done with good response for 3 years. When headache recurred, she was reevaluated and was correctly diagnosed as PLML.
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PMID:Primary leptomeningeal lymphoma with long-term survival: a case report. 1102 96

A 71-year-old man developed dysarthria and difficulty of swallowing in December 1997. He was diagnosed as having the bulbar type of amyotrophic lateral sclerosis (ALS). In November 1998, he was admitted to our hospital to undergo treatment for bulbar palsy and respiratory discomfort. In January 1999, ventilatory support (synchronous intermittent mandatory ventilation) during sleep at night was initiated. Severe progressive hypotension and loss of consciousness were observed soon after the start of artificial respiration, and both symptoms disappeared after artificial respiration was discontinued. This phenomenon was observed consistently during ventilatory support, while unpleasant stimuli such as bronchoscopy and replacement of the cannula tube induced severe hypertension. To clarify the mechanism of underlying these abnormal changes in blood pressure, autonomic function tests were performed while awake during the daytime. Ventilatory support induced a drop in blood pressure accompanied by a decrease in influx speed to the right ventriculum, the latter of which suggested a reduction in venous return. These values returned to the baseline following detachment of the ventilator. A 60 degrees head-up tilt (HUT) angle and standing from a supine position produced orthostatic hypotension, the latter of which was accompanied by a compensatory increase in pulse rate. The basal supine plasma noradrenaline (NA) level was high and the HUT showed a slight elevation of NA. The basal supine plasma arginine vasopressin (AVP) level was within the normal range, whereas the AVP level did not increase during HUT. Urinary secretion rates of NA and 3-methoxy-4-hydroxy-phenylglycol were elevated. A cold pressor test demonstrated reflex hypertension. The oculovagal reflex, coefficient of variation of R-R intervals. (CVR-R) and increase in pulse rate in response to atropine administration were within the normal range. The combination of midodrine, L-dihydroxyphenylserine (DOPS) and increasing intravascular volume via continuous intravenous drip infusion relieved the circulatory collapse during artificial respiration. In conclusion, the present case of ALS had sympathetic hyperactivity, somatosympathetic reflex and dysregulation of the baroreflex arc. Degeneration of central autonomic network, including the hypothalamus and the central nucleus of the amygdala, which has been shown in some ALS patients, might underlie the autonomic abnormalities in this patient.
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PMID:[A case of amyotrophic lateral sclerosis presenting with circulatory collapse during artificial respiration]. 1125 87

A 56-year-old right-handed male with a history of hypertension and diabetes presented two episodes of stroke: The first affected territory was the left anterior coroidal artery (capsular and paracapsular infarcts at the level of the genu and posterior arm of the internal capsule) and the second was the right thalamus, due to a hematoma. Following the first stroke, the patient developed severe dysarthria and after the second stroke remained anarthric. The pathophysiology of the disorder is discussed, and the role of the left and right thalamus as far as speech is concerned is reviewed.
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PMID:Subcortical anarthria: a case report. 1141 14

We report the case of a 44 year old man who presented with a two-month history of dysarthria, ataxia and leg weakness whilst on maintenance lithium for bipolar disorder. Examination revealed significant cerebellar and pyramidal dysfunction. Serum lithium was 1.5 mmol/l, a moderate elevation above his usual stable levels of 0.4-0.8 mmol/l. The patient's past history included hypertension and chronic renal impairment and the development of neurological symptoms coincided with the recent onset of heart failure. On cessation of lithium he partially recovered, the main residuum being persistent cerebellar ataxia. The case is an example of lithium neurotoxicity developing insidiously in the absence of an overt acute phase syndrome, and highlights the need for keen observation of the patient in the hope of preventing permanent deficits.
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PMID:Lithium neurotoxicity: the development of irreversible neurological impairment despite standard monitoring of serum lithium levels. 1209 41

Stroke is the main manifestation of cerebrovascular disease (CVD). Few studies report the insidious and progressive development of CVD. The aim of this study was the characterization of a CVD form without stroke in association with vascular subtypes and risk factors (VRF). From 105 CVD patients, 65 had stroke (62%), 13 of them had more than one stroke (20%), and 40 patients had a chronic progressive form (CPF) (38%). Mean evolution times up to maximum neurological deficiency were 1.57+/-0.94 and 344.25+/-210.96 days, respectively. Group results significantly associated with VRFs: hypertension (p=0.0046), hyperlipemia (p=0.0046) and atrial fibrillation (p=0.0173); with clinical manifestations: aphasia (p=0.0018), pyramidal syndrome (p=0.0000001) and small vessel disease (SVD) (p=0.0000001); and with MRI: bilateral infarctions (p=0.00009) and incomplete white matter lesions (IWMLs) (p=0.0061). Within the CPF group, dysarthria and complete infarctions were associated (p=0.00036). Most neurological disorders associated with CVD are related to CPF. The significant correlations of SVD, bilateral infarcts, IWMLs, dysarthria, several VRFs and the strong difference in evolution time up to maximum neurological deficiency values characterize CPF as a separate entity within CVD.
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PMID:Stroke vs. chronic progressive cerebrovascular disease: a magnetic resonance imaging study of symptomatic outpatients. 1241 59

Vascular dementia is the second most common type of dementia. The subcortical ischaemic form (SIVD) frequently causes cognitive impairment and dementia in elderly people. SIVD results from small-vessel disease, which produces either arteriolar occlusion and lacunes or widespread incomplete infarction of white matter due to critical stenosis of medullary arterioles and hypoperfusion (Binswanger's disease). Symptoms include motor and cognitive dysexecutive slowing, forgetfulness, dysarthria, mood changes, urinary symptoms, and short-stepped gait. These manifestations probably result from ischaemic interruption of parallel circuits from the prefrontal cortex to the basal ganglia and corresponding thalamocortical connections. Brain imaging (computed tomography and magnetic resonance imaging) is essential for correct diagnosis. The main risk factors are advanced age, hypertension, diabetes, smoking, hyperhomocysteinaemia, hyperfibrinogenaemia, and other conditions that can cause brain hypoperfusion such as obstructive sleep apnoea, congestive heart failure, cardiac arrhythmias, and orthostatic hypotension. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL)and some forms of cerebral amyloid angiopathy have a genetic basis. Treatment is symptomatic and prevention requires control of treatable risk factors.
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PMID:Subcortical ischaemic vascular dementia. 1284 65

Carbamazepine is a well-established, effective treatment of complex partial seizures and is well tolerated in most patients. The adverse effects of carbamazepine include aplastic anemia, agranulocytosis, pancytopenia, bone marrow depression, thrombocytopenia, cardiac conduction abnormalities, congestive heart failure, and peripheral edema. Hypertension or hypotension has also rarely been documented in patients with either therapeutic or toxic blood levels of carbamazepine. It is possible that carbamazepine-induced hypertension in those with therapeutic blood levels is rarely seen because most of the patients who begin treatment are young and do not have baseline hypertension. The authors describe a patient of African-American descent with a history of controlled essential hypertension who developed severe uncontrolled hypertension when started on carbamazepine. Treatment with additional antihypertensive medications did not reduce his blood pressure. In addition, he developed two episodes of transient neurologic deficits, the symptoms of which consisted of dysarthria, vertigo, and unstable gait. A substantial reduction of his carbamazepine dose resulted in the control of his blood pressure and no recurrence of his symptoms.
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PMID:Transient neurologic deficits associated with carbamazepine-induced hypertension. 1289 34

The baroreflex maintains blood pressure through the glossopharyngeal (IX) cranial nerve. We report a 54-year-old man who developed a left sided headache, hoarseness, dysarthria, dysphagia, and sustained hypertension from a left internal carotid artery dissection. We hypothesise that interruption of the left IX nerve caused hypertension in this patient.
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PMID:Left internal carotid artery dissection presenting with headache, Collet-Sicard syndrome and sustained hypertension. 1464 21


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