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)

Effects of intracerebroventricular (third ventricle) injection of N-methyl-D-aspartate (NMDA) on arterial blood pressure, on heart rate, on arginine vasopressin (AVP) and levels of catecholamines in plasma and on the behaviour of normotensive freely-moving rats have been evaluated. N-Methyl-D-aspartate significantly (P less than 0.01) increased arterial blood pressure and levels of catecholamines and AVP in plasma. With 0.1-1.0 micrograms/rat all animals presented psychomotor agitation, stereotyped movements, hyperexcitability, exophthalmus, dyspnoea, jumping, rearing and teething. The selective antagonist for NMDA receptors, 2-APV injected in the third ventricle, significantly (P less than 0.01) antagonized the hypertension, the increase in levels of catecholamines and AVP in plasma and behavioural effects. An antagonist of alpha 1 adrenergic receptors, prazosin (i.v.), an agonist of alpha 2 adrenergic receptors, clonidine (i.c.v.) and a relatively selective antagonist of V1 subtype of receptor of AVP, CGP 25838 (i.c.v. and i.v.), 15 min before NMDA, significantly (P less than 0.01) decreased the effects induced by the injections of NMDA. On the contrary, an antagonist of opiate receptors, naloxone (i.v.), 15 min before NMDA, significantly (P less than 0.01) increased the NMDA-induced modifications. Pretreatment with the antagonists at these doses, did not significantly modify the basal values of arterial blood pressure and behaviour. Only 2-APV sometimes induced ataxia, lasting about 5 min. This study points out an increase in the central sympathetic efferent activity and in release of AVP involved in the NMDA-induced cardiovascular and behavioural effects.
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PMID:Participation of arginine vasopressin-mediated and adrenergic system-mediated mechanisms in the hypertension induced by intracerebroventricular administration of NMDA in freely moving rats. 135 1

A mother and two of her daughters had deafness and cortical reflex myoclonus; the mother also had mild truncal ataxia. Muscle and skin biopsy specimens revealed abundant ragged-red fibres and abnormal mitochondria. The son of one of the daughters had sensorineural deafness. Three other grandchildren were asymptomatic. The two daughters also had diabetes mellitus, hypertension and cardiomyopathy. Another daughter died of renal failure. The mother lost her hearing in her 70s, one daughter in her 30s, and the other daughter and the grandson in their 20s. The mother has had transient episodes (24-48 hours) of temporal disorientation, severe action myoclonus, and ataxia for about eight years. This is the first reported family with inherited deafness, myoclonus, and ataxia with mitochondrial pathology.
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PMID:Abnormal muscle and skin mitochondria in family with myoclonus, ataxia, and deafness (May and White syndrome). 153 18

The term "papilledema" describes optic disc swelling resulting from increased intracranial pressure. A complete history and direct funduscopic examination of the optic nerve head and adjacent vessels are necessary to differentiate papilledema from optic disc swelling due to other conditions. Signs of optic disc swelling include elevation and blurring of the disc and its margins, venous congestion, and retinal hard exudates, splinter hemorrhages and infarcts. Patients with papilledema usually present with signs or symptoms of elevated intracranial pressure, such as headache, nausea, vomiting, diplopia, ataxia or altered consciousness. Causes of papilledema include intracranial tumors, idiopathic intracranial hypertension (pseudotumor cerebri), subarachnoid hemorrhage, subdural hematoma and intracranial inflammation. Optic disc edema may also occur from many conditions other than papilledema, including central retinal artery or vein occlusion, congenital structural anomalies and optic neuritis.
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PMID:Papilledema: clinical clues and differential diagnosis. 154 98

In 1986, we reported two anatomoclinical observations of a familial condition that we called "fatal familial insomnia" (FFI). We now present the pedigree as well as the clinical and neuropathologic findings in five new subjects. The pedigree includes 288 members from six generations. Men and women are affected in a pattern consistent with an autosomal dominant inheritance. The age of onset of the disease varies between 37 and 61 years; the course averages 13 months with a range of 7 to 25 months. Progressive insomnia (polygraphically proven in two cases); autonomic disturbances including hyperhidrosis, hyperthermia, tachycardia, and hypertension; and motor abnormalities including ataxia, myoclonus, and pyramidal dysfunction, were present in every case, but with variable severity and time of presentation. Sleep and autonomic disorders were the earliest signs in two subjects, motor abnormalities were dominant in one, and others had intermediate clinical patterns. Pathologically, all the cases had severe atrophy of the anterior ventral and mediodorsal thalamic nuclei. Other thalamic nuclei were less severely and inconsistently affected. In addition, most of the cases had gliosis of the cerebral cortex, a moderate degree of cerebellar atrophy with "torpedoes," and severe atrophy of the inferior olivary nuclei. One case also showed spongy degeneration of the cerebral cortex. We conclude that all the lesions were primary, and that FFI is a multisystem disease in which the different structures are primarily affected with different severity. The insomnia appears to correlate best with the major thalamic pathology. The possibility that FFI belongs to the group identified as prion diseases or diseases transmitted by unconventional agents is examined.
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PMID:Fatal familial insomnia: clinical and pathologic study of five new cases. 173 58

In 45 cases of porencephaly 35 were male and 10 female. Their age ranged from 80 days to 58 years (mean 14 years). In this series, symptoms were observed 80 days to 22 years before diagnosis. twenty-four cases were premature delivery, difficult labour or birth trauma. 14 cases had a history of head injury. 36 cases had congenital porencephalic cyst and 9 had post-traumatic porencephaly. The main symptoms and signs of porencephaly were dementia, speech defect, intracranial hypertension, hydrocephalus, epilepsy, ataxia or paralysis. etc. It is suggested that CT scan is very useful in the diagnosis of porencephaly, and section of cerebral cortex, opening of cyst, continuous drainage or shunting operation should be done as soon as the diagnosis was made.
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PMID:[Porencephaly. A report of 45 cases]. 187 15

During 1984-1989, 19 Bedouin children, 4-8 years old, were hospitalized because of henbane plant (Hyoscyamus reticulatus) poisoning. There were 14 cases in the autumn, 3 in the spring and 2 in the summer. The most prominent signs were altered state of consciousness (including deep coma in 3) and flushed dry, warm skin in all. Pupils were dilated in 18 of the 19 and restlessness and hallucinations were present in 17. Less common were vomiting, increased tendon reflexes, convulsions, involuntary movements, ataxia, hypertension, hyperpyrexia and tachycardia. Therapy included intravenous physostigmine in 7 and sedatives (diazepam and triclofos) in 6. All were free of symptoms within 24 hours of admission. Henbane may grow as an annual or biennial. Renewed growth of leaf rosettes occurs before the first rains and they attract attention in the fields. The parts of the plant eaten by most of the children were the roots, which are easily mistaken for the edible roots of other plants. The main alkaloids in henbane are atropine (hyoscyamine) and scopolamine (hyoscine) which explains the clinical picture of mixed stimulation and depression of the brain. Educational measures should be undertaken to prevent poisoning of Bedouin children by eating such plants.
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PMID:[Henbane (Hyoscyamus reticulatus) poisoning in children in the Negev]. 195 6

The records of 483 patients admitted to the emergency room because of syncope were reviewed. Thirty seven patients (7.7%) were found to suffer from transient ischemic attack- (TIA) related syncope. This group is the subject of this report. Of these patients, 28 (76%) were men (mean age 71 years). Seven patients reported previous syncopal episodes. Past history revealed a high rate of ischemic heart disease (70%) and hypertension (68%). Concurrent neurologic symptoms, which led to the diagnosis of TIA-related syncope, included mainly vertebrobasilar symptoms: vertigo (in 55% of the patients), ataxia (46%), parasthesia (41%). Two patients most probably were presenting bilateral carotid artery disease. Various diagnostic tests (including electroencephalography, computed tomography, sonography, and cerebral angiography) were used to exclude other causes of syncope. During follow-up (mean 14.5 months) four patients (11%) had an additional episode of TIA and in three of them syncope reappeared. One patient had a complete stroke. We conclude that TIA is a much more frequent explanation for syncope than has been previously argued. These patients tend to be elderly males with high incidence of ischemic heart disease and hypertension. The concurrent neurologic symptoms, leading to the diagnosis, represent mainly vertebrobasilar territory ischemia.
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PMID:Transient ischemic attack-related syncope. 204 43

Computerized tomography of the head was done in 5021 patients aged 21 to 81 years from various neurological, neurosurgical and neurotraumatological indications. Brain atrophy as an only finding (primary) was noted in 11.5%- and in 5.4% of cases it was associated with other changes. The neurological-radiological correlations were established in 200 cases of primary strophy. History data included: headaches in 54.5%, dizziness in 15.0%, epilepsy in 24.5%. Objective examination showed: slight hemiparesis in 37.5%, spastic-atactic gait disturbances in 31.5%, isolated damage to the corticospinal tracts with signs limited to one side of the body was more frequent in cortical atrophy, and these signs associated with ataxia were more frequent in subcortional atrophy. The authors explain this as a loss of cortical cells or damage to the paraventricularly coursing nerve fibres. A probable aetiology of "primary" atrophy was established in 405% of cases (hypertension, atherosclerosis, minor craniocerebral trauma). No signs or neurological syndromes were observed which could be regarded as more or less characteristic of brain atrophy.
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PMID:[Brain atrophy: radiological-neurological correlations]. 213 53

The authors describe a family (mother, son and two daughters) with mitochondrial myopathy. The mother was asymptomatic. Two daughters had lactic acidosis and myoclonic epilepsy, mild dementia, ataxia, weakness and sensory neuropathy. The son suffered one acute hemiplegic episode due to an ischemic infarct in the right temporal region. All the patients studied had hypertension. EEG disclosed photomyoclonic response in the proband patient. Muscle biopsy disclosed ragged-red fibers and abnormal mitochondria by electron microscopy. Biochemical analysis showed a defect of cytochrome C oxidase in mitochondria isolated from skeletal muscle. Several clinical and genetic aspects of the mitochondrial encephalomyopathies are discussed.
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PMID:Mitochondrial myopathy and myoclonic epilepsy. 216 73

The powdered bark of Maquira sclerophylla is consumed as snuff in north Brazil. Both the crude and the purified hydrosoluble extract (WP) injected i.p. in the dose range of 0.05-0.5 g/kg induced hyperexcitability, tremors, motor incoordination, ataxia, quietness and muscle relaxation in rats. The effects were progressive, dose-related and reversed after 30 min. Anesthetized rats, guinea-pigs and dogs injected with the purified extract (10-50 mg/kg, i.v.) showed a biphasic change of carotid blood pressure. The early and transient hypotension was blocked by atropine but not by vagotomy: the secondary hypertension was long lasting and sustained for over 30 min. The hypertension was shortened but not blocked after ganglionic blockade or reserpine treatment. Either pithing or alpha receptor blockade with yohimbine reduced both effects of the extract. Guinea-pigs and dogs were more responsive than rats and died by heart arrest. Incubation of WP (20 micrograms/ml) increased both the rate and force of contraction of isolated guinea-pig right atria by 2 and 5 times, respectively. Propranolol (4 micrograms/ml) blocked the chronotropic effect but did not decrease the inotropic effect. In electrically driven guinea-pig left atria, WP (10 micrograms/ml) increased the force of contraction by 80% and the maximum rate of force development by 60%, but did not change the time to peak tension, the time to 50% relaxation, or the rate of relaxation. These cardiovascular effects resemble those of digitalis-like drugs. Cardenolides were detected in WP by phytochemical screening.
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PMID:Pharmacology of an Indian-snuff obtained from Amazonian Maquira sclerophylla. 221 23


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