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

The cerebrovascular permeability to protein was studied in hypercapnic rats and in rats with epileptic seizures induced by bicuculline and homocysteine. Despite the differences of the basic pathophysiological mechanisms involved in these models, the blood-brain barrier (BBB) dysfunction was clearly related to the combined effects of high blood pressure and cerebral vasodilatation, thus indicating mechanical factors to be predominantly involved. The BBB changes were most frequent in central and basal regions in contrast to those induced by acute hypertension, which are most common in cortical areas.
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PMID:The pathophysiology of the blood-brain barrier dysfunction induced by severe hypercapnia and by epileptic brain activity. 87 51

The influence of shortlasting (less than 1 min) epileptic seizures on the permeability to protein of the blood-brain barrier (BBB) was studied in rats. The protein tracer, horseradish peroxidase (HRP) was used as marker substance. Monitoring arterial blood pressure (BP) and electroencephalogramme (EEG) seizures were induced electrically after HRP was given intravenously. Following a single electroshock seizure slight staining of brain tissue was seen, while after 10 electroshock stimuli followed by sustained seizure activity, this phenomenon was more pronounced. If 10 electroshock stimuli were preceded by transsection of the spinal cord, blood pressure increase was abolished and no tissue staining was seen in spite of epileptic seizure activity recorded on EEG. This means that the acute hypertension and not the seizure activity per se is the mechanism behind the breakdown of the BBB during epileptic seizures. Electron microscopy revealed an increased vesicular transport (pinocytosis) across the endothelial cells, while the vascular structure remained intact.
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PMID:Acute hypertension causing blood-brain barrier breakdown during epileptic seizures. 92 Jan 12

Acute subdural hematoma in infants is characterized by convulsive seizure, disturbance of consciousness, vomiting and irritability soon after mild head injury. The majority of cases have tence or bulged anterior fontanel and preretinal hemorrhage. Eleven cases, all traumatic in etiology and male under the age of one year were reported. Nine of them were treated by percutaneous subdural tapping alone, i.e., "Tapping Only Method". For the first several days, tappings were carried out daily. The subdural content was liquefied old dark blood or liquefied fresh-appearing blood in most cases. After that taps were performed only in the presence of intracranial hypertension. Vomiting and irritability were fairly reliable indicaters of intracranial hypertension but the most consistent signs were the fontanel tension to palpation and the measurement of head circumference. As soon as it could be determined that increased pressure did not recur within ten days after the last tap or that dry tap was confirmed the infant was discharged and follow as an outpatient. Follow-up studies on this series by cerebral angiography, EEG, skull measurement and Denver developmental screening test revealed normal physical and mental development in nine cases, although three out of nine cases showed mild but persistent avascular area. The remaining two cases showed more or less physically and mentally retarded developments: the initial treatment for both of them was delayed more than ten days. Acute infantile subdural hematoma due to mild head injury should be divided into the following two types: "Fulminant type", which rapidly falls in coma and may be fatal. The another, "Mild type" manifests only signs and symptoms of mild intracranial hypertension. This mild type should be treated by tapping only method without delay. There is a possibility that some mild type cases are overlooked and later progress to chronic infantile subdural hematoma. For comparison, thirteen cases of acute infantile subdural hematoma treated by trephination and/or craniotomy were reviewed. Pathological study revealed that early formation of capsular membrane is one of the characteristic findings.
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PMID:[Treatment of acute subdural hematoma in infancy-tapping only method and a follow-up study (author's transl)]. 94 81

Oppenheimer and Fischberg's vasoconstriction-hypothesis on the pathogenesis of hypertensive encephalopathy was subsequently supported by animal experiments. Later on the role of decompensation of the autoregulatory mechanism of the cerebral blood flow was revealed. The transient symptomatology comprises headache, seizures, focal cerebral symptoms (hemiplegia etc.), visual disturbances, mental disorders, papiledema etc. The age-dependency of the influence of edema is probably expressed by the predominance of seizures in childhood and the long duration of the symptoms in our third and fourth patient. The differentiation between hypertensive encephalopathy and a local complication of hypertension (hemorrhage) can be difficult, not at least because the first disturbance may be followed by the second (patient 3). Hypertension is not always present as initial symptom (patient 1 and 2). Hence a series of blood pressure readings is required in acute cerebral incidents in childhood. Steroid-treatment may lead, especially in patients suffering from a hypocomplementemic form of membranoproliferative glomerulonephritis, to a sudden rise of the blood pressure and subsequently to hypertensive encephalopathy (patients 2 and 3). Hypertensive encephalopathy is a neuropediatric emergency. The urgent treatment with dioxaside, fursemide and sodium nitroprusside is shortly reviewed.
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PMID:Hypertensive encephalopathy in childhood. Diagnostic problems. 98 19

Twenty-six patients with the syndrome of inappropriate secretion of antidiuretic hormone were reviewed. The underlying diseases were bronchogenic carcinoma (12 cases); myxoedema (five cases); diseases of the nervous system (five cases); bronchopneumonia, carcinoma of the oesophagus, acute intermittent porphria and chlorpropamide therapy (each one case). Serum sodium levels ranged between 104 and 125 mEq per litre. Eighteen patients presented neurological manifestations, which in 14 were considered to be due to hyponatraemia. Neurological signs included disorders of consciousness (stage I and II coma), extrapyramidal signs, asterixis and epileptic seizures. An hyponatraemic coma was the first manifestation of the syndrome in five cases. In all cases where the EEG was recorded it showed non-specific signs of metabolic coma. The fundi never showed signs of intracranial hypertension. Blood urea and creatinine levels were invariably low in the euthyroid patients; these values were normal or elevated in patients with myxoedema and hyponatraemia. Hypokalaemia was frequent, and hypocalcaemia constant. In eleven cases an excess of water intake revealed the clinical syndrome: six patients were excessive beer drinkers and five had received extensive intravenous infusions. In one case the deleterious effect of diuretics was evident, and in another, the syndrome became evident during radiotherapy of an oesophageal tumour. Treatment of the syndrome was successful in all cases. A review of the literature concerning the various pathogenic mechanisms corresponding to the different underlying diseases is presented. The concept of aberrant hormonal production by a tumour is illustrated by an electron microscopic study.
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PMID:Clinical, biological and pathogenic features of the syndrome of inappropriate secretion of antidiuretic hormone. A review of 26 cases with marked hyponatraemia. 100 53

Two hundred eighty patients were admitted to an intensive care stroke unit over a one-year period. Subsequent investigation indicated that only 199 of these patients actually had cerebral ischemic or hemorrhagic lesions, 10 had other cerebrovascular lesions, and the remaining 71 patients had unrelated diseases, predominantly seizures. Detailed analysis of 103 stroke patients revealed an overall incidence of 59% hypertension, and 72% had hypertensive, ischemic or valvular heart disease. Fifty percent of the patients had various cardiac arrhythmias, some of which were responsible for the acute cerebrovascular lesion. Fourteen patients died during the acute phase, 11 from apparently irreversible cerebral selling, mainly due to cerebral hemorrhage. Secondary complications such as pneumonia, pulmonary embolism, pressure sores and urinary infection were almost nonexistent, but beneficial effects on the primary cerebral lesions were more difficult to demonstrate.
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PMID:Intensive care management of stroke patients. 100 32

Neuropathologic findings in 2 cases of cerebral lymphomatoid granulomatosis with sequelae are presented. A 30-year old male with macular rash and pulmonary lymphomatoid granulomatosis responded to Prednisone terapy but developed acute intracranial hypertension with coma. A necrotizing hemorrhagic lesion was evident in the left putamen surrounded by diffuse and perivascular atypical lymphoplasmacytic infiltration. An 18-year old girl developed pulmonary lymphomatoid granulomatosis, diplopia, slurred speech and right hemiparesis. Brain scan, angiography and EEG suggested a left fronto-parietal mass assumed to represent lymphomatoid granulomatosis. She responded well to cerebral irradiation, intrathecal methotrexate and cytoxan but relapsed with seizures and increasing respiratory insufficiency. At autopsy, stigmata of cerebral lymphomatoid granulomatosis were absent but a parenchymatous degeneration consistent with disseminated necrotizing leukoencephalopathy following antileukemic therapy in children, was found.
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PMID:Cerebral lymphomatoid granulomatosis. A report of two cases, with disseminated necrotizing leukoencephalopathy in one. 100 3

Cardiovascular responses were elicited from 372 histologically verified sites in the amygdala and closely adjacent structures in 82 rats under urethan or chloralose anesthesia. Arterial hypotension was elicited at low current intensities from the medial, central, lateral, and basal nuclei of rats under either anesthetic; the hypotension was still elicited in artificially respired paralyzed rats. Stimulation of the cortical nucleus produced variable changes in arterial pressure. The hypotension elicited under urethan was not found to be correlated with changes in the frequency of electrical activity of hippocampus, amygdala, or septum or to be associated with electrical seizures. Hypertension was usually elicited from the medial nucleus at high current intensities and was attributed to current spread to the cortex ventral to the medial nucleus from which hypertension was elicited at low current intensities. Stimulation of the central, basal, and lateral nuclei under chloralose elicited bradycardia. Lesions of the stria terminalis had no effect on the hypotension, whereas lesions of the ipsilateral medial forebrain bundle abolished this response.
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PMID:Pathway mediating hypotension elicited by stimulation of the amygdala in the rat. 113 May 39

The authors report a boy aged 9 years in whom a giant meningioma of the small wing of the sphenoidal bone was removed surgically. Attention is called to the rarity of these tumours in the first decade of life. Developmental retardation, speech beginning at the age of 4 years, large head and epileptic seizures developing at the age of 7 years without signs of intracranial hypertension suggested the possibility of organic brain disease and development of massive hemiparesis, speech disturbances and choked disc in the last period of the disease were the cause of referral of the child to a neurosurgical unit. Plain skull films and angiography demonstrated changes typical of raised intracranial pressure and presence of an expanding lesion in the left cerebral hemisphere. Meningioma was found on operation hidden within the left frontal and temporal lobes but connected by means of a narrow band to the dura of the small wing of the sphenoidal bone. A good result was obtained. Follow-up examination after 2 years demonstrated slight neurological abnormalities and a very good general state of the child.
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PMID:[Case of giant meningioma of the small wing of the sphenoid bone in a 9-year-old boy]. 118 62

Phencyclidine is now one of the most frequently used main ingredients of "street drug" preparations. Its effects are highly dose dependent and three varieties of acute intoxication have been seen clinically associated with different dosages and routes of administration. Most persons using phencyclidine smoke it sprinkled on parsley in low doses. The presence of horizontal and vertical nystagmus associated with hypertension in a patient who is agitated or comatose are diagnostic of a phencyclidine intoxicated state. Sensory isolation and intravenous administration of diazepam in the event of seizure activity have proved effective in the treatment of acute intoxicated states. Phencyclidine has pronounced behavioral toxicity and several deaths due to this agent have now been documented. It is unknown whether seizure activity or respiratory depression is the primary cause of death in pharmacological overdoses.
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PMID:Phencyclidine--states of acute intoxication and fatalities. 121 Mar 29


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