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

Intracranial hypertension with papilledema occurred in two patients receiving danazol therapy for either cyclic neutropenia or immune hemolytic anemia. Results of clinical, laboratory, and neuroradiologic studies showed no apparent cause for the condition in Case 1 and the papilledema resolved one month after discontinuing danazol. Carotid angiography in Case 2 demonstrated cerebral venous sinus thrombosis; the papilledema showed gradual improvement after cessation of danazol. An additional seven cases of pseudotumor cerebri presumed secondary to danazol therapy have been reported to the Food and Drug Administration. The papilledema resolved in all seven cases soon after discontinuing danazol. A drug-induced complication should be suspected, and alternative therapy sought, in patients who develop intracranial hypertension associated with administration of danazol.
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PMID:Pseudotumor cerebri induced by danazol. 291 2

The functional and morphological aspects of craniosynostoses are reviewed, based on a series of 462 operations, 350 intra-cranial pressure recordings and 300 I.Q. assessments. Increased intracranial pressure and mental impairment are linked. The frequency of intracranial hypertension is higher when more than one suture is involved, but even monosutural craniosynostoses can be affected. Increased intracranial pressure had mental deficiency are more frequent after one year of age than before. Surgery lowers the intracranial pressure and halts the mental regression. The younger the patient is at the time of surgery, the better the results. Surgery does not improve the I.Q. once it is already impaired. Morphological results of frontocranial remodeling are good and remain so with growth. Facial anomalies associated with craniosynostoses improve after early frontocranial remodeling, except for the severe midface retrusion of Crouzon's disease and Apert's syndrome that need in most cases a supplementary midface advancement.
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PMID:Craniofacial surgery for craniosynostosis: functional and morphological results. 306 4

To determine the importance of intracranial hypertension in central nervous system acute infections, we studied intracranial pressure (ICP) in 27 patients, aged 45 days to 13 years. Fourteen had meningitis and 13 had encephalitis; all were in deep coma with a Glasgow Coma Scale 7 or less. Intracranial hypertension defined by a mean ICP above 15 mm Hg was observed in 12 patients with meningitis (86%) and in 9 with encephalitis (69%). Patients with meningitis exhibited a very early and severe intracranial hypertension. A striking difference is noted between survivors and non-survivors who had a very high maximal ICP with a severe reduction in cerebral perfusion pressure. Intracranial hypertension occurred in all patients with acute primitive encephalitis but only in 3/7 patients with post-infectious encephalitis. ICP monitoring seems to be important in the comatose forms of bacterial meningitis in the early period, herpes encephalitis and postinfectious encephalitis with severe status epilepticus.
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PMID:[Intracranial pressure in comatose meningitis and encephalitis in children]. 318 25

Thirty four patients with cryptococcal meningitis seen in the University of Malaya medical centre since 1980 were reviewed. Eleven patients had bilateral papilloedema and visual impairment but eventually survived. Seven patients had intensive aggressive measures, including shunting to reduce intracranial hypertension irrespective of ventricular size shown in CT scan, and showed substantial improvement in vision. It is concluded that papilloedema and visual failure in cryptococcal meningitis reflects raised intracranial pressure and that this should be treated vigorously.
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PMID:Intracranial hypertension causing visual failure in cryptococcus meningitis. 320 3

In some cases of dural arteriovenous malformations (dural AVMs) of the transverse-sigmoid sinuses, the presence of an occlusion or hypoplasia on the sinus contralateral to the affected side may significantly contribute to the development of intracranial hypertension. For these cases, closure of AV shunts or removal of the affected sinus may not be sufficient to improve intracranial hypertension. We encountered 2 cases of intracranial hypertension caused by dural AVMs at the transverse-sigmoid sinuses associated with disturbance of venous outflow contralateral to the lesion. Reconstruction of venous outflow using a saphenous vein graft was performed between the transverse sinus and the subclavian or external jugular vein after the dural AVMs were partially occluded by catheter embolization. Intracranial hypertension was relieved in both cases. In one case dural AVM was obstructed by both embolization and radical surgery after the bypass was confirmed unobstructed several weeks later. The bypass remained patent at the follow-up 4 months later. In the other case, patency of the bypass lasted only for approximately 1 month. In both cases clinical improvements were not remarkable. It is considered that the presence of AV shunt in the case of dural AVM may facilitate the patency of a graft placed between the venous systems. Reconstruction of the venous outflow may deserve further trial for the treatment of intracranial hypertension associated with some types of dural AVM.
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PMID:[Reconstruction of the venous outflow using a vein graft in dural arteriovenous malformation associated with sinus occlusion]. 321 Dec 76

To determinate the importance of intracranial hypertension in central nervous system (CNS) acute infections, we studied intracranial pressure (ICP) in 27 patients, age 45 days to 13 years. Fourteen had meningitis and 13 had encephalitis; all were in deep coma with Glasgow Coma Scale 7 or less. Intracranial hypertension defined by a mean ICP above 15 mmHg, was observed in 12 patients with meningitis (86%) and in 9 with encephalitis (69%). Patients with meningitis exhibited a sudden and severe intracranial hypertension. A striking difference was noted between survivors and non survivors who had a very high maximal ICP with a severe reduction of cerebral perfusion pressure (CPP). Intracranial hypertension occurred in all patients with acute primary encephalitis but in only 3/7 patients with post-infectious encephalitis. ICP monitoring seems to be important in the comatose forms of: (1) bacterial meningitis in the early period (2) herpes encephalitis (3) post-infectious encephalitis with severe status epilepticus.
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PMID:Intracranial pressure in childhood central nervous system infections. 322 Oct 7

The cerebrospinal fluid (CSF) concentrations of arginine vasopressin (AVP) and oxytocin (OT) were investigated both in patients with benign intracranial hypertension and in age and sex matched controls. Twenty eight lumbar punctures were performed on 15 patients with benign intracranial hypertension as part of their routine investigation and therapy. All patients had raised intracranial pressure (27.4, SE 1.7 cm.CSF). CSF AVP levels were significantly elevated in benign intracranial hypertension (2.1, SE 0.3 pmol/l) compared with controls (0.7, SE 0.1 pmol/l, p less than 0.001) but CSF OT concentrations were similar in both groups. CSF osmolality and plasma AVP and osmolality were identical in patients and controls. There was no correlation between CSF AVP concentration and intracranial pressure. The selective elevation of AVP in CSF may be of importance in the pathogenesis of raised intracranial pressure in benign intracranial hypertension.
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PMID:Cerebrospinal fluid neurohypophysial peptides in benign intracranial hypertension. 322 Dec 20

Intracranial hypertension is a dangerous condition and is common in patients suffering from a severe head injury or from a variety of pathological problems. Measurement of intracranial pressure (ICP) is considered by many to be a valuable aid in the management of such patients. Despite the invasive nature of the more widely-used measurement techniques, and hence their associated risks, results from many centres have convincingly shown that ICP measurement enables management of intracranial hypertension to be rationally approached, and a direct measure of the progress and outcome of treatment to be obtained. This paper begins with a description of normal cerebrospinal fluid (c.s.f.) pressure. This is followed by an account of the pressure-volume relationship of the intracranial system, and the control mechanisms that regulate the ICP during limited increases in mass volume within the cranium. The consequences of these for patient management are discussed. Reasons why ICP is monitored, and the benefits arising, are described. The paper then concentrates upon the methods of measuring ICP and discusses their relative merits and limitations. A selection of typical pressure sensors is described. Finally, methods that have been devised to monitor ICP and to anticipate intracranial hypertension are reviewed, and the direction of work in this area is assessed.
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PMID:Intracranial pressure: a review of clinical problems, measurement techniques and monitoring methods. 354 97

Twenty-three infants suffering the effects of moderate or severe hypoxic-ischaemic encephalopathy were continuously monitored for intracranial pressure (ICP) by means of a subarachnoid catheter for a total of 1083 hours. Cerebral perfusion pressure (CPP) was also continuously monitored for 21 of the infants. The median age at the start of ICP monitoring was 17 hours, and the opening pressure correlated poorly with maximum sustained pressures. Maximum sustained ICP allowed the infants to be divided into three groups: (1) those with no elevation of ICP (nine), of whom two died and five had a normal outcome; (2) those with sustained rises in ICP which were resistent to treatment (nine), of whom seven died and two survivors are severely handicapped; and (3) those in whom the pressure was elevated but could be controlled medically (five), of whom two survived to be quite normal. No infant with a sustained elevation of ICP of 15mmHg or more survived to be normal, nor any who had had a CPP below 20mmHg for one hour or more. Hypotension was the cause of low CPP in most cases. There was a highly significant correlation between sustained elevation of ICP above 10mmHg and poor outcome, but no correlation between outcome and minimum CPP. It was not possible to predict clinically which infants would develop intracranial hypertension, and some infants with very severe perinatal asphyxia did not develop intracranial hypertension, and some infants with very severe perinatal asphyxia did not develop raised intracranial pressure at any time.
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PMID:Value of intracranial pressure monitoring of asphyxiated newborn infants. 359 67

Neuropsychological outcome within 1 year after severe head injury was examined in 42 conscious survivors and correlated with acute measurements of cerebral blood flow (CBF) and intracranial pressure (ICP). During acute coma, CBF was elevated in 23 patients, indicating hyperemia, and was reduced in the remaining 19 cases. Intracranial hypertension (ICP 20 mm Hg or greater) was present acutely in 15 patients and absent in 27. Occurrences of hyperemia and intracranial hypertension were significantly related. During chronic recovery, neuropsychological dysfunction was found in all cases. However, patients with hyperemia revealed greater impairment of overall intellectual and memory functions than did those with reduced flow, while patients with intracranial hypertension showed greater memory deficit than did those without ICP elevations. The results suggest that early pathophysiological events can influence subsequent neuropsychological outcome, and that chronic recovery is not homogeneous in young severely head-injured adults.
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PMID:Relationship of acute CBF and ICP findings to neuropsychological outcome in severe head injury. 377 50


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