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)

The causes of death and neurological sequelae in African children with cerebral malaria are obscure. Intracranial pressure (ICP) was monitored and cerebral perfusion pressure (CPP) calculated in 23 Kenyan children with cerebral malaria. Four children had severe intracranial hypertension (ICP > 40 mm Hg, CPP < 40 mm Hg): two died, one with an ICP of 158 mm Hg and signs of transtentorial herniation, the other one with an ICP of 42 mm Hg and cardiorespiratory arrest. The other two survived with severe neurological sequelae. Nine had intermediate intracranial hypertension (ICP > 20 mm Hg, CPP < 50 mm Hg) and 10 had mild intracranial hypertension (maximum ICP 10-20 mm Hg); all survived without severe sequelae. Mannitol controlled the ICP in children with intermediate intracranial hypertension, but it did not prevent the development of intractable intracranial hypertension in children with severe intracranial hypertension. Intracranial hypertension is a feature of Kenyan children with cerebral malaria and severe intracranial hypertension is associated with a poor outcome.
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PMID:Intracranial hypertension in Africans with cerebral malaria. 913 62

An 11-year-old girl developed signs of intracranial hypertension after status epilepticus with convulsive movements of her right upper limb. Computerized tomography revealed left hemispheric hypodensity with mass effect, attributed to vasogenic edema. Intracranial hypertension was controlled under intracranial pressure monitoring and clinical status slowly improved. The patient was aphasic and right hemiplegic when she recovered consciousness but she remarkably recovered from her neurological deficits during the following two years despite neuroradiological evolution demonstrating extensive destruction of the left cortex and white matter. Two positron emission tomography (PET) scans were performed respectively six weeks and eight months after status epilepticus, and both demonstrated profound left hemispheric hypometabolism except in the lenticular nucleus and a restricted area of motor/premotor cortex. On the other hand, glucose metabolism in the right hemisphere was heterogeneously increased on the second PET when compared with the first PET. We concluded that, in this case, clinical recovery might have implicated functional reorganization arising from the intact hemisphere.
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PMID:[Cerebral lesions following convulsive partial status epilepticus. Clinical, neuroradiologic and PET study of a case]. 919 Mar 70

Raised intracranial pressure leads to increased pressure around the optic nerve (ON), which underlies the formation of papilledema and the enlargement of the dural optic nerve sheath (ONS). In clinical practice, the presence of widened ONSs is demonstrable on neuroimaging, but their relationship to cerebrospinal fluid (CSF) pressure remains unknown. The authors investigated the ONS response to pressure during CSF absorption studies in 12 patients undergoing neurological testing. The ONS diameter was evaluated by serial B-mode ultrasound scans of the anterior ON near its entry into the globe. All patients tested showed ONS diameter changes that exhibited covariance with the alteration of lumbar CSF pressure and were completely reversible during the infusion tests. The maximum difference in ONS diameter between baseline and peak pressure conditions was 1.8 mm on average (range 0.7-3.1 mm), corresponding to an average ONS diameter variation of 45% (range 15-89%). Regression analysis yielded a linear covariance between ONS diameter and CSF pressure with different slopes across subjects (0.019-0.071 mm/mm Hg, mean r = 0.78). However, this linear relationship was only present within a CSF pressure interval. This interval differed between patients: ONS dilation commenced at pressure thresholds between 15 mm Hg and 30 mm Hg and in some patients saturation of the response (constant ONS diameter) occurred between 30 mm Hg and 40 mm Hg. With a single exception, definitely enlarged ONS diameters (> 5 mm) were present when CSF pressure exceeded levels of 30 mm Hg. Retrospectively, discrimination between normal and elevated outflow resistance was possible on the basis of the ONS response to intrathecal infusion alone. It is concluded that the human ONS has sufficient elasticity to allow a detectable dilation in response to intracranial hypertension. Because of a variable pressure-diameter relationship, the subarachnoid pressure cannot be predicted exactly by single scans. Therefore, the clinical relevance of this method relies on the demonstration of pathologically enlarged sheaths or ongoing enlargement on serial ultrasonography studies.
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PMID:Validation of the optic nerve sheath response to changing cerebrospinal fluid pressure: ultrasound findings during intrathecal infusion tests. 920 62

Intracranial hypertension with papilledema has been reported in renal patients, but a survey of the literature suggests that the incidence rate is low. We present reports of 15 of approximately 1,670 patients with renal disorders, who were treated with growth hormone for impaired growth and subsequently developed symptoms and/or signs of intracranial hypertension. The male:female ratio was 6.5:1, and the median age was 12 years. The median duration of growth hormone treatment before onset of symptoms or signs was 13 weeks. All but 2 patients were symptomatic. In the patients in whom growth hormone therapy is known to have been discontinued, the symptoms and signs of intracranial hypertension abated. At least 4 of these patients experienced a recurrence when re-exposed to growth hormone. Many of the affected patients presented with predisposing conditions, but growth hormone appears to have been the precipitating factor. Prospective funduscopic evaluation may be warranted in patients with renal disorders who are receiving growth hormone.
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PMID:Papilledema in 15 renally compromised patients treated with growth hormone. 926 Feb 44

Stereotactic aspiration is well known for its simplicity and safety in the surgical treatment of hypertensive intracerebral hemorrhage. Postoperative fibrinolytic infusion with urokinase or recombinant tissue plasminogen activator and drainage of liquified hematoma are often used to improve the removal of hematoma. We evaluated the safety and effectiveness of streptokinase in this treatment modality in patients with hypertensive intracerebral hemorrhage or cerebellar hemorrhage. Twelve patients with hypertensive intracerebral hemorrhage underwent stereotactic aspiration using streptokinase as a fibrinolytic agent. There were six cases of putaminal hemorrhage, three of thalamic hemorrhage, and three of cerebellar hemorrhage. All but one patient had a large hematoma and presented with intracranial hypertension. Stereotactic aspiration was undertaken to remove the hematoma. Postoperatively, streptokinase was infused into the residual hematoma every 6 to 12 hours via a catheter implanted during the operation. Liquified hematoma was aspirated by syringe manually just before each infusion of streptokinase. The average duration of the entire treatment was 6 days (range 1-7). The residual hematoma at the end of treatment was less than 10 mL in all patients. Intracranial hypertension also subsided significantly in all patients. Only one patient had aspiration-induced bleeding during the operation. We conclude that stereotactic aspiration of hypertensive intracerebral hemorrhage is relatively safe and simple. Streptokinase can be infused intracerebrally to drain residual hematoma without severe side-effects.
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PMID:Combined use of stereotactic aspiration and intracerebral streptokinase infusion in the surgical treatment of hypertensive intracerebral hemorrhage. 944 15

Remodelling the cranial vault in an attempt to increase the intracranial volume and thus control intracranial hypertension, whilst at the same time improving the patient's appearance, has been the mainstay of surgery for syndromic craniosynostosis. We report a case of craniosynostosis in whom cranial vault expansion was followed by the development of hind-brain herniation and hydrocephalus. This prompted a review of our other cases of craniosynostosis who had been evaluated by magnetic resonance imaging following surgery in order to assess the frequency of hind-brain herniation and hydrocephalus in these children. Magnetic resonance imaging had been performed in the postoperative evaluation of 34 cases of craniosynostosis who had undergone procedures intended to increase the intracranial volume. The position of the cerebellar tonsils and the presence or otherwise of hydrocephalus was recorded for all cases. The effectiveness of surgery in treating raised intracranial pressure (ICP) was evaluated by means of postoperative ICP monitoring and had been performed in 22 cases. Herniation of the hind-brain below the level of the foramen magnum was observed in 18 cases (53%). Hydrocephalus, requiring the insertion of a ventriculoperitoneal shunt, was present in 14 cases (41%) and had developed after the cranial vault procedure in 9. The mean sleeping ICP measured postoperatively was normal (<10 mm Hg) in 5, borderline (10-15) in 7, and raised (>15 mm Hg) in 10 cases. Cranial vault expansion in complex craniosynostosis may fail to address the underlying aetiology of intracranial hypertension. Furthermore, both hydrocephalus and hind-brain herniation may develop following such surgery. Neither the increase in intracranial volume afforded by cranial vault expansion nor the shunting of hydrocephalus precludes the persistence of abnormal ICP. These findings are discussed in the light of possible mechanisms, in addition to cephalocranial disproportion responsible for intracranial hypertension in complex craniosynostosis. The implications for the surgical management of complex craniosynostosis are reviewed.
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PMID:Consequences of cranial vault expansion surgery for craniosynostosis. 948 57

A series of 72 severely head injured patients are reported, 24 (33%) with surgical intracranial hematomas. All patients were intensively cared for under the same therapeutic regime; intracranial pressure (ICP) was monitored and treated if increased. The series mortality was 39%. Uncontrollable increase of ICP (UI-ICP), always fatal, was observed in 18% of patients and in 13 of 28 deaths (46%); the incidence of UI-ICP among deaths was higher in patients less than in those more than 40 years old (55% vs 25%). Patients with UI-ICP were frequently deeply comatose and with arterial hypotension on admission; almost all died in the first days. Patients directly admitted from the scene with well staffed Life Flight Helicopter Emergency Care compared with those directly admitted from the scene with different type of ambulance service (paramedics, police, firemen and private) had a mortality rate significantly less (20% vs 54%) and an incidence of UI-ICP strongly lower both among patients (5% vs 29%) and among deaths (25% vs 54%). Thus in this small series intensive care after admission was not effective to obtain good results if patients had received poor preadmission emergency care. Review of the literature on main clinical predictors of outcome in severe head injury, have made possible some observations. Ischemic and intracranial hypertension brain lesions were generally present in patients killed by head trauma; while diffuse axonal injury, frequently responsible for vegetative, severe disability survival and late deaths, was observed only in 20-30% of postmortem examinations. Old age, poor neurological status and cardiocirculatory and respiratory disturbances prior to and upon admission positively worsened the outcome, while intracranial hematomas had a more variable predictive value. Intracranial hypertension was a definitively ominous predictor only if very high when the risk to be or become uncontrollable seems to be much elevated. UI-ICP, often fatal despite any aggressive therapy, was the single most frequent killer after severe head injury, responsible for about half of all deaths after admission. The different outcome among severe head injury series could be conceivably related to a different frequency of UI-ICP. Besides the severity of head injury and delay and mode of admission, we suggest that preadmission respiratory and cardiocirculatory and the quality of emergency medical system could strongly affect the incidence of uncontrollable increase of ICP in admitted patients and thus the mortality rate and favorable recovery of the series. The advanced preadmission emergency care service with intensive care after admission could significantly explain the better results often observed in severe head injury series.
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PMID:Severe head trauma. Review of the factors influencing the prognosis. 955 61

The present series of experiments was performed to investigate the influence of acute intracranial hypertension on the upper limit (UL) of cerebral blood flow (CBF) autoregulation. Three groups of eight rats each--one with normal intracranial pressure (ICP) (2 mmHg), one with ICP = 30 mmHg, and one with ICP = 50 mmHg--were investigated. Intracranial hypertension was maintained by continuous infusion of lactated Ringer's solution into the cisterna magna, where the pressure was used as ICP. Cerebral perfusion pressure (CPP), calculated as mean arterial blood pressure (MABP)-ICP, was increased stepwise by continuous intravenous infusion of norepinephrine. CBF was calculated by the intracarotid 133Xe method. In all three groups the corresponding CBF/CPP curve included a plateau where CBF was independent of changes in CPP, showing intact autoregulation. At normal ICP the UL was found at a CPP of 141 +/-2 mmHg, at ICP = 30 mmHg the UL was 103+/-5 mmHg, and at ICP = 50 mmHg the UL was found at 88+/-7 mmHg. This shift of the UL was more pronounced than the shift of the lower limit (LL) of the CBF autoregulation found previously. We conclude that intracranial hypertension is followed by both a shift toward lower CPP values and a narrowing of the autoregulated interval between the LL and the UL.
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PMID:The upper limit of cerebral blood flow autoregulation in acute intracranial hypertension. 955 69

The visual function of 35 patients with a diagnosis of idiopathic intracranial hypertension was assessed prospectively over a 3 year period. In assessing the visual function of cases of idiopathic intracranial hypertension a number of tests were employed including visual field assessment with Humphrey and Goldmann perimeters and documentation of visual acuity and contrast sensitivity. Loss of visual function is the only serious complication and may occur early or late in the course of the condition. An appropriate and sensitive clinical assessment regime is therefore of importance in the outpatient situation. Visual field assessment was documented as the most sensitive to detection of visual loss, with statistically greater sensitivity in comparison with visual acuity and contrast sensitivity testing. Detection of asymptomatic visual loss indicates the necessity for visual monitoring to ensure detection of insidious visual loss. The types of visual field defects noted in this study were typical of anterior optic nerve pathology of raised intracranial pressure and commonly included arcuate defects, nasal steps and global constriction. Visual loss was noted at presentation and during follow-up in up to 87% of patients using Goldmann perimetry and up to 82% of patients using Humphrey perimetry. The visual status improved significantly throughout the follow-up period and the final visual outcome was excellent or good in 83% of patients.
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PMID:Assessment of visual function in idiopathic intracranial hypertension: a prospective study. 961 26

Intracranial hypertension is a serious consequence of the impaired intracranial volume homeostasis. It can be encountered in practically all fields of clinical praxis. The article reviews bibliographic data of the mechanisms of the intracranial hypertension development: Intracranial expansion, Brain edema, Hemodynamic brain edema, Liquor accumulation--hydrocephalus. A pathophysiological approach to the hypotheses of edema and brain swelling is stressed. Outlines of the modern diagnostics and therapy of the intracranial hypertension are presented.
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PMID:[Intracranial hypertension]. 965 Apr 17


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