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)

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

We present the clinical and pathologic findings in an atypical case of idiopathic intracranial hypertension. A 51-year-old man had headaches, visual deterioration, papilloedema, and deafness. Neuroimaging was normal, and cerebrospinal fluid pressure monitoring confirmed increased intracranial pressure. The patient was treated with a ventriculo-peritoneal shunt. Histopathology revealed grossly atrophic optic nerves with almost complete axonal loss. The prelaminar portion of the optic nerves was thickened by gliosis and hyalinized capillaries, which have not been described previously.
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PMID:Idiopathic intracranial hypertension: a case report with optic nerve histopathology. 1049 48

A morphological study, macro and microscopical, was made of brain lesions in 120 victims of fatal road traffic accidents. Burst lobes were identified in 12 (10.0%) of the patients. It occurred in the frontal lobe in 6 (50.0%) patients, in the temporal lobe in 2 (16.7%) and in both lobes in 4 (33.3%) patients. A skull fracture occurred in 8 (66.7%) patients and intracranial hypertension occurred in half of cases. Nine patients were admitted in coma and three patients died immediately after the road traffic accident. All cases of burst lobes were associated with diffuse axonal injury, which explains the severe alteration of consciousness observed at the patients' admission.
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PMID:[Burst lobe in victims of fatal road traffic accident. Frequency and association with other head injury]. 1068 88

In order to study the pathophysiology and the intracranial hemodynamics of traumatic brain injury, we have developed a modified closed-head injury model of impact-acceleration that expresses several features of severe head injury in humans, including acute and long-lasting intracranial hypertension, diffuse axonal injury, neuronal necrosis, bleeding, and edema. In view of the clinical relevance of impaired autoregulation of cerebral blood flow after traumatic brain injury, and aiming at further characterization of the model, we investigated the autoregulation efficiency 24 h after experimental closed-head injury. Cortical blood flow was continuously monitored with a laser-Doppler flowmeter, and the mean arterial blood pressure was progressively decreased by controlled hemorrhage. Relative laser-Doppler flow was plotted against the corresponding mean arterial blood pressure, and a two-line segmented model was applied to determine the break point and slopes of the autoregulation curves. The slope of the curve at the right hand of the break point was significantly increased in the closed head injury group (0.751 +/- 0.966%/mm Hg versus -0.104 +/- 0.425%/mm Hg,p = 0.028). The break point tended towards higher values in the closed head injury group (62.2 +/- 20.8 mm Hg versus 46.9 +/- 12.7 mm Hg; mean +/- SD, p = 0.198). It is concluded that cerebral autoregulation in this modified closed head injury model is impaired 24 h after traumatic brain injury. This finding, in addition to other characteristic features of severe head injury established earlier in this model, significantly contributes to its clinical relevance.
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PMID:Impaired autoregulation of cerebral blood flow in an experimental model of traumatic brain injury. 1097 43

Neurofilaments (NFP) are components of neuronal cytoskeleton involved primarily in axonal transport and in the regulation of dynamic activities of nerve cells. NFP consist of three subunits denominated high- (200 kDa, NFP-H), intermediate- (160 kDa, NFP-I), and low-molecular weight (68 kDa, NFP-L) neurofilament proteins. Their function and polymerization depends on phosphorylation status, and is regulated by Ca2+ influx. Ca2+ overload enhances degradation of NFP and may compromise axonal transport. An increased susceptibility to ischemia occurs in hypertension, which is also a cause of brain damage. In this study, the expression of phosphorylated NFP (P-NFP) was investigated in the brain of spontaneously hypertensive rats (SHR) using immunohistochemical techniques with antibodies against the phosphorylated epitope of NFP RT-97. Microanatomical analysis included frontal cortex, occipital cortex, hippocampus and cerebellar cortex. The effect of long-term treatment with the dihydropyridine-type Ca2+ antagonist nicardipine on the expression of P-NFP was investigated as well. In hypertension a decreased P-NFP immunoreactivity was observed in frontal and occipital cortex, in the CA1 subfield of hippocampus and in the dentate gyrus, but not in the CA3 subfield of hippocampus or in the cerebellar cortex. Treatment with a daily dose of 3 mg/kg of nicardipine and 10 mg/kg of hydralazine significantly reduced systolic pressure in SHR. The above dose of nicardipine and to a lesser extent a non-hypotensive dose of the compound (0.1 mg/kg/day), but not hydralazine, increased P-NFP immunoreactivity in the cerebral cortex and hippocampus, except the CA3 subfield. The possibility that rescued P-NFP immunoreactivity by treatment with nicardipine depends on improved brain perfusion caused by the compound and/or by countering neuronal Ca2+ overload is discussed.
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PMID:Effect of nicardipine treatment on the expression of neurofilament 200 KDa immunoreactivity in the brain of spontaneously hypertensive rats. 1127 May 80

We report on a 10-year old previously healthy boy who exhibited a fulminant and nearly monophasic clinical course of demyelinating encephalitis with relapsing intracranial hypertension syndrome. Histologic examination of a diagnostic brain biopsy revealed an inflammatory demyelinating process with perivascular T lymphocytic infiltration and axonal damage reminiscent of multiple sclerosis-like lesions. In the brain, the DNA of human Herpes virus 6 (HHV6) was detectable. Eleven months after the initial symptoms and on maintainance with oral steroids, MRI showed demyelination of both hemispheres as well as demyelination of the brain stem and Wallerian degeneration. The boy exhibited a severe neurologic defect syndrome. The clinical and radiological course is unusual because of the asymmetric progression of the encephalitis and the extensive confluent lesions without demarcated border or enhancement of the rim after injection of gadolinium. The clinical course showed no definite steroid response. The pathogenetic relevance of HHV6 remains elusive. Although single patients with HHV6-associated encephalomyelitis have been reported, HHV6 DNA is occasionally detected in brains of healthy individuals.
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PMID:Fulminant course in a case of diffuse myelinoclastic encephalitis-- a case report. 1131 1

We report dizygotic twins who first presented at the age of 6 months with severe diaphragmatic weakness and marked abnormalities of autonomic function. A female sibling had earlier died from a disorder with similar clinical features. Both twins had a severe axonal polyneuropathy with generalized hypotonic limb weakness together with diaphragmatic paralysis resulting in respiratory failure. Associated features were tachycardia, increased sweating, elevated body temperature, and hypertension, suggesting autonomic dysfunction. Nerve conduction studies indicated an axonopathy affecting both motor and sensory nerve fibres. Sural nerve biopsy in one twin performed at the age of 7 months showed a reduced population of myelinated nerve fibres, particularly those of larger diameter, with no indication of hypomyelination, demyelination or axonal atrophy. Examples of axonal forms of hereditary motor and sensory neuropathy (HMSN) with onset in infancy are very rare and autonomic involvement associated with this condition has not so far been described.
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PMID:Inherited early onset severe axonal polyneuropathy with respiratory failure and autonomic involvement. 1136 91

To study pharmacotherapy of traumatic brain injury in rats, a modified closed head injury model was used that expresses clinically relevant features including intracranial hypertension and morphological alterations. Long-term survival under ethically acceptable conditions would greatly improve its clinical relevance. To ensure this goal with great reproducibility, the experimental protocol was adapted, in particular the impact-acceleration kinetics. Variations in impact-acceleration conditions were obtained by modifying the stiffness of the impact site and changing the height of a 400 g weight dropped from 51.5 to 31.5 cm (51.5/400; 31.5/400). Impact and acceleration were measured with a force sensor incorporated in a rigid dummy-rat and an accelerometer mounted on the platform onto which the animals are positioned. Significant correlation was shown between impact and acceleration. Accelerations obtained in rats were significantly lower than those in the dummy. Unlike the 51.5/400 group, in the 31.5/400 group no mortality or cranial fractures were observed. In both groups intracranial pressure rose to pathological values immediately after trauma and remained elevated longer than 24 h. Diffuse axonal injury developed in all groups and remained present for at least 7 days. By reducing the impact-acceleration conditions, post-traumatic complications were diminished, while the clinically important features were maintained.
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PMID:Validation of a closed head injury model for use in long-term studies. 1145 56

POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, skin disorders) is a rare multisystemic disease associated with plasma cell dyscrasia. A 68-year-old woman with chronic renal insufficiency and arterial hypertension included in her medical history was admitted to the hospital with confusion, somnolence and asthenia. She presented ascites, hepatosplenomegaly, leg oedema, distal dysesthesias, leuconychia and multiple nodular purple red angiomas on the trunk, upper limbs and fingers. Hypothyroidism was revealed in the laboratory investigations and monoclonal IgG peak in immunoelectrophoresis. Electromyography showed both demyelinisating and axonal degenerative neuropathy. The diagnosis of POEMS syndrome was based on the dermatopathological examination of a cutaneous angioma; histology revealed features of glomeruloid angioma, a specific marker of this syndrome.
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PMID:POEMS syndrome revealed by multiple glomeruloid angiomas. 1207 35

To study plasticity of central autonomic circuits that develops after spinal cord injury (SCI), we have characterized a mouse model of autonomic dysreflexia. Autonomic dysreflexia is a condition in which episodic hypertension occurs after injuries above the midthoracic segments of the spinal cord. As synaptic plasticity may be triggered by axonal degeneration, we investigated whether autonomic dysreflexia is reduced in mice when axonal degeneration is delayed after SCI. We subjected three strains of mice, Wld(S), C57BL, and 129Sv, to either spinal cord transection (SCT) or severe clip-compression injury (CCI). The Wld(S) mouse is a well-characterized mutant that exhibits delayed Wallerian degeneration. The CCI model is an injury paradigm in which significant the axonal degeneration is due to secondary events and therefore delayed relative to the time of the initial injury. We herein demonstrate that the incidence of autonomic dysreflexia is reduced in Wld(S) mice after SCT and in all mice after CCI. To determine if differences in afferent arbor sprouting could explain our observations, we assessed changes in the afferent arbor in each mouse strain after both SCT and CCI. We show that independent of the type of injury, 129Sv mice but not C57BL or Wld(S) mice demonstrated an increased small-diameter CGRP-immunoreactive afferent arbor after SCI. Our work thus suggests a role for Wallerian degeneration in the development of autonomic dysreflexia and demonstrates that the choice of mouse strain and injury model has important consequences to the generalizations that may be drawn from studies of SCI in mice.
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PMID:Autonomic dysreflexia after spinal cord transection or compression in 129Sv, C57BL, and Wallerian degeneration slow mutant mice. 1295 97


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