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

After a stroke, recovery that continues beyond 3 or 4 weeks has been attributed to plasticity, a reorganization of the brain in which functions previously performed by the ischemic area are assumed by other ipsilateral or contralateral brain areas. Neuronal plasticity has been variously attributed to redundancy (parallel distributed pathways), changes in synaptic strength, axonal sprouting with formation of new synapses, assumption of function by contralateral homologous cortex, and substitution of uncrossed pathways. Transcranial magnetic stimulation, positron emission tomography (PET), functional magnetic resonance imaging (fMRI), and 128-electrode high-resolution electroencephalography have been successfully applied to demonstrate cortical reorganization after hemiplegia. Recording the motor potential is a promising noninvasive method for the localization of motor control after hemispheric lesions. Most patients with hemiparetic stroke show some improvement, usually during the first 3 to 6 months after the ictus. Improvement and prognosis depend on a number of variables including volume and location of the infarction, age of the patient, and the elimination of risk factors to avoid future episodes (i.e., dietary control of lipids, the elimination of tobacco, and the control of diabetes and hypertension). Currently, emphasis has been placed on fibrinolytic treatment in the first 3 hours to prevent or minimize neurological deficit. Aside from the above listed factors, improvement after stroke may be due to reorganization of the brain, particularly the cerebral cortex, and repair of damaged tissue and recanalization. It is also important to relate such changes to functional improvement and successful rehabilitation.
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PMID:Brain reorganization after stroke. 1468 16

According to a recent epidemiological study done in Japan, 2 or 3 million Japanese people are thought to be suffering from glaucoma, and 70-80% of them have not been examined or diagnosed by ophthalmologists. Therefore, the problem is how to find these untreated and undiagnosed people. At present, treatment of glaucoma continues to be directed at lowering intraocular pressure to prevent progression of glaucomatous optic neuropathy. However, theoretically, there are three stages in the prevention of progression of glaucoma. In the first stage, diagnosis of glaucoma can be done by genetic examination, before occurrence of glaucoma. The MYOCILIN/trabecular meshwork-inducible glucocorticoid response gene and the optineurin gene were identified as the genes that cause open angle glaucoma. Although some Japanese patients have sequence changes in the myocilin gene, there are no apparent specific mutations in Japanese glaucoma patients, in the MYOCILIN/TIGR and optineurin genes. Secondary glaucoma such as steroid glaucoma, induced by allergic diseases, and neovascular glaucoma, induced by retinal circulatory insufficiency, are preventable by improving the causal diseases, diabetes and hypertension. The education of doctors and laymen is important to reduce the occurrence of diabetes, and hypertension to prevent diabetic retinopathy, and retinal vessel occlusion. The second stage in preventing progression of glaucoma is to find the disease as early as possible. In Japan, a physical examination system is in place for everybody over 40 years old, in companies and local districts. Therefore, ocular examination, specially non-mydriatic fundus photographs should be taken in these examinations, and the film should be evaluated by an ophthalmologist, to search for retinal and optic disc abnormalities. Primary open angle glaucoma can be detected through this system in early stages. In primary angle closure glaucoma, instruments for estimating anterior chamber rapidly and accurately are necessary for the diagnosis. There is a special machine which can be handled easily, safely, and economically for detecting angle closure glaucoma, has been developed by Yamanashi University. This machine might help to reduce the number of angle closure glaucoma patients in the world. In the near future, a glaucoma network system should be put in place all over Japan. This organization consists of central headquarter and local central office. Most hospitals and private offices will belong to a local central office, and several glaucoma specialists will work in central and local offices. All glaucoma patients will be registered in local glaucoma office. The information on glaucoma patients will be communicated in the system the through light fiber cables or a satellite system. The patients can ask about their own disease through this glaucoma center system. In the third stage of glaucoma prevention, progression of glaucomatous optic neuropathy is retarded by conventional IOP lowering treatment or neuroprotective drugs. This stage compromises rehabilitation of visual function, implant of artificial visual systems, and regeneration of retinal ganglion cells(RGC). The disturbances of axonal flow in guinea pig optic nerve fibers was demonstrated electromicroscopically by quick-freeze, deep-etching method and, the decrease in numbers of motor proteins like "Kinesin" "Dynein" and "MAP-1" was shown in guinea pig eyes with elevated intraocular pressure by immunohistochemistry. Retinal glanglion cells have been isolated and new findings have been reported using this RGC culture system. Therefore, new neuroprotective drugs will be developed through this culture system.
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PMID:[21st century management of glaucoma]. 1473 29

Hypertension is one of the major risk factors of stroke and vascular dementia (VaD). We used stroke prone spontaneous hypertensive rats (SPSHRs) as a model for neuronal degeneration frequently occurring in humans with vascular disease. Recently, high b value q-space diffusion-weighted imaging (DWI) was shown to be very sensitive to the pathophysiological state of the white matter. We studied the spinal cords of SPSHR rats ex vivo after the appearance of motor impairments using diffusion anisotropy and q-space diffusion imaging (measured at a high b value of up to 1 x 10(5) s/mm(2)). The diffusion anisotropy images computed from low b value data set (b(max) approximately 2500 s/mm(2)) showed a small but statistically significant decrease (approximately 12%, P < 0.05) in the diffusion anisotropy in the spinal cords of the SPSHR group as compared to control rats. However, more significant changes were found in the high b value q-space diffusion images. The q-space displacement values in the white matter of the SPSHR group were found to be higher by more than 70% (P < 0.002) than that of the control group. These observations concurred with electron microscopy (EM) that showed significant demyelination in the spinal cords of the SPSHR group. These results seem to indicate that high b value q-space DWI might be a sensitive method for following demyelination and axonal loss associated with vascular insults.
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PMID:Hypertension and neuronal degeneration in excised rat spinal cord studied by high-b value q-space diffusion magnetic resonance imaging. 1476 64

The morphology and function of sciatic nerve were investigated in spontaneously hypertensive rats (SHR), either control or hydralazine-treated, and in normotensive Wistar Kyoto rats of 6 months of age. In control SHR decreased percentages of class I fibers (20-15 microm in diameter), of axonal NFP-H 200 kDa neurofilament protein immunoreactivity and of nerve conduction velocity were found. The percentages of class III (10-5 microm in diameter) and IV (<5 microm in diameter) and of S100beta-immunoreactive Schwann cell profiles were increased. Treatment with the hypotensive drug hydralazine countered sciatic nerve changes. The shift of nerve composition vs. smaller fibers is probably the cause of reduced nerve conduction velocity found in SHR and is consistent with the occurrence of a sympathetic hyper innervation in this animal model of hypertension. Our findings support the hypothesis that arterial hypertension may represent a risk factor of neuropathy.
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PMID:Morphological and conduction changes in the sciatic nerve of spontaneously hypertensive rats. 1519 70

The effect of interferon alpha in chronic viral hepatitis and common side effects are well known, but axonal polyneuropathy and hearing loss have been rarely reported. A 58-year-old woman was administered interferon alpha-2a (9 MU/3 times a week) and lamividin (100 mg daily) with the diagnosis of chronic hepatitis B. At the fifth month of the treatment gait disturbance and tinnitus developed. In her neurological examination tandem gait was ataxic on the right side. Cerebral magnetic resonance imaging performed to elucidate a probable cerebral pathology revealed nonspecific millimetric hyperintense lesions thought to be related with her hypertension anamnesis. Electroneuromyography demonstrated mild axonal polyneuropathy. The finding of pure-tone audiometry was sensorineural hearing loss in her left ear. Our diagnosis was axonal polyneuropathy and sensorineural type hearing loss as a side effect of interferon. In conclusion, the development of polyneuropathy and sensorineural hearing loss in the same patient may suggest autoimmunity as the cause of these side effects.
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PMID:Axonal neuropathy and hearing loss associated with alpha interferon treatment in chronic hepatitis B: a case report. 1533 19

Accurate radiographic diagnosis is a cornerstone of the clinical management and outcome prediction of the head-injured patient. New technological advances, such as multi-detector computed tomography (MDCT) scanning and diffusion-weighted magnetic resonance imaging (MRI) have influenced imaging strategy. In this article we review the impact of these developments on the neuroradiological diagnosis of acute head injury. In the acute phase, multi-detector CT has supplanted plain X-ray films of the skull as the initial imaging study of choice. MRI, including fluid-attenuated inversion recovery, gradient echo T2* and diffusion-weighted sequences, is useful in determining the severity of acute brain tissue injury and may help to predict outcome. The role of MRI in showing diffuse axonal injuries is emphasized. We review the different patterns of primary and secondary extra-axial and intra-axial traumatic brain lesions and integrate new insights. Assessment of intracranial hypertension and cerebral herniation are of major clinical importance in patient management. We discuss the issue of pediatric brain trauma and stress the importance of MRI in non-accidental injury. In summary, new developments in imaging technology have advanced our understanding of the pathophysiology of brain trauma and contribute to improving the survival of patients with craniocerebral injuries.
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PMID:New developments in the neuroradiological diagnosis of craniocerebral trauma. 1569 94

Until relatively recently, depression has been considered a purely "mental" disorder and therefore in the natural domain of psychologists and psychiatrists. However, recent epidemiological studies have revealed that aging, physical and psychological stress, chronic pain, several metabolic disorders such as insulin resistance and established diabetes, alcoholism, inflammatory conditions, and vascular disorders such as arterial hypertension all may be associated with depression. The present review examines some of these depression-associated factors and the mechanisms by which they might give rise to vascular disorders such as atherosclerosis, microcirculation endothelial dysfunction, and interstitial disturbances leading to organ damage. A number of disorders involving the circulation can lead progressively and insidiously to large artery rigidity, remodeling of peripheral arteries, and alterations of the microcirculation of large blood vessels. Perturbations in vasa vasorum blood flow may contribute to atherogenesis, in addition to the influence of numerous cellular events involved in inflammation (tumor necrosis factor alpha, interleukin 1 beta, etc). Since Hans Selye first described the neuroendocrine cascade generated by experimentally induced stress half a century ago, phenomena such as the axonal release of neurotransmitters (including serotonin), accumulation of metabolites such as homocysteine, platelet-activating factor, and nitric oxide also have been implicated in the pathogenesis of depression. Moreover, vascular consequences of depression such as heart rate and pulse pressure variations may lead to endothelial dysfunction in critical microcirculation networks (cerebral, myocardial, and renal) and initiate physicochemical alterations in interstitial compartments adjacent to vital organs. The appropriate use of ambulatory monitoring of vascular parameters, such as heart rate and pulse pressure, and eventually, early identification of genetic and metabolic markers may prove helpful in the early detection of events preceding and predicting the clinical manifestations of depression.
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PMID:Depression and cardiovascular disease: a reciprocal relationship. 1587 13

Three-modality evoked potentials (EPs) have been used for several years in association with the electroencephalogram (EEG) as a diagnostic and prognostic tool in acute traumatic or nontraumatic coma. In 1993 we proposed to combine these in two indices: the index of global cortical function (IGCF) and the index of brain-stem conduction (IBSC). Four EP patterns based on both indices emerge at the acute stage of severe head trauma. These are easily explainable by pathophysiology. Pattern 1 corresponds to alterations in the index of global cortical function without changes in the index of brain-stem conduction. Its prognosis is good (80 to 90% of these patients recover). Pattern 2 is characterized by alterations of somatosensory EPs that are suggestive of midbrain dysfunction. The prognosis depends both on the reversibility of the midbrain dysfunction and on the extent of associated diffuse axonal lesions, whose evaluation requires MRI. Patients who recovered from Pattern 2 sometimes did so after a long interval during which they remained vegetative. Pattern 3 is characterized by alterations of brain-stem auditory EPs that are suggestive of pontine involvement. It usually follows uncontrolled intracranial hypertension and corresponds to evolving transtentorial herniation. All patients with that transient pattern eventually died. Pattern 4 is categorized by the disappearance of all activities of intracranial origin, contrasting with the preservation of all activities of retinal, spinal-cord, and peripheral-nerve origin. This pattern corresponds to brain death. In our experience, three-modality EPs are currently the best bedside brain-death confirmatory tool.
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PMID:Evoked potentials in severe brain injury. 1618 39

Autonomic dysreflexia is a potentially life-threatening condition in which episodic hypertension occurs after injuries above the mid-thoracic segments of the spinal cord. Despite the seriousness of this condition, little is known of the molecular mechanisms that lead to its development. The completed sequencing of the mouse genome, its dense genetic map, and the large repository of engineered and spontaneous mouse mutants, make the mouse an ideal model organism in which to study the molecular mechanisms underlying autonomic dysreflexia. We subjected two wild-type strains of mice, 129Sv and C57BL/6, and one spontaneous mouse mutant, Wallerian degeneration slow (Wld s), to spinal cord transection and clip-compression injury. We found that the incidence of autonomic dysreflexia is greatly reduced, compared to spinal cord-transected wild-type mice, in Wld s mice after both injury paradigms and in 129Sv and C57BL/6 that have undergone the clip-compression injury. We also found that the amplitude of the dysreflexic response was greater in cord-compressed 129Sv than in C57BL/6 mice. These results implicate axonal degeneration as an important source of signals that trigger the development of autonomic dysreflexia and are discussed in the context of mouse genetics, interstrain differences and possible molecular mechanisms underlying autonomic dysreflexia after spinal cord injury.
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PMID:Genetic approaches to autonomic dysreflexia. 1619 9

The term paroxysmal sympathetic storms is used to define episodic alterations in body temperature, blood pressure, heart and respiratory rate, size of pupil, and level of consciousness coinciding with hyperhidrosis, excessive salivation and extensor posturing. All the cases were presented after severe diffuse axonal head injury. We present two young patients with diffuse axonal head injury that develop in their evolution hypertension, tachycardia and fever without evidence during the episodes of epileptiform activity and without any infectious cause with excellent answer to the treatment with beta-blockers and morphine. We consider that the correct diagnosis of this entity minimizes the application of unnecessary studies allowing an appropriate treatment.
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PMID:[Paroxysmal sympathetic storm after diffuse axonal head injury]. 1713 74


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