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

The anteroventral part of the hypothalamus adjacent to the third ventricle (AV3V) has been implicated in electrolytic lesion studies as a site crucial to the development and maintenance of hypertension. Cryoblockade is known to alter synaptic and axonal transmission differently at different temperatures. In this study, cooling of the hypothalamus, including the AV3V area, to the temperature known to block only synaptic function did not alter blood pressure in two different models of experimental hypertension in the rat. Cooling sufficient to block both synaptic and axonal transmission, however, reduced blood pressure elevations to near normotensive levels. Synaptic cryoblockade in the ventromedial portion of the frontal cortex lowered experimental hypertension by 21 +/- 3 mm Hg (p less than 0.05). In normotensive controls, blood pressure was not altered by cryoblockade in either the frontal cortex or hypothalamus. Anatomical evidence provided by others shows that cells in the ventromedial frontal cortex project, in part, through the AV3V region to the brainstem cardioregulatory structures. These results indicate that neural activity arising in frontal cortex is axonally projected through the hypothalamus to maintain elevated blood pressure in experimental hypertension.
Hypertension 1987 Jun
PMID:Cryoblockade of the ventromedial frontal cortex reverses hypertension in the rat. 358

A 52-year-old woman presented with increasing pain, weakness, and paraesthesiae of four months' duration in the lower limbs. She suffered from chronic obstructive airways disease and hypertension. Neurological examination revealed wasting of the quadriceps muscles, weakness of the lower limbs, and absent ankle jerks. The sensory examination was normal. Full blood count, ESR, biochemical, immunological, and viral studies, urinary heavy metal assays, and cerebrospinal fluid examination were normal. Nerve conduction studies were consistent with a sensorimotor neuropathy, and electromyographic sampling was consistent with acute denervation. A sural nerve biopsy showed axonal degeneration and segmental demyelination. One month after admission, she developed carbon dioxide retention. Her weakness spread to affect the upper limbs, and she could not be resuscitated after a cardiac arrest three months after admission. General autopsy examination revealed bronchopneumonia. Neuropathological examination showed a lymphocytic infiltrate in the nerve roots of the cauda equina, the lumbosacral plexus, and the sural and vagal nerves. Increased cellularity and collagen were evident in these nerves. A diagnosis of chronic inflammatory polyneuropathy was made. The neuropathology of this entity is discussed.
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PMID:Neuropathological findings in a case of chronic inflammatory polyneuropathy. 384 15

Accelerated renovascular hypertension produces optic nerve changes ranging from optic disc edema to optic atrophy. To elucidate the pathogenesis of hypertensive optic neuropathy, the optic nerves from 12 monkeys (23 eyes) with accelerated renovascular systemic hypertension were studied by electron and light microscopy. Within 21 months, the animals demonstrated the entire spectrum of pathologic changes. In the optic nerves with optic disc edema, the prelaminar optic nerve exhibited vasoconstriction with subsequent axonal hydropic swelling, axolemma disruption, and glial swelling. In retrolaminar myelinated optic nerve, vasoconstriction was more severe, with endothelial swelling and pericytic degeneration resulting in intramyelinic vacuoles and glial swelling. Optic disc edema appeared to result from axonal hydropic swelling secondary to ischemic infarct, followed by loss of axons and gliosis in the prelaminar optic nerve. The retrolaminar myelinated nerve showed prominent microglial reaction and eventual atrophy of axons and glia. Ischemia seemed to play a major role in hypertensive optic neuropathy, which represents anterior ischemic optic neuropathy.
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PMID:Fundus lesions in malignant hypertension. II. A pathologic study of experimental hypertensive optic neuropathy. 402 51

The transmitter depletion of the myocardium in hypertrophy and especially insufficiency has formerly been attributed to a decrease of certain enzymes that are involved in the neurotransmitter synthesis. However, we could show in human auricles recently that one main reason for the catecholamine depletion is the distension of the adrenergic ground plexus in the course of hypertrophy of the myocardial muscle cells. At the same time, electron microscope investigations revealed various changes of the axonal ultrastructure, especially in heart insufficiency. Additional experimental work in renal hypertension of rats should answer the question whether this process occurs also in other parts of the heart and whether it can be followed sequentially during the development of hypertension. In this preliminary report about these studies, attention is drawn to focal transmitter depletion in areas of severe vascular necrosis and inflammation, especially in the right ventricular wall. During the first three months after the beginning of the experiment, the total noradrenaline content decreased only slightly, whereas the concentration of this transmitter is lowered significantly by myocardial growth in both ventricles. It is concluded that there are essential differences between hypertrophy in experimental renal hypertension and human cardiac hypertrophy.
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PMID:Differences between transmitter depletion in human heart hypertrophy and experimental cardiac hypertrophy in Goldblatt rats. 610 85

A 32-year-old obese woman with hypertension and a three-year history of pseudotumor cerebri developed bilateral juxtapapillary subretinal neovascular membranes. To our knowledge, this is the first reported case of bilateral subretinal neovascular membranes complicating the course of this disease. The subretinal neovascular membrane in the left eye spontaneously involuted, but because the membrane in the right eye threatened the foveola, the patient underwent argon-laser photocoagulation. The subretinal fluid and hemorrhage progressively resolved, the membrane was replaced by fibrous tissue, and visual acuity improved. The pathogenesis of the subretinal neovascular membranes was presumably secondary to pressure deformity of the border of Bruch's membrane at the optic disk, creating a discontinuity of normal anatomic apposition of the chorioretinal layers. This anatomic dehiscence, coupled with hypoxia created by axonal tissue swelling and resultant impaired vascular perfusion of the tissues, led to the development of subretinal neovascular membranes.
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PMID:Bilateral juxtapapillary subretinal neovascularization associated with pseudotumor cerebri. 616 60

Central catecholamine (CA) neurons in the nucleus tractus solitarius (NTS) and paraventricular hypothalamic nucleus (PVN) were studied in Wistar rats that had been unilaterally nephrectomized. The experimental animals were then treated with deoxycorticosterone acetate (DOCA) and salt water. The control animals were treated with the vehicle and tap water. Blood pressure of animals 4 weeks after DOCA/salt treatment was significantly elevated when compared to control rats. Morphologically, CA terminals showed no noticeable changes in the DOCA/salt hypertensive rats. Furthermore, the density of CA terminals either in the NTS or in the PVN of the DOCA/salt hypertensive rats was not statistically different from that of normotensive controls, suggesting that salt does not cause lesions or destruction of CA terminals. However, an extensive electron-microscopic morphometric analysis indicated that there was an enhancement of CA synaptogenesis (expressed by increased synaptic frequency among all CA boutons labeled with 5-hydroxydopamine) in the PVN, but not in the NTS of DOCA/salt hypertensive rats. In addition, the high-performance liquid chromatography revealed decreased CA contents in the PVN, but not in the NTS, of DOCA/salt hypertensive animals. Since synapses are primary sites for neurotransmitter release, the above results collectively suggest that more CA synapses formed in the PVN may reflect a net CA release from CA terminals resulting in the decreased CA content in the axonal terminals. Such an increased CA release and enhanced CA synaptogenesis may consequently enhance CA function in the PVN of hypertensive rats 4 weeks after DOCA/salt treatment, and relate to the development and/or maintenance of hypertension in the DOCA/salt rats.
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PMID:Catecholamine synapses and contents in the paraventricular hypothalamic nucleus and nucleus tractus solitarius of DOCA-salt hypertensive rats. 647 21

Nine children treated for acute leukemia or lymphosarcoma developed subacute encephalopathy starting with listlessness, depression and impairment of speech. Walking difficulties, ataxia, spasticity and sphincter disorders developed later. Transient intracranial hypertension and abnormal movements respectively developed in two patients. EEG frontal slow waves, raised CSF protein, abnormal white matter radioisotope uptake and CT scan hypodensity with patchy contrast enhancement were evident at the onset. Later, dilated ventricles and calcification appeared in the younger patients. Post-mortem neuropathological studies of three patients disclosed predominantly perivascular myelin loss in areas of white matter necrosis, abnormalities of small vessels and numerous axonal swellings. The spinal cord showed secondary degeneration of the corticospinal tracts. Analysis of the aetiological factors in this series points to the prevailing danger of cranial radiotherapy, probably increased by the young age of patients and by associated drug administration.
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PMID:Necrotising leukoencephalopathy complicating treatment of childhood leukaemia. 669 15

In the past few years, considerable progress has been made in describing patients with head injuries in such a manner that comparisons in morbidity and mortality can be made among neurosurgical centers according to the seriousness of the injury. Less progress had been made in classifying the type of pathology, especially by computerized tomography. The authors have introduced a classification that includes both the type and the seriousness of the injury. There appear to be two principal causes of the brian damage produced by head injury: 1) mechanical damage to neurons and their processes, especially axons and 2) ischemia. Mechanical damage produces axonal degeneration. Although central regeneration generally is quite limited, perhaps many of the axons damaged by head injury degenerate in continuity, a circumstance in which functional regeneration by axoplasmic outgrowth is much more likely to occur than in most experimental situations where the axons are physically divided. The ischemic brain damage that is so common in head injury appears to be mass lesions and brain swelling that both cause intracranial hypertension. The more the brain swells, and the higher the intracranial pressure, the more difficult it is to control the swelling and the pressure. In patients with acute subdural hematoma in particular, the brian swelling and the high mortality appear to be due to ischemic brain damage. There is recent evidence that the mortality rate in patients with acute subdural hematoma is a function of the time from injury to evacuation of the hematoma. Therefore, outcome from head injury can be improved by the earliest possible removal of space-occupying hematomas and by early, vigorous management of intracranial hypertension.
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PMID:Can the out come from head injury be improved? 705 18

A previously healthy 10-year-old girl suffered sudden, binocular visual deterioration. During the next few years her neurologic and visual condition progressively worsened and she developed hypertension, seizures, ataxia, and lactic acidemia, leading to death at the age of 16 years. Bilateral optic disk pallor was followed by the loss of the foveal reflex and pigmentary maculopathy, manifested as disorganization of the retinal layers, loss of ganglion cells, degeneration of the photoreceptors and nuclei, and irregular infiltration of the retina by pigment epithelial cells. The optic nerves and tracts showed central axonal loss. Bilateral, multifocal symmetric areas of cerebral atrophy and necrosis of the neuropil and neurons in the cerebral cortex, basal ganglia, and thalamus were observed; neurons persisted in the dorsal medulla, despite neuropil degeneration.
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PMID:Pigmentary macular degeneration with multifocal necrotizing encephalopathy. 729 3

Multiple Sclerosis (MS) cases found at autopsy in patients who had died from other diseases and in whom no sign or symptom could be related to MS are called "asymptomatic". Three cases are reported. The first patient was a 62 year old man who presented with a slowly progressive disturbance of gait, incontinence and deterioration of intellectual function. A falx meningioma was surgically removed. The patient died 3 years later with an acute respiratory illness. Examination of the brain disclosed evidence of the operation and numerous old plaques disseminated through the cerebral hemispheres (centrum semi-ovale, periventricular regions, internal thalamus and junction between cortex and white matter) and in the brain stem. The second case, a 77 year old woman with diabetes mellitus and hypertension, presented with cortical blindness and disturbances of memory of acute onset. She died one year later. Examination of the brain showed multiple infarcts involving the territories of both posterior cerebral arteries and the left middle cerebral artery. Numerous old plaques were seen in the periventricular regions, in the corpus callosum and in the left middle cerebellar peduncle. The third case, a 60 year old woman with mitral and aortic stenosis, presented with cortical deafness and transient right hemiparesis. She died 5 years later. Brain examination showed infarcts involving both middle cerebral artery territories. There was also many old plaques in the periventricular areas, thalamus, internal capsule, centrum semi-ovale, brain stem and right nucleus dentatus. In the 3 cases, the optic tracts were normal. The spinal cord, examined only in the first case, was also normal. The asymptomatic character of these MS cases can be explained first by the location of the plaques and the lack of spinal cord and optic tract involvement. It could also be due to the small size of the plaques and to axonal preservation. Such features are rare since our 3 observations have been selected from a pathological collection of 125 MS cases and 9,300 general neuropathological records. Six other cases have been previously reported by other authors.
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PMID:[Asymptomatic multiple sclerosis - 3 cases (author's transl)]. 733 73


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