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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the relationships between gastric change accompanying patients with acute stroke and the function of the autonomic nervous system and pituitary-adrenal system, studies on the gastroendoscopic technique and biochemical observations were done in 122 patients. The mean urinary noradrenalin and adrenalin excretions were elevated in patients with acute gastric changes, especially in patients with multiple erosions and acute ulcers. An elevation of the mean fasting serum gastrin concentration was found in patients with acute ulcers and no acute gastric changes. The mean urinary 17-OHCS excretion was increased in patients with multiple erosions, petechiae and acute ulcers. In conclusion, the sympathetic and parasympathetic nervous system and the pituitary-adrenal system have respectively different roles in the production of various types of acute gastric changes in patients.
Stroke
PMID:Acute gastric changes in patients with acute stroke. Part 2: gastroendoscopic findings and biochemical observation of urinary noradrenalin, adrenalin, 17-OHCS and serum gastrin. 96 Jan 67

A gastroendoscopic study was performed on 177 patients with acute stroke. Gastric changes were found in 92 among them (52%), including ten with acute ulcer. A high frequency of gastric changes was found in patients with serious stroke and/or in patients whose cerebral lesions were located close to the hypothalamus or its centrifugal tract. The mortality in patients with gastric changes was high, especially in patients with acute ulcers, multiple erosions and petechiae. The frequency of brown gastric juice and coffee grounds at gastroendoscopic examination (gastric hemorrhage) was three times as high as that of melena and/or hematoemesis. On the other hand, the mortality of patients with gastric hemorrhage differed little from that of patients with melena and/or hematoemesis.
Stroke
PMID:Acute gastric changes in patients with acute stroke. Part 1: with reference to gastroendoscopic findings. 108 8

We report an autopsy case of infant death due to heat stroke. On a winter day, a 52-day-old female baby was placed under a Japanese electric foot warmer with a coverlet (kotatsu) on an electric carpet warmer in a heated room at home. After about 5 h, the mother noticed that the baby was unconscious and took her to a hospital. Spontaneous respiration, however, was already absent, and the pupils were dilated. The trunk was hot; body temperature was 41.3 degrees C. The skin of the whole body was dry. Autopsy revealed second-degree burn injuries on the left side of the face and the dorsum of the left hand. Numerous marked petechiae and ecchymoses were found in the thymus (capsule and parenchyma), pleurae (visceral and parietal), pericardial cavity (internal and external surfaces), epicardium, and beneath the serosa at the origin of the aorta. In addition, there was congestion in various organs, edema in the brain and lungs, and hemorrhage in the lungs. Histopathologically, macrophages without hemosiderin granules were present in the alveoli. When the heating conditions at the accident were reproduced experimentally, the temperature in the electric kotatsu warmer rose to 50-60 degrees C. Thus, we concluded that misuse of the electric kotatsu caused heat stroke in this infant.
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PMID:An autopsy case of infant death due to heat stroke. 147 26

Male and female, spontaneously hypertensive rats (SHR) with blood pressures ranging from 190-210 mmHg were subjected unilateral or bilateral carotid artery ligation. Representative numbers of animals were killed 2, 4, 6, 8, 10, 12, 24 and 48 hours later. Severe cerebral ischemia caused a significant and protracted increase in the pre-existent high blood pressure, the enzymes CPK, SGOT and LDH triglycerides, free fatty acids, glucose, and corticosterone. Despite these marked pathophysiologic changes, the brains of these animals were free of real damage except for cerebral edema and scattered petechiae. Some of the animals developed massive atrial thrombi and myocardial infarcts. It is suggested that severe cerebral ischemia precipitated the myocardial infarcts through the aegis of the hypothalamic-pituitary-adrenal stress response.
Stroke
PMID:Comparative effects of unilateral and bilateral carotid artery ligation in the spontaneously hypertensive rat. 735 34

Multiple cerebral petechiae associated with intravascular globules of neutral fat and localized primarily within the white matter are distinctive lesions which secure the pathologic diagnosis of cerebral fat embolism. The abundance of these lesions in an unknown, but presumably small, percentage of cases of fat embolism, along with the even more widespread distribution of embolic fat droplets throughout both white and gray matter, suggest that these lesions and emboli must have a profound effect on neurologic function. Nevertheless, respiratory insufficiency is by far a more common clinical manifestation of the fat embolism syndrome and the neurologic involvement of such patients is often attributed to the secondary effects of generalized hypoxia. The following patient with overt respiratory and neurologic symptoms re-emphasizes the direct primary effect of fat emboli within the central nervous system as a cause of white matter hemorrhages and neurologic deterioration. Explantations for the selectivity of the lesions for the cerebral white matter are explored.
Stroke
PMID:Cerebral fat embolism: a neuropathological study of a microembolic state. 742 78

To obtain information about changes of basic fibroblast growth factor (bFGF) in the brain under a chronic hypertensive condition, we immunohistochemically studied the distribution and level of bFGF in the brain of stroke-prone spontaneously hypertensive rats (SHRSPs). The advanced cerebral lesions in SHRSPs demonstrated massive bleeding, cavity formation and diffuse degeneration of the white matter, whereas the early changes were petechiae, edema and massive glial accumulation around fibrin deposition containing necrotized microvessels. In the control normotensive rats, immunoreactivity for bFGF was demonstrated in nerve cells, especially in selective neuronal populations, ependymal cells and epithelial cells of the choroid plexus, while there was almost no reactivity in astrocytes. In SHRSPs, on the other hand, there was marked immunoreactivity in the densely accumulated reactive cells, particularly astrocytes, in and around cerebral cortical lesions. Slightly increased reaction for bFGF was found in the nerve cells around lesions. Astrocytes in the subcortical white matter on both ipsi- and contralateral sides of the cortical lesion also showed immunoreactivity for bFGF. The location of increased bFGF expression in SHRSPs corresponded very well with the site of extravasated plasma fluid demonstrated by anti-fibrinogen antibody. Electron microscopically, bFGF was shown in astrocytes along the rough endoplasmic reticulum, suggesting that the growth factor was produced in the cells and not taken up from the surroundings. These findings indicate the possibility that edema and the simultaneously generated free radicals or some extravasated plasma components express bFGF in astrocytes and probably in nerve cells, and that the thus expressed bFGF plays some role in the sequence of developmental events of hypertensive cerebral lesions.
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PMID:Increased basic fibroblast growth factor immunoreactivity in the brain of stroke-prone spontaneously hypertensive rats. 794 75

To obtain information about the role of nitric oxide (NO) in the development of hypertensive cerebral lesions, we used immunohistochemical methods to study the distribution and level of nitric oxide synthase (NOS) in the brain of stroke-prone spontaneously hypertensive rats (SHRSPs). The early changes in the brain of SHRSPs were petechiae, edema and massive glial accumulation around fibrin deposits, which contained necrotized microvessels, whereas advanced cerebral lesions comprised massive bleeding, cavity formation and diffuse degeneration of the white matter. In the normotensive control rats, immunoreactivity for NOS was demonstrated in scattered neuronal cells, as has been reported previously, but there was no reactivity in glial cells. In the present study in SHRSPs, however, considerable NOS immunoreactivity was observed in most reactive astrocytes and in a proportion of the microglial cells and macrophages in the vicinity of the cortical lesions and in the subcortical white matter both ipsi- and contralateral to the cortical lesion. The nerve cells in the edematous region also showed weak immunoreactivity for NOS. The distribution of increased NOS in SHRSP brains corresponded well with the sites of extravasated plasma fluid as demonstrated by anti-fibrinogen antibody. Based on these findings, we postulate that edema and the simultaneously generated free radicals or some extravasated plasma components may induce expression of NOS in the reactive cells and nerve cells, and that the NO thus generated may be involved in the development of hypertensive cerebral lesions.
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PMID:Altered nitric oxide synthase immunoreactivity in the brain of stroke-prone spontaneously hypertensive rats. 884 57

Infant and early childhood death caused by environmental hyperthermia (fatal heat stroke) is a rare event, typically occurring in vehicles or beds. The aims of this study were to describe the demographics, circumstances, pathology, and manner of death in infants and young children who died of environmental hyperthermia and to compare these cases with those reported in the literature. Scene investigation, autopsy reports, and the microscopic slides of cases from three jurisdictions were reviewed. The subjects in 10 identified cases ranged in age from 53 days to 9 years. Eight were discovered in vehicles and 2 in beds. When the authors' cases were grouped with reported cases, the profile of those in vehicles differed from those in beds. The former were older, were exposed to rapidly reached higher temperatures, and often had more severe skin damage. The latter were mostly infants and were exposed to lower environmental temperatures. Hepatocellular necrosis and disseminated intravascular coagulation were reported in victims who survived at least 6 hours after the hyperthermic exposure. The consistent postmortem finding among nearly all victims was intrathoracic petechiae, suggesting terminal gasping in an attempt at autoresuscitation before death. The manner of death was either accident or homicide. Recommendations for the scene investigation are made.
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PMID:Environmental hyperthermic infant and early childhood death: circumstances, pathologic changes, and manner of death. 1176 5

Haemorrhagic transformation of cerebral infarction is a common and potentially serious occurrence following acute ischaemic stroke. Though often a "natural" evolution, particularly in acute embolic stroke, haemorrhagic transformation is a prime concern with the use of thrombolytic therapy for acute ischaemic stroke. The severity of haemorrhage may range from a few petechiae to a large haematoma with space occupying effect. The pathogenesis of haemorrhagic transformation is not well established, though ischaemia and reperfusion have been proposed to cause disruption of the blood-brain barrier leading to extravasation of blood. At the molecular level, free radicals and proteolotic enzymes (metalloproteinases) may cause tissue injury. Studies have identified a number of clinical, radiological, and biochemical parameters that may serve as potential predictors of increased risk for haemorrhagic transformation. The knowledge of these factors may help in improving patient selection for thrombolytic therapy.
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PMID:Haemorrhagic transformation in acute ischaemic stroke following thrombolysis therapy: classification, pathogenesis and risk factors. 1871 15

Cerebral venous thrombosis (CVT) was formerly considered a rare disorder, associated with an unfavorable outcome. More recent data based on modern imaging techniques, however, have changed our perception of this disorder. The use of angiography and, especially, MRI have allowed an early diagnosis and have proved that the incidence of CVT is, in fact, higher than previously thought, approximately 3-4 cases per million people per year, and that the majority of patients have a favorable outcome. At present, the most frequent causes are oral contraceptives assumption and pregnancy/puerperium; as a consequence, 75% of patients are females. CVT may cause isolated intracranial hypertension or lead to an ischemic stroke, which does not follow the distribution of an arterial vessel and has a relevant vasogenic edema. Venous strokes often have a hemorrhagic component, ranging from small petechiae to an actual intracerebral hemorrhage; the latter is associated with a worse clinical course. The clinical presentation of CVT is highly variable and includes patients with just a mild headache, others with focal neurological deficits and a few with a dramatic syndrome with coma; seizures are a frequent presenting symptom. The best radiological examination to confirm the suspicion of CVT is MRI of the brain, which can both demonstrate parenchymal lesions and directly show evidence of sinus occlusions. The available evidence suggests that anticoagulants are effective in reducing mortality and dependency in CVT patients; the possible role of systemic or localized thrombolysis is still to be established.
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PMID:Cerebral venous thrombosis. 1934 6


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