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N Heye

Publications and source records attributed to N Heye.

At least 37 records · Page 2Linked to original sources
PubMed1993

Morphometrical evaluation of triflusal in brain infarction.

MCA occlusion in animals is a common model for experimental stroke. In previous studies we have shown that one of the factors, which influence evolution of an infarct is microthrombosis in the area of infarction and in the surrounding brain tissue. The present study was undertaken for assessment of the number of microthrombi and of the size of brain infarcting in rats treated with the antiaggregatory substance Triflusal. 7 groups of Sprague-Dawley rats, each group consisting of 6 animals, underwent transsphenoidal MCA occlusion. The animals received Triflusal in various amounts from day 2 till day 6. At day 7 animals were decapitated and the brains were fixed in formaldehyde. The brain was dissected at the level of the optic chiasm and embedded in paraffin. Fresh microthrombi were detected py PTAH (Phosphotungstic acid hematoxylin) staining. In each animal the hemisphere with the ischemic lesion as well as the contralateral hemisphere were examined. The area of both hemispheres was calculated by subtraction of the ventricle area from the total brain area of a section. Infarct was defined as the region of necrosis which was sharply demarcated from normal brain. The infarcted area was planimetrically measured to obtain a ratio of infarcted to normal brain. A correlation between the effect of Triflusal, number of microthrombi and size of the infarcted area could be demonstrated. The pathogenetic role of the microthrombi in the evolution of cerebral infarction as well as the effect of Triflusal in different dosages on the number of microthrombi could be clearly assessed by quantitative morphometry.

Animals↗
PubMed1993

[Thalamic form of Creutzfeldt-Jakob disease].

We report a patient presenting with rapid progressive dementia. Neuropathological findings indicative for Creutzfeldt-Jakob disease--vacuolisation, nerve cell loss and gliosis--were found isolated in the thalamus and the basal ganglia. Clinical, neurophysiological and pathological findings in thalamic form of Creutzfeldt-Jakob disease differentiate significantly to other forms of Creutzfeldt-Jakob disease.

Aged↗
PubMed1993

[Topodiagnosis of Creutzfeldt-Jakob disease using HMPAO-SPECT].

An 80-year old female presented with early stage Creutzfeldt-Jakob disease with clinical, neurophysiological and neuropathological findings suggesting a focal involvement of the brain. HMPAO SPECT disclosed asymmetries of regional cerebral perfusion, thus suggesting that it may be a further diagnostic instrument in this disease.

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PubMed1992

The topography of microthrombi in ischemic brain infarct.

Following cerebral ischemia a tendency to increased coagulation can be detected. Vascular occlusion may develop either as a result of local thrombus formation or from emboli caused by circulating platelet aggregates. We studied the localization of microthrombi and their effects on tissue in double-hemisphere sections. Fresh brain infarcts showed a large number of microthrombi limited to the ischemic region. In more advanced infarcts they were found mainly at the border of the necrosis and diffusely distributed over both hemispheres. Older, subsiding infarcts showed only isolated microthrombi limited to the area of the necrosis. This indicates that great importance must be attached to microthrombi in infarct progression.

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PubMed1992

Focal involvement and lateralization in Creutzfeldt-Jakob disease: correlation of clinical, electroencephalographic and neuropathological findings.

Focal involvement can be assumed in the initial stage of Creutzfeldt-Jakob disease (CJD). We correlated the clinical, electroencephalographic and neuropathological findings in 13 cases of CJD with special reference to focal or lateralized changes. Eight cases showed clinical and 9 electroencephalographic signs of asymmetry. Four cases with a course of the disease shorter than 12 months presented circumscribed tissue alterations at autopsy. Cases with a clinical duration longer than 12 months had pathological changes involving both hemispheres symmetrically. The infectious agent seems to spread through the entire brain within a period of 12 months.

Adult↗
PubMed1991

The role of microthrombi and microcirculatory factors in localization and evolution of focal cerebral ischemia.

Ischemic cerebral infarction is caused primarily by occlusion of a large arterial vessel. Local circulatory disturbances in the center of ischemic tissue and in ischemic penumbra and the degree of sensitivity to ischemia in different brain regions influence subsequent ischemic progression. Postischemic recirculation is impaired by hemodynamic disturbances and formation of microthrombi, hemorrheologic changes and degeneratively altered vessels of microcirculation. Increased postischemic coagulation can be demonstrated in laboratory tests of few minutes extending up to two weeks after the onset of ischemia. Morphological observations on microthrombi after experimental focal ischemia as well as in patients with cerebral infarction show that formation of microthrombi is dependent on the duration of ischemia and the extent of infarcted tissue. Microthrombi are most prevalent in early stages of tissue damage. This suggests that microthrombi have an effect on the progression of ischemic necrosis. On the basis of our results, we can state that 1) microcirculatory disturbances are triggered by focal cerebral ischemia, 2) formation of microthrombi is a contributing factor to the evolution of postischemic microcirculatory disturbances, and 3) microthrombi promote the progression of ischemic necrosis.

Animals↗
PubMed1991

Oxalate-induced encephalitis after infusions of sugar surrogates.

The case of a 55-year-old female with oxalate-induced lethal encephalitis following infusions of sugar surrogates is reported. Renal failure and subsequent central coma developed following the use of xylitol, fructose and sorbitol above the recommended dosages. The patient died due to raised intracranial pressure. Cerebral damage was caused by encephalitis due to calcium oxalate crystals. Oxalosis induced by sugar surrogates may be explained either by dose-dependent toxic effects or genetically fixed intolerance.

Biopsy↗
PubMed1991

Effects of triflusal and acetylsalicylic acid on microthrombi formation in experimental brain ischemia.

Ischemic cerebral infarcts induce hypercoagulation and microthrombosis, thus leading to vessel occlusion and reduction of local cerebral blood flow. Antiaggregant therapy can reduce the formation of microthrombi. We tested the effect of acetylsalicylic acid (ASA) and triflusal (2-acetoxy-4-tri-fluoromethylbenzonic acid) on the formation of microthrombi after middle cerebral artery (MCA) occlusion. Six groups of rats, each consisting of six animals received either ASA or triflusal at dosages of 12.5, 25 or 50 mg/1,000 g b.wt./day. One control group was sham-operated, in another control group MCA occlusion was performed; both groups received no therapy. The number of microthrombi was counted 7 days after MCA occlusion on paraffin sections. The highest number of microthrombi was found in the group with MCAO and without therapy (mean 28 microthrombi/animal). In treated groups a reduction of the number of microthrombi could be stated. The strongest reduction was achieved in the group treated with 12.5 mg triflusal (mean 5.2). No statistic significant difference in the number of microthrombi was found between the groups treated with 12.5 mg triflusal and 50 mg ASA (mean 8.7) compared to sham-operated control animals (mean 4.3, p greater than 0.05). Treatment with 12.5 mg triflusal was superior to 50 mg ASA in preventing microthrombi formation (p less than 0.05). These results indicate, that in experimental brain ischemia the number of microthrombi can be effectively reduced by application of antiaggregatory drugs.

Animals↗
PubMed1991

[Sturge-Weber syndrome. Diagnostic imaging relative to neuropathology].

Clinical presentation of a child with port-wine stain and seizures leads to the suspicion of Sturge-Weber disease (SWD). This diagnosis can be confirmed by the detection of a meningeal angiomatosis. In rare cases, early detection of meningeal pathology by ultrasound has been reported. Key findings are brain atrophy, gyriform cortical calcifications demonstrated by skull radiographs after the first year of life or earlier by cranial CT, and dys- or aplasia of the deep cerebral veins on angiography. Radionuclide imaging shows focal or diffuse tracer accumulation over the affected brain regions. MR demonstrates an abnormal appearance of the affected meninges, especially thickening and pathologically increased signal intensity after Gd-DTPA application. This, in association with the demonstration of abnormal enhancement in deep medullary veins, is the most characteristic finding. Contrast-enhanced MR allows early and non-invasive diagnosis of SWD, mainly by revealing leptomeningeal angiomatosis and abnormal venous vessels.

Adolescent↗
PubMed1990

Primary leptomeningeal gliomatosis with predominant involvement of the spinal cord.

The authors report on a 43-year-old male with apparent myelomeningeal encephalitis. The most important clinical symptoms included severe lymphocytosis of the CSF, cranial nerve palsies, obstructive hydrocephalus, progressive coma, and presence of an intramedullary mass causing paraplegia. Neither CSF analysis, nor the intraoperative findings gave evidence of a neoplastic process. Regarding the paraclinical data we supposed a CNS inflammatory process, but autopsy revealed the diagnosis of an intraspinal, leptomeningeal gliomatosis.

Adult↗
PubMed1990

Focal-unilateral accentuation of changes observed in the early stage of Creutzfeldt-Jakob disease.

We report on a 67-year-old male patient with progressive right-sided hemiparesis predominating in the arm and right-sided myoclonias. The EEG showed periodic delta activity in the left hemisphere. The patient died of pulmonary embolism 10 weeks after the onset of the symptoms. The neuropathological examination was indicative of Creutzfeldt-Jakob disease: distinct spongiform changes, nerve cell loss and proliferation of astroglia in the left hemisphere were found; in the right hemisphere, however, only a few circumscribed spongiform foci were seen. There was a clear correlation between the unilateral predominance of the EEG abnormality and neuropathological changes. The hypothesized spread of infection along commissural projection pathways is supported by this pattern of lesions.

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