Biomedical subjects
N Heldt
Publications and source records attributed to N Heldt.
[Congenital astrocytoma of the brain stem].
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Variations in the drainage of the lateral mesencephalic vein.
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The visualization of the anterior spinal artery and its blood-stream direction during brachial vertrebral angiography.
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Normal and pathological radioanatomy of the superior choroid vein.
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[Neurological symptomatology of vertebro-basilar sacculated aneurysms, apropos of 2 cases].
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Neuropathological epidemiology of cerebral aging: a study of two genetic polymorphisms.
We studied whether ApoE and -219 GT (ApoE promoter) polymorphism modulates neurofibrillary tangle (NFT) and senile plaque (SP) development in aging among 190 non-institutionalized individuals (mean age 79.5 years). Analysis revealed that the mean Braak stage was higher in epsilon4 allele carriers. Once individuals with Braak stage V were excluded (n = 5), relationships between NFT and the two genotypes studied were weak, whereas in epsilon4 allele carriers, the risk of SP was multiplied by 4 to 7 in four areas (CA1, subiculum, isocortex and entorhinal cortex). This association was more pronounced in subjects under 80 years and was also observed when analysis was restricted to Braak stages 0, I and II. Epsilon 2 allele carriers appeared to have fewer lesions but, due to limited numbers, this trend was not significant. In two regions (CA1, subiculum), the number of SP increased significantly for individuals who were homozygous for the T allele of -219 GT. However the association was no longer significant when controlling for ApoE epsilon4. It should be noted that the brain of elderly subjects carrying one epsilon4 allele may not undergo senile changes.
[Progressive multifocal leukoencephalopathy. Contribution of nuclear magnetic resonance imaging].
Progressive multifocal leucoencephalopathy is a white matter infection caused by a papovavirus. Immunocompromised patients are predominantly affected. We report the case of a 74-year old woman with abdominal lymphoma resistant to chemotherapy. The diagnosis was suggested by cerebral CT and NMR images and was confirmed at postmortem pathological examination. The contribution of complementary examinations to the diagnosis is discussed in the light of recently published studies.
Hemimegalencephaly: a clinicopathological study of four cases.
Pathological findings in four cases of hemimegalencephaly are presented. These cases demonstrated diffuse enlargement of the cortex with disappearance of horizontal layering of the neurons restricted to one hemisphere. In all cases there was marked enlargement of a high percentage of neurons. The nosological situation is discussed and is considered to be heterogeneous; cases 1-3 had cerebral lesions without lesions of the skin or viscera. In these three cases, significant glial abnormalities were found in only one. These cases and others quoted in the literature were considered to be a separate entity completely different from Bourneville's tuberous sclerosis. The aetiology of this developmental malformation remains unknown; genetic factors were not found. Case 4 was associated with a cardiac lesion and with a linear sebaceous naevus characteristic of Solomon's syndrome. Periventricular tumours resembling candlewax drippings were noted. This case, close to Bourneville's disease, could be incorporated into the framework of neuroectodermoses together with tuberous sclerosis.
[Infantile neuroaxonal dystrophy or Seitelberger's disease].
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[Proceedings: Cerebral tumors of germinal origin].
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[Germinomas of the pineal region. Indications for direct approach].
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[Granular-cell tumors of the neurohypophysis. Apropos of a case].
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[Facial hemispasm from vascular compression].
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[2nd case of mycetoma due to Nocardia in Tunisia].
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[Apropos of neuro-ophthalmologic forms of Hodgkin's disease].
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[Primary reticulosarcoma of bone with an orbito-cranial localization].
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Gerstmann-Sträussler-Scheinker disease with A117V mutation in a second French-Alsatian family.
We report a kindred of French/Alsatian origin with symptoms of Gerstmann-Sträussler-Scheinker disease over 3 generations. In the propositus, cerebellar signs and memory disturbance were the presenting features, followed by other neurological manifestations. Biopsy of the cerebral cortex showed numerous multicentric and "kuru"-type amyloid plaques that on immuno-light and electron microscopy stained with antibody to prion protein. Molecular genetic analysis revealed an A117V mutation in the open reading frame of the prion protein gene. Questions as to pathology and spread of this mutation are discussed.