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Biomedical subjects

K Schmidtke

Publications and source records attributed to K Schmidtke.

23 records · Page 2Linked to original sources

[Striato-nigral degeneration (SND): a multisystem atrophy?].

Two cases of striato-nigral degeneration are reported. In case 1 the female patient showed a Parkinson syndrome, cardiac arrhythmias and vasomotor disturbances. Morphologically mainly the putamen and substantia nigra revealed severe atrophic changes according to the restricted form of striato-nigral degeneration (SND). In case 2 there was a disorder of the upper and lower motor neuron in a female patient. Morphologically this case was an example of a multisystem atrophy with changes in the striato-nigral, olivo-ponto-cerebellar systems and spinal motor and autonomic neurons. These cases demonstrate the variability of the striato-nigral degenerations which are met with in two forms: a "pure" form as in case one and as a part of multisystem atrophies. This is underlined in a review of 69 literature cases, which also shows that SND, Shy-Drager syndrome and olivo-ponto-cerebellar atrophy represent very probably different varieties of one and the same degenerative process.

Aged↗

Pena-Shokeir phenotype with major CNS-malformations: clinicopathological report of two siblings.

Clinical and pathological features of two siblings of opposite sex with the Pena-Shokeir phenotype are reported. A detailed account of the prenatal and dysmorphological findings is given in one case. A broad range of deformations regarded as secondary to fetal hypokinesia was present, including a number of yet unreported findings. One case showed additional endocrine hyperplasia and left lung trilobation. Both siblings displayed extensive, highly similar CNS-abnormalities. The type and convergence of these malformations differ from previously reported cases and characterize a new familial subtype of the Pena-Shokeir phenotype.

Abnormalities, Multiple↗

Cell groups of the medial longitudinal fasciculus and paramedian tracts.

The aim of this article is to introduce the reader to a continuum of cell clusters which may play an important role in the maintenance of eye position. They lie interspersed between the fascicles of the medial longitudinal fasciculus (MLF) and paramedian tracts in the caudal pons and medulla, and they also constitute the rostral part of the classical abducens nucleus. Previous workers showed that these 'cell groups of the paramedian tracts' (pmt cell groups) project to the flocculus, and receive afferents from several horizontal premotor cell groups. Results of neuroanatomical tracer experiments reported here demonstrate that they also receive a direct input from the vertical premotor gaze neurons in the mesencephalon (rostral iMLF and the interstitial nucleus of Cajal), as well as from some groups of oculomotor internuclear neurons. The projecting fibres descend to the cell groups of the paramedian tracts in the MLF. It is suggested that deficits in gaze-holding seen in internuclear ophthalmoplegia, for example, may result from damage to afferents of this paramedian cell continuum.

Abducens Nerve↗

Evaluation of intracerebral lesions in patients with acquired immunodeficiency syndrome. Neuropathological findings and experimental data.

In this paper we present the results of post-mortem examinations of the central nervous system in 61 male patients who died with Acquired Immunodeficiency Syndrome (AIDS); it includes 23 patients with reported neurological abnormalities at the time of presentation. The analysis revealed central nervous system (CNS) neoplasms (lymphoma, Kaposi's sarcoma) and a variety of inflammatory lesions (bacterial, fungal, protozoal and viral) in 32 cases. A total of 11 patients without opportunistic infections showed significant brain abnormalities characterized by microglial nodules and/or multinucleated giant cells, changes which are probably related to infection by human immunodeficiency virus (HIV). In addition, we describes results from a series of experiments designed to define the target cell population of HIV in the brain. The expression of CD4 complex--putative receptor for HIV--was investigated using short-term cultured brain cells taken from embryonic brain anlage and from different regions of fetal brain; glioma cells were also used. Cells derived from normal embryonic and fetal brain, as well as glioma cells, were examined with respect to their susceptibility to HIV. CD4 antigen expression could be demonstrated only on glioma cells of the permanent glioma line 85HG-59 comprised of cells with properties characteristic of astrocytes. Nevertheless, normal embryonic and fetal brain cells as well as glioma cells could be infected by HIV as documented by immunocytochemical methods and southern blot analysis. HIV infected brain cells showed reduced growth rate and altered growth pattern. This study emphasizes the diversity of HIV conditioned CNS impairments, suggesting that genomic variability of HIV may result in varying cell type preference of the virus. The experimental data indicate that CD4 expression in brain cells is probably not 'conditio sine qua non' for HIV susceptibility. The alterations of HIV-infected brain cells demonstrated provide further evidence for a direct involvement of HIV in the pathogenesis of AIDS-related neurological syndromes.

Acquired Immunodeficiency Syndrome↗

Sarcoidosis of the spinal cord and medulla oblongata. A pathological and neuroradiological case report.

A case of 68-year-old woman with symptoms of slowly progressive diffuse myelopathy, is presented, which could only temporally be reversed by immunosuppression. Contrast enhanced magnetic resonance (MR) scan demonstrated multifocal patchy enhancing lesions from cervical to mild thoracic segment and a circumscribed lesion of the whole medulla oblongata. Postmorten examination disclosed a histological confirmed, multifocal sarcoidosis of the spinal cord and medulla oblongata, with few sarcoid granulomas in one hilar lymph node and skeletal muscle of the upper extremities. Only nine similar cases of intramedullary sarcoidosis confirmed by autopsy with symptoms solely attributable to the spinal cord have been reported. A review of the pathological manifestations, diagnostic and treatment of intramedullary sarcoidosis is given.

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