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Biomedical subjects

G Stoltenburg

Publications and source records attributed to G Stoltenburg.

26 records · Page 2Linked to original sources
PubMed1979

Chronic and acute transtentorial herniation with tumours of the posterior cranial fossa.

In patients with expanding lesions of the posterior fossa general hyper-reflexia (and bilateral latency shifts of auditory evoked brain stem potentials) have been noted as possible symptoms of chronic ascending transtentorial herniation. After ventricular tap, this chronic herniation may evolve into acute herniation with progressive reduction of consciousness which in our experience can only be survived by decompression of the compressed brain stem. The chronic transtentorial herniation is related morphologically to demyelination of the pyramidal tracts and the auditory pathways, whereas the acute transtentorial herniation is related to microcirculatory disturbances in the reticular formation of the mesencephalo-pontine junction.

Auditory Pathways↗
PubMed1978

Experimental studies on hydrocarbon neuropathies induced by methyl-ethyl-ketone (MEK).

An outbreak of neuropathies among Berlin solvent sniffers was closely related to the denaturation by methyl-ethyl-ketone (MEK) of the mixture used. The solvent was composed of n-hexane, toluene and ethyl-acetate. Nervous system responses to chronic repeated exposure to 10,000 ppm pure n-hexane, 10,000 ppm MEK/n-hexane (ratio 1:9) and 6000 ppm pure MEK were investigated in rats. Motor neuropathy of the dying back type with giant swelling of axons in the peripheral and central nervous system developed in animals exposed to MEK/n-hexane and n-hexane. Severe potentiation of n-hexane neurotoxicity and shortened onset of morphological and clinical signs were demonstrated in animals exposed to MEK/n-hexane. MEK alone did not produce neuropathy under these conditions. The findings suggest that commercial solvent mixtures containing MEK/n-hexane should be avoided.

Administration, Intranasal↗
PubMed1977

Toxic polyneuropathies after sniffing a glue thinner.

In West Berlin in the autumn of 1975 through the following 5 months we observed 18 juvenile patients who had a toxic polyneuropathy and had sniffed a glue thinner. The neurological picture consisted of a symmetrical, progressive, ascending, mainly motor, polyneuropathy with pronounced muscle atrophy and characteristic vegetative alterations. The height of the disease was reached after 1 1/2-2 1/2 months and was characterized by tetraplegia in 7 patients. After 8 months all patients still had a motor deficit. Nerve biopsy showed paranodal axon swelling, dense masses of neurofilaments and secondary myelin retraction. The neurological and morphological data correspond to the "glue sniffer's neuropathy" and the n-hexane and MBK polyneuropathy after industrial exposure, as described in 10 cases to date. However, there was no MBK in the glue thinner. The polyneuropathies occurred in close time relation with the denaturation of the thinner with MEK (2-butanone). It is concluded from the data n-hexane and MBK have a common toxic mechanism with primary axonal changes and that there is an additional synergistic effect of MEK.

Adolescent↗
PubMed1974

[The use of stereologic image analysis in medicine (peripheral nerves)].

The use of image plane scanning for the purpose of quantification of data is becoming increasingly important in medicine and biology. Such equipment allows complex geometric-statistical relationships to be investigated by reduction to a counting process in which picture elements are counted (using a photocell), stored, and evaluated. Various absolute values of interest can then be computed using certain mathematical relationships. These methods, using automatically controlled sampling, are fast, and, since they are able to detect small variations in light intensity, very accurate. Furthermore, even in the presence of highly complex patterns, an accurate surface area measurement can be made. Peripheral nerve cells, for example, lend themselves well to such methods, since the strong contrast between individual structural elements provides excellent conditions for automatic measurement.

Axons↗
PubMedDate not supplied

Tuberous sclerosis complex with disseminated telencephalic distribution of atypical cells and their relation to corticogenesis.

In 2 cases of tuberous sclerosis complex (TSC), a disseminated distribution of atypical cells throughout the white matter and cortex of the telencephalon has been found. No cortical tubera were observed. In 1 of the cases, ventricular wall tumors (giant astrocytomas) were present. Stripes and candle guttering excrescences of groups of atypical cells perpendicular to the ventricular wall and to the cortical surface indicate erroneous genetic information in sets of neuroepithelial germ cells. This is compatible with the somatic second hit hypothesis effective in addition to the basic defect of TSC1 and TSC2 genes. The normal age-correspondend corticogenesis with regular layering and regular differentiation of neurons and glia without any cortical malformation or dysplasia and the sparing of allocortical parts of the telencephalon (hippocampus) as well as of basal ganglia, cerebellum, brain stem and spinal cord point to the rather late appearance of atypical cells which manifest in loco and do not interfere with corticogenesis. The bidirectional potential of atypical cells is obvious by their strong GFAP and APP surface staining. This coexpression indicates glial as well as neuronal features and emphasizes the relatively low level of differentiation of these cells. In their disseminated localization in our cases, these cells do not form tumors in the telencephalic white matter or cortex thus escaping sonographic detection before birth.

Biomarkers, Tumor↗
PubMedDate not supplied

Clinical data on three cases of occupationally induced PCB-intoxication.

Since the ban of PCBs at the end of the 1970s, extensive measures have been undertaken in Germany to dispose of PCB contaminated transformers. We report on three patients with considerable skin exposure to PCBs, in particular to Clophen A 30, while repairing or dismounting transformers. The periods of exposure range from 4 and 5 to 20 years. All patients presented with distal-symmetrical sensorimotor polyneuropathy as well as encephalopathy. In one of the cases, the neuropathy and encephalopathy progressed for a period of over 8 years after termination of exposure. In the two other cases the neurological deficits persisted over an observed period of 2-3 years. The reported clinical results may suggest that the long half-life of Clophen and its accumulation in fatty tissue can lead to persistence of PNS and CNS impairment long after the period of exposure.

Aged↗