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Biomedical subjects

E Gibbels

Publications and source records attributed to E Gibbels.

At least 37 records · Page 2Linked to original sources

[Tabular instructions for differential diagnosis of polyneuropathies (author's transl)].

Following a brief review of the nosological system a comprehensive table containing diseases in which polyneuropathies can occur is presented. The tables list the typical neurological syndrome, affections of other organ systems, diagnostical aids from history, clinical course and additional findings and finally the most important differential diagnoses and specific treatment. A list of diseases which show similar accentuation of polyneuropathy is added.

Diagnosis, Differential↗

[Fiber type disproportion, a subtype of so-called nonprogressive myopathies (author's transl)].

The clinical course, serological, and electromyographic findings, and also histological, histochemical, and electron microscopic abnormalities of two patients with congenital fiber type disproportion, a subtype of the so-called congenital nonprogressive myopathies, are described in this study. Other important subgroups are discussed regarding both variation and overlapping. As these diseases neither belong to the "classical" myopathies nor to the neuropathies, other possible factors such as a distrubed trophic function of the nerve or abnormalities of the reflex arc are under consideration.

Biopsy↗

[McArdle's disease--description based on three own observations (author's transl)].

The paper reports on three observations made by the authors of McArdle's Disease. Characteristic symptoms are a premature tiring of the musculature and painful muscle contractions; in the late stage of the disease, mild muscle atrophy can also occur. The ischemia test is is pathologic. Myoglobinuria often occurs after major strain. Studies by light microscope and the electron-microscope result in an increased glycogen deposit in the muscle fiber. The diagnosis is verfied by the histochemical and biochemical proof of muscle phosphorylase deficiency. Routine histologic investigation of muscle biopsy is not sufficient to identify the disease. Despite the established enzyme defect and the resulting impairment of anerobic energy availability, the genesis of the disease or syndrome has not yet been fully clarified.

Adult↗

[Unmyelinated nerve fibers in senile nerves and in late thalidomide neuropathy: a quantitative electron microscopic study (author's transl)].

Sural nerve biopsies of four patients, aged 54--76 years, with a predominantly sensory type of neuropathy following high dosages of thalidomide were examined by light and electron microscopy. The present study includes a qualitative and quantitative evaluation of unmyelinated nerve fibers. Despite severe neuropathy, increased numbers of small unmyelinated axons per endoneurial area were noted in all patients. This numerical increase appeared to be independent of aging, since it was not seen in two senile controls, studied at the age of 83 and 88 years. The increase in the endoneurial density of unmyelinated axons, especially of small sized fibers, is likely to be related to regeneration following degeneration of unmyelinated axons although endoneurial shrinkage secondary to loss of large myelinated fibers could have caused an additional increase in the number of axons per endoneurial area. Axonal sprouting, despite degeneration of large numbers of myelinated and unmyelinated fibers, appears to be consistent with some of the characteristic clinical features of thalidomide neuropathy such as paresthesias, hyperesthesia for pain and temperature, and disturbances of autonomic functions. On the other hand, a variable number of empty Schwann cells (bands of Büngner) and pockets at the surface of many Schwann cells noted in the four patients with neuropathy were also seen in both senile controls with no signs of neuropathy. Thus, it is obvious that pockets and empty Schwann cells may be related to aging or other causes of slow axonal wasting with Schwann cell proliferation and are not necessarily associated with clinically manifest neuropathy.

Aged↗

[Subclinical diabetes and polyneuropathy (author's transl)].

By investigation of the carbohydrate metabolism in 357 patients with polyneuropathy observed in hospital in recent years, and by statistical comparison with a control group in the literature, an attempt was made to find out whether subclinical diabetes can cause diabetic polyneuropathy to a greater extent. In spite of the more frequent occurrence in the total number of patients, a more significant etiological role for this type of metabolic disorder in polyneuropathy cannot be concluded from the results. Whether a more unspecific, general polyneuropathy-promoting influence is to be ascribed to it must remain open.

Adult↗

Cylindrical spirals in skeletal muscle: a further observation with clinical, morphological, and biochemical analysis.

Cylindrical spirals are abnormal uniform membranous inclusions in skeletal muscle, usually confined to type 2 fibers. Hitherto, only five cases have been published with various clinical syndromes. Here, a case is presented for the first time with detailed electrophysiological, histometrical, and biochemical analysis: a 60-year-old man with slowly progressing polyneuropathy confirmed by electrophysiological findings, and a history of diabetes, alcoholism, nicotine abuse, and weight reduction. In various muscle biopsies, large aggregates of cylindrical spirals were found almost exclusively in type 2B fibers. Obviously, the aggregates were derived from abnormal perinuclear and, therefore, mainly subsarcolemmal tubulovesicular structures. Morphometrical, histochemical, and biochemical analysis of muscle revealed no further information about the nature of these inclusions. They were not present in skin biopsy containing subcutaneous nerves.

Biopsy↗

Morphometry of unmyelinated nerve fibers.

Based on the literature and personal experiences, methods for planning, performing, and evaluating morphometric studies of unmyelinated nerve fibers (UF) in nerve biopsies are recommended and available control values presented. UF assessment should include total endoneurial area of the entire nerve specimen, size of the evaluated area, number of fascicles studied, final magnification of the respective electron micrographs, counts of registered UF, number per nerve and density per mm2 of all UF as well as of original UF, the respective histograms, and counts of degenerating UF, UF-type Schwann cell nuclei and "empty" UF-type Schwann cell complexes.

Cell Nucleus↗