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Biomedical subjects

H Feistner

Publications and source records attributed to H Feistner.

50 records · Page 3Linked to original sources
PubMed1989

Post-irradiation lesions of the caudal roots.

The article reports on 3 patients suffering from muscular atrophy after radiotherapy of the para-aortal lymph nodes for malignant testicular tumor without any sensory, bladder, or bowel disturbances. By neurophysiological examination, a lesion of the lumbal plexus and the peripheral nerves of the lower extremities were excluded. On EMG-examination there were no giant motor unit potentials, as they can be found in anterior horn cell lesions. Though there were no sensory deficits, a distinct prolongation of latencies and reduction of amplitudes could be found for lumbar dermatomal somatosensory evoked potentials (SSEP) and those after stimulation of some peripheral nerves of the lower extremities.

Adult↗
PubMed1986

[Familial polyneuropathy with a disposition to pressure paralyses. A contribution to the differential diagnosis of mononeuropathies].

When a young woman admitted for recurrent peripheral nerve palsies was suspected to suffer from hereditary polyneuropathy with liability to pressure palsies, 8 members of her family were examined diagnostically. Only one of these had a history of a transient mononeuropathy. A neurophysiological examination demonstrated peripheral nerve lesions not only in the patients father but also in 5 of her brothers and sisters. In presenting the data for this family the characteristics of hereditary polyneuropathy with liability to pressure palsies and the most important differential diagnostic aspects are discussed.

Adult↗
PubMed1979

Semliki forest virus: cause of a fatal case of human encephalitis.

A fatal case of human encephalitis has been observed for which our results indicate that Semliki Forest virus (SFV) was the etiologic agent. This is surprising in view of the fact that this virus, which has been widely studied, was believed to be one of the arboviruses nonpathogenic for man. Described are the clinical course, the virological examinations performed, and the histopathological findings in the central nervous system.

Adult↗
PubMedDate not supplied

Rapid on-line estimation of responses to transcranial magnetic and peripheral nerve electrical stimulation in single human motoneurons.

Cross-correlation experiments allow to obtain information about synaptic potentials in human motoneurons. However, recording cross-correlation responses of one motoneuron to transcranial magnetic and electrical peripheral nerve stimulation requires a considerable recording time when both responses are recorded consecutively. In this paper a method is introduced yielding the same information about the responses of a single motoneuron to both types of stimuli while requiring only a fraction of the recording time necessary for a conventional cross-correlation experiment. The main features of the method introduced were: (i) use of the recharging time of the magnetic stimulator for response recording to the electrical stimulus, (ii) use of specific stimulus timing with respect to the motor unit discharges, and (iii) on-line display with statistical testing of the response functions allowing to stop stimulus application, if the responses to both types of stimuli had reached statistical significance. Application of the method is demonstrated with response recording of 70 tibialis anterior motor units from five healthy volunteers to transcranial magnetic and peroneal nerve electrical stimulation.

Adult↗
PubMedDate not supplied

Mitochondrial tRNA(Cys) mutation A5823G in a patient with motor neuron disease and temporal lobe epilepsy.

We discovered a new homoplasmic mutation in the mitochondrial cysteine tRNA of a 60-year-old Caucasian male suffering from asymmetrical pure lower motor neuron disease (MND) and temporal lobe epilepsy (TLE). Furthermore, titrations with Amytal, an inhibitor of NADH:CoQ oxidoreductase, revealed mild mitochondrial dysfunction in skeletal muscle tissue, which was described in patients with MND in an earlier report. The mutation was undetectable in 155 Caucasian controls of both sexes, in 40 MND patients and in 13 individuals suffering from TLE. It was, however, detected in a heteroplasmic state in the patient's mother, who did not suffer from a neurological disorder. Since this rare mutation affected a nonconserved base position and was not observed in MND or TLE materials, its relation to disease remains unclear.

Blotting, Southern↗
PubMedDate not supplied

Spinal motoneuron function in lower motor neuron disease: normal corticomotoneuronal and peripheral Ia EPSPs in patients with spinal muscular atrophy.

Responses of single tibialis anterior motor units to transcranial magnetic stimulation and to a synchronized Ia volley evoked by peripheral electrical nerve stimulation were obtained in patients with distal spinal muscular atrophy and compared to normal controls. Estimations of excitatory postsynaptic potential (EPSPs) by cross-correlations revealed no difference in rise time of EPSPs for both groups of subjects despite considerable changes in macro-EMG parameters of the motor units studied in patients with spinal muscular atrophy (SMA). The results indicate that voluntarily activated spinal motoneurons in SMA are capable of normal excitatory responses to transcranial magnetic as well as peripheral Ia stimulation.

Action Potentials↗
PubMedDate not supplied

Stiff-man syndrome: possible autoimmune etiology targeted against GABA-ergic cells.

We report the case of a female patient, who died at the age of 66 years. Besides an insulin-dependent diabetes mellitus (IDDM) she had developed the clinical symptoms of stiff-man-syndrome (SMS) and harbored autoantibodies against glutamate-decarboxylase (GAD) in blood and liquor. GAD catalyzes the biosynthesis of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). The autopsy revealed typical alterations observed in diabetes mellitus including an incomplete fibrosis of pancreatic Langerhans islets. A decrease of GABA-ergic cells in the cerebellar cortex was observed, and a size reduction of Renshaw cells in the spinal cord. Furthermore, a dilution series of a polyclonal GABA antibody delivered a reduced immunofluorescence in the cerebellum. In skeletal muscle a neurogenic atrophy was observed. As described in literature, the clinical symptoms decayed following clonazepam administration. We suggest that this case including GAD autoantibodies, dramatic loss of GAD-expressing pancreatic cells, and loss or atrophy of GABA secretory neurons, supports the hypothesis that SMS may be an autoimmune disease directed against GABA-ergic cells. Furthermore, we suggest a neuronal hypersensitivity at the spinal cord level caused by the atrophic Renshaw cells.

Aged↗