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Biomedical subjects

F Gerstenbrand

Publications and source records attributed to F Gerstenbrand.

At least 127 records · Page 7Linked to original sources
PubMed1978

Myotonic myopathy with painful muscle contractions and decrease of symptoms by cold.

Myotonic reaction and paresis accompanied by painful muscle contractions limited to the upper limbs, which decrease remarkably in the cold, were observed in a 29 year old man. The histological investigation revealed minimal non-specific signs of myopathy. The biochemical studies of muscular tissue contained a normal amount of myophosphorylase, acid maltase and glycogen. Ischemic work induced normal elevation of venous lactate. The activities of CPK, LDH and SGOT in the blood serum were occasionally increased. The EMG showed typical myotonic bursts and electrical silence during painful muscle contractions. Repetitive high frequency stimulation demonstrated a clear initial increase of the amplitude of action potentials followed by a decrease in the contracted muscle. The father of the patient suffered from dystrophia myotonica. This coincidnece suggests that this myotonic myopathy is a variant of dystrophia myotonica.

Cold Temperature↗
PubMed1978

[The application of guanidine hydrochloride to the treatment of degenerative nervous and muscular diseases. I. Clinical results (author's transl)].

This paper reports the results obtained on using guanidine hydrochloride in the treatment of patients with amyotrophic lateral sclerosis, degenerative diseases of the spinocerebellar system or the peripheral nervous system and dystrophic muscle diseases. A long-term effect of the substance was a diminution in the rate of progression of the diseases, with the exception of the group with dystrophic muscle diseases. Initial clinical improvement occurred in certain patients of both groups. The substance seems to be more effective in less-advanced cases than on administration in the later stages of the disease. The therapeutic dosage was 20 to 40 mg/kg/day. The most frequent side-effect was paraesthesia and sometimes gastric disturbance was reported. Therapy had to be discontinued in 3 patients due to leucopenia. In these patients the symptoms rapidly increased in severity after discontinuation of treatment. This supports the assumption that guanidine hydrochloride treatment slows down the progress of the disease.

Adult↗
PubMed1978

[Transitory burst-suppression pattern in endogenous-exogenous encephalopathy (author's transl)].

A status epilepticus was observed in a 22 year old female patient during endotoxinshock. The status epilepticus was treated with a high dosage of diazepame. The EEG showed a burst suppression pattern, in our case mixed by anoxia and diazepame. The burst-suppression pattern and the clinical suspicion of delayed degradation of diazepame caused by toxic hepatic failure suggested the therapy of forced diuresis. This therapy was followed by decreasing suppression periods, indicating the dominante influence of the hypnotic drug. This result shows the diagnostic as well as the therapeutic value of forced diuresis in this case.

Adult↗
PubMed1977

[The efficacy of guanidine hydrochloride in the treatment of Werdnig-Hoffmann disease (author's transl)].

The use of guanidine hydrochloride is reported in the treatment of 4 cases of Werdnig-Hoffmann disease. Improvement was achieved in two cases. Amelioration was initially observed in the third patient, but a relapse occurred during temporary discontinuation of therapy and the disease progressed, albeit at a slower rate, after resumption of therapy. The final case was a terminal one in which, however, slight temporary improvement occurred in response to therapy. A maximum dosage of 0.4 g (based on the assumption of an average body weight of 15 kg in these children) was reached by gradual increments. Side effects like shortlasting vomiting were observed only in case 1. The pharmacological action of guanidine hydrochloride is discussed. According to Otsuka and Endon the mechanism of action may be based on an increase in the end-plate potential amplitude. However, an augmented supply of spinal transmitters may also play a role in the mediation to the pharmacological action.

Child, Preschool↗
PubMed1977

Apallic syndrome in chronic mercury poisoning.

This report includes five cases afflicted by chronic mercury poisoning which was observed in Iraq in 1972. All five cases showed the symptomatology of a severe cerebral damage combined with peripheral nerve lesion. The clinical picture reveals an apallic syndrome or a prestage ensuring in the full-blown picture. The combination of CNS lesions with polyneuropathy is typical of mercury poisoning with failure of all brain functions and the appearance of brain stem automatism, combined with severe muscular atrophy. When such conditions are established the remission seems to be impossible. The historical as well as the clinical and morphological facts of the Minamata disease is reviewed. The different stages of chronic mercury poisoning in Iraq are described.

Adolescent↗