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Biomedical subjects

F Gerstenbrand

Publications and source records attributed to F Gerstenbrand.

At least 145 records · Page 8Linked to original sources
PubMed1977

[Electrophysiogical and neuropharmacological studies in a patient with progressive myoclonus-epilepsy (author's transl)].

A progressive form of myoclonus-epilepsy was described in an 21 year old girl. Electrophysiological and neuropharmacological studies were carried out. The typical EEG-pattern, the close association of cortical discharges and myoclonic jerks, the form of myoclonus indicated a "pyramidal" myoclonus. Pharmacological data suggested that two possible mechanisms--a partial deafferentation of cortical neurones and a failure of thalamic, extrapyramidal and brain stem reticular formations--might be responsible for the EEG-abnormalities and concomitant myoclonus. Results from neuropharmacological studies demonstrated a suppressive effect (on EEG-discharges and myoclonic jerks) of clonazepam, diazepam, phenobarbital, taurine, levodopa and budipin. Taurine, levodopa and budipin might induce a new aspect in therapy of progressive myoclonus epilepsy and of myoclonus caused by other etiologic factors.

Adult↗
PubMed1976

[Motor nerve conduction velocity in uraemic polyneuropathy: correlation with metabolic factors (author's transl)].

The following parameters have been examined in twenty-one patients suffering from chronic renal failure (creatinine level between 4.5 and 18.8 mg/100 ml serum): maximum motor nerve conduction of the peroneal nerve, amplitude of the compound muscle action potential of the extensor digitorum brevis muscle, serum creatiine, total protein, serum globulins, serum albumins, alkali reserve, time of increase of serum creatinine above 4 mg/100 ml up to time of determination of the maximum motor nerve conduction, daily urinary excretion, mean blood pressure, (p less than 0.01) was found between maximum motor nerve conduction, as well as amplitude of the compound muscle action potential, and the serum albumin level only. Decreased levels of serum albumin, is correlated with diminished nerve conduction and a lower amplitude. The relationship between the electrophysiological data and serum albumin levels maybe explained on the basis of progression of a pre-existing polyneuropathy due to additional dietary malnutrition. A different interpretation is the assumption of an inactivation of neurotoxin on binding by albumins. A decrease in the albumin level would, therefore, result in an increased amount of unbound toxic agent. The values of the maximum motor nerve conduction were between 16 m/sec and 51 m/sec (mean value 42.2 m/sec), pointing to a polyneuropathy of primary axonal type rather that to primary demyelinization. The amplitudes of the compound muscle action potentials were not greatly reduced and thus the uraemic polyneuropathy seems to be of mixed type. In uraemic polyneuropathy different aetiological factors have to assumed. According to the prevalent factor a polyneuropathy of predominantly axonal or predominantly demyelinizing type may result.

Action Potentials↗
PubMed1976

[Augmented indication field for Convulex therapy (author's transl)].

The therapeutic effect of n-dipropylacetate (DPA) is described in 20 patients with cerebral or spinal spasticity. Improvement was ween in 8 out of 11 patients with cerebral spasticity, 3 out of 5 patients with spinal spasticity and 3 out of 4 cases who had sustained perinatal damage. Satisfactory clinical amelioration and improvement in the EEG was observed in myoclonia, particularly of the Unverricht-Lundborg type.

Adolescent↗
PubMed1976

[The severest form of CO poisoning (author's transl)].

The case histories of four patients with severe cerebral manifestations as a result of CO poisoning are reported. All patients displayed an acute mesencephalic syndrome in the initial stage. One case developed a fatal bulbar syndrome following a transitional phase. Autopsy showed cerebral oedema, in addition to necrotic areas in the basal ganglia and cerebellar haemorrhage. The other 3 patients developed an apallic syndrome with all the typical features and symptoms. Two of these patients died without showing any improvement, displaying not only necroses in the basal ganglia, but also diffuse destruction of the white matter and, in one case, even of the cortex. The third patient recovered. His recovery took a similar course to that of a case of traumatic apallic syndrome and he was subsequently able to take up normal activities. It is concluded from these four cases that secondary brain oedema precedes the development of the most serious form of CO poisoning and is of grave prognostic significance.

Adolescent↗
PubMed1976

[Cerebral involvement in the Sézary syndrome (author's transl)].

Two foci of histologically verified mycosis fungoides were found in the left parietal region of a 45-year-old man with involvement of the brain during an exacerbation of leukemia. There was perivascular and diffuse infiltration with lymphoma-like cells and occasional giant (Lutzner) cells but no involvement of the meninges. Both before and after operation the CSF contained a few atypical lymphocytes and mononuclear cells, one of which showed ultrastructurally the deeply clefted nucleus of Sézary cells. Atypical cells were confirmed morphologically in the peripheral blood, as well as by cytochemical (beta-glucuronidase) and immunological (rosettes with SRBC) markers, after the postoperative leucocytosis had subsided. It is suggested that this CNS involvement during a leukemic conversion phase of mycosis fungoides is consistent with the Sézary syndrome.

Brain Neoplasms↗
PubMed1975

[Infusion therapy with mif (melanocyte inhibiting factor) in Parkinson's disease (author's transl)].

On the basis of reports in the literature and of our own clinical experience it appears that melanocyte inhibiting factor (MIF) is a very promising therapeutic agent in the management of Parkinson's disease. Besides theoretical considerations relating to biochemical and pathophysiological spheres, the question of the current dosage for clinical usage seems to be of the utmost importance. We are of the opinion that the currently-employed dosage of 400 mg daily is still too low. Hence, the present investigation will be continued with a view to establishing the optimum dosage for maximal therapeutic effect.

Aged↗
PubMed1975

[The activity of aminotransferases in serum and cerebrospinal fluid in neurological diseases (author's transl)].

The activities of the aminotransferases, GOT and GPT, were determined in the serum and cerebrospinal fluid of patients with Parkinson's disease, Huntington's chorea, Wilson's disease, amyotrophic lateral sclerosis (ALS), Friedreich's ataxia, phenylketonuria, and head injuries. 1. In patients with Huntington's chorea the activity of SGOT was lower than in controls (P = 0.02); in Friedreich's ataxia LGPT activity was decreased (P less than 0.001); in patients suffering from ALS SGOT (P = 0.005), SGPT (P less than 0.001) and LGOT (P less than 0.001) activities were increased. 2. Long-term treatment of Parkinson's disease and Wilson's disease with L-dopa resulted in an increase in SGOT, LGOT, and SGPT activity over approximately 2 months, with subsequent normalization of these enzyme activities in spite of continued therapy. Guanidine treatment led to an increase in aminotransferase activities in patients with ALS. Penicillamine caused a decrease in SGOT and SGPT activities in Wilson's disease. These results illustrate the necessity of taking therapeutic measures into account in the interpretation of data on aminotransferase activities.

Alanine Transaminase↗
PubMed1975

Urinary catecholamine excretion and thyroid hormone blood level in the course of severe acute brain damage.

Urinary catecholamine excretion and thyroid hormone blood level were studied in 16 patients following severe cerebral trauma. Increased excretion rates of epinephrine and norepinephrine were found. There was no significant difference in the catecholamine excretion when compared with generally traumatized patients. The relationships between catecholamine excretion, increased metabolic rates, and negative nitrogen balance indicate that in patients with a midbrain syndrome there exists an additional diencephalic metabolic factor, which leads to a rise in fat oxidation and perpetuation of catabolism. Early high caloric parenteral nutrition seems to inhibit the initial increase of catecholamine excretion and thus protects the body from an unnecessary breakdown of its own reserves. If the course is classified according to neurological stages, it can be shown that patients with a traumatic apallic syndrome in poor condition have a high increase of catecholamine excretion. Secretion of thyroid hormones is not influenced significantly by cerebral trauma.

Adolescent↗