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Biomedical subjects

T Stober

Publications and source records attributed to T Stober.

32 records · Page 2Linked to original sources
PubMed1985

Intrathecal thyrotropin-releasing hormone therapy of amyotrophic lateral sclerosis.

Six patients with amyotrophic lateral sclerosis were given from 800 to 4000 micrograms of thyrotropin-releasing hormone (TRH) intrathecally for a period of 2-6 months. The progressive course of this disease, manifested by increasing atrophy, paralysis and disability score, was not altered. This supports the hypothesis that the decrease in TRH content in the anterior horn region is secondary to the cellular destruction. TRH appears to play no significant role in the pathogenesis of amyotrophic lateral sclerosis.

Amyotrophic Lateral Sclerosis↗
PubMed1985

Blood distribution in computer cranial tomograms after subarachnoid hemorrhage with and without an aneurysm on angiography.

This is a comparative study of the blood distribution in computer cranial tomograms after spontaneous subarachnoid hemorrhage in 51 patients with saccular aneurysms and 34 patients with no evidence of a source of bleeding in cerebral panangiography. There was often less blood observed at all sites when aneurysms were not present. This was, however, significant only in the interhemispheric fissure, the Sylvian cisterns, the parietal sulci as well as intracerebrally. Thus, 79.4% of patients without an aneurysm were in grades I and II of the Hunt and Hess scale as opposed to 47.0% of those patients with evidence of an aneurysm.

Adult↗
PubMed1985

[Early auditory evoked potentials and clinical course parameters in Friedreich ataxia].

The previously published reports of early auditory evoked potentials in collectives of Freidreich's ataxia show a discrepancy of the results. On the other side clinically and theoretically in this disease there are some interesting aspects. For example there is a decrease of amplitudes in patients suffering from a disturbance of discrimination as far as various sources of noise are concerned. The examined patients show pathological as well as normal results with a high degree of correlation in clinical criteria and the sum of amplitudes. All patients with slowered nerve conduction velocity showed pathological early auditory evoked potentials. More importance can be attributed to the early diagnostics in addition to the previously described differential diagnostic application of the early auditory evoked potentials.

Adolescent↗
PubMed1985

[Creatine kinase BB activity in the serum of patients with cerebrovascular diseases].

There are conflicting reports of an increase in the activity of creatine kinase BB isoenzyme (CK-BB) in the serum of patients with cerebrovascular disease. The serum CK-BB activity of 33 patients with ischemic brain infarction, subarachnoid hemorrhage or intracerebral hemorrhage was measured with a bioluminescence method (CK-B Kit, LKB-Wallac) in combination with immunoprecipitation. The results were compared with lesions determined by computed tomography. In the control group (N = 19) there was a mean activity of 0.35 +/- 0.26 U/l (means +/- SE). In patients with small lesions (N = 11) the activity was 0.41 +/- 0.21 U/l, which was not significantly elevated when compared to the control group (Mann/Whitney U test). Therefore, patients with more extensive lesions (N = 12) and the group with severe lesions (N = 10) showed a significant elevation, with a mean activity of 0.61 +/- 0.34 U/l and 1.12 +/- 0.52 U/l, respectively. The group with severe lesions had a maximum activity on the first day after the initial symptoms.

Adult↗
PubMed1984

[Incidence of ventricular arrhythmia relative to the QT interval in spontaneous intracranial hemorrhages].

A prospective study was done in 54 patients with acute spontaneous intracranial haemorrhage, 27 of them with subarachnoid bleeding and 27 with primary intracerebral haemorrhage. The frequency of ventricular arrhythmias was registered by continuous long-term ECG and the incidence of QT prolongation by daily standard ECG registration. Prolongation of frequency-corrected QT-interval (QTc) developed in 9 patients with subarachnoid haemorrhage and in 10 with intracerebral haemorrhage. For assessment of time-relation between QT-interval and ventricular arrhythmias the results of corresponding long-term ECG and standard ECG were used and two groups were defined: group A (149 tapes) = QTc less than or equal to 450 ms, group B (43 tapes) = QTc greater than 450 ms. In group B singular frequent ventricular extrasystoles, couplets and non-persistent ventricular tachycardias occurred more frequently though not significantly so. Persistent ventricular tachycardias occurred significantly more frequently in group B (14% vs. 1%, P less than 0.01). In three tapes of group B, all of them with QTc prolongation of more than 550 ms persistent ventricular tachycardias with typical "torsade de pointes " morphology were seen. The results show that QTc prolongation of more than 450 ms occurs in a third and significant ventricular arrhythmia in nearly half of patients with spontaneous intracranial haemorrhage. Persistent ventricular tachycardias occur almost only in cases of QTc-prolongation. Pronounced QTc prolongation of more than 550 ms is rare. However, it can give rise to torsade de pointes and ventricular fibrillation.

Adult↗
PubMed1984

Recurrent torsade de pointes type ventricular tachycardia in intracranial hemorrhage.

Two out of 72 cases of intracranial hemorrhage-induced polymorphous ventricular tachycardia with typical Torsade de Pointes morphology are presented. Both patients had marked QTc prolongation more than 550 ms. In one patient (QTc: 669 ms) Torsade de Pointes degenerated into fatal ventricular fibrillation. Even though polymorphous Torsade de Pointes type ventricular tachycardia is rare during the clinical course of intracranial hemorrhage, attention should be given to the QT interval. QTc prolongation more than 550 ms may carry a high risk of Torsade de Pointes type ventricular tachycardia and ventricular fibrillation.

Adult↗
PubMed1984

Bicaudate diameter--the most specific and simple CT parameter in the diagnosis of Huntington's disease.

In addition to the neurological findings, the functional capacity of 12 patients with Huntington's disease was evaluated quantitatively according to the Shoulson and Fahn scale [1]. This parameter was related to the following computed tomographic measurements: the greatest distance between the frontal horns (FH), the shortest distance between the heads of the caudate nuclei (bicaudate diameter, CC) and the quotient FH/CC. The ratio of the bicaudate diameter and the external diameter of the skull across the narrowest point of the heads of the caudate nuclei (CC/OTcc) was also used as well as the bicaudate diameter and the maximum internal diameter of the skull (CC/ITmax). The best correlation was found between the bicaudate diameter and functional capacity (r = -0.64, P less than 0.05). All the quotients containing the bicaudate diameter likewise showed a correlation with functional capacity, though to a less marked degree. Thus the bicaudate diameter appears to be the most specific and simple computed tomographic parameter for the differentiation of Huntington's disease from normal states or choreatic syndromes of different origin.

Brain↗
PubMed1983

Quantitative evaluation of functional capacity during isoniazid therapy in Huntington's disease.

Eleven patients with Huntington's disease were treated with high doses of isoniazid. In addition to clinical assessment, the functional capacity was evaluated quantitatively. The symptoms of four of the patients showed a marked improvement and their functional capacity increased. The condition of one patient with the rigid form (Westphal's variant) deteriorated, and the remaining six patients showed no change. Patients with prominent mental disturbances appeared to respond best to isoniazid therapy.

Adult↗
PubMed1983

Lead concentrations in blood, plasma, erythrocytes, and cerebrospinal fluid in amyotrophic lateral sclerosis.

The purpose of the investigation was to elucidate the repeatedly discussed relationship between chronic lead intoxication and ALS. The following mean lead concentrations were determined in 9 patients with ALS: 8.65 +/- 3,91 micrograms/100 ml in the blood, 0.97 +/- 0.78 microgram/100 ml in the plasma, 19.15 +/- 5.0 micrograms/100 ml in the erythrocytes, and 0.89 +/- 0.44 microgram/100 ml in the cerebrospinal fluid. These values did not differ appreciably from the controls with 7.91 +/- 3.83 micrograms/100 ml (n = 14) in the blood, 1.13 +/- 0.46 microgram/100 ml (n = 10) in the plasma, 18.96 +/- 12.63 micrograms/100 ml (n = 10) in the erythrocytes, and 0.85 +/- 0.91 microgram/100 ml (n = 15) in the cerebrospinal fluid. These findings do not support the assumption of lead poisoning as a pathogenetic factor in ALS.

Amyotrophic Lateral Sclerosis↗
PubMed1982

Electrocardiographic alterations in subarachnoid haemorrhage. Correlation between spasm of the arteries of the left side on the brain and T inversion and QT prolongation.

In a retrospective study of 89 patients with subarachnoid haemorrhage (SAH), the frequency and specificity of changes in the electrocardiogram (ECG) were determined, as well as electrocardiographically established arrhythmias. The ECG changes were correlated with neurological as well as angiographic findings (localization of the aneurysm and vascular spasm). Abnormal ECGs were found in about 80% of the patients. The following abnormalities were found with decreasing frequency: depression and elevation of the ST segment, prolongation of the QT interval, flattening and inversion of the T wave, U waves and TU fusion waves, and arrhythmias (sinus tachycardia and bradycardia, extrasystole). A verified correlation (chi-square test) was shown between angiographically demonstrated spasm of the brain arteries of the left side and negative T waves as well as a prolongation of the QT interval. These results are related to the causal role of the left stellate ganglion in the generation of ECG changes and arrhythmias (animal experiments, and the success by blockade or surgical removal of the stellate ganglion in hereditary QT prolongation.

Adolescent↗