Clinical Neuroscience - 1968;21(12)

Clinical Neuroscience

DECEMBER 01, 1968

Principal stages in studying the problem of physiological mechanisms of mental activity in man

N. P. Bechtereva, A. Tchernysheva

Much of what happens in the brain during mental activity - especially in the most complex living tissue, the human brain - is still unclear. A major merit of the Pavlovian school is the elucidation of the physiological mechanisms that determine the diverse manifestations of the probable brain anatomofunctional schema of conditioned reflex activity, shedding light on the trait-, environment- and organism-dependent specificities of these mechanisms. An attempt has been made to adapt the conditional reflex methodology to humans in order to study higher nervous activity.

ENG 1968;21(12)

Clinical Neuroscience

DECEMBER 01, 1968

[Seduxen treatment in certain neurological diseases (neurosis, pain, muscle spasm)]

LEHOCZKY Tibor

[Seduxen 5 mg tabl., produced by Kőbánya Pharmaceuticals, has been used in clinical therapeutic trials. Out of 100 patients in the ward, 77 were in different groups of neurasthenia, - neurosis, 7 patients were treated for pain caused by organic disease, 16 for muscle spasm and contracture. He discusses the 8 groups of neurasthenia-neurosis listed and finds that the highest improvement rates were in the reactiv and vasovegetative groups, 82.7% in the former and 83.3% in the latter. The overall improvement rate for all groups was 77.8%. The 75% improvement in neurasthenia anxiosa is highlighted, following the anxiolytic effect of diazepam highlighted by both foreign and national researchers. These results suggest that Seduxen is a very good tranquillant drug, which, at the right dose (3 X 14, 3 X 12, 3 X 1 tablets daily), has a sedative effect without side effects. Seduxen also has a direct analgesic and analgesic effect, not only in arthritis and arthrosis of various types, but also in polyneuritis, neuritis and neuralgia. Seduxen is an excellent muscle relaxant, which has been observed in 13 of its 16 organic patients to a marked degree and in three to a moderate degree; by reducing the dose sufficiently, a detrimental degree of muscle weakness can be avoided. Dose: 3x1/2 tablets daily is recommended as the initial dose, but in the vast majority of patients 3x1 tablets daily was adequate; in some cases 3x 14 tablets daily proved beneficial. Experience has shown that the side effects of Seduxen are mild, exceeding those of known tranquillant drugs only in cases of overdose or individual hypersensitivity. A certain degree of drowsiness is relatively common, but this, like muscle hypotension in paretic patients, can be avoided by reducing the dose appropriately. ]

HUN 1968;21(12)

Clinical Neuroscience

DECEMBER 01, 1968

[Serum glutamic acid oxaloacetic acid transaminase activity in muscle diseases]

LIPCSEY Attila, SZABADI Elemér, FEKETE Istvánné

[The authors measured GOT enzyme activity in serum from patients with muscle atrophy of various origins (myogenic and neurogenic atrophy) and in serum from individuals with various neurological diseases. Their experience has shown that in myogenic diseases, if the presence of other diseases associated with parenchymal breakdown can be excluded, the measurement of GOT activation can be used to support the myogenic nature of the process.]

HUN 1968;21(12)

Clinical Neuroscience

DECEMBER 01, 1968

[Further studies to detect human-brain corticosteroid fractions]

FAZEKAS I. Gyula, FAZEKAS Attila

[1. Lobar pneumonia, sudden cardiac death from paralysis, sudden cardiac death from paralysis in alcoholic state, self-harm, lightning strike, apoplexy cerebri, carcinosis peritonei, isonicide poisoning, cyanide poisoning, barbiturate poisoning, CO poisoning, Wofatox poisoning, alcohol poisoning+freezing deaths 26-92 years of age from 5 brain areas of 18 people (11 males and 7 females) were extracted 1 1/2-10 h after death, paper chromatographed in Bush 5 system, followed by chromatography in 2 n NaOH and 0.1% tetrasolium blue 9: 1. Evaluation was based on the tetrasolium blue reaction, NaOH fluorescence, Rf. values, standards and native blue fluorescence. 2 Brain extracts were run with different amounts of tetrahydrocortisol, tetrahydrocortisol, cortisol, cortisone, corticosterone and 11-dehydrocorticosterone as standards. The brain areas tested were : 1. bridge+brain, 2. cerebellum, 3. cerebellar nuclei, 4. cerebral cortex, 5. cerebral white matter. 3. 10 corticosteroid fractions were identified in total, 6 fractions were all identical to the standards, the other 4 unidentified steroids were labelled X1, X2, X3, X4. 4. These steroids were detected in different qualities and quantities in different brain areas depending on the deaths. 5. cortisol (=hydrocortisone) was detected in almost all brain areas tested in all 18 cases. Cortisol was found in most brain areas of those who died of heart failure, self-harm, lightning, apoplexy cerebri and various poisonings, but could not be detected in brain areas of those who died of heart failure in an alcoholic state and of cyanide poisoning. Other fractions were present in varying numbers and quantities in different brain areas. 6. Most fractures and the largest number were found in the brain areas of those who died of carcinosis peritonei and pneumonia. Fewest fractures and least amount were found in brain areas of those who died of cardiac arrest in alcoholic state and various intoxications in alcoholic state, and alcohol poisoning + frostbite. 7. Consistent with our previous animal studies and our studies on human subjects, we observed in the present study that alcohol induced significantly fewer corticosteroid fractions and quantities in all areas of the human brain compared to those in the non-alcoholic state. 8. In the cases studied, the total steroid content of each brain area does not show a consistent quantitative pattern that is characteristic of each death. 9. No lawful correlations between age, sex, adrenal weight, body weight, body height and the quantity and quality of corticosteroid content in the brain were found. 10. No decrease in brain corticosteroid content within 10 hours after death was observed with increasing time.]

HUN 1968;21(12)

Clinical Neuroscience

DECEMBER 01, 1968

[Tuberous sclerosis and Sturge - Weber disease co-incidence]

SZILÁRD János, MÉSZÁROS Endre

[Data from an in vivo 14-year-old female patient with predominant symptoms of tuberous sclerosis and concomitant lesions suggestive of Sturge-Weber disease are presented, along with a family history of multiple neurological lesions and tumour formation. In the context of the co-detection of two very rare conditions, we wished to draw attention to the importance of dealing with neuroectodermal disorders. We also review the literature on the various dysgenetic abnormalities associated with the two disorders. ]

HUN 1968;21(12)

Clinical Neuroscience

DECEMBER 01, 1968

[Book review]

GOMBI Róza

[The author presents Bechtereva, N. P., Bondarchuk, A. N., Smirnov, B. M. and Trohachev, A. 1.: Physiology and pathophysiology of deep structures of the human brain.]

HUN 1968;21(12)