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At least 181 records · Page 10Linked to original sources
PubMed1993

Erythema multiforme-like eruption in association with severe headache following pyritinol.

A 46-year-old woman presented with an unusual erythema multiforme-like eruption and severe headache 10 days after treatment with pyritinol for cerebral concussion. Histopathologic findings were consistent with erythema multiforme. Skin lesions and headache cleared after withdrawal of the drug. According to neurological examination and magnetic resonance imaging of the brain, the headache may have resulted from a slight, pyritinol-induced vasculitis. Previous reports on severe pyritinol-induced side effects and possible pathogenetic mechanisms are reviewed. Since pyritinol cannot be considered as an essential drug for cerebral concussion, adverse effects as described here raise doubts as to its general use in the given indication.

Brain↗
PubMed1978

Treatment of the alcoholic organic brain syndrome with EMD 21657. A derivative of a pyritinolmetabolite: double-blind clinical, quantitative EEG and psychometric studies.

The efficacy of EMD 21657--a derivative of a pyritinolmetabolite--with regard to the improvement of the organic brain syndrome (OBS) of chronic alcoholics was investigated in a double-blind study utilizing clinical, psychometric and quantitative EEG evaluation. Nineteen patients received 3 x 300 mg EMD and 21 patients 3 x 1 dragee placebo for 6 weeks. The groups did not differ in regard to age, sex, weight, height, alcohol anamnesis or IQ. The hospitalized patients were examined before as well as at the end of the second, fourth and sixth week of drug treatment. While the overall evaluation by the psychiatrist and patients at the end of the period of treatment did not show marked intergroup differences, the clinical global impression scale and the OBS rating scale demonstrated that both groups showed a significant reduction in their OBS and that improvement with EMD 21657 therapy was significantly superior to the one with placebo. Psychometric analysis also exhibited a significant superiority of EMD in regard to the general, associative, numeric and total verbal memory, concentration and attention variability. Psychovisual memory and the quantative aspects of attention showed opposite findings. Flickerlight fusion frequency, reaction time and after-image did not change significantly. The psychomotor activity improved significantly more with EMD than placebo; this was especially pronounced in the left hand. Affect and mood improved also more with EMD than placebo. Side effects were observed more frequently under active treatment and were characterized by temporary headaches. Power spectral density analysis of the EEG revealed in both groups a decrease of delta, fast alpha and beta activities and an increase in theta and slow alpha activity, but changes during EMD treatment more frequently reached the level of statistical significance than with placebo. The most consistant finding was the theta augmentation under EMD treatment. It was concluded that EMD 21657 is a CNS-effective drug with pronounced nootropic and slight thymotropic properties.

Adult↗
PubMed1980

Neurotropic drugs as co-medication to psychotropics. Combined administration of a neurotropic drug and a tetracyclic antidepressant.

Interactions of EMD 21 657 - a neurotropic drug - and maprotiline were studied in 40 depressive outpatients. Patients were assigned at random to an experimental or a control group. 20 patients of the experimental group received EMD 21 657 (3 X 400 mg/day p.o.) in addition to maprotiline (75 mg/day p.o.) during an initial treatment of 10 days. 20 patients of the control group were treated during this period with maprotiline of the same dosage but did not received EMD 21 657 as co-medication. During the 10-day period of treatment and observation, subjective information on the first day of improvement of depressive symptoms and severity of side effects were recorded. Under supplementary treatment with EMD 21 657 the onset of antidepressant action occurred sooner than in the control group receiving maprotiline alone. The earlier improvement in the experimental group was statistically significant in the target symptom 'obsessive rumination' (p less than 0.01). Undesirable effects of maprotiline treatment were seldom observed or were mild in terms of severity. A decrease in the rate of side effects in the experimental group could not be shown statistically.

Adolescent↗
PubMed1981

Therapeutic effect of pyritinol on sequelae of head injuries.

Two hundred and seventy patients suffering from the sequelae of different forms of brain injury have been treated orally with pyritinol 200 mg three times a day for a period of 6 weeks. It has been shown that, compared with placebo therapy, pyritinol produces statistically significant improvement in the clinical and psychoneurological manifestations. It is concluded that pyritinol is a drug of therapeutic benefit in the treatment of the sequelae of cerebral trauma.

Adolescent↗
PubMed1975

Pyritinol hydrochloride and cognitive functions: influence on children in slow learner classes.

Pyritinol-HCl was tested for its impact on the cognitive functions of children with learning disabilities. This study is a contribution to scientific discussion on the complicated methodologic problems in evaluating the clinical efficacy of psychopharmacologic agents. Sixty-seven pupils of slow learner classes between the ages of 11 and 16 years were treated for 6 months with 300 mg pyritinol-HCl/24 hr or placebo under strict double-blind conditions. Drug intake was stimulated and controlled by means of intense psychosocial interaction with the mothers of the subjects. The dependence variables used to test medication effects were 22 parameters of cognitive performance measured in psychologic tests for perceptual and intellectual functions which were administered immediately before and after the medication phase. First the gainscores before and after treatment with pyritinol or placebo within the 22 cognitive parameters were statistically compared. In addition, an analysis of covariance on the corrected results of the second test (treating the results of first testing as covariates) and a two group discriminant analysis for overall differences were performed. None of the 22 parameters showed statistically significant treatment effects with respect to average performance (t (pyritinol - placebo) = 1.96 to 1.31), neither could the two groups be separated by discriminant analysis (Hotelling's T2 = 35.4, df - 22 and 43, P = 0.465). With respect to a variability of gainscores, however, in four parameters there was a significantly higher variance in the pyritinol group (F = 1.85-2.33, P less than 0.05, less than 0.02, respectively). This fact may signify that pyritinol-HCl had different effects on different subjects. By means of prognostic stratification we therefore attempted to define objective criteria for a selection of subjects with probable positive treatment effects. None of the 15 tested criteria, such as body weight, age, perceptual handicaps, or reduced short term memory, IQ range, proved, however, to be critical for a prognosis of pyritinol effects within the present test population.

Adolescent↗
PubMed2007

Stability-indicating electrochemical methods for the determination of meclophenoxate hydrochloride and pyritinol dihydrochloride using ion-selective membrane electrodes.

The construction and electrochemical response characteristics of polyvinyl chloride (PVC) membrane sensors for the determination of meclophenoxate hydrochloride (I) and pyritinol dihydrochloride (II) in presence of their degradation products are described. The sensors are based on the use of the ion-association complexes of (I) and (II) cation with sodium tetraphenyl borate and ammonium reineckate counteranions as ion-exchange sites in the PVC matrix. In addition beta-cyclodextrin (beta-CD) membranes were used in the determination of I and II. These ion pairs and beta-CD were then incorporated as electroactive species with ortho nitrophenyl octyl ether (oNPOE) as a plasticizer. Three PVC sensors were fabricated for each drug, i.e. meclophenoxate tetraphenyl borate (meclo-TPB), meclophenoxate reineckate (meclo-RNC) and meclophenoxate beta-cyclodextrin (meclo-beta-CD), and the same was done for pyritinol (pyrit-TPB), (pyrit-RNC) and (pyrit-beta-CD). They showed near Nernestian responses for meclophenoxate over the concentration range 10(-5)-10(-2) with slopes of 52.73, 51.64 and 54.05 per concentration decade with average recoveries of 99.92+/-1.077, 99.96+/-0.502 and 100.03+/-0.763 for meclo-TPB, meclo-RNC and meclo-beta-CD respectively. Pyritinol also showed near Nernestian responses over the concentration range of 3.162 x 10(-6) - 3.162 x 10(-4) for pyrit-TPB and pyrit-RNC, and 10(-6) - 3.162 x 10(-4) for pyrit-beta-CD with slopes of 30.60, 31.10 and 32.89 per concentration decade and average recoveries of 99.99+/-0.827, 100.00+/-0.775 and 99.99+/-0.680 for pyrit-TPB, pyrit-RNC and pyrit-beta-CD respectively. The sensors were used successfully for the determination of I and II in laboratory prepared mixtures with their degradation products, in pharmaceutical dosage forms and in plasma.

Dosage Forms↗
PubMed1978

[The effect of pyritinol on the human cerebrovascular circulation (author's transl)].

The change in global and regional cerebral circulation after intravenous administration of pyritinol was investigated in 14 patients with acute or subchronic cerebral ischemia. The measurement of the cerebral circulation was performed by intraarterial isotope clearance with 133xenon using a multidetector apparatus. With a single administration of pyritinol (400 mg) there was a statistically significant increase in the cerebral circulation in the gray matter by 6.7 ml/100 g/min corresponding to 9.7% (p less than 0.01) 10 minutes after the end of the drug injection. In the areas of all portions of the brain with defective circulation there was a significant increase in blood flow by 8.9, 0.8 and 3.2 ml/100 g/min (gray matter, white matter, total substance), corresponding to 12.3%, 4.4% and 8.1%. In areas with a normal initial status, the increase in blood flow attained statistical significance in the gray matter only (p less than 0.05).

Brain Ischemia↗
PubMedDate not supplied

[Characteristics of the antivitamin effect of pyriditol, a disulfide pyridoxine derivative, on animal body].

Intraperitoneal administration of disulphide pyridoxine (pyriditol) to albino mice in a dose of 300 mg/kg brings down the GABA level and the GABA-transaminase activity in the brain, the glutamic acid content and the glutamate-decarboxylase activity remaining unchanged. In the liver and, especially, in the kidneys of test animals the activity of aspartate-and alanine-aminotransferase goes down. The diurnal urinary output of the animals shows a decreased passage of 4-pyridoxic acid. These results are interpreted to be consequent upon the antivitamin action of pyriditol with respect to pyridoxine.

4-Aminobutyrate Transaminase↗
PubMed2001

[Current strategies of pathogenetic therapy of Alzheimer's disease].

This is a review of the data available in the literature and the authors' own findings on pathogenetical rationale for the use and clinical study of current treatments for Alzheimer's disease (AD) (synonym: Alzheimer-type dementia). In the past decade many attempts have been made at targeting different links of the pathogenesis of a neurodegenerative process that underlie AD. Several areas of pathogenetical therapy for AD have been developed on the basis of experimental studies and pilot clinical tests. The most developed areas are as follows: various compensatory (replacement) treatments aimed at overcoming neurotransmitter deficit in different neuronal systems that are damaged in AD to a greater or lesser extent; neuroprotective therapy promoting increased viability (survival) of neurons and their plasticity, and vasoactive therapy. Rather new directions of AD pathogenetic therapy, such as antiinflammatory and hormonal therapy along with antiamyloid therapeutic strategies are still under study.

Aged↗
PubMed1975

[Neurophysiologic control during treatment of cerebral ischaemia with danaden retard (author's transl)].

After a three month treatment with Danaden retard (Encephabol + nicotinic acid) a group of patients suffering from cerebral ischaemia showed (in contrast to an untreated group) a significant reduction of slow waves in the EEG, a significant improvement of the audiogram, a reduction of the optic and acoustic reaction time and of the peak latency of the visual evoked potentials.

Brain↗