Pyritinol
WHAT IS IT?
Pyritinol is derived from natural sources. It is two pyridoxine (vitamin B6) molecules linked with sulfur bonds. It has no B6 activity, however.
WHAT DOES IT DO?
Pyritinol is one of the oldest nootropic (intelligence enhancing) substances around. It has been used in Europe for many conditions such as organic psychoses, cerebral circulatory disorders, alcoholism, dyslexic factors, behavior and intellect disorders in children and post-cerebral infarction (stroke) states. It is also useful for brain aging, ADD, and learning disabilities associated with retardation.
Pyritinol is a strong antioxidant, superior to DMAE or Piracetam in the brain. It is especially effective against the dangerous hydroxyl radical.
This substance increases brain cell energy by enhancing blood glucose transport through the blood-brain barrier and by increasing brain cells utilization of glucose, the sugar the body burns for energy. In a double-blind, placebo controlled, study of 87 patients with various brain disorders, it was found that they used only about 50% of the normally available glucose. Those taking Pyritinol returned to normal in the glucose uptake and their clinical symptoms similarly improved. Most dementias such as Alzheimer’s, stroke, or drug toxicities are characterized by impaired brain carbohydrate metabolism (BCM.) The degree of impairment corresponds to the severity of symptoms.
A study compared Pyritinol with Hydergine™, (a drug used for Alzheimer’s) and Pyritinol was found to be associated with a continuous and significant improvement in symptoms. Hydergine’s results were more modest and tended to plateau early in the treatment.
In the immune system, Pyritinol increases neutrophil chemotaxis. This means that the white blood cell called a neutrophil travels to the site of an infection and releases free radicals to kill germs. Most of the pus that forms in wounds is made from neutrophils. In the process it promotes an inflammatory reaction, which can become severe. Pyritinol not only increases the number of neutrophils traveling to the infection, it prevents the inflammation from becoming too severe. Interestingly enough, it also prevents the sugar-induced loss of immune function. Normally, the sugar in a can of soda can inhibit immune function by stopping neutrophils from killing germs. This can be so severe that a loss of 50 to 80% function for up to five hours can take place. Pyritinol prevents this immune dysfunction.
Pyritinol also increases mental vigilance by increasing nerve activity in the locus coeruleus of the brain. This part of the brain is especially prone to damage in Alzheimer’s Disease. Pyritinol literally increases brain power as measured by an electroencephalogram (EEG) which also results in better memory according to studies.
CAUTIONS
Very few side effects have been noted with Pyritinol.
DOSE
A wide range of doses has been used in Pyritinol studies. These have ranged from as low as 100 mg twice daily to 200 mg three time’s daily or 200 mg four times daily. For anti-aging, cognition enhancing or antioxidant purposes, 100 mg Pyritinol two or three times daily is generally safe and adequate. Higher doses (400 - 1000 mg daily) should probably be used only occasionally. Pyritinol may be taken either on empty stomach or after food, as desired. Persons only prone to insomnia should probably only take Pyritinol morning and early afternoon. There may be a mutual enhancement of action between Pyritinol and other nootropic substances, allowing/requiring lower doses of some or all the drugs in order to avoid an over-excitation effect.
[Above info from Natural Health Consultants - Home page]
Pyritinol: The European Smart Drug
The drug Pyritinol is used in Europe for the treatment of several forms of neurologic impairment. Based upon published research, this therapy shows benefits in the treatment of early stage Alzheimer’s disease, stroke, vertigo, head trauma, and age-associated mental impairment.
The evidence shows that pyritinol enhances neuronal metabolic function. It works by increasing brain-cell energy levels so that youthful, cognitive function can be at least partially restored. There is a large volume of human clinical data supporting the safety and efficacy of this European therapy.
The pyritinol molecule is structurally similar to vitamin B6, but functions in the brain in a different way. The dose of pyritinol used in most of the human clinical studies is one 200-mg capsule taken 3 times a day.
(In referring to the studies described below, a "double-blind" trial is one in which neither the subjects nor the persons administering the treatment know which treatment a subject is receiving. When a trial is "randomized," it means that subjects are assigned to treatment groups in a known probability distribution, to produce more accurate results.)
The journal Alzheimer’s Research (2/3 1996) reported on a double-blind study conducted in the United States in which pyritinol was compared to Hydergine and placebo (a dummy treatment) in treating 100 patients with Alzheimer’s disease. Two measures of cognitive function were used to assess treatment effects.
After 12 weeks of treatment, "the results indicated that treatment with pyritinol was associated with a significant and continuous improvement in cognitive functioning over the course of the study, while treatment with Hydergine was associated with a more modest improvement that tended to plateau early in the treatment phase."
In the journal Neuropsychobiology (26(1-2) 1992), a 12-week, double-blind clinical trial was performed to investigate the benefit of pyritinol in the treatment of several forms of senile dementia. A total of 156 patients were allocated to either of two groups: the "senile dementia of the Alzheimer’s type" group, or the "multi- infarct dementia (stroke)" group.
In a 12-week, double-blind treatment, the researchers used three well-established tests to evaluate cognitive function. In addition, EEG brain mapping was employed to measure brain-cell function.
The doctors stated, "The therapeutic efficacy of pyritinol was clearly demonstrated by confirmatory analysis as the drug was statistically significantly superior to placebo in all three target variables. The EEG mapping demonstrated significant differences between placebo and pyritinol.
Based on the results of this trial, it can be accepted that the therapeutic effect of pyritinol is superior to placebo in patients with mild to moderate dementia of both degenerative (Alzheimer’s) and vascular (stroke) etiology."
As reported in a study in the British journal International Clinical Psychopharmacology (January, 1989), 26 patients with Alzheimer’s disease were randomly assigned in a double- blind trial of pyritinol versus placebo. The patients had a mild to moderate degree of dementia.
The results of the study showed that "pyritinol was associated with a significant improvement in cognitive performance. Regional cerebral blood-flow data showed that treatment with pyritinol normalized the pattern of blood flow increase during activation and improved the score on the test used for activation."
In the German journal Pharmacopsychiatry (September 1986), the effects of pyritinol were investigated in a placebo-controlled, randomized, double-blind study in geriatric patients suffering from cerebral functional disorders, with a moderate to severe degree of chronic brain syndrome. In a previous study, a rise in the vigilance (wakefulness, alertness) level was demonstrated in patients undergoing pyritinol treatment. Data from 107 patients were included in the statistical analysis, 54 on pyritinol and 53 on placebo. No notable adverse drug reactions were observed.
The doctors reported, "Statistically significant results were found in favor of pyritinol, compared with placebo, in both the level of clinical symptomatology & the performance level. Particularly impressive was the superiority of pyritinol in the factor ‘social behavior.’"
In the journal Neuropsychobiology (24(3) 1990), 12 healthy male volunteers received pyritinol in doses of 600 or 1,200 mg per day, or placebo for three days according to a randomized, double-blind design. On the first and third days of each of the three treatment periods, subjects completed a battery of psychological tests. The doctors reported, "Significant improvements in the Critical Flicker Fusion test and the Choice Reaction Time test were found after pyritinol."
In a study conducted at the Max-Planck-Institute of Neurology and published in Annals of the New York Academy of Sciences (640, 1991), pyritinol was tested along with piracetam and phosphatidylserine in Alzheimer’s patients. Positron emission tomography (PET) was used to measure the brain’s energy metabolism (brain functioning).
The doctors noted that glucose metabolism decreases slightly with age, but Alzheimer’s disease shows severe deficits in glucose metabolism. In the assessment of the effects of pyritinol on disturbed glucose metabolism, the doctors stated, "PET studies showed general increases in glucose utilization with piracetam, pyritinol and phosphatidylserine.
In the Journal of International Medical Research (9/3, 1981) 270 patients suffering from different forms of brain injury were treated with pyritinol for 6 weeks. It was shown that, "compared with placebo therapy, pyritinol produces statistically significant improvement in clinical and psycho neurological manifestations. It is concluded that pyritinol is a drug of therapeutic benefit in the treatment of the [results] of cerebral trauma."
In Pharmatherapeutica (England, 2/5, 1980) a double-blind, placebo- controlled trial was carried out on 40 patients suffering from moderately advanced dementia. The patients were allocated randomly either to pyritinol or placebo for three months. Assessments of cognitive function were made pre-treatment and monthly up to three months, and then at follow-up at six months. The doctors concluded, "Patients on pyritinol showed significantly higher levels of improvement than did those on placebo. Laboratory tests conducted throughout remained within normal limits for both groups."
In the German journal Med. Klin. (73/31 1978), 161 patients with chronic organic brain syndrome (average age 64 years) were treated with various doses of pyritinol for different periods of time. The doctors stated, "Statistical analysis of the data showed the success rate of treatment increases significantly with increasing dose & duration of [Pyritinol].
In the French journal Ouest Medicine (29/1 1976), pyritinol was tested on people who suffered from vertigo. The doctors described a complicated mechanism by which pyritinol was effective against vertigo, and reported the following:
"In a clinical experience with 60 cases of vertigo, the author obtained a cure rate of 83.33 percent, accompanied by an improvement in the patients’ mental and social state. The drug was tolerated well by patients of all ages."
The Czech journal Cs. Pediat. (29/10 1974) reported that pyritinol was tested on 41 children (28 boys and 13 girls) with various diseases of the central nervous system. The doctors reported, "In severe contusions of the skull with apallic syndrome (a total of 9 children), improvement was recorded in the majority, & marked improvement in 33%.
In meningo-encephalitis (8 children), treatment was successful in 50% the patients; in infantile cerebral palsy and malformations on the brain (19 children), treatment was successful in about 33% of cases. In minor disorders of the brain (5 children), the effect was smallest. According to these results, pyritinol treatment offers a certain contribution to treatment used in pediatric neurological practice."
Those with any of the neurological impairments that pyritinol has been documented to alleviate should consider taking 200 mg 3 times a day under the care of a physician, preferably a neurologist. It appears that pyritinol can produce both an immediate and a cumulative beneficial effect on neurologic function.
Those seeking to preserve and enhance cognitive function may consider trying two 200-mg capsules of pyritinol early in the day in place of drugs such as Hydergine. It is suggested that pyritinol be taken early in the day because its cerebral-energizing benefits can interfere with sleep if taken too close to bedtime.
[Info adapted from Vitamins and Supplements Rooted in Science - Life Extension]
Pyritinol In Dementia
Neuropsychobiology 1992;26(1-2):65-70
Therapeutic efficacy of pyritinol in patients with senile dementia of the Alzheimer type (SDAT) and multi-infarct dementia (MID).
Fischhof PK, Saletu B, Ruther E, Litschauer G, Moslinger-Gehmayr R, Herrmann WM. Psychiatric Hospital Baumgartner Hohe, Vienna, Austria.
This trial was performed to investigate the efficacy of pyritinol in the treatment of senile dementia. Initially, a total of 183 inpatients were screened for eligibility. Of 164 patients who met the inclusion criteria, 156 completed the trial. Allocation of the patients to the Senile Dementia of the Alzheimer Type group or the Multi-Infarct Dementia group was based on the Hachinski Ischemic Score, computed tomography scans and electroencephalographic (EEG) findings. In a 12-week double-blind treatment phase either 200 mg pyritinol dihydrochloride-monohydrate or placebo was given 3 times daily. Confirmatory statistics included item 2 of the Clinical Global Impression, the total score of the Short Cognitive Performance Test (Syndrom Kurz Test) and the factor ‘cognitive disturbances’ of the Sandoz Clinical Assessment Geriatric scale. In addition, data on tolerance, of EEG brain mapping and of a responder analysis were evaluated based on descriptive statistics. The therapeutic efficacy of pyritinol was clearly demonstrated by confirmatory analysis, as the drug was statistically significantly superior to placebo in all 3-target variables. The clinical relevance of the outcome was underlined by the analysis of the descriptive variables and by the convergence found at the different observation levels. The EEG mapping demonstrated significant differences between placebo and pyritinol, with the latter decreasing slow and increasing fast alpha and beta activity, which reflects improvement of vigilance. Based on the results of this trial, it can be accepted that the therapeutic effect of pyritinol is superior to placebo in patients with mild to moderate dementia of both degenerative and vascular etiology.
Clin Psychopharmacol 1989 Jan;4(1):25-38
Pyritinol treatment of SDAT patients: evaluation by psychiatric and neurological examination, psychometric testing and rCBF measurements.
Knezevic S, Mubrin Z, Risberg J, Vucinic G, Spilich G, Gubarev N, Wannenmacher W. Department of Neurology, University Hospital Centre, Zagreb, Yugoslavia.
A group of 26 patients with the diagnosis of Senile Dementia of Alzheimer type (SDAT) was included by random assignment in a double-blind, cross-over trial of pyritinol versus placebo. The patients had a mild to moderate degree of dementia. Psychiatric and neurological examination, psychometric testing, and measurement of the regional cerebral blood flow (rCBF) at rest and during mental activation were used to assess treatment effects. The results of the study showed that pyritinol was associated with a significant improvement in cognitive performance. RCBF data showed that treatment with pyritinol normalized the pattern of blood flow increase during activation and improved the score on the test used for activation.
Pharmatherapeutica 1980;2(5):317-22
A placebo-controlled study of pyritinol (‘Encephabol’) in dementia.
Cooper AJ, Magnus RV.
A double blind, placebo-controlled trial was carried out on 40 patients suffering from moderately advanced dementia. The patients were allocated randomly either pyritinol (800 mg daily) or identical placebo for 3 months. Assessments using a modified Crichton Geriatric Behavioral Rating Scale were made pre-treatment and monthly up to 3 months, and then at follow-up at 6 months. Patients on pyritinol showed significantly higher levels of improvement than did those on placebo. Laboratory tests conducted throughout remained within normal limits for both groups.
Alzheimer’s Research, 1996; 2(3):79-84
Efficacy of Pyritinol versus Hydergine upon cognitive performance in patients with Senile Dementia of the Alzheimer’s type: A double-blind multi-center trial.
George J. Spilich, Wolfgang Wannenmacher, Antonio Duarte, Marco Buendia, J. Toro Gómez, Sergio Ramirez, Amalia Anaya, and Enrique Otero.
In this multi-center trial, 100 patients with the diagnosis of Senile Dementia of the Alzheimer’s type (SDAT) of mild to moderate severity were randomly divided into two treatment groups and, following a placebo wash-out phase, were administered either pyritinol or hydergine for 12 weeks in a double-blind, randomized parallel comparison. Two measures of cognitive functioning were employed to assess treatment effects. The results indicated that treatment with pyritinol was associated with a significant and continuous improvement in cognitive functioning over the course of the study while treatment with hydergine was associated with a more modest improvement that tended to plateau early in the treatment phase. We interpret our results to indicate that treatment of mild to moderate Alzheimer’s disease with pyritinol is more likely to result in an improvement in cognitive performance than is a similar course of treatment with hydergine. Our results also suggest that continued treatment with pyritinol is often accompanied by continued improvement in cognitive function, while treatment effects with hydergine are mostly limited to those observed in the initial 6 weeks of intervention.
Pyritinol In Children
Pediatr Res 1975 Sep;9(9):717-21
Pyritinol hydrochloride and cognitive functions: influence on children in slow learner classes.
Walti U, Kuenzler M, Schild J, Vassella F, Pavlincova E, Bircher J, Herschkowitz N.
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 that 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.
Zh Nevropatol Psikhiatr Im S S Korsakova 1979;79(10):1431-4
Analysis of the effectiveness of treating children with different forms of intellectual deficiency with piriditol
Lupandin VM, Ermolina LA, Zykov MV, Korobeinikova II, Dzhebrailova TD.
The clinical efficacy of piriditol treatment in children with intellectual insufficiency was studied by means of special techniques, determining the velocity of visual information processing (VVIP) and short-time visual memory (SVM), which reflects the functional state of the brain. Piriditol was administered to 50 children aged from 7 to 12 years. The clinical state was characterized as mental retardation, due to mild organic brain lesions or oligophrenia in the form of mild debility. The use of special techniques (VVIP and SVM) for the study of intellectual activity permitted to analyze more differentially the stimulating and sedative effect of piriditol, to detect the new property of the drug, i.e. to remove the processes of fatigue in the brain tissues. A positive effect of the treatment was most marked in children with mental retardation rather than in oligophrenic patients.
Pharmatherapeutica 1981;3(1):40-5
Tamitinol in paedopsychiatric out-patient therapy.
Sanz R, Bettschart W, Reinhardt B.
A study was carried out in 11 children, ranging in age from 7 to 12 years, to determine the clinical effect of tamitinol, in addition to psychotherapy, in alleviating disturbances of learning and behaviour. Tamitinol was administered as one 100 mg tablet per 10 kg body weight daily for 8 weeks. Assessments were made of the patients’ mental condition using a 7-point rating scale, before and during treatment. Global response to treatment and tolerance were evaluated at the end of the trial by the clinician and the patients (or parents). Significant improvement was noted in 7 of the 10 children who completed the study. Six of the 13 psychiatric symptoms evaluated by the clinician were significantly improved (p less than 0.01). The drug was well tolerated by all patients.
Cs.pediat. (Czechoslovakia), 1974, 29/10 (562-564)
Neurologic Diseases in Children
41 patients (28 boys & 13 girls) with various diseases of the central nervous system were treated by oral administration of pyritinol in addition to the usual therapy. Before, during and after termination of treatment, neurological, psychological and EEG examinations were made to evaluate the effect of pyritinol. The patients were divided into 4 main groups. In severe contusions of the skull with apallic syndrome (9), improvement was recorded in the majority, & marked improvement in one-third. In meningoencephalitis (8), treatment was successful in half the patients; in infantile cerebral palsy and malformations on the brain (19), treatment was successful in about one-third of cases. In minor disorders of the brain (5), the effect was smallest. According to these results, pyritinol treatment offers a certain contribution to treatment used in pediatric neurological practice.
J Hyg Epidemiol Microbiol Immunol 1983;27(4):373-80
Brain maldevelopment and delayed neuro-behavioural deviations, induced by perinatal insults, and possibilities of their prevention.
Benesova O.
Noxious insults interfering perinatally lead to disorganization of normal perinatal brain development characterized by growth acceleration and intensive histogenesis and known as a sensitive "vulnerable" period of CNS development. Thus induced abnormities, sometimes very discrete, give rise to functional pathology that becomes apparent gradually during maturation as neurobehavioural deviations. For the study of these pathogenetic processes, two experimental models were established. Rat was chosen as an advantageous model animal since the "brain growth spurt" occurring in man in the third trimester of gravidity is shifted postnatally in this altricial species. Prolonged neonatal malnutrition (days 1-40) lead in adult rats to behavioural abnormities (hyperactivity, stereotypy, decreased adaptability, aggressivity) associated with biochemical and electrophysiological alterations in the brain. But this multifactorial and long-term insult was not suitable for more precise analysis. Therefore short-term inhibition of protein synthesis was induced in 7-day-old rats by cycloheximide that resulted in delayed behavioural deviations (hyperactivity, decreased habituation, learning deficit, motor incoordination) connected with permanent morphological, biochemical and endocrinological alterations. These models were used for testing brain maldevelopment-regulatory action of nootropics. Pyritinol administered for 7-10 days following the noxious intervention prevented the brain maldevelopment and functional disturbances in both experimental models. Favourable effects of early and long-term pyritinol treatment on neuro-psycho-pathological sequels of perinatal distress were confirmed in clinical controlled prospective study of 128 high-risk newborns.
Pyritinol Studies
Neurol Neurochir Pol 1981 Jul-Aug;15(4):447-51
Comparative evaluation of psychoactive drugs used in patients with subacute and chronic cerebrovascular disorders
Wasilewski R, Lebiediewa N, Kozlowa E, Wolkow W.
The report is based on 315 patients with subacute and chronic cerebral circulatory disturbances caused mostly by atherosclerosis aged 30 to 82 years, treated for 1-6 months. In 90 cases Piracetam (Nootropil) was given, 107 received Piritinol (Encephabol, Enerbol), 77 Piriditol, 41 Centrophenoxin. The patients were allocated randomly to these groups. In the treated patients improvement was achieved in a considerable proportion of cases (44-82%) treated with different drugs. This improvement manifested itself as regression or decreased intensity of neurotic complaints, labyrinthine-cerebellar signs, pyramidal signs, anxiety and fears, improvement of recent memory, attention, psychomotor activity. The best results were obtained with Nootropil, moderately good with Centrophenoxin, Encephabol, and poor with Piriditol. Drug tolerance was best with Encephabol, while that of other drugs was slightly worse. The only disquieting symptoms was activation of epileptic seizures in several patients treated with Nootropil or Centrophenoxin. The best way of administration was giving the drugs in two doses in the morning hours and at noon. The authors regard as useful the treatment of patients with subacute and chronic cerebral circulatory failure with psychoenergizing drugs.
Farmakol Toksikol 1980 Jul-Aug;43(4):417-21
Effect of pyriditol on drug metabolism
Avakumov VM, Kovler MA.
Pyriditol (encephabol, enerobol, pyrithioxin, etc.), a disulfide derivative of pyridoxin, exerts an inhibitory effect on hexobarbital and amphetamine metabolism i vivo and on ethylmorphine N-demethylation in vitro. In the latter case the inhibition proceeds according to the mixed type of action. Pyriditol potentiates the hypnotic action of hexobarbital and barbital as well as the effects of amphetamine stereotypy. The mechanism of the potentiating of hexobarbital and amphetamine effects is of combined character and is conditioned both by the physiological properties of pyriditol and its inhibitory effect on hexobarbital and amphetamine metabolism.
Neuropsychobiology 1990-91;24(3):159-64
Psychopharmacological effects of pyritinol in normal volunteers.
Hindmarch I, Coleston DM, Kerr JS. HPRU, Robens Institute, University of Surrey, Guildford, UK.
Twelve healthy male volunteers received pyritinol 600 or 1,200 mg or placebo for 3 days according to a randomised, double-blind crossover design. On the 1st and 3rd days of each of the three treatment periods subjects completed a battery of psychological tests including Critical Flicker Fusion (CFFT), Choice Reaction Time (CRT), tests of memory and subjective drug effects at 1, 2, 4 and 6 h after dosing. Significant improvements in CFFT and CRT were found after pyritinol. There were no significant differences on the other tests; however, the observed enhancement in performance could be attributed to the effect of the drug.
J Int Med Res 1981;9(3):215-21
Therapeutic effect of pyritinol on sequelae of head injuries.
Kitamura K.
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.
Anaesthesist 1979 Nov;28(11):530-2
Use of encephabol in anaesthesia and post-anaesthesia resuscitation.
Papatheodossiou N.
On the basis of good results in a pilot study of 40 patients who had undergone anaesthesia for various surgical operations, infusions of pyritinol was tested under controlled double-blind conditions on 60 further patients. Pyritinol 600 mg was infused immediately after anaesthesia. The aim of this study was to verify the favourable effect on the post-anaesthesia phase. It was shown that pyritinol significantly shortens the wakening time and, furthermore, positively influences the subjective feeling of the patients after anaesthesia.
MMW Munch Med Wochenschr 1978 Sep 29;120(39):1263-8
The effect of pyritinol on the human cerebrovascular circulation (author’s transl)
Herrschaft H.
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).
Electroencephalogr Clin Neurophysiol 1978 Jan;44(1):1-7
N1—P2 component of the auditory evoked potential during alcohol intoxication and interaction of pyrithioxine in healthy adults.
Krogh HJ, Khan MA, Fosvig L, Jensen K, Kellerup P.
The auditory evoked potential was used to assess the effect of alcohol intoxication (1 g/kg) and pyrithioxine (7 mg/kg) on 9 adult subjects. Its components in the latency range 50—250 msec (N1—P2) were studied for 6 g 30 min, during a constant level of alertness. Four periods were considered: alcohol alone, alcohol plus pyrithioxine, pyrithioxine plus alcohol and placebo. With alcohol alone the N1—P2 amplitude was small in the first part of the test and large in the second part as compared to placebo values. Pyrithioxine antagonism was greatest after alcohol had been resorbed. The placebo period indicated that amplitude changes were not due to long-term habituation, when the subject was kept alert.
Med Klin 1975 Jun 27;70(26):1133-8
Neurophysiologic control during treatment of cerebral ischaemia with danaden retard (author’s transl)
Klensch H, Hoffmann HR.
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.
Eur Neurol 1975;13(4):285-303
Facilitation through hyperventilation of therapeutic effect of pyrithioxin in cerebral infarct patients.
Stoica E, Enulescu O, Gheorghiu M.
A method of treatment consisting in administration of a neurodynamic drug, pyrithioxin, combined with a short period of hyperventilation (HV) was applied in cerebral infarct patients with hemiplegia. The combination was superior to pyrithioxin alone for the motor recovery of these patients. In some cases, it induced immediately a partial restoration of motility. The combination constantly brought about an increase in urinary excretion of norepinephrine and vanilmandelic acid, which failed to occur after pyrithioxin or HV alone. HV appears to facilitate the neural effects of the drug by promoting its transfer into the CNS.
