Therapeutic Efficacy of Pyritinol in Patients with Senile Dementia of the Alzheimer Type (SDAT) and Multi-infarct Dementia (MID)

Abstract

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.

Objective Assessment of the Degree of Dementia by Means of EEG

“…However, the spectral analysis of the Brunovsky/Matousek/Edman/Cervena/ Krajca EEG can contribute to reveal the small EEG abnormalities, consisting of a slowing of the alpha activity and an increase in power in the theta band [11]. An improved method, informing on the topographic changes of the EEG activity, was successfully applied in pharmacological studies in dementia [12][13][14].…”

Propentofylline in Adult-Onset Cognitive Disorders: Double-Blind, Placebo-Controlled, Clinical, Psychometric and Brain Mapping Studies

“…Based on the CT, primarily vascular etiology of the con dition could be assumed in only a smaller part of the patients, although in this context it is of interest that in the subsample of patients undergoing EEG brain map ping the MRI showed vascular findings much more often than the CT. Anyhow, several investigators have de scribed similar therapeutic outcomes in dementias of different etiologies treated by the same drug such as xantinolnicotinate [29,30], denbufylline [31 ], pyritinol [32], nimodipin [33].…”

Demência vascular: dificuldades diagnósticas e tratamento

“…• Métodos de neuroimagem (TC, RM -volume lesional, número e topografia das lesões, gravidade de leucoaraiose, grau de atrofia e dilatação ventricular) 7,9,20,76 • Eletrofisiológicos (EEG espectral, coerência eletrencefalográfica, eletro-oculografia, análise do ciclo sonovigília, potenciais cognitivos, potenciais motores) 1,19,23,35,44,45,48,67,72,76 • Bioquímicos e hormonais (interleucina-1, histamina, fator de necrose tissular, complexos imunes circulantes, alfa-1-antitripsina e alfa-2-macroglobulina, GH, PRL, androsterona, cortisol urinário; CRH, neuropeptídeos, endotelina-1 e colinesterase no LCR) 5,[11][12][13][14]37,47,57,58,71,82 • Neuropsicológicos (vários conjuntos de testes, baterias de testes, escalas de gravidade de demê-ncia) 6,8,26,35,53,59,60,67,68,79 • Provas funcionais (SPECT, PET, espectroscopia por RM) 10,20,21,49,50,81…”