This paper is another one presenting the influence of neuroleptics on human EEG. There were performed routine EEG recordings of 41 non-medicated schizophrenic patients. The same patients were examined one e again on the l0-14th day of pharmacotherapy. The EEG recordings were evaluated visually as well as using automatic analysis of chosen channels (FFT). The results were analysed statistically.
The visual estimation revealed the slowing of alpha rhythm and increase of abnormalities in EEG in the patients under the therapy with neuroleptics. The bioelectrical activity was desorganised particularly by atypical neuroleptics.
The automatic analysis also showed the slowing of alpha rhythm, particularly in the right parieto-occipital region, as well as increase of fast theta activity in the left fronto-temporal region.
This article reviews the literature about secondary forms of restless legs syndrome induced by psychopharmacotherapy (RLS). Drug-induced forms of RLS were observed during treatment with neuroleptics, lithium, tricyclic and tetracyclic antidepressants, selective serotonin reuptake inhibitors, anticonvulsants, centrally acting antiemetic, histamine receptor H2 antagonists and after cessation of hypnotics, sedatives, anxiolytics and opioid analgesics. In addition, alcohol and caffeine were reported to increase RLS symptom s in susceptible individuals.
In this paper we present the up-to-date knowledge on the mechanisms of action of selective serotonin reuptake inhibitors (SSRIs) and their use in anxiety disorders. Furthermore, we describe changes in serotonergic, GABAergic, peptidergic (CCK), adrenergic and dopaminergic systems along with changes in the RPA axis, observed both in animal and human studies, after the administration of SSRIs. Finally, we discuss the influence of SSRIs on Fos expression in different brain areas.
Many lines of evidence suggest that mitochondrial oxidative stress is important in pathogenesis of dementias. Superoxide anion generated by mitochondria induces lipid peroxidation, synthesis of hydro gen peroxide and betaamyloid plaques formation. Tocopherol the inhibitor of lipid peroxidation and deprenyl the inhibitor of monoaminooxidase prevent the oxidative injury of human brain mitochondria. A placebo-controlled, c1inical trial of tocopherol and deprenyl in subjects with moderately advanced Alzheimer disease indicated, that group treated with tocopherol (2000 lU) or deprenyl (10 mg) may slow functional and mental deterioration.
Ginkgo biloba extracts such as EGb-761 have been suggested to have a multitude of beneficial effects on brain function, from enhancing cognitive function in dementia. Several mechanisms of action are useful in explaining how EGb 761 benefits patients with AD and other age-related, neurodegenerative disorders. The EGb 761 possesses antioxidant and free radical-scavenging activities and inhibits membrane lipid peroxidation. Flavonoids purchased from EGb 761 may inhibit the monoaminooxidase activity in brain and they increase the respiratory control ratio of brain mitochondria. EGb 761 is useful drug in dementia and other neurodegenerative diseases.