The impact of neurological comorbidities on sleep and the pharmacotherapy of terminal hyposomnia

Abstract

Introduction. Neurological comorbidities are sometimes trigger factors for terminal hyposomnia and other sleep disorders. Tissue hypoxia in the hypothalamus, hippocampus, limbic system release a metabolic hyperexcitation of the whole body during sleep and wakefulness, increases cortisol and adrenocorticotropic hormone during the early sleep period, parasympathetic tone decreases in heart rate variability and electroencephalographic activity is high during NREM sleep. Aim of study. The influence of neurological comorbidities on sleep and the approach of contemporary pharmacotherapeutic management in sleep disorders. Methods and materials. I conducted a retrospective study, analyzing the indication sheets of the observation sheets of 50 patients diagnosed with terminal hyposomnia in common with neurological comorbidities, hospitalized in the Department of Vascular and Extrapyramidal Neurology of the IMSP of the Institute of Neurology and Neurosurgery, Chisinau, during the period 2019-2020. Results. It was determined that vertebrobasilar syndrome and cerebral atherosclerosis have the highest share of sleep disorders, with the same level, representing 78% of patients. Depressive anxiety disorders were reported in 52% of patients, followed by migraine with a rate of 40%, tension-type headache with 30% and epilepsy with 4% of patients. The study showed that sleep disorders are closely correlated with vertebrobasilar syndrome and cerebral atherosclerosis having a high impact and favoring the occurrence of terminal hyposomnia because they have a common pathophysiology that leads to a marked deterioration of the brain, due to insufficient blood flow and as a result affects the posterior cerebral circulation followed by impaired sleep-wake circadian rhythm and the appearance of sleep disorders. The preparations used in terminal hyposomnia were listed: benzodiazepines (clonazepam, alprazolam), imidazopyridine derivatives (zolpidem) and associated with preparations of neurological comorbidities: MgSO4, mildronate, cyanocobalamin, piracetam and others. International guidelines also recommend preparations that help nourish neurons, brain vessels and ensure a smooth flow of blood. For example, atherosclerotic plaques or cerebral vasoconstriction will significantly improve the sleep-wake cycle, and the quality and quantity of sleep will be within the limits of the norm. Conclusion. Ensuring proper pharmacotherapeutic management, including neurometabolic preparations significantly reduces the risk of terminal hyposomnia, and comorbidities are an important guide for formulating an individualized treatment that offers therapeutic opportunities and limitations.