Abstract

Many classes of medications, such as antipsychotics, anticonvulsants, anticholinergics, and other commonly prescribed drugs, can cause cognitive impairment (CI). The negative effect of drugs on cognitive functions is due to the following pathophysiological mechanisms: a reduction in neuronal excitability, an increase in gamma-aminobutyric acid activity, and decreases in enzyme activity, the number of receptors, cerebral perfusion, as well as brain atrophy; moreover, a number of mechanisms have not been fully studied. An important role in the development of drug-induced CI is played by predisposing (senility or childhood, brain damage, chronic diseases, functional disorders, genetic causes, initial cognitive decline, polypragmasia), and precipitating (acute diseases, infections, metabolic disorders, dehydration, acute urinary retention, malnutrition, environmental influences, etc.) factors. The dose of a drug, the duration of its use is of absolute value. There is a need for the differential diagnosis of CI induced by drugs and CI directly related to the diseases, for which these drugs are prescribed. Drug-induced CI should be suspected if an association is established between a decline of cognitive functions and the start of drug intake. The treatment of this CI involves primarily dose withdrawal or reduction and the use of sustained-release dosage forms, if available. In some cases, cognitive training and/or special drug therapy may be required to correct the CI that has occurred. The measures to prevent drug-induced KI include the choice of the lowest-risk drugs, the use of current side-effect rating scales, in particular an anticholinergic burden scale.

Highlights

  • Many classes of medications, such as antipsychotics, anticonvulsants, anticholinergics, and other commonly prescribed drugs, can cause cognitive impairment (CI)

  • The negative effect of drugs on cognitive functions is due to the following pathophysiological mechanisms: a reduction in neuronal excitability, an increase in gamma-aminobutyric acid activity, and decreases in enzyme activity, the number of receptors, cerebral perfusion, as well as brain atrophy; a number of mechanisms have not been fully studied

  • There is a need for the differential diagnosis of CI induced by drugs and CI directly related to the diseases, for which these drugs are prescribed

Read more

Summary

Для андрогендепривационной терапии

Дигидротестостерон является мощным метаболитом тестостерона, B связывающимся с более высокой аффинностью с рецепторами андрогена, которые функционируют как фактор транскрипции. РНК рецептора андрогена экспрессируется в префронтальной коре, теменной доле и гиппокампе – областях мозга, ответственных за память и высшие когнитивные функции. Мужской эстроген (образующийся в результате ароматизации тестостерона) также связывается с участками в гиппокампе и префронтальной коре, увеличивая серотонинергическую и холинергическую активность, которая поддерживает нервную систему и изменяет уровень липопротеинов с целью снижения риска церебральной ишемии. Возраст-ассоциированная потеря ацетилхолина и холинергических A нейронов в базальном ядре Мейнерта; аккумуляция бета-амилоидных пептидов в коре, гиппокампе, миндалевидном теле. Предполагается, что причиной является повышение концентрации 9-карбоксиметоксиметилгуанина, основного метаболита ацикловира. Уменьшение концентрации ГАМК вследствие ингибирования метаболизма пиридоксина и накопления глутаминовой кислоты; нейротоксическое действие метаболита

Антиретровирусные Неизвестна
Уровень доказательности С В
Амантадин Карбамазепин Меперидин Препараты белладонны
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call