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Treatment of dementia and cognitive impairment

Medical expert of the article

Psychiatrist, psychotherapist
, medical expert
Last reviewed: 06.07.2025

Treatment of dementia and other cognitive disorders

Optimal management of patients with cognitive impairment includes the following measures:

  • early detection of cognitive impairment;
  • determination of their nature and severity of disorders, establishment of a nosological diagnosis;
  • dynamic observation of the patient;
  • early initiation of treatment using (if possible) pathogenetic therapy;
  • duration and continuity of the therapy;
  • treatment of concomitant neurological, mental and somatic disorders;
  • medical, social and professional rehabilitation of patients;
  • psychological support and (if necessary) behavioral correction for the patient’s immediate relatives.

The choice of therapeutic tactics depends on the cause (nosological diagnosis) and severity of cognitive impairment. In the stage of mild and moderate dementia associated with Alzheimer's disease, vascular and mixed (vascular-degenerative) dementia, dementia with Lewy bodies and Parkinson's disease with dementia, acetylcholinergic and glutamatergic drugs have proven themselves well.

Currently, 4 drugs from the acetylcholinesterase inhibitor group are used in the treatment of dementia: donepezil, rivastigmine, galantamine and ipidacrine. The use of these drugs helps to reduce the severity of cognitive impairment, normalize behavior, improve adaptation in everyday life, which ultimately leads to an improvement in the quality of life of patients and their immediate environment.

Another approach to pathogenetic therapy of dementia is the use of memantine, a reversible non-competitive blocker of N-methyl-O-aspartate receptors to glutamate. It is used in the same diseases as acetylcholinesterase inhibitors. In severe dementia, memantine is the drug of first choice, since the effectiveness of acetylcholinergic drugs at this stage has not been sufficiently studied. Contraindications to the use of memantine are epilepsy and renal failure. Side effects are extremely rare.

If monotherapy is insufficiently effective, combined use of an acetylcholinesterase inhibitor and memantine is acceptable and advisable.

Neuroleptics are used to control behavioral and psychotic disorders in patients with dementia when pathogenetic therapy is ineffective. The most preferable are those that do not have extrapyramidal side effects (atypical neuroleptics), such as quetiapine and olanzapine. The tendency to complications of neuroleptic therapy is especially high in patients with movement disorders (e.g.,

Indications, contraindications and side effects of acetylcholinergic therapy (donepezil, rivastigmine, galantamine, ipidacrine) Alzheimer's disease with extrapyramidal symptoms, dementia with Lewy bodies, Parkinson's disease with dementia).

Indications

Absolute contraindications

Relative contraindications

Side effects

Alzheimer's disease

Vascular dementia

Mixed dementia

Dementia with Lewy bodies

Dementia in Parkinson's disease

Liver diseases

Sick sinus syndrome

Bradycardia {<55/min)

Severe bronchial asthma

Exacerbation of gastric ulcer or duodenal ulcer

Uncontrolled epilepsy

Renal failure

Dizziness

Nausea

Vomit

Diarrhea

Anorexia

Weight loss

In the non-dementia (mild and moderate) cognitive impairment stage, drugs with neuroprotective action are preferable, as they can potentially prevent or delay the development of dementia. However, in practice, it is very difficult to assess the preventive effect of a particular drug. Therefore, there is no single approach to managing patients with mild or moderate cognitive impairment. In everyday clinical practice, drugs with vasoactive and metabolic action (phosphodiesterase inhibitors, calcium channel blockers, pyrrolidone derivatives, peptidergic and amino acid drugs, ginkgo biloba leaf extract) are widely used. Against the background of the use of vascular and metabolic drugs, a decrease in the severity of cognitive and emotional disorders, an improvement in the well-being of patients are noted. The question of the duration of use of these drugs remains open. The empirically accepted intermittent (course) treatment of non-dementia cognitive impairment does not have sufficient justification.

As in dementia, in mild and moderate cognitive impairment, it is very promising to influence neurotransmitter systems in order to optimize synaptic transmission processes, which play a key role in the formation of cognitive functions. Regression of cognitive impairment in patients without dementia is noted against the background of the use of piribedil (an agonist of D 2 /D 3 receptors to dopamine and an antagonist of presynaptic alpha-adrenergic receptors, stimulating dopaminergic and noradrenergic transmission). At the same time, the use of acetylcholinergic drugs should apparently be limited to the initial stages of dementia, but is not justified in patients with mild and moderate cognitive impairment.


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