Treatment of the post-stroke speech disorders in the patients with cardiac and cerebrovascular pathology

Abstract

the Russian Academy of the Medical Sciences, by the end of the acute period of the blood-stroke aphasia is reported in 36% of the cases, while dysarthria is reported only in 14% of the cases.13–17 Speech disorder is the cause of the social and mental maladjustment of the patients, it significantly reduces their communicative capabilities, everyday vitality, contributes to their social exclusion. Recovery after the post-stroke speech disorder is a daunting task and depends on many factors. Unfortunately, the speech disorder is very persistent and the full recovery usually takes from 2 to 6 years.14–16,18,19 The presence of the gross total sensorimotor aphasia of the patients having the acute period of the blood-stroke (especially, if these defects are refractory during 3-4 months) is an adverse factor for the speech disorder recovery.20,21 With no regard of the severity of the blood-stroke and the starting date of the speech corrective therapy, speech function recovery in usually poor. In most cases, providing the long systematic psychological corrective therapy by the speech therapist-afasiologist can only induce the limited improvement of the speech function.21 In view of all these factors, the drug treatment plays a major role in the process of the post-stroke patients’ rehabilitation. There are no specific recommendations concerning the treatment of such patients in the present literature on the post-stroke cognitive defects. That’s why, specialists follow general approaches to treat the patients with bloodstroke (vascular risk factors correction, antihypertensive therapy, statins etc.). There are a lot of medications used for the recovery of the cognitive functions of the patients with the acute cerebrovascular accident but all of them could be divided into 4 groups: 1) medications that effect on the certain neurotransmitter systems; 2) medications with neurotrophic action; 3) medications with neurometabolic action; 4) medications with vasoactive action. Unfortunately, most of the medications used in Russian clinical practice have no evidencebased guidelines there are no results of placebo-controlled studies, that’s why, there is no objective evidence of the effectiveness. Today there is no consensus on the effectiveness of speech disorder’s drug therapy. In recent years many researches, studying the effect of the number of medications on neurorehabilitation’s effectiveness, are carried out. The series of scientific researches have proved positive effect of the Paricetam. The Paricetam administration at a dose of 2400 mg twice per day had a positive effect on the expressive speech indicators.22,23 According to Berthier et al.,24 Donepezil use at a dose of 10 mg once daily combined with weekly two hour speech corrective therapy improved the parameters of the nominal speech function and reduced the severity of post-stroke aphasia.24 According to the results of the randomized placebo-controlled studies that were performed by Walker-Batson et al.25 in 2001, 10 courses of speech therapy combined with 10 mg of the amphetamine during 5 weeks improved the recovery of speech disorder in blood-stroke’s recovery phase.25 With respect to the effectiveness of the antiparkinsonian medications in case of post-stroke aphasia the contradicting results were obtained: the bromocriptine administration did not have a positive effect on the speech functions recovery, but within this study the speech therapy for the patients was not conducted, however, the levodopa administration had a positive effect especially in case of the coronal position of the ischemic foci, but in combination with the speech corrective therapy.22,26 Akatinol memantine is one of the most advanced modern medications for the cognitive defect recovery. NMDA receptormediated excitotoxicity is considered to be an important factor for the neuron death in the ischemic penumbra.4,27–32 In case of the cerebrovascular pathology there has been observed the enhanced release of the glutamate from the ischemic neurons that causes the increasing of the glutamate activity and the synaptic transmission failure, contributes to the additional damage and untimely cell death. Memantine refers to the uncompetitive low affinity use-dependent NMDA receptor antagonists. Memantine blocks the cation channel of the neuron in the resting state, with the development of membrane depolarization processes the memantine is removed from the channel that provides normal synaptic transmission and recovery of the signal-to-noise ratio.33–38 Blocking the intracellular calcium current, the memantine has a neuroprotective effect.33,39–41 For a while this