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Neurogenic dysphagia is a disorder with impaired swallowing, which is caused by various disorders of the central and peripheral nervous systems, neuromuscular transmission, or muscles. Dysphagia is one of the most common and at the same time the most dangerous symptoms of many neurological disorders. Patients with dysphagia often have severe disability, a higher risk of aspiration pneumonia, and significantly increased mortality rate. Despite the availability of many diagnostic screening methods, clinical scales, questionnaires, and instrumental diagnostic methods, the issue of neurogenic dysphagia is underestimated, especially in the early stages. As a result, patients do not receive timely treatment and prevention of dysphagia and associated complications. Validation of available diagnostic scales, development of international protocols and standards for the diagnosis, treatment, and prevention of dysphagia and associated complications are important to establish a unified and evidence-based approach for patients with dysphagia.

Background. Type 2 diabetes (Т2DM) both directly and indirectly impacts the development of morphological and functional changes of the central nervous system. Aim. The study was to determine clinical and neurophysiological patterns of cognitive impairment (CI) in patients with chronic cerebrovascular diseases (CCD) and Т2DM. Materials and methods. We examined 132 patients with CCD. First group included 58 patients without Т2DM aged 64.5 [58; 72], second group 74 patients with CCD and Т2DM 63 [57; 70]. Clinical, neurological, neuropsychological, neurophysiological (cognitive evoked potentials (EP) and neurovisualisation (brain MRI) examination was carried out to all patients. Results. Somatic and neurological characteristics of the patients were similar in both groups with the exception of more distinct metabolic changes in Т2DM patients. Neurovisualisation study of the brain MRI in Т2DM patients revealed more distinct changes in the form of white matter hyperintensity and subarachnoidal spaces enlargement. Neuropsychological examination in patients revealed the reduction of intellectual flexibility, constructive praxis disruption, optical spatial dysfunction and deteoration of delayed word recall. Significant disorders in the way of overall cognitive impairment, lobar dysfunction and impaired verbal associative productivity, proved by statistically lower amplitude and higher latency of P300 EP peak were noted in Т2DM patients. Correlation links were detected: for P300 amplitude and direct and inverse number listing test (r=0.366 and r=0.520; p=0.006 and p0.001 respectively); P300 latency and HbA1c (r=0.32; р0.05) in group 2 and glucose levels in both groups (r=0.30; p0.05); inverse relationship of latency with control functions evaluation (r=-0.34; p=0.008). Conclusion. CCD especially with Т2DM manifests with neurocognitive imbalance, including control functions disruption and are accompanied by neurophysiological and neurovisualistion changes.