Cerebral small vessel disease (CSVD) is the most common, chronic and progressive vascular disease. The changes affect arterioles, capillaries and small veins supplying the white matter and deep structures of the brain. It is the most common incidental finding on brain scans, especially in people over 80 years of age. Magnetic resonance imaging (MRI) plays a key role in the diagnosis of CSVD. The nomenclature and radiological phenotypes of CSVD were published in 2013 based on the unified position of the so-called Centres of Excellence in Neurodegeneration. The disease is characterized by a diverse clinical and radiological picture. It is primarily responsible for stroke incidents, gait disturbances, depression, cognitive impairment, and dementia in the elderly. The CSVD contributes to about 20% of strokes, including 25% of ischemic strokes and 45% of dementias. Common causes of CSVD include arteriosclerosis, cerebral amyloid angiopathy (CAA), genetic small vessel angiopathy, inflammation and immune-mediated small vessel diseases, and venous collagenosis. There is no causal treatment and management is mainly based on combating known risk factors for cardiovascular disease (CVD).

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Thyroid dysfunction is very often accompanied by cognitive and affective disorders. The frequency of these disorders in patients with compensated Hashimoto’s thyroiditis (HT) is unknown. The aim of the present study was to evaluate brain dysfunction in euthyroid HT patients by means of event-related potentials (ERP) and magnetic resonance spectroscopy (MRS) and to correlate it with cognitive function. 68 patients with HT (59 female, 9 male) and 45 healthy controls were included in the study. All the patients underwent ERP including an analysis of N200 and P300 response parameters. MRS voxels were located in the posterior cingulate gyrus (PCG) and the left parietal white matter (PWM). The NAA/Cr, mI/Cr, and Cho/Cr ratios were analysed. The ERP parameters, MRS metabolite ratios and hormonal concentrations (TSH, fT3, fT4) as well as TGAb and TPOAb titer were also correlated. There was a significant prolongation of the latencies of N200 and P300 potentials and a significant decrease of P300 amplitude in HT patients than in the control group. There was a significant positive correlation between the mI/Cr ratio in the PCG area and P300 latencies. NAA/Cr ratio in the PCG region showed significant negative correlations with all N200 latencies. The results may suggest brain dysfunction in neurologically asymptomatic HT patients. ERPs undergo significant changes in patients with HT and may, in combination with MRS, constitute an important element in the recognition and monitoring of cognitive functions in this group of patients.

Chronic inflammatory demyelinating polyneuropathy (CIDP) is the most common form of autoimmune polyneuropathy. It is a chronic disease and may be monophasic, progressive or recurrent with exacerbations and incomplete remissions, causing accumulating disability. In recent years, there has been rapid progress in understanding the background of CIDP, which allowed us to distinguish specific phenotypes of this disease. This in turn allowed us to better understand the mechanism of response or non-response to various forms of therapy. On the basis of a review of the relevant literature, the authors present the current state of knowledge concerning the pathophysiology of the different clinical phenotypes of CIDP as well as ongoing research in this field, with reference to key points of immune-mediated processes involved in the background of CIDP.