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).

We present six cases of extra-axial lesions: three meningiomas [including one intraventricular and one cerebellopontine angle (CPA) meningioma], one dural metastasis, one CPA schwannoma and one choroid plexus papilloma which were chosen from a larger cohort of extra-axial tumors evaluated in our institution. Apart from conventional MR examinations, all the patients also underwent perfusion-weighted imaging (PWI) using dynamic susceptibility contrast method on a 1.5 T MR unit (contrast: 0.3 mmol/kg, rate 5 ml/s). Though the presented tumors showed very similar appearance on conventional MR images, they differed significantly in perfusion examinations. The article draws special attention to the usefulness of PWI in the differentiation of various extra-axial tumors and its contribution in reaching final correct diagnoses. Finding a dural lesion with low perfusion parameters strongly argues against the diagnosis of meningioma and should raise a suspicion of a dural metastasis. In cases of CPA tumors, a lesion with low relative cerebral blood volume values should be suspected to be schwannoma, allowing exclusion of meningioma to be made. In intraventricular tumors arising from choroid plexus, low perfusion parameters can exclude a diagnosis of meningioma. In our opinion, PWI as an easy and quick to perform functional technique should be incorporated into the MR protocol of all intracranial tumors including extra-axial neoplasms.

The purpose of this study was to assess metabolic, perfusion, and microstructural changes within the posterior cingulate area in patients with Alzheimer's disease (AD) and amnestic mild cognitive impairment (aMCI) using advanced MR techniques such as: spectroscopy (MRS), perfusion weighted imaging (PWI), and diffusion tensor imaging (DTI). Thirty patients with AD (mean age 71.5 y, MMSE 18), 23 with aMCI (mean age 66 y, MMSE 27.4), and 15 age-matched normal controls (mean age 69 y, MMSE 29.5) underwent conventional MRI followed by MRS, PWI, and DTI on 1.5 Tesla MR unit. Several metabolite ratios (N-acetylaspartate [NAA]/creatine [Cr], choline [Ch]/Cr, myoinositol [mI]/Cr, mI/NAA, mI/Cho) as well as parameters of cerebral blood volume relative to cerebellum and fractional anisotropy were obtained in the posterior cingulate region. The above parameters were correlated with the results of neuropsychological tests. AD patients showed significant abnormalities in all evaluated parameters while subjects with aMCI showed only perfusion and diffusion changes in the posterior cingulate area. Only PWI and DTI measurements revealed significant differences among the three evaluated subject groups. DTI, PWI, and MRS results showed significant correlations with neuropsychological tests. DTI changes correlated with both PWI and MRS abnormalities. Of neuroimaging methods, DTI revealed the highest accuracy in diagnosis of AD and aMCI (0.95, 0.79) followed by PWI (0.87, 0.67) and MRS (0.82, 0.47), respectively. In conclusion, AD is a complex pathology regarding both grey and white matter. DTI seems to be the most useful imaging modality to distinguish between AD, aMCI, and control group, followed by PWI and MRS.

A complex picture of factors influencing cognition is necessary to be drawn for a better understanding of the role of potentially modifiable factors in dementia. The aim was to assess the prevalence and determinants of cognitive impairment, including the role of cerebral small vessel disease (CSVD) in Polish middle-aged cohort. A comprehensive set of clinical (hypertension, coronary heart disease, diabetes mellitus, hyperlipidaemia, body mass index, smoking status, alcohol intake) and socio-demographic data was collected in the PURE study in years 2007–2016, which was the basis for detailed analysis of risk factors of cognitive impairments in years 2016–2018 in the PURE-MIND sub-study. Five hundred forty-seven subjects (age range 39–65, mean 56.2 ± 6.5) underwent neuropsychological assessment with Montreal Cognitive Assessment (MoCA), Trail Making Test (TMT) and Digit Symbol Substitution Test (DSST) followed by brain MRI. Mean MoCA score was 26.29 and 33% participants met criteria for mild cognitive impairment (MCI) (MoCA< 26). Seventy-three percent showed findings related to CSVD. Higher WMH burden and lacunar infarcts were associated with lower MoCA and DSST scores. Severe CSVD was associated with twofold incidence of MCI, and obesity increased its probability by 53% and hypertension by 37%. The likelihood of MCI was reduced in nonsmokers. One factor analysis showed the important role of lower level of education, older age, rural area of residence and hypertension. MCI and CSVD are highly prevalent in the middle-aged population in Poland. A greater importance should be given to potentially modifiable risk factors of dementia which are already present in mid-life.

Primary progressive multiple sclerosis (PPMS), the least frequent type of multiple sclerosis (MS), is characterized by a specific course and clinical symptoms, and it is associated with a poor prognosis. It requires extensive differential diagnosis and often a long-term follow-up before its correct recognition. Despite recent progress in research into and treatment for progressive MS, the diagnosis and management of this type of disease still poses a challenge. Considering the modern concept of progression “smoldering” throughout all the stages of disease, a thorough exploration of PPMS may provide a better insight into mechanisms of progression in MS, with potential clinical implications. The goal of this study was to review the current evidence from investigations of PPMS, including its background, clinical characteristics, potential biomarkers and therapeutic opportunities. Processes underlying CNS damage in PPMS are discussed, including chronic immune-mediated inflammation, neurodegeneration, and remyelination failure. A review of potential clinical, biochemical and radiological biomarkers is presented, which is useful in monitoring and predicting the progression of PPMS. Therapeutic options for PPMS are summarized, with approved therapies, ongoing clinical trials and future directions of investigations. The clinical implications of findings from PPMS research would be associated with reliable assessments of disease outcomes, improvements in individualized therapeutic approaches and, hopefully, novel therapeutic targets, relevant for the management of progression.

Background. Parkinson's disease (PD) is a progressive neurodegenerative disorder with a characteristic clinical picture. Apart from classical movement disorders, a significant role is also played by non-motor symptoms, in particular cognitive impairments, which have a significant impact on the quality of life of the patients. Tau protein and amyloid beta are well-known non-specific biomarkers in Alzheimer's disease (AD). Objectives. The study assessed the practical value of determining tau protein and amyloid beta (A beta 42) in the blood serum of patients with PD and their relationship with cognitive impairments, radiographic image and the used dose of L-DOPA. Material and methods. The neuropsychological assessment was carried for 64 patients with PD. The levels of amyloid beta 1-42 (A beta 42) and tau proteins in serum were also measured. Results. The A beta 42 level in the serum was statistically higher in patients with longer duration of the disease (p < 0.05) and those who were taking a higher dose of L-DOPA (p < 0.05). The average level of tau protein in the serum was slightly lower in the study groups than in the control group and showed no statistical significance. No correlation was found between the levels of tau protein and A beta 42 and the results of neuropsychological tests. Tau protein correlated with hippocampal atrophy (p < 0.05). Conclusions. Serum levels of A beta 42 and tau protein in PD may be a useful marker for the assessment of cognitive impairments. The role of L-DOPA in the process of dementia in PD remains unclear.