**4. Cognitive abilities and imaging methods**

Magnetic resonance imaging (MRI) is used as one of the basic methods for diagnostics, visualization, and monitoring of the inflammatory lesion dynamics in the brain and spinal cord. The first MRI studies in patients with MS were published in 1981. It was found that inflammatory lesions occur 5–10 times more than MS clinical attacks. Commonly used images for the diagnosis of MS are those in which lesions of hyperintense signal of size from 1 mm to several cm are apparent, located in the white matter of both hemispheres, mostly in the cerebral ventricles, as well as in the brain stem, medulla, cerebellum, and upper cervical spinal cord. If the radiologist wants to depict the active lesions, he/she applies gadolinium. The range of lesions visible in this way does not correlate with clinical disability as it is not known whether the lesion is currently in the stage of reparation or destruction.

The only areas described as hypodensities ("black holes") are areas where a loss of axons, thus the definitive loss of tissue, has occurred. The typical brain damage in the white matter in MS patients is clearly associated with a loss of axons [23]. Loss of axons is also a natural sign of brain aging, and its verification is only possible postmortem.

Recent neuropsychological studies especially use functional magnetic resonance imaging (fMRI) to assess the plasticity of functional cognitive deficits in patients with MS. The method consists of recording the activation of brain areas during the presentation of various simple neuropsychological tests. Compensatory mechanisms of cognitive functions already in the early stages of chronic MS are described. The results of fMRI scans in a group of MS patients with mild cognitive impairment and a healthy control group were compared. The functional activation areas of the brain were completely distinct during the presentation of the verbal naming test in each group (in MS patients in the frontal part of the right cortex and in the left Brodmann's area, and in the right cingulate gyrus in the healthy group). The functional reorganizations of motor functions are also described in fMRI assessments of MS patients, when compared to healthy subjects. MS patients with mild cognitive deficits assessed by neuropsychological tests were presented with auditory memory tests during an fMRI and were found to display heightened activity in different areas. Patients with greater neuropsycholog‐ ical deficits were found to exhibit lower activation of brain areas during the fMRI assessment, which probably supports the theory of adaptive mechanisms resulting from neural disorga‐ nization or inhibition associated with MS [24]. It is therefore also possible to explain the unproven relationship between the extent of morphological findings of gliosis and plaques in the white matter, and the severity and location of neuropsychological deficits in terms of this plasticity of neuropsychological functions. The range of specific cognitive deficits, such as memory disorders, reduced processing speed, and attention disorders, can be better explained by the cortical gray matter lesions (lesions and atrophy) than subcortical white matter lesions [25]. It has been shown that neocortical atrophy is associated with impaired verbal memory, visual episodic and working memory, verbal fluency, attention/concentration, and processing speed [26]. It is also possible that the neocortical atrophy is further responsible for slight personality changes, such as euphoria, that are seen in MS patients [27]. The left frontal atrophy occurs in patients with impaired verbal/auditory memory, while the right frontal atrophy is associated with impaired visual episodic and working memories. The medial temporal cortex atrophy is associated with a decrease in processing speed and impaired episodic and verbal memories. The most important within the subcortical gray mater are atrophy, structural changes, and an altered metabolism of the thalamus, which are associated with the impairment of many cognitive domains [28]. Generally, it can be concluded that the cognitive impairment observed in MS patients is caused by inflammatory lesions and a widespread loss of gray matter. Although it is not possible to define the neuropsychological profile of MS patients as strictly "cortical" or "subcortical", it seems that it is the disruption of the cortical gray matter which determines the degree and nature of cognitive dysfunction. Instead of the term sub‐ cortical dementia, often associated with a severe multi‐domain cognitive impairment, the term multiple disconnection syndrome is also used for cognitive deficits in MS [29].
