Objectives: No widely available, adequately sensitive diagnostic test to establish prognosis in stroke patients has been developed thus far. The aim of this study was to analyse changes in plasma levels of MMP-9 and MMP-2 as potential prognostic factors in patients with ischaemic stroke. Methods: The study included 56 patients presenting with the signs of ischaemic stroke for less than 24 hours, and 60 healthy controls without a history of neurological and/or inflammatory disorders. Plasma concentrations of MMP-2 and MMP-9 were determined immunoenzymatically at admission (i.e. within 24 hours of the cerebrovascular episode) and on the 7th day of hospital stay. Results: Median concentrations of MMP-9 in stroke patients were significantly lower than in the controls, both at admission and on the 7th day of hospital stay. No significant changes in the concentration of MMP-2 in ischaemic stroke patients were observed during the course of hospital stay. No significant association was found between both MMP concentrations and neurological status of patients with cerebrovascular episodes. Conclusions: The lack of significant associations between plasma concentrations of MMP-2/MMP-9 and clinical status suggests that these metalloproteinases should not be used as prognostic factors in patients with ischaemic cerebral episodes.
Multiple sclerosis is a chronic demyelinating disease of the central nervous system. At diagnosis, about 85% of patients with multiple sclerosis have a relapsing-remitting form of the disease. Relapses are the typical multiple sclerosis manifestation, yet their frequency during the disease’s course is variable and unpredictable. Usually at the disease onset relapse symptoms resolve totally, whereas in the later period relapses leave permanent residual neurological deficits. Neurological worsening in the course of multiple sclerosis may have aetiology other than relapse. Recurrence of pre-existing symptoms of multiple sclerosis in the context of infection or stress is termed a pseudo-relapse. Glucocorticosteroids are used to improve neurological recovery after a relapse. In the light of the current knowledge they act exclusively to counteract the symptoms, and do not affect disability progression in long-term observation, nor do they prevent subsequent relapses. The use of glucocorticosteroids is not necessary with every case of neurological worsening. Other reasons for exacerbation or occurrence of symptoms should be excluded, such as infection, stress or disease fluctuation. Benefits and risk, including adverse effects, comorbidities and contraindications should be considered before applying glucocorticosteroids for multiple sclerosis relapses. There is no universal dosing regimen. The article presents general rules for glucocorticosteroid use in multiple sclerosis, discussing its advantages and limitations.
Multiple sclerosis is a progressive inflammatory and demyelinating disease of the central nervous system. Although the primary cause of this disease has not been established yet, it is known that destruction of myelin sheaths and loss of neurons and oligodendrocytes can be observed as disease progresses. It has been suggested that a possible link between neuroinflammation and neurodegeneration could be the phenomenon of oxidative stress. Oxidative stress develops when there are too many free radicals produced within the cell, and the natural antioxidative mechanisms are not effective enough to dispose of them. It has been proven to contribute to the pathomechanism of such neurodegenerative disorders as Parkinson’s disease or Alzheimer’s disease. The role of oxidative stress in the pathogenesis of multiple sclerosis has also been recently confirmed, establishing it as a new target in the disease’s management. Even though the efficacy of such antioxidants as polyphenols, vitamins (A, C, E) and alpha-lipoic acid has been confirmed in many preclinical experiments, no significant effect has been shown in clinical trials. However, some clinical trials related to the use of antioxidants in multiple sclerosis treatment are still in progress. One compound with antioxidant potential that has been proven effective and safe in both preclinical and clinical trials is dimethyl fumarate. It was licensed for the treatment of multiple sclerosis in 2013. Even though its mechanism of action has not been fully established, one of its known effects is the induction of antioxidant pathway related to Nrf2 transcription factor and synthesis of antioxidant enzymes, leading to decrease in oxidative stress.
A growing number of people with dementia translates into the necessity to use modern imaging methods. Function tests assessing glucose metabolism in the brain, such as 18F-FDG PET/CT, are conducted in the case of clinical doubts and facilitate the differential diagnostics of dementia. In the case of the Alzheimer’s disease, glucose metabolism disorders become visible, above all, in the area of both the parietotemporal areas, posterior parts of the callosal gyrus, the precuneus as well as medial temporal lobe. In the case of dementia with the Lewy bodies, glucose metabolism disorders relate to the occipital lobes and both the parietotemporal areas. In the case of frontotemporal dementia, lesions are observed, above all, in the frontal lobes and poles of the anterior temporal lobes. On the other hand, in the case of vasogenic dementia, there are numerous, spread deficits visible in collecting a marker within the brain – both the cortex and the subcortical nuclei. Characteristic glucose metabolism disorders are present also in the case of other, less common neurodegenerative diseases, such as corticobasal degeneration and the atrophy of the posterior part of the brain. In the case of corticobasal degeneration, one can observe a decreased collection of 18F-FDG within the sensory-motor cortex, in the subcortical nuclei and the thalamus on the side with the disease, while in the case of atrophy of the posterior part of the brain – within both the parieto-occipital areas. Besides glucose metabolism, it is possible to assess the presence of β amyloid in the brain. It is deemed that a negative result of PET/CT for β amyloid enables to exclude the Alzheimer’s disease as being the cause of dementia. The utilisation of non-invasive PET/CT makes it possible to early diagnose dementia and determine the prognosis.
Working memory is the foundation of a well-functioning brain system, ensuring proper execution of complex cognitive problems. According to numerous researchers, emotions, in particular negative ones, impact the quality of working memory function. Patients with depressive disorders tend to display impaired working memory, experiencing difficulties with controlling or removing negative emotions and retaining positive information. The alterations in the capacity of working memory present in patients struggling with affective disorders have their neurobiological correlates. The literature regarding studies which have utilised neuroimaging techniques does not hold a congruent view as to the presence of a common pattern of brain dysfunction in patients with affective disorders. Mood disorders are most typically associated with abnormalities in the activity of both cortical and subcortical regions of the brain while solving tasks that involve working memory. Working memory dysfunctions play a major role in producing and fuelling the symptoms of affective disorders. Moreover, neuropsychological deficits present in patients diagnosed with bipolar affective disorder tend to be perceived as very characteristic for their functioning. This paper presents the most relevant current information concerning the issue in question. Further research into the area is much called for, with additional attention paid to the effect of the course and the clinical picture of the disease on the functioning of working memory, as it could potentially improve the quality of the diagnostic and therapeutic process for the patients.
The doctor–patient relationship is special as it addresses issues directly related to dignity and intimacy. Patients share information about their problems and, in turn, the doctor has the knowledge and skills that can help to solve these problems. It should be noted, however, that there is a clear disparity in this relationship: at some point the patient must trust the doctor and comply with the proposed instructions. As a result of this imbalance, the notion of patient rights was developed. It was pointed out that patients should be treated in a manner respectful of their dignity. This has resulted in an increasingly popular approach, according to which the patient has become a partner in the therapeutic process. In recent years, however, a disturbing phenomenon may be observed. Some patients have changed their attitude to doctors, regarding them exclusively as specialists in a given field. The expectations and demands of patients have increased and are sometimes accompanied by verbal and/or physical aggression. Therefore, some important issues that arise at this point: Does the occurrence of aggressive behaviour stem from a specific cause? Perhaps only a certain group of patients are likely to show this type of behaviour? Is it possible to become addicted to aggression? How should doctors react to verbal and/or physical violence?