The specific of sclerosis multiplex (SM) – young patient’s age, heterogeneity of symptoms, not prediction of disease course – inflict that the rehabilitation of persons with SM is one of the most difficult questions of neurological rehabilitation. So the wide spectrum of symptoms in sclerosis multiplex caused that this is chronic disease, which we struggle every day. Sclerosis multiplex is chronic disease of the central nervous system, which occurrence with 30-100 frequency incidents on 100 000 occupants. However, the possession knowledge about this disease, and the possible therapeutic forms can in many cases soften stepping symptoms and have positive effects in many parameters. In last years growth of number scientific reports documenting the effectiveness rehabilitation in sclerosis multiplex was observed. The rehabilitation in multiple sclerosis remains the symptomatic treatment and deals with all the range of motor disturbances caused by this illness (form vegetative to smooth coordination problems). The management of the therapeutic process effectively reduce the disease effects, helping the same pharmacological treatment. Independently of the diagnosis form, the results of SM is self-independently and the lowering quality of life, what make difficult gradually independence, self-service and degree of moving in every conditions. The stabilisation by physiotherapist defects of function and the qualification of proceeding aims, gives the possibility reducing the sizes of occurrence symptoms in measure of disease progress. In this work the authors presents the chosen forms of motive exercises, physical procedures, and some principles of procedures during rehabilitation activities in patient’s with SM.
Fatigue syndrome, depression and cognitive function impairment are very frequent in multiple sclerosis. Investigations of symptoms of these disturbances were not examined routine. They require time and clinical experience. These sufferings can step out on every stage of the disease, also outdistancing physical symptoms, as well in clinically isolated syndrome. Unfortunately, they undergo remission seldom. Fatigue syndrome is one of the most frequent and the most serious problem in multiple sclerosis. It is the cause of serious motor and mental handicap and intellectual, the causing the greater depth the disability and deterioration quality of life. Moreover, it is unusually difficult to clinically effective treatment. The impairment of cognitive functions, and especially the fresh memory, belongs to deficits observed already in initial phase of disease. Depression among the patient with multiple sclerosis is result of many complicated processes. It can be result of chronicity of disease, as also the lack of possibility of effective treatment and the unforeseeable course of the disease or the effect of therapy of disease. Depression is intensified at the beginning of the disease, mainly in the relapsing-remitting form and influences on negative perceptions of neurological symptoms of the disease. It poorly correlates with clinical severity of multiple sclerosis. Fatigue syndrome, depression and cognitive function impairment more often were observed in primary progressive form of the disease than in relapsing-remitting, although this has not been a constant finding.
Multiple sclerosis is chronic and progressive disorder of central nervous system, in which different psychiatric diagnosis comorbit in 75% with neurological symptoms. The reasons of depressive disorders are still not precisely known. Psychiatric disorders are often comorbid with neurological disorders and also influence diagnosis and treatment, more often than in other somatic illnesses. It is worth to emphasize that psychic disturbances are a consequence of neurological disorders but can also be primary sign of the disease. Especially emotional disorders and cognitive impairment are characteristic to patients with multiple sclerosis. Emotional, behavioural disorders and cognition dysfunction are often a result of pharmacotherapy of neurological disorders. Psychiatric disorders are often met in patients with autoimmunological disorders, what is more corticosteroid treatment may worsen the symptoms. Depressive disorders, especially serious and moderate episodes, occur twice more frequent than in general population. Following some authors patients suffering from multiple sclerosis and psychiatric disorders present deeper cognitive function impairment, poorer life quality and motor abilities as well as have worse treatment response. Although cognitive functions’ worsening occurs in half number of multiple sclerosis patients, dementia appears in few cases. Psychiatric disorders commonly comorbit with multiple sclerosis have adverse influence on everyday functioning.
Apolipoprotein E plays an important role in metabolism of cholesterol and in modulation of inflammatory reaction, processes of significance in pathology of multiple sclerosis. Therefore great interest is noted in the impact of ApoE on the pathophysiology of multiple sclerosis. The role of APOE as a gene associated with incidence of multiple sclerosis was a subject of many studies. The basic question whether a particular genotype of APOE or presence of particular alleles is predisposing the host to development of multiple sclerosis received till now no positive answer. The relatively high frequency of APOE genotype in multiple sclerosis patients did not reach statistical significance. Also the results demonstrating the influence of particular APOE genotypes or alleles on development of multiple sclerosis subgroups (relapsing-remitting form or primarily progressing form) proved to be insignificant and the association between the APOE alleles and frequency of relapses was not definitely established. The positive correlation was noted only in individual studies. The association between APOE allele and intensified progression of multiple sclerosis seems to be established. Most important were the results demonstrating an association between APOE ε4 and rapid disease progression in studies using magnetic resonance imaging but the apolipoprotein E genotype was not directly associated with severity of the disease, tested using the multiple sclerosis severity scale. The presence of APOE ε4 allele as a factor predisposing for development of cognitive deficit in multiple sclerosis, especially in learning and recent memory, seems to be well documented. The severe cognitive deficit in victims of multiple sclerosis was evidently associated with the ε4 allele and promotor polymorphism. It was even linked to a five-fold increase in the relative risk of cognitive impairment. The results obtained in Polish population were identical.
Multiple sclerosis (MS) is a rare disease of the central nervous system in the patients at developmental age. The onset of MS occurring in childhood constitutes less than 10% of the cases. The majority of data originating from the publications concerns the clinical course and laboratory investigations. At present not much is known about the sufficient competence in the histopathological findings, immunopathogenesis and genetic factors in the aforementioned age group. The suitable diagnostic criteria for the paediatric MS have not been defined yet, but many attempts have been made. At present McDonald’s criteria are obligatory, but they are less specific and sensitive for the children. To distinguish acute disseminated encephalomyelitis (ADEM) from the first attack of MS is still a challenging problem. In the differential diagnosis of paediatric MS it should be also taken into account: borreliosis, vasculitis, mitochondrial and metabolic disorders. Paediatric MS is associated with a more favourable course compared to adult MS, however, children can become disabled at a younger age. The relapsing-remitting course in paediatric MS concerns about 90% cases. The primary progressive course occurs rarely. The application of immunomodulatory therapies for children have been recommended, but still there is a lack of prospective investigations and long-term observations. Tolerability and efficacy of interferon β and glatiramer acetate appear to be similar to those observed at adults. In this paper we present the individualities of the childhood MS based on the literature available over the past decade. In particular, the authors present the symptoms, diagnostic and therapeutic difficulties of paediatric MS.
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS). It affects usually young people between 20 and 40 years of age, predominantly women. According to Lublin and Riengold classification there are four major clinical patterns of MS course: remitting-relapsing, primary progressive, secondary progressive and progressive-relapsing. Making definite diagnosis of MS is becoming recently very important because of development of some new immunomodulatory therapies of MS with proven effectiveness when used at the early stage of the disease. Because of the huge diversity of MS clinical signs and symptoms as well as the course of the disease, there are several other diseases with similar clinical picture. Differential diagnosis of MS includes such disease as: acute disseminated encephalomyelitis (ADEM), neuroboreliosis, neurosarcoidosis, systemic lupus erythematosus (SLE), Sjögren’s syndrome, CNS vasculitis, Behçet’s disease, antiphospholipid syndrome and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Very important in MS differential diagnosis are some laboratory findings. The most useful techniques are magnetic resonance imaging (MRI), cerebrospinal fluid (CSF) examination, visual evoked potentials (VEP) and some blood tests. They often facilitate differential diagnosis of MS at the early stage of the disease. This is very important because the proper treatment can be initiated early.
In its classical meaning multiple sclerosis (MS) denotes a demyelinating disease of the central nervous system, resulting in a multifocal, multistage and, less frequently, chronic progressive neurological syndrome. Currently, MS is treated largely as a generalised degenerative disease of the brain and spiral cord, in which an inflammatory process leads to not only demyelination and injury of axons but also to loss of neurons and cerebral atrophy. In its anatomical patterns at the beginning a subacute inflammatory process prevails, which becomes transformed into a chronic inflammation, linked to manifestation of foci (plaques) of variable numbers, size and distribution. The lesions may be observed using magnetic resonance tomography in T1- and T2-dependent patterns. The methods demonstrate also atrophy of the grey matter, particularly within the cerebral cortex, which is of a high clinical significance, determining several signs/symptoms of the disease. Several morphological, mainly immunohistochemical studies, demonstrated extensive lesions not only to the myelin but also to axons, already in fresh lesions. In the cellular infiltrates numerous lymphocytes T and B are encountered, of a high significance for the immunological pathomechanism of the disease. Several data indicate that the pathological process in MS reflects to a significant extent apoptosis, particularly apoptosis of oligodendroglia cells. Neuropathological investigations, performed largely on peripheral blood lymphocytes suggest that a retrovirus associated with MS may play a role in aetiology of MS. The extensive discussion whether MS is a uniform nosological unit still continues and, until now, only certain variability of neuropathological lesions, mainly demyelination, has been proven.
Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS). Aetiology of SM is still unknown. Two pathological processes: inflammation and neurodegeneration are present from the beginning of MS. Autoreactive myelin-specific T cells can mediate the inflammatory response. Final stage of the development of MS is demyelination and axonal damage, which leads to the appearance of neurological symptoms. Several experimental models of MS were developed to get information about the mechanisms of the disease development. Those models include knockout mice (known as myelin mutants), chemically induced inflammation in the CNS, viral and autoimmune models. Knockout animals with blocked gene for myelin basic protein (MBP), mice Rumpshaker and Jimpy without genes for proteolipid protein (PLP), and mice with blocked gene for myelin associated glycoprotein (MAG) have been used to study the mechanisms of demyelination. The use of various toxins such as ethidium bromide or cuprizone also allows the study of the mechanisms of de-/remyelinization in the CNS. Viral models of MS can be induced by Semliki Forest virus and Theiler’s virus. The well-known and widely used experimental model of MS is experimental autoimmune encephalomyelitis (EAE). None of the mentioned above models perfectly initiate development and course of this disease. However, thanks to them the pathological mechanisms leading to development of MS can be studied.