Functional recovery of patients with intracerebral haemorrhage and cerebral infarction after rehabilitation.

To investigate potential differences in functional recovery after rehabilitation between intracerebral haemorrhage and cerebral infarction, we retrospectively compared the outcomes of patients with intracerebral haemorrhage (N = 208) and cerebral infarction (N = 480) who were consecutively discharged from our convalescent rehabilitation hospital between January 2013 and December 2018. Functional improvement was estimated by functional independence effectiveness measurements (proportion of potential for improvement achieved) upon discharge. Univariate analysis showed no significant differences in functional improvement between the two groups possibly because of the demographic variations upon admission.

Functional recoveries of patients with branch atheromatous disease after rehabilitation: Comparison with other types of cerebral infarction and importance of stratification by clinical categories.

Background: Functional recoveries after rehabilitation of patients with branch atheromatous disease (BAD) have not been well investigated, however, clinical category of cerebral infarction including BAD itself could be a potential predictive factor for functional outcome.

Objective: To describe characteristics of functional recoveries of patients with BAD through comparison with other types of cerebral infarction.

Methods: We retrospectively compared outcomes of patients with BAD (N = 222), cardioembolic cerebral infarction (CE: N = 177) and atherothrombotic cerebral infarction (AT: N = 219) by using functional independence measure (FIM) and FIM effectiveness (the proportion of potential for improvement achieved).

Effect of intensive rehabilitation on improvement of activity of daily living after intracerebral hemorrhage: a retrospective observational study.

Between 2008 and 2012, the intensity of rehabilitation therapy for the recovery phase of stroke was gradually increased at our hospital in line with the policy of Japan's National Insurance System. Training hours increased from 0.8 to 2.

Apoptosis of T cells in peripheral blood and cerebrospinal fluid is associated with disease activity of multiple sclerosis.

Apoptotic elimination of pathogenic T cells is considered to be one of regulatory mechanisms in multiple sclerosis (MS). To explore the potential relationship between Fas-mediated apoptosis and the disease course of MS, we examined apoptosis, defined by annexin V (AV) binding, and Fas (CD95) expression in CD4+ and in CD8+ T cells in MS patients by using five-color flow cytometry. The percentage of AV+CD4+CD3+ cells and CD95+AV+CD4+CD3+ cells in peripheral blood and cerebrospinal fluid (CSF) were significantly decreased in active MS patients compared with inactive MS patients.

The activation of memory CD4(+) T cells and CD8(+) T cells in patients with multiple sclerosis.

To reevaluate whether an association exists between the clinical course of multiple sclerosis (MS) and the activation of memory T cells, we investigated the phenotype of T cells in peripheral blood and cerebrospinal fluid (CSF) of patients with MS using five-color flow cytometry. A cross-sectional study with 39 relapsing-remitting MS patients demonstrated that the percentage of CD25(+)CD45RO(+)CD4(+)CD3(+) cells was significantly increased in peripheral blood as well as in CSF of active MS patients compared with inactive MS patients. A longitudinal study with 11 relapsing-remitting MS patients also showed a higher percentage of CD25(+)CD45RO(+)CD4(+)CD3(+) cells in peripheral blood at the phase of exacerbation than during remission.

[The role of apoptosis in autoimmune encephalomyelitis].

Experimental autoimmune encephalomyelitis(EAE), an inflammatory demyelinating disease of the central nervous system(CNS) provoked by myelin antigens, is widely used as a model for multiple sclerosis. Recent studies have shown that apoptosis may contribute to the death of oligodendrocytes and/or neurons, a pathological event leading to neurological deficits. On the other hand, the apoptotic elimination of inflammatory cells such as T cells and macrophages from the CNS is generally believed to contribute to the spontaneous recovery of EAE.

Regulatory role of p53 in experimental autoimmune encephalomyelitis.

The role of p53, a pro-apoptotic protein, in experimental autoimmune encephalomyelitis (EAE) was investigated using p53-deficient C57BL/6J mice. p53-deficient mice immunised with myelin oligodendrocyte glycoprotein (MOG) exhibited a more severe clinical course of EAE with more severe inflammation in the central nervous system (CNS) compared to wild-type littermates. While T and B cell responses of p53-deficient mice to MOG were comparable to those of wild-type littermates, significantly higher production of IL-6, granulocyte macrophage colony-stimulating factor and IL-10 was observed in lymphocytes exposed to MOG from p53-deficient mice than those from wild-type littermates.

The suppression of T cell apoptosis influences the severity of disease during the chronic phase but not the recovery from the acute phase of experimental autoimmune encephalomyelitis in mice.

The elimination of T cells by apoptosis is considered to be one of the regulatory factors in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. To address further the role of apoptotic T cell death in EAE, we investigated myelin oligodendrocyte glycoprotein (MOG)-induced EAE in transgenic mice overexpressing the anti-apoptotic gene, bcl-2, in T cells. During the acute phase of EAE, no significant difference was observed in the clinical course, pathology and T cell response to MOG between bcl-2 transgenic mice and wild-type littermates.

Gender does not influence the susceptibility of C57BL/6 mice to develop chronic experimental autoimmune encephalomyelitis induced by myelin oligodendrocyte glycoprotein.

Multiple sclerosis (MS), an inflammatory demyelinating disease of the central nervous system (CNS), is more prevalent in females than males. It is well documented that a significant gender difference exits in the susceptibility of mice to develop experimental autoimmune encephalomyelitis (EAE), a model of MS, induced by myelin basic protein or proteolipid protein. In contrast, we report here that no significant difference between female mice and male mice with myelin oligodendrocyte glycoprotein (MOG)-induced EAE was observed in the incidence of disease, clinical course, histological findings in the CNS, T cell response and cytokine production of spleen cells to MOG, and anti-MOG IgG level in serum.