The effect of low-frequency repetitive transcranial magnetic stimulation (rTMS) on the treatment of aphasia caused by cerebrovascular accident (CVA).

Background: Aphasia is a common outcome of Cerebrovascular Accident (CVA) in which clinical interventions have limited effectiveness. Some evidence suggests that noninvasive stimulation of the brain can have beneficial effects in the treatment of CVA induced aphasia. In patients with motor aphasia, repetitive Transcranial Magnetic Stimulation (rTMS) is used to facilitate long-term improvement in speech ability. Since identifying effective methods for treating CVA induced aphasia can be very important in subsequent decision-making and treatment interventions, the objective of this study was to evaluate the effect of low-frequency TMS in Broca's area in the right hemisphere on the treatment of CVA induced motor aphasia. Methods: This clinical trial enrolled 24 patients with a clinical diagnosis of motor aphasia caused by CVA using convenient sampling. In this study, the effect of stimulation of Broca's area in the right hemisphere was examined by low-frequency rTMS (one Hz) on aphasia caused by CVA. To conduct verbal fluency test in patients, their correct responses to the selected images before and after rTMS during a certain time were recorded and compared by non-parametric Wilcoxon test using SPSS16 and the significance level was considered <0.05. Registration ID of this research in IRCT is IRCT2014052417814N1. Results: The study findings suggested a significant difference between Wilcoxon test results of patients before and after rTMS (z= -4.401), and it was found that using low-frequency rTMS in the right hemisphere was effective on improving dysarthria in the study population with 95 percent confidence interval (p<0.001). Conclusion: According to the findings, low-frequency rTMS has the potential to be considered as a treatment for patients with nonfluent aphasia caused by CVA.

The effect of low-frequency repetitive transcranial magnetic stimulation (rTMS) on the treatment of aphasia caused by cerebrovascular accident (CVA).

Background: Aphasia is a common outcome of Cerebrovascular Accident (CVA) in which clinical interventions have limited effectiveness. Some evidence suggests that noninvasive stimulation of the brain can have beneficial effects in the treatment of CVA induced aphasia. In patients with motor aphasia, repetitive Transcranial Magnetic Stimulation (rTMS) is used to facilitate long-term improvement in speech ability. Since identifying effective methods for treating CVA induced aphasia can be very important in subsequent decision-making and treatment interventions, the objective of this study was to evaluate the effect of low-frequency TMS in Broca's area in the right hemisphere on the treatment of CVA induced motor aphasia. Methods: This clinical trial enrolled 24 patients with a clinical diagnosis of motor aphasia caused by CVA using convenient sampling. In this study, the effect of stimulation of Broca's area in the right hemisphere was examined by low-frequency rTMS (one Hz) on aphasia caused by CVA. To conduct verbal fluency test in patients, their correct responses to the selected images before and after rTMS during a certain time were recorded and compared by non-parametric Wilcoxon test using SPSS16 and the significance level was considered <0.05. Registration ID of this research in IRCT is IRCT2014052417814N1. Results: The study findings suggested a significant difference between Wilcoxon test results of patients before and after rTMS (z= -4.401), and it was found that using low-frequency rTMS in the right hemisphere was effective on improving dysarthria in the study population with 95 percent confidence interval (p<0.001). Conclusion: According to the findings, low-frequency rTMS has the potential to be considered as a treatment for patients with nonfluent aphasia caused by CVA.

A mutation causes MuSK reduced sensitivity to agrin and congenital myasthenia.

Congenital myasthenic syndromes (CMSs) are a heterogeneous group of genetic disorders affecting neuromuscular transmission. The agrin/muscle-specific kinase (MuSK) pathway is critical for proper development and maintenance of the neuromuscular junction (NMJ). We report here an Iranian patient in whom CMS was diagnosed since he presented with congenital and fluctuating bilateral symmetric ptosis, upward gaze palsy and slowly progressive muscle weakness leading to loss of ambulation. Genetic analysis of the patient revealed a homozygous missense mutation c.2503A>G in the coding sequence of MUSK leading to the p.Met835Val substitution. The mutation was inherited from the two parents who were heterozygous according to the notion of consanguinity. Immunocytochemical and electron microscopy studies of biopsied deltoid muscle showed dramatic changes in pre- and post-synaptic elements of the NMJs. These changes induced a process of denervation/reinnervation in native NMJs and the formation, by an adaptive mechanism, of newly formed and ectopic NMJs. Aberrant axonal outgrowth, decreased nerve terminal ramification and nodal axonal sprouting were also noted. In vivo electroporation of the mutated MuSK in a mouse model showed disorganized NMJs and aberrant axonal growth reproducing a phenotype similar to that observed in the patient's biopsy specimen. In vitro experiments showed that the mutation alters agrin-dependent acetylcholine receptor aggregation, causes a constitutive activation of MuSK and a decrease in its agrin- and Dok-7-dependent phosphorylation.

Myasthenia gravis development and crisis subsequent to multiple sclerosis.

During the last decade, sporadic combination of multiple sclerosis (MS) and myasthenia gravis (MG) has been reported repeatedly. Although these are anecdotal, they are important enough to raise concerns about co-occurrence of MG and MS. Here, we present a case of an MS patient who developed an MG crisis. She had received interferon for relapsing remitting MS. Interestingly, she developed an MG crisis 4 years after the diagnosis of MS. MS and MG have relatively the same distribution for age, corresponding to the younger peak of the bimodal age distribution in MG. They also share some HLA typing characteristics. Furthermore, some evidences support the role of systemic immune dysregulation due to a genetic susceptibility that is common to these two diseases. The association may be underdiagnosed because of the possible overlap of symptoms especially bulbar manifestations in which either MG or MS can mimic each other, leading to underestimating incidence of the combination. The evidence warrants physicians, especially neurologists, to always consider the possibility of the other disease when encountering any patients either with MS or MG. Anecdotal and sporadic reports of combination of multiple sclerosis (MS) and myasthenia gravis (MG) have been raised concerns about co-occurrence of them.