Rinshō shinkeigaku = Clinical neurology
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A 55-year-old woman with a 3-year and 4-month history of liver metastasis from breast cancer underwent chemotherapy with capecitabine and cyclophosphamide for following 10-months. She did not have hypertension and was not pregnant. She showed dysarthria and mild somnolence, and her conscious level developed to semicoma after 6 days. ⋯ Combination of these drugs was considered for the possible cause to induce leukoencephalopathy like PRES. Usually leukoencephalopathy occurs in relatively early time after start of chemotherapy with capecitabine or cyclophosphamide, but we consider that late-onset leukoencephalopathy can be induced by long-term chemotherapy with these drugs. It is necessary to observe leukoencephalopathy by brain MRI regularly when these drugs are used.
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Randomized Controlled Trial
[Stimulation of primary motor cortex and reorganization of cortical function].
The use of electrical motor cortex stimulation (EMCS) for post-stroke pain was established in Japan and has spread globally. EMCS has been used for the treatment of neuropathic pain, Parkinson's syndrome, and recovery of motor paresis. Since 2000, repetitive transcranial magnetic stimulation (rTMS) has been developed for the treatment of various neurological disorders. rTMS is a non-invasive method with almost no adverse effects. ⋯ For 'Kaifukuki' rehabilitation, high-frequency rTMS of affected M1 seemed to be effective for recovery of hand function. And even after cessation of rTMS, the recovery would be better than usual rehabilitation for two weeks. New methods and devices for rTMS therapy are under development, and rTMS of the M1 is likely to be established as an effective therapy for some neurological disorders.
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There are growing experimental and clinical data on the pathophysiological roles of antiganglioside antibodies in Guillain-Barré syndrome (GBS) and Fisher syndrome (FS). Antibodies to a ganglioside complex (GSC) consisting of two different gangliosides are detected in some GBS and FS sera. Recently, anti-GM1/GalNAc-GD1a complex antibodies, anti-GA1/GQ1b antibodies with no reaction against GM1/GQ1b, and anti-GM1/LM1 antibodies have been detected in GBS or FS sera. ⋯ Complement-independent pathophysiology such as blockade of voltage-gated Ca channels, the apoptotic mechanism of neurons, and alteration of microdomains in the nerve cell membrane should also be considered. Complex glycolipid environments in the cell membrane may govern the accessibility and avidity of antiganglioside antibodies for target gangliosides. Thus, the pathogenic effect of antiganglioside antibodies may depend on the local glycolipid environment in the nerve membrane, as well as on the antibody specificity.
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A 36-year-old man presented with cognitive impairment and disturbance of short-term memory functions with character change. Cerebrospinal fluid analysis revealed no abnormalities; however, brain MRI revealed high-signal intensity from bilateral hippocampus lesions on fluid attenuated inversion recovery (FLAIR) images and T(2) weighted images. The 18F-fluorodeoxyglucose PET demonstrated high glucose uptake in the bilateral hippocampus lesions. ⋯ The pathological findings were seminoma. We experienced a case of paraneoplastic limbic encephalitis associated with seminoma with short-term memory disturbance. The occurrence of paraneoplastic limbic encephalitis with antibodies against cell membrane (NMDA-receptor antibody and GluRε2 antibody) and intracellular (Ma2 antibody) is rare even in the literature.
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Review Case Reports
[Neurological decompression illness in a Japanese breath-held diver: a case report].
We report a Japanese breath-hold diver (Ama) who presented neurological disorders after diving. He repeated diving into 25-30 meters depth in the sea for 6 hours. After diving, he felt dizziness and unsteady gait. ⋯ He was diagnosed as having neurological decompression illness and therefore underwent hyperbaric oxygen therapy. The pathogenesis of this case was considered to be microbubbles induced by decompression. The present case suggests that repetitive rapid surfacing from the deep sea causes neurological decompression illness even in the breath-hold diver.