Brain and nerve = Shinkei kenkyū no shinpo
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In this review study, second-generation antiepileptic drugs (AEDs) (levetiracetam, gabapentin, topiramate, lamotrigine, zonisamide, oxcarbazepine, vigabatrin, pregabalin, rufinamide, tiagabine, lacosamide, and felbamate) and injectable AEDs (levetiracetam, lacosamide, fosphenytoin, lorazepam, and valproic acid) available in North America were compared with those available in Japan. Three second-generation AEDs (gabapentin, topiramate, and lamotrigine) were recently approved in Japan. Levetiracetam is currently under review for approval by the Japanese regulatory agency. ⋯ The effects of this drug are more prolonged than those of diazepam. Intravenous administration of valproic acid is regarded as a new treatment option for patients with status epilepticus, because sedative and negative effects on the cardiorespiratory system of this drug are lesser than those of the traditional injectable AEDs. These novel medications will aid the improvement of the quality of life of epileptic patients through improved seizure control and reduced adverse effects.
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Review
[Stiff-person syndrome and other myelopathies constitute paraneoplastic neurological syndromes].
Stiff-person syndrome (SPS) is an autoimmune neurological disorder characterized by rigidity of the trunk and proximal limb muscles, intermittent superimposed spasms, and increased sensitivity to external stimuli. It has been more than 50 years since Moerch and Woltman reported the first 14 cases with this syndrome. During the last half century, many autoantibodies discovered, such as anti-glutamic acid decarboxylase (GAD), anti-amphiphysin, anti-gephyrin, and anti-gamma-aminobutyric acid A receptor-associated protein (GABARAP) antibodies. ⋯ Although the understanding and treatment of SPS have evolved, the disease remains underdiagnosed. In the past, some patients with SPS have been diagnosed with psychiatric disorders. Therefore, it is important to increase awareness of SPS among practicing physicians.
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Neuromyotonia occurs due to several causes such as hereditary, immune-mediated and degenerative neurological disorders. Isaacs' syndrome (immune-mediated neuromyotonia) is an antibody-mediated potassium channel disorder (channelopathy). Clinical symptoms of Isaacs' syndrome are characterized by muscle cramp, slow relaxation following muscle contraction (pseudomyotonia), and hyperhidrosis; these symptoms are due to hyperexcitability of the peripheral nerve, including autonomic nerve. ⋯ Thus, an increasing number of immune-mediated neurological disorders with anti-VGKC antibodies are being identified. However, except in Morvan's syndrome, it is rare to find symptoms pertaining to involvement of both the peripheral and central nervous system in the same patient with anti-VGKC antibodies. The differences in the pathomechanism of Isaacs' syndrome and limbic encephalitis are still unclear.
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Traumatic brain injury is one of the subjects that always arouse intense attention from emergency medicine. In the latter half of the 1960s, death by traffic accidents had drastically increased in Japan and, this period was called "the age of traffic war". Traumatic brain injury was considered to be one of the major causes of traffic death, and the need for neurosurgeons was widely recognized. ⋯ This time, we report on actual incidences of traumatic brain injury in Japan. We have compared 1,002 cases from Project 1998 with other 1,101 cases from Project 2004. We think that it is essential for neurosurgeons engaging in emergency medicine to make a continuous effort to wards accumulating data regarding traumatic brain injury and improving the guideline.
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Cerebral salt wasting syndrome (CSWS) in patients with aneurysmal subarachnoid hemorrhage (SAH) is considered to correlate with delayed ischemic neurological deficits (DIND) induced by cerebral vasospasm; however, its exact mechanism is still not well-known. The purpose of the present study is to evaluate the relationship between hyponatremia caused by CSWS and the increase of the urinary sodium excretion in early phase following SAH. Fifty-four patients with SAH were divided into 2 groups, normonatremia group and hyponatremia group which suffered hyponatremia after SAH. ⋯ Further, excretion of sodium in the urine tended to increase 3 days after SAH and significantly increased 7 days after SAH. In conclusion, the increased urinary sodium excretion in the early phase of SAH would serve as a predictive factor for CSWS after SAH. We consider that it is important to start sodium and fluid supplementation and inhibit natriuresis by fludrocortisone acetate administration before hyponatremia occurs in order to prevention delayed ischemic neurological deficits in SAH patients.