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An acute febrile disease, scrub typhus is caused by rickettsial nfection transferred by a bite of the chigger larvae infected with rientia tsutsugamushi. It is also known as tsutsugamushi disase and is characterized by focal or disseminated vasculitis and erivasculitis, which may involve the lung, heart, liver, spleen nd central nervous system [1–3]. The main pathologic change s focal or disseminated vasculitis caused by the destruction of ndothelial cells and the perivascular infiltration of leukocytes 1]. Scrub typhus occurs in a wide area of eastern Asia and he western pacific region [3]. It occurs in persons who ngage in occupational or recreational behavior that brings hem into contact with mite-infested habitats such as bush and rass. Scrub typhus can present with neurologic signs resembling septic meningitis or encephalitis syndrome. According to a study y Pai et al., twelve (48%) of 25 patientswith scrub typhus hadmild SF pleocytosis [7]. However, focal neurologic signs and abnormal euroradiologic findings in scrub typhus are rarely reported. We eport a case of scrub typhusmeningo-encephalitis with focal neuologic signs and associated neuroradiologic abnormalities along ith a review of the literature.

We report on a 32-year-old woman who developed reversible cortical blindness and right-sided weakness after cesarean section at 36 weeks of gestation, due to preeclampsia. An initial brain MRI demonstrated high signal intensity lesions in the bilateral occipito-parietal and left frontal lobes on T2-weighted and diffusion-weighted imaging. All of the lesions showed low signal intensity on apparent diffusion coefficient (ADC) map, which were compatible with cytotoxic edema, and MR angiography (MRA) showed diffuse vasospasm of the intracranial vessels. A follow-up brain MRI showed that most of the lesions disappeared and the vasospasm also resolved. This case suggests that the cytotoxic edema in preeclampsia may evolve differently from the pattern in cerebral infarction and explains the relatively benign course of the neurological signs in preeclampsia.

Eosinophilic vasculitis has been described as part of Churg-Strauss syndrome (CSS), but it also affects the central nervous system in

Oculomotor nerve palsy frequently occurs because of external compression by an internal carotid-posterior communicating artery aneurysm and diabetes mellitus. In addition, pontine infarction, cavernous sinus tumors, demyelinating disease, and autoimmune disorder are well-known causes of oculomotor nerve palsy. However, cases of complete oculomotor nerve palsy by neurovascular conflicts presented with a sudden onset of clinical symptoms are extremely rare. We experienced a rare case of complete oculomotor nerve palsy because of direct vascular compression of the oculomotor nerve by the posterior cerebral artery.

A healthy, 66-year-old, right-handed man was admitted to our university hospital and diagnosed with herpes zoster ophthalmicus (HZO). After 4 weeks, he complained of hemichorea on his left side. Brain MRI showed a focal hemorrhage in the right subthalamic area. No evidence of aneurysmal lesion or cerebral angiitis was observed on cerebral angiography.

The underlying cause of myasthenia gravis is unknown, although there is probably a genetic component to it. We sought to identify the genetic variants associated with an increased or decreased risk of developing myasthenia gravis in the Korean Multicenter MG Cohort samples. To find new genetic targets that are related to autoimmune myasthenia gravis, a whole genome-based SNP analysis was performed using an Axiom Genome-Wide ASI 1 Array plate containing 598,375 SNPs and samples from 109 MG patients and 150 neurologically normal controls. The p values of association between these SNPs and autoimmune myasthenia gravis were calculated in all the available genetic modes such as allele, dominant, recessive, and co-dominant mode using (1) MG and Control, (2) AChR-antibody positive MG and Control, (3) AChR-antibody negative MG and Control, (4) Ocular MG and Control, and (5) Generalized MG and Control samples, respectively. A total of 641 SNPs from five case–control associations showed p values of less than 0.00001. From regional analysis, we selected seven genes (RYR3, CACNA1S, SLAMF1, SOX5, FHOD3, GABRB1, SACS) for further analysis. Fatigue in MG patients was caused not only by abnormal neuromuscular transmission but also by the impairment of excitation–contraction (E–C) coupling. In the process of E–C coupling in skeletal muscle, ryanodine receptor (RyR) and dihydropyridine receptor (DHPR/CACNA1S) function as Ca2+ channels. SLAMF1 leads to IFN- α production of CD4+ T cells. IFN- α production of CD4+ T cells is associated with pathogenesis and immunoregulation of MG. However, speculating the plausibility and the biological significance of these candidate loci is premature because additional genetic data is needed to confirm the notion that these E–C coupling gene or SLAMF1 gene are associated with autoimmune MG. The present study suggests that some genetic polymorphisms might be related to autoimmune myasthenia gravis.