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Background: Although antidepressants are still a commonly used treatment for social anxiety disorder (SAD), a significant proportion of patients fail to remit following antidepressants. However, no standard approach has been established for managing such patients. This study aimed to examine the effectiveness of cognitive behavioral therapy (CBT) as an adjunct to usual care (UC) compared with UC alone in SAD patients who remain symptomatic following antidepressant treatment., Methods: This was a prospective randomized open-blinded end-point study with two parallel groups (CBT + UC, and UC alone, both for 16 weeks) conducted from June 2012 to March 2014. SAD patients who remain symptomatic following antidepressant treatment were recruited, and a total sample size of 42 was set based on pilot results., Results: Patients were randomly allocated to CBT + UC (n = 21) or UC alone (n = 21). After 16 weeks, adjusted mean reduction in the Liebowitz Social Anxiety Scale from baseline for CBT + UC and UC alone was -40.87 and 0.68, respectively; the between-group difference was -41.55 (-53.68 to -29.42, p < 0.0001). Response rates were 85.7 and 10.0% for CBT + UC and UC alone, respectively (p < 0.0001). The corresponding remission rates were 47.6 and 0.0%, respectively (p = 0.0005). Significant differences were also found in favor of CBT + UC for social anxiety symptoms, depressive symptoms, and functional impairment., Conclusions: Our results suggest that in SAD patients who have been ineffectively treated with antidepressants, CBT is an effective treatment adjunct to UC over 16 weeks in reducing social anxiety and related symptoms., (© 2016 S. Karger AG, Basel.)

Background: Cognitive behavior therapy (CBT) is regarded as an effective treatment for social anxiety disorder (SAD) in Europe and North America. Individual CBT might be acceptable and effective for patients with SAD even in non-Western cultures; therefore, we conducted a feasibility study of individual CBT for SAD in Japanese clinical settings. We also examined the baseline predictors of outcomes associated with receiving CBT., Methods: This single-arm trial employed a 14-week individual CBT intervention. The primary outcome was the self-rated Liebowitz Social Anxiety Scale, with secondary measurements of other social anxiety and depressive severity. Assessments were conducted at baseline, after a waiting period before CBT, during CBT, and after CBT., Results: Of the 19 subjects screened, 15 were eligible for the study and completed the outcome measures at all assessment points. Receiving CBT led to significant improvements in primary and secondary SAD severity (ps < .001). The mean total score on the Liebowitz Social Anxiety Scale improved from 91.8 to 51.7 (before CBT to after CBT), and the within-group effect size at the end-point assessment was large (Cohen's d = 1.71). After CBT, 73% of participants were judged to be treatment responders, and 40% met the criteria for remission. We found no significant baseline predictors of those outcomes., Conclusion: Despite several limitations, our treatment-which comprises a 14-week, individual CBT program-seems feasible and may achieve favorable treatment outcomes for SAD in Japanese clinical settings. Further controlled trials are required in order to address the limitations of this study., Trial Registration: UMIN-CTR UMIN000005897.

Introduction: Pharmacotherapy and cognitive behavioural therapy (CBT) are consistently effective as first-line treatments for social anxiety disorders (SADs). Nevertheless, pharmacotherapy is often the first choice in clinical practice. In many countries, the first line of pharmacotherapy involves the administration of a selective serotonin reuptake inhibitor (SSRI). Although a significant proportion of patients with SAD fail to respond to the initial SSRI administration, there is no standard approach to the management of SSRI-resistant SAD. This paper describes the study protocol for a randomised controlled trial to evaluate the clinical effectiveness of CBT as a next-step strategy, concomitant with conventional treatment, for patients with SSRI-resistant SAD., Methods and Analysis: This Prospective Randomized Open Blinded End-point study is designed with two parallel groups, with dynamic allocation at the individual level. The interventions for the two groups are conventional treatment, alone, and CBT combined with conventional treatment, for 16 weeks. The primary end-point of SAD severity will be assessed by an independent assessor using the Liebowitz Social Anxiety Scale, and secondary end-points include severity of other social anxieties, depressive severity and functional impairment. All measures will be assessed at weeks 0 (baseline), 8 (halfway point) and 16 (postintervention) and the outcomes will be analysed based on the intent-to-treat. Statistical analyses are planned for the study design stage so that field materials can be appropriately designed., Ethics and Dissemination: This study will be conducted at the academic outpatient clinic of Chiba University Hospital. Ethics approval was granted by the Institutional Review Board of Chiba University Hospital. All participants will be required to provide written informed consent. The trial will be implemented and reported in accordance with the recommendations of CONSORT., Clinical Trial Registration Number: UMIN000007552.

Introduction: The aim of this study was to investigate whether the outline of the hippocampal body becomes rounded on coronal magnetic resonance imaging (MRI) as the volume of the hippocampal formation decreases in Alzheimer's disease (AD)., Methods: Institutional review board approval of the study protocol was obtained, and all subjects provided informed consent for the mini-mental state examination (MMSE) and MRI. The MRI and MMSE were prospectively performed in all 103 subjects (27 men and 76 women; mean age ± standard deviation, 77.7 ± 7.8 years) who had AD or were concerned about having of dementia and who consulted our institute over 1 year. The subjects included 14 non-dementia cases (MMSE score ≥ 28) and 89 AD cases (MMSE score ≤ 27). The total volume of the bilateral hippocampal formation (VHF) was assessed with a tracing method, and the ratio of the VHF to the intracranial volume (RVHF) and the rounding ratio (RR) of the hippocampal body (mean ratio of its short dimension to the long dimension in the bilateral hippocampal body) were calculated. Using Spearman's correlation coefficient, the correlations between RR and VHF and between RR and RVHF were assessed., Results: Correlation coefficients between RR and VHF and between RR and RVHF were -0.419 (p < 0.01) and -0.418 (p < 0.01), respectively. There was a significant negative correlation between RR and the volume of the hippocampal formation., Conclusion: The outline of the body of the hippocampal formation becomes rounded on coronal images as its volume decreases in AD.

Purpose: On routine coronal images, we have recognized atrophied hippocampi that appear round in patients with Alzheimer's disease (AD). The purpose of this study was to evaluate rounding of the hippocampus in patients with AD and to elucidate whether this change is a useful radiological marker of atrophy of the hippocampus., Materials and Methods: We enrolled 14 patients with moderate AD (Mini-Mental State Examination score 16.2 +/- 3.3) and 15 patients without dementia or neurological deficits as the control group. For measurement of the hippocampus, we used T2-weighted coronal images parallel to the floor of the fourth ventricle. Two observers measured the dimensions of the long and short axes of the hippocampal body of 28 hippocampi from 14 patients with AD and 30 hippocampi from 15 controls. As a marker of rounding of the hippocampal body, we calculated the ratio of the short axis length to the long axis length (the rounding ratio) of the hippocampus., Results: We observed apparent atrophy of the long axis of the hippocampus in patients with AD. An unpaired t-test indicated significant differences in the long axis length and the rounding ratio between the control and AD groups (P < 0.01) in the measurements of both observers. However, there was no significant difference in the short axis length. With a threshold of 0.7 in the rounding ratio, the sensitivity was 85.7% and the specificity was 66.7%., Conclusion: The hippocampus appears round on coronal images in the presence of moderate AD. The rounding ratio of the hippocampus is a useful and facile indicator of hippocampal atrophy.

Purpose: On magnetic resonance imaging (MRI) sagittal sections, we sometimes encounter abnormal aspects of the superior profile of the midbrain and the cingulate sulcus in patients with dementia. In this preliminary study, we refer to these findings as the "upper midbrain profile sign" and the "cingulate sulcus sign." We prospectively evaluated the usefulness of these signs for the diagnosis of idiopathic normal-pressure hydrocephalus (iNPH), Alzheimer's disease (AD) and progressive supranuclear palsy (PSP)., Materials and Methods: We evaluated the upper midbrain profile sign and the cingulate sulcus sign on MRI sagittal images obtained from 21 people with headaches but no neurological deficit (controls), 10 iNPH patients, 11 AD patients, and 5 PSP patients. The upper midbrain profile sign indicated a concave shape to the superior profile of the midbrain on mid-sagittal images, and the cingulate sulcus sign indicated a narrow, tight aspect of the posterior part of the cingulate sulcus on paramedian-sagittal images., Results: These signs were never seen in any images from the controls. The upper midbrain profile sign was seen in 7 of 10 patients with iNPH, 5 of 11 with AD, and 3 of 5 with PSP. The cingulate sulcus sign was seen in all 10 patients with iNPH but was never seen in any patient with AD or PSP., Conclusion: The upper midbrain profile sign could support a diagnosis of PSP but cannot discriminate among iNPH, AD, and PSP. In contrast, the cingulate sulcus sign has a very high sensitivity for iNPH and should facilitate the distinction of iNPH from other dementias. In the clinical setting, it is momentous to evaluate these signs easily by one simple MRI sequence.

The characteristic magnetic resonance (MR) findings of Cockayne syndrome have been reported; however, the corresponding characteristics on diffusion-weighted and fluid-attenuated inversion recovery (FLAIR) imaging are yet to be documented. In this adult case with Cockayne syndrome, we identified small patchy subcortical lesions visualized as areas of high intensity on diffusion-weighted images and low intensity on FLAIR images. It is possible that these findings reflect active demyelinating lesions.

The opportunistic fungal pathogens Candida inconspicua and C. norvegensis are very rarely isolated from patients and are resistant to fluconazole. We collected 38 strains of the two microorganisms isolated from Europe and Japan, and compared the polymorphism of the rRNA intergenic spacer (IGS) and internal transcribed spacer (ITS) regions, antifungal drug susceptibility, and extracellular enzyme production as a potential virulence factor. While the IGS sequences of C. norvegensis were not very divergent (more than 96.7% sequence similarity among the strains), those of C. inconspicua showed remarkable diversity, and were divided into four genotypes with three subtypes. In the ITS region, no variation was found in either species. Since the sequence similarity of the two species is approximately 70% at the ITS region, they are closely related phylogenetically. Fluconazole resistance was reconfirmed for the two microorganisms but they were susceptible to micafungin and amphotericin B. No strain of either species secreted aspartyl proteinase or phospholipase B. These results provide basal information for accurate identification, which is of benefit to global molecular epidemiological studies and facilitates our understanding of the medical mycological characteristics of C. inconspicua and C. norvegensis.

A 59-year-old man with an 8-years history of diabetes mellitus had an acute onset of sharp pain in the anterior part of right lower leg. One month later, the pain changed to deep dull nature in the deeper site of the peroneal region. The pain increased, when he stood up, walked, and stayed in the cold room and decreased by rest. It was more painful in the evening than in the morning. The first sharp pain was thought to be caused by ischemia due to diabetic vascular neuropathy. The next dull pain was considered to be originated from ephaptic transmission between sympathetic efferent fibers to group IV and afferent ones from the skeletal muscle. The latter dull pain was selectively suppressed by nerve block when it became effective to the branch of deep peroneal nerve to extensor digitorum longus muscle. The hypothesis of ephaptic transmission was supported by meaningful decrease of muscle sympathetic activity detected by microneurography before and after the dosage of L-DOPS, which effectively suppressed the pain as well as other alpha-stimulant, midodrine hydrochloride. We concluded that the ephaptic pain caused by muscle sympathetic activity could be suppressed by the vasoconstrictive drugs through the mechanism of baroreflex control.

A 26-year-old woman was admitted to our hospital because of fever of unknown origin. She had been treated with prednisolone, elcatonin and alfacalcidol under the diagnosis of systemic lupus erythematosus (SLE) and aseptic necrosis of femoral bone head. Six months ago she began to have a fever and subsequently left low back pain, for which extensive examinations were performed in other hospital but their causes remained unclear. She was referred to our hospital for further evaluation and therapy in October 1995. Bacteriological, immunological or serological examinations did not reveal the origin of fever. CT and ultrasonic examination did not show any abnormality. However, MRI, which was taken for the evaluation of aseptic necrosis of femoral bone head, showed the abscess shadow in sacroiliac joint. Open biopsy was performed and Mycobacterium tuberculosis bacilli were detected from the abscess. To our best knowledge, this is the first report of SEE with tuberculosis sacroiliac arthritis.

A case of flunarizine hydrochloride (FZ)-induced severe urinary retention and meteorism which resulted from sphincter spasm of the urinary bladder and the anus is presented. An 81-year-old female had received 10 mg/day FZ orally for 12 months before hypokinesia and general fatigue developed. Physical examination revealed slight rigidity of the extremities, abdominal distention and spasm of the anal sphincter muscle. Laboratory examinations showed uremia (BUN 88 mg/dl, Creatinine 16.8 mg/dl) and abdominal X-ray demonstrated marked distention of the small and large bowels. Renal failure improved within 2 days after massive urination using a urethral catheter. Abdominal distention was improved by the ileus and anal tubes. The difficulties of urination and defecation and decreased mobility of the extremities were resolved one month after the cessation of FZ. No organic changes were detected in urinary, intestinal and neurological systems by cystoscopy, CT, MRI and gastrointestinal fiberscopy. Serum concentration of FZ was 42.5 ng/ml on admission but decreased slowly to 17.9 ng/ml 80 days later. Serum half life was calculated to be 55 days which was 3 times longer than that healthy younger volunteers.

alpha-Bungarotoxin is known to bind with nicotinic acetylcholine receptors of skeletal muscle. Binding of iodine 125-labeled alpha bungarotoxin to the murine thymus, muscle, and liver was estimated. The toxin was bound to the muscle. The thymus was also capable of binding a considerable amount of the toxin, and the binding was obviously blocked by tubocurarine chloride. Binding to the liver, an organ containing no nicotinic acetylcholine receptor, was very slight. These results may indicate the presence of nicotinic acetylcholine receptors in the thymus, which could have implications in the pathogenesis of myasthenia gravis. Degenerating myoid cells and their receptors may represent autoantigens that induce an immunological cross-reaction with the receptors of skeletal muscles, giving rise to myasthenia gravis.