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The patient was a 31-year-old female with no previous health problems; however, during a health checkup in 2013, a nodule (2.5 cm in diameter) was identified in the S10 area of the left lung. No clinical symptoms were apparent. Positron emission tomography/computed tomography revealed an accumulation in the same region. The patient was suspected of having lung cancer, and video-assisted thoracoscopic surgery was performed. A histopathological examination of the resected specimen revealed epithelioid granulomas accompanied by caseous necrosis in the lesion. The culture was positive for Mycobacterium tuberculosis, which led to the final diagnosis of tuberculoma. Initially, the patient underwent anti-M. tuberculosis treatment [isoniazid (INH) + rifampicin (RFP) + ethambutol (EB) + pyrazinamide (PZA)]. However, two weeks later, the development of epatic dysfunction necessitated suspension of the medication. Treatment was resumed following improvement of the hepatic function. However, this relapsed two weeks later, resulting in discontinuation of the treatment. The patient was negative for each of the four drugs in the drug-induced lymphocyte stimulation test (DLST), and drug-induced hepatotoxicity (DIH) attributable to the anti-tuberculous drugs that were administered. Therefore, desensitization therapy was initiated. EB + PZA were changed to levofloxacin (LVFX) at an initial dose of 250 mg/day (dose level increased to the maintenance dose). Subsequently, desensitization therapy with RFP and INH was applied in accordance with the Japanese Society for Tuberculosis protocol. After each drug dose level reached the maintenance dose level, the therapy was completed following administration of the drugs for the recommended duration of 6 months. There were no signs of relapse 6 months following completion of the therapy. Therefore, the patient responded well to the substitute therapy with LVFX and desensitization therapy, and the present case report provided information regarding the treatment of tuberculoma.

Olanzapine is one of the most widely prescribed atypical antipsychotic drugs in the treatment of schizophrenia. Besides its well-known side effect on weight gain, it may also impair human parental behavior. In this study, we took a preclinical approach to examine the behavioral effects of olanzapine on rat maternal behavior and investigated the associated neural basis using the c-Fos immunohistochemistry. On postpartum days 6-8, Sprague-Dawley mother rats were given a single injection of sterile water or olanzapine (1.0, 3.0 or 5.0 mg/kg, sc). Maternal behavior was tested 2 h later, after which rats were sacrificed and brain tissues were collected. Ten brain regions that were either implicated in the action of antipsychotic drugs and/or in the regulation of maternal behavior were examined for c-Fos immunoreactivity. Acute olanzapine treatment dose-dependently disrupted various components of maternal behavior (e.g., pup retrieval, pup licking, nest building, crouching) and increased c-Fos immunoreactivity in the medial prefrontal cortex (mPFC), nucleus accumbens shell and core (NAs and NAc), dorsolateral striatum (DLSt), ventral lateral septum (LSv), central amygdala (CeA) and ventral tegmental area (VTA), important brain areas generally implicated in the incentive motivation and reward processing. In contrast, olanzapine treatment did not alter c-Fos in the medial preoptic nucleus (MPN), ventral bed nucleus of the stria terminalis (vBST) and medial amygdala (MeA), the core brain areas directly involved in the mediation of rat maternal behavior. These findings suggest that olanzapine disrupts rat maternal behavior primarily by suppressing incentive motivation and reward processing via its action on the mesocorticolimbic dopamine systems, other limbic and striatal areas, but not by disrupting the core processes involved in the mediation of maternal behavior in particular. (C) 2012 Elsevier Inc. All rights reserved.