We described a rare case of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and severe unconsciousness accompanied by bilateral hypothalamic and anterior thalamic lesions with positive serum antiaquaporin 4 (AQP4) antibody. A 29-year-old man was admitted to our hospital due to the subacute progression of an unconscious state. He was observed to be hyponatraemic secondary to SIADH. Brain MRI showed bilateral hypothalamic and anterior thalamic lesions. Anti-AQP4 antibody was detected in his serum. After the administration of intravenous methylprednisolone pulse therapy, his symptoms improved with complete recovery from SIADH and regression of the hypothalamic and anterior thalamic lesions. The patient was transferred to another hospital for rehabilitation with 20 mg/day of oral prednisolone 127 days after admission. This case highlights the importance of testing for anti-AQP4 antibody in patients with unexplainable SIADH, subacute progressive unconsciousness and bilateral hypothalamic and anterior thalamic lesions.

An 80‐year‐old woman presented with loss of appetite. At age 78, she was diagnosed as familial neuronal intranuclear inclusion disease (NIID) based on (i) leukoencephalopathy with hyperintensities along the corticomedullary junction on diffusion‐weighted imaging (DWI) revealed by brain magnetic resonance imaging (MRI), (ii) skin biopsy samples showing ubiquitin‐positive intranuclear inclusions in adipocytes, and (iii) family history. Her cognitive function was preserved while apathy was apparent. However, on this admission, her cognitive function got worse. Afterward, the patient developed subcortical hemorrhage, and the risk for the hemorrhage was not identified. NIID might be associated with intracranial hemorrhage. In addition, brain MRI after the bleeding showed the rapid expansion of hyperintense lesions on DWI even in the frontal lobe where bleeding was irrelevant. Intracranial hemorrhage might have affected the enlarged hyperintense lesions.

We present a case of communicating hydrocephalus associated with neurosarcoidosis in which the patient was diagnosed by endoscopic biopsy and successfully treated with corticosteroid therapy. The patient was a 53‐year‐old woman who presented with vertigo and nausea. Brain MRI revealed hydrocephalus and contrast‐enhancing areas only on the interthalamic adhesion. Sarcoidosis was suspected based on hilar lymphadenopathy and her past history of uveitis; however, there was no other organ involvement appropriate for biopsy. We performed endoscopic third ventriculocisternostomy and performed biopsy of nodular lesions of the interthalamic adhesion. Interestingly, endoscopy revealed numerous lesions on ventricular walls, which were not detected on contrast‐enhanced MRI. The histopathological examination revealed findings consistent with sarcoidosis. The patient was started on corticosteroid therapy, and her hydrocephalus improved conspicuously. Our case reinforces the notion that endoscopic biopsy is helpful in the definite diagnosis of neurosarcoidosis.