川合 謙介

Delusional misidentification, a rare syndrome in which a patient displays persistent delusional misidentification of individuals or objects, occurs in several types of dementia. However, the pathology of delusional misidentification is still unclear, and there was no data pertaining to striate-frontal projection. Here, we report a case of delusional misidentification following frontotemporal dementia in which complex striate-frontal and some specific frontal gyrus dysfunction were observed. In our presented case, delusional misidentification progressed following frontal atrophy. Believing that her actual daughter had been replaced by her niece, her symptoms of delusional misidentification and frontal atrophy progressed in the short term, and social arrangement was necessary three months after the onset. There were no abnormal neurological findings including parkinsonism and general cognitive function test scores were preserved. Validated by dopamine transporter single-photon emission computed tomography, right unilateral striatal uptake decreased significantly without parkinsonism or Parkinson's disease. In addition, of specific concern, functional magnetic resonance images showed left opercular inferior frontal gyrus and right superior frontal gyrus dysfunctions. Our case study highlights complex striate-frontal projection and specific frontal gyrus dysfunctions associated with the pathology of delusional misidentification syndrome.

BACKGROUND: Chronic inflammation of the thorax, as in tuberculosis-related pyothorax, can cause secondary malignant lymphomas. However, primary malignant lymphoma of the central nervous system, specifically of the dura mater, developing after intracranial infection or inflammation has rarely been reported. Herein, the authors describe a case of primary dural lymphoma that developed secondary to subdural empyema, with an initial presentation mimicking a chronic subdural hematoma. OBSERVATIONS: A 51-year-old man had undergone single burr hole drainage for subdural empyema 2 years prior. The patient subsequently underwent multiple craniotomy and drainage procedures, with successful remission of the subdural empyema. He was subsequently referred to the authors' hospital approximately a year after his initial treatment because of a recollection of subdural fluid, which was suspected to be recurrent empyema. After another single burr hole drainage, which revealed only a subdural hematoma, a histopathological diagnosis of B-cell lymphoma of the dural/subdural membrane was made. Subsequent radiation therapy was completed, with good local control and no recurrence of the subdural hematoma confirmed at 2 months posttreatment. LESSONS: Intracranial lymphoma triggered by chronic inflammation is rare but should be considered a differential diagnosis in subdural hematomas for which the background pathology is unclear. https://thejns.org/doi/10.3171/CASE24153.

It is established that neurogenesis of dentate gyrus is increased after ischemic insult, although the regulatory mechanisms have not yet been elucidated. In this study, we focused on Ezh2 which suppresses gene expression through catalyzing trimethylation of lysine 27 of histone 3. Male gerbils were injected with adeno-associated virus (AAV) carrying shRNA targeting to Ezh2 into right dentate gyrus 2 weeks prior to forebrain ischemia. One week after ischemia, animals were injected with thymidine analogue to label proliferating cells. Three weeks after ischemia, animals were killed for histological analysis. AAV-mediated knockdown of Ezh2 significantly decreased the ischemia-induced increment of proliferating cells, and the proliferated cells after ischemia showed significantly longer migration from subgranular zone (SGZ), compared to the control group. Furthermore, the number of neural stem cells in SGZ significantly decreased after ischemia with Ezh2 knockdown group. Of note, Ezh2 knockdown did not affect the number of proliferating cells or the migration from SGZ in the non-ischemic condition. Our data showed that, specifically after ischemia, Ezh2 knockdown shifted the balance between self-renewal and differentiation toward differentiation in adult dentate gyrus.

Endoscopic third ventriculostomy (ETV) is a safe treatment option for chronic obstructive hydrocephalus. However, we encountered a case of chronic subdural hematoma (CSDH) with bilateral large hematoma volumes after ETV for chronic obstructive hydrocephalus. We herein report a rare complication of ETV. The patient was a 53-year-old woman who had been diagnosed with asymptomatic ventricular enlargement with aqueductal stenosis 5 years previously. However, over the course of 5 years, her gait and cognitive function gradually declined. ETV was administered to relieve symptoms. Head Magnetic resonance imaging performed 1 week after ETV indicated bilateral subdural hygroma. Three weeks after ETV, she presented with headache and left incomplete paralysis, and head Computed tomography (CT) demonstrated bilateral CSDH with a large volume hematoma. Burr-hole evacuation and drainage of the bilateral CSDH were performed, after which the symptoms resolved. However, 7 weeks after ETV, she again presented with headache and incomplete right paralysis, and CT revealed bilateral CSDH re-enlargement. After the second burr-hole evacuation and drainage of bilateral CSDH, her symptoms resolved. The bilateral CSDH continued to shrink following the second hematoma evacuation surgery and completely disappeared on CT scan performed 3 months after ETV. Ventricular enlargement due to chronic obstructive hydrocephalus stretches the brain mantle for several years. This long-term stretching may have diminished the brain compliance and led to the development, growth, and recurrence of CSDH. In ETV for chronic obstructive hydrocephalus, surgeons should consider the risk of postoperative CSDH with a high hematoma volume and tendency to recur.