Mechanism of Corpus Callosum Infarction Associated with Acute Hydrocephalus: Clinical, Surgical, and Radiological Evaluations for Pathophysiology.

Background: Corpus callosum (CC) infarction has been reported to be rare because of the rich blood supply in the CC. The pathophysiology of CC infarction associated with acute hydrocephalus is unknown. The aim of the present study was to clarify the characteristics and mechanism of CC infarction associated with acute noncommunicating hydrocephalus (ANCH).

A case of pathology-proven neuromyelitis optica spectrum disorder with Sjögren syndrome manifesting aphasia and apraxia due to a localized cerebral white matter lesion.

A woman with Sjögren syndrome manifesting as aphasia with a left deep cerebral white matter lesion tested positive for anti-aquaporin 4 (AQP4) antibody. Open biopsy of the lesion revealed active demyelination with edematous changes and the preservation of most axons, indicating a non-necrotic demyelinating lesion. Immunostaining for AQP4 was diffusely lost, whereas the loss of glial fibrillary acidic protein immunostaining was limited but with highly degenerated astrocytic foot processes in perivascular areas.

Hydrocephalus due to diffuse villous hyperplasia of the choroid plexus.

An 8-month-old female presented with hydrocephalus caused by cerebrospinal fluid (CSF) overproduction due to bilateral choroid plexus enlargement, which was clinically diagnosed as diffuse villous hyperplasia of the choroid plexus, but differentiation from bilateral choroid plexus papilloma was difficult. She initially underwent ventriculoperitoneal shunt surgery, but developed marked retention of ascites. Therefore, the peritoneal end of the shunt was removed for external drainage, but excessive CSF (1,500 ml/day) was collected.

[A case of brain herniation due to delayed bone flap sinking].

Marked depression of the skin flap after external decompressive craniotomy, affecting the brain function, is known as sinking flap syndrome. However, to our knowledge, there have been no reports of delayed sinking of the entire bone flap after the procedure, inducing neurological symptoms. We encountered a patient with neurological symptoms due to sinking of the entire bone flap 15 years after the first operation.