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). METHODS: We reviewed clinical the data from all patients who had undergone surgical intervention for ANCH at Chiba University Hospital from January 2008 to March 2018. Patients with vascular lesions, a history of hydrocephalus, and lacking magnetic resonance imaging studies were excluded. The clinical, surgical, and radiological parameters were obtained retrospectively for pathophysiological analysis. RESULTS: A total of 23 patients with ANCH who had undergone surgical intervention and had met the inclusion criteria were included in the present study. Of the 23 patients, 6 (23%) had developed CC infarction. All CC infarctions were located in the splenium. Although no clinical or surgical features were associated with splenial infarction, the radiological parameters of lateral ventricle enlargement and a narrower callosal angle at the posterior commissure and the foramen of Monro were significantly associated with splenial infarction. CONCLUSION: The present study has presented evidence that increased intraventricular pressure by ANCH applied transversely in the splenium will directly induce compression of the superior branch of the posterior callosal artery and pericallosal pial plexus, resulting in splenium-specific infarction in patients with 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. These results suggested neuromyelitis optica spectrum disorder (NMOSD) pathology rather than Sjögren-related vasculitis. Only cerebral cortical symptoms with a cerebral white matter lesion could be observed in NMOSDs.

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. Computed tomography and magnetic resonance imaging revealed marked symmetric enhancement of the choroid plexuses in the bilateral lateral ventricles. Thallium-201 chloride single-photon emission computed tomography showed pronounced uptake on both early and delayed images, and good washout. CSF examination revealed no abnormalities such as atypical cells, and a ventriculoatrial shunt was inserted, achieving good control of the hydrocephalus.

[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. A 59-year-old male underwent clipping by craniotomy due to subarachnoid hemorrhage resulting from the rupture of a left internal carotid aneurysm 15 years earlier. He was discharged, but developed paresis in the right upper and lower limbs 6 months before symptom onset. CT showed sinking of the free bone flap, while MRI revealed left uncal herniation. After uncal resection and free flap fixation, the symptoms improved. This case confirmed the necessity of firm bone flap fixation at the time of cranial closure.