Junya Jito

Maturational changes in diffusion anisotropy in the rat corpus callosum: Comparison with quantitative histological evaluation

To determine the main histological components that affect fractional anisotropy (FA) in postnatal development of the rat corpus callosum and compare FA values with histological changes evaluated quantitatively.

Microscopic anatomy of the brain-meningioma interface.

We analyzed the relation between meningioma and the brain in 50 surgical cases. So-called capsule formation was seen in 20 meningiomas, of which 13 were categorized as thin and 7 as thick. In 21 meningiomas the arachnoid membrane was intact, and 10 meningiomas had no underlying arachnoid membrane. The other 19 tumors showed partial disruption of the arachnoid membrane. The degree of arachnoid disruption correlated with the tumor grade, perifocal edema, pial blood supply on angiography, and tumor size. The existence of brain invasion correlated with the tumor grade and partially with tumor size. In case of invasive tumor, GFAP-positive cells were found deep in the tumor, usually in contact with blood vessels. The axons in gliotic brain often showed degenerative changes such as ballooning or varicose swelling. Meningiomas were usually demarcated by a basement membrane that was collagen type 4 (Col4)-positive. However, atypical and anaplastic meningiomas usually lacked Col4 staining at the interface. In two benign meningiomas that looked like an invasive growth, Col4 staining was seen above the brain. A pia mater-like structure covered the tumor surface in both cases. We could not demonstrate a relation between the expression of matrix metalloproteinase (MMP)-2 or MMP-9 and arachnoid disruption or brain invasion.

Treatment strategies for cerebellar hemangioblastomas: simple or further studies?

emangioblastomas are hypervascular benign neoplasms; they account for <3% of all central nervous H system tumors and are mainly located in the cerebellum, the brainstem, and the spinal cord. Sporadic hemangioblastomas account for approximately 75% of all hemangioblastomas; they usually occur as a solitary lesion in patients in the fourth and fifth decades of life, which is older than patients who have hemangioblastomas associated with von Hippel-Lindau (VHL) disease (1). The first-line treatment for sporadic, especially solitary, cerebellar hemangioblastomas is total resection of the lesion because complete resection is feasible, and most of the lesion does not recur. When the tumor shows apparent enlargement in size, invades vital structures, or becomes symptomatic with or without neurologic deficit, some intervention should be considered. The authors of the present article analyzed the relationship between several clinical factors and long-term outcomes of 36 patients with sporadic cerebellar hemangioblastomas after resection and concluded that the solid configuration observed on preoperative images was one of the most important clinical factors related to both immediate and long-term outcomes after surgery. Several clinical studies have been reported about clinical outcomes in hemangioblastomas associated with VHL disease and sporadic-type hemangioblastomas, but a few previously published studies described the outcome only in sporadic cerebellar hemangioblastomas. The conclusion from these studies is clear and coincides well with our clinical impressions.

Treatment of spontaneous intradural vertebral artery dissections.

Spontaneous intradural vertebral artery dissections may cause subarachnoid hemorrhage and often result in devastating damage. Increased use of noninvasive imaging studies has allowed larger numbers of patients to be diagnosed. In addition, intracranial vertebral artery dissection tends to induce multiple lesions affecting both intracranial vertebral arteries recurrently. Although unruptured dissections in this area usually have a benign nature, some authors have reported on the incidence of rupture from this lesion. Once hemorrhage from a dissecting vessel wall has occurred, it needs to be treated in the acute phase because of the high risk of rebleeding resulting in high morbidity and mortality. From December 2004 to July 2010, we managed 47 patients with spontaneous vertebral artery dissection, 31 patients were ruptured and 16 were unruptured. All patients who suffered from subarachnoid hemorrhage were treated with endovascular procedures. Most of the patients with unruptured dissection received medical therapy, but if the aneurysmal dilatation persisted or grew, surgical interventions were performed. Stenting with or without coils was deployed for 13 patients with posterior inferior cerebellar artery involvement at the site of dissection and/or were affected on the dominant side. In some patients, stenting was performed even if they were in the acute phase. For other ruptured patients, internal coil trappings were performed. Six patients died due to severe initial subarachnoid hemorrhage and one patient, who underwent stent deployment with coils for the dominant vertebral artery, with bilateral dissection continuing to the basilar artery died due to rerupture while the next additional coiling was planning. There were two cases of complications related to the intervention. During the follow-up period no bleeding occurred in any of the patients except for the previously mentioned patient. In conclusion, internal coil trapping or stent placement with or without coils was effective in preventing rebleeding of ruptured vertebral artery dissection. If the dissection is unruptured, it is necessary to detect the risk of bleeding with careful watching and when progress appears to be made, patients should be treated promptly. Stent-assisted therapy for preserving the patency of the parent artery and major branches is a promising treatment for vertebral artery dissection, even in the acute stage of subarachnoid hemorrhage. However, the risk of acute rerupture and recurrence remains even with the porous stent placement with or without coils.

Trigeminal Neuralgia Attributable to Intraneural Trigeminocerebellar Artery: Case Report and Review of the Literature.

BACKGROUND The trigeminocerebellar artery (TCA) is a branch of the basilar artery supplying both the trigeminal nerve root and the cerebellar hemisphere. Despite its proximity to the trigeminal nerve, only a few cases of trigeminal neuralgia (TN) caused by TCA compression of the trigeminal nerve have been reported. Moreover, TN caused by blood vessel penetration of the trigeminal nerve is very rare. CASE DESCRIPTION We present a case of an 82-year-old female patient with typical episodes of TN. The radiologic studies showed that the offending artery was a unique branch of the basilar artery originating at a higher level than that of the usual anterior inferior cerebellar artery. During microvascular decompression surgery we were able to identify the offending vessel supplying the trigeminal nerve root and traveling between the sensory and motor root of the trigeminal nerve as an intraneural TCA. To shift the TCA away from the root entry zone, we dissected the epineurium of trigeminal nerve parallel to its axis and anchored the proximal portion of the TCA to the petrous dura. The patients pain was completely gone immediately after the operation, with no neurologic deficits reported. CONCLUSIONS The TCA is a potential offending vessel in TN because of trigeminal nerve compression, and the longitudinal dissection of the trigeminal nerve to make space between the vessel and the nerve roots may be an effective procedure to relieve TN caused by pressing intraneural vessels.

Recurrent subdural hematoma secondary to headbanging: A case report.

Background: “Headbanging” is the slang term used to denote violent shaking of ones head in time with the music. This abrupt flexion-extension movement of the head to rock music extremely rarely causes a subdural hematoma. Case Description: A 24-year-old female was admitted to our department because of right sided partial seizure and acute or subacute subdural hematoma over the left cerebral convexity. She had no history of recent head trauma but performed headbanging at a punk rock concert at 3 days before admission. Since, she had a previous acute subdural hematoma on the same side after an accidental fall from a baby buggy when she was 11 months old, the present was recurrent subdural hematoma probably due to headbanging. Conclusions: Headbanging has the hazardous potential to cause a subdural hematoma.