Meningiomas sometimes appear to stop growing after attaining a large size. Commonly used exponential growth models do not reflect this phenomenon. We attempted to find the best curve to simulate their growth. Fifty-two patients with meningioma were followed up for 3.1-21.7 years (mean 7.5 years) with four or more imaging studies each. Thirty-one patients had asymptomatic tumors. The other 21 patients with residual or recurrent tumor were followed up after surgery. Time-volume curves for each tumor were plotted. Nonlinear regression analyses were performed against power, exponential, logistic, and Gompertzian curves. Time-volume curves corresponded to the Gompertzian and logistic growth curves better than to power or exponential curves. When simulating time-volume curves with Gompertzian curves, the majority of benign meningiomas began to slow their growth before patient age of 80 years. Twenty-three of 31 asymptomatic meningiomas had already passed the inflection point before diagnosis. In contrast, this happened less frequently in symptomatic tumors. Especially, all six atypical meningiomas continued to grow quasi-exponentially. Sigmoid curves that approach a plateau were better descriptors of the growth of benign meningiomas than were curves of unlimited growth. However, atypical meningiomas were unlikely to slow their growth.

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.

Purpose: 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. Materials and Methods:Diffusion tensor image (DTI) data of the rat (postnatal 1-10 weeks) corpus callosum were obtained with a 7.0 T MR scanner. Histological parameters were quantitatively assessed in toluidine blue-stained semithin sections. Simple and multiple linear regression analyses were performed to investigate relationships between FA values and histological variables. Results:The mean FA value (mFA) increased significantly in the early growth stages, whereas the change became smaller after postnatal week 4. Simple regression analysis showed a high correlation between the area of myelin sheath and mFA (r ϭ 0.856; P Ͻ 0.01). The area of extracellular space correlated negatively with mFA (r ϭ Ϫ0.813; P Ͻ 0.01). In a forward stepwise analysis, the area of myelin sheath had the strongest influence on mFA (P Ͻ 0.001), followed by the number of unmyelinated axons (P ϭ 0.113). Multiple linear regression analysis revealed that both parameters predicted mFA with a highly significant adjusted correlation coefficient (r 2 adj. ϭ 0.738, P Ͻ 0.001). Conclusion:During the early development stage in the rat corpus callosum, the strongest contribution to FA value is the area of myelin sheath.

Background:“Headbanging” is the slang term used to denote violent shaking of one's 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.

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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.

A polyethylene glycol (PEG) hydrogel sealant recently has been approved as an adjunct to sutured dural closure in Japan. We treated consecutive six patients with PEG hydrogel sealant in posterior fossa operation. Three of six cases suffered delayed cerebrospinal fl uid (CSF) leak after watertight dural closure with the PEG hydrogel sealant, although there was no leak case which was treated with fi brin glue, before 2 years until the adoption of the new material. These patients underwent posterior fossa craniotomy and discharged without remarkable CSF leak. The pseudomeningocele under the occipital wound caused the CSF leak occurr from 5th to 7th week postoperatively. All CSF leak cases needed surgical repair. At the repair, the PEG hydrogel was liquefi ed and almost absorbed. A fi stula on the closure line and a dead space after the absorption of the PEG hydrogel was observed. When the absorbable PEG hydrogel sealant plugs in small gaps of sutured dura, its properties to prevent adhesion might suppress healing process of dural closure, so that CSF could leak through the gaps and collect as a pseudomeningocele in the dead space after absorption of the PEG hydrogel. In posterior fossa surgery a PEG hydrogel sealant should be applied when dural edges are closed tightly without any gaps.

A 57-year-old man presented with a transient ischemic attack due to dissection of the middle cerebral artery. He suffered total aphasia and clouding of consciousness for several minutes. On admission, he was alert without neurological deficit. Magnetic resonance (MR) angiography and conventional angiography depicted irregularity and double lumen of the left middle cerebral artery. The diagnosis was dissection of the middle cerebral artery. After 1 month, he left our institute with no neurological deficit. Transient ischemic attack associated with dissection of an intracranial artery is unusual. The source images of MR angiography are useful for the essential follow up of dissection.