Statins have pleiotropic effects that are considered beneficial in preventing cerebral vasospasm and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage (aSAH). Many studies using statins have been performed but failed to show remarkable effects. We hypothesized that a long-acting statin would be more effective, due to a longer half-life and stronger pleiotropic effects. Patients with aSAH were randomly assigned to a pitavastatin group (4 mg daily; n = 54) and a placebo group ( n = 54) after repair of a ruptured aneurysm. The primary efficacy end point was vasospasm-related delayed ischemic neurological deficits (DIND), and the secondary end points were cerebral vasospasm evaluated by digital subtraction angiography (DSA), vasospasm-related new cerebral infarctions, and outcome at three months. Severe cerebral vasospasms on DSA were statistically fewer in the pitavastatin group than in the placebo group (14.8% vs. 33.3%; odds ratio, 0.32; 95% confidence interval, 0.11-0.87, p = 0.042); however, the occurrence of DIND and new infarctions and outcome showed no statistically significant differences between the groups. The present study is the first to prove the definite, statin-induced amelioration of cerebral vasospasm on DSA. However, administration of any type of statin at the acute phase of aSAH is not recommended.

Background: Several clinical studies have indicated the efficacy of cilostazol, a selective inhibitor of phosphodiesterase 3, in preventing cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). They were not double-blinded trial resulting in disunited results on assessment of end points among the studies. The randomized, double-blind, placebo-controlled study was performed to assess the effectiveness of cilostazol on cerebral vasospasm. Methods: Patients with aneurysmal SAH admitted within 24 h after the ictus who met the following criteria were enrolled in this study: SAH on CT scan was diffuse thick, diffuse thin, or local thick, Hunt and Hess score was less than 4, administration of cilostazol or placebo could be started within 48 h of SAH. Patients were randomly allocated to placebo or cilostazol after repair of a ruptured saccular aneurysm by aneurysmal neck clipping or endovascular coiling, and the administration of cilostazol or placebo was continued up to 14 days after initiation of treatment. The primary end point was the occurrence of symptomatic vasospasm (sVS), and secondary end points were angiographic vasospasm (aVS) evaluated on digital subtraction angiography, vasospasm-related new cerebral infarction evaluated on CT scan or MRI, and clinical outcome at 3 months of SAH as assessed by Glasgow Outcome Scale, in which poor outcome was defined as severe disability, vegetative state, and death. All end points were evaluated with blinded assessment. Results: One hundred forty eight patients were randomly allocated to the cilostazol group (n = 74) or the control group (n = 74). The occurrence of sVS was significantly lower in the cilostazol group than in the control group (10.8 vs. 24.3%, p = 0.031), and multiple logistic analysis showed that cilostazol use was an independent factor reducing sVS (OR 0.293, 95% CI 0.099-0.568, p = 0.027). The incidence of aVS and vasospasm-related cerebral infarction were not significantly different between the groups. Poor outcome was significantly lower in the cilostazol group than in the control group (5.4 vs. 17.6%, p = 0.011), and multiple logistic analyses demonstrated that cilostazol use was an independent factor that reduced the incidence of poor outcome (OR 0.221, 95% CI 0.054-0.903, p = 0.035). Severe adverse events due to cilostazol administration did not occur during the study period. Conclusions: Cilostazol administration is effective in preventing sVS and improving outcomes without severe adverse events. A larger-scale study including more cases was necessary to confirm this efficacy of cilostazol.

The relatively high rate of post-operative recurrence in the treatment of chronic subdural hematoma (CSDH) is a significant problem. Goreisan is an herbal medicine that exhibits a hydragogue effect by inhibiting the expression of aquaporins, and its efficacy in preventing post-operative CSDH recurrence has been suggested by several case trials. This multi-center prospective randomized controlled trial was performed to investigate the preventative effect of goreisan on post-operative CSDH recurrence. Patients with symptomatic CSDH over 60 years old undergoing burr hole surgery were enrolled in this study. The patients were randomly allocated to the control group or the goreisan group, in which oral administration of goreisan (7.5 g daily) was continued for 12 weeks. The primary end-point was the post-operative recurrence rate at 12 weeks and the secondary end-point was hematoma volume reduction rates on computed tomography scan at 12 weeks. The analyses were performed not only on patients of all ages older than 60 years, but also on patients divided into those over or under 75 years old. One hundred and eighty patients were followed and analyzed (the control group, n = 88; the goreisan group, n = 92). The recurrence rates considering patients of all ages and patients under 75 years old were relatively low in the goreisan group but without a significant difference. The hematoma volume reduction rates showed no significant difference. Based on the results of the present study, a larger-scale study including more cases is necessary in future to confirm the efficacy of goreisan.

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A 72-year-old man developed left facial palsy at age 14 and left-sided hearing loss at age 20. At the age of 59, he presented with gait disturbance, and a large left cerebellopontine angle tumor was detected, which had markedly destroyed the pyramidal bone. The tumor was subtotally resected, but he required two more operations at the ages of 64 and 69 because of tumor regrowth. At the present time, recurrent tumor has destroyed the occipital bone and is invading the scalp. However, even though he has several cranial nerve palsies and cerebellar ataxia, he remains in stable condition and demonstrates long-term survival. The patient's surgical specimens revealed a papillary adenoma, which was recently thought to be of endolymphatic sac origin, although the origin of this kind of tumor, whether arising from the middle ear or from the endolymphatic sac, has not been established with certainty so far. In this paper, we provide further evidence that this tumor originates from the endolymphatic sac, based on anatomical, histopathological, and embryological evidence.

The surgical treatment of ruptured blister-like dissecting aneurysm on the internal carotid artery (ICA) is still controversial. We report a case of this disease successfully managed by a staged treatment: GDC packing into the blister-like aneurysm in the acute stage followed by proximal occlusion in the chronic stage. The merit of this staged treatment is to prevent rerupture in the acute stage and to allow the proximal occlusion in the chronic stage with or without an extracranial-intracranial bypass, after assessment of tolerance of the ICA occlusion.

We reviewed reports about the postoperative course of hemifacial spasm (HFS) after microvascular decompression (MVD), including in our own patients, and investigated treatment for delayed resolution or recurrence of HFS. Symptoms of HFS disappear after surgery in many patients, but spasm persists postoperatively in about 10–40%. Residual spasm also gradually decreases, with rates of 1–13% at 1 year postoperatively. However, because delayed resolution is uncommon after 1 year postoperatively, the following is advised: (1) In patients with residual spasms after 1 year postoperatively (incomplete cure) or who again experience spasm ≥ 1 year postoperatively (recurrence), re-operation is recommended if the spasms are worse than before MVD. (2) When re-operation is considered, preoperative magnetic resonance imaging (MRI) findings and intraoperative videos should be reviewed to ensure that no compression due to a small artery or vein was missed, and to confirm that adhesions with the prosthesis are not causing compression. If any suspicious findings are identified, the cause must be eliminated. Moreover, because of the risk of nerve injury, decompression of the distal portion of the facial nerve should be performed only in patients in whom distal compression is strongly suspected to be the cause of symptoms. (3) Cure rates after re-operation are high, but complications such as hearing impairment and facial weakness have been reported in 10–20% of cases, so surgery must be performed with great care.

Various kinds of hyperthermic treatment for malignant glioma had been inhibited due to both their incomplete feverish action and strict cooling effect of the brain. The author shows an effective results of hyperthermia for the treatment of malignant glioma in an in vivo study using stick type carboxymethylcellulose (CMC)-magnetite, a newly manufactured magnetite-product. A stick type CMC-magnetite, containing magnetite particles, was inserted into the T-9 glioma in the rat brain stereotactically, and the rats were exposed to an alternative magnetic field (AMF). The application time of AMF, which measured 88.9 kHz and 380 Oe, was 30 min a day. The rats were divided into three groups: three AMF applications (group I), one AMF application (group II) and no application but only injection of CMC-magnetite (control). As a result, the mean survival in days of these three groups measured 44.2+/-10.9 (group I), 17.0+/-1.5 (group II) and 14.4+/-1.5 (control). This investigation showed both significant effectiveness in attacking malignant glioma and significant prolonging of the survival time in rats. It is also a characteristic feature of the magnetite particles to spread through the tumor diffusely after three applications of AMF. This feature seemed to be one of the main factors that caused greater hyperthermic effect on glioma in this study. This method of hyperthermic treatment could be a useful strategy in the treatment of malignant glioma.