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Parkinson's disease(PD)is a degenerative disorder of the central nervous system. Its cardinal features are resting tremor, rigidity, bradykinesia, and postural instability. Several years after disease onset, many patients with PD exhibit postural deformities, including camptocormia, Pisa syndrome, and dropped head syndrome, which can lead to spinal deformities. In addition, spinal degenerative disorders are frequently associated with PD and can further impact the patients' quality of life. Current evidence suggests a multifactorial etiology for postural deformities and spinal degenerative disorders in PD, which includes abnormal stress on the spine(biomechanical factors), postural instability and impairment of postural compensation(physiological factors), and imbalance of dopaminergic signals(pharmacological factors). The relative contribution of these factors varies between patients and across symptoms. Consequently, neurologists have difficulty treating these axial problems. Moreover, many studies have reported poor outcomes and high complication rates of spinal surgery in patients with PD, which embarrasses spinal surgeons. An improved understanding of the mechanisms underlying spinal problems in PD might ultimately lead to more effective management of these disabling complications.

Ependymoma is the most common primary intramedullary tumor of the spinal cord, accounting for a quarter of these tumors. We experienced a case of 'ependymoma of the spinal cord with a cystic lesion that presented as an intradural extramedullary tumor extending from the thoracic to lumbar vertebrae. In review of past literature on reports of spinal intradural extramedullary ependymoma, lesions spanning three or more vertebrae with cystic lesions were frequent, and about half were World Health Organization grade II or higher. Dissemination or recurrence of these tumors may occur after surgery. There is no consensus on postoperative adjuvant therapy for intradural extramedullary spinal ependymoma, but careful consideration should be given to the intraoperative findings and the characteristics of the tumor.

A 56-year-old man complained of gait disturbance and confused thinking. Magnetic resonance imaging(MRI)revealed an arteriovenous malformation(AVM)of the cerebellar vermis(Spetzler-Martin grade IV)causing hydrocephalus. One dilated precentral cerebellar vein was compressing the aqueduct. After feeder embolization over 3 sessions using N-butyl cyanoacrylate(NBCA), the nidus was reduced to one-third in size. However, symptoms remained unimproved, and endoscopic third ventriculostomy(ETV)was performed. The third ventricle showed thinning of the floor, with a fenestration in part of the floor. Radiological findings and clinical symptoms improved, and the patient returned home after rehabilitation. The condition of the patient remained stable as of six months later. On angiography, the draining vein showed a pressure of 20 mmHg with no change in the residual AVM. Embolization alone achieved a reduction in nidus volume, but could not reduce venous pressure, and combination therapy including ETV proved necessary. Cases with hydrocephalus due to aqueductal stenosis by AVM are extremely rare. This pathology is discussed with reference to the literature.

Sturge-Weber syndrome (SWS) is a rare neurocutaneous syndrome characterized by intracranial leptomeningeal angioma, facial port-wine nevi, and glaucoma. Diagnosis is relatively easy because of the facial angioma and MRI findings, but evaluating severity is difficult. Predictors of SWS's prognosis are epilepsy and brain dysfunction under the leptomeningeal angioma. Therefore, active research has been intensely conducted with electrophysiological, neuroimaging, and neuropsychological methods. Final goals of this research are to define the therapeutic strategy. In this review, we focus on recent advances in neuroimaging and EEG analysis to discover the epileptogenesis, the most adequate therapy, and prospective topics of investigation in SWS.

A 68-year-old female presented with the disturbance of brainstem function. Brain T2 weighted and FLAIR (fluid-attenuated inversion recovery) magnetic resonance imaging revealed the hyperintensity signal of the medulla oblongata, which led to diagnosis of brainstem infarction. Diagnostic cerebral angiography showed the dural arteriovenous fistula (DAVF) developed on the left transverse sinus (TS). Venous drainage route was consisted of retrograde leptomeningieal venous reflux of the cerebrum and spinal perimedullary vein via superior petrosal sinus. Venous hypertension of the brainstem was relieved by transvenous platinum coil selective embolization of superior petrosal sinus. The correct analysis of venous drainage pattern is essential for the curative endovascular surgery.

Subclavian artery aneurysm is relatively rare, but, we can scarcely find mention in the literature of a subclavian-vertebral junction aneurysm. We report a case of a 73-year-old man with a left subclavian-vertebral junction arterial aneurysm of 11 mm in diameter which caused a brain stem thromboembolism. He showed right hemiparesis and dysarthria on admission. On the 5th day after admission, his hemiparesis worsened and he could not even walk. In order to prevent further embolic attack on the vertebro-basilar system and rupture from the aneurysm, we embolized the aneurysm successfully with some GDC coils. During the operation, no further brain infarction occurred, and we maintained blood circulation in the left subclavian-vertebral artery. This aneurysm appeared on angiography to be atherosclerotic in its clinical characteristics, and we have scheduled follow-up angiography in two years time. As his hemiparesis had improved, he was discharged from the hospital on foot.