Eye opening apraxia (EOA) has been described in literature as a complication of deep brain stimulation (DBS), especially after electrode implantation in the subthalamic nucleus (STN). EOA can be either worsened or alleviated by DBS depending on the etiology. Herein, we report a rare case where the progression of brain atrophy may have contributed to the delayed onset of EOA. The patient, a 73-year-old woman, had previously undergone bilateral STN-DBS for advanced Parkinson’s disease (PD), which was performed by another DBS team, at the age of 68 years. She initially experienced a dramatic improvement in her motor symptoms, with no adverse events. However, she had difficulty in opening her right eye 3 years after the DBS surgery. Imaging studies showed that the brain atrophy had progressed over the past 5 years, and that the DBS electrodes were implanted through the far anterior entry points. We considered that the relative movement of the DBS might have been caused by the progression of the brain atrophy to the posterior limb of the internal capsule (IC) where the corticobulbar tract exists, and this was enhanced by the lower implantation angle. The present case illustrates the importance of the DBS insertion angle considering the a+ trophic effect and the follow-up imaging studies after DBS.

POEMS (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes) syndrome is a rare paraneoplastic syndrome elicited by plasma cell dyscrasia. Its clinical manifestations are multiple and stroke is not a recognized feature. A 44-year-old woman with a 3-month history of bilateral lower extremity sensorimotor disturbance was admitted to our hospital. Examinations revealed polyneuropathy, organomegaly, hypothyroidism, monoclonal gammopathy, pelvic plasmacytoma, and elevated serum vascular endothelial growth factor (VEGF) levels. A diagnosis of POEMS was made. Her condition was improved by radiation therapy of her pelvic plasmacytoma and she continued to be seen on an outpatient basis. Five years after her first admission she was re-admitted with sudden-onset right hemiparesis. A brain computed tomography (CT) scan revealed a left intracranial hemorrhage and magnetic resonance (MR) angiography and cerebral angiography showed occlusion of the proximal portion of the bilateral middle cerebral artery and narrowing of the bilateral internal carotid artery at the terminal portion; moyamoya vessels were seen. This is the first report of a patient whose intracranial hemorrhage was attributable to quasi-moyamoya disease associated with POEMS syndrome. We suggest that the POEMS syndrome be ruled out in the differential diagnosis of patients presenting with atypical stroke, multivessel stenotic lesions (moyamoya vessels), and polyneuropathy.

Hemophilia is an X-linked hemorrhagic disease due to coagulation factor VIII or IX deficiency with approximately 5–10% incidence of central nervous system bleeding. We present an intriguing case of a refractory subacute subdural hematoma (SDH) controlled with endovascular embolization in a hemophilic patient. A 5-year-old severe hemophilic A boy presented with a life threatening left parietal subcortical hemorrhage, for which he underwent craniotomy and evacuation of the hematoma. Recurrent hemorrhage necessitated a repeat craniotomy. This was followed by three episodes of SDH development at the craniotomy site that were treated surgically, and finally controlled with embolization in the subacute period. This case presents a novel option for treating a refractory SDH in patients with coagulation disorders.

Crowned dens syndrome (CDS) is a rare disease which presents with neck pain and rigidity. A 74-year-old man with right chronic subdural hematoma (CSDH) underwent hematoma drainage. After the operation, he complained of neck pain and laboratory test revealed elevation of C-reactive protein (CRP) and white blood cell (WBC). Suspecting localized infection, wound irrigation was performed. Neck pain relieved after irrigation, but we could not find the source of infection. CDS was diagnosed by computed tomography (CT). CDS is frequently misdiagnosed as meningitis and localized infection. CT is useful for diagnosis. Neurosurgeons need to be aware of CDS after operation.

We report the case of a 40-year-old man presenting with focal headache and a bulge at the right parietal bone, diagnosed as an intradiploic arachnoid cyst. The cyst wall included “meningothelial hyperplasia,” which is a rare finding. While over 40 cases of intradiploic arachnoid cysts have been reported to date, meningothelial hyperplasia in an intradiploic arachnoid cyst does not appear to have been reported. We also discuss the pathological findings of arachnoid cysts with meningothelial hyperplasia and mechanisms of enlargement of the arachnoid cyst.

The lateral transpsoas approach to access the vertebrae obviates the need for an approach surgeon and minimizes muscular disruption, thus allowing for quicker recovery. Several reports on the lateral transpsoas procedure have described few complications. However, the development of an unsightly and painful abdominal flank bulge is a largely under-recognized and very rare complication of the lateral transpsoas approach. A 59-year-old man suffered from back pain and bilateral posterior leg pain. Computed tomography (CT) scan and MRI showed retrolisthesis at L3-4, L2 wedge vertebrae with kyphosis, left L4 screw loosening, and L3-4 disc herniation with central canal stenosis. L2 corpectomy and L3-4 DLIF and posterior fusion to T12 for kyphosis correction were performed. For the lateral approach, resection of the T11 rib was performed. One month later, he developed left abdominal flank bulging below the lateral approach site, which was aggravated by walking, coughing, defecating, constipation, and eating. CT scan showed left abdominal flank bulging accompanied by abdominal muscle thinning. We believe that this complication is caused by denervation of the abdominal musculature after injury to the T11 intercostal nerves.

Few papers have reported detailed accounts of intracerebral hemorrhage caused by cerebral hyperperfusion after superficial temporal artery to middle cerebral artery bypass (STA-MCA) bypass for atherosclerotic occlusive cerebrovascular disease. We report a case of vasogenic edema and subsequent intracerebral hemorrhage caused by the cerebral hyperperfusion syndrome (CHS) after STA-MCA bypass for atherosclerotic occlusive cerebrovascular disease disease without intense postoperative blood pressure control. A 63-year-old man with repeating left hemiparesis underwent magnetic resonance angiography (MRA), which revealed right internal carotid artery (ICA) occlusion. We performed a double bypass superficial temporal artery (STA)–middle cerebral artery (MCA) bypass surgery for the M2 and M3 branches. While the patient’s postoperative course was relatively uneventful, he suffered generalized convulsions, and computed tomography revealed a low area in the right frontal lobe on Day 4 after surgery. We considered this lesion to be pure vasogenic edema caused by cerebral hyperperfusion after revascularization. Intravenous drip infusion of a free radical scavenger (edaravone) and efforts to reduce systolic blood pressure to <120 mmHg were continued. The patient experienced severe left hemiparesis and disturbance of consciousness on Day 8 after surgery, due to intracerebral hemorrhage in the right frontal lobe at the site of the earlier vasogenic edema. Brain edema associated with cerebral hyperperfusion after STA-MCA bypass for atherosclerotic occlusive cerebrovascular disease should be recognized as a risk factor for intracerebral hemorrhage. The development of brain edema associated with CHS after STA-MCA bypass for atherosclerotic occlusive cerebrovascular disease requires not only intensive control of blood pressure, but also consideration of sedation therapy with propofol.

A traumatic internal carotid artery (ICA) aneurysm is rare and difficult to treat. Trapping of ICA is commonly performed owing to the difficulty of directly approaching ICA aneurysms. Recently, coiling the aneurysm itself was recommended if possible. However, it is controversial which of methods are best to completely treat aneurysm. We present the case of a 74-year-old man, who had experienced a head injury 8 years previously, with recurrent severe epistaxis. An ICA aneurysm was detected on computed tomography. The trapping and bypass was planned. However, sudden epistaxis occurred, we performed trapping to stop the bleeding and save his life. After the operation, no right ICA or aneurysm was detected. However, severe epistaxis recurred two months after the operation. In the second operation, a ligation of the common −/− external carotid artery and a severance of an ICA portion between the ophthalmic artery and the aneurysm were insufficient to stop the bleeding. This case indicates ICA trapping, even if a trapping portion is below an ophthalmic artery, is insufficient to treat an ICA aneurysm. ICA aneurysms should be suspected when a patient present with recurrent −/− massive epistaxis, who has a head injury history, even if it is far past.

Herein, safe and reliable neuroendoscopic biopsy via an extremely narrow foramen of Monro (ENFM) for a non-hydrocephalic patient with hypothalamic and pineal region tumors was successfully applied. A 17-year-old boy presented with hypothalamic manifestations attributed to hypothalamic and pineal region tumors. Small ventricles were seen. Intraoperatively, to advance different diameter steerable fiberscopes via ENFM, the third ventricle was flushed to induce a moment increase in the intraventricular pressure with subsequent dilatation of FM. Postoperative course was uneventful. Histopathological studies revealed a yolk sac tumor. Adjuvant therapy was applied. Follow-up neuroimaging disclosed marvellous improvement of the condition. His symptoms gradually improved.