Hinge technique is a new method for cerebral decompression that allows the bone flap to move outward in response to brain swelling and essentially allows reconstruction of the cranial vault as a minor procedure under local anesthesia. This retrospective study assessed outcomes following the use of this new decompressive technique. During an approximately 7-year period (June 2004 to March 2011), 58 patients who had suffered head trauma or stroke underwent cerebral decompression using the hinge technique or conventional decompressive craniectomy. Patients were assessed with the Glasgow Coma Scale (GCS), the Glasgow Outcome Scale (GOS), and the modified Rankin scale (mRS). Twenty-one patients (16 males, 5 females; age range, 21-78 yrs; mean age, 57.4 ± 15.5 yrs) underwent cerebral decompression using the hinge technique, and 37 patients (18 males, 19 females; age range, 5-83 yrs; mean age, 54.1 ± 20.9 yrs) underwent conventional decompressive craniectomy. There was no significant difference in preoperative GCS or postoperative GOS or mRS between the two groups. Six patients in the decompressive craniectomy group and none of the patients in the hinge technique group developed bone flap infection (p ＝ 0.02). The bone flap was removed in two cases in the hinge technique group due to low cerebral perfusion pressure as well as elevated intracranial pressure (ICP). The hinge technique with ICP monitoring was effective and safe for management for head trauma or stroke and was not associated with bone flap infection.

A 64-year-old female presented with rapid onset of left ophthalmoplegia and truncal ataxia, after experiencing diplopia due to left abducens nerve palsy for a year. She had undergone surgery twice for left trigeminal neuralgia caused by a large intracranial epidermoid cyst at the age of 48 and 52 years. The intracranial epidermoid cyst grew and became predominantly enhanced by contrast medium on computed tomography (CT) and T 1 -weighted magnetic resonance (MR) imaging, which had not been observed earlier. The tumor was partially removed and the histological diagnosis was squamous cell carcinoma (SCC). Radiation therapy was administered, but she presented with paraplegia of the bilateral lower extremities and anesthesia due to spinal multiple metastases of SCC one year later. Radiation therapy was administered for the spinal lesions, but she died of multiple metastases to the cerebellum and medulla oblongata with hydrocephalus 2 years after the third surgery. Transformation of intracranial epidermoid cysts to SCC appears as predominant enhancement on CT or T 1 -weighted MR imaging with rapid deterioration of neurological features. All reported cases of malignant transformation of intracranial epithelial cysts to SCC with leptomeningeal carcinomatosis have occurred in intracranial epidermoid cysts.

A 29-year-old woman presented with a severe headache. Computed tomography revealed a large cystic lesion with a mural nodule-like mass homogeneously enhanced with contrast medium in the right cerebellum. The tumor was removed, and pathological studies revealed a cerebellar astrocytoma corresponding to World Health Organization grade II. When she was 35 years old, or 6 years after the surgery, magnetic resonance imaging revealed a recurrence of the tumor in the right cerebellum, and subtotal removal of the recurrent tumor was performed. Pathological studies revealed a mixed glioblastoma multiforme and anaplastic ependymoma. Chemotherapy (Paraplatin and VePeside-S) and focal radiation therapy at 60 Gy were administered following surgery. Thereafter, at 39 years of age, or 4 years after radiation therapy, magnetic resonance imaging again revealed a recurrence of the tumor, which was heterogeneously enhanced with gadoliniumdiethylenetriamine pentaacetic acid in the right cerebellum. Subtotal removal of the tumor was performed; pathological studies revealed an anaplastic ependymoma with sarcomatous components. Immunohistochemical findings showed some parts of the sarcomatous components to stain positively for glial fibrillary acidic protein and, as a result, these sarcomatous components were diagnosed to be gliosarcoma.

A 6-year-old boy had undergone ventriculoperitoneal (VP) shunt for acute hydrocephalus because of a brain tumor at the age of 11 months, and presented with vomiting and somnolence after the shunt malfunctioned 6 days after VP shunt reconstruction, during which the right external jugular vein was injured during the tunneling process and the peritoneal catheter was not fixed to the peritoneum with a purse string suture. Radiography revealed an abnormal route of the peritoneal catheter, suggesting that the distal VP shunt catheter had migrated into venous vasculature through the right external jugular vein. Computed tomography revealed that the peritoneal catheter had migrated into the internal jugular vein and the right atrium. At surgery, the peritoneal catheter was exposed through a small incision on the subclavicular region, was easily extracted from the internal jugular vein and the heart as there was no coiling or adhesion of the distal catheter to the vascular tissues, and was repositioned into the peritoneum with weak fixing between the subcutaneous tissues of the right subclavicular region and the right abdominal rectus muscle fascia as a temporary emergency measure. Peritoneal shunt migration into the internal jugular vein and the heart through the external jugular vein can be lethal because of pulmonary infarction or arrhythmia, and must be detected as soon as possible. Periodic follow-up radiography should be scheduled after VP shunt placement, even in the absence of symptoms.

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