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Background Although most neurovascular diseases can be treated either by microsurgical or endovascular means, a subset of patients may require a combined approach. Patient transfer from the operating room (OR) to the angiosuite has been a fundamental drawback of this type of approach. Objective The purpose of this study is to report our clinical experience performing combined surgical and endovascular procedures for neurovascular diseases in the hybrid OR. Methods 29 patients with neurovascular diseases underwent combined endovascular and surgical procedures in a single session: 16 were scheduled combined treatment and 13 were emergency combined procedures. Of the emergency cases, three were rescue surgeries after endovascular complications. Three patients had ruptured intracranial aneurysms, eight had unruptured intracranial aneurysms, eight had arteriovenous malformations and eight had arteriovenous fistulae; two patients had either a spinal tumor or dural arteriovenous fistulae. Results All combined procedures were performed in a single session without changing the patient9s surgical position. In cases of ruptured arteriovenous malformations or aneurysms with hematoma, an emergency embolization was performed to assist the surgical procedure. Combined superficial temporal artery–middle cerebral artery (STA–MCA) bypass followed by endovascular parent artery trapping were successfully performed for complex large or giant aneurysms. There were two periprocedural ischemic complications. Of the three patients who underwent surgical rescue after endovascular complications, two remained intact and one died despite immediate surgical procedures. Conclusion A combined endovascular and surgical approach conducted in a hybrid OR provides a new strategy for the treatment of complex neurovascular diseases.

With the availability of new techniques, such as intravascular embolisation and radiosurgery, the therapeutic approach to arteriovenous malformations (AVMs) of the brain has recently been modified. The present study reports the authors, experiences in treating AVMs over the past 13 years. Spetzler-Martin grading of AVMs was I and II in 19 cases, III in 12, IV in 5 and V in 1 case. Four therapeutic regimens were utilised: surgical resection alone, embolisation and resection, and radiosurgery alone or after surgical resection. Generally, for low-grade AVMs (Spetzler-Martin grades I, II and III), the therapeutic choice was surgical resection in 27 cases, in combination with pre-operative embolisation in two of these patients. Two cases received radiotherapy only and one case received radiosurgery after embolisation, while one case was treated conservatively. Of the five cases of grade IV, four required surgical treatment, whereas the fifth case was treated conservatively. Favourable results (good recovery and moderate disability) were obtained in 96% of the low-grade AVMs as compared with the high-grade AVMs (66%) that had a poor outcome (due to primary brain damage resulting from haemorrhage at the onset in three cases and due to postoperative re-bleeding in one case). This report summarises preliminary experience in treating intracranial AVMs by surgical resection, intravascular embolisation and radiotherapy. Good therapeutic results can be expected by combining these therapeutic modalities.

Age is an important factor influencing outcome after severe traumatic brain injury (TBI). In general, the older the victim, the higher the probability of a poor outcome. To investigate the mechanism underlying the link between age and outcome, the data for 797 patients enrolled in the Japan Neurotrauma Data Bank (JNTDB), aged 6 years or older, with Glasgow Coma Scale (GCS) scores of 8 or less on admission or deterioration to that level within 48 h of impact were analyzed. Thirty-eight percent of the patients were between the ages of 40 and 69 years, and 24% of the patients were older than 69 years. Older patients had higher rates of mortality and lower rates of favorable outcome. The frequency of mass lesions which were associated with poorer outcomes significantly increased with age, but regardless of the intracranial lesion type, older patients had poorer outcomes. The GCS score and the occurrence of systemic complications did not differ significantly according to age. Multiple systemic injury was less frequent in older patients. The varied occurrence of intracranial lesion types according to age is likely caused by the disparity between the young and aged brain in the progression of secondary brain injury. Alteration in the pathophysiological response, which is related to the development of secondary brain injury in the aging brain, probably contributes to more severe and irreversible brain damage in older patients, and is thus associated with poor outcomes.

A 4-year study (Japan Neurotrauma Data Bank) of the medical treatment of 1002 cases of traumatic brain injuries in Japan was conducted from 1998 to 2001 at 10 emergency medical centers. Patients with severe head injury were eligible for entry with a Glasgow Coma Scale score of 8 or less at admission. Patients who underwent craniotomy were also included. Children under 5 years old were excluded. An original data sheet with 392 items from multi-focal viewpoints, such as etiology of injury, pre-hospital care, initial treatment including neuro-intensive care unit, and surgical treatment, was created. The results show that the patient's age and mechanism of injury are the most important factors in the outcome.

Cerebral angiography demonstrated an ACoA aneurysm in a 63-year-old man with subarachnoid haemorrhage (Fig. 1 a). Although the left OA was clearly seen, the right OA could not be identified. The anomalous OA, which was found later during surgery, had not been seen on the common carotid angiograms in any phases in multiple views. A right pterional craniotomy was performed. An artery 1 mm in diameter was found above the right optic nerve. This artery arose from the proximal (A1) segment of the ACA and entered the optic canal, and was identified as an anomalous OA (Fig. 1 b). Since this artery anchored the A1 segment firmly at its origin, retraction of the frontal lobe was restricted. Thus neck clipping was unavoidably performed through the space behind the right ACA with extensive resection of the gyrus rectus. Post-operative angiography confirmed completely satisfactory clipping, but the anomalous OA was not demonstrated.

A case of a traumatic middle cerebral artery occlusion resulting from a boxing injury is presented. A 22-year-old man, an amateur boxer, was admitted because of difficulty in speaking, that had appeared a day after a sparring fight. A computed tomographic scan showed low-density areas in the left globus pallidus and corona radiata. A carotid angiogram indicated complete occlusion of the left middle cerebral artery at its origin and an irregularity and narrowing of the left internal carotid artery in its supraclinoid portion. The patient was discharged 4 weeks after the admission with some persistent expressive dysphasia that diminished during the next month. The clinical features and mechanisms of the traumatic middle cerebral artery occlusion are discussed.

A case is presented in which Escherichia coli seeded a pre-existing chronic subdural hematoma. A 77-year-old woman was admitted to our hospital because of lethargy, left hemiparesis and fever. Drainage through a burr hole was performed with the diagnosis of bilateral chronic subdural hematoma. Operative findings revealed the infected subdural hematoma on the right side and non-infected subdural hematoma on the left side. Cultures of the subdural hematoma grew Escherichia coli. In view of the pyuria, the etiology of the infected subdural hematoma was postulated to be a urinary tract infection. In the majority of 14 reported cases, the causative organisms were Escherichia coli, Salmonella, and the systemic sources of infection included the urinary tract, gastrointestinal disease, or were unknown. The possibility of infected subdural hematoma should be considered when computed tomography findings suggestive of chronic subdural hematoma exist in a patient with signs of infection.

A case of multiple intracranial epidermoids is reported. A 38-year-old woman who had a three-year history of hemihypesthesia on the right side of her body, diplopia, gait disturbance, dysarthria, and visual field defect, was admitted. Neurological examination revealed right hemiparesis, bilateral abducens palsies, and cerebellar dysfunction. A computed tomography (CT) scan demonstrated a huge low density area in the left middle cranial fossa and heterogeneous density area in the brain stem. She was diagnosed tentatively as epidermoid in the middle fossa and intraaxial mass of the brain stem. Surgery was performed twice. In the first operation, the temporal mass was removed subtotally. Secondarily, only suboccipital craniectomy was performed. After the second operation, her condition deteriorated due to recurrent aseptic meningitis and aspiration pneumonia. She died three months later. Autopsy revealed that an epidermoid was situated in the brain stem intraaxially and another epidermoid was located in the temporal region independently. An intraaxial epidermoid is a rare entity, especially in the brain stem. There is no report of multiple intracranial epidermoids in the literature. The authors emphasize the necessity to rule out epidermoid, when CT shows a high or heterogeneous density area, even if multiple and/or contrast enhanced.

This study was carried out to clarify the biochemical changes in the cold injured brain and their relationship to pathological changes. The cold lesion was produced by application of a cryoprobe containing liquid nitrogen to the exposed left temporal surface for 1 minute in rats anesthetized with a halothane and oxygen gas mixture. The brain edema developed by this procedure was localized in one hemisphere. The animals were guillotined at scheduled times after the cold injury. The brains were rapidly removed and divided exactly between the two hemispheres. Changes in specific gravity of the brain tissue were measured by the dry-weight method until 4 weeks after the injury. Hematoxylin-eosin and Kliiver-Barrera stains were applied to pathological specimens. Free amino acid and uric acid levels were measured chronologically by using Iriyama's method. Catecholamine levels were analyzed by using high-performance liquid chromatography with electrochemical detection. Water content in the injured hemisphere reached a peak level at 12 hours after the injury, then decreased gradually, and entered the normal range at 1 week after the injury. This results was similar to the previous report. Multiple small hemorrhagic lesions were disclosed 2 hours after the injury. This suggests that a mechanism similar to hemorrhagic infarction might play a role in the development of cold injury. Essential amino acids were increased in the injured hemisphere, while those in the contralateral side remained within normal ranges. This result suggests that, in the injured hemisphere, there was not only nonutilization of the essential amino acids but also disturbance of the blood brain barrier, and that the aerobic glycolytic pathway was maintained normally in the contralateral hemisphere. Norepinephrine and dopamine were lowered, while tyrosine was increased in the early stage of cold injury. This suggests impairment of the catecholamine synthesis followed by nonutilization of catecholamine precursors. Uric acid level was increased immediately after the injury, especially on the injured side, and lowered to near baseline level at 4 weeks after the insult. Although biosynthesis of uric acid in the brain is not fully understood, it seems to be a fine parameter of brain damage.