We report a rare intracisternal C1 posterior root neurinoma in a 35-year-old man without neurofibromatosis who presented with headache, nuchal pain, bilateral motor weakness of the upper extremities, and numbness in the right distal upper extremity. CT and MRI study showed a 20-mm intracisternal lesion at the foramen magnum. At surgery, there was an anastomosis between the C1 posterior root and a spinal accessory nerve at the site of the tumor; the root from the collateral sulcus of this C1 root was absent. Postoperatively, the patient remains free of symptoms. Foramen magnum neurinomas have been described as accessory nerve tumors. We present new anatomical consideration regarding this lesion.

Summary We report a rare intracisternal C1 posterior root neurinoma in a 35-year-old man without neurofibromatosis who presented with headache, nuchal pain, bilateral motor weakness of the upper extremities, and numbness in the right distal upper extremity. CT and MRI study showed a 20-mm intracisternal lesion at the foramen magnum. At surgery, there was an anastomosis between the C1 posterior root and a spinal accessory nerve at the site of the tumor; the root from the collateral sulcus of this C1 root was absent. Postoperatively, the patient remains free of symptoms. Foramen magnum neurinomas have been described as accessory nerve tumors. We present new anatomical consideration regarding this lesion.

救急医療体制の下, 高度救命救急センターにおける最近のクモ膜下出血(SAH)の症例を分析し, SAH急性期における患者管理について検討した.対象は最近2年間に当センターに搬入された連続200例のSAHである.搬入時心肺停止を含めたpoor grade症例が半数以上を占め, 積極的な神経集中管理の下, 脳保護を図る重要性が指摘された.急性期管理をprehospital phase, hospital phaseの各phaseに分けた対応と工夫が必要であり, 特にprehospital phaseにおける搬送時の降圧, 鎮静化の徹底化, さらに3次元CTアンギオをSAH周術期の管理(術前, 術後, 脳血管攣縮の評価)に使用し, 診断の低侵襲化を図ることも重要と考えられた.

It is rare to encounter subarachnoid hemorrhage (SAH) whose origin cannot be detected by cerebral angiography. Occasionally, the detection is prevented by initial disappearance of the cerebral aneurysm as soon as it has ruptured. The collapse of cerebral aneurysm might be caused by perianeurysmal hematoma and brain, the thrombosed aneurysm, early cerebral vasospasm, and unknown etiology. We encountered a ruptured aneurysm that was finally detected by cerebral angiography in the third examination. The aneurysm was partially thrombosed pathologically. We speculate on the management of SAH whose origin cannot be detected by cerebral angiography.

A retrospective analysis has been investigated about the optimal perioperative management of 200 consective subarachnoid hemorrhage (SAH) patients admitted to the Advanced Critical Care Emergency Center of Nippon Medical School in recent two years. 82 cases were males and 118 cases were females. Of the 200 patients, 130 were in poor grade (grade IV and V) including 27 patients in cardiopulmonary arrest (CPA) condition. 89% of the patients were group 3 and 4 according to Fisher CT classification. The algorithm in the acute management of SAH can be classified into prehospital phase and hospital phase. The hospital phase can be further classified into resuscitative phase, diagnostic phase, operative phase and postoperative neurointensive care phase. Of 21 patients with rebleeding, 6 cases were in prehospital phase and 6 cases were in diagnostic phase. Based on these findings, in prehospital phase strict control of blood pressure and sedation is recommended during transfer. Three dimentional CT angiography is less invasive and very useful in the perioperative management of SAH. The introduction of endovascular occlusion with GDC coil and brain hypothermial treatment will have the possibility of improving the overall prognosis of severe SAH.

It is ideal for the occlusion of chief cerebral artery to perform revascularization safely by some means in the ultraacute stage. Unfortunately, when the revascularization cannot be carried out, massive cerebral edema often occurs. Massive cerebral edema often causes lethal transtentorial herniation. Three patients with extensive cerebral infarction underwent decompressive craniectomy at the moment low density area was found on the computed tomography, that is, before massive cerebral edema occurred. This avoided complications of not only lethal transtentorial herniation but also secondary neurological deficits due to cerebral edama. Early decompressive craniectomy may have positive therapeutic significance in prevention of secondary neurological deficits due to massive cerebral edema.

急性硬膜下血腫(ASDH)の外減圧術中に著明な脳腫脹を来した13症例をもとに,致死的ASDHの治療限界について考察した。術前のGCSは3-4点7例,5-8点6例,瞳孔は散大4例,不同8例だった。CTで10例が脳挫傷や外傷性クモ膜下出血(T-SAH)を伴い,10例は脚間槽が描出されていなかった。手術は受傷後平均2時間41分で開始された。術後は適宜,低体温療法やバルビツレート療法を導入した。12例は平均5.2日目に死亡した。2歳女児の1例は神経脱落症状を残すことなく退院した。CTで脚間槽が描出されない,またT-SAHで脳底槽が充満しているASDHはきわめて救命困難であるが,小児例は積極的治療の対象とすべきである。

The effect of the 21-aminosteroid U74006F, an inhibitor of iron-dependent lipid peroxidation, on neurologic outcome and cerebral edema was evaluated in adult male Sprague-Dawley rats subjected to a fluid percussion temporal brain injury followed by 45 min of hypoxia (PaO2 = 30.0 mm Hg). The rats were divided randomly into five groups. Bolus injections of a control drug or U74006F (1.0, 3.0, 10.0, or 30.0 mg/kg) were given 3 min and 3 h after the injury. Twenty-four hours after the injury, the neurologic status was evaluated, the rats were killed, and brain water content was determined by microgravimetry. U74006F did not significantly reduce brain water content at any dose level, nor did it affect rotorod walking or activity scores. However, rats treated with U74006F at a dose of 10.0 mg/kg had significantly better motor function scores (p < 0.05) than rats in the control group. These findings demonstrate the usefulness of U74006F as a cerebroprotective agent in this model of experimental head injury.

Background and Purpose: Accurate and reproducible determination of the size and location of cerebral infarcts is critical for the evaluation of experimental focal cerebral ischemia. The purpose of this study was to compare intracardiac perfusion of 2,3,5-triphenyltetrazolium chloride with immersion of brain tissue in 2,3,5-triphenyltetrazolium chloride to delineate brain infarcts in rats.Methods: After 6, 24, or 48 hours of ischemia induced by permanent middle cerebral artery occlusion, some rats were perfused with 2,3,5-triphenyltetrazolium chloride; other rats were given an overdose of barbiturates, after which brain sections were immersed in 2,3,5-triphenyltetrazolium chloride. Coronal sections were taken 4, 6, and 8 mm from the frontal pole, and infarct areas in perfused and immersed sections were compared; subsequently, the same sections were stained with hematoxylin and eosin.Results: In rats subjected to 24 or 48 hours of occlusion, areas of infarction were clearly defined with both 2,3,5-triphenyltetrazolium chloride staining techniques, and the infarct sizes correlated well with the results of hematoxylin and eosin staining (r = 0.85-0.94).Conclusions: These results demonstrate that intracardiac perfusion of 2,3,5-triphenyltetrazolium chloride is an accurate, inexpensive, and efficient staining method to detect infarcted tissue 24 and 48 hours after the onset of ischemia in rats.

Calcium is critically important in the normal and in the pathological metabolism of cerebrovascular cells, glial cells, and neurons, and elevated concentrations of intracellular calcium may cause cell death by activation of proteolytic and lipolytic enzymes. Traumatic spinal cord [25] and brain injuries [22] cause rapid falls in extracellular calcium, with sudden rises in intracellular calcium which likely contribute to overall cell injury and death. Antagonists of both voltage-sensitive and receptor-operated calcium channels have been shown to improve outcome after a variety of central nervous system insults including focal cerebral ischemia [7, 9, 18], spinal cord injury [6, 20], and experimental brain trauma [17]. The present study was performed to examine the effect of the dihydropyridine voltage-sensitive calcium channel antagonist nimodipine on outcome after a combination of fluid percussion brain impact and postimpact hypoxia.