✓ The authors review their 2-year experience with a rhinoseptal transsphenoidal approach to skull-base tumors of various pathologies involving both the sphenoid and cavernous sinuses. Eight patients with cranial nerve palsies attributable to compression of the contents of the cavernous sinus and/or optic canal are included in this report. Among these patients, a total of 17 cranial nerves were affected. Postoperative normalization was achieved in eight nerves, significant improvement in seven nerves, and no improvement in two nerves. There were no operative complications of aggravation of cranial nerve palsies in this series. In spite of the limited operating field, the results demonstrate the effectiveness and safety of this approach. The authors recommend that this approach be considered before more aggressive surgery is undertaken.
Nobuo Hashimoto and Haruhiko Kikuchi
Nobuo Hashimoto, Hajime Handa and Shogo Nishi
✓ A 48-year-old woman developed multiple intracranial and intraspinal metastases from an invasive growth hormone-secreting pituitary adenoma after surgery and radiation therapy. This is the first reported case to show that the cells in the metastatic tumors and in the cerebrospinal fluid contained growth hormone.
Nobuo Hashimoto, Hajime Handa and Tatsuhito Yamagami
✓ Two years' experience with an extracapsular transsphenoidal approach to pituitary adenomas is presented. Some pituitary tumors contain an inordinate amount of connective tissue that often makes transsphenoidal resection difficult. By opening the tumor capsule and adjacent arachnoid membrane, such tumors with suprasellar extension can be safely removed. In some cases of functioning adenoma, resection of the diaphragma sellae and adjacent arachnoid membrane results in hormonal control. Among 62 cases of transsphenoidal surgery for pituitary adenomas, eight cases required this procedure. The surgical procedure is described and the cases are summarized. The indication and limitations of this procedure are discussed.
Jun-Ichiro Hamada, Nobuo Hashimoto and Tetsuya Tsukahara
✓ Two cases of moyamoya disease associated with repeated intraventricular hemorrhage are reported. The origin of bleeding was thought to be a distal aneurysm of the choroidal artery. The aneurysms were confirmed radiologically and histologically. The relationship between moyamoya disease and aneurysms is discussed, and a treatment proposed.
Hideki Hayashi, Shun-ichi Kihara, Minoru Hoshimaru and Nobuo Hashimoto
✓ The authors describe a rare case of diaphragmatic paralysis caused by cervical spondylosis. A 64-year-old man presented with dyspnea as well as cervical radicular pain and left-sided upper-extremity motor weakness. Chest radiography revealed elevation of both sides of the diaphragm. All symptoms were ameliorated immediately after cervical laminoplasty, and spirometry revealed improvement of ventilatory function 6 months after surgery. Cervical spondylosis should be considered a factor that can cause respiratory dysfunction.
Yoo Kang, Nobuo Hashimoto, Haruhiko Kikuchi, Naohiro Yamazoe and Fumitada Hazama
✓ Pathological and experimental studies have shown that cerebral aneurysms develop in part as a result of injury to the blood vessel wall. One of the peculiar aspects of aneurysm development is a defective proliferative or healing response to such injury. To examine this phenomenon, blood coagulation Factor XIII, which is known to enhance the healing process of wounds in general, was given to rats to induce experimental cerebral aneurysms. The rats were subjected to ligation of one common carotid artery and induction of hypertension, and were fed beta-aminoproprionitrile. Two weeks thereafter, Factor XIII was injected intravenously daily for 5 days (10 U/100 gm body weight/day). Twelve days after the start of Factor XIII injections, the rats were sacrificed and examined under light and electron microscopy. In seven of 12 bifurcations which developed small aneurysms, prominent intimal thickening was observed in the aneurysm lumen. In the most advanced cases, the aneurysm lumen was completely filled with proliferated smooth-muscle cells and collagen. In five of nine bifurcations that showed no aneurysm development, apparent intimal thickening was found at the site where aneurysms might be expected to grow. In the group of rats studied for induction of cerebral aneurysms but not given Factor XIII, none of 11 bifurcations with or without aneurysms showed such intimal thickening. The results indicated that the proliferative response at the sites of aneurysm development was modified by exogenous Factor XIII.
Yoshifumi Kawanabe, Tomoh Masaki and Nobuo Hashimoto
Object. The Ca++ influx into vascular smooth-muscle cells (VSMCs) plays a fundamental role in the development and chronic effects of vasospasm after subarachnoid hemorrhage (SAH). The Ca++-permeable nonselective cation channels (NSCCs) are activated by several endothelium-derived constricting factors such as endothelin 1 (ET-1) and thromboxane A2. Moreover, the receptor-operated Ca++ channel blocker LOE 908 inhibits ET-1—induced extracellular Ca++ influx via NSCCs in the VSMCs of the basilar artery (BA) and the NSCC-dependent part of ET-1—induced vasoconstriction of BA rings. The purpose of the present study was to evaluate the in vivo role of LOE 908 on SAH-induced vasospasm.
Methods. Forty-two Japanese white rabbits were assigned to seven groups. Treatment groups consisted of the following: 1) control rabbits without SAH that received a cisternal injection of saline; 2) rabbits with SAH that were subjected to the intravenous administration of saline; 3 through 6) rabbits with SAH that underwent the intravenous administration of 0.01, 0.1, 1, or 10 mg/kg LOE 908, respectively; and 7) rabbits without SAH that underwent the intravenous administration of 10 mg/kg LOE 908. Autologous blood was injected into the cisterna magna. The caliber of the BA was measured on angiographic studies before and after the cisternal injection of autologous blood.
The intravenous injection of LOE 908 inhibited the magnitude of an SAH-induced vasosapsm. In addition, the concentration of LOE 908 required to relax vasospasm (1 mg/kg) correlated with that required to block Ca++ influx into VSMCs.
Conclusions. The Ca++ channel blocker LOE 908 may inhibit the magnitude of an SAH-induced vasospasm by blocking the influx of Ca++ through NSCCs in rabbit BAs. Blocking the NSCCs may represent a new treatment for cerebral vasospasm after SAH.
Yoshifumi Kawanabe, Tomoh Masaki and Nobuo Hashimoto
Object. Endothelin-1 (ET-1) is one of the major inducers of vasospasm following subarachnoid hemorrhage (SAH). It is generally accepted that extracellular signal—regulated kinase 1 and 2 (ERK1/2) are involved in ET-1—induced vascular contraction. In addition, ET-1 transactivates epidermal growth factor receptor (EGFR) protein tyrosine kinase (PTK), which leads to ERK1/2 stimulation. Therefore, the authors examined whether EGFR—PTK transactivation contributes to ET-1—induced vascular contraction in this study.
Methods. Mitogen-activated protein kinase inhibitor, PD98059, inhibited ET-1—induced ERK1/2 stimulation in rabbit basilar artery (BA) vascular smooth-muscle cells (VSMCs). Moreover, PD98059 inhibited ET-1—induced contraction of rabbit BA rings. A specific inhibitor of EGFR PTK, AG1478, inhibited ET-1—induced EGFR—PTK transactivation, ERK1/2 stimulation, and contraction of BA rings in a concentration-dependent manner. The concentration of AG1478 required for 50% inhibition of the ET-1—induced contraction of BA rings was similar to that for ET-1—induced EGFR—PTK transactivation. Furthermore, AG1478 also inhibited ET-1—induced BA vasospasm in vivo.
Conclusion. The results indicate that EGFR—PTK transactivation pathway plays an important role in ET-1—induced vascular contraction.
Toru Iwama, Kohei Hayashida, Jun C. Takahashi, Izumi Nagata and Nobuo Hashimoto
Object. The purpose of this study was to evaluate cerebral hemodynamic and metabolic features in patients with arteriovenous malformations (AVMs) by using positron emission tomography (PET) scanning.
Methods. Twenty-four patients with supratentorial cerebral AVMs participated in PET studies in which 15O inhalation steady-state methods were used. The authors recorded the values of regional cerebral blood flow (rCBF), regional cerebral blood volume (rCBV), the regional oxygen extraction fraction (rOEF), and the regional cerebral metabolic rate of O2 (rCMRO2) at three designated regions of interest (ROIs) in each patient. These ROIs included perilesional (ROI-p), ipsilateral remote (ROI-i), and contralateral symmetrical (ROI-c) brain regions. To identify the factors that exert a direct effect on the hemodynamics of brains affected by AVM, we also separated the lesions according to their size and flow type shown on angiograms, and grouped the patients according to the presence or absence of progressive neurological deficits. We then compared the PET parameters at different ROIs in individual patients and evaluated the mean values obtained for all 24 patients according to AVM flow type and size, and the presence or absence of progressive neurological deficits.
Conclusions. Overall, mean rCBV and rOEF values were significantly higher in ROI-p than in ROI-c (p = 0.00046 and p = 0.015, respectively). No significant differences were seen between the ROI-i and ROI-c with respect to rCBF, rCBV, and rOEF. Mean rCMRO2 values were similar in the three ROIs; however, the mean rCBF was significantly lower in the ROI-p than in the ROI-c in patients with high-flow AVMs (p = 0.019), large AVMs (p = 0.017), and progressive neurological deficits (p = 0.021). Furthermore, the mean rOEF values were significantly higher in the ROI-p than in the ROI-c in patients with high-flow AVMs (p = 0.005), large AVMs (p = 0.019), and progressive neurological deficits (p = 0.017). The PET studies revealed hemodynamic impairment characterized by decreased rCBF and increased rOEF and rCBV values in the ROI-p of patients with large, high-flow AVMs regardless of whether they exhibited progressive neurological deficits.