Yoshihisa Oka

Evaluation of prognostic factors following expansive laminoplasty for cervical spinal stenotic myelopathy

BACKGROUND Expansive laminoplasty of several types has been proposed for patients with cervical multisegmental stenotic myelopathy to reduce postlaminectomy complications. Its effectiveness has not been fully explored by evaluating long-term results and magnetic resonance imaging (MRI) findings before and after surgery. METHODS We conducted a 5-year follow-up study of 22 patients with cervical spondylotic myelopathy and/or ossification of the posterior longitudinal ligament surgically treated with expansive laminoplasty. The operative results were examined using the Japanese Orthopedic Association (JOA) disability scale, with reference to the findings of MRI, computed tomography, and radiography. RESULTS Postoperative improvement was observed in 18 (81.8%) of the 22 patients. In 11 patients the percentage recovery of the JOA score was higher than 50% (average: 83.1%), while in the remaining 11 patients it was lower than 50% (average: 20.1%). Factors contributing to incomplete recovery appear to be related mainly to cord degeneration with atrophy (depicted as a T2-high intensity area) and to specific factors such as long symptom duration, age higher than 70 years, deterioration due to trauma, severe cord compression, radiculopathy, and kyphotic cervical curvature. CONCLUSIONS In cervical myelopathy, patients with multisegmental stenosis, expansive laminoplasty can be expected to provide a favorable outcome by providing sufficient cord decompression and stabilization of the cervical spine, when the stenotic cervical canal is enlarged to the normal range (over 12 mm residual anteroposterior diameter and 200 mm2 residual canal area). The efficacy can be restricted by various factors, especially irreparable cord degeneration.

Cerebral Blood Flow Measurement as an Indicator for an Indirect Revascularization Procedure for Adult Patients with Moyamoya Disease

OBJECTIVE Some adult patients with moyamoya disease have been treated successfully by indirect revascularization alone, although surgical indications and hemodynamic changes for these patients have not been fully explored. To examine surgical indications for this procedure, we studied the regional cerebral blood flow (rCBF) and angiographic findings in adult patients with moyamoya disease preoperatively and postoperatively. METHODS On 17 hemispheric sides of 12 adult patients with moyamoya disease treated surgically with a combination of various indirect procedures, mainly by encephaloduroarteriosynangiosis, we retrospectively evaluated changes in rCBF using xenon-133 single photon emission computed tomography, angiographic collateral formation, and clinical results. RESULTS Preoperatively, the rCBF values in the cortices at the bypass site at rest and after acetazolamide loading were lower than normal. The rCBF values were significantly increased after revascularization, approaching normal, except for incomplete recovery of vascular reactivity. The extent of postoperative neovascularization from implanted tissues fed by the external carotid artery system was more developed, in parallel with the preoperative decrease in resting and loading rCBF values. One-third of the operated sides exhibiting both a low rCBF at rest and impaired vascular reactivity in the noninfarcted cortices achieved good revascularization over two-thirds of the middle cerebral artery territory, accompanied by rCBF improvement and moyamoya vessel regression. Enough potential for neovascularization in the noninfarcted cortices was indicated that the resting rCBF was lower than 50 ml/100 g per minute (below the normal value by 2 standard deviations) and did not increase more than that value after loading, even in a 40-year-old patient who presented with a hemorrhage. Clinically, 11 patients (92%) had good results at the 4-year follow-up, whereas 1 patient (8%) with unsatisfactory neovascularization and a lesser extent of moyamoya vessel reduction experienced rebleeding. CONCLUSION We conclude that for the surgical treatment of adult patients with moyamoya disease, indirect procedures, mainly encephaloduroarteriosynangiosis, are recommended for patients with lower rCBF and no or negative vascular reactivity in the noninfarcted cortices, as well as for those who have no indication for the direct procedure. It is possible to determine these indications by a xenon-133 inhalation single photon emission computed tomographic study including an acetazolamide challenge test.

Endothelial nitric oxide synthase expression in tumor vasculature is correlated with malignancy in human supratentorial astrocytic tumors

OBJECTIVE Endothelial nitric oxide synthase (eNOS) may play an important role in the regulation of tumor blood flow and vascular permeability. However, there have been no reports describing alterations of eNOS expression in relation to malignant progression in human astrocytic tumors. We immunohistochemically studied the relationship between eNOS expression in tumor vasculature and malignancy in supratentorial astrocytic tumors. METHODS Tissue samples were obtained from 12 patients with low-grade astrocytomas, 10 with anaplastic astrocytomas, and 17 with glioblastomas. Normal brain tissue samples were obtained from four patients with other brain diseases. Immunohistochemical staining was performed using the avidin-biotin complex method, with polyclonal anti-eNOS antibody, and the levels of eNOS expression in endothelial cells were evaluated as slight, moderate, or intense on the basis of eNOS immunoreactivity. The proliferative potential was assessed as the MIB-1 staining index for tumor cells. RESULTS The expression of eNOS was slight in all specimens of normal brain tissue, slight in 7 and moderate in 5 specimens of low-grade astrocytoma, slight in 2, moderate in 6, and intense in 2 specimens of anaplastic astrocytoma, and moderate in 5 and intense in 12 specimens of glioblastoma. The MIB-1 staining index (mean+/-standard deviation) was 0.2+/-0.2% for normal specimens, 1.8+/-0.6% for low-grade astrocytomas, 9.6+/-6.9% for anaplastic astrocytomas, and 18.5+/-7.7% for glioblastomas. The MIB-1 staining indices for slight, moderate, and intense eNOS expression were 2.0+/-2.3%, 10.8+/-9.8%, and 16.9+/-7.7%, respectively. CONCLUSION Expression of eNOS in tumor vessels was significantly correlated with histological grade and proliferative potential. These findings suggest that astrocytic tumor vessels possess higher activity for nitric oxide production than do normal vessels.

Protein synthesis and immunoreactivities of contraction-related proteins in smooth muscle cells of canine basilar artery after experimental subarachnoid hemorrhage

We examined time-dependent changes in protein synthesis and in the immunoreactivities of representative contraction-related structural proteins in smooth muscle cells of canine basilar arteries after experimental subarachnoid hemorrhage (SAH). Protein synthesis was assessed by the percentage of polyribosome-forming ribosomes to total ribosomes (aggregation rate), a morphological index of the activity of protein synthesis. The aggregation rates in prostaglandin F2α- (PGF2α) and 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced contracted basilar arteries were 70.0 ± 7.0% and 71.4 ± 8.7%, respectively, quite similar to the value in normal basilar artery (73.0 ± 8.0%). In the single-SAH group with little delayed histological changes in the basilar arteries, the aggregation rate was significantly decreased to 30.5 ± 6.4% by 24 h after the SAH, and recovered to 52.3 ± 9.0% and 70.2 ± 7.6% at 7 and 14 days postSAH, respectively, when the vasospasm was moderately and completely ameliorated. In contrast, in the double-SAH group in which the basilar arteries developed delayed smooth muscle cell death and long-lasting arterial contraction, a significant decrease in the aggregation rate (25.0 ± 5.0% on day 4) persisted for 14 days. The in vitro incorporation of [3H]-leucine in the basilar arterial cells was also significantly suppressed 4 and 7 days after the initial SAH (1.2 ± 0.4 and 1.4 ± 0.3 × 103 dpm/mg protein) in the double-SAH group, as opposed to no significant decrease in the basilar artery at 7 days postSAH in the single-SAH group (1.9 ± 0.6 × 103 dpm/mg protein). The immunoreactivity of α-smooth muscle actin, a contractile protein, demonstrated by immunohistochemistry and immunoblots, was not altered for up to 14 days even in the double-SAH group, but that of calponin and of h-caldesmon, contraction-inhibiting proteins, was markedly reduced 4–14 days after the initial SAH. Persistent impairment of protein synthesis and relative reduction of immunoreactivities of the contraction-inhibiting proteins were observed in arteries with severe vasospasm and loss of smooth muscle cells, as noted in the double-SAH subjects. These abnormalities may cooperate to cause cerebral arterial narrowing accompanied by degeneration of smooth muscle cells after SAH.

Possible mechanism to induce protein kinase C-dependent arterial smooth muscle contraction after subarachnoid haemorrhage

SummaryA possible mechanism for the induction of protein kinase C (PKC)-dependent vascular contraction independent to the increase of intracellular Ca++ was investigated in the pathogenesis of cerebral vasospasm in the double subarachnoid haemorrhage (SAH) model. The level of 1,2-diacylglycerol (DAG), which is an intrinsic PKC activator, significantly increased from days 4 to 7 in the basilar artery after the initial SAH, and the continuous administration of 1,2-bis(nicotinamido)-propane (AVS), a novel free radical scavenger, not only lowered the concentration of lipid peroxides in the CSF but also successfully suppressed the basilar arterial narrowing and the increase of DAG in the basilar arterial wall in the same model. It was suggested that lipid peroxides generated in the subarachnoid clot affect the DAG content of the cerebral artery. Analysis of hydroxy-eicosatetraenoic acids (HETEs) with high performance liquid chromatography (HPLC) revealed the production of relatively large amount of 12-HETE in the subarachnoid clot. To examine the potential effect of exogenous 12-HETE on the DAG content of the cerebral artery, the basilar artery was incubated with 12-HETE in vitro. 12-HETE induced a concentration-dependent slow increase in DAG content in the arterial wall after 6 hours of incubation. Under conditions in which DAG formation was facilitated by the Ca++-ionophore, DAG accumulation in the basilar artery was enhanced in the presence of 12-HETE. It was suggested that 12-HETE generated in the subarachnoid clot, induced DAG accumulation in the arterial wall by inhibition of DAG metabolism, resulting in the induction of prolonged PKC-dependent smooth muscle contraction in the pathogenesis of cerebral vasospasm.