Chronic kidney disease (CKD) is a major risk factor for poor prognosis in patients with cardiovascular diseases. We previously showed that renal artery stenosis (RAS) was often found in patients with cardiovascular diseases such as myocardial infarction. The aim of the present study was to evaluate the incidence and risk factors of RAS in patients with stroke or severe carotid artery stenosis. (1) From 2,167 autopsy patients during the 17-year period between 1980 and 1997, we studied 346 cases with stroke. RAS was found in 36 patients (10.4%), and the patients with RAS were older and had worse kidney function. Multiple logistic regression analysis identified kidney function, hypertension, and carotid artery stenosis as independent predictors of RAS. (2) From February to August 2006, 41 consecutive patients with severe carotid artery stenosis were admitted to the department of Neurosurgery of National Cardiovascular Center. Kidney function, urinary albumin excretion and renal artery duplex scanning were performed in all patients. They were classified into two groups according to the findings of renal artery duplex scanning, 11 patients with RAS and 30 patients without RAS. We evaluated the differences in clinical findings and renal function between the groups and clarified the risk factors for RAS. In the patients with RAS, smoking and incidence of cardiovascular diseases were evident, and kidney function was impaired significantly compared with the patients without RAS. Multivariate logistic regression showed that smoking, the presence of cardiovascular diseases and kidney function were significant clinical predictors for RAS. (3) Carotid endarterectomy was performed in 42 patients with RAS (n=11) and without RAS (n=31) in our hospital. Transient increase of serum creatinine and decrease of urine output was observed in the patients with RAS. In conclusion, RAS was frequently detected in the patients with stroke or severe carotid artery stenosis. The risks of RAS were smoking, the presence of cardiovascular diseases and kidney dysfunction. Since RAS was the underlying cause of hypertension and renal failure, it is important to consider the presence of RAS in patients with stroke or carotid artery stenosis.

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Aortogenic and paradoxical embolisms have been recognized as possible causes of cryptogenic stroke. For the diagnosis of both conditions, transesophageal echocardiography has been widely used in the routine examination of ischemic stroke patients. An aortic IMT>4mm, mobile plaques and ulcers were defined as complex lesions and could be a potential risk for ischemic stroke. For medical treatment of aortogenic embolism, combination of statin and anti-thrombotic therapy (either antiplatelet or anticoagulation therapy) is recommended. For diagnosis of paradoxical embolism, confirmation of a right-to-left shunt through the patent foramen ovale is not sufficient enough because almost 20% of healthy adults have a right-to-left shunt. A diagnosis of deep vein thrombosis or pulmonary embolism is also required. For cryptogenic stroke patients with patent foramen ovale, antiplatelet therapy is usually recommended to prevent a recurrent event while warfarin is reasonable for high-risk patients who have other indications for anticoagulation such as venous thrombosis.

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An anticoagulant turns procoagulant. This is the fundamental paradox of heparin-induced thrombocytopenia (HIT), an immune-mediated, life-threatening side effect of heparin therapy. Antibodies against complexes of platelet factor 4 and heparin induced by heparin administration, when they have the high levels of platelet-activating properties (HIT antibodies), are the major cause of HIT. HIT antibodies stimulate platelets and endothelial cells resulting in thrombocytopenia, increased thrombin generation, and associated venous and arterial thrombosis. HIT typically occurs 5 to 14 days after heparin administration (typical-onset HIT). HIT antibodies are transient but can be detected for about 100 days after cessation of heparin treatment. Thus, some patients develop HIT several days after discontinuing heparin (delayed-onset HIT) or soon after the re-administration of heparin (rapid-onset HIT), that is caused by the residual circulating HIT antibodies that resulted from the recent heparin treatment. HIT should be considered as a clinicopathologic syndrome and must be diagnosed through a combination of clinical pretest probability (e.g. the 4T's scoring system) and the detection of HIT antibodies by a serological assay. Several clinical research studies performed in Western countries have revealed that the prevalence of HIT is 0.5 to 5%, which varies depending on the clinical settings. HIT is life threatening, especially when unrecognized or untreated. Thromboembolic events can occur in 25 to 50% of HIT patients, and the thombotic death rate can reach to about 5%. All heparin administration including heparin flushes should be discontinued in patients strongly suspected of having HIT and substituted with a thrombin inhibitor. Recognition of HIT has improved in Japan since manufacturers' prescribing information (package insert) on heparin was revised to mention HIT in April, 2006. In addition, argatroban, a direct thrombin inhibitor, was recently approved by Japanese regulators in July, 2008 as the first drug for the treatment of HIT, based on the results of a multicenter, non-randomized, open-label trial performed at 20 institutes. Several retrospective studies and a multicenter, prospective cohort study suggest lower incidences of HIT in Japan than what is diagnosed in Western countries, probably due to ethnic factors and/or different clinical practices. Based on these results, we will seek to establish Japanese guidelines for the diagnosis and treatment of HIT.

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The technologies for the diagnosis of unstable plaque in the carotid artery are developing and the imaging modalities are also increasing. However, the evidence levels are not so high. Some reports suggest that the ultrasound findings of low echoic plaque, ulcer formation and heterogeneous plaque are the signs of vulnerable plaque. Recently, I have found that some types of plaque have mobility on part of the plaque surface. I call such plaque "mobile plaque". I believe that after comparison with the pathological specimens, this finding reflects a rupture of the plaque and fresh intra-plaque hemorrhage. Especially, symptomatic patients with this condition tend to suffer relapse strokes, so rapid action is needed to prevent it from worsening. Detection of the micro-embolic signals by trans-cranial Doppler method can evaluate the vulnerability of carotid artery plaque indirectly, because micro-embolic signals reflect any attached fragile thrombus on the plaque or plaque rupture. Stroke patients with a lot of micro-embolic signals need careful treatment, because these patients also tend to relapse. Plaque imaging by MRI is a useful method to evaluate vulnerability of the carotid artery plaque. I think combined MRI and ultrasound examinations can cover any weaknesses in either system alone. Now, there is no established guideline for the diagnosis of unstable plaque, so it is necessary to match-up modalities according to need.

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Internal carotid artery stenosis is a systemic vascular disease that is frequently complicated with hypertension, diabetes mellitus, obesity, ischemic heart disease and arteriosclerosis obliterans. Patients undergoing hemodialysis are also frequently complicated with internal carotid artery stenosis. To determine individual indications for carotid endarterectomy, carotid artery stenting, and medical treatment based not only on internal carotid stenosis but also on systemic vascular disease is important and strict perioperative management is required to prevent postoperative complications in high-risk patients. We describe the problems associated with carotid endarterectomy among high-risk patients and their management.

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Carotid artery stenting (CAS) is indicated even for high-risk carotid endarterectomy patients. However, CAS carries its own high-risk and difficulties due to access route problems such as atherosclerosis, tortuousity, nearly total occlusion and aneurysms, as well as those posed by lesion characteristics such as circled calcification, dangerous plaque, and floating thrombus. The added complications of elderly patients, hypercoagulopathy and intimal fragility due to diabetes mellitus are troublesome in both treatment options. Particularly, cholesterol crystal embolization is a rare but fetal ischemic complication. Patients with severe coronary ischemic disease should be carefully managed for postoperative hypotension. General risk management based on the preoperative evaluation of each patient's general condition, access route, lesion, plaque, collateral pathway and cerebral blood flow and the operator's technical capabilities, as determined by national qualification system rating, is mandatory for the treatment of such high-risk patients. Anti-platelet therapy and certain protection methods are particularly important to avoid ischemic complications. It is also important to take measures for an adequate treatment strategy, to have high quality skill and to be capable of rapid trouble shooting for any unexpected accidents.

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Experience with dissection of the cavernous sinus (CS), one of the most complicated structures in the brain, is essential for understanding its anatomy and training in CS-related skull base surgery, but only a limited number of neurosurgical residents have the opportunity of cadaver dissection. A three-dimensional (3D) skull model is proposed for such surgical training which incorporates artificial dura mater, the CS, and the cranial nerves. The 3D skull model was produced by a selective laser sintering method. The CS and double-layer dura mater were modeled with silicone, cranial nerves with rubber fibers or sponge, and the internal carotid artery with vinyl tube. The model could be dissected, and the anterior clinoidectomy and peeling of the meningeal dura (dura propria) from the lateral wall of the CS were performed in almost the same way as in actual surgery. The process of making the skull model with CS-related structures and observation of the dissected CS model facilitate further understanding of the stereoscopic anatomy of the CS.

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Isolated congenital cervical block vertebrae, known as the Type 2 Klippel-Feil syndrome, is rarely presented with symptoms of spondylotic myelopathy. Here, we report on 5 patients who developed spondylotic myelopathy. Not only the adjacent nonfused segments but also the other nonfused segments may became hypermobile and subject to significantly increased stress. For multilevel spondylosis, laminoplasty is effective treatment. This has the advantage of both decompression and the preservation of some cervical movement.

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