Prevalence rates of antiphospholipid antibodies in ischemic stroke patients.
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Biomedical subjects
Publications and source records attributed to Yasuhisa Kitagawa.
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According to an epidemiological study in Japan, there are as many as 22 million patients with tension headache and 8.4 million with migraine. Furthermore, patients suffering from both types of headache concurrently are estimated to account for more than 50% of headache patients. We studied the efficacy of drug therapy for migraine accompanied by tension headache-like symptoms, focusing principally on neck stiffness. We evaluated the efficacy of rizatriptan by comparison of findings before and after therapy in 34 migraine patients, consisting of 16 without neck stiffness (migraine without neck factor: WONF) and 18 with it (migraine with neck factor: WNF), who received treatment at our neurology/internal medicine department from 1 March 2004 to 31 May 2005. In the study, all the patients were asked to keep a record of their migraine status. The severity of migraine was classified by physicians according to the International Headache Society diagnostic criteria, based on which drug efficacy was evaluated. We selected rizatriptan for migraine treatment in our study based on Dr. Ferrari's report. In the efficacy study of rizatriptan, in the group of 34 migraine patients, the pain relief rate (79.4%) and pain-free rate (41.2%) at two hours after treatment were as high as those reported in the meta-analysis performed by Ferrari et al., indicating high efficacy of rizatriptan. In the efficacy comparison between the WONF and WNF groups, the painfree rates were 56.3% and 27.8%, and cumulative pain relief rates were 100% and 61.1%, respectively, with better results in the WONF group. A test result was also significantly better (p=0.0076) in the WONF group. Rizatriptan was proved effective in treating migraine patients accompanied by tension headache-like symptoms. Comparison of efficacy rates between patient groups with and without tension headache-like symptoms showed that the pain relief rate in the group without neck stiffness was higher.
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OBJECTIVE: We examined the effects of drug therapy with pravastatin (P) or bezafibrate (B) and diet (D) therapy on serum lipids and soluble intercellular adhesion molecule-1 (sICAM-1) in hyperlipidemic cerebrovascular disease (CVD) patients in the chronic stage. METHODS: This study included 36 patients (28 with cerebral infarction and hyperlipidemia and eight with cerebral hemorrhage and hyperlipidemia) divided into three groups: Group P (12 patients), Group B (10 patients), and Group D (14 patients). Before and after treatment, total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) and sICAM-1 levels were measured. RESULTS: In Group P, Group B and Group D, TC levels were decreased by 30% (p < 0.005), 21% (p < 0.01), and 21% (p < 0.001), LDL-C levels were decreased by 38% (p < 0.005), 18% (not significant), and 25% (p < 0.005) and TG levels were decreased by 27% (p < 0.05), 53% (p < 0.005) and 22% (p < 0.05), respectively. sICAM-1 levels were decreased by 20% (p < 0.005) in Group P, but were not decreased in Group B or Group D. There was no correlation between deltaTC and delta sICAM-1 (r = 0.172). CONCLUSION: Administration of pravastatin significantly reduced sICAM-1 levels, independently of its decreasing effect on TC and TG in chronic CVD patients. Pravastatin may exert anti-atherosclerotic activity via two distinct mechanisms.
We discuss here the epidemiology of chronic headache. Headache is a widespread and costly public health problem. Few people do not experience headache: in men, the lifetime prevalence for headache of any kind is 93 %, and for women it is up to 99%. Approximately 8.4 million people in Japan suffer from migraine, and 22 million have tension-type headache. Despite the painful, costly, and disabling impact of headache, many patients with headache do not seek medical advice. It is important to recognize the incidence of various kinds of chronic headache, and to diagnose and treat them correctly. In this article, we review the incidence, precipitating factors, regional prevalence, and age dependence of the incidence of each type of chronic headache.
Oxidized low-density lipoprotein cholesterol (Ox-LDL) is considered to play a critical role in the pathogenesis of atherosclerosis. We investigated the role of malondialdehyde-modified LDL (MDA-LDL), an indicator of Ox-LDL, in cerebral infarction. We also investigated the relationship between MDA-LDL and atherosclerotic change of the carotid artery. Subjects were 30 patients with lacunar infarction (LA), 19 patients with atherothrombotic infarction (AT) and 48 controls. Carotid arteries were evaluated with B-mode Doppler ultrasonography. The intima-media thickness (IMT) was considered to be increased if its value was more than 1.1 mm. The level of MDA-LDL concentration was significantly (P < 0.05) elevated in AT patients (129.96 +/- 27.88 U/I) than in LA patients (99.35 +/- 34.06 U/l) and controls (97.65 +/- 32.61 U/l). Among AT patients, plasma level of MDA-LDL concentration was statistically significantly elevated in the group with increased IMT (139.7 +/- 24.5 U/l) than in the group without increased IMT (102.7 +/- 17.2 U/l). No statistically significant difference was found among LA patients. However, there was no difference in LDL-C concentration between the patients with and without IMT thickening among LA or AT patients. The concentration of MDA-LDL was significantly decreased (P < 0.05) after statin administration for 5-6 months. MDA-LDL, namely degraded or qualitatively changed LDL-C, appears to be related to atherosclerotic change of the carotid artery in AT patients.
Antiphospholipid syndrome is characterized by arterial or venous thrombosis, and the presence of antiphospholipid antibodies (aPL). APL are considered to be a cause of an acquired hypercoagulable state leading to stroke and transient ischemic attack (TIA). We examined the causes in 50 young patients with ischemic stroke. The most prevalent cause was atherosclerosis and the incidence of APS was 12.5%. APL comprise a heterogeneous group of autoantibodies, such as beta2-glycoprotein I dependent anticardiolipin antibody (beta2-GPIaCL), lupus anticoagulant (LA), and other antiphospholid-protein antibodies. We examined the incidence and the pathogenic role of antiphospholipid protein antibodies. The subjects comprised 250 patients (155 male, 95 females) with ischemic stroke, aged 26 to 92 years (mean 72 years). We measured beta2-GPI aCL, IgG aCL, LA, phosphatidyserine dependent antiprothrtombin antibody (PS-PT), antiphosphatidyl-serine antibody (PS), antiphosphatidyl-inositol antibody (PI) in each patient. The incidence of beta2-GPI aCL, IgG aCL, LA, phosphatidyserine, PS-PT, PS, and PI was 2.8%, 12%, 9.2%, 7.2%, 9.6%, and 8.8%, respectively. The incidence of young stroke patients under 50 years was 5.2%. Among 13 young stroke patients, 5 had SLE. Among 23 patients with LA., 18 (78%) patients had PS-PT. Anti-PS-PT antibody is closely related to LA. Antinuclear antibody was detected in 79% of the patients with aPS and/or aPI. We compared the carotid ultrasonographic findings in positive aPI or aPS patients with those in negative ones. Increased IMT, plaque score and carotid stenosis were more common in aPI and aPS-positive patients than in negative ones Three of 5 patients who showed positive beta2-GPI, aCL and LA, simulataneously, had sysyemic lupus erythematosus as an immulological background. Two of 3 patients with PI and/or PS and beta2-GPI and/or LA were patients with SLE. Antiphospholipid antibody was considered to be a risk factor of stroke, especially in SLE and/or young female patients. The incidence of lupus anticoagulant is more common than beta2-GPI aCL in ischemic stroke. In SLE patients with stroke, multi-antiphospholipid-protein antibodies was inclined to be present. LA is closely related to ant-PS-PT and aPI and aPS are associated with anti-nuclear antibody and precipitation of atherosclerosis.
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A 39-year-old man presented with multiple intracranial cavernous malformations manifesting as intractable seizures persisting for more than 20 years. He underwent gamma knife radiosurgery (GKRS) for right frontal and left temporal cavernous malformations. He began to suffer from progressive left hemiparesis and inattention 2 years 5 months after the GKRS. Magnetic resonance imaging showed abnormal ring enhancement and extensive brain edema around the right frontal lesion. Conservative therapies such as external decompression, low-dose barbiturates, and mild hypothermia had no effect on his clinical status. Stereotactic biopsy of the ring-enhanced area demonstrated gliosis. Signs of cerebral herniation appeared, so we performed partial resection of the right frontal lobe. His symptoms recovered immediately. Subsequent hyperbaric oxygen (HBO) therapy significantly improved the extensive brain edema. Delayed radiation necrosis associated with potentially fatal brain edema may occur after GKRS for cavernous malformations. Internal decompression and subsequent HBO therapy were very effective for the treatment of these lesions.
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Antiphospholipid syndrome is considered to be a cause of an acquired hypercoagulable state leading to stroke and transient ischemic attack. Antiphospholipid antibodies (aPL) comprise a heterogeneous group of autoantibodies. Among them, lupus anticoagulant (LA) and beta 2-glycoprotein I dependent anticardiolipin antibody (beta 2-GPI aCL) are important and commonly measured. Recently, LA has been considered to be closely related to phosphatidylserine anti-prothrombin antibody. APL is an independent risk factor for first-ever ischemic stroke and a prognostic marker of recurrent stroke. The precipitating factors for the occurrence of stroke are the presence of beta 2-GPI-dependent aCL, a GPL aCL level of more than 40, and the simultaneous presence of lupus anticoagulant. Several mechanisms are believed to be involved in the thrombotic process in patients with antiphospholipid antibodies. Human activated protein C functions as a potent anticoagulant in human plasma by inhibiting the activity of coagulation cofactors Va and VIIIa. Activation of protein C is impaired in patients with aPL. Recently, the presence of aPL has been considered to be contributory factor for the development of atherosclerotic lesions. Transgenic mouse lacking the LDL receptor develop accelerated arteriosclerosis upon immunization with beta 2-GPL Several therapeutic options are available for the prevention of ischemic stroke in patients with aPL, such as antiplatelet, anticoagulant, and immunosuppressive therapy. The rate of recurrence in patients undergoing antiplatelet and anticoagulation combination therapy was found to be lower than that in patients receiving other forms of therapy. The WARSS-APASS collaborative study showed that there was no difference in the recurrence rate between aPL patients receiving antiplatelet or anticoagulation therapy alone. APL has been investigated in other neurological disorders such as multiple sclerosis, chorea, migraine and convulsion. The association of aPL with multiple sclerosis remains debatable. APL could be a contributory factor for the development of convulsion, but not for migraine.