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Purpose Antiplatelet drugs are essential in patients with cardiovascular disease who undergo stent placement. We hypothesized that risks of mortality would differ according to adherence to antiplatelet agents, number of antiplatelet agents, and antiplatelet regimens in patients undergoing stent placement or angioplasty. Materials and methods Between 2002 and 2013, we initially enrolled 8671 subjects who underwent stent placement or angioplasty in the National Health Insurance Service-National Sample Cohort in Korea. Using the International Classification of Diseases, 10th revision, the incidence of all-cause death, including cardiovascular disease, cerebrovascular disease, and cancer, was defined. Using a nested case-control study design, controls were matched to cases at a ratio of 4:1, and a total of 5415 subjects were eligible for this study. Results During a median follow-up period of 3.51 years, the incidence rate of all-cause death was 40 per 1000 person-years. We found that adherence to antiplatelet monotherapy significantly decreased risk of death by cerebro-cardiovascular disease, compared with discontinuation of antiplatelets [adjusted odds ratio (OR) 0.62, 95% confidence interval (CI) (0.41-0.96)]. Compared with dual antiplatelet therapy (DAPT), aspirin and clopidogrel monotherapy significantly reduced death by cerebro-cardiovascular disease [adjusted OR 0.65, 95% CI (0.44-0.95) and adjusted OR 0.58, 95% CI (0.35-0.96), respectively]. There was no significant difference of mortality between aspirin monotherapy and clopidogrel monotherapy. Conclusion Our study demonstrated that adherence to antiplatelet therapy and antiplatelet monotherapy, compared with DAPT, in patients with stent placement or angioplasty may have a beneficial effect on mortality in cerebro-cardiovascular disease.

Purpose Cerebral ischemic lesions are frequently observed after carotid artery stenting (CAS), and anti-platelet agents are used to prevent stent thrombosis and peri-procedural complications. However, despite the premedication, cerebral ischemic lesions are observed, suggesting that they may rather be related to anti-platelet resistance. We, therefore, investigated the effects of anti-platelet resistance on the development of cerebral ischemic lesions after CAS. Materials and methods We retrospectively reviewed patients who received CAS and selected patients for whom brain MRI was performed within 24 hours after CAS and for whom anti-platelet resistance was checked. Anti-platelet resistance was examined by the VerifyNow system. We analyzed the correlation between anti-platelet resistance and cerebral ischemic lesions detected on follow-up MRI. Results Among 76 patients, 45 (59.2%) developed new ischemic lesions after CAS. Twelve (15.8%) patients showed aspirin resistance and 50 (65.8%) patients showed clopidogrel resistance. Patients with a new ischemic lesion demonstrated a significantly greater frequency of clopidogrel resistance than those who had no new ischemic lesion (82.2% versus 41.9%, p=0.001). The frequency of aspirin resistance was not significantly different between the groups of patients with and without new ischemic lesions (20.0% versus 9.7%, p=0.340). In multivariate analysis, clopidogrel resistance was a significant risk factor for post-procedural cerebral ischemia. Conclusion Anti-platelet resistance can be used to predict new ischemic lesions after CAS. Anti-platelet resistance should be evaluated in all patients prior to CAS to prevent ischemic complications related to CAS.

Purpose Abnormalities in hemostasis and coagulation have been suggested in chronic renal failure (CRF). In this study, we compared processes of thrombus formation between rats with CRF and those with normal kidney function. Materials and methods CRF was induced by 5/6 ablation/infarction of the kidneys in Sprague-Dawley rats, and surviving rats after 4 weeks were used. Ferric chloride (FeCl₃)-induced thrombosis in the carotid artery was induced to assess thrombus formation. Whole blood clot formation was evaluated using rotational thromboelastometry (ROTEM). Platelet aggregation was assessed with impedance platelet aggregometry. Results FeCl₃-induced thrombus formation was initiated faster in the CRF group than in the control group (13.2±1.1 sec vs. 17.8±1.0 sec, p=0.027). On histological examination, the maximal diameters of thrombi were larger in the CRF group than in the control group (394.2±201.1 μm vs. 114.0±145.1 μm, p=0.039). In extrinsic pathway ROTEM, the CRF group showed faster clot initiation (clotting time, 59.0±7.3 sec vs. 72.8±5.0 sec, p=0.032) and increased clot growth kinetics (α angle, 84.8±0.2° vs. 82.0±0.6°, p=0.008), compared to the control group. Maximal platelet aggregation rate was higher in the CRF group than in the control group (58.2±0.2% vs. 44.6±1.2%, p=0.006). Conclusion Our study demonstrated that thrombogenicity is increased in rats with CRF. An activated extrinsic coagulation pathway may play an important role in increasing thrombogenicity in CRF.

We report herein a case of hyperacute onset of spontaneous cervical spinal subdural hematoma treated with methylprednisolone pulse therapy that showed good results. A 57-year-old man was admitted for posterior neck pain and paraparesis which occurred an hour ago. MRI revealed a ventral subdural hematoma distributed from the level of C1 down to T3, compressing the spinal cord. Conservative management with methylprednisolone pulse therapy was administered considering the patient's poor general condition. Although emergent surgical decompression is necessary in most cases of spinal subdural hematoma, conservative management with steroid therapy could be effective.

Rapid arterial rethrombosis is associated with high-grade residual stenosis and usually occurs at the site of the initial occlusion, resulting in reocclusion of the recanalized artery. Platelets may play an active role in such rethrombosis after thrombolytic-induced clot lysis. Given that glycoprotein IIb/IIIa receptor blockers, like tirofiban, prevent thrombus formation by inhibiting the final common pathway of platelet aggregation, they may be helpful for treating rethrombosis after thrombolysis. A 64-year-old man presented with an acute ischemic stroke due to internal carotid artery (ICA) occlusion. The ICA was recanalized by intravenous thrombolysis but reoccluded shortly after recanalization. The reoccluded ICA was successfully recanalized using intra-arterial tirofiban. A carotid stent was subsequently inserted to relieve severe stenosis and to prevent recurrent stroke. Here, we report a case of rescue treatment of a successfully recanalized ICA by intra- arterial tirofiban. We suggest that rescue use of intra-arterial tirofiban may be effective and safe, especially in hemorrhage prone situations, due to the relatively lower dose of tirofiban compared with intravenous doses.

This study was carried out to assess the effects of intracavitary injection of urokinase in the early liver abscess (ELA) of the rabbits. ELAs were induced on 25 in 47 New Zealand rabbits, which were divided into two groups, with 15 in group A, and 10 in group B. Urokinase was injected into the ELA of group A, and normal physiologic saline into those of group B. One and a half hours after the injections, the rabbits were sacrificed and evaluated by pathologists for the degree of fibrosis of the ELA wall, and fibrinolysis in the ELA itself. Statistical analyses were performed between the two groups. The following ELA sizes for each group were obtained: Group A, 4.3 x 2.9-10.1 x 7.2 mm (mean 7.1 x 4.1 mm); Group B, 4.6 x 2.7-15.0 x 9.7 mm (mean 8.5 x 4.57 mm). Eleven (73%) in group A showed grade II fibrosis of ELA wall, and 8 (80%) in group B showed grade III fibrosis of ELA wall (p=0.002). On pathological analysis, 5 (46%) in group A showed grade II fibrin, and 8 (80%) in group B showed grade III fibrin, of the ELA (p=0.09). In conclusion, injection of urokinase, into the ELAs, can reduce the degree of fibrosis of abscess walls.

Claude's syndrome is a distinctive brainstem syndrome characterized by ipsilateral third cranial nerve palsy with contralateral hemiataxia and is due to an intrinsic or extrinsic lesion in the midbrain. We report a case of Claude's syndrome caused by neurocysticercosis infection. A 68 year-old Asian man was admitted to our hospital because of ataxia, left ptosis, and diplopia. Brain magnetic resonance imaging (MRI) showed a cystic lesion in the midbrain, which was surrounded by ring enhancement and peripheral edema. Neurocysticercosis infection was diagnosed by the cerebral spinal fluid study. The patient was treated with albendazole and steroids. A follow-up brain MRI three months later demonstrated the disappearance of a surrounding brain edema and rim enhancement. The most common cause of Claude's syndrome is cerebrovascular disease and malignancy. However, there is no report caused by neurocysticercosis infection. Therefore, if we encounter Claude's syndrome, we should consider neurocysticercosis infection as one of the etiologic factors.

Purpose Late diagnosis and treatment lead to high mortality and poor prognosis in tuberculous meningitis (TbM). A rapid and accurate diagnosis is necessary for a good prognosis. Neuron-specific enolase (NSE) has been investigated as a biochemical marker of nervous tissue damage. In the present study, the usefulness of NSE was evaluated, and a cut-off value for the differential diagnosis of TbM was proposed. Materials and Methods Patient charts were reviewed for levels of serum and cerebrospinal fluid (CSF) NSE, obtained from a diagnostic CSF study of samples in age- and gender-matched TbM (n=15), aseptic meningitis (n=28) and control (n=37) patients. Results CSF/serum NSE ratio was higher in the TbM group than those of the control and aseptic groups (p=0.001). In binary logistic regression, CSF white blood cell count and CSF/serum NSE ratio were significant factors for diagnosis of TbM. When the cut-off value of the CSF/serum NSE ratio was 1.21, the sensitivity was 86.7% and the specificity was 75.4%. Conclusion The CSF/serum NSE ratio could be a useful parameter for the early diagnosis of TbM. In addition, the authors of the present study suggest a cut-off value of 1.21 for CSF/serum NSE ratio.

Duchenne muscular dystrophy usually affects males. However, females are also affected in rare instances. Approximately 8% of female Duchenne muscular dystrophy (DMD) carriers are manifesting carriers and have muscle weakness to some extent. We investigated the clinical features of 3 female patients with dystrophinopathy diagnosed by clinical, pathological, and genetic studies at our neuromuscular disease clinic. The onset age of manifesting symptoms varied (8-28 years). Muscle weakness grade varied as follows: patient 1 showed asymmetrical bilateral proximal upper and lower extremities weakness, patient 2 showed asymmetrical bilateral upper extremities weakness similar to scapulohumoral muscular dystrophy, and patient 3 had only bilateral asymmetric proximal lower extremities weakness. Two patients had familial histories of DMD (their sons were diagnosed with DMD), but the 1 remaining patient had no familial history of DMD. The serum creatine kinase level was elevated in all patients, but it was not correlated with muscular weakness. An electromyography study showed findings of myopathy in all patients. One patient was diagnosed with a DMD carrier by a muscle biopsy with an immunohistochemical stain (dystrophin). The remaining 2 patients with familial history of DMD were diagnosed by multiplex ligation-dependent probe amplification (MLPA). There were inconsistent clinical features in the female carriers. An immunohistochemical analysis of dystrophin could be useful for female carrier patients. Also, multiplex ligation-dependent probe amplification is essential for the diagnosis of a manifesting female carrier DMD in female myopathic patients because conventional multiplex PCR could not detect the duplication and is less accurate compared to MLPA.