Switch to Semont maneuver is no better than repetition of Epley maneuver in treating refractory BPPV.

The objectives of this study is to compare the efficacy between repetition of Epley maneuver and switch to alternate Semont maneuver in treating posterior canal benign paroxysmal positional vertigo (PC-BPPV) that does not respond to the initial Epley maneuver. In the nationwide, seven dizziness clinics of Korea, 506 consecutive patients (303 women, age range 22-87, mean age ± SD = 64 ± 12, median = 61) with idiopathic PC-BPPV were initially treated with a single Epley maneuver. Of those, 144 (28.5%) patients, who did not respond to the therapy, were randomized to the repetition of Epley maneuver (n = 70) or switch to Semont maneuver (n = 74). The therapeutic efficacy was determined within 1 h by a blinded examiner after the trial of each second maneuver. The efficacy did not differ between the repetition of Epley maneuver and switch to Semont maneuver groups (38.6 vs. 27.0%, p = 0.14, Chi-square test). However, the patients with a long duration (p < 0.001, linear regression) and latency (p = 0.01) of the positional nystagmus during Dix-Hallpike maneuver showed a higher rate of the initial and second treatment failures. Either Epley or Semont maneuver may be applied as a second treatment to the patients with PC-BPPV refractory to the initial Epley maneuver. This study provides Class I evidence that repeated Epley and switch to Semont maneuver shows a similar efficacy in treating PC-BPPV that does not respond to the initial Epley maneuver. CLINICAL TRIAL REGISTRATION: NCT01822002.

Stroke awareness in Korean high school students.

Public awareness is essential for the early diagnosis, treatment, and prevention of stroke. In particular, young adults represent an important avenue for increasing awareness and precluding the adoption of unhealthy, risk-increasing behaviors. This study was the first to investigate the basic knowledge of Korean adolescents about stroke and evaluate the improvement of this knowledge after an educational lecture. In total, 1269 high school students were instructed on the risk factors, symptoms, diagnosis, and management of stroke. Knowledge was evaluated before education (Pre-E), immediately after the lecture (Post-E1), and during a 2-week follow-up (Post-E2), using a questionnaire. Overall, we found that students' knowledge increased after the educational session. On the questionnaire section pertaining to stroke risk factors, out of nine possible points, the mean scores were 3.97, 5.28, and 5.10, on the Pre-E, Post-E1, and Post-E2 tests, respectively, indicating a significant improvement (p < 0.001). Additionally, students who reported that they paid attention during the lecture performed better, and scored 4.29, 6.32, and 6.40, on the Pre-E, Post-E1, and Post-E2 tests, respectively, again indicating a significant improvement (p < 0.001). Our findings indicate that incorporating a stroke education program into school curriculums will enhance the knowledge of Korean adolescents. Implementing this type of program is critical as it may reduce behavior associated with increased stroke risk, and more effort is needed to develop educational methods for engaging students and increasing their concentration during these programs.

[Development of guide to clinical performance and basic clinical skills for medical students].

The aim of this report was to discuss the development and content of a guide on clinical performance and basic clinical skills for medical students. We published the first edition of this guide in 2010 and will publish the second edition in 2016. Initially, we took a survey on important clinical presentations and fundamental clinical and technical skills in 41 medical schools in Korea. Ultimately, we chose 80 core clinical presentations and 56 clinical skills. In the guide to basic clinical skills, we described the physical examination and technical skills according to the preprocedural preparation, procedure, and postprocedural process. In the guide on clinical performance, we reviewed patient encounters-from history taking and the physical examination to patient education. We included communication skills, principles of patient safety, and clinical reasoning schemes into the guides. In total, 43 academic faculty members helped develop the basic clinical skills guide, 75 participated in establishing the clinical performance guide, and 16 advisors from 14 medical specialty societies contributed to the guide. These guides can help medical students approach patients holistically and safely.

Aristolochic Acid I induces ovarian toxicity by inhibition of akt phosphorylation.

Aristolochic acids are natural products found in Chinese herbs of the Aristolochiaceae family. Aristolochic acid I (AAI) is a potent carcinogen and was found to be toxic in animal and clinical studies. Apoptosis is a rapid, selective process of physiological cell deletion that regulates the balance between cell proliferation and cell death and is induced by various kinds of damage. However, the toxicity of AAI during ovarian maturation in the mouse is unclear and is the subject of the present investigation. We used Chinese hamster ovary-K1 (CHO-K1) cells and an AAI injection mouse model: MTT assay was used to assess AA toxicity to cells; ovary size and weight were measured to determine the toxicity of AA to mouse ovary; western blot was used to assess apoptosis; TUNEL assay was used to evaluate apoptotic cell death; and immunohistochemistry was used to examine the local expression of apoptotic proteins in ovary tissue. We found that AAI significantly inhibits the viability of CHO-K1 cells and strongly induces apoptotic cell death in CHO-K1 cells and in mouse ovary. In addition, we observed that AAI markedly increases the expression of pro-apoptotic proteins, including Bax, caspase-3, caspase-9, and poly(ADP) ribose polymerase (PARP). In contrast, anti-apoptotic proteins, such as Bcl-2 and survivin, were decreased by AAI treatment. Furthermore, we observed that ovary size and weight were significantly reduced and that the number of ovulated oocytes was markedly suppressed in AAI-treated mice. These results suggest that AAI strongly induces toxic damage during ovarian maturation by inhibiting Akt phosphorylation-mediated suppression of apoptosis.

Tooth loss may predict poor cognitive function in community-dwelling adults without dementia or stroke: the PRESENT project.

Periodontal disease is a potential predictor of stroke and cognitive impairment. However, this association is unclear in adults aged 50 yr and above without a history of stroke or dementia. We evaluated the association between the number of teeth lost, indicating periodontal disease, and cognitive impairment in community-dwelling adults without any history of dementia or stroke. Dental examinations were performed on 438 adults older than 50 yr (315 females, mean age 63±7.8 yr; 123 males, mean age 61.5±8.5 yr) between January 2009 and December 2010. In the unadjusted analysis, odds ratios (OR) of cognitive impairment based on MMSE score were 2.46 (95% CI, 1.38-4.39) and 2.7 (95% CI, 1.57-4.64) for subjects who had lost 6-10 teeth and those who had lost more than 10 teeth, respectively, when compared with subjects who had lost 0-5 teeth. After adjusting for age, education level, hypertension, diabetes, hyperlipidemia, and smoking, the relationship remained significant (OR, 2.0; 95% CI, 1.08-3.69, P=0.027 for those with 6-10 teeth lost; OR, 2.26; 95% CI, 1.27-4.02, P=0.006 for those with more than 10 teeth lost). The number of teeth lost is correlated with cognitive impairment among community-dwelling adults aged 50 and above without any medical history of stroke or dementia.

Serum YKL-40 levels correlate with infarct volume, stroke severity, and functional outcome in acute ischemic stroke patients.

BACKGROUND AND PURPOSE: YKL-40 is associated with various neurological disorders. However, circulatory YKL-40 levels early after onset of acute ischemic stroke (AIS) have not been systematically assessed. We aimed to identify the temporal changes and clinical usefulness of measuring serum YKL-40 immediately following AIS. METHODS: Serum YKL-40 and C-reactive protein (CRP) levels were monitored over time in AIS patients (n = 105) and compared with those of stroke-free controls (n = 34). Infarct volume and stroke severity (National Institutes of Health Stroke Scale; NIHSS) were measured within 48 hours of symptom onset, and functional outcome (modified Rankin Scale; mRS) was measured 3 months after AIS. RESULTS: Within 12 hours of symptom onset, levels of YKL-40 (251 vs. 41 ng/mL) and CRP (1.50 vs. 0.96 µg/mL) were elevated in AIS patients compared to controls. The power of YKL-40 for discriminating AIS patients from controls was superior to that of CRP (area under the curve 0.84 vs. 0.64) and YKL-40 (r = 0.26, P<0.001) but not CRP levels were correlated with mRS. On day 2 of admission (D2), YKL-40 levels correlated with infarct volume and NIHSS. High YKL-40 levels predicted poor functional outcome (odds ratio 5.73, P = 0.03). YKL-40 levels peaked on D2 and declined on D3, whereas CRP levels were highest on D3. CONCLUSIONS: Our results demonstrate serial changes in serum YKL-40 levels immediately following AIS and provide the first evidence that it is a valid indicator of AIS extent and an early predictor of functional outcome.

Multifocal strokes as the initial manifestation of metastatic tumors.

Patients with cancer are hypercoagulable and at a significant risk for ischemic stroke, but rarely present with stroke as the first manifestation of an underlying malignancy. We report on 2 patients with bihemispheric, multiterritorial infarctions in the absence of a cardioembolic source.

Medial vestibulospinal tract lesions impair sacculo-collic reflexes.

The medial vestibulospinal tract (VST) is known to mediate the vestibular-evoked myogenic potential (VEMP) in the contracting sternocleidomastoid muscle (SCM). To determine whether disruption of the medial VST in the medulla impairs formation of VEMP, we measured VEMP in 14 patients with medial medullary infarction (MMI). VEMP was induced by a short tone burst and was recorded in contracting SCM while patients turned their heads forcefully to the contralateral side against resistance. Normative data were obtained from 47 healthy volunteers. Seven patients (50%) had abnormal VEMP in the side of the MMI lesion, absent in two, decreased in four, and delayed in two. One patient showed both decreased and delayed response. Of the seven patients with abnormal VEMP, five had the lesions that extended to the dorsal tegmentum while five of the seven patients with normal VEMP showed restricted anteromedial lesions mainly involving the pyramids. Spontaneous nystagmus (4/7, 57%), gaze-evoked nystagmus (6/7, 86%), and ocular tilt reaction/tilt of the subjective visual vertical (4/7, 57%) were frequently observed in the patients with abnormal VEMP. The abnormal VEMP in patients with infarctions involving the medullary tegmentum supports that VEMP is mediated by the medial VST descending within the medial longitudinal fasciculus.

Abnormal vestibular evoked myogenic potentials in medial medullary infarction.

BACKGROUND: The medial vestibulospinal tract (MVST), which descends in the medial longitudinal fasciculus (MLF), may mediate the vestibular evoked myogenic potentials (VEMPs) in the contracting sternocleidomastoid muscle. We report herein abnormal VEMPs in a patient with medial medullary infarction (MMI) that appeared to involve the MLF. CASE REPORT: A patient with infarction involving the right medial medulla showed decreased p13-n23 amplitude and increased p13/n23 latencies of the VEMPs on the right side. These abnormal VEMPs recorded in an MMI patient support the theory that VEMPs are mediated by the MVST contained within the MLF. CONCLUSIONS: VEMPs may represent a valuable tool for investigating vestibular dysfunction originating from the saccule, even in patients with central vestibulopathies, which is not readily defined by conventional vestibular function tests.

Endothelial function in lacunar infarction: a comparison of lacunar infarction, cerebral atherosclerosis and control group.

BACKGROUND: There are conflicting evidences on endothelial function in lacunar infarction. This may be attributed to the effects of risk factors on the vascular smooth muscle. To test endothelial function only in patients with lacunar infarction, we evaluated the endothelium-dependent and -independent vasodilatation of the brachial artery. METHODS: We enrolled consecutive patients with lacunar infarction defined by clinical characteristics and MRI findings. The control group included age- and sex-matched patients with hypertension who do not have any history of clinical stroke, coronary artery disease or peripheral vascular disease. Endothelial function was evaluated using flow-mediated dilatation (FMD) and nitrogen-mediated dilatation (NMD) of the brachial artery. FMD and NMD were examined by an experienced vascular sonographer using a high-resolution ultrasound. Intracranial stenosis was defined as flow gap or >50% reduction in vessel diameter on MRA. RESULTS: FMD was 6.6 +/- 4.5% in the lacunar infarction group and 12.2 +/- 4.6% in the control group (p = 0.000). NMD was 14.3 +/- 4.9% in the lacunar infarction group and 13.8 +/- 4.9% in the control group (p = 0.37). FMD in patients with lacunar infarction and intracranial arterial stenosis was 6.4 +/- 3.9%, and FMD in patients with lacunar infarction was only 6.9 +/- 5.5%. In the control group, it was 12.2 +/- 4.6%. CONCLUSION: FMD was low in patients with lacunar infarction. NMD was similar between the lacunar infarction group and the control group. These results are suggestive of pure endothelial dysfunction in lacunar infarction. Endothelial dysfunction was as severe in lacunar infarction as in intracranial arterial stenosis.

Isolated nodular infarction.

BACKGROUND AND PURPOSE: Isolated nodular infarction has rarely been described in human. The purpose of this study is to report clinical and laboratory findings of isolated nodular infarction. METHODS: Eight patients with isolated nodular infarction were recruited from 6 hospitals in Korea. All patients underwent a complete and standardized neurotological evaluation including ocular torsion, bithermal caloric tests, and rotatory chair test in addition to MRI and MR angiography. RESULTS: All patients presented with isolated vertigo and moderate to severe imbalance. The most common manifestation was unilateral nystagmus and falling in the opposite direction, which mimicked peripheral vestibulopathy. Six patients had unilateral lesion, and 2 showed bilateral lesions. The direction of the spontaneous nystagmus was all ipsilesional in the unilateral lesion. However, head impulse and bithermal caloric tests were normal. Other findings include periodic alternating nystagmus, perverted head shaking nystagmus, paroxysmal positional nystagmus, and impaired tilt suppression of the postrotatory nystagmus. Hypoplasia of the ipsilesional vertebral artery was the only abnormal finding on MR angiography in 3 patients. The prognosis was excellent. CONCLUSIONS: Isolated nodular infarction mostly presents with isolated vertigo mimicking acute peripheral vestibulopathy. However, severe imbalance and a negative head impulse test are important clinical discriminants between nodular infarcts and peripheral vestibular dysfunction. The findings of isolated nodular infarctions are consistent with impaired gravito-inertial processing of the vestibular signals and disrupted nodular inhibition on the vestibular secondary neurons and the velocity storage mechanism.

Correlation between insulin resistance and intracranial atherosclerosis in patients with ischemic stroke without diabetes.

BACKGROUND: Insulin resistance (IR) is associated with an increased risk for cardiovascular morbidity and mortality including ischemic stroke. Its final complications are cardiovascular and cerebrovascular disease caused by atherosclerosis. However, few studies on the relationship between IR and intracranial (IC) atherosclerosis have been reported. METHODS: We analyzed 110 patients with acute stroke without diabetes who underwent brain magnetic resonance angiography and cerebral angiography. Patients were divided into 3 equal groups according to the tertiles of homeostasis model assessment of IR (HOMA-IR): group I (n = 36; HOMA-IR < 0.92), group II (n = 37; 0.92 or= 1.55). Cerebral artery atherosclerosis was classified as either IC or extracranial (EC). RESULTS: Patients with IC or EC atherosclerosis showed higher level of HOMA-IR than those without. When the association was assessed according to the site of atherosclerosis, HOMA-IR showed a significant association with the site of atherosclerosis (IC + EC > IC > EC, P < .01). Multivariate analysis revealed that HOMA-IR was an independent predictor of IC atherosclerosis. CONCLUSIONS: Although the association between IR and stroke patterns in patients with atherosclerosis remains uncertain, IR is associated with IC atherosclerosis in patients with acute ischemic stroke without diabetes.