ObjectivesThe correlation of optic nerve sheath diameter (ONSD) as seen on ultrasonography (US) and directly measured intracranial pressure (ICP) has been well described. Nevertheless, differences in ethnicity and type of ICP monitor used are obstacles to the interpretation. Therefore, we investigated the direct correlation between ONSD and ventricular ICP and defined an optimal cut-off point for identifying increased ICP (IICP) in Korean adults with brain lesions.MethodsThis prospective study included patients who required an external ventricular drainage (EVD) catheter for ICP control. IICP was defined as an opening pressure over 20 mmHg. ONSD was measured using a 13 MHz US probe before the procedure. Linear regression analysis and receiver operator characteristic (ROC) curve were used to assess the association between ONSD and ICP. Optimal cut-off value for identifying IICP was defined.ResultsA total of 62 patients who underwent ONSD measurement with simultaneous EVD catheter placement were enrolled in this study. Thirty-two patients (51.6%) were found to have IICP. ONSD in patients with IICP (5.80 ± 0.45 mm) was significantly higher than in those without IICP (5.30 ± 0.61 mm) (P < 0.01). The IICP group showed more significant linear correlation with ONSD (r = 0.57, P < 0.01) compared to the non-IICP group (r = 0.42, P = 0.02). ONSD > 5.6 mm disclosed a sensitivity of 93.75% and a specificity of 86.67% for identifying IICP.ConclusionONSD as seen on bedside US correlated well with directly measured ICP in Korean adults with brain lesions. The optimal cut-off point of ONSD for detecting IICP was 5.6 mm.
Genome-wide association studies found genetic variations with modulatory effects for intracranial aneurysm (IA) formations in European and Japanese populations. We aimed to identify the susceptibility of single nucleotide polymorphisms (SNPs) to IA in a Korean population consisting of 250 patients, and 294 controls using the Asian-specific Axiom Precision Medicine Research Array. Twenty-nine SNPs reached a genome-wide significance threshold (5 × 10−8). The rs371331393 SNP, with a stop-gain function of ARHGAP32 (11q24.3), showed the most significant association with the risk of IA (OR = 43.57, 95% CI: 21.84–86.95; p = 9.3 × 10−27). Eight out of 29 SNPs—GBA (rs75822236), TCF24 (rs112859779), OLFML2A (rs79134766), ARHGAP32 (rs371331393), CD163L1 (rs138525217), CUL4A (rs74115822), LOC102724084 (rs75861150), and LRRC3 (rs116969723)—demonstrated sufficient statistical power greater than or equal to 0.8. Two previously reported SNPs, rs700651 (BOLL, 2q33.1) and rs6841581 (EDNRA, 4q31.22), were validated in our GWAS (Genome-wide association study). In a subsequent analysis, three SNPs showed a significant difference in expressions: the rs6741819 (RNF144A, 2p25.1) was down-regulated in the adrenal gland tissue (p = 1.5 × 10−6), the rs1052270 (TMOD1. 9q22.33) was up-regulated in the testis tissue (p = 8.6 × 10−10), and rs6841581 (EDNRA, 4q31.22) was up-regulated in both the esophagus (p = 5.2 × 10−12) and skin tissues (1.2 × 10−6). Our GWAS showed novel candidate genes with Korean-specific variations in IA formations. Large population based studies are thus warranted.
ObjectivePosture induced common peroneal nerve (CPN) palsy is usually produced during the prolonged squatting or habitual leg crossing while seated, especially in Asian culture and is manifested by the onset of foot drop. Because of its similarity to discogenic foot drop, patients may be diagnosed with a lumbar disc disorder, and in some patients, surgeons may perform unnecessary examinations and even spine surgery. The purpose of our study is to establish the clinical characteristics and diagnostic assessment of posture induced CPN palsy.MethodsFrom June 2008 to June 2012, a retrospective study was performed on 26 patients diagnosed with peroneal nerve palsy in neurophysiologic study among patients experiencing foot drop after maintaining a certain posture for a long time.ResultsThe inducing postures were squatting (14 patients), sitting cross-legged (6 patients), lying down (4 patients), walking and driving. The mean prolonged neural injury time was 124.2 minutes. The most common clinical presentation was foot drop and the most affected sensory area was dorsum of the foot with tingling sensation (14 patients), numbness (8 patients), and burning sensation (4 patients). The clinical improvement began after a mean 6 weeks, which is not related to neural injury times. Electrophysiology evaluation was performed after 2 weeks later and showed delayed CPN nerve conduction study (NCS) in 24 patients and deep peroneal nerve in 2 patients.ConclusionWe suggest that an awareness of these clinical characteristics and diagnostic assessment methods may help clinicians make a diagnosis of posture induced CPN palsy and preclude unnecessary studies or inappropriate treatment in foot drop patients.
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