Hakjae Roh

Gender differences in the functional recovery after acute stroke.

Background and Purpose PurposezzInterest in gender differences in the effects of acute stroke is growing worldwide. However, gender differences in functional recovery after acute stroke in the Korean population have yet to be evaluated. The aim of this investigation was to compare long-term functional outcomes between male and female after acute stroke. Methods Patients with acute stroke were enrolled prospectively between January 2005 and January 2009. Baseline characteristics, risk factors, stroke subtypes, time delay from onset to arrival at a hospital, active treatment, and stroke severity were compared between male and female. Differences in mortality and disability at discharge, and at 3 months and 1 year after stroke onset were also investigated. Functional disabilities were categorized into two groups: good outcome (score on modified Rankin scale ≤2) and poor outcome (score on modified Rankin scale >2). Results Among 1,055 patients with acute stroke, 575 were male (aged 64.83±11.98 years, mean±SD) and 480 were female (aged 70.09±13.02 years). There were no gender differences in mortality at 3 months and 1 year after stroke. The frequency of poor outcomes was higher in female patients than in male patients at discharge (39.8% versus 30.9%, respectively; p=0.003), the 3 months follow-up (32.3% versus 20.8%, respectively; p<0.001), and the 1 year follow-up (31.1% versus 18.7%, respectively; p=0.001). After adjusting for multiple confounding factors including age and stroke severity, the female gender persisted as a predictor of poor functional outcome at 3 months and 1 year after stroke. Conclusions Female patients have greater difficulty than male patients in recovering from a disabled state after acute stroke. Future studies should investigate the causes of this gender difference.

Low Glomerular Filtration Rate Increases Hemorrhagic Transformation in Acute Ischemic Stroke

Background: Decreased glomerular filtration rate (GFR) can increase the risk of bleeding tendency and hemorrhagic stroke. However, the relationship between the levels of GFR and hemorrhagic transformation (HT) after acute ischemic stroke is largely unknown. The aim of this study was to assess whether GFR level is associated with HT in acute ischemic stroke. Methods: We reviewed 770 consecutive patients with acute ischemic stroke within 7 days from September 2007 to February 2012 in a prospective stroke registry database. We calculated the patient’s GFR using the Cockcroft-Gault equation, and divided them into 3 groups: ≥60, 30–59 and <30 ml/min/1.73 m2. HTs were identified by follow-up computed tomography (CT) or magnetic resonance imaging, and were defined as (1) any degree of high density within the area of low attenuation of vascular territory on noncontrast brain CT, or (2) low-signal intensity area in gradient echo within high-signal intensity meaning acute infarct on diffusion-weighted imaging. Multivariable logistic regression analyses were used to estimate the risk of GFR for HT. Stratification analyses were done according to the presence of HT high risk factors: atrial fibrillation (AF), thrombolysis and large size infarction. Additional logistic regression model for symptomatic HTs was established with the same variables. Results: HTs were noted in 131 patients (17.0%) and symptomatic HTs in 63 patients (8.2%). In univariate analysis, HTs were more frequent in patients with AF (51.9 vs. 16.7%, p < 0.001) and large-size infarction (42.0 vs. 5.3%, p < 0.001). The risk of HT was associated with decreased GFR among 3 subgroups classified according to the value of estimated GFR: 49/394 (12.4%) in the GFR ≥60 group, 66/312 (21.2%) in the 30≤ GFR <59 group and 16/64 (25.0%) in the GFR <30 group (p = 0.002). We found a significant association between the GFR <30 group and HTs in acute ischemic stroke (OR 2.90; 95% CI 1.26–6.68, p = 0.012) after adjusting for other risk factors. Moreover, the incidence of HTs was higher in the subgroups without thrombolysis (OR 3.49; 95% CI 1.44–8.46) and without AF (OR 3.44; 95% CI 1.10–10.76). Decreased GFR also had a tendency of increasing symptomatic HTs (OR 2.39; 95% CI 0.72–7.94, p = 0.154). Conclusions: Low levels of GFR are associated with a high risk of HT after acute ischemic stroke. Further studies are needed to elucidate whether HT in the patients with renal insufficiency are related to a worse outcome after acute ischemic stroke.

Associations of cigarette smoking with intracranial atherosclerosis in the patients with acute ischemic stroke

BACKGROUND Although cigarette smoking has been established as an important risk factor for stroke, the effect on the atherosclerotic stenosis, which are based on observational studies, have been controversial. We set out to examine the differences in the risk factors between smokers and nonsmokers and to investigate the association of cigarette smoking with cerebral arterial stenosis. METHODS A total of 989 consecutive patients with acute noncardioembolic ischemic stroke were prospectively enrolled from June 2004 to January 2010. The risk factor profiles were compared between smokers and nonsmokers. We analyzed the degree of stenosis in all MRA, and evaluated influencing factors in the patients with intracranial atherosclerosis (ICAS) and extracranial atherosclerosis (ECAS) who were randomly matched by age and sex. RESULTS There were differences in the distribution of risk factors between the 467 (70.0%) nonsmokers and the 215 (30.0%) smokers. Nonsmokers were older (71.7±11.0 versus 61.7±12.0, p<0.001) and had a higher frequency of hypertension than smokers had (75.4% versus 64.0%, p=0.002). When smokers and nonsmokers were age- and sex-matched, smoking was more prevalent in patients with ICAS than with ECAS (32.9% versus 28.2%). Conditional regression analysis revealed that smoking and hypertension increased the odds of ICAS [smoking, odds ratio (OR): 1.83, p=0.026; hypertension, OR: 1.84, p=0.01], whereas hyperlipidemia increased the odds of ECAS (OR: 1.87, p=0.034). CONCLUSION The distributions of the major risk factors for ischemic stroke were different between smokers and nonsmokers. Cigarette smoking may be more associated with ICAS than with ECAS after adjusting for potential risk factors.

Implication of Left Ventricular Diastolic Dysfunction in Cryptogenic Ischemic Stroke

Background and Purpose— Left ventricular diastolic dysfunction (LVDD) is a predictor for atrial fibrillation (AF). This study was aimed to investigate whether LVDD in cryptogenic ischemic stroke (CS) could be a clue to stroke mechanism. Methods— The clinical and echocardiographic findings of 1589 consecutive patients with acute ischemic stroke or transient ischemic attack between 2004 and 2013 were reviewed. LVDDs among stroke subtypes were graded by transthoracic echocardiography into 4 groups by severity: normal, abnormal relaxation (grade I), pseudonormal (grade II), and restrictive diastolic filling (grade III), whereas severe LVDD was defined as grade III. We classified the lesion pattern of CS into cardioembolism-mimic or non–cardioembolism-mimic and determined whether cardioembolism-mimic lesions were associated with severe LVDD. Results— The fraction of severe LVDD in CS was not different from that of stroke with AF (27.3% versus 37.1%; P=0.173) but was significantly higher than that of stroke without AF (27.3% versus 13.4%; P=0.008). Cardioembolism-mimic CS had more severe LVDD than non–cardioembolism-mimic CS (41.4% versus 11.5%; P=0.013). LVDD of grade II (odds ratio, 4.37; 95% confidence interval, 2.99–6.41) and grade III (odds ratio, 5.60; 95% confidence interval, 3.42–9.17) were independently related to stroke with AF after adjusting covariates. Conclusions— The severe LVDD could be a predictor of stroke with AF, and its frequency was similar between CS and stroke with AF. Cardioembolism-mimic CS had significantly more severe LVDD than non–cardioembolism-mimic CS. LVDD could be helpful to discriminate the stroke mechanism in the patients with acute CS.

Driving with polyneuropathy

Polyneuropathy may result in pain, numbness, and weakness, which may in turn affect driving ability. Medications used to treat neuropathic pain may alter cognition, which may further affect driving. Although such impairments have engendered questions about the driving safety in this group of patients, the rate of motor vehicle accidents (MVAs) in patients with neuropathy has not been studied rigorously. We surveyed patients with neuropathy from three medical centers for reported accident rate, and we analyzed variables related to increased risk for accidents compared to National Highway Traffic Safety Administration data. Surveys from 260 subjects demonstrated that 40.6% were involved in traffic accidents (0.11 accidents/year). Their accident rate was 10.8 MVAs per million vehicle miles traveled (MVA/MVMT), compared to 3.71 MVA/MVMT in 55–59‐year‐old drivers and 3.72 in 60–64‐year‐olds (National Highway Traffic Safety Administration data). In all, 72.4% cited their neuropathy and 55.2% cited their medications as playing a role in their accidents, and 51.6% changed their driving habits after developing neuropathy. Independently, elevated levels of pain, motor weakness, and ambulation difficulty met statistical significance for increased MVA frequency. We conclude that accident frequency and discomfort with driving are higher in neuropathy patients compared to age‐matched national statistics. However, most patients seem to change habits according to their ability to drive; as such, driving issues should be addressed with caution and on a case‐by‐case basis. Muscle Nerve, 2009

Utility of the cutaneous silent period in patients with diabetes mellitus

We performed this study to evaluate whether or not the cutaneous silent period (CSP) is a useful metric to identify small-fiber neuropathy in diabetic patients. The CSP was measured from the abductor pollicis brevis muscle in 30 healthy controls and 110 diabetic patients, who in turn were divided into 3 subgroups (patients with large-fiber neuropathy, patients with small-fiber neuropathy, and asymptomatic patients). The measured CSP and clinical characteristics were compared among the groups. The power of the CSP in discriminating patients from controls and any correlation with other clinical variables were analyzed. Each patient subgroup had a significantly delayed CSP latency compared to the controls. The latency of patients with large-fiber neuropathy was also significantly prolonged compared to the other subgroups of patients. The CSP latency was the only variable to discriminate patients. The latency showed a significant correlation with the late responses in nerve conduction studies. Thus, the CSP latency may be a useful tool in evaluating small neural fiber function in diabetic patients.

Transient urinary retention in acute right lateral medullary infarction.

Urinary disturbance has rarely been reported in patients with a medullary lesion. We evaluated a patient with acute infarction in the right lateral medulla who had voiding difficulty as an initial manifestation. Urodynamic study showed detrusor areflexia on voiding, and the voiding symptom completely recovered 2 weeks after the stroke onset. The urinary retention in this patient might be caused by interruption of descending fibers from facilitatory pontine tegmentum micturition centers.

Can We Discriminate Stroke Mechanisms by Analyzing the Infarct Patterns in the Striatocapsular Region

Background and Aims: The aims of our study were to elucidate the differences in the distribution of acute middle cerebral artery (MCA) infarctions involving the striatocapsular region and to compare those following embolic striatocapsular infarctions with those originating from MCA disease (MCAD). Methods: We prospectively enrolled patients with acute large infarcts located in the lenticulostriate artery territory. Brain coronal diffusion-weighted imaging (DWI) and magnetic resonance angiography were carried out in all patients. The types of infarct distribution were divided into 3 categories: (1) dominant in the distal territory (DD), (2) distributed equally between the distal and proximal territories (DE) and (3) dominant in the proximal territory. Stroke mechanisms were classified into stroke from proximal embolism, MCAD and stroke of undetermined etiology. Results: A total of 71 patients were recruited. Proximal embolic sources were significantly more prevalent in patients with a DE lesion, but symptomatic MCA stenoses were more common in patients with a DD lesion than in those with a DE lesion. Conclusion: These results suggest that the dominant area of striatocapsular infarctions on coronal DWI can be an important clue for stroke etiology.

Clinical Manifestations in Paroxysmal Kinesigenic Dyskinesia Patients with Proline-Rich Transmembrane Protein 2 Gene Mutation

Background and Purpose Given the diverse phenotypes including combined non-dyskinetic symptoms in patients harboring mutations of the gene encoding proline-rich transmembrane protein 2 (PRRT2), the clinical significance of these mutations in paroxysmal kinesigenic dyskinesia (PKD) is questionable. In this study, we investigated the clinical characteristics of PKD patients with PRRT2 mutations. Methods Familial and sporadic PKD patients were enrolled and PRRT2 gene sequencing was performed. Demographic and clinical data were compared between PKD patients with and without a PRRT2 mutation. Results Among the enrolled PKD patients (8 patients from 5 PKD families and 19 sporadic patients), PRRT2 mutations were detected in 3 PKD families (60%) and 2 sporadic cases (10.5%). All familial patients with a PRRT2 gene mutation had the c.649dupC mutation, which is the most commonly reported mutation. Two uncommon mutations (c.649delC and c.629dupC) were detected only in the sporadic cases. PKD patients with PRRT2 mutation were younger at symptom onset and had more non-dyskinetic symptoms than those without PRRT2 mutation. However, the characteristics of dyskinetic movement did not differ between the two groups. Conclusions This is the first study of PRRT2 mutations in Korea. The presence of a PRRT2 mutation was more strongly related to familial PKD, and was clinically related with earlier age of onset and common non-dyskinetic symptoms in PKD patients.

Association between Hypertriglyceridemia and Lacunar Infarction in Type 2 Diabetes Mellitus

BACKGROUND Although recent studies have shown that the elevation of serum triglyceride (TG) is related to the increased incidence of ischemic stroke, the relationship between hypertriglyceridemia and subtypes of ischemic stroke is largely unknown. This study attempted to evaluate whether hypertriglyceridemia is associated with lacunar stroke in diabetes mellitus (DM). METHODS A total of 2141 consecutive patients with acute ischemic stroke were enrolled from March 2005 to April 2014, excluding the subjects with undetermined/other determined etiology or no lipid data. We compared the lipid profiles among stroke subtypes. The estimated serum TG levels and the interaction between DM and stroke subtypes were determined by analysis of covariance (ANCOVA) and Tukeys multiple comparison. RESULTS In ANCOVA test, the difference of estimated TG between DM and non-DM patients was largest in small-vessel occlusion (SVO; 159.7 [95% confidence interval {CI}, 143.2-176.2] versus 122.4 [95% CI, 106.1-138.7]), and a significant interaction was observed between DM and stroke subtypes for TG levels (P = .013) but not for total cholesterol (P = .363), low-density lipoprotein cholesterol (P = .171), or high-density lipoprotein cholesterol (P = .231). By Tukeys multiple comparison, SVO was consistently associated with DM for serum TG levels (P < .001). CONCLUSIONS In acute ischemic stroke with DM, serum TG level was significantly associated with lacunar infarction adjusting for other lipid profiles and vascular risk factors. Further studies are warranted to reveal the pathophysiologic implication of hypertriglyceridemia for lacunar infarction in type 2 DM.