Patent foramen ovale (PFO) is growing in clinical interest because of a renewed focus on embolic stroke of undetermined source (ESUS), the PFO attributable fraction (the 10-point Risk of Paradoxical Embolism score), technical advances in PFO diagnosis, and the emergence of endovascular device closure as a treatment option. However, recent randomized controlled trials of the management of patients with ESUS and PFO failed to demonstrate the superiority of closure over medical treatment. The mechanisms of stroke other than paradoxical embolism may be important in patients with ESUS and PFO. This paper reviews the current understanding of the pathophysiology of stroke and therapeutic options in patients with PFO and ESUS.
Diagnosis ; Embolism, Paradoxical ; Foramen Ovale, Patent* ; Humans ; Stroke

BACKGROUND AND PURPOSE: Oxidative stress is involved in the pathophysiological mechanisms of stroke (e.g., atherosclerosis) and brain injury after ischemic stroke. Statins, which inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, have both pleiotropic and low-density lipoprotein (LDL)-lowering properties. Recent trials have shown that high-dose statins reduce the risk of cerebrovascular events. However, there is a paucity of data regarding the changes in the oxidative stress markers in patients with atherosclerotic stroke after statin use. This study evaluated changes in oxidative stress markers after short-term use of a high-dose statin in patients with atherosclerotic stroke. METHODS: Rosuvastatin was administered at a dose of 20 mg/day to 99 patients who had suffered an atherosclerotic stroke and no prior statin use. Blood samples were collected before and 1 month after dosing, and the serum levels of four oxidative stress markers-malondialdehyde (MDA), oxidized LDL (oxLDL), protein carbonyl content (PCO), and 8-hydroxy-2'-deoxyguanosine (8-OHdG)-were evaluated to determine the oxidation of MDA and lipids, proteins, and DNA, respectively, at both of those time points. RESULTS: The baseline levels and the degrees of reduction after statin use differed among the oxidative stress markers measured. MDA and PCO levels were associated with infarct volumes on diffusion-weighted imaging (r=0.551, p<0.05, and r=0.444, p=0.05, respectively). Statin use decreased MDA and oxLDL levels (both p<0.05) but not the PCO or 8-OHdG level. While the reduction in MDA levels after statin use was not associated with changes in cholesterol, that in oxLDL levels was proportional to the reductions in cholesterol (r=0.479, p<0.01), LDL (r=0.459, p<0.01), and apolipoprotein B (r=0.444, p<0.05). CONCLUSIONS: The impact of individual oxidative stress markers differs with time after ischemic stroke, suggesting that different oxidative markers reflect different aspects of oxidative stress. In addition, short-term use of a statin exerts antioxidant effects against lipid peroxidation via lipid-lowering-dependent and -independent mechanisms, but not against protein or DNA oxidation in atherosclerotic stroke patients.
Antioxidants* ; Apolipoproteins ; Atherosclerosis ; Brain Injuries ; Cholesterol ; Coenzyme A ; DNA ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors* ; Lipid Peroxidation ; Lipoproteins ; Oxidative Stress ; Oxidoreductases ; Stroke ; Rosuvastatin Calcium

Atonic seizure shows characteristic features such as head drop because postural muscle tone is suddenly lost. Atonia of the seizure means no muscle tone and loss of electromyographic activities were reported. We report a left parietal lobe epilepsy patient with atonic seizure showing hypotonia on electromyography. A 27 year-old woman had intractable head drop seizures since 6 years old. Her brain MRI demonstrated cortical dysplasia in the left parietal lobe. During the video-EEG monitoring, she had 21 epileptic seizures which were atonic seizures. During her atonic seizures, simultaneous EMG recordings showed decreased muscle activities during the head drop attacks, instead of no muscle tone. This is the first case showing transient hypotonia during the atonic seizure, instead of atonia.
Brain ; Electromyography ; Epilepsy ; Female ; Head ; Humans ; Malformations of Cortical Development ; Muscle Hypotonia ; Muscles ; Parietal Lobe ; Seizures ; Syncope

BACKGROUND AND PURPOSE: Left atrial dysfunction has been reported in patients with patent foramen ovale (PFO). Here we investigated the role of left atrial dysfunction in the development of embolic stroke in patients with PFO. METHODS: We identified consecutive patients with embolic stroke of undetermined sources except for PFO (PFO+ESUS). Healthy subjects with PFO served as controls (PFO+control). A stratified analysis by 10-year age group and an age- and sex- matching analysis were performed to compare echocardiographic markers between groups. In the PFO+ESUS group, infarct patterns of PFO-related stroke were determined (cortical vs. cortico-subcortical) and analyzed in correlation with left atrial function parameters. RESULTS: A total of 118 patients and 231 controls were included. The left atrial volume indices (LAVIs) of the PFO+ESUS patients were higher than those of the PFO+controls in age groups of 40–49, 50–59, and 60–69 years (P<0.001, P=0.003, and P=0.027, respectively), and in the age- and sex-matched analysis (P=0.001). In the PFO+ESUS patients, a higher (>28 mL/m2) LAVI was more associated with the cortical infarct pattern (P=0.043 for an acute infarction and P=0.024 for a chronic infarction, both adjusted for age and shunt amount). The degree of right-to-left shunting was not associated with infarct patterns, but with the posterior location of acute infarcts (P=0.028). CONCLUSIONS: Left atrial enlargement was associated with embolic stroke in subjects with PFO. Left atrial physiology might contribute to the development of PFO-related stroke and need to be taken into consideration for optimal prevention of PFO-related stroke.
Atrial Function, Left ; Echocardiography ; Embolism ; Embolism, Paradoxical ; Foramen Ovale, Patent* ; Healthy Volunteers ; Heart Atria ; Humans ; Infarction* ; Physiology ; Stroke