Hypereosinophilic syndrome presenting as acute ischemic stroke, myocardial infarction, and arterial involvement: A case report.

BACKGROUND: Simultaneous cerebral and myocardial infarction with arterial involvement has not been reported in hypereosinophilic syndrome (HES). Here, we report a patient with HES that was also associated with acute ischemic stroke, myocardial infarction, and arterial involvement of the left common carotid artery, vertebral arteries, posterior cerebral artery, and coronary artery. CASE SUMMARY: A 64-year-old male patient was admitted with headache and right lower extremity weakness. Laboratory tests indicated eosinophilia. Brain magnetic resonance imaging (MRI) showed bilateral and multiple acute infarcts in the border zones. Electrocardiography revealed that T wave was inverted and that the concentration of troponin I was significantly elevated above normal levels. Cardiac echocardiography showed an ejection fraction of 69% with mitral and tricuspid mild regurgitation. Computed tomography angiography detected multiple and localized instances of mild stenosis in the left common carotid artery bifurcation, bilateral vertebral arteries (V5 segment), and the posterior cerebral artery (P2 segment). These were observed together with multiple non-calcified and mixed plaques as well as luminal stenosis in the left circumflex artery, left anterior descending artery, and right coronary artery. The patient was treated with oral methylprednisolone and clopidogrel, after which the absolute eosinophil count fell rapidly to a normal level. After one month, a second brain MRI showed a partial reduction in the size and number of the lesions. CONCLUSION: HES can masquerade as ischemic stroke, myocardial infarction, and arterial vascular involvement. The patient reported here recovered very quickly when his eosinophil blood count returned to normal. Early diagnosis and rapid reduction of eosinophils may lead to a good prognosis.

Local thrombolytic therapy in severe cerebral venous sinus thrombosis during puerperium.

This study is to explore and evaluate the efficacy and safety of local thrombolytic therapy in superior sagittal sinus in patients with severe cerebral venous sinus thrombosis during puerperium, as well as the efficacy and safety of anti-platelet aggregation treatment for preventing recurrence. Twelve patients during postpartum period with cerebral venous sinus thrombosis were received local thrombolytic therapy by placing a micro-catheter at the distal end of superior sagittal sinus from January 2008 to December 2013. All the patients accepted mechanical thrombus maceration before local intrasinus thrombolytic therapy, and were treated with low molecular weight heparin in the acute phase. After local thrombolytic therapy, anti-platelet aggregation treatment was performed for 6 months. Follow-up data included lumber puncture, fundus examination and magnetic resonance venography (MRV) once per half year for 6-70 months. At discharge, the intracranial pressure of 12 patients reduced to below 200 mmH2O. DSA or MRV confirmed that superior sagittal sinus of 9 patients were smooth. The cortex venous and deep venous were recovered to normal. Superior sagittal sinus of 3 patients recanalized partly. Cortex venous and deep venous was compensated. The follow-up study indicated that no thrombosis and new neurological symptoms occurred among all patients. Local thrombolytic treatment is safe and effective in patients with severe cerebral venous sinus thrombosis during puerperium. The collateral circulation compensation is the main recovery factor. And it is also safe and effective for anti-platelet aggregation treatment to prevent recurrence of cerebral venous sinus thrombosis.

Postural sway in idiopathic rapid eye movement sleep behavior disorder: a potential marker of prodromal Parkinson's disease.

There is compelling evidence that postural instability occurs at very early clinical stages of Parkinson's disease (PD), making it tempting to speculate that changes in postural sway may even occur at a prodromal phase. Studies estimate that approximately half of patients with idiopathic rapid eye movement (REM) sleep behavior disorder (RBD) will eventually develop PD, so RBD may be an indicator of prodromal PD. This study was undertaken to investigate postural sway and its relation to stereopsis function in patients with RBD. We examined 24 patients with polysomnography-confirmed RBD and 23 healthy, sex-and age-matched control subjects. Postural sway was measured with an accelerometer at the center of mass at the lower spine. Subjects were asked to stand quietly for 30s under two usual conditions (eyes open and eyes closed) and three challenging conditions (eyes open with dual task, eyes closed with dual task, and tandem standing). Stereopsis was assessed using the Titmus fly test. RBD patients showed an increased variability of trunk acceleration and a decrease of smoothness of sway, compared to control subjects. These differences reached significance in the challenging conditions. RBD patients demonstrated significant impairment in stereopsis. There were statistically significant correlations between log seconds of arc of the Titmus test and some sway parameters within the RBD group. RBD patients with abnormal stereopsis showed a significant increase of JERK values compared to patients with normal stereopsis in the challenging conditions. Our results indicate that idiopathic RBD patients, especially with abnormal stereopsis, have subtle signs of postural instability under challenging conditions. Postural sway performance may serve as a biological marker for prodromal PD.