Takaya Kitano

Multiple Infarcts Are Associated With Long-Term Stroke Recurrence and All-Cause Mortality in Cryptogenic Stroke Patients.

Background and Purpose— Brain infarct patterns that are observed via diffusion-weighted imaging are useful for classifying stroke subtypes. However, it is unclear whether infarct patterns can predict long-term outcomes in cryptogenic stroke patients. Herein, we investigated the association between acute brain infarct patterns and long-term stroke outcomes in cryptogenic stroke patients. Methods— Acute cryptogenic stroke patients were consecutively enrolled between April 2008 and March 2012. Diffusion-weighted imaging ischemic lesion patterns were classified as single lesions, scattered lesions in one vascular territory, or multiple lesions in multiple vascular territories. Survivors (at discharge) were followed up for 3 years after stroke onset. Results— A total of 272 cryptogenic stroke patients (132 women; aged 72±13 years) were enrolled. Among these patients, 169 (62.1%) had a single lesion, 38 (14.0%) had scattered lesions, and 65 (23.9%) had multiple lesions. Next, 261 patients (96.0%) were evaluated to assess right-to-left shunting, and 61 patients (23.4%) exhibited right-to-left shunting. On patient admission, right-to-left shunting and increased D-dimer levels were independently associated with multiple lesions but not single or scattered lesions. During the follow-up period (median, 1093 days), 30 patients (11.0%) developed recurrent stroke and 35 patients (12.9%) died. Multivariate Cox proportional hazard analyses showed that multiple infarcts were independently associated with recurrent stroke and all-cause mortality (hazard ratio, 3.79; 95% confidence interval, 2.24–6.37; P<0.001). Conclusions— Multiple brain infarcts on diffusion-weighted imaging were independently associated with long-term stroke outcomes in cryptogenic stroke patients.

Association Between Absolute Eosinophil Count and Complex Aortic Arch Plaque in Patients With Acute Ischemic Stroke

Background and Purpose— Eosinophil counts are thought to be associated with atherosclerosis and aortic arch plaques. However, whether these associations exist among patients with acute ischemic stroke remains unclear. We aimed to evaluate the association between absolute eosinophil count (AEC) and aortic arch plaques among these patients. Methods— Consecutive acute ischemic stroke patients undergoing transesophageal echocardiography were retrospectively analyzed. Complex aortic arch plaques (CAPs) were defined as plaques ≥4 mm in thickness, with ulcer, or with mobile component. Results— A total of 430 patients (289 male, mean age 69.8±11.4 years) were enrolled. Patients with CAPs (n=169) showed higher mean AEC than those without (167±174/µL versus 127±127/µL; P=0.007). Multivariate analysis showed that increased AEC was independently associated with the presence of CAPs (odds ratio, 2.09; 95% confidence interval, 1.21–3.65). Conclusions— Among patients with acute ischemic stroke, increased AEC was independently associated with the presence of CAPs. Our results suggest that AEC may be a useful predictor for the presence of CAPs in these patients.

A Case of Hypertensive Encephalopathy with Enlarged Optic Nerve Sheath Measured by Transorbital Sonography.

This case report describes our experience in using transorbital sonography to evaluate pathological changes in the central nervous system in hypertensive encephalopathy. A 49-year-old man with nausea, headache, and mild confusion was diagnosed with hypertensive encephalopathy by brain magnetic resonance imaging (MRI), which revealed vasogenic edema in the bilateral thalamus and the brain stem. Lumbar puncture showed no severe intracranial hypertension. Transorbital sonography showed an increase in the optic nerve sheath diameter (ONSD). Repeated examination revealed a return of the ONSD to an almost normal range after a reduction in blood pressure and a resolution of symptoms. An improvement in cerebral vasogenic edema was confirmed by brain MRI. ONSD might be related to the severity of cerebral vasogenic edema. Repeated measurement of ONSD by transorbital sonography may be useful to assess the pathological course and the effect of treatment in hypertensive encephalopathy.

In-stent thrombosis after carotid artery stenting in a patient with protein C deficiency

Dear Editor: In-stent thrombosis (IST) is a rare but serious complication of carotid artery stenting (CAS) [1]. However, the risk factors for IST have not been determined. We present a case of IST following CAS in a patient with protein C deficiency. A 40-year-old otherwise healthy woman was admitted to our hospital because of weakness in her left upper limb. She had cerebral infarction in her early thirties, but no sequelae remained, and she was not on anti-thrombotic agents. She had started taking oral contraceptives 7 days prior to her presentation. On admission, the neurological examination revealed left hemiparesis, hemihypoesthesia, and unilateral spatial neglect. Magnetic resonance imaging revealed an acute cerebral infarction and occlusion in the horizontal segment of the right middle cerebral artery (Fig. 1a, b). Thus, an emergent mechanical thrombectomy was planned. A right carotid angiography that was performed prior to thrombectomy revealed a filling defect at the origin of the right internal carotid artery, which indicated a mural thrombus (Fig. 1c). We performed CAS in advance (WALLSTENT; Boston Scientific, Natick, MA), following the administration of dual antiplatelet therapy. The filling defect disappeared after CAS (Fig. 1d). Subsequently, we deployed the Solitaire FR/2 stent (4 × 20 mm, Medtronic, Irvine, California, USA) to the occluded middle cerebral artery, and immediate flow restoration was observed. One pass of the stent retriever successfully recanalized the vessel, and a red thrombus was retrieved. The patient’s symptoms improved; however, a slight left unilateral spatial neglect remained. Eight thousand units of unfiltered heparin per day (continuous injection) and dual antiplatelet therapy were continued following thrombectomy. Contrast-enhanced ultrasonography is a routine evaluation procedure performed after CAS at our institution as it helps visualize intra-stent abnormalities [2, 3]. After 2 days, contrast-enhanced ultrasonography detected a circular contrast defect in the distal part of the stent (Fig. 1e). We considered the defect as an IST and thus increased the dose of heparin to 11,000 units per day under activated partial thromboplastin monitoring. No significant decrease in the patient’s platelet count was observed. Plasma protein C activity and total protein C antigen levels, which were sampled before initiating the treatment, were found to be low (48% in the clotting-time based assay and 50% in the latex photometric immunoassay). Other markers of thrombophilia, including protein S (levels of free antigen and total antigen) and antithrombin III levels, and plasminogen activity were not significantly decreased. We did not test factor V Leiden or prothrombin G20210A mutation in this patient because these abnormalities are extremely rare among Japanese population. Testing with antiphospholipid antibodies yielded negative results. Repeated examinations for protein C on day 10 also showed significantly decreased values. Other examinations for potential stroke risks showed negative results: atrial fibrillation was not detected via electrocardiogram monitoring during admission; transthoracic and transesophageal echocardiography detected no embolic source in her heart or aorta; rightto-left shunt was negative; and ultrasonography of the lower extremity veins revealed no deep venous thrombosis. On the 12th-day follow-up, the thrombosis had disappeared without stroke recurrence.Warfarin was initiated under heparin injection. Several conditions could be considered as the pathology of the initial filling defect in the carotid artery. Slight abnormalities such as injury of the intima or rupture of small atheromatous plaques might have caused the clot formation. Carotid dissectionwas also a possible cause, although she had no pain in her neck. It was quite unlikely that the chronic carotid artery stenosis had caused * Takaya Kitano takayakitano@neurol.med.osaka-u.ac.jp