Ozlem Ozkul-Wermester

Increased blood-brain barrier permeability on perfusion computed tomography predicts hemorrhagic transformation in acute ischemic stroke.

Background/Purpose: Perfusion computed tomography (CT) is capable of measuring the permeability surface product (PS). PS reflects the permeability of the blood-brain barrier, involved in the pathophysiology of hemorrhagic transformation (HT) of ischemic stroke. The aim of our study was to determine if an increased PS can predict HT. Methods: A total of 86 patients with ischemic stroke were included. They underwent multimodality CT, including the measurement of PS. We compared the clinical and radiological characteristics of patients who developed HT to those who did not, using univariate analysis. Multivariate regression analyses were then used to determine HT predictors. Results: HT was observed in 27 patients (31%). Infarct PS was significantly associated with HT (p = 0.047), as were atrial fibrillation (p = 0.03), admission National Institute of Health Stroke Scale score (p = 0.02), infarct volume (p = 0.0004), presence of large-vessel occlusion (p = 0.0005) and a poorer collateral status (p = 0.003). Using logistic regression modeling, an infarct PS >0.84 ml/100 g/min was an independent predictor of HT (OR 28, 95% CI 1.75-452.98; p = 0.02). Other independent predictors of HT were infarct volume and a history of atrial fibrillation. Conclusions: Our findings suggest that infarct PS can be a predictor of HT and may help clinicians to improve patient care around thrombolysis decisions in the acute phase of ischemic stroke.

Proportion of single-chain recombinant tissue plasminogen activator and outcome after stroke

Objective: To determine whether the ratio single chain (sc)/(sc + 2 chain [tc]) recombinant tissue plasminogen activator (rtPA) influences outcomes in patients with cerebral ischemia. Methods: We prospectively included consecutive patients treated with IV rtPA for cerebral ischemia in 13 stroke centers and determined the sc/(sc + tc) ratio in the treatment administered to each patient. We evaluated the outcome with the modified Rankin Scale (mRS) at 3 months (prespecified analysis) and occurrence of epileptic seizures (post hoc analysis). We registered Outcome of Patients Treated by IV Rt-PA for Cerebral Ischaemia According to the Ratio Sc-tPA/Tc-tPA (OPHELIE) under ClinicalTrials.gov identifier no. NCT01614080. Results: We recruited 1,004 patients (515 men, median age 75 years, median onset-to-needle time 170 minutes, median NIH Stroke Scale score 10). We found no statistical association between sc/(sc + tc) ratios and handicap (mRS > 1), dependency (mRS > 2), or death at 3 months. Patients with symptomatic intracerebral hemorrhages had lower ratios (median 69% vs 72%, adjusted p = 0.003). The sc/(sc + tc) rtPA ratio did not differ between patients with and without seizures, but patients with early seizures were more likely to have received a sc/(sc + tc) rtPA ratio >80.5% (odds ratio 3.61; 95% confidence interval 1.26–10.34). Conclusions: The sc/(sc + tc) rtPA ratio does not influence outcomes in patients with cerebral ischemia. The capacity of rtPA to modulate NMDA receptor signaling might be associated with early seizures, but we observed this effect only in patients with a ratio of sc/(sc + tc) rtPA >80.5% in a post hoc analysis.

Cervical osteophyte causing cerebellar infarction.

A 59-year-old man presented with sudden onset of vertigo, headache, nausea, and left-hand clumsiness. Neurological examination showed multidirectional nystagmus and left kinetic cerebellar syndrome. The patient did not have neck injury. Brain MRI showed acute infarction in the region of the left posterior inferior cerebellar artery (fi gure A). CT angiography showed left vertebral artery stenosis caused by extrinsic compression by an osteophyte of the superior articular process of the fourth cervical vertebra, compromising the foramen transversarium, with a downstream occlusion of the left vertebral artery in its extracranial segment (fi gure B, C). Extrinsic compression of the vertebral artery is a rare complication of cervical osteophytes. Embolic infarction rarely occurs. Surgical treatment can be proposed to decompress the artery.

Leucoencephalopathy following abuse of sniffed heroin

A 29-year-old man was admitted for acute cognitive impairment. Three weeks earlier, he had been admitted for coma due to sniffed heroin abuse responsive to naloxone infusion. At admission, the patient presented with apraxia, severe memory impairment and anosognosia. Brain MRI revealed symmetric hyperintensities of supratentorial white matter, sparing brainstem and cerebellum, on FLAIR and B1000 sequences. Four months later, repeated neuropsychological assessment revealed dramatic improvement of global cognitive functions. Toxic leucoencephalopathy excluding the cerebellum and brainstem is a rare complication of heroin abuse, and seems to concern especially patients that use heroin by sniff or injection. In these patients, cognitive troubles are predominant, prognosis seems better and infratentorial brain structures can be spared. In conclusion, our observation emphasizes that heroin-induced encephalopathy can have a favourable outcome and that imaging and clinical patterns can indicate the mode of drug administration.

Brain developmental venous anomaly thrombosis

A 62-year-old man was admitted for partial motor seizures and headaches. His medical history included arterial hypertension, obstructive sleep apnea syndrome and migraine. Because of his migraine, he had received an MRI 4 years earlier on which a right frontal developmental venous anomaly (DVA) had been fortuitously discovered. At admission, the patient presented with headaches since 2 weeks, different from his usual migraine headaches. The headache was permanent, more painful, and not relieved by usual analgesics. He had no focal neurological deficits. Brain MRI (Fig. 1a–d) revealed a filling defect in the collecting vein of the known right frontal DVA with limited perifocal edema on FLAIR and intravascular hypointensity on T2*, compatible with the diagnosis of DVA thrombosis. Brain MRI revealed no additional vascular malformations. Standard biological data were normal. Extensive laboratory investigations revealed isolated elevate D-dimer (730 ng/ml; N\ 500). Protein C, protein S, antithrombin III, antiphospholipid and anticardiolipin b2glycoprotein-1 complex antibodies were within the normal range. Factor V Leiden, prothrombin, and Janus Kinase 2 mutations were absent. Intravenous heparin infusion was rapidly introduced followed by daily oral vitamin K antagonists (fluindione 20 mg per day). Levetiracetam (500 mg twice per day) was also introduced. Three months later, repeated brain MRI (Fig. 1e–h) showed complete resolution of DVA thrombosis with complete recanalization of the DVA. Six months later, levetiracetam and fluindione were definitively stopped and the patient had no seizure or thrombosis recurrence. DVAs are the most commonly observed cerebral vascular malformations, with an incidence rate of[2 % [1]. Two-thirds of DVAs have a supratentorial location [2]. In the vast majority of cases, DVAs follow a benign clinical course and do not require follow-up imaging studies or specific medical management. Hemorrhagic risk associated with DVAs is very low and is estimated approximately 0.22–0.68 % per year [3]. Thrombosis of DVAs or their collecting veins is rare [4, 5] and may lead to a variety of complications including venous ischemic infarction, parenchymal hemorrhage, venous congestive edema, or subarachnoid hemorrhage. Pathophysiological mechanisms of DVAs thrombosis remain unclear. Risk factors for venous thrombosis, altered venous flow and lack of smooth muscle cells and elastic connective tissue increasing venous pressure in DVAs may play a role in the thrombotic process [1, 2]. There are no clear guidelines on DVA thrombosis treatment but many authors recommend that thrombosed DVAs must be approached with the same workup and treatment regimen as cerebral venous thrombosis [2]. When a compressive brain hematoma or edema requires surgical management, DVA collecting vein must be spared to avoid venous infarction [2]. Of note is that DVAs can be associated with other vascular malformations and, in cases of hemorrhage related to DVAs, cavernous malformations (CMs) are the most often encountered causative malformation. CMs are associated with DVAs in 13–40 % of cases [2]. CMs may be difficult to identify in the setting of a DVA presenting with & Romain Lefaucheur romain.lefaucheur@chu-rouen.fr

Stroke mimicking relapse in a patient with CLIPPERS syndrome.

Chronic lymphocytic inflammation with pontine/pontocerebellar perivascular enhancement responsive to steroids (CLIPPERS) is a novel type of brainstem encephalomyelitis recently described [1]. The pathophysiology remains unknown, and an autoimmune hypothesis has been proposed. We report a patient with CLIPPERS presenting suggestive signs of relapse and whose MRI revealed mesencephalic stroke. A 52-year-old man was referred for binocular diplopia and ataxia that had begun 3 days earlier. His medical history included CLIPPERS syndrome diagnosed 4 years earlier (already published, cf Ref. [2]; Fig. 1a) and chronic sinusitis. CLIPPERS had been diagnosed when the patient had presented progressive ataxia, dysarthria and binocular diplopia; brain MRI had shown characteristic punctuate and curvilinear enhancement peppering the pons (Fig. 1a). Further investigations had excluded neurosarcoidosis, CNS lymphoma, granulomatosis, paraneoplastic and chronic infectious processes. Since treatment with oral prednisolone secondarily relayed by methotrexate (per os 12.5 mg per week) had been introduced, neurological examination was normal and he had presented no relapses. Brain biopsy had not been performed because of typical brain imaging and dramatic response with steroids. At admission, he presented with ataxia associated with pupil-sparing left partial third nerve palsy. Brain MRI showed a left paramedian mesencephalic hypersignal in FLAIR and diffusion-weighted sequences, without gadolinium enhancement, compatible with the diagnosis of stroke (Fig. 1b1, 2, 3). MR angiography revealed no signs of brain vasculitis. The patient did not present arterial hypertension. He was not smoker. Biological data revealed a high rate of A1C hemoglobin (10.3 %; N\ 6 %) and LDL cholesterol (5.60 mmol/l). Others biological samples revealed no other abnormalities, especially no signs of systemic inflammation. Doppler ultrasonography of the supra-aortic trunks and transcranial sonography revealed mild atherosclerosis without hemodynamically relevant stenosis. Continuous ECG monitoring was normal. Polysomnography revealed severe sleep apnea syndrome. Cardiac ultrasonography was normal. Oral aspirin (160 mg per day), simvastatine (40 mg per day), metformin (3000 mg per day) and positive airway pressure therapy were introduced. The patient had no recurrence of stroke.

Suspected subdural hematoma.

A 71-year-old woman was admitted for 3 inaugural right-sided focal seizures. Shortly before, she had experienced a minor head trauma. Her neurological examination finding was normal. A brain computed tomographic scan and magnetic resonance imaging (MRI) showed abnormalities supporting the diagnosis of chronic subdural hematoma (SDH), with a subcutaneous collection regarding this subdural hematoma (Figure, A-C). She did not undergo surgery, and monitoring with brain MRI was recommended. Three months later, while partial seizures persisted despite anti-epileptic treatment (levitiracetam, 2000 mg/d), follow-up brain MRI showed increased extra-axial and subcutaneous gadolinium-enhanced masses (Figure, D and E). Given this unusual subdural hematoma evolution and radiological worsening of the suspected hematoma, craniotomy and biopsies were performed. The histopathology findings revealed a low-grade B-cell marginal zone lymphoma involving dura with bone and scalp invasion. The patient underwent radiotherapy after surgery, which reduced the residual mass. Six months later, her neurological condition deteriorated with progressive appearance of a right hemiparesis, aphasia, and drug-resistant epilepsy.

In-hospital delays to stroke thrombolysis: Out of hours versus regular hours and reduction in treatment times through the creation of a 24/7 mobile thrombolysis team

BACKGROUND The main aim of this study was to evaluate the impact of the implementation of a mobile thrombolysis team (MTT) on time to thrombolysis treatment depending on patient admission time: regular hours (RH) or out of hours (OH). METHODS 504 consecutive patients treated with IV tPA or with combined IV tPA and mechanical thrombectomy for acute ischemic stroke were retrospectively included between 1st January 2013 and 31st December 2017. Three sub-periods were identified: 2013-2014, 2015-2016, and 2017 during which patients were treated with the usual care (UC), by the MTT or with UC according to their time of admission, or by the MTT, in the three time periods respectively. We compared in-hospital delays according to patient admission time. RESULTS In 2013-2014, 133 patients were included. Both median door-to-needle (DTN) and imaging to needle (ITN) times were shorter for patients admitted during RH than OH, respectively 75 min versus 85 min and 52 min versus 57 min (P < 0.05), and the proportion of patients with DTN ≤ 60 min was 23% versus 9% (P < 0.05), respectively. In 2015-2016, 223 patients were included. DTN and ITN times were shorter for patients admitted during RH and treated by the MTT than during OH with UC, respectively 54 min versus 78 min and 24 min versus 47 min (P < 0.001), and the proportion of patients with DTN ≤ 60 min was 64% versus 21% (P < 0.001), respectively. In 2017, there was no difference concerning in-hospital delays regardless of patient admission time (P > 0.05). DISCUSSION DTN time was significantly longer for patients admitted OH. We suggest that the implementation of an around-the-clock MTT would allow a reduction of in-hospital delays and similar times to thrombolysis treatment regardless of admission time.

Innominate artery dissection and stroke after rifle recoil

Cervical artery dissection is a frequent cause of stroke, more so in young patients. Innominate artery (IA) dissection is uncommon, and most often associated with dissection of other major arteries like the aorta. The leading cause of IA injury is high-energy thoracic trauma, as in motor vehicle crash. IA dissection after blunt trauma is rare. We described here the unusual case and iconography of an isolated IA dissection after rifle recoil initially presenting as a stroke.

Suspected stroke in a pregnant woman: Usefulness of arterial spin labeling MRI sequences

La Presse Medicale - In Press.Proof corrected by the author Available online since jeudi 18 aout 2016