Apparent diffusion coefficient signature of ischemic tissue predicts neurological progression in isolated pontine infarcts.

Background: Early neurological deterioration is encountered in up to a third of patients with isolated pontine infarcts. A limited number of clinical and imaging features have been suggested as predictors of neurological progression in this setting. In this study, we assessed whether quantitative apparent diffusion coefficient (ADC) measurements within the ischemic pontine region could be used as a radiomic feature to forecast clinical deterioration. Methods: We calculated the mean ADC value of ischemic voxels within the ischemic region and normalized them to the contralateral non-ischemic tissue (relative ADC, rADC) in patients with isolated pontine infarcts. This imaging signature was then compared among patients with neurological progression (n = 21) and a propensity matched cohort of non-progressors (n = 42), together with other clinical and imaging features in bivariate and multivariate statistical models. Results: The rADCmean was significantly lower among patients with progression (p = 0.008). Female gender and extension of the ischemic lesion to the ventral pontine surface were other features significantly associated with progression. The association between rADCmean and progression persisted in multivariate models with an odds ratio of 13.7 (95% CI 2.6-72.8; p = 0.002) for progression among patients with rADCmean ≤ 0.67 in their ischemic tissue. The probability for worsening was 80% among patients who had an ischemic lesion extending to the ventral pontine surface with a mean rADC ≤ 0.67. Conclusion: The mean rADC value within the ischemic lesion is closely related with early neurological deterioration in patients with isolated pontine infarcts.

Dual Testing to Achieve Low On-treatment Platelet Reactivity for Aneurysm Embolization.

BACKGROUND AND PURPOSE: Although point-of-care tests are used extensively to test platelet function before endovascular aneurysm treatment, their use and validity are still debated. We compared the results of two point-of-care tests (VerifyNow® and Multiplate®) for assessing patients treated with stents and flow diverters and determined their relation to periprocedural complications. METHODS: All patients undergoing treatment of intracranial aneurysms were tested using both methods and were retrospectively evaluated. Patients with acute subarachnoid hemorrhage and those who had to be maintained on anticoagulants for unrelated diseases were excluded. An acceptable level of platelet inhibition was required on both tests to commence with treatment, otherwise antiplatelet medication was adjusted to reach this level. RESULTS: Mean PRU (platelet reactivity units) and ADP AUC (adenosine diphosphate area under the aggregation curve) were 68 ± 66 and 23 ± 15, respectively, in 295 patients. Both tests showed a good correlation (r = 0.45). Both tests were able to predict hemorrhagic events but not ischemic events. When patients with very low reactivity (PRU < 60) were compared to the rest of the group, there were more hemorrhagic events in the first group but the overall rate of complications were similar (p = 0.27). CONCLUSION: In this largest study comparing two widely used commercial platelet function tests, the correlation between the tests were less than ideal; however, the very low platelet reactivity attained by the help of dual platelet testing did not result in an increased overall complication rate.

Post-stroke inflammatory response is linked to volume loss in the contralateral hemisphere.

OBJECTIVES: There is a delicate homeostatic balance between the central nervous system and immune system. Stroke triggers an immunodepressive state to suppress a potential immune reaction directed against neuroglial tissue; however, this supposedly protective response inadvertently results in an infection-prone, and thereby a pro-inflammatory setting. In this study, we assessed the magnitude of cerebral volume loss in the unaffected contralateral hemisphere following stroke, and determined its relationship with inflammatory cascades. METHODS: The volume of the hemisphere contralateral to the ischemic insult was measured on admission and follow-up MRI's in 50 ischemic stroke patients. Information related to clinical features, infectious complications, and markers of inflammation (erythrocyte sedimentation rate, neutrophil/lymphocyte ratio, C-reactive protein) were prospectively collected, and their relationship with hemispheric volume change was evaluated using bivariate and multivariate statistics. RESULTS: The contralateral hemisphere volume decreased by a median (interquartile range) of 14 (4-32) mL after a follow-up duration of 101 (63-123) days (p < .001); the volume reduction was 0.8 (0.2-1.8) % per month with respect to baseline. Old age, atrial fibrillation, stroke severity, C-reactive protein level, neutrophil/lymphocyte ratio, and development of infections during hospitalization were significantly associated with volume loss (p < .05). Stroke severity (NIHSS score or infarct volume) and inflammation related parameters (neutrophil/lymphocyte ratio or systemic infections) remained independently and positively associated with volume loss in multivariate regression models. CONCLUSIONS: Cerebral tissue changes following stroke are not limited to the ischemic hemisphere. Apart from stroke severity, a pro-inflammatory state and post-stroke infections contribute to cerebral volume loss in the non-ischemic hemisphere.

The effect of carotid artery stenting on capillary transit time heterogeneity in patients with carotid artery stenosis.

INTRODUCTION: Carotid revascularisation improves haemodynamic compromise in cerebral circulation as an additional benefit to the primary goal of reducing future thromboembolic risk. We determined the effect of carotid artery stenting on cerebral perfusion and oxygenation using a perfusion-weighted MRI algorithm that is based on assessment of capillary transit-time heterogeneity together with other perfusion and metabolism-related metrics. PATIENTS AND METHODS: A consecutive series of 33 patients were evaluated by dynamic susceptibility contrast perfusion-weighted MRI prior to and within 24 h of the endovascular procedure. The level of relative change induced by stenting, and relationship of these changes with respect to baseline stenosis degree were analysed. RESULTS: Stenting led to significant increase in cerebral blood flow (p < 0.001), and decrease in cerebral blood volume (p = 0.001) and mean transit time (p < 0.001); this was accompanied by reduction in oxygen extraction fraction (p < 0.001) and capillary transit-time heterogeneity (p < 0.001), but an overall increase in relative capillary transit-time heterogeneity (RTH: CTH divided by MTT; p = 0.008). No significant change was observed with respect to cerebral metabolic rate of oxygen. The median volume of tissue with MTT > 2s decreased from 24 ml to 12 ml (p = 0.009), with CTH > 2s from 29 ml to 19 ml (p = 0.041), and with RTH < 0.9 from 61 ml to 39 ml (p = 0.037) following stenting. These changes were correlated with the baseline degree of stenosis.Discussion: Stenting improved the moderate stage of haemodynamic compromise at baseline in our cohort. The decreased relative transit-time heterogeneity, which increases following stenting, is probably a reflection of decreased functional capillary density secondary to chronic hypoperfusion induced by the proximal stenosis.Conclusion: Carotid artery stenting, is not only important for prophylaxis of future vascular events, but also is critical for restoration of microvascular function in the cerebral tissue.

Recrudescence of Deficits After Stroke: Clinical and Imaging Phenotype, Triggers, and Risk Factors.

Importance: Reemergence of previous stroke-related deficits (or poststroke recrudescence [PSR]) is an underrecognized and inadequately characterized phenomenon. Objective: To investigate the clinical features, triggers, and risk factors for PSR. Design, Setting, and Participants: This retrospective study incorporated a crossover cohort study to identify triggers and a case-control study to identify risk factors. The study used the Massachusetts General Hospital Research Patient Data Repository to identify patients for the period January 1, 2000, to November 30, 2015, who had a primary or secondary diagnosis of cerebrovascular disease, who underwent magnetic resonance imaging of the brain at least once, and whose inpatient or outpatient clinician note or discharge summary stated the term recrudescence. In all, 153 patients met the preliminary diagnostic criteria for PSR: transient worsening of residual poststroke focal neurologic deficits or transient recurrence of prior stroke-related focal deficits, admission magnetic resonance imaging showing a chronic stroke but no acute infarct or hemorrhage, no evidence of transient ischemic attack or seizure, no acute lesion on diffusion-weighted imaging, and no clinical or electroencephalographic evidence of seizure around the time of the event. Main Outcomes and Measures: Clinical and imaging features of PSR; triggers (identified by comparing PSR admissions with adjacent admissions without PSR); and risk factors (identified by comparing PSR cases with control cases from the Massachusetts General Hospital Stroke Registry). Results: Of the 153 patients, 145 had prior infarct, 8 had hypertensive brain hemorrhage, and 164 admissions for PSR were identified. The patients' mean (SD) age was 67 (16) years, and 92 (60%) were women. Recrudescence occurred a mean (SD) of 3.9 (0.6) years after the stroke, lasted 18.4 (20.4) hours, and was resolved on day 1 for 91 of the 131 episodes with documented resolution time (69%). Deficits were typically abrupt and mild and affected motor-sensory or language function. No patient had isolated gaze paresis, hemianopia, or neglect. During PSR, the National Institutes of Health Stroke Scale (NIHSS) score worsened by a mean (SD) 2.5 (1.9) points, and deficits were limited to a single NIHSS item in 62 episodes (38%). The underlying chronic strokes were variably sized, predominantly affected white matter tracts, and involved the middle cerebral artery territory for 112 patients (73%). Infection, hypotension, hyponatremia, insomnia or stress, and benzodiazepine use were higher during PSR admissions. Compared with the control group (patients who did not experience recrudescence), the PSR group (patients who were hospitalized for recrudescence) had more women, African American individuals, and those who self-identified as being from "other" race. The PSR group also had more diabetes, dyslipidemia, smoking, infarcts from small-vessel disease, and "other definite" causes and worse onset NIHSS scores. Six patients (4%) received intravenous tissue plasminogen activator without complications. Conclusions and Relevance: The PSR features identified in the study should enable prompt diagnosis and distinguish recrudescence from mimics, such as transient ischemic attacks, migraine, Todd paralysis, and Uhthoff phenomenon. Prospective studies are required to validate the proposed diagnostic criteria and to decipher underlying mechanisms.

Hemorrhagic primary CNS angiitis and vasoconstrictive drug exposure.

BACKGROUND: Primary angiitis of the CNS (PACNS) typically manifests with accumulating neurologic deficits from ischemic strokes. Intracerebral hemorrhage (ICH) is an uncommon complication. There is limited knowledge about the risk factors and features of hemorrhagic PACNS. METHODS: We identified 49 patients (20 biopsy-proven) with PACNS diagnosed at our hospital from 1993 to 2015. We compared the features of hemorrhagic and nonhemorrhagic PACNS and analyzed the hemorrhagic PACNS cases in detail. RESULTS: The mean age was 51 ± 15 years; 13 patients were men. Five patients had ICH (mean age 52 ± 14 years; 4 men) including 4 where ICH was the first manifestation of PACNS. All ICH patients reported recent exposure to sympathomimetic drugs (e.g., diet pills, nasal decongestants). Patients with ICH had higher rates of headache (100% vs 43%, p = 0.022), especially thunderclap headache (60% vs 0%, p = 0.001), and eosinophilic vascular infiltrates on brain biopsy (50% vs 9%, p = 0.084). In all ICH patients, brain MRI showed lobar hemorrhages with concurrent punctate diffusion-restricted lesions, suggesting an acute inflammatory process. Four received a short course of immunosuppressive therapy. All patients showed complete clinical resolution or significant improvement within weeks. CONCLUSIONS: In this study, hemorrhagic PACNS was exclusively associated with sympathomimetic drug exposure. The high rate of thunderclap headache, lobar hemorrhages, and the self-limited clinical course suggests a shared mechanism between hemorrhagic PACNS and the reversible cerebral vasoconstriction syndrome (RCVS), a PACNS mimic. This RCVS-PACNS overlap syndrome may result from sympathomimetic drug-induced prolonged distal vasoconstriction, culminating in inflammation.

Glucocorticoid-associated worsening in reversible cerebral vasoconstriction syndrome.

OBJECTIVE: Factors predicting poor outcome in patients with the reversible cerebral vasoconstriction syndrome (RCVS) have not been identified. METHODS: In this single-center retrospective study, we analyzed the clinical, brain imaging, and angiography data in 162 patients with RCVS. Univariable and multivariable regression analysis were performed to identify predictors of persistent (nontransient) clinical worsening, radiologic worsening, early angiographic progression, and poor discharge outcome (modified Rankin Scale score 4-6). RESULTS: The mean age was 44 ± 13 years; 78% of patients were women. Persistent clinical worsening occurred in 14% at 6.6 ± 4.1 days after symptom onset, radiologic worsening in 27% (mainly new infarcts), and angiographic progression in 15%. Clinical worsening correlated with angiographic progression and new nonhemorrhagic lesions. Age and sex did not independently predict any type of worsening. Infarction on baseline imaging predicted poor outcome. Prior serotonergic antidepressant use predicted clinical and angiographic worsening but not poor outcome. Intra-arterial vasodilator therapy independently predicted clinical worsening and poor discharge outcome but was offered to more severe cases. Glucocorticoid treatment proved to be an independent predictor of clinical, imaging, and angiographic worsening and poor outcome. Of the 23 patients with clinical worsening, 17 received glucocorticoids (15 within the preceding 2 days). There were no significant differences in baseline brain lesions and angiographic abnormalities between glucocorticoid-treated and untreated patients. CONCLUSION: Patients with RCVS at risk for worsening can be identified on basis of baseline features. Iatrogenic factors such as glucocorticoid exposure may contribute to worsening.

High-flow oxygen therapy for treatment of acute migraine: A randomized crossover trial.

Background Impaired oxygen utilization and cerebrovascular dysfunction are implicated in migraine. High-flow oxygen is effective in cluster headache and has shown promise in animal models of migraine, but has not been adequately studied in patients with migraine. Methods In this randomized, crossover-design, placebo-controlled trial, adult migraineurs self-administered high-flow oxygen or medical air at 10-15 l/min via face mask in blinded fashion starting soon after symptom onset for 30 minutes, for a total of four migraine attacks. Participants recorded the severity of headache, nausea, and visual symptoms on visual analog scales periodically up to 60 minutes. Results We enrolled 22 individuals (mean age 36 years, 20 women) who self-treated 64 migraine attacks (33 oxygen, 31 air). The pre-specified primary endpoint (mean decrease in pain score from baseline to 30 minutes) was 1.38 ± 1.42 in oxygen-treated and 1.22 ± 1.61 in air-treated attacks ( p = 0.674). Oxygen therapy resulted in relief (severity score 0-1) of pain (24% versus 6%, p = 0.05), nausea (42% versus 23%, p = 0.08) and visual symptoms (36% versus 7%, p = 0.004) at 60 minutes. Exploratory analysis showed that in moderately severe attacks (baseline pain score <6), pain relief was achieved in six of 13 (46%) oxygen versus one of 15 (7%) air ( p = 0.02). Gas therapy was used per protocol in 91% of attacks. There were no significant adverse events. Conclusion High-flow oxygen may be a feasible and safe strategy to treat acute migraine. Further studies are required to determine if this relatively inexpensive, widely available treatment can be used as an adjunct or alternative migraine therapy.

Hemorrhagic Reversible Cerebral Vasoconstriction Syndrome: Features and Mechanisms.

BACKGROUND AND PURPOSE: To compare hemorrhagic and nonhemorrhagic reversible cerebral vasoconstriction syndromes (RCVS) with a view to understand mechanisms. METHODS: This single-center retrospective study included 162 patients with RCVS. Clinical, brain imaging, and angiography data were analyzed. RESULTS: The mean age was 44±13 years, 78% women. Hemorrhages occurred in 43% including 21 patients with intracerebral hemorrhage (ICH) and 62 with convexal subarachnoid hemorrhage (cSAH). The frequency of triggers (eg, vasoconstrictive drugs) and risk factors (eg, migraine) were not significantly different between hemorrhagic and nonhemorrhagic RCVS or between subgroups (ICH versus non-ICH, isolated cSAH versus normal scan). Hemorrhagic lesions occurred within the first week, whereas infarcts and vasogenic edema accumulated during 2 to 3 weeks (P<0.001). Although all ICHs occurred before cSAH, their time course was not significantly different (P=0.11). ICH and cSAH occurred earlier than infarcts (P≤0.001), and ICH earlier than vasogenic edema (P=0.009). Angiogram analysis showed more severe vasoconstriction in distal versus proximal segments in all lesion types (ICH, cSAH, infarction, vasogenic edema, and normal scan). The isolated infarction group had more severe proximal vasoconstriction, and those with normal imaging had significantly less vasoconstriction. Multivariable analysis failed to uncover independent predictors of hemorrhagic RCVS; however, female sex predicted ICH (P=0.048), and angiographic severity predicted infarction (P=0.043). CONCLUSIONS: ICH and cSAH are common complications of RCVS. Triggers and risk factors do not predict lesion subtype but may alter central vasomotor control mechanisms resulting in centripetal angiographic evolution. Early distal vasoconstriction is associated with lobar ICH and cSAH, and delayed proximal vasoconstriction with infarction.

Reversible cerebral vasoconstriction syndromes and primary angiitis of the central nervous system: clinical, imaging, and angiographic comparison.

Reversible cerebral vasoconstriction syndromes (RCVS) and primary angiitis of the central nervous system (PACNS) are invariably considered in the differential diagnosis of new cerebral arteriopathies. However, prompt and accurate diagnosis remains challenging. Here we compared the features of 159 RCVS to 47 PACNS patients and developed criteria for prompt bedside diagnosis. Recurrent thunderclap headache (TCH), and single TCH combined with either normal neuroimaging, border zone infarcts, or vasogenic edema, have 100% positive predictive value for diagnosing RCVS or RCVS-spectrum disorders. In patients without TCH and positive angiography, neuroimaging can discriminate RCVS (no lesion) from PACNS (deep/brainstem infarcts). Ann Neurol 2016;79:882-894.

Gender and hormonal influences in reversible cerebral vasoconstriction syndrome.

INTRODUCTION: The reversible cerebral vasoconstriction syndromes, including postpartum angiopathy, have been characterized over the last decade. Women are predominantly affected. Some studies suggest that postpartum angiopathy carries a worse prognosis. PATIENTS AND METHODS: We compared the clinical, neuroimaging, and angiographic features of 36 men, 110 non-pregnant women and 16 postpartum women included in our single-center cohort of patients with reversible cerebral vasoconstriction syndromes encountered from 1998 to 2016. RESULTS: As compared to men, non-pregnant women were older (48 ± 11 vs. 34 ± 13 years, p < 0.001), had more underlying migraine (49% vs. 19%, p = 0.002), depression (53% vs. 14%, p < 0.001) and serotonergic antidepressant use (45% vs. 11%, p < 0.001), developed more clinical worsening (18% vs. 3%, p = 0.022), more infarcts (39% vs. 20%, p = 0.031) and worse angiographic severity scores (23 ± 14 vs. 10.9 ± 10.3, p < 0.001), but had similar discharge outcomes (modified Rankin scale scores 0-3, 90% vs. 91%, p = 0.768). Sexual activity was an important trigger in men (22% vs. 4%, p = 0.002). As compared to non-pregnant women, postpartum angiopathy patients were younger (33 ± 6 years, p < 0.001) and had less vasoconstrictive drug exposure (25% vs. 67%, p = 0.002) but showed similar clinical, radiological and angiographic findings and similar discharge outcomes (modified Rankin scale scores 0-3 in 94%, p = 0.633). There were no significant differences between pre- and post-menopausal women, or those with and without hysterectomy. DISCUSSION/CONCLUSION: The observed gender differences in reversible cerebral vasoconstriction syndromes may result from hormonal or non-hormonal factors. Hormonal imbalances may trigger reversible cerebral vasoconstriction syndromes. Given the absence of significant differences in the female subgroups, hormonal factors do not appear to significantly affect the course or outcome of reversible cerebral vasoconstriction syndromes.

Clot characteristics on computed tomography and response to thrombolysis in acute middle cerebral artery stroke.

BACKGROUND: Clinical and computer tomography angiography (CTA) correlates of hyperdense middle cerebral artery sign (HMCAS) and dot sign were revisited in patients treated for acute MCA stroke. Temporal evolution of these signs over 24 hours was assessed quantitatively by density (Hounsfield unit [HU]) measurements. METHODS: Maximum pixel-sized HUs throughout proximal MCA and its insular fissure branches were determined in 131 patients with acute MCA stroke treated by intravenous thrombolysis and/or interventional thrombolysis/thrombectomy; 14 patients treated for vertebrobasilar stroke (VBS) and 42 nonstroke control subjects. Utility of visually determined HMCAS and dot sign, absolute HU of proximal and distal MCA, side-to-side HU ratio and difference, and hyperdense MCA burden score for the prediction of early dramatic recovery (EDR) and third-month favorable prognosis were evaluated. The clinical value of the changes in vessel hyperdensity over 24 hours was identified in subjects who received intravenous thrombolysis (99 MCA stoke and 11 VBS). A multivariate model with adjustment for age, baseline stroke severity (National Institutes of Health Stroke Scale [NIHSS]), and CTA-based modified clot burden score (mCBS) was used to determine independent predictors of short- and long-term clinical outcome. RESULTS: The presence of HMCAS and dot sign, their density indices (maximum HU, ipsilateral-to-contralateral HU ratio, and difference), and changes in quantitative attenuation over 24 hours were not significantly associated with EDR and favorable third-month outcome in the multiple regression models, whereas NIHSS and mCBS were found to be significant independent "negative predictors" of both EDR and favorable prognosis, while age was a strong "negative indicator" only for 3-month good outcome. Average HU decrease over the first day was 5.7 HU in HMCAS (+) and 2.9 HU in dot sign (+) arteries. The densities of thrombi in MCA and insular branches were not different in subjects with and without cardioembolism. CONCLUSIONS: CTA provides dependable (high sensitivity and specificity) information regarding clot size and location, whereas hyperdense artery signs have low sensitivity and just acceptable specificity levels in this regard. However, the prognostic and diagnostic information generated by the presence of hyperdense artery signs and temporal change in attenuation can be useful in acute stroke settings where CTA is not readily available. Quantitative measures, rather than qualitative evaluation have a higher yield in determination of temporal change of the hyperdensity signs and its possible clinical correlates.

Transorbital Ultrasonographic Measurement of Optic Nerve Sheath Diameter in Brain Death.

BACKGROUND: Ultrasonographic measurement of optic nerve sheath diameter (ONSD) can successfully be used to estimate intracranial pressure (ICP) elevation. Its utility in corroboration of brain death (BD) was herein studied. METHODS: ONSD was measured in 29 subjects with BD; in 19 comatose patients (with raised ICP in 11), 20 patients with various neurological diseases, and 40 healthy control subjects. The distance between the inner and outer edges of the echolucent lines around hyperechoic area surrounding the optic nerve (ON) was identified as ONSD external (ONSDe) and ONSD internal (ONSDi). RESULTS: Compared to patients with neurological diseases (5.75 ± .79 mm) or healthy controls (5.98 ± .63 mm), ONSDe was significantly higher in comatose patients (7.61 ± .97 and 6.71 ± 1.07 mm in those with and without raised ICP) and BD subjects (8.34 ± .66 mm). ONSDi showed similar trends across the groups: 6.09 ± .71 mm in BD; 5.89 ± .37 mm in comatose control with elevated ICP; 5.16 ± .49 mm in comatose control with normal ICP; 4.36 ± .68 mm in neurological control; 4.69 ± .67 mm in healthy control. The accuracy of ONSDe measurements in differentiating patients with ICP elevation (n = 40) was .965 as determined by area under the curve (AUC) of receiver-operator characteristics curves. Similarly, accuracy in discrimination of BD was .952. However, ONSDe showed limited yield to identify BD cases among comatose patients with Glasgow coma scale score of 3, where accuracy was .803 (95% CI: .709-.816) and decreased further to .722 (95% CI: .610-.816) when analyses were restricted to comatose patients with ICP elevation. AUC values for ONSDi was similar or lower. CONCLUSION: ONSD is significantly greater in subjects with BD. However, quantification of ONSD cannot discriminate BD subjects from comatose ones with raised ICP with 100% certainty.

Ischemic stroke phenotype in patients with nonsustained atrial fibrillation.

BACKGROUND AND PURPOSE: The widespread use of ambulatory cardiac monitoring has not only increased the detection of high-risk arrhythmias like persistent and paroxysmal atrial fibrillation (AF), but also made it possible to identify other aberrations such as short-lasting (<30 seconds) irregular runs of supraventricular tachycardia. Ischemic stroke phenotype might be helpful in understanding whether these nonsustained episodes play a similar role in stroke pathophysiology like their persistent and paroxysmal counterparts. METHODS: In a consecutive series of patients with ischemic stroke, we retrospectively determined clinical and imaging features associated with nonsustained AF (n=126), defined as <30-second-lasting supraventricular tachyarrhythmias with irregular RR interval on 24-hour Holter monitoring, and compared them to patients with persistent/paroxysmal AF (n=239) and no AF (n=246). RESULTS: Patients with persistent/paroxysmal AF significantly differed from patients with nonsustained AF by a higher prevalence of female sex (odds ratio [95% confidence interval], 1.8 [1.1-2.9]), coronary artery disease (1.9 [1.1-3.0]), and embolic imaging features (2.7 [1.1-6.5]), and lower frequency of smoking (0.4 [0.2-0.8]) and hyperlipidemia (0.5 [0.3-0.8]). In contrast, patients with no AF were younger (0.5 [0.4-0.6] per decade) and more likely to be male (1.7 [1.0-2.8]) in comparison with nonsustained AF population. The prevalence of nonsustained AF was similar among cryptogenic and noncryptogenic stroke patients (32% versus 29%). Voxel-wise comparison of lesion probability maps revealed no significant difference between cryptogenic stroke patients with and without nonsustained AF. CONCLUSIONS: Clinical features of patients with nonsustained AF exhibited an intermediary phenotype in between patients with persistent/paroxysmal AF and no AF. Furthermore, imaging features did not entirely resemble patterns observed in patients with longer durations of AF.

The utility of middle cerebral artery clot density and burden assessment by noncontrast computed tomography in acute ischemic stroke patients treated with thrombolysis.

BACKGROUND: Quantitative and qualitative evaluation of middle cerebral artery (MCA) density, together with extent of thrombi, was assessed on plain computerized tomography (CT) to delineate better the prognostic value of the hyperdense MCA sign (HMCAS) in a cohort of patients who underwent intravenous or intra-arterial thrombolysis. METHODS: Density of MCA was quantified by maximum pixel-sized measurement of Hounsfield unit (HU) in 105 patients with acute MCA proximal segment occlusion, 15 patients with vertebrobasilar circulation stroke (VBS) and 44 nonstroke control subjects. Predictive value of HMCAS, absolute HU value of within MCA, side-to-side HU ratio, and difference along with a newly introduced hyperdense MCA burden score in early dramatic recovery (EDR) and third-month favorable prognosis were determined with multivariate adjustment for age, baseline stroke severity, and thrombus length as measured on CT angiography. Receiver operator characteristics (ROC) curves were used to determine the cutoffs of quantitative indices to determine HMCAS and their prognostic significance. RESULTS: Higher HU was present in the ipsilateral MCA of the patients compared with their contralateral side and basilar tip and any MCA of VBS stroke and control subjects (area under the curve [AUC] of ROC curves was .753). Symptomatic-to-asymptomatic HU difference and ratio of MCA stroke were also significantly higher than side-to-side difference calculated in VBS stroke and control groups (AUC of ROC curves: .770 and .764, respectively). Optimal thresholds of absolute HU (44), side-to-side HU difference (2), and ratio (1.0588) showed borderline sensitivity and specificity. HMCAS and its quantitative indices were not significantly associated with EDR and favorable third-month outcome. Furthermore, there was no difference in terms of cardioembolic and atherothrombotic thrombi HU. CONCLUSIONS: Utility of the HMCAS as a prognostic marker in stroke thrombolysis is not high in the CT angiography era. Previous observation regarding its positive prognostic role can be attributed to its association with proximal location and extent of clot burden, which are detectable reliably with current CT angiography techniques. Neither quantification nor extent of increased density seems to have clinical utility for treatment decision making in MCA strokes and prediction of emboli composition and response to recanalization attempt.

Differentiating reversible cerebral vasoconstriction syndrome with subarachnoid hemorrhage from other causes of subarachnoid hemorrhage.

IMPORTANCE: Reversible cerebral vasoconstriction syndrome (RCVS) is a clinical-angiographic syndrome characterized by recurrent thunderclap headaches and reversible segmental multifocal cerebral artery narrowing. More than 30% of patients with RCVS develop subarachnoid hemorrhage (SAH). Patients with RCVS with SAH (RCVS-SAH) are often misdiagnosed as having potentially ominous conditions such as aneurysmal SAH (aSAH) or cryptogenic "angiogram-negative" SAH (cSAH) owing to overlapping clinical and imaging features. OBJECTIVE: To identify predictors that can distinguish RCVS-SAH from aSAH and cSAH at the time of clinical presentation. DESIGN: Retrospective analysis of 3 patient cohorts: patients with RCVS (1998-2009), patients with aSAH (1995-2003), and patients with cSAH (1995-2003). SETTING: Academic hospital and tertiary referral center. PARTICIPANTS: Consecutive patients with RCVS-SAH (n = 38), aSAH (n = 515), or cSAH (n = 93) whose conditions were diagnosed using standard criteria. MAIN OUTCOMES AND MEASURES: Multivariate logistic regression analysis was used to identify predictors that differentiate RCVS-SAH from aSAH and cSAH. RESULTS: Predictors differentiating RCVS-SAH from aSAH were younger age, chronic headache disorder, prior depression, prior chronic obstructive pulmonary disease, lower Hunt-Hess grade, lower Fisher SAH group, higher number of affected arteries, and the presence of bilateral arterial narrowing. Predictors differentiating RCVS-SAH from cSAH were younger age, female sex, prior hypertension, chronic headache disorder, lower Hunt-Hess grade, lower Fisher SAH group, and the presence of bilateral arterial narrowing. CONCLUSIONS AND RELEVANCE: We identified important clinical and imaging differences between RCVS-SAH, aSAH, and cSAH that may be useful for improving diagnostic accuracy, clinical management, and resource utilization.

Aortic interruption presenting with recurrent ischemic strokes in an adult.

Presentation of an interrupted aortic arch (IAA) in adulthood is extremely rare. Nonhemorrhagic stroke has not been reported previously in any adult with IAA. We, herein, describe a formerly asymptomatic 52-year-old male presenting with recurrent vertebrobasilar circulation ischemic strokes resulting from accelerated atherosclerotic arteriopathy secondary to IAA associated upper body hypertension. Surgical correction of IAA led to treatment of hypertension and cessation of ischemic attacks together with regression of collateral arterial networks as shown by computer tomography angiography.

Reversible cerebral vasoconstriction syndromes: analysis of 139 cases.

OBJECTIVES: To compare the clinical, laboratory, and imaging features of patients with reversible cerebral vasoconstriction syndromes evaluated at 2 academic centers, compare subgroups, and investigate treatment effects. DESIGN: Retrospective analysis. SETTING: Massachusetts General Hospital (n = 84) or Cleveland Clinic (n = 55). PATIENTS: One hundred thirty-nine patients with reversible cerebral vasoconstriction syndromes. MAIN OUTCOME MEASURES: Clinical, laboratory, and imaging features; treatment; and outcomes. RESULTS: The mean age was 42.5 years, and 81% were women. Onset with thunderclap headache was documented in 85% and 43% developed neurological deficits. Prior migraine was documented in 40%, vasoconstrictive drug exposure in 42%, and recent pregnancy in 9%. Admission computed tomography or magnetic resonance imaging was normal in 55%; however, 81% ultimately developed brain lesions including infarcts (39%), convexity subarachnoid hemorrhage (34%), lobar hemorrhage (20%), and brain edema (38%). Cerebral angiographic abnormalities typically normalized within 2 months. Nearly 90% had good clinical outcome; 9% developed severe deficits; and 2% died. In the combined cohort, calcium channel blocker therapy and symptomatic therapy alone showed no significant effect on outcome; however, glucocorticoid therapy showed a trend for poor outcome (P = .08). Subgroup comparisons based on prior headache status and identified triggers (vasoconstrictive drugs, pregnancy, other) showed no major differences. CONCLUSION: Patients with reversible cerebral vasoconstriction syndromes have a unique set of clinical imaging features, with no significant differences between subgroups. Prospective studies are warranted to determine the effects of empirical treatment with calcium channel blockers and glucocorticoids.