CPSP patients present with diverse sensory symptoms and its pathophysiology is still poorly understood. Amitriptyline and lamotrigine are effective treatments. Further studies are needed to understand the pathophysiology and investigate newer therapeutic modalities.

C erebral vasospasm is a major cause of poor outcomes in aneurysmal subarachnoid hemorrhage (aSAH), resulting in cerebral ischemia, infarction, disability, and death. 20,25 Cerebral vasospasm is noted on angiography in as many as 70% of patients following aSAH and is predicted by high mean flow velocities (MFVs) on transcranial Doppler (TCD) ultrasonography. 19,24,26,35 Vasospasm is strongly associated with delayed cerebral ischemia (DCI) 12 and cerebral infarction, 11,39,49 although poor outcomes can still occur in its absence. Of the current techniques available for diagnosing cerebral vasospasm, catheter angiography and CT angiography are invasive, and require contrast-dye injection and radiation exposure, and therefore do not allow dynamic monitoring of vasospasm. 31The radiation exposure and invasive nature of angiography implies that it is not useful for identifying subclinical vasospasm prior to the onset of the condition, and that its use is frequently restricted to confirm prevalent vasospasm abbreviatioNs aSAH = aneurysmal subarachnoid hemorrhage; CI = confidence interval; DCI = delayed cerebral ischemia; df = degrees of freedom; MFV = mean flow velocity; MWE = mean weighted estimate; NPV = negative predictive value; PPV = positive predictive value; TCD = transcranial Doppler. obJective The impact of transcranial Doppler (TCD) ultrasonography evidence of vasospasm on patient-centered clinical outcomes following aneurysmal subarachnoid hemorrhage (aSAH) is unknown. Vasospasm is known to lead to delayed cerebral ischemia (DCI) and poor outcomes. This systematic review and meta-analysis evaluates the predictive value of vasospasm on DCI, as diagnosed on TCD. methods MEDLINE, Scopus, the Cochrane trial register, and clinicaltrials.gov were searched through September 2014 using key words and the terms "subarachnoid hemorrhage," "aneurysm," "aneurysmal," "cerebral vasospasm," "vasospasm," "transcranial Doppler," and "TCD." Sensitivities, specificities, and positive and negative predictive values were pooled by a DerSimonian and Laird random-effects model. results Seventeen studies (n = 2870 patients) met inclusion criteria. The amount of variance attributable to heterogeneity was significant (I 2 > 50%) for all syntheses. No studies reported the impact of TCD evidence of vasospasm on functional outcome or mortality. TCD evidence of vasospasm was found to be highly predictive of DCI. Pooled estimates for TCD diagnosis of vasospasm (for DCI) were sensitivity 90% (95% confidence interval [CI] 77%-96%), specificity 71% (95% CI 51%-84%), positive predictive value 57% (95% CI 38%-71%), and negative predictive value 92% (95% CI 83%-96%). coNclusioNs TCD evidence of vasospasm is predictive of DCI with high accuracy. Although high sensitivity and negative predictive value make TCD an ideal monitoring device, it is not a mandated standard of care in aSAH due to the paucity of evidence on clinically relevant outcomes, despite recommendation by national guidelines. High-quality randomized trials evaluating the impact ...

Recanalization of acute BAO leads to reduction in mortality by two-fold and reduction in the risk of DoD by 1.5-fold. This study underscores the equipoise in acute BAO for comparing systemic and endovascular therapies, and testing different time windows through RCTs.

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Background and Purpose Penumbral biomarkers promise to individualize treatment windows in acute ischemic stroke. We used a novel MRI approach which measures oxygen metabolic index (OMI), a parameter closely related to PET-derived cerebral metabolic rate of oxygen utilization, to derive a pair of ischemic thresholds: (1) an irreversible-injury threshold which differentiates ischemic core from penumbra and (2) a reversible-injury threshold which differentiates penumbra from tissue not-at-risk for infarction. Methods Forty acute ischemic stroke patients underwent MRI at three time-points after stroke onset: < 4.5 hours (for OMI threshold derivation), 6 hours (to determine reperfusion status), and 1 month (for infarct probability determination). A dynamic susceptibility contrast method measured CBF, and an asymmetric spin echo sequence measured OEF, to derive OMI (OMI=CBF*OEF). Putative ischemic threshold pairs were iteratively tested using a computation-intensive method to derive infarct probabilities in three tissue groups defined by the thresholds (core, penumbra, and not-at-risk tissue). An optimal threshold pair was chosen based on its ability to predict: infarction in the core, reperfusion-dependent survival in the penumbra, and survival in not-at-risk tissue. The predictive abilities of the thresholds were then tested within the same cohort using a 10-fold cross-validation method. Results The optimal OMI ischemic thresholds were found to be 0.28 and 0.42 of normal values in the contralateral hemisphere. Using the 10-fold cross-validation method, median infarct probabilities were 90.6% for core, 89.7% for non-reperfused penumbra, 9.95% for reperfused penumbra, and 6.28% for not-at-risk tissue. Conclusions OMI thresholds, derived using voxel-based, reperfusion-dependent infarct probabilities, delineated the ischemic penumbra with high predictive ability. These thresholds will require confirmation in an independent patient sample.

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