The dual origin of lexical perseverations in aphasia: Residual activation and incremental learning

Lexical perseveration, the inappropriate repetition of a previous response, is common in aphasia. Two underlying mechanisms have been proposed: residual activation and incremental learning. Previous attempts to differentiate the two have relied on experimental paradigms that encourage semantically related errors and analysis techniques designed to detect perseverations over short distances, resulting in a bias towards detecting short-lag, semantically related perseverations that both mechanisms can account for. Two key predictions that differentiate these accounts remain untested: only residual activation can explain short-lag, semantically unrelated perseverations, whereas only incremental learning can explain long-lag, semantically related perseverations. In this paper, we used a large set of picture naming trials and a novel analysis technique to test these key predictions in a multi-session study involving six individuals with aphasia. We found clear evidence for both mechanisms in different individuals, demonstrating that either one is sufficient to cause perseveration. Importantly, perseverations due to residual activation were associated with more severely impaired systems than those due to incremental learning, suggesting that a certain degree of structural and functional integrity was necessary for incremental learning. Finally, the results supported a key prediction of the incremental learning account by showing perseverations over longer lags than have previously been reported.

Effect of antiplatelet therapy on thromboembolism after flow diversion with the Pipeline Embolization Device

Object Flow-diverting stents offer a novel treatment approach to intracranial aneurysms. Data regarding the incidence of acute procedure-related thromboembolic complications following deployment of the Pipeline Embolization Device (PED) remain scant. The authors sought to determine the rate of embolic events in a bid to identify potential risk factors and assess the role of platelet inhibition. Methods Data in all patients receiving a PED for treatment of an intracranial aneurysm were prospectively maintained in a database. Diffusion-weighted 3-T MRI was performed within 24 hours of PED deployment. The incident rate of procedural embolism was established, and univariate analysis was then performed to determine any associations of embolic events with measured variables. The degree of platelet inhibition in response to aspirin and clopidogrel was evaluated by challenging the platelet samples with arachidonic acid and adenosine diphosphate, respectively, and then performing formal light transmission platelet aggregometry. Results Twenty-three patients with 26 aneurysms were eligible for inclusion in the study. Thirty-one PEDs were deployed in 25 procedures. All ischemic lesions detected on diffusion-weighted 3-T MRI were identified as embolic based on their location and distribution, with none appearing to be due to perforator artery occlusion. Procedural embolic events were found in the target parent vessel territory in 13 (52%) of 25 procedures, with no patients harboring lesions contralateral to the deployed PED. The number of embolic events per procedure ranged from 3 to 16, with a mean of 5.4. There was no significant difference between cases with and without procedural embolism in platelet inhibition by aspirin (mean 15% vs 12% residual activation; p = 0.28), platelet inhibition by clopidogrel (mean 41% vs 41% residual activation; p = 0.98), or intraprocedural heparin-induced anticoagulation (mean activated clotting time 235 seconds vs 237 seconds; p = 0.81). By multivariate analysis, the authors identified larger aneurysm size (p = 0.03) as the single variable significantly associated with procedural embolism. There was no significant relationship between aneurysm size and the number of embolic events (p = 0.32) or the total burden of the embolism lesion area (p = 0.53). Conclusions Acute embolism following use of the PED for treatment of intracranial aneurysms is more common than hypothesized. The only identifiable risk factor for embolism appears to be greater aneurysm size, perhaps indicating significant disturbed flow across the aneurysm neck with ingress and egress through the PED struts. The strength of antiplatelet therapy, as measured by residual platelet aggregation, did not appear to be associated with cases of procedural embolism. Further work is needed to determine the implications of these findings and whether anticoagulation regimens can be altered to lower the rate of complications following PED deployment.