Iodine-stained fragmented thromboembolism.

AIM: Iodine-stained fragmented thromboembolism (ISFT) is a rare phenomenon encountered in the immediate aftermath of mechanical thrombectomy or rarely as a complication of post-carotid stenting. The aim was to describe the imaging appearance and discuss its pathophysiology. METHOD: This is a retrospective review of patients who underwent mechanical thrombectomy for acute stroke at a single institution over the period of one year. All patients underwent the standard acute stroke imaging protocol (CT head, CT angiogram (CTA) and CT brain perfusion) and when clinically appropriate followed by catheter angiogram and mechanical thrombectomy. ISFT was defined as an arterial luminal filling defect with Hounsfield density equal to or greater than iodine seen on the biplanar CT or conventional CT. The presence and location of ISFT were documented. Standard CT angiogram (CTA) or magnetic resonance angiogram (MRA) was performed 24-48 hours after the neurointerventional procedure to assess for recanalization, volume of infarction and the fate of the ISFT. RESULTS: ISFTs were identified in eight (five males and three females, age range 18-80 years) out of 49 patients in the following locations: distal M1 (n = 1), M2 (n = 4), M3 (n = 1), A1 (n = 1), distal A2 (n = 1). ISFT and vessel recanalization occurred in five patients on follow-up. ISFT and vessel occlusion persisted in two patients. CONCLUSION: ISFT is likely the result of mechanical disruption of a thromboembolus, and porosity of the thromboembolus fragment may transiently retain iodinated contrast. Recognition of this entity may be important to aid detection of residual thromboembolism and avoid misinterpretation as calcified thromboembolism.

Acute treatment with the 5-HT(1A) receptor agonist 8-OH-DPAT and chronic environmental enrichment confer neurobehavioral benefit after experimental brain trauma.

Acute treatment with the 5-HT(1A) receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) or chronic environmental enrichment (EE) hasten behavioral recovery after experimental traumatic brain injury (TBI). The aim of this study was to determine if combining these interventions would confer additional benefit. Anesthetized adult male rats received either a cortical impact or sham injury followed 15min later by a single intraperitoneal injection of 8-OH-DPAT (0.5mg/kg) or saline vehicle (1.0mL/kg) and then randomly assigned to either enriched or standard (STD) housing. Behavioral assessments were conducted utilizing established motor and cognitive tests on post-injury days 1-5 and 14-18, respectively. Hippocampal CA(1)/CA(3) neurons were quantified at 3 weeks. Both 8-OH-DPAT and EE attenuated CA(3) cell loss. 8-OH-DPAT enhanced spatial learning in a Morris water maze (MWM) as revealed by differences between the TBI+8-OH-DPAT+STD and TBI+VEHICLE+STD groups (P=0.0014). EE improved motor function as demonstrated by reduced time to traverse an elevated narrow beam in both the TBI+8-OH-DPAT+EE and TBI+VEHICLE+EE groups versus the TBI+VEHICLE+STD group (P=0.0007 and 0.0016, respectively). EE also facilitated MWM learning as evidenced by both the TBI+8-OH-DPAT+EE and TBI+VEHICLE+EE groups locating the escape platform quicker than the TBI+VEHICLE+STD group (P's<0.0001). MWM differences were also observed between the TBI+8-OH-DPAT+EE and TBI+8-OH-DPAT+STD groups (P=0.0004) suggesting that EE enhanced the effect of 8-OH-DPAT. However, there was no difference between the TBI+8-OH-DPAT+EE and TBI+VEHICLE+EE groups. These data replicate previous results from our laboratory showing that both a single systemic administration of 8-OH-DPAT and EE improve recovery after TBI and extend those findings by elucidating that the combination of treatments in this particular paradigm did not confer additional benefit. One explanation for the lack of an additive effect is that EE is a very effective treatment and thus there is very little room for 8-OH-DPAT to confer additional statistically significant improvement.