Arterial Collapse during Thrombectomy for Stroke: Clinical Evidence and Experimental Findings in Human Brains and In Vivo Models.

BACKGROUND AND PURPOSE: Aspiration thrombectomy has become a preferred approach to recanalize large-vessel occlusion in stroke with a growing trend toward using larger-bore catheters and stronger vacuum pumps. However, the mechanical response of the delicate cerebral arteries to aspiration force has not been evaluated. Here, we provide preclinical and clinical evidence of intracranial arterial collapse in aspiration thrombectomy. MATERIALS AND METHODS: We presented a clinical case of arterial collapse with previously implanted flow diverters. We then evaluated the effect of vacuum with conventional aspiration catheters (with and without stent retrievers) in a rabbit model (n = 3) using fluoroscopy and intravascular optical coherence tomography. Then, in a validated human cadaveric brain model, we conducted 168 tests of direct aspiration thrombectomy following an experimental design modifying the catheter inner diameter (0.064 inch, 0.068 inch, and 0.070 inch), cerebral perfusion pressures (mean around 60 and 90 mm Hg), and anterior-versus-posterior circulation. Arterial wall response was recorded and graded via direct transluminal observation. RESULTS: Arterial collapse was observed in both the patient and preclinical experimental models. In the human brain model, arterial collapse was observed in 98% of cases in the M2 and in all the cases with complete proximal flow arrest. A larger bore size of the aspiration catheter, a lower cerebral perfusion pressure, and the posterior circulation in comparison with the anterior circulation were associated with a higher probability of arterial collapse. CONCLUSIONS: Arterial collapse does occur during aspiration thrombectomy and is more likely to happen with larger catheters, lower perfusion pressure, and smaller arteries.

A Thrombectomy Model Based on Ex Vivo Whole Human Brains.

BACKGROUND AND PURPOSE: The persistent challenges in thrombectomy for large-vessel occlusion, such as suboptimal complete recanalization and first-pass effect imply an insufficient understanding of the artery-clot-device interaction. In this study, we present a thrombectomy model using fresh human brains, which can capture the artery-clot-device interaction through concurrent transmural and angiographic visualizations. MATERIALS AND METHODS: Fresh nonfrozen whole adult human brains were collected and connected to a customized pump system tuned to deliver saline flow at a physiologic flow rate and pressure. Angiography was performed to verify the flow in the anterior-posterior and vertebrobasilar circulations and collaterals. Large-vessel occlusion was simulated by embolizing a radiopaque clot analog. Thrombectomy was tested, and the artery-clot-device interactions were recorded by transmural and angiographic videos. RESULTS: Baseline cerebral angiography revealed excellent penetration of contrast in the anterior-posterior and vertebrobasilar circulations without notable arterial cutoffs and with robust collaterals. Small branches (<0.5 mm) and perforating arteries were consistently opacified with good patency. Three device passes were performed to achieve recanalization, with failure modes including elongation, fragmentation, and distal embolization. CONCLUSIONS: This model enables concurrent transmural and angiographic analysis of artery-clot-device interaction in a human brain and provides critical insights into the action mechanism and failure modes of current and upcoming thrombectomy devices.

Multifocal motor sensory demyelinating neuropathy: inflammatory demyelinating polyradiculoneuropathy.

The authors present two cases that provide the first autopsy findings in multifocal acquired demyelinating sensory and motor neuropathy (MADSAMN). Both cases documented multifocal but asymmetric demyelinating neuropathy with rare axonal degeneration. One case clearly documented an inflammatory polyradiculoplexoneuropathy, confirming the inflammatory nature of this neuropathy. This study showed that MADSAMN is an inflammatory demyelinating polyradiculoneuropathy that shares histologic features observed in chronic inflammatory demyelinating polyradiculoneuropathy and multifocal motor neuropathy (MMN), suggesting a similar immunopathogenesis for these entities.