Do patients with large vessel occlusion ischemic stroke harboring prestroke disability benefit from thrombectomy?

OBJECTIVES: Evidence of endovascular treatment (EVT) for acute large vessel occlusion (LVO) ischemic stroke in patients harboring substantial prestroke disability is lacking due to their exclusion from randomized trials. Here, we used routine care observational data to compare outcomes in patients with and without prestroke disability receiving EVT for LVO ischemic stroke. METHODS: Consecutive patients undergoing EVT for acute LVO ischemic stroke at the Sahlgrenska University Hospital from January 1st, 2015 to March 31st, 2018 were registered in the Sahlgrenska Stroke Recanalization Registry. Pre- and poststroke functional levels were assessed by the modified Rankin Scale (mRS). Outcomes were recanalization rate (mTICI = 2b/3), symptomatic intracranial hemorrhage [sICH], complications during hospital stay, and return to prestroke functional level and mortality at 3 months. RESULTS: Among 591 patients, 90 had prestroke disability (mRS ≥ 3). The latter group were older, more often female, had more comorbidities and higher NIHSS scores before intervention compared to patients without prestroke disability. Recanalization rates (80.0% vs 85.0%, p = 0.211), sICH (2.2% vs 6.3% p = 0.086) and the proportion of patients returning to prestroke functional level (22.7% vs 14.8% p = 0.062) did not significantly differ between those with and without prestroke disability. Patients with prestroke disability had higher complication rates during hospital stay (55.2% vs 40.1% p < 0.01) and mortality at 3 months (48.9% vs 24.3% p < 0.001). CONCLUSION: One of five with prestroke disability treated with thrombectomy for a LVO ischemic stroke returned to their prestroke functional level. However, compared to patients without prestroke disability, mortality at 3 months was higher.

Role of sympathetic nervous system in activity-induced cerebral perfusion.

Several studies have suggested that autonomic neural control plays a role in regulation of cerebral blood flow (CBF), although the exact role of the sympathetic nervous system on CBF remains debated. The effects of sympathetic innervation on activity-induced cerebral perfusion changes in humans have not been studied. The aims of this study were therefore (a) to investigate patients with an "intrinsic" sympathetic deficit after stroke and healthy controls with regard to activity-induced cerebral perfusion changes, and (b) to investigate possible differences in functional CBF regulation between the anterior and posterior circulation. Cerebral blood flow velocity in the medial cerebral artery (MCA) and posterior cerebral artery (PCA) was investigated in 21 healthy controls and 17 patients with Wallenberg's syndrome using transcranial Doppler sonography during cortical activation of MCA and PCA territories, respectively. Patients with a central sympathetic deficit had a prolonged decrease of resistance in the MCA and showed a slower and less pronounced decrease of resistance in the PCA upon cortical activation. No difference was observed between the side with and without sympathetic deficit. Results suggest that (a) sympathetic efferents are involved in economisation of activity-induced changes of cerebral perfusion in the anterior circulation, (b) activity-induced sympathetic regulation of blood flow differs between the anterior and posterior vascular territories in humans and (c) a possible resting sympathetic tonus on extraparenchymal vessel might exist in the posterior circulation.

Effect of sympathetic muscle vasoconstrictor activity on capsaicin-induced muscle pain.

Neuropathic pain syndromes with sympathetically maintained pain are often associated with a deep somatic pain component. An adrenergic interaction between sympathetic vasoconstrictor neurons and cutaneous afferents has been demonstrated. To determine whether a sympathetic-afferent interaction exists in deep somatic tissues, we investigated the effect of sympathetic muscle vasoconstrictor activity on experimentally induced pain. In 12 healthy volunteers, capsaicin was infused into the anterior tibial muscle. Intensity and quality of muscle and referred pain were assessed. The analyses were performed during the presence of low sympathetic muscle vasoconstrictor activity induced by breathing 100% O(2) gas (normocapnia), and during high activity induced by inspiration of 95% O(2) and 5% CO(2) (hypercapnia). The degree of sympathetic muscle vasoconstrictor discharge was monitored indirectly by measuring systemic blood pressure and end-expiratory CO(2) and by performing duplex sonography of muscle resistance vessels. The intensity, quality, and spatial distribution of muscle and referred pain were not significantly different during resting and increased sympathetic muscle vasoconstrictor discharge, indicating that such activity does not influence pain after intramuscular infusion of capsaicin.