Acute Cortical Stroke Research Articles

Abstract TP42: Risk of Acute Ischemic Stroke in Monocular Vision Loss of Vascular Etiology

Purpose: To evaluate the risk of concurrent acute cortical ischemic stroke in the setting of monocular vision loss of vascular etiology. Design: Retrospective and prospective, cross-sectional study. Subjects: Patients age 18 or older diagnosed with monocular vision loss of suspected or confirmed vascular etiology who had no other neurologic deficits and who received brain magnetic resonance imaging (MRI) within 7 days of onset of visual symptoms. Methods: Medical record review was performed from 2013-2016 at Yale-New Haven Hospital. Subjects were included if vision loss was unilateral, permanent or transient, and thought to be due to a vascular etiology such as central retinal artery occlusion (CRAO) or branch retinal artery occlusion (BRAO). Any subjects with neurologic deficits other than vision loss were excluded. Other exclusion criteria were positive visual phenomena, non-vascular intraocular pathology, and intracranial pathology other than ischemic stroke. Institutional Review Board/Ethics Committee approval was obtained. Main Outcome Measures: Presence or absence of acute cortical stroke on diffusion weighted imaging (DWI) sequence on brain MRI. Results: A total of 641 records were reviewed, with 293 subjects found to have monocular vision loss. After excluding subjects with focal neurologic deficits, there were 41 subjects who met inclusion criteria and received a brain MRI. 8 of the 41 subjects (19.5%) were found to have brain MRI positive for acute cortical strokes. The proportion of lesion positive MRI was 1/23 (4.3%) in transient monocular vision loss subjects, 4/12 (33.3%) in patients with CRAO, and 2/5 (40%) in BRAO. Conclusions: Patients with transient or permanent monocular vision loss of vascular etiology such as CRAO or BRAO may have up to 19.5% risk of concurrent cortical ischemic stroke, even when there are no other neurologic deficits. This highlights the importance of urgent stroke evaluation in this patient population.

Event-related desynchronization of sensorimotor EEG rhythms in hemiparetic patients with acute stroke

Previous neuroimaging studies based on neurovascular coupling have shown that stroke affects both, strength and spatial extent of brain activation during upper limb movements. Here, we investigated the sub-second amplitude dynamics of a direct neuronal measure, i.e., event-related desynchronization (ERD) of EEG oscillations during finger movements, in patients with acute cortical and subcortical stroke. Acute cortical strokes were found to decrease the ERD of alpha oscillations for the affected pericentral sensorimotor areas compared to a control group. Within the cortical stroke group, the affected hemisphere showed a smaller alpha-ERD compared to the unaffected hemisphere when each was contralateral to the acting hand. Furthermore, when cortical stroke patients moved their paretic hand, the ipsilateral (i.e., contralesional) alpha-ERD was stronger than the contralateral (ipsilesional) ERD. Interestingly, the alpha-ERD amplitude in a hemisphere with a cortical stroke was relatively well preserved for non-paretic hand movements compared to alpha-ERD amplitude for paretic hand movements. This finding provides a new perspective for assessing the rehabilitative potential, which could be utilized through training of the still responsive cortical network, e.g., via enforced use of the paretic hand.

Cardiac chronotropic organization of the rat insular cortex

Clinical evidence implicates the cerebral cortex in the genesis of ECG changes and cardiac arrhythmias. Such findings are not infrequent following acute cortical stroke and during partial seizures. Electrical stimulation of the cerebral cortex, however, only rarely and inconsistently results in cardiac changes. When encountered, attendant alterations in blood pressure and respiration occur; consequently, it is unclear whether the cardiac effects are primary or secondary to these. Phasic insular cortex microstimulation linked to the ECG cycle, a new technique, elicits only heart rate effects, eliminating confounding variables. The insular cortex was chosen for study because of its profuse autonomic and limbic connectivity. Cardiac chronotropic sites were demonstrated in 37 chloralose-anesthetized rats, with tachycardia represented in the rostral posterior insula, and bradycardia in the caudal posterior insula. Both effects were abolished by atenolol but not by atropine, implying their mediation by respective increases or decreases in sympathetic activity. This is the first report of the demonstration of a cortical region wherein stimulation affects heart rate and no other parameter.