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ObjectiveWhile clinical benefit from thrombolysis decreases with increase in time from stroke onset, the relationship of acute physiologic tissue compartments and collateral response to stroke onset time remains unclear.MethodsWe studied consecutive patients with proximal arterial occlusions (n = 355) with whole-brain perfusion CT with CT angiography within 6 hours of stroke onset. Penumbra and core were defined using voxel-based thresholds. Tissue mismatch was defined as the ratio of penumbra to core. Collateral scores were assessed using a previously validated visual score.ResultsMean (SD) age was 72.1 (12.4) years, median (interquartile range) NIH Stroke Scale score 16 (4), mean (SD) time to imaging 152.5 (69.7) minutes. Penumbra volume (Spearman ρ = 0.119, p = 0.026) and mismatch increased (Spearman ρ = 0.115, p = 0.030) with time from onset. Core volume decreased (Spearman ρ = −0.112, p = 0.035) while collateral scores increased with time (Spearman ρ = 0.117, p = 0.028). On multivariable regression, good collateral scores predicted longer time since onset (β = 0.101, p = 0.039) while mismatch was not a predictor (β = 0.001, p = 0.351). Good collateral score was the strongest independent predictor of final infarct volume and improvement in clinical deficit.ConclusionsIn our large patient cohort study of proximal arterial occlusions, we found an incremental collateral response and preserved penumbral volume with time. Thus, tissue viability can be maintained in this time window (0–6 hours) after stroke if leptomeningeal collaterals are able to sustain the penumbra. Our findings suggest that a longer therapeutic window may exist for intra-arterial intervention and that multimodal imaging may have a role in strokes of unknown onset time.

{#article-title-2} To the Editor: We read with interest the article by Larrue et al.1 We recently assessed the impact of newer stroke classification systems on stroke subtypes.2 We also agree with the conclusion regarding the contribution of atrial septal abnormalities to stroke in younger people. Despite the thorough cardiac investigation, Larrue et al. report a relatively low proportion of patients with unexplained stroke with patent foramen ovale (PFO). Of 160 cases investigated, 67 (41.2%) had a PFO (24 isolated, 43 with an atrial septal aneurysm [ASA]). In our institution, of those with …

Objective: We report an unusual case of a dominant hemisphere, medial occipital and medial temporal cortical infarction precipitating Korsakoff9s psychosis and a disinhibition syndrome, reminiscent of a frontal lobe phenotype. A 66 year-old, right handed man, while driving to watch the Monaco Grand Prix, developed acute headache and amnesia accompanied by emotional lability, disinhibited behavior, inappropriate laughter and a right homonymous hemianopia. He had deficits in both episodic and working memory, a mild degree of executive dysfunction and a tendency to confabulate. There were no other focal neurological signs. He had been well previously, except for moderately high alcohol consumption. The cognitive deficits persisted 6 months after presentation, despite thiamine replacement. Acute imaging demonstrated restricted diffusion in the medial occipital and temporal lobes involving the fusiform and parahippocampal gyri with sparing of thalamus and other deeper structures. The rest of the parenchymal structures were normal and there was no evidence of small vessel ischaemia. An occlusion of P2 segment of the left posterior cerebral artery and its cortical branches was seen on vascular imaging. Cognitive deficits associated with posterior cerebral artery infarctions include a constellation of behavioural symptoms including transcortical aphasia, alexia without agraphia, Gerstmann syndrome, episodic memory deficit, visual agnosia, prosopagnosia and rarely acute delirium with/without aggressive behavior. Disinhibition syndromes of frontal phenotype have rarely been reported and may be associated with cortical deafferentation following a non-dominant thalamic lesion. This case demonstrates that behavioural deficits after cortical PCA territory infarction are not restricted to memory, language and vision and may occur without thalamic involvement. We hypothesise that the Korsakoff9s syndrome may have been the result of a functional disruption of mamillothalamic connections, as previously described, whereas the frontal behavioural features may be caused by a disruption of occipito temporal and occipito frontal connectivity. Disclosure: Dr. Agarwal has nothing to disclose. Dr. Manford has received personal compensation for activities with UCB Pharma and Eisai.