Delayed cerebral atrophy after cerebellar stroke: topographical relation and clinical impact

• Published in: Brain communications 2021-10, Vol.3 (4), p.fcab279-fcab279
• Main Authors: van Niftrik, Christiaan H B, Visser, Thomas F, Sebök, Martina, Muscas, Giovanni, El Amki, Mohamad, Serra, Carlo, Regli, Luca, Wegener, Susanne, Fierstra, Jorn
• Format: Article
• Language: English
• Subjects: Original
• ISSN: 2632-1297; 2632-1297
• DOI: 10.1093/braincomms/fcab279

Abstract Remote dysconnectivity following cerebellar ischaemic stroke may have a negative impact on supratentorial brain tissue. Since the cerebellum is connected to the individual cerebral lobes via contralateral tracts, cerebellar lesion topography might determine the distribution of contralateral supratentorial brain tissue changes. We investigated (i) the occurrence of delayed cerebral atrophy after cerebellar ischaemic stroke and its relationship to infarct volume; (ii) whether cerebellar stroke topography determines supratentorial atrophy location; and (iii) how cortical atrophy after cerebellar stroke impacts clinical outcome. We performed longitudinal volumetric MRI analysis of patients with isolated cerebellar stroke from the Swiss Stroke Registry database. Stroke location and volume were determined at baseline MRI. Delayed cerebral atrophy was measured as supratentorial cortical volumetric change at follow-up, in contralateral target as compared to ipsilateral reference-areas. In patients with bilateral stroke, both hemispheres were analysed separately. We obtained maps of how cerebellar lesion topography, determines the probability of delayed atrophy per distinct cerebral lobe. Clinical performance was measured with the National Institutes of Health Stroke Scale and modified Rankin Scale. In 29 patients (age 58 ± 18; 9 females; median follow-up: 6.2 months), with 36 datasets (7 patients with bilateral cerebellar stroke), delayed cerebral atrophy occurred in 28 (78%) datasets. A multivariable generalized linear model for a Poisson distribution showed that infarct volume (milliliter) in bilateral stroke patients was positively associated with the number of atrophic target areas (Rate ratio = 1.08; P = 0.01). Lobe-specific cerebral atrophy related to distinct topographical cerebellar stroke patterns. By ordinal logistic regression (shift analysis), more atrophic areas predicted higher 3-month mRS scores in patients with low baseline scores (baseline score 3–5: Odds ratio = 1.34; P = 0.02; baseline score 0–2: OR = 0.71; P = 0.19). Our results indicate that (i) isolated cerebellar ischaemic stroke commonly results in delayed cerebral atrophy and stroke volume determines the severity of cerebral atrophy in patients with bilateral stroke; (ii) cerebellar stroke topography affects the location of delayed cerebral atrophy; and (iii) delayed cerebral atrophy negatively impacts clinical outcome. Van Niftrik et al. show that cerebellar stroke commonly resul