Abstract

PurposeIpsilateral thalamic diaschisis (ITD) refers to the phenomenon of thalamic hypoperfusion or hypometabolism due to a distant cerebral injury. To further investigate the characteristics and spectrum of ITD, we analyzed quantitative measurements of thalamic hypoperfusion in acute anterior circulation stroke. MethodsWe selected consecutive patients with large-vessel occlusion (LVO) anterior circulation stroke and available CT perfusion (CTP) examination on admission who underwent endovascular thrombectomy. Thalamic perfusion parameters on CTP were tested between ipsi- and contralesional thalamus and ischemic territory. Values were compared with thresholds from CTP analysis software. Associations of thalamic perfusion parameters with acute imaging and clinical data were determined in uni- and multivariate logistic regression analyses. ResultsNinety-nine patients were included. All perfusion parameters indicated significant non-ischemic hypoperfusion of the thalamus, not reaching the levels of ischemia in the middle cerebral artery territory due to LVO (all p < 0.002). Multiple perfusion parameters exhibited significant association with ischemic lesion extent (relative cerebral blood flow [CBF]: β = − 0.23, p = 0.022; Δtime to drain: β = 0.33, p < 0.001; ΔTmax: β = − 0.36, p < 0.001) and involvement of the Lentiform Nucleus (Δmean transit time: β = 0.64, p = 0.04; Δtime to drain: β = 0.81, p = 0.01; ΔTmax: β = − 0.82, p = 0.01). Symptom severity on admission exhibited minor significant association with reduction of thalamic CBF in uncorrected analysis (Odds ratio: 0.05, p = 0.049), but short- and long-term outcomes were unaffected by perfusion status. ITD reached guideline-based software-threshold levels in only one patient. ConclusionsITD in acute stroke is a non-binary phenomenon affected by lesion extent and involvement of the lentiform nucleus. We found uncorrected association of ITD with early clinical presentation, but no association with short- or long-term outcome was evident. Relevant misclassification of ITD by guideline-based CTP software was not indicated, which needs further dedicated testing.

Highlights

  • Ipsilateral thalamic diaschisis (ITD) refers to the phenomenon of thalamic hypoperfusion, hypometabolism, hypofunction and loss of volume ipsilateral to a distant cerebral injury. (Carrera and Tononi, 2014) ITD is especially known to occur due to supratentorial cerebrovascular injury (Fiorelli et al, 1991; Ogawa et al, 1997; Sakashita et al, 1993; De Reuck et al, 1995; Craig et al, 2019; Hendrik, 2020)

  • Numerous studies established the use of positron emission tomography (PET) or magnet resonance imaging (MRI) to examine diaschisis phenomena, predominantly in later phases (Baron et al, 1981; Sebok et al, 2018)

  • All parameters indicate significant hypoperfusion of the ipsilesional thalamus compared to the contralesional side with reduction of cerebral blood flow (CBF) and cerebral blood volume (CBV) (p < 0.001) and elevation of MTT (p = 0.001), TTD and TMAX

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Summary

Introduction

Ipsilateral thalamic diaschisis (ITD) refers to the phenomenon of thalamic hypoperfusion, hypometabolism, hypofunction and loss of volume ipsilateral to a distant cerebral injury. (Carrera and Tononi, 2014) ITD is especially known to occur due to supratentorial cerebrovascular injury (Fiorelli et al, 1991; Ogawa et al, 1997; Sakashita et al, 1993; De Reuck et al, 1995; Craig et al, 2019; Hendrik, 2020). Ipsilesional thalamic hypoperfusion and hypometabolism can be found in the acute (Reidler et al, 2018), subacute (Fiorelli et al, 1991; Sakashita et al, 1993; Hendrik, 2020) and chronic (De Reuck et al, 1995) phase of stroke. Numerous studies established the use of positron emission tomography (PET) or magnet resonance imaging (MRI) to examine diaschisis phenomena, predominantly in later phases (Baron et al, 1981; Sebok et al, 2018) Alongside these modalities, 4-dimensional, dynamic CT perfusion (CTP), as used in critical stroke care, advanced the visualization of diaschisis phenomena to the acute stroke phase by sampling contrast enhancement dynamics of brain tissue (Sommer et al, 2016; Kunz et al, 2017; Reidler et al, 2018)

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