Cortical Thickness of Brain Areas Beyond Stroke Lesions and Sensory-Motor Recovery: A Systematic Review

 Useless, absolutely nothing on how to recover, knowing cortical thickness does nothing at all. The mentors and senior researchers need remedial training on the only goal in stroke; 100% recovery.

Cortical Thickness of Brain Areas Beyond Stroke Lesions and Sensory-Motor Recovery: A Systematic Review

Anna Maria Cortese^1*, Luisa Cacciante¹, Anna-Lisa Schuler², Andrea Turolla¹ and Giovanni Pellegrino²

• ¹Laboratory of Rehabilitation Technologies, San Camillo Istituto di Ricovero e Cura a Carattere Scientifico, Venice, Italy
• ²Laboratory of Clinical Imaging and Stimulation, San Camillo Istituto di Ricovero e Cura a Carattere Scientifico, Venice, Italy

Background: The clinical outcome of patients suffering from stroke is dependent on multiple factors. The features of the lesion itself play an important role but clinical recovery is remarkably influenced by the plasticity mechanisms triggered by the stroke and occurring at a distance from the lesion. The latter translate into functional and structural changes of which cortical thickness might be easy to quantify one of the main players. However, studies on the changes of cortical thickness in brain areas beyond stroke lesion and their relationship to sensory-motor recovery are sparse.

Objectives: To evaluate the effects of cerebral stroke on cortical thickness (CT) beyond the stroke lesion and its association with sensory-motor recovery.

Materials and Methods: Five electronic databases (PubMed, Embase, Web of Science, Scopus and the Cochrane Library) were searched. Methodological quality of the included studies was assessed with the Newcastle-Ottawa Scale for non-randomized controlled trials and the Risk of Bias Cochrane tool for randomized controlled trials.

Results: The search strategy retrieved 821 records, 12 studies were included and risk of bias assessed. In most of the included studies, cortical thinning was seen at the ipsilesional motor area (M1). Cortical thinning can occur beyond the stroke lesion, typically in regions anatomically connected because of anterograde degeneration. Nonetheless, studies also reported cortical thickening of regions of the unaffected hemisphere, likely related to compensatory plasticity. Some studies revealed a significant correlation between changes in cortical thickness of M1 or somatosensory (S1) cortical areas and motor function recovery.

Discussion and Conclusions: Following a stroke, changes in cortical thickness occur both in regions directly connected to the stroke lesion and in contralateral hemisphere areas as well as in the cerebellum. The underlying mechanisms leading to these changes in cortical thickness are still to be fully understood and further research in the field is needed.

Systematic Review Registration: https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42020200539; PROSPERO 2020, identifier: CRD42020200539.

Introduction

Stroke is the leading cause of disability in western countries, with more than 3 million people left with a disability every year (Dobkin, 2005; Vos et al., 2016).

Stroke lesion triggers a multitude of systemic and cerebral effects, such as neurogenesis, gliogenesis and axonal sprouting, which, together with genetic (e.g., polymorphisms, transcriptome) and environmental factors (e.g., time point and intensity of rehabilitation), ultimately determine the long-term outcome and the degree of disability after rehabilitation (Cramer, 2008; Murphy and Corbett, 2009; Cramer et al., 2011; Di Pino et al., 2014, 2016; Di Lazzaro et al., 2015, 2016a; Bernhardt et al., 2017).

Direct contribution of lesion properties (e.g., side, location, etiology) to clinical outcome is limited and a significant role is played by alterations of brain areas beyond the lesion site (Dromerick and Reding, 1995; Pantano et al., 1996; Löuvbld et al., 1997; Miyai et al., 1997; Barber et al., 1998; Beaulieu et al., 1999; Chen et al., 2000; Vogt et al., 2012; Munsch et al., 2016; Dodd et al., 2017; Ernst et al., 2018; Pellegrino et al., 2019a). The latter mechanism is a solid concept in clinical and experimental neurology, introduced more than a century ago, and termed diaschisis (Carrera and Tononi, 2014).

The introduction of neuroimaging techniques allowing for whole brain functional mapping in vivo has demonstrated that behavioral impairments and potential recovery are linked to complex and distributed changes of brain functional activity and connectivity (Pellegrino et al., 2012, 2021; Silasi and Murphy, 2014; Burke Quinlan et al., 2015; Adhikari et al., 2017; Siegel et al., 2018). An overall rearrangement of brain function seems to occur in all stroke cases and is more pronounced in brain regions interconnected with the lesion site (Pellegrino et al., 2012; Di Lazzaro et al., 2014; Di Pino et al., 2014).

However, while a remarkable amount of research effort has been devoted to understanding changes of brain function, the effects of stroke on brain morphology, cortical thickness (CT) and cortical volume have not been fully characterized. It might be expected that regions beyond the lesion site may undergo cortical atrophy due to neuronal loss caused by disconnection (Carrera and Tononi, 2014; Di Pino et al., 2014). Conversely, brain regions may be expected to show cortical thickening of the areas participating during recovery via compensatory mechanisms, increased activity and consequently cortical plasticity (Di Pino et al., 2014). Alike functional changes, which show a dynamic evolution over time, potential changes of CT are expected to occur in a time period ranging from a few weeks to years after stroke lesion (Streitbürger et al., 2012).

The aim of this study is to systematically review the literature on the effects of stroke on CT beyond the lesion site and their potential relationship with clinical outcome in terms of sensory-motor function.

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