Thalamic atrophy and cognition in multiple sclerosis

Abstract

These findings suggest that thalamic atrophy is a clinically relevant biomarker of the neurodegenerative disease process in multiple sclerosis.

Thalamic Anisotropy and Functional Disability

“…[5][6][7] In particular, thalamic involvement is becoming increasingly recognized as a significant step in the development of clinical disability and memory impairment in multiple sclerosis. 8 Tovar-Moll et al 9 in an article published in the current issue of the American Journal of Neuroradiology demonstrate thalamic abnormalities in diffusion tensor metrics that correlate with clinical disability scores, in keeping with similar studies published on the subject. 10,11 Most interesting, Tovar-Moll et al reported increased fractional anisotropy (FA) and mean diffusivity (MD) values in the thalamus in comparison with matched controls.…”

Explaining the heterogeneity of functional connectivity findings in multiple sclerosis: An empirically informed modeling study

“…Given the strong clinical relevance of cortico‐thalamic involvement for cognition in MS (Houtchens et al, 2007; Schoonheim et al, 2015a), we employ a well‐known cortico‐thalamic mean field model in this study (Abeysuriya, Rennie, & Robinson, 2014; Robinson, Loxley, O'connor, & Rennie, 2001; Robinson, Rennie, Rowe, & O'Connor, 2004). This model is informed by empirical data and optimized to produce realistic power spectra mimicking electroencephalogram/magnetoencephalography recordings.…”

Superior Cerebellar Peduncle Atrophy Predicts Cognitive Impairment in Relapsing Remitting Multiple Sclerosis Patients with Cerebellar Symptoms: A DTI Study

“…Disconnections of the fibers to the thalamus, negatively involve the limbic circuitry avoiding the mediation and regulation of many cognitive functions [14,15]. Although many studies have shown a strong association between thalamic atrophy and cognitive function [16][17][18], no one focused on its microstructural changes, as well as on abnormalities of MCP, SCP and DN, and on their relationships to cognitive functions in MS.…”

“…The feed forward loop (Figure 1 in blue) connects cortical areas via middle cerebellar peduncle (MCP) with deep cerebellar nuclei, including the dentate nucleus (DN) (afferent pathway). The feedback loop (Figure 1 in orange) connects the deep cerebellar nuclei with motor cortex, via the superior cerebellar peduncle (SCP), the red nucleus and the thalamus (Th) (efferent pathway) [12,13].Disconnections of the fibers to the thalamus, negatively involve the limbic circuitry avoiding the mediation and regulation of many cognitive functions [14,15]. Although many studies have shown a strong association between thalamic atrophy and cognitive function [16][17][18], no one focused on its microstructural changes, as well as on abnormalities of MCP, SCP and DN, and on their relationships to cognitive functions in MS.…”