Understanding the role of the primary somatosensory cortex: Opportunities for rehabilitation

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Understanding the role of the primary somatosensory cortex: Opportunities for rehabilitation

2015, Neuropsychologia

 

M.R. Borich a,n, 

S.M. Brodie b, 

W.A. Gray a, 

S. Ionta c, 

L.A. Boyd a,d
a Division of Physical Therapy, Department of Rehabilitation Medicine, Emory University School of Medicine, Atlanta, USA
b Department of Physical Therapy, Faculty of Medicine, University of British Columbia, Vancouver, Canada
c The Laboratory for Investigative Neurophysiology (The LINE), Department of Radiology and Department of Clinical Neurosciences, University HospitalCenter and University of Lausanne, Lausanne, Switzerland
d Brain Behaviour Laboratory & Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, BC, Canada
a r t i c l e i n f o
 Article history:
Received 31 March 2015Received in revised form19 June 2015Accepted 7 July 2015

a b s t r a c t

Emerging evidence indicates impairments in somatosensory function may be a major contributor tomotor dysfunction associated with neurologic injury or disorders. However, the neuroanatomical substrates underlying the connection between aberrant sensory input and ineffective motor output are still under investigation. The primary somatosensory cortex (S1) plays a critical role in processing afferent somatosensory input and contributes to the integration of sensory and motor signals necessary forskilled movement. Neuroimaging and neurostimulation approaches provide unique opportunities to noninvasively study S1 structure and function including connectivity with other cortical regions. These research techniques have begun to illuminate casual contributions of abnormal S1 activity and connectivity to motor dysfunction and poorer recovery of motor function in neurologic patient populations.This review synthesizes recent evidence illustrating the role of S1 in motor control, motor learning and functional recovery with an emphasis on how information from these investigations may be exploited to inform stroke rehabilitation to reduce motor dysfunction and improve therapeutic outcomes.
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 2015 Elsevier Ltd. All rights reserved.

1. Introduction

The planning, execution, and control of motor behaviors is a complex neural process in part dependent on correct sampling of multiple sensory modalities from the body periphery (e.g., somatosensation, vestibular, etc.) and external environment (e.g., vision,hearing, etc.) (Hummelsheim et al., 1988; Riemann and Lephart, 2002; Wolpert et al., 2013; Zarzecki et al., 1978). Without correct processing and translation of sensory input, both before and during movement, motor outputs are abnormal and/or inaccurate.Thus, there is a tight link between sensory processing and movement production. Accordingly, emerging evidence suggests abnormal processing of somatosensory information by the primary somatosensory cortex (S1) contributes to deficits seen in neurological disorders typically classified by motor dysfunction (e.g.stroke, Parkinson's disease, dystonia, ataxia, etc.) (Elbert et al., 1998; Hummelsheim et al., 1988; Jacobs et al., 2012; Konczak and Abbruzzese, 2013; Rub et al., 2003; Wolpert et al., 2013). There is a growing body of literature regarding the effects of altered S1 function on M1 activity and the control of movement.Increased M1 excitability has been noted in animal models of neurological conditions involving S1 damage, such as stroke(Harrison et al., 2013; Winship and Murphy, 2009) and idiopathic dystonia (Domenech et al., 2013). Focal lesions to sensorimotor areas, similar to injuries resulting from stroke, have resulted in difficulty with a battery of motor behavioral tasks assessing gross motor function and reflexes in rats (Gerlai et al., 2000; Kleim et al., 2007; McIntosh et al., 1996), and impaired fine motor skills involving small objects in monkeys (Brinkman et al.,1985; Hikosaka et al., 1985). Motor deficits observed after S1 lesions may not always be due to difficulty with executing motor commands but rather attributed to disrupted learning of new motor tasks, as motor deficits are attenuated if the task had been learned prior to S1 injury (Pavlides et al.,1993; Sakamoto et al.,1989,1987). Another phenomenon that could affect motor function is the alteration of somatosensory maps within S1. Studies in rodents have found a shift in the sensory map after experimentally-induced stroke that results in an overlap with a portion of the motor representation where the  neurons originally devoted to encode exclusively motor commands take on a small role in sensory processing, reducing their capacity for involvement in the motor system (Harrison et al., 2013; Winship and Murphy, 2009). In the following sections, the importance of S1 to motor function will be considered using theoretical models, neuroimaging approaches, non-invasive neural stimulation technologies, and combined neuroimaging
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neurostimulation paradigms. Finally, future clinical implications of a comprehensive understanding of the relationship between motor functioning and S1 structure, function, and connectivity will be discussed.