Discussion: Neuroplasticity and rehabilitation

Discussion: Neuroplasticity and rehabilitation ORDER NOW FOR CUSTOMIZED AND ORIGINAL ESSAY PAPERS ON Discussion: Neuroplasticity and rehabilitation This assignment explores current evidence on neurological intervention in contemporary practice. Discussion: Neuroplasticity and rehabilitation Instructions: Discuss findings of a study on neuroplasticity and rehabilitation .You will provide a synthesis that consists of the following: Research question Methods Effectiveness Healthcare implications Future inquiry Note: 1. Paper should be up to 1-2 pages in length. I attach the article below. attachment_1 Perspective Addressing Neuroplastic Changes in Distributed Areas of the Nervous System Associated With Chronic Musculoskeletal Disorders Rene? Pelletier, Johanne Higgins, Daniel Bourbonnais R. Pelletier, MSc, Sciences de la Re?adaptation, E?cole de Re?adaptation, Faculte? de Me?decine, Universite? de Montre?al, Montreal, Quebec, Canada. J. Higgins, PhD, E?cole de Re?adaptation, Faculte? de Me?decine, Universite? de Montre?al, CP 6128, Succursale Centre-ville, Montre?al, Que?bec, Canada H3C 3J7, and Centre for Interdisciplinary Research in Rehabilitation of Greater Montreal, Montreal, Quebec, Canada. Address all correspondence to Dr Higgins at: [email protected]. D. Bourbonnais, PhD, E?cole de Re?adaptation, Faculte? de Me?decine, Universite? de Montre?al, and Centre for Interdisciplinary Research in Rehabilitation of Greater Montreal. [Pelletier R, Higgins J, Bourbonnais D. Addressing neuroplastic changes in distributed areas of the nervous system associated with chronic musculoskeletal disorders. Phys Ther. 2015;95:1582–1591.] © 2015 American Physical Therapy Association Present interventions utilized in musculoskeletal rehabilitation are guided, in large part, by a biomedical model where peripheral structural injury is believed to be the sole driver of the disorder. There are, however, neurophysiological changes across different areas of the peripheral and central nervous systems, including peripheral receptors, dorsal horn of the spinal cord, brain stem, sensorimotor cortical areas, and the mesolimbic and prefrontal areas associated with chronic musculoskeletal disorders, including chronic low back pain, osteoarthritis, and tendon injuries. These neurophysiological changes appear not only to be a consequence of peripheral structural injury but also to play a part in the pathophysiology of chronic musculoskeletal disorders. Neurophysiological changes are consistent with a biopsychosocial formulation reflecting the underlying mechanisms associated with sensory and motor findings, psychological traits, and perceptual changes associated with chronic musculoskeletal conditions. These changes, therefore, have important implications in the clinical manifestation, pathophysiology, and treatment of chronic musculoskeletal disorders. Musculoskeletal rehabilitation professionals have at their disposal tools to address these neuroplastic changes, including top-down cognitive-based interventions (eg, education, cognitive-behavioral therapy, mindfulness meditation, motor imagery) and bottom-up physical interventions (eg, motor learning, peripheral sensory stimulation, manual therapy) that induce neuroplastic changes across distributed areas of the nervous system and affect outcomes in patients with chronic musculoskeletal disorders. Furthermore, novel approaches such as the use of transcranial direct current stimulation and repetitive transcranial magnetic stimulation may be utilized to help renormalize neurological function. Comprehensive treatment addressing peripheral structural injury as well as neurophysiological changes occurring across distributed areas of the nervous system may help to improve outcomes in patients with chronic musculoskeletal disorders. Published Ahead of Print: May 7, 2015 Accepted: May 1, 2015 Submitted: December 23, 2014 Post a Rapid Response to this article at: ptjournal.apta.org 1582 f Physical Therapy Volume 95 Number 11 Downloaded from http://ptjournal.apta.org/ by Kimber Gerlich on November 1, 2015 November 2015 Neuroplastic Changes and Chronic Musculoskeletal Disorders Discussion: Neuroplasticity and rehabilitation T raditionally, treatments for chronic musculoskeletal disorders (CMSDs) such as chronic low back pain (CLBP) have been anchored in a biomedical model. This model is based on a structuralpathology paradigm where insult to anatomical structures is believed to be the sole driver of the condition. Over the last 2 decades, evidence has emerged of neurophysiological changes within the peripheral and central nervous systems associated with CMSDs. Studies suggest that CMSDs do not simply result from ongoing structural pathology to peripheral tissues but involve a complex interplay among peripheral structural injury; altered afferent information conveyed from peripheral receptors toward the spinal cord, brain stem, and cortical areas; changes in neuronal processing of noxious stimuli; and psychosocial factors.1 These neurophysiological changes are consistent with experimental and clinical findings of altered sensory transmission, including sensory amplification of pain; motor control changes such as altered muscle recruitment patterns; changes in perceptual processes, including altered body image; psychological traits such as catastophization and somatization; and behavioral changes such as fear avoidance that appear to be implicated both in the clinical manifestation and the pathophysiology of CMSDs (Table). Neurophysiological changes, or neuroplasticity, refer to changes in structure, function, and organization within the nervous system that occur continuously throughout our lifetimes in response to internal stressors such as cognitive processes, internal changes in sensory afference, and external stressors such as motor learning and peripheral sensory stimulation.2 Neuroplasticity is the method by which the brain encodes new experiences, learns, November 2015 and develops new behaviors. Neuroplastic changes associated with CMSDs have been demonstrated in the: (1) peripheral nervous system and spinal cord, (2) brain stem, (3) sensorimotor areas, and (4) mesolimbic and prefrontal areas of the cortex.1,3 Neurophysiological changes occurring within peripheral receptors and the dorsal horn of the spinal cord include increased responsiveness to nociceptive stimuli resulting from anatomical insult to musculoskeletal structures and neuropathic stimuli in sensory amplification, a process called sensitization, resulting in hyperalgesia, increased pain perception, and allodynia; innocuous stimuli are perceived as painful.4 Peripheral sensitization, involving increased responsiveness of the peripheral nociceptors, and central sensitization, involving changes in the spinal cord amplifying the transmission of pain, are natural processes that have a biological advantage in helping to protect the injury from reinjury.4 However, sensitization should be transient, and peripheral and dorsal horn plastic changes should return to their preinjury state, with normalized afferent peripheral input associated with tissue repair.4 Neuroplastic changes also occur within the brain stem, specifically in areas involved in the descending modulation of nociceptive and neuropathic stimuli, including the periaqueductal gray (PAG)5 and the rostral ventral medulla (RVM).6 The PAG and RVM are influenced by the mesolimbic and opioid systems, which, in turn, influence the transmission of noxious stimuli in the dorsal horn of the spinal cord.7 Evidence suggests that these descending modulatory systems are affected in chronic pain states and may perpetuate sensitization within the spinal cord.6,8 The sensory discriminative areas involved in the transmission and processing of noxious stimuli include the primary and secondary somatosensory cortices (S1 and S2, respectively) and the insula.Discussion: Neuroplasticity and rehabilitation 7 The insula appears to be at the crossroads between the sensory discriminative and affective aspects related to pain sensation in the caudal portion and pain affect in the anterior portion.7 Changes in structure, function, and somatotopic organization of S19 and the primary motor cortex (M1)10 have been demonstrated in chronic pain conditions, including CLBP and complex regional pain syndrome (CRPS), and have been found in patellofemoral pain syndrome, patellar tendinopathy,11 osteoarthritis (OA), and rotator cuff pathology.1 Changes in pressure pain thresholds12 and bilateral findings, including decreased strength13 and range of motion14 and presence of inflammatory mediators in the contralateral homologous structure,15 also allude to the presence of altered neural transmission and processing in a number of CMSDs. The neuroplastic changes in the cortical sensorimotor areas are consistent with sensory disturbances (ie, changes in tactile acuity), perceptual disturbances (ie, altered body image), and motor disturbances (ie, motor control) apparent in different CMSDs. The neurophysiological changes in the sensorimotor cortical areas often correlate with pain intensity and symptom duration.9,10 Evidence suggests a 2-way causality between pain or injury and cortical plasticity in S1 and M1, as the elimination of pain may result in cortical reorganization, and interventions that address cortical reorganization may result in decreased pain and improved function.16 The cognitive-affective-motivational areas involved in pain processing receive input from ascending projec- Volume 95 Number 11 Physical Therapy f Downloaded from http://ptjournal.apta.org/ by Kimber Gerlich on November 1, 2015 1583 Neuroplastic Changes and Chronic Musculoskeletal Disorders Table. Areas of Neuroplastic Changes Associated With CMSD and Possible Signs and Symptoms Manifested by the Patienta Possible Physiological Consequences of Neuroplastic Changes in These Areas Mesolimbic and prefrontal areas Areas demonstrated to have been affected include: insula, cingulate cortex, amygdala, medial and dorsolateral prefrontal cortex, and nucleus accumbens Altered neuronal responses to pain, especially in regard to the “unpleasantness” associated with pain Implicit and explicit learning associating pain with movement and negative outcomes Spontaneous fluctuations in pain Problems in affective, cognitive, and motivational aspects in relation to pain These changes may be associated with psychological aspects related to pain, including fear avoidance, anxiety, depression, catastrophization, somatization, worry, and increased vigilance Descending pain modulatory systems, PAG-RVM pathway Descending modulatory systems receive input from prefrontal and mesolimbic structures, including the cingulate cortex, amygdala, and mPFC Decreased descending inhibition of pain (disturbed conditioned pain modulation) Central sensitization (hyperalgesia and allodynia) Pain thresholds may be decreased (pressure and thermal) Peripheral receptors Increased transduction of nociceptive stimuli Increased pain transmission in the area of injury resulting from changes in input and output characteristics in peripheral nociceptors (peripheral sensitization) Contributes to central sensitization (hyperalgesia and allodynia) Dorsal horn of the spinal cord Increased transmission of nociceptive and neuropathic stimuli Results from changes in membrane permeability, decreased inhibition Influenced by descending modulation pathways, including the PAG-RVM Central sensitization (hyperalgesia and allodynia) Pain thresholds may be decreased (pressure and thermal) Somatosensory cortex Altered somatosensory maps, including expansion, retraction, or shifting of representation Increased 2-point discrimination Impaired performance of laterality recognition Change in perception of body image, including size of the limb, altered body midline Primary motor cortex Changes in muscle/movement representations in motor areas of the brain and corticospinal excitability Changes in motor control, including cocontraction and loss of ability to selectively recruit individual muscles Somatosensory associative areas a Signs and Symptoms That May Possibly Indicate Neuroplastic Changes in Discussion: Neuroplasticity and rehabilitation These Areas Neurophysiological Changes Associated With CMSD Perceptual disturbances in body image, including altered size and altered body midline Impaired performance of laterality recognition CMSD?chronic musculoskeletal disorder, PAG-RVM?periaqueductal gray-rostral ventral medulla, mPFC?medial prefrontal cortex. tions via the brain stem and the thalamus.7 The cognitive-affectivemotivational areas involved in pain processing include the structures within the mesolimbic and prefrontal areas such as the insula, anterior cingulate cortex (ACC), amygdala, and prefrontal cortex (PFC).7 Arguably, the most important neuroplastic changes associated with CMSDs occur within the mesolimbic and prefrontal areas, regions associated with threat, fear, aversive conditioning, attention, motivation engagement or disengagement, and executive control.17 The best biomarker 1584 f identified for the transition from acute to chronic conditions,18 and for the presence of chronicity in people with low back pain and OA, involves activity within these regions.3 Altered structure, function, and activity within the mesolimbic and prefrontal areas correlate with psychological traits that are often implicated in chronic conditions such as fear avoidance and catastrophization (a tendency to focus on and magnify actual or anticipated pain experience and to feel hopeless in the face of such experience19).20,21 Mesolimbic structures, specifically the PFC, ACC, and amygdala, also influence motor areas and functioning of the descending modulatory systems, including the PAG-RVM pathway, that are affected in chronic pain states.6,7 The PFC and mesolimbic activity appear to lay the foundation for increased vigilance, attention, and salience attributed to the injury and, therefore, may contribute to central sensitization, resulting in hyperalgesia and allodynia, and provide conditions ripe for inducing neuroplastic changes in the sensorimotor and subcortical areas. Increasing attention Physical Therapy Volume 95 Number 11 Downloaded from http://ptjournal.apta.org/ by Kimber Gerlich on November 1, 2015 November 2015 Neuroplastic Changes and Chronic Musculoskeletal Disorders and salience directed to the injury, threat, and perception of pain appear to result in implicit and explicit learning linking movement with pain.16 In summary, neurophysiological changes associated with CMSDs include alterations in structure (decrease in gray matter in mesolimbic and prefrontal areas),22,23 function, organization (ie, changes in response properties and cortical representation in S1 and M1),1 and neurobiology (changes in brain chemistry concentrations have been found in people with CLBP in an area of the PFC and in M1).24 Implications of Distributed Neuroplastic Changes Associated With CMSD for Rehabilitation Neuroplasticity associated with CMSDs has important implications for the treatment of conditions such as CLBP, OA, and possibly other CMSDs.25 Conventional rehabilitation interventions, in large part, are directed toward input mechanisms (ie, mechanisms addressing inflammation, repair, and remodeling in peripheral structural injury) and output mechanisms (ie, muscle strength, endurance, motor control, and proprioception) associated with CMSDs.26 Although these interventions may have an impact on peripheral structures, they—in themselves—may not be sufficient to restore cortical properties and function and alleviate pain, particularly in chronic injuries.27 In musculoskeletal rehabilitation, limited resources have been directed to the problems of transmission, processing, and control mediating afferent stimuli and motor output. Discussion: Neuroplasticity and rehabilitation 26 Failure to effectively treat conditions such as CLBP may stem from the fact that the central neuroplastic changes occurring across distributed areas associated with this condition have largely been November 2015 ignored and may explain why treatment effects are consistently small regardless of the type of intervention.1,28 Principles of neuroplasticity emerging from animal and human studies can be harnessed to induce positive neuroplastic changes. Studies in people with and without neurological injury suggest that the stimuli necessary to promote neuroplastic changes, at least in sensorimotor cortical areas, must be repetitive, of sufficient intensity to stimulate adaptive changes, require attention and behavioral salience, and involve learning.2,29 These studies also suggest that changes will be specific to the neuronal structures implicated in the task.2,29 Neuroplasticity is stimulus driven, and the stimuli can be mediated by top-down (from higher to lower hierarchical structures within the nervous system) and bottom-up (from peripheral to central structures of the nervous system) processes.30 As CMSDs involve neuroplastic changes within distributed areas, it is logical to believe that treatment should be directed across the different affected structures in the nervous system, including the sensorimotor areas and the mesolimbic prefrontal areas. Although this area of study is in its infancy, it appears that rehabilitation professionals have at their disposal tools and resources to promote adaptive changes in the sensorimotor areas as well as the mesolimbic and prefrontal areas associated with CMSDs. Interventions Top-down Reconceptualizing pain. Health care practitioners and people with CMSDs tend to view pain with a biomedical focus31 despite the failings of this model to explain clinical and experimental findings and to guide effective rehabilitative strategies. Studies indicate that the relationship between threat and tissue damage is altered in chronic pain states, the stimulus-response relationship between structural injury and pain perception is nebulous, and neuroplastic changes associated with chronic pain are maladaptive and no longer perform the biological function of protection.1,3,4,16 It is imperative that updated and current knowledge regarding pain and a biopsychosocial perspective stemming from the wealth of research findings that have emerged over the last 2 decades be transferred to health care professionals and the health care curriculum.32,33 Recognition of misguided beliefs, values, and behavioral strategies that people with CMSDs may display regarding pain and their injury that are incongruent with the rehabilitation principles of graded activity to promote mobilization and positive adaptive changes should be addressed early and continuously in the rehabilitative process.33 The conceptualization that pain and movement are associated with structural damage and the belief that the structural insult to anatomical structures is the source of all pain need to be reformulated.34 Experimental findings demonstrate that neurophysiology education of pain (NEP), which includes information regarding the anatomy, physiology, and processing of noxious stimuli; the perceptual nature of pain; and the altered processing with chronic pain, is associated with improvement in function and attenuation of pain.35 The information and concepts presented in the NEP programs are accessible to patients experiencing chronic pain34 and can have an immediate impact on behavior.35 Although the scientific literature is limited in regard to these programs, they would appear to perform better than educational programs that stem from a biomedical model to explain structural pathol- Volume 95 Number 11 Physical Therapy f Downloaded from http://ptjournal.apta.org/ by Kimber Gerlich on November 1, 2015 1585 Neuroplastic Changes and Chronic Musculoskeletal Disorders ogy and biomechanics as the drivers of the CMSD.36,37 A single session of neurophysiology education of pain in people with CLBP has proven to result in a transient decrease in pain and improvement in function35 and may be associated with changes in brain activation patterns.38 For more permanent changes in belief and behavior, the concepts stemming from neurophysiology education will probably need to be repeated consistently in the rehabilitation program.32 Although education has been demonstrated to be beneficial in outcome for chronic back pain,39 recent meta-analyses and systematic reviews of NEP demonstrate that these programs are promising but that results are currently tenuous due to the limited number of studies.36,37 Addressing maladaptive thoughts and behavior. 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