Neuroplasticity:a camouflaged cardinal in musculoskeletal rehabilitation

Srishti Banerjee

1L.J institute of physiotherapy,L.J University,L.J campus,sarkhej-gandhinagar highway,ahmedabad,Gujarat 382210,India.

Abstract The rehabilitation of musculoskeletal dysfunctions (MSD) such as osteoarthritis, anterior cruciate ligament injuries and low back pain focuses on symptomatic management of pain followed by stretching and strengthening. However, these interventions focus just on symptomatic pain management and addressing musculoskeletal impairments. But it has been found that neuroplastic changes continue to occur throughout these pathologies and sometimes even are persistent,as conventional rehabilitation doesn’t focus on these changes therefore chances of reinjury increase. Therefore this article discusses underlying neuroplastic changes associated with MSD and neuroplasticity-based interventions for better clinical outcomes.

Keywords:neuroplasticity; musculoskeletal dysfunction; rehabilitation

Introduction

The current rehabilitation of musculoskeletal dysfunction (MSD) is based on the biomedical model, which functions based on the structural pathology paradigm that is sufficient to explain acute injury but in chronic injury presence of neuroplastic changes. There are emerging evidence of the presence of neuroplastic changes in response to musculoskeletal injury which are responsible for the chronic stage changes. Following any MSD, the neuroplastic changes occur across central and peripheral nervous system [1].

Neuroplastic changes in spinal cord and peripheral nervous system includes [2-4]

· Slow stimuli processing, transmission and incorrect localization

· Allodynia and hyperalgesia due to an increase in the receptor field of nociceptors in the dorsal horn.

Neuroplastic changes in the brainstem includes

Changes in periaqueductal gray matter, rostral ventral medulla and their connections which modulate nociception which is even suggestive of poorer surgical prognosis. It is found that in patients with chronic low back pain the blood flow to these areas reduces,suggesting a reduced neuronal activity [2-5].

Neuroplastic changes in cortex

Occur in response to pain and are specific to pathology. Such as medial prefrontal cortex (PFC) is activated in chronic low back pain(LBP),and insula in osteoarthritis.Similarly,the area representing the low back in the somatosensory cortex shifts medially directly proportional to the chronicity of the condition. In addition to this,there are neurochemical changes seen in the right thalamus in patients with left sciatica[6, 7].

Neuroplastic changes in mesolimbic system and prefrontal cortex

It is associated with[8]

· Psychological traits of pain such as fear, avoidance and catastrophization

· Transit from acute to chronic states

· Magnitude of chronicity

· Presence of biomarkers of brain such as increased insular activation is associated with pain duration, activation of medial PFC is associated with pain intensity.

About then, the first cry of a Grand Slam! hit the air. Everyone joined in. When Harry reached home plate, about to collapse19, his teammates lifted him as high as they could and chanted, Harry, Harry, Harry!

Neuroplastic changes in primary motor cortex

It includes alteration in corticospinal recruitment with greater activation of superficial muscles in chronic LBP[9].

Interventions with a neuroplastic basis in MSDs

The neuroplastic changes occurring, especially in the cortex, are reversible once the pain reduces.

Principles of application of neuroplasticity-based exercises [1,10]

· The exercises,either done as part or as a whole practice,should be focused on functional application of the exercise done i.e. it should be task specific and parameters such as amplitude and speed should resemble real-life activities.

· Neural change can only be induced if sufficient repetitions of a particular exercise are done.

· The learner should be shifted to external focus of attention by providing feedback.

Neuroplastic interventions address pain in chronic MSDs

Neuroplastic based interventions, such as cognitive behavioural therapy (CBT) addresses catastrophisation of pain by incorporating cognitive restructuring, problem-solving skills and interventions to address maladaptive behaviors. CBT is found to address concerns originating due to activation of PFC, such as anxiety, depression, and reduced activity. In addition, CBT modulates mesolimbic system function which is clinically evident by an increased executive function. Evidences suggest that CBT can reduce the connectivity between the PFC and anterior cingulate cortex (ACC), which is clinically evident in reduction in pain and improved self-efficacy in patients with chronic LBP. CBT influences on PFC, mesolimbic system and its influence on descending pain modulation system within the brainstem and sensorimotor cortex [11-13]. In addition to traditional CBT, approaches like acceptance commitment therapy (ACT) and mindfulness-based stress reduction (MBSR). ACT focuses on acceptance of positive and negative experiences, clarity in the values and commitment to these values, followed by setting goals and taking actions supporting these values [14, 15]. Where are MBSR focuses on interventions such as yoga, meditation, relaxation techniques to manage stress, minimises anxiety and its effects on pain. MSBR also focuses on transferring this skill into activities of daily living. MSBR interventions focus on the frontal structures and its connections to the mesolimbic system [16-18].

Interventions to address neuroplastic changes in the sensorimotor areas

Interventions such as peripheral electrical stimulation (PES) and sensory discriminative training are useful in addressing altered processing and organization of sensation in S1. Studies have shown in patients with chronic regional pain syndrome, tactile acuity specifically two point discrimination addresses pain, improves function, and renormalizes the properties and organization within S1 areas provided the patients being fully attentive during the session.PES, can cause alteration in the somatotopic map and improves the sensation.The parameters for stimulation of a mixed healthy nerve are frequencies > 10 Hz, duration 120 minutes and intensity close to the motor threshold results in increase in corticospinal excitability[19-21].

Interventions to address neuroplastic changes in motor cortex[22, 23]

In a patient with a painful shoulder, shoulder elevation can be retrained as follows.

· Part practice:the patient practices shoulder elevation in a pain-free range in the scapular plane and the therapist enables this by application of a sustained glenohumeral posterolateral glide.

· Whole practice:the patient independently performs a full range of pain free shoulder elevation.

· Repetition:the part practice should be repeated for 2-4 sets with 6-10 repetitions. The whole practice should be repeated 3 sets of 6-10 repetitions, three times a day. For a pain free motion, a taping technique can be used for shoulder and following which the functional movements involving shoulder elevation can be incorporated.

· Task-specific training:shoulder elevation to reach for overhead objects.

· External focus of attention:focus on environmental cues for a correct pain-free shoulder movement can provide with a shift to the external focus.Virtual reality computer gaming is one of the excellent tools for shifting to an external focus.

If the movements are too painful, which limits physical repetitions,in such cases mental imagery can be used. In patients experiencing chronic pain, mental imagery improves physical performance and addresses cortical changes in PFC and mesolimbic system.

Conclusion

Considering the extensive neuroplastic changes in response to most the MSDs, it is important to incorporate neuroplasticity based interventions for better outcomes.