What Happens When the Brain’s Map Changes?

Neuroplasticity describes the capacity of the nervous system to modify its structure, connectivity or function in response to activity and experience. Cortical reorganization is one possible expression of this capacity. It may involve changes in cortical excitability, the location or overlap of functional representations, connectivity among regions, or recruitment of different networks during a task. These changes are not automatically pathological. Learning a skill, adapting to changing sensory conditions and recovering after neural injury all require plasticity. The same biological capacity may contribute to persistent dysfunction when repeated nociceptive input, altered movement, disuse or protective behaviour reinforces a pattern that is no longer well calibrated to current conditions.

The primary somatosensory cortex contains multiple organized representations of the body.[1] These representations are influenced by the sensory information reaching them and by their interactions with thalamic, parietal and motor networks. Pain may alter the type and volume of sensory information associated with a body region. It may also change attention, movement and use of the affected area. Each of these changes can modify the activity of the neural systems representing the body. This does not establish one universal form of pain-related remapping. Neuropathic pain, low back pain, complex regional pain syndrome and fibromyalgia do not necessarily produce the same neural findings. Different research methods may also measure different aspects of neural organization.

The primary motor cortex is organized somatotopically, although its organization is considerably more overlapping and functionally complex than a simple map of individual muscles.[2] Its representations can change with learning, altered sensory input and changes in movement. Tsao et al. (2008) found that the cortical representation of the transversus abdominis muscle was displaced in people with recurrent low back pain.[3] Massé-Alarie et al. (2016) subsequently described impaired corticomotor control involving the lumbar multifidus in chronic low back pain.[4] Li et al. (2021) also identified differences in the cortical representations of the transversus abdominis and multifidus muscles in people with chronic low back pain.[5] These findings suggest that persistent low back pain may be associated with changes in the cortical control of muscles involved in spinal stability. The direction of causation remains difficult to determine. Pain may change movement and cortical organization, altered motor control may influence loading and sensory input, or both processes may interact over time.

Complex regional pain syndrome may include pain, sensory disturbances, autonomic changes, reduced movement, weakness, tremor and dystonia. Although research initially emphasized changes within the primary and supplementary motor cortices, literature discussed in my thesis also described changes involving the putamen, insula and thalamocortical networks.[6,7] Di Pietro et al. (2020) reported altered resting activity and connectivity in people with complex regional pain syndrome.[6] Azqueta-Gavaldon et al. (2020) identified structural and functional changes involving the putamen and related these findings to pain and motor deficits.[7] These observations support the conclusion that persistent pain cannot always be localized to one cortical map or isolated brain region.

An association between pain and altered cortical organization does not establish whether reorganization caused the pain, resulted from the pain or developed through a reciprocal process. Persistent pain changes movement, attention, sensory input and behaviour. Each of these factors can influence neural activity. Cortical findings also represent group averages. A statistically significant difference between a pain population and a control group does not mean that every person with the condition has the same neural alteration. Neuroimaging and transcranial magnetic stimulation findings should not be treated as individual diagnostic tests unless they have been validated for that purpose.

The possibility of altered body representation creates opportunities for rehabilitation, but it should not be reduced to the claim that pain can simply be “rewired.” Sensory discrimination, visual feedback and progressive movement may provide information capable of influencing sensorimotor processing. Their usefulness is likely to depend upon the individual, the pain condition and the wider clinical context. Treatment should continue to consider tissue pathology, neurological disease, inflammation and other medical causes. A cortical explanation should expand clinical reasoning rather than replace careful examination of the body.

The following phantom-limb and cortical-representation publications were used during development of the Academy Lesson but were not included in my thesis. Flor (2003) reported that the magnitude of cortical reorganization correlated with pain intensity in phantom-limb pain and other neuropathic pain syndromes.[CU1] Moseley and Flor (2012) subsequently reviewed evidence of altered sensory and motor representations across several persistent-pain conditions.[CU2] The later review also examined rehabilitation approaches intended to influence sensory and motor representations. These findings extend the mechanisms discussed in my thesis, but they do not establish that representational change is present in every person with persistent pain.

Plasticity allows the nervous system to learn from repeated experience. When pain changes how a person senses, attends to or moves a body region, those repeated patterns may become biologically reinforced. Tissue healing alone may not automatically restore the previous sensorimotor pattern. Rehabilitation can provide structured opportunities for updating. Repeated, accurately guided and tolerable sensory and motor experiences may help the nervous system develop patterns that are better calibrated to the person’s present condition and capacity.

When the nervous system reorganizes, function may change—even when the body itself has not.

Cortical and subcortical organization may change in persistent pain, but these changes are diverse and condition-dependent. They may affect bodily perception, motor control and sensory processing. The appropriate conclusion is not that every persistent-pain condition results from a distorted brain map. It is that pain and neural representation can influence one another through plasticity.

The main Paper is derived exclusively from my thesis discussions of somatosensory organization, chronic low back pain, complex regional pain syndrome and motor-cortical plasticity. Literature not contained in my thesis appears only within the Current Evidence Update.

Delhaye, B. P., Long, K. H., & Bensmaia, S. J. (2018). Neural basis of touch and proprioception in primate cortex. Comprehensive Physiology, 8(4), 1575–1602. https://doi.org/10.1002/cphy.c170033 Geyer, S., Matelli, M., Luppino, G., & Zilles, K. (2000). Functional neuroanatomy of the primate isocortical motor system. Anatomy and Embryology, 202(6), 443–474. https://doi.org/10.1007/s004290000127 Tsao, H., Galea, M. P., & Hodges, P. W. (2008). Reorganization of the motor cortex is associated with postural control deficits in recurrent low back pain. Brain, 131(8), 2161–2171. https://doi.org/10.1093/brain/awn154 Massé-Alarie, H., Beaulieu, L. D., Preuss, R., & Schneider, C. (2016). Corticomotor control of lumbar multifidus muscles is impaired in chronic low back pain. Experimental Brain Research, 234(4), 1033–1045. https://doi.org/10.1007/s00221-015-4528-x Li, X., Liu, H., Ge, L., Yan, Y., Lo, W. L. A., Li, L., & Wang, C. (2021). Cortical representations of transversus abdominis and multifidus muscles were discrete in patients with chronic low back pain. Neural Plasticity, 2021, 6666024. https://doi.org/10.1155/2021/6666024 Di Pietro, F., Lee, B., & Henderson, L. A. (2020). Altered resting activity patterns and connectivity in individuals with complex regional pain syndrome. Human Brain Mapping, 41(13), 3781–3793. https://doi.org/10.1002/hbm.25087 Azqueta-Gavaldon, M., Youssef, A. M., Storz, C., Lemme, J., Schulte-Göcking, H., Becerra, L., Azad, S. C., Reiners, A., Ertl-Wagner, B., Borsook, D., Upadhyay, J., & Kraft, E. (2020). Implications of the putamen in pain and motor deficits in complex regional pain syndrome. Pain, 161(3), 595–608. https://doi.org/10.1097/j.pain.0000000000001745

CU1. Flor, H. (2003). Cortical reorganisation and chronic pain: Implications for rehabilitation. Journal of Rehabilitation Medicine, Supplement 41, 66–72. https://doi.org/10.1080/16501960310010179 CU2. Moseley, G. L., & Flor, H. (2012). Targeting cortical representations in the treatment of chronic pain: A review. Neurorehabilitation and Neural Repair, 26(6), 646–652. https://doi.org/10.1177/1545968311433209