Investigation of the Relationship Between Central Sensitization and Neuropathic Pain in Lumbar Disc Herniation

Does Central Sensitization Mediate Neuropathic Complaints in Lumbar Disc Herniation? A Cross-sectional Observational Study

Central sensitization (CS) is as increased response to normal or sub-threshold stimuli of central nervous system and its close relationship with in many musculoskeletal diseases with chronic pain has been demonstrated in several studies. CS is also one of the main mechanisms proposed in the generation of neuropathic pain, and the relationship between pain sensitization and neuropathic complaints has been shown in different diseases.In this study, it was aimed to investigate the effect of central sensitization on the distribution pattern and neuropathic character of pain in patients with lumbar disc herniation who applied to the physical medicine and rehabilitation outpatient clinic.

Lumbar disc herniation (LDH) is one of the leading causes of musculoskeletal pain and its lifetime prevalence is around 80%. Different types of pain can be seen in patients with LDH, which are classified by the International Association for the Study of Pain (IASP) as nociceptive low back pain, somatic referred pain, radicular pain, and radiculopathy. While nociceptive low back pain originates from the structures in the lumbar spine, this pain is characterized as somatic referred pain when it spreads to the lower extremities. Radicular pain is different from these two pains in mechanism and character, and neuropathic complaints accompany axial pain. LDH is also the most common cause of lumbar radicular pain and causes neuropathic pain by irritation of the spinal nerve or dorsal root ganglion. In recent studies, it has been shown that nociceptor hyperexcitability and continuous stimulus discharge into the central nervous system play an important role in the formation of neuropathic pain. This mechanism is also encountered in central sensitization (CS), which is well-known to be associated with chronic pain and characterized by increased response to painful stimuli. Although there are many definitions of CS in the literature, one of the most comprehensive definitions was made as "Changes in the membrane excitability of the central pain pathways and changes in the synaptic transmission of the dorsal anterior horn cells and a decrease in the inhibition of the descending pathways". In animal models, inflammation-mediated spinal microglia activation has been shown to play a role in chronic radicular pain secondary to disc herniation, which has been associated with the development of central sensitization. A study showed that the frequency of CS is increased in patients with chronic low back pain, and this rate is variable in patients with LDH. In addition, data on the role of CS in LDH-related pain, especially radicular pain, are increasing.Considering all these data, CS is likely to affect pain in various ways in patients with LDH, particularly in its severity, extent, and neuropathic component. Therefore, in this study, it was aimed to investigate the relationship between CS accompanying LDH patients with pain characteristics and neuropathic pain development.

Inclusion Criteria:

Having a diagnosis of lumbar disc herniation Accepting to participate in the study

Exclusion Criteria:

Concomitant active systemic inflammatory disease, infection and malignancy Having disease that will cause neuropathic pain in the other lower extremity, such as polyneuropathy, multiple sclerosis etc Refusing to participate in the study