Digging Deeper

CHRONIC LOW BACK PAIN AND CENTRAL SENSITISATION STUDY

Sahebalam M, Hatef B, Pirzad Jahromi G. Central Sensitization Severity in Chronic Low Back Pain: Associations with Sleep, Distress, Cortisol, and Visuospatial Working Memory. J Pain Res. 2026;19:1-13
https://lnkd.in/eMb65dAv

Chronic low back pain (CLBP) is one of the leading causes of disability worldwide. Most cases are “non‑specific,” meaning no clear structural or neurological cause can be identified. Increasing evidence shows that symptoms in many patients arise not only from peripheral tissues but also from altered central nervous system processing. Central sensitization (CS) is a key mechanism in this process, involving heightened responsiveness of pain pathways and amplified pain perception. This helps explain why some individuals experience widespread or disproportionate pain and respond poorly to treatments focused solely on the spine or musculoskeletal structures.

CS is also linked to dysregulation of stress‑related systems, particularly the hypothalamic–pituitary–adrenal (HPA) axis. Chronic stress and persistent pain can alter cortisol patterns, influencing mood, immune activity, and pain sensitivity. Neuroinflammatory pathways, including cytokines such as interleukin‑6, may also contribute, although findings remain inconsistent. Sleep disturbance and psychological distress are highly prevalent in chronic pain and interact bidirectionally with pain intensity, often creating a cycle of worsening symptoms.

Cognitive changes—such as difficulties with attention, working memory, and executive function—are increasingly recognised in chronic pain and may reflect overlapping neural circuits involved in pain, emotion, and cognition. Despite this, few studies have examined sleep, emotional distress, neuroendocrine markers, and cognition together in CLBP populations stratified by CS severity.

This study examined how pain, central sensitization (CS), sleep, mood, and cognition interact in adults with chronic low back pain (CLBP).

FINDINGS:
– Participants with CLBP and high CS reported greater pain, poorer sleep, higher emotional distress, and subtle working‑memory deficits compared with pain‑free controls.

– Sleep disturbance strongly correlated with pain and CS symptoms, reinforcing its role as a core treatment target.

– Psychological distress was also elevated, supporting a biopsychosocial understanding of CS.

– Biological markers showed only modest differences: morning cortisol was slightly higher, while IL‑6 did not differ, highlighting the limits of single time‑point sampling. Cognitive testing revealed reduced visuospatial working memory in high‑CS participants, with planning ability preserved.

Overall, CLBP with probable CS reflects a multidimensional pattern of sensory, emotional, sleep‑related, and cognitive changes, underscoring the need for integrated, CS‑informed assessment and management