Chronic Back Pain: Corticolimbic Brain Structure Changes, Involvement Over Time

In patients with chronic back pain, changes in gray matter volume (GMV) in the corticolimbic structures of the brain measured over a period of 7 years revealed increased involvement of areas responsible for emotion and motivation in pain maintenance, according to study results published in Pain.

Chronic pain has been associated with reorganization of gray matter in the brain that may represent a prognostic or diagnostic biomarker. In patients with chronic back pain, however, studies have shown both less and more GMV in different brain areas over time, compared with that in those without chronic back pain.

To determine how development and maintenance of chronic back pain is associated with structural changes in the gray matter of corticolimbic brain structures, researchers conducted a population-based longitudinal study that measured GMV in various brain structures among patients with chronic back pain. They compared this volume with GMV in individuals without chronic pain (control group) at 2 time points separated by 7 years. Their hypothesis was that, compared with those in the control group, people who developed chronic back pain would have less GMV in limbic structures such as the medial prefrontal cortex, hippocampus, amygdala, and ventral striatum.

Data were collected from the population-based Study of Health in Pomerania (SHIP), which was conducted in 2 independent cohorts of a population at high risk for disease in northeast Germany. Data were obtained from the baseline examination, performed between 2008 and 2012, and the follow-up examination, performed between 2014 and 2018. Only the 1215 SHIP patients who had both baseline and follow-up examinations and underwent magnetic resonance imaging of the brain were selected for inclusion in the current study.

Patients were selected for analysis if, at follow-up, they reported radiating back pain on most days that had lasted at least 3 months (ie, chronic back pain). Average pain intensity had to be at least 3 on a scale between 0 (signifying no pain) and 10 (signifying the greatest pain imaginable). This group was subdivided to separately evaluate patients who had established chronic back pain at baseline and developed chronic back pain with a radiating character and pain lasting more than 3 months within the last 12 months vs those who had emerging chronic back pain, defined as back pain that did not fulfill the criteria for chronicity at baseline. Patients in the control group had to report no chronic pain, and no back pain or occasional pain with an intensity of less than 2 at baseline and follow-up. Excluded were individuals with a history of stroke, multiple sclerosis, epilepsy, Parkinson disease, dementia, cerebral tumor, intracranial cyst, or hydrocephalus.

Ultimately, 168 patients with chronic back pain and 323 individuals without chronic back pain (control group) were included in the study.

Patients who indicated chronic back pain at follow-up had less GMV in the right entorhinal area, right amygdala, and left medial frontal cortex at baseline, compared with individuals in the control group. More intense pain and higher BMI and depression scores were noted in patients who had back pain at baseline and later developed chronic back pain.

At follow up, patients with chronic back pain had an increase of GMV in the left ventral striatum, but those without chronic back pain showed a decrease in GMV in this area. Participants with chronic back pain also had a GMV decrease in the left parahippocampal gyrus at 7 years’ follow up.

Additionally, among patients with chronic back pain, pain duration was negatively associated with GMV in the left caudate.

Limitations of this study include those related to sample selection from a population-based cohort. Because the collection of SHIP data was not specifically aimed at investigating chronic back pain, pain was not assessed clinically but instead based on self-reports, which may lack validity. The exact duration of pain was not available at baseline. Participants with chronic back pain differed in several variables vs those in the control group; therefore, these 2 groups are not entirely comparable. Additionally, individuals taking antidepressants (except for pain intensity analysis), antiepileptics, benzodiazepines, and opioids were not excluded from participation, to preserve the sample size and representativeness of the groups.

The researchers concluded, “[T]hese findings are in accordance with the notion that limbic brain properties are both predisposing risk factors and drivers of brain reorganization during the development of [chronic back pain].”

This article originally appeared on Clinical Pain Advisor