Overall, there is moderate evidence for regional changes in gray and white matter, together with an altered functional connectivity during rest and increased activity in pain-related areas following painful stimulation, evidencing an upregulated pain matrix. More longitudinal research is needed to clarify the temporal relationship regarding pain and neuroplastic changes, and integration of different brain imaging techniques is warranted.
Lumbar muscle degeneration is a common feature in non-specific low back pain (LBP). It is hypothesized that degenerated muscles might compromise spinal stability and lead to further injury/pain. However, little is known about lumbar muscle morphometry after resolution of LBP. Therefore, this study investigated the extent of lumbar muscle atrophy and fatty infiltration in individuals who are at risk for a recurrence of LBP. Thirteen participants in remission of unilateral recurrent LBP were compared to 13 healthy controls, comparable for age, weight, length and level of physical activity. Total, lean muscle and fat cross-sectional area (CSA) of lumbar multifidus (MF), erector spinae (ES) and psoas (PS) were investigated on T1-weighted Magnetic Resonance Imaging (MRI), bilaterally and at 3 lumbar levels (L3 upper, L4 upper and L4 lower endplate). In addition, a muscle-fat-index (MFI) was calculated reflecting the amount of fatty infiltration in lean muscle tissue. No significant differences for total, lean muscle and fat CSA were found between people in remission of recurrent LBP and the control group. Conversely, MFI was increased bilaterally at the 2 lowest lumbar levels. There were no differences between the previously painful and non-painful side of the LBP group for any of the parameters. These results show a generalized increase in intramuscular fatty infiltration in lean muscle tissue in the absence of macroscopical signs of muscle degeneration after resolution of LBP. These findings reflect a decreased muscle quality, but not quantity, and might indicate a pathophysiological mechanism contributing to recurrence of LBP.
An emerging technique in chronic pain research is MRI, which has led to the understanding that chronic pain patients display brain structure and function alterations. Many of these altered brain regions and networks are not just involved in pain processing, but also in other sensory and particularly cognitive tasks. Therefore, the next step is to investigate the relation between brain alterations and pain related cognitive and emotional factors. This review aims at providing an overview of the existing literature on this subject. Pubmed, Web of Science and Embase were searched for original research reports. Twenty eight eligible papers were included, with information on the association of brain alterations with pain catastrophizing, fear-avoidance, anxiety and depressive symptoms. Methodological quality of eligible papers was checked by two independent researchers. Evidence on the direction of these associations is inconclusive. Pain catastrophizing is related to brain areas involved in pain processing, attention to pain, emotion and motor activity, and to reduced top-down pain inhibition. In contrast to pain catastrophizing, evidence on anxiety and depressive symptoms shows no clear association with brain characteristics. However, all included cognitive or emotional factors showed significant associations with resting state fMRI data, providing that even at rest the brain reserves a certain activity for these pain-related factors. Brain changes associated with illness perceptions, pain attention, attitudes and beliefs seem to receive less attention in literature. Significance: This review shows that maladaptive cognitive and emotional factors are associated with several brain regions involved in chronic pain. Targeting these factors in these patients might normalize specific brain alterations.
Chronic spinal pain (CSP) is a severely disabling disorder, including nontraumatic chronic low back and neck pain, failed back surgery, and chronic whiplash-associated disorders. Much of the current therapy is focused on input mechanisms (treating peripheral elements such as muscles and joints) and output mechanisms (addressing motor control), while there is less attention to processing (central) mechanisms. In addition to the compelling evidence for impaired motor control of spinal muscles in patients with CSP, there is increasing evidence that central mechanisms (ie, hyperexcitability of the central nervous system and brain abnormalities) play a role in CSP. Hence, treatments for CSP should address not only peripheral dysfunctions but also the brain. Therefore, a modern neuroscience approach, comprising therapeutic pain neuroscience education followed by cognition-targeted motor control training, is proposed. This perspective article explains why and how such an approach to CSP can be applied in physical therapist practice.
The CSI was weakly associated with PPTs and not with CPM efficacy in CSP patients. Moderate to strong associations were found with current pain intensity, quality of life, disability, and catastrophizing. The current results illustrate that the CSI does not reflect a direct measure of CS, yet is a representation of general distress, possible originating from CS symptoms.
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