One of the key contributors to peripheral nerve disease in patients with diabetes is the central nervous system (CNS), a new report suggests.
Published in the journal Pain, the study, conducted by Dr Solomon Tesfaye of Sheffield (UK) Teaching Hospitals NHS Foundation Trust and colleagues, outlines additional insights that examine the role of the CNS in the development of diabetic peripheral neuropathy (DPN).
“Although DPN has been considered a disease of the peripheral nerve, from numerous studies it is becoming apparent that there are indeed changes within the CNS that … appear to be concomitant with the evolution of painful and painless DPN,” the authors write.
Reviewing evidence resulting from the use of advanced imaging techniques in several studies, Dr Tesfaye and colleagues determined that CNS factors might explain the development of DNP.
Key findings from the report include the following:
- Differences in the cross-sectional area (width) of the spinal cord, particularly before symptoms of DPN have appeared.
- Loss of volume (atrophy) in the primary sensory cortex — the main brain area involved in sense of touch.
- Differences in blood supply in a part of the brain called the thalamus — oversupply (hyperperfusion) in painful DPN, compared with undersupply (hypoperfusion) in painless DPN.
- Changes in higher brain areas, specifically the “pain processing matrix” — thought to be involved not only in detecting the location and intensity of pain but also the emotional responses.
- Reductions in the brain gray matter, particularly in areas where “somatosensory perceptions” are processed.
“Imaging may help us to unravel one of the fundamental unanswered questions — where can the primary pathophysiology of the painful symptomatology of DPN be found?” the researchers write. “They hope that further detailed MRI studies “may lead to development of more rational therapies to help reduce the burden of DPN.”
Tesfaye S, Selvarajah D, Gandhi R, et al. Diabetic peripheral neuropathy may not be as its name suggests: evidence from magnetic resonance imaging. Pain. 2016; 157:S72-S80 doi: 10.1097/j.pain.0000000000000465.