Connect with us
  • Elysium

Spinal injury news

Antibodies ‘could propagate pain after SCI’

‘We know about antibody-mediated autoimmune syndromes developing in patients with cancer – but that it can also occur in patients after SCI is striking’



Antibodies that develop after spinal cord injury may help to propagate pain after severe forms of SCI, new research has revealed. 

Patients recovering from severe SCI can develop an autoimmune response directed against spinal cord proteins that may associate with pain development, the study reveals. 

Researchers found that after SCI, the immune system of some patients produces antibodies that bind to the spinal cord and living neurons. Such autoantibodies could lead to the development of pain or even interfere with the response to rehabilitation, they state.  

The findings could lead to new treatments for SCI patients who have certain antibody profiles.

“To our knowledge, this is the first study to demonstrate that, after SCI, patients may increasingly develop autoantibodies that bind to the spinal cord and to the surface of neurons,” said corresponding author Dr Jan Schwab, professor of neurology and neurosciences at Ohio State University. 

“As such, our findings indicate that antibody-mediated autoimmune responses may emerge in some patients about three weeks after SCI. 

“So far, we know about antibody-mediated autoimmune syndromes developing in patients with cancer, but that it can also occur in patients after SCI is striking.”

The study, by Ohio State University Wexner Medical Centre and College of Medicine, alongside the Medical University in Vienna, applied and extended diagnostic methods which were earlier established to detect autoimmune diseases of the brain, such as autoimmune encephalitis. 

“Here, the ability to become able to diagnose patients with autoimmune encephalitis was crucial,” said Dr Schwab. 

“After reaching a diagnosis, these patients can now be successfully treated, which was not possible 15 years ago. 

“In analogy, extending this clinically validated toolbox enabled us to reveal novel autoimmune signatures after SCI, as a first and necessary step.”

Dr Schwab and his collaborators compared blood-serum antibodies from patients with severe (motor complete and motor incomplete) SCI and from control patients over time. The capacity of antibodies to recognise and bind to spinal cord tissue proteins as well as living dorsal root ganglia neurons was tested in a blinded manner.

In addition, the researchers examined archival human spinal tissue samples at time points ranging from the time of injury to several months later. They looked for B- and Plasma cells as cellular origin of the antibody synthesis at the lesion site in spinal-cord injury compared to unaltered control cord tissue.

Key findings included:

  • Robust and emerging autoantibody binding was restricted to only a subpopulation (16 per cent) of SCI patients; it was absent in controls
  • Autoantibody binding was detected mainly in a specific region of the spinal cord involved in sensory-motor integration (i.e., the substantia gelatinosa)
  • Autoantibody binding was associated with patients who required neuropathic pain medication
  • The study of archival spinal-tissue lesions showed B-cell infiltration in 27 per cent of the SCI patients, the presence of plasma cells in nine per cent, synthesising both IgG and IgM antibodies in areas of activated complement deposition. Antibody synthesis in an area of complement deposition if self-sufficient mechanism to propagate cell death
  • Analysis of cerebral spinal fluid from an additional single patient demonstrated IgM antibody synthesis with late re-opening of the blood spinal cord barrier.

“Overall, our study revealed a new and unexpected autoimmune signature that affects a subpopulation of patients after SCI and qualifies as modifiable, potential mechanism to reduce pain and improve quality of life in spinal cord injured patients,” Dr Schwab said.