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Published on: April 9, 2011
Evidence for peripheral neuroinflammation after acute whiplash
Colette Ridehalgh1,2, Joel Fundaun3,4, Stephen Bremner5
1Department of Clinical Neuroscience, Brighton and Sussex Medical School, Trafford Centre, University of Sussex, Falmer, Brighton, United Kingdom.
Whiplash-associated disorder grade II (WADII) may involve peripheral neuroinflammation, indicated by MRI changes and heightened nerve sensitivity. This suggests a need to rethink WADII management strategies.
Area of Science:
- Neuroscience
- Musculoskeletal Medicine
- Radiology
Background:
- Whiplash-associated disorder grade II (WADII) presents with neck complaints and musculoskeletal signs, often without clear neurological deficits.
- A subset of WADII patients may have underlying peripheral neuroinflammation, contributing to poor prognosis and high socioeconomic costs.
Purpose of the Study:
- To investigate the presence of peripheral neuroinflammation in acute WADII.
- To correlate neuroinflammation indicators with clinical presentations and imaging findings.
Main Methods:
- Recruited 122 WADII participants and 43 healthy controls (HCs).
- Utilized T2-weighted MRI of the brachial plexus, dorsal root ganglia, and median nerve.
- Assessed clinical surrogates: heightened nerve mechanosensitivity (HNM), serum inflammatory mediators, and quantitative sensory testing for somatosensory hyperalgesia.
Main Results:
- Increased T2 signal ratio in the C5 brachial plexus root and C5-C8 dorsal root ganglia in WADII patients compared to HCs.
- 55% of WADII participants exhibited HNM, with associated cold/pressure hyperalgesia and increased neuropathic pain.
- Elevated serum inflammatory mediators and somatosensory changes (47% of WADII) were observed.
Conclusions:
- Acute WADII exhibits a complex phenotype with evidence of peripheral neuroinflammation in a subgroup of individuals.
- Findings suggest that neuroinflammation should be considered in WADII, necessitating a re-evaluation of current management approaches.
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