Traumatic Brain Injury

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This article focuses on chronic pain following traumatic brain injury. See open access article by Irvine et al.[1]

Epidemiology

Global incidence of TBI is 106 per 100,000 people.[1]

Classification

Classification of Traumatic Brain Injury[1]
Feature Mild Moderate Severe
Loss of consciousness <30 min 30 min - 24 h > 24 h
Amnesia <24 h 1-7 d >7 d
Glasgow Coma Score 13-15 9-12 1-9
Structural Imaging Normal Abnormal, transient changes Abnormal, lasting changes

Clinical Features

Among 23 studies with 4200 patients, 51.5% had chronic pain, 57.8% of those had post-traumatic headache (some studies up to 81%). Headache at the time of injury was 71%, and by one year this had dropped to 41%. 12% had CRPS with severe TBI. Post-traumatic stress disorder can occur.[1]

Mechanisms

  • Descending regulation of pain.
    • Lower pressure pain thresholds, decreased conditioned pain modulation (similar to post-stroke, post-surgical, fibromyalgia), reduced firing LC, dysregulation PAG output.
    • Treatment alpha-2 agonists, selective serotonin-NA reuptake inhibitors.
  • Ascending pathways. STT (post thalamic stroke pain), demonstrated on diffusion tensor tractography.
    • Treatment deep brain and motor cortex stimulation, or target posterior limb capsule.
  • Dopamine & Substantia Nigra. Injury to substantia nigra and other dopaminergic centres.
    • Treatment levodopa.
  • Neuroinflammation
  • Neurodegeneration
  • Axonal damage.

All of these areas are potential mechanisms for persistent post-traumatic headache, not cervical pain.

See Also

References

  1. โ†‘ 1.0 1.1 1.2 1.3 Irvine & Clark. Chronic Pain After Traumatic Brain Injury: Pathophysiology and Pain Mechanisms. Pain medicine (Malden, Mass.) 2018. 19:1315-1333. PMID: 29025157. DOI.