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Traumatic Brain Injury: Difference between revisions
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See open access article by Irvine et al | {{stub}} | ||
This article focuses on chronic pain following traumatic brain injury. See open access article by Irvine et al.{{#pmid:29025157|irvine}} | |||
==Epidemiology== | |||
Global incidence of TBI is 106 per 100,000 people.<ref name="irvine"/> | |||
==Classification== | |||
{| class="wikitable" | |||
|+ Classification of Traumatic Brain Injury<ref name="irvine"/> | |||
|- | |||
! 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.<ref name="irvine"/> | |||
==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== | |||
*[[Chronic Post-Traumatic Neck Pain]] | |||
==References== | ==References== | ||
[[Category:Cervical Spine]] | [[Category:Cervical Spine Conditions]] | ||
[[Category:Head and Jaw]] | <references /> | ||
[[Category:Head and Jaw Conditions]] | |||
Latest revision as of 19:43, 6 January 2023
This article is a stub.
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
| 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.
