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Network dysfunction after traumatic brain injury
Sharp DJ, Scott G, Leech R.. Nature reviews. Neurology, 2014-02-11
Topic: Risk, prevention and care in population studies
Diffuse axonal injury after traumatic brain injury (TBI) produces neurological impairment by disconnecting brain networks. This structural damage can be mapped using diffusion MRI, and its functional effects can be investigated in large-scale intrinsic connectivity networks (ICNs). Here, we review evidence that TBI substantially disrupts ICN function, and that this disruption predicts cognitive impairment. We focus on two ICNs--the salience network and the default mode network. The activity of these ICNs is normally tightly coupled, which is important for attentional control. Damage to the structural connectivity of these networks produces predictable abnormalities of network function and cognitive control. For example, the brain normally shows a 'small-world architecture' that is optimized for information processing, but TBI shifts network function away from this organization. The effects of TBI on network function are likely to be complex, and we discuss how advanced approaches to modelling brain dynamics can provide insights into the network dysfunction. We highlight how structural network damage caused by axonal injury might interact with neuroinflammation and neurodegeneration in the pathogenesis of Alzheimer disease and chronic traumatic encephalopathy, which are late complications of TBI. Finally, we discuss how network-level diagnostics could inform diagnosis, prognosis and treatment development following TBI.
Key findings
- Damage to the structural connectivity of these networks produces predictable abnormalities of network function and cognitive control.
- For example, the brain normally shows a 'small-world architecture' that is optimized for information processing, but TBI shifts network function away from this organization.
- The effects of TBI on network function are likely to be complex, and we discuss how advanced approaches to modelling brain dynamics can provide insights into the network dysfunction.
- We highlight how structural network damage caused by axonal injury might interact with neuroinflammation and neurodegeneration in the pathogenesis of Alzheimer disease and chronic traumatic encephalopathy, which are late complications of TBI.
- Finally, we discuss how network-level diagnostics could inform diagnosis, prognosis and treatment development following TBI.
Why it matters
This review describes how traumatic brain injury disrupts large-scale brain networks and discusses how such damage might interact with inflammation and neurodegeneration in the later development of Alzheimer's disease. It is a review of mechanisms and reports no treatment that cures or prevents Alzheimer's disease.
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Study details
- Evidence strengthLow
How this study scored 47/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Nature reviews. Neurology) |
| Journal's citation record | 3 / 4 | Nature Reviews Neurology: journal h-index 269 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2014 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 647 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 46.2 citations a year over 14 year(s) since 2014 |
| Impact for its field and year | 3 / 6 | Cited 5.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 3 / 4 | Cited 140 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Robert Leech: h-index 69 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Imperial College London: institution h-index 1,744 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 24514870) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 47 / 100 | — |
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APA 7th
Sharp, D. J., Scott, G., & Leech, R. (2014). Network dysfunction after traumatic brain injury. Nature reviews. Neurology. https://doi.org/10.1038/nrneurol.2014.15
Vancouver
Sharp DJ, Scott G, Leech R. Network dysfunction after traumatic brain injury. Nature reviews. Neurology. 2014. doi:10.1038/nrneurol.2014.15. PMID: 24514870.
BibTeX
@article{sharp2014-24514870,
author = {Sharp, D. J. and Scott, G. and Leech, R.},
title = {{Network dysfunction after traumatic brain injury}},
journal = {Nature reviews. Neurology},
year = {2014},
doi = {10.1038/nrneurol.2014.15},
pmid = {24514870},
url = {https://doi.org/10.1038/nrneurol.2014.15}
}
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