The DOI matches its Crossref record; 124 of the 124 references it cites were found in a registry or an index.
Traumatic Brain Injury: A Disease Process, Not an Event
Abstract
Traumatic brain injury (TBI) is seen by the insurance industry and many health care providers as an "event." Once treated and provided with a brief period of rehabilitation, the perception exists that patients with a TBI require little further treatment and face no lasting effects on the central nervous system or other organ systems. In fact, TBI is a chronic disease process, one that fits the World Health Organization definition as having one or more of the following characteristics: it is permanent, caused by non-reversible pathological alterations, requires special training of the patient for rehabilitation, and/or may require a long period of observation, supervision, or care. TBI increases long-term mortality and reduces life expectancy. It is associated with increased incidences of seizures, sleep disorders, neurodegenerative diseases, neuroendocrine dysregulation, and psychiatric diseases, as well as non-neurological disorders such as sexual dysfunction, bladder and bowel incontinence, and systemic metabolic dysregulation that may arise and/or persist for months to years post-injury. The purpose of this article is to encourage the classification of TBI as the beginning of an ongoing, perhaps lifelong process, that impacts multiple organ systems and may be disease causative and accelerative. Our intent is not to discourage patients with TBI or their families and caregivers, but rather to emphasize that TBI should be managed as a chronic disease and defined as such by health care and insurance providers. Furthermore, if the chronic nature of TBI is recognized by government and private funding agencies, research can be directed at discovering therapies that may interrupt the disease processes months or even years after the initiating event.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Neuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123 · cited 1×
“Ab plaques and neurofibrillary tangles comprised of tau protein are pathological characteristics of AD (Braak and Braak, 1991; Forman et al., 2004).”
BackgroundAlzheimer's Disease: Genes, Proteins, and Therapy
Selkoe, D. J. (2001) · Physiological Reviews · doi:10.1152/physrev.2001.81.2.741 · Cited by 6,063
Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein
De Strooper, B., Saftig, P., Craessaerts, K., Vanderstichele, H., Guhde, G., Annaert, W., Von Figura, K., & Van Leuven, F. (1998) · Nature · doi:10.1038/34910 · Cited by 1,818
Premature mortality due to cardiovascular disease in hypopituitarism
Rosén, T., & Bengtsson, B.-Å. (1990) · The Lancet · doi:10.1016/0140-6736(90)91812-o · Cited by 1,402
(1999) · doi:10.1097/00001199-199912000-00009 · Cited by 1,387
Systemic inflammation and disease progression in Alzheimer disease
Holmes, C., Cunningham, C., Zotova, E., Woolford, J., Dean, C., Kerr, S., Culliford, D., & Perry, V. H. (2009) · Neurology · doi:10.1212/wnl.0b013e3181b6bb95 · Cited by 1,139 · cited 1×
“Those with high baseline TNF-a levels had a fourfold increase in the rate of cognitive decline (Holmes et al., 2009).”
A population-based study of seizures after traumatic brain injuries
Annegers, J. F., Hauser, W. A., Coan, S. P., & Rocca, W. A. (1998) · New England Journal of Medicine · doi:10.1056/nejm199801013380104 · Cited by 1,090 · cited 1×
“Individuals with a TBI are 1.5–17 times (depending on the severity of the TBI) more likely than the general population to develop seizures (Annegers et al., 1998).”
InfluentialDocumented head injury in early adulthood and risk of Alzheimer’s disease and other dementias
Plassman, B. L., Havlik, R. J., Steffens, D. C., Helms, M. J., Newman, T. N., Drosdick, D., Phillips, C., Gau, B. A., Welsh–Bohmer, K. A., Burke, J. R., et al. (2000) · Neurology · doi:10.1212/wnl.55.8.1158 · Cited by 896
Prevalence of Epilepsy in Rochester, Minnesota: 1940–1980
Hauser, W. A., Annegers, J. F., & Kurland, L. T. (1991) · Epilepsia · doi:10.1111/j.1528-1157.1991.tb04675.x · Cited by 841
Fleminger, S. (2003) · Journal of Neurology, Neurosurgery & Psychiatry · doi:10.1136/jnnp.74.7.857 · Cited by 719
Cited by
Traumatic brain injury: integrated approaches to improve prevention, clinical care, and research
Maas, A. I. R., Menon, D. K., Adelson, P. D., Andelic, N., Bell, M. J., Belli, A., Bragge, P., Brazinova, A., Büki, A., Chesnut, R. M., et al. (2017) · The Lancet Neurology · doi:10.1016/s1474-4422(17)30371-x · Cited by 2,609
The chronic and evolving neurological consequences of traumatic brain injury
Wilson, L., Stewart, W., Dams-O'Connor, K., Diaz-Arrastia, R., Horton, L., Menon, D. K., & Polinder, S. (2017) · The Lancet Neurology · doi:10.1016/s1474-4422(17)30279-x · Cited by 607
Traumatic brain injury: neuropathological, neurocognitive and neurobehavioral sequelae
Pavlovic, D., Pekic, S., Stojanovic, M., & Popovic, V. (2019) · Pituitary · doi:10.1007/s11102-019-00957-9 · Cited by 369
Epidemiology of Chronic Effects of Traumatic Brain Injury
Haarbauer-Krupa, J., Pugh, M. J., Prager, E. M., Harmon, N., Wolfe, J., & Yaffe, K. (2021) · Journal of Neurotrauma · doi:10.1089/neu.2021.0062 · Cited by 341
Traumatic brain injury: sex, gender and intersecting vulnerabilities
Mollayeva, T., Mollayeva, S., & Colantonio, A. (2018) · Nature Reviews Neurology · doi:10.1038/s41582-018-0091-y · Cited by 328
Metadata
- Authors
- Masel, B. E., & DeWitt, D. S.
- Venue
- Journal of Neurotrauma
- Publisher
- SAGE Publications
- Published
- 2010-08
- Volume
- 27
- Issue
- 8
- Pages
- 1529-1540
- ISSN
- 0897-7151 (ISSN-L)
- 1557-9042
- OpenAlex
- W1997435185
- Cited by
- 955
- References
- 124
- FWCI
- 22.64
- Type
- journal article
- Language
- en
- Open access
- closed
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Traumatic Brain Injury: A Disease Process, Not an Event. https://app.cochat.ai/papers/10.1089/neu.2010.1358
- The paper
- Masel, B. E., & DeWitt, D. S. (2010). Traumatic Brain Injury: A Disease Process, Not an Event. Journal of Neurotrauma. https://doi.org/10.1089/neu.2010.1358
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.