scholarly journals Traumatic brain injury as a risk factor for dementia

2019 ◽  
Vol 29 (Supplement_4) ◽  
Author(s):  
E Mezzalira ◽  
B Stopa ◽  
A Khawaja ◽  
S Izzy ◽  
W Gormley

Abstract Introduction The Centers for Disease Control and Prevention (CDC) reports that there were 2.87 million cases of traumatic brain injury (TBI) in the United States in 2014, 69 million worldwide. Some studies suggest a connection between TBI and increased risk of dementia, but it remains unclear whether the risk increases with age and TBI severity. Given our aging population, it is essential to better characterize the link between TBI and dementia. Methods We conducted a retrospective cohort study of two major academic medical centers for years 2000-2015. We identified all patients with TBI, aged 45 and older. Variables included age, TBI severity, pre-existing dementia, dementia diagnosed after TBI, years to dementia, and follow-up time. TBI severity was determined by head/neck AIS score, using ICD-PIC software. Mild TBI was defined as AIS 0-2, and Moderate/Severe as AIS 3-6. Analysis was done in R.v.3.0.1 software. Results Overall, there were 14,199 patients with TBI, of which 9,938 (70%) were mild and 4,261 (30%) were moderate/severe. Mean age was 70.5 (±14.0). There were 1,422 cases (10%) of pre-existing dementia, and 850 (6%) cases of dementia diagnosed after TBI. The mean follow-up time was 1,129 (±1,474) days. The 75-84 age group had the highest incidence of TBI (28%). When compared by age group and TBI severity, the proportion of moderate/severe TBI increased with increasing age. The proportion of pre-existing dementia increased with age, as expected. Notably, there is increased incidence of dementia after TBI in patients aged 65 and older (7-10%, p < 0.001). There was no observed effect of TBI severity on the risk of dementia after TBI. Conclusions Our results indicate that TBI is a risk factor for the development of dementia, especially in patients aged 65 and older. Given the global public health burden of these two diseases it is critical to develop effective TBI primary prevention strategies. Key messages TBI is a risk factor for the development of dementia. Need for public health measures to mitigate the risk of TBI in the patient population 65 and older.

Neurosurgery ◽  
2019 ◽  
Vol 66 (Supplement_1) ◽  
Author(s):  
Brittany M Stopa ◽  
Elisabetta Mezzalira ◽  
Ajaz Khawaja ◽  
Saef Izzy ◽  
William B Gormley

Abstract INTRODUCTION The Centers for Disease Control and Prevention (CDC) reports that there were 2.87 million cases of traumatic brain injury (TBI) in the United States in 2014. Some studies suggest a connection between TBI and increased risk of dementia, but it remains unclear whether the risk increases with age and TBI severity. Given our aging population, it is essential to better characterize the link between TBI and dementia. METHODS We conducted a retrospective cohort study of 2 major academic medical centers for years 2000 to 2015. We identified all patients with TBI, aged 45 and older. Variables included age, TBI severity, pre-existing dementia, dementia diagnosed after TBI, years to dementia, and follow-up time. TBI severity was determined by head/neck AIS score, using ICD-PIC software. Mild TBI was defined as AIS 0 to 2, and moderate/severe as AIS 3 to 6. Analysis was done in R.v.3.0.1 software. RESULTS Overall, there were 14 199 patients with TBI, of which 9938 (70%) were mild and 4261 (30%) were moderate/severe. Mean age was 70.5 (± 14.0). There were 1422 cases (10%) of pre-existing dementia, and 850 (6%) cases of dementia diagnosed after TBI. The mean follow-up time was 1129 (± 1,474) d. The 75 to 84 age group had the highest incidence of TBI (28%). When compared by age group and TBI severity, the proportion of moderate/severe TBI increased with increasing age. The proportion of pre-existing dementia increased with age, as expected. Notably, there is increased incidence of dementia after TBI in patients aged 65 and older (7%-10%, P < .001). There was no observed effect of TBI severity on the risk of dementia after TBI. CONCLUSION Our results indicate that TBI is a risk factor for the development of dementia, especially in patients aged 65 and older. This points to the need for public health measures to mitigate the risk of TBI in this patient population.


2021 ◽  
Author(s):  
Max T Eyre ◽  
Fábio N Souza ◽  
Ticiana S. A. Carvalho-Pereira ◽  
Nivison Nery ◽  
Daiana de Oliveira ◽  
...  

Background: Zoonotic spillover from animal reservoirs is responsible for a significant global public health burden, but the processes that promote spillover events are poorly understood in complex urban settings. Endemic transmission of Leptospira, the agent of leptospirosis, in marginalised urban communities occurs through human exposure to an environment contaminated by bacteria shed in the urine of the rat reservoir. However, it is unclear to what extent transmission is driven by variation in the distribution of rats or by the dispersal of bacteria in rainwater runoff and overflow from open sewer systems. <br /><br />Methods: We conducted an eco-epidemiological study in a high-risk community in Salvador, Brazil, by prospectively following a cohort of 1,401 residents to ascertain serological evidence for leptospiral infections. A concurrent rat ecology study was used to collect information on the fine-scale spatial distribution of ‘rattiness’, our proxy for rat abundance and exposure of interest. We developed and applied a novel geostatistical framework for joint spatial modelling of multiple indices of disease reservoir abundance and human infection risk. <br /><br />Results: The estimated infection rate was 51.4 (95\%CI 40.4, 64.2) infections per 1,000 follow-up events. Infection risk increased with age until 30 years of age and was associated with male gender. Rattiness was positively associated with infection risk for residents across the entire study area, but this effect was stronger in higher elevation areas (OR 3.27 95\%CI 1.68, 19.07) than in lower elevation areas (OR 1.14 95\%CI 1.05, 1.53). <br /><br />Conclusions: These findings suggest that, while frequent flooding events may disperse bacteria in regions of low elevation, environmental risk in higher elevation areas is more localised and directly driven by the distribution of local rat populations. The modelling framework developed may have broad applications in delineating complex animal-environment-human interactions during zoonotic spillover and identifying opportunities for public health intervention.<br /><br />Funding: This work was supported by the Oswaldo Cruz Foundation and Secretariat of Health Surveillance, Brazilian Ministry of Health, the National Institutes of Health of the United States (grant numbers F31 AI114245, R01 AI052473, U01 AI088752, R01 TW009504 and R25 TW009338); the Wellcome Trust (102330/Z/13/Z), and by the Fundação de Amparo à Pesquisa do Estado da Bahia (FAPESB/JCB0020/2016). M.T.E is supported by an MRC doctorate studentship. F.N.S. participated in this study under a FAPESB doctorate scholarship.


2020 ◽  
Vol 64 (10) ◽  
Author(s):  
Gisele Peirano ◽  
Liang Chen ◽  
Barry N. Kreiswirth ◽  
Johann D. D. Pitout

ABSTRACT There is an enormous global public health burden due to antimicrobial-resistant (AMR) Klebsiella pneumoniae high-risk clones. K. pneumoniae ST307 and ST147 are recent additions to the family of successful clones in the species. Both clones likely emerged in Europe during the early to mid-1990s and, in a relatively short time, became prominent global pathogens, spreading to all continents (with the exception of Antarctica). ST307 and ST147 consist of multiple clades/clusters and are associated with various carbapenemases (i.e., KPCs, NDMs, OXA-48-like, and VIMs). ST307 is endemic in Italy, Colombia, the United States (Texas), and South Africa, while ST147 is endemic in India, Italy, Greece, and certain North African countries. Both clones have been introduced into regions of nonendemicity, leading to worldwide nosocomial outbreaks. Genomic studies showed ST307 and ST147 contain identical gyrA and parC mutations and likely obtained plasmids with blaCTX-M-15 during the early to mid-2000s, which aided in their global distribution. ST307 and ST147 then acquired plasmids with various carbapenemases during the late 2000s, establishing themselves as important AMR pathogens in certain regions. Both clones are likely underreported due to restricted detection methodologies. ST307 and ST147 have the ability to become major threats to public health due to their worldwide distribution, ability to cause serious infections, and association with AMR, including panresistance. The medical community at large, especially those concerned with antimicrobial resistance, should be aware of the looming threat posed by emerging AMR high-risk clones such as K. pneumoniae ST307 and ST147.


2017 ◽  
Vol 38 (06) ◽  
pp. 768-774 ◽  
Author(s):  
Annie Chiu ◽  
Holly Hinson

AbstractTraumatic brain injury (TBI) is a serious health care problem on both individual and public health levels. As a major cause of death and disability in the United States, it is associated with a significant economic and public health burden. Although the evidence to support the use of induced hypothermia on neurologic outcome after cardiac arrest is well established, its use in treating TBI remains controversial. Hypothermia has the potential to mitigate some of the destructive processes that occur as part of secondary brain injury after TBI. Hypothermia can be helpful in lowering intracranial pressure, for example, but its influence on functional outcome is unclear. There is insufficient evidence to support the broad use of prophylactic hypothermia for neuroprotection after TBI. Investigators are beginning to more carefully select patients for temperature modulating therapies, in a more personalized approach. Examples include targeting immunomodulation and scaling hypothermia to achieve metabolic targets. This review will summarize the clinical evidence for the use of hypothermia to limit secondary brain injury following acute TBI.


Biomedicines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1650
Author(s):  
Pei-Wen Cheng ◽  
Yi-Chung Wu ◽  
Tzyy-Yue Wong ◽  
Gwo-Ching Sun ◽  
Ching-Jiunn Tseng

Traumatic brain injury confers a significant and growing public health burden. It is a major environmental risk factor for dementia. Nonetheless, the mechanism by which primary mechanical injury leads to neurodegeneration and an increased risk of dementia-related diseases is unclear. Thus, we aimed to investigate the effect of stretching on SH-SY5Y neuroblastoma cells that proliferate in vitro. These cells retain the dopamine-β-hydroxylase activity, thus being suitable for neuromechanistic studies. SH-SY5Y cells were cultured on stretchable membranes. The culture conditions contained two groups, namely non-stretched (control) and stretched. They were subjected to cyclic stretching (6 and 24 h) and 25% elongation at 1 Hz. Following stretching at 25% and 1 Hz for 6 h, the mechanical injury changed the mitochondrial membrane potential and triggered oxidative DNA damage at 24 h. Stretching decreased the level of brain-derived neurotrophic factors and increased amyloid-β, thus indicating neuronal stress. Moreover, the mechanical injury downregulated the insulin pathway and upregulated glycogen synthase kinase 3β (GSK-3β)S9/p-Tau protein levels, which caused a neuronal injury. Following 6 and 24 h of stretching, GSK-3βS9 was directly bound to p-TauS396. In contrast, the neuronal injury was improved using GSK-3β inhibitor TWS119, which downregulated amyloid-β/p-Taus396 phosphorylation by enhancing ERK1/2T202/Y204 and AktS473 phosphorylation. Our findings imply that the neurons were under stress and that the inactivation of the GSK3β could alleviate this defect.


Neurology ◽  
2021 ◽  
Vol 96 (13) ◽  
pp. e1792-e1799
Author(s):  
Yue Leng ◽  
Amy L. Byers ◽  
Deborah E. Barnes ◽  
Carrie B. Peltz ◽  
Yixia Li ◽  
...  

ObjectiveTo test the hypothesis that veterans with traumatic brain injury (TBI) have an increased subsequent risk of sleep disorders, we studied the longitudinal association between TBI and incident sleep disorders in nearly 200,000 veterans.MethodsWe performed a cohort study of all patients diagnosed with a TBI in the Veterans Health Administration system from October 1, 2001, to September 30, 2015, who were age-matched 1:1 to veterans without TBI. Veterans with prevalent sleep disorders at baseline were excluded. Development of sleep disorders was defined as any inpatient or outpatient diagnosis of sleep apnea, hypersomnia, insomnia, or sleep-related movement disorders based on ICD-9 codes after the first TBI diagnosis or the random selection date for those without TBI. We restricted the analysis to those with at least 1 year of follow-up. We used Cox proportional hazards models to examine the association between TBI and subsequent risk of sleep disorders.ResultsThe study included 98,709 veterans with TBI and 98,709 age-matched veterans without TBI (age 49 ± 20 years). After an average follow-up of 5 (1–14) years, 23,127 (19.6%) veterans developed sleep disorders. After adjustment for demographics, education, income, and medical and psychiatric conditions, those who had TBI compared to those without TBI were 41% more likely to develop any sleep disorders (hazard ratio 1.41 [95% confidence interval 1.37–1.44]), including sleep apnea (1.28 [1.24–1.32]), insomnia (1.50 [1.45–1.55]), hypersomnia (1.50 [1.39–1.61]), and sleep-related movement disorders (1.33 [1.16–1.52]). The association was stronger for mild TBIs, did not differ appreciably by presence of posttraumatic stress disorder, and remained after a 2-year time lag.ConclusionIn 197,418 veterans without sleep disorders, those with diagnosed TBI had an increased risk of incident sleep disorders over 14 years. Improved prevention and long-term management strategies for sleep are needed for veterans with TBI.


2020 ◽  
Vol 110 (6) ◽  
pp. 897-899
Author(s):  
Gabrielle F. Miller ◽  
Scott R. Kegler ◽  
Deborah M. Stone

Objectives. To document the increasing influence of firearm suicide on the incidence of traumatic brain injury (TBI)–related death in the United States. Methods. We used national vital statistics data from 2008 to 2017 to identify TBI-related deaths, overall and by cause, among US residents. National counts stratified by year, sex, and age group (to facilitate age adjustment) were merged with corresponding population estimates to calculate incidence rates. Results. During the 10-year period beginning in 2008, when it became the leading cause of TBI-related death in the United States, firearm suicide accounted for nearly half (48.3%) of the increase in the absolute incidence of TBI-related death when combining all injury categories showing absolute increases. Rates of TBI-related firearm suicide increased among both males and females. Conclusions. Safe storage of firearms among people at risk and training of health care providers and community members to identify and support people who may be thinking of suicide are part of a comprehensive public health approach to suicide prevention. Public Health Implications. States, communities, and health care systems can save lives by prioritizing comprehensive suicide prevention.


2020 ◽  
Vol 11 (5) ◽  
pp. 77-82
Author(s):  
Ambarish Ghosh ◽  
Birva Desai ◽  
Arghya Halder ◽  
Aniruddha Ghosh ◽  
Priyanka Das ◽  
...  

Background: Traumatic brain injury (TBI), a leading cause of morbidity and mortality worldwide, is an alteration in brain function, caused by an external force. With rapid surge in urbanization, motorization and economic liberalization in India, risk of TBI is increased, raising a cause for concern about its neurological as well as psychiatric sequelae. Aims and Objectives: This study was planned to understand the magnitude of the problem which could give us insights to manage/ rehabilitate it in a more comprehensive manner. Materials and Methods: The current study included 50 patients aged 18-60 years at DY Patil Medical College, Pune. GCS scores were noted for severity of TBI. Patients were assessed through MMSE, BCRS, HAM-A & BDI. Results: On GCS, 20% cases had severe head injury; 22% moderate and 58% had mild. On MMSE initially, at six months and one year; 26.19%, 21.88% & 11.1% cases had cognitive impairment respectively. On BCRS, 38.10%, 34.4% & 37.10% cases had cognitive deterioration initially, at six month & at one year respectively. On HAM-A, mild & moderate to severe anxiety was found in 64.3% & 35.7% cases respectively. On BDI, initially 7.14% cases had depression, 25% at six months and 37.05% after one year. No statistically significant change was seen in BCRS score during follow up. Comparison of the mean scores at first interview and at six months demonstrated statistically significant (P-value p<0.005) differences in MMSE as well as BDI. Conclusion: TBI is associated with n increased risk of psychiatric disorders and may need psychiatric interventions later.


2010 ◽  
Vol 41 (6) ◽  
pp. 1271-1277 ◽  
Author(s):  
Yi-Hua Chen ◽  
Wen-Ta Chiu ◽  
Shu-Fen Chu ◽  
Herng-Ching Lin

BackgroundWhether traumatic brain injury (TBI) is an independent risk factor for the subsequent development of schizophrenia has evoked considerable controversy. No evidence has been previously reported from Asia. This study estimated the risk of schizophrenia during a 5-year period following hospital admission for TBI relative to a comparison group of non-TBI patients during the same period in Taiwan.MethodTwo datasets were linked: the Traumatic Brain Injury Registry and the Taiwan National Health Insurance Research Dataset. A total of 3495 patients hospitalized with a diagnosis of TBI from 2001 to 2002 were included, together with 17 475 non-TBI patients as the comparison group, matched on sex, age, and year of TBI hospitalization. Each individual was followed for 5 years to identify any later diagnosis of schizophrenia. Cox proportional hazard regressions were performed for analysis.ResultsDuring the 5-year follow-up period, patients who had suffered TBI were independently associated with a 1.99-fold (95% confidence interval 1.28–3.08) increased risk of subsequent schizophrenia, after adjusting for monthly income and residential geographical location. The severity and type of TBI was not associated with the subsequent development of schizophrenia.ConclusionsOur findings add important evidence from Asia and suggest a potential link between TBI and schizophrenia. Our study suggests that clinicians and family members should be alert to possible neuropsychiatric conditions following TBI.


2016 ◽  
Vol 22 (3) ◽  
Author(s):  
Ahmad Imran ◽  
Abid Ali Qureshi ◽  
Amna Tariq

<p>The study was aimed at documenting the relationship between Glasgow coma score with imaging findings on computed tomography in children with traumatic brain injury. Un-necessary radiation exposure can be detrimental in pediatric age group and can lead to an increased risk of radiation induced malignancies.</p><p><strong>Patients and Methods:</strong><strong>  </strong>This retrospective study was conducted in Department of Radiology Lahore from 15.8.11 to 15.11.11. It included 48 children who presented in emergency department with history of fall or trauma to head. These patients underwent computed tomography using standard imaging protocols. All the data was analyzed by using SPSS version 17.</p><p><strong>Results:</strong><strong>  </strong>A total of 48 patients from 6 months to 15 years of age with history of fall or trauma to head who underwent CT scan were included in study. 20 (42%) patients revealed normal study. Extra/intra axial bleed is noted in 11 (23%), evidence of cerebral edema was</p><p>noted in 4 (8%) patients. 9 (19%) patients had fracture of skull bones and cephalhematoma was noted among 4 (8%) patients. Imaging findings were seen in majority of the patients with GCS less than 13/15.</p><p><strong>Conclusion:</strong><strong>  </strong>Neuroimaging can serve as a useful guide regarding management of traumatic brain injury however un-necessary radiation exposure is detrimental in pediatric age group. A correlation between GCS and decision regarding imaging can serve as an effective approach to decrease rates of neuro imaging after pediatric head trauma.</p>


Sign in / Sign up

Export Citation Format

Share Document