Severe traumatic brain injury treatment

Severe traumatic brain injury treatment

There are currently no established treatments for the underlying pathophysiology in TBI and while neuro-rehabilitation efforts are promising, there are currently is a lack of consensus regarding rehabilitation following TBI of any severity 1).

see Severe traumatic brain injury guidelines.

see also Pediatric traumatic brain injury guidelines.

Severe traumatic brain injury (TBI) is currently managed in the intensive care unit with a combined medical-surgical approach. Treatment aims to prevent additional brain damage and to optimise conditions for brain recovery. TBI is typically considered and treated as one pathological entity, although in fact it is a syndrome comprising a range of lesions that can require different therapies and physiological goals. Owing to advances in monitoring and imaging, there is now the potential to identify specific mechanisms of brain damage and to better target treatment to individuals or subsets of patients. Targeted treatment is especially relevant for elderly people-who now represent an increasing proportion of patients with TBI-as preinjury comorbidities and their therapies demand tailored management strategies. Progress in monitoring and in understanding pathophysiological mechanisms of TBI could change current management in the intensive care unit, enabling targeted interventions that could ultimately improve outcomes 2).

Monitoring

see Intracranial pressure monitoring for severe traumatic brain injury.

Hormonal replacement

Hormonal analysis should be considered in patients with moderate-to-severe traumatic brain injury, so that appropriate hormonal replacement can be done to optimize the clinical outcome 3).

Case series

Data from 729 severe traumatic brain injury patients admitted between 1996 and 2016 were used. Treatment was guided by controlling intracranial pressure and cerebral perfusion pressure according to a local protocol.

Cerebral perfusion pressurepressure reactivity index curves were fitted automatically using a previously published curve-fitting heuristic from the relationship between pressure reactivity index and cerebral perfusion pressure. The cerebral perfusion pressure values at which this “U-shaped curve” crossed the fixed threshold from intact to impaired pressure reactivity (pressure reactivity index = 0.3) were denoted automatically the “lower” and “upper” cerebral perfusion pressure limits of reactivity, respectively. The percentage of time with cerebral perfusion pressure below (%cerebral perfusion pressure < lower limit of reactivity), above (%cerebral perfusion pressure > upper limit of reactivity), or within these reactivity limits (%cerebral perfusion pressure within limits of reactivity) was calculated for each patient and compared across dichotomized Glasgow Outcome Scores. After adjusting for age, initial Glasgow Coma Scale, and mean intracranial pressure, percentage of time with cerebral perfusion pressure less than lower limit of reactivity was associated with unfavorable outcome (odds ratio %cerebral perfusion pressure < lower limit of reactivity, 1.04; 95% CI, 1.02-1.06; p < 0.001) and mortality (odds ratio, 1.06; 95% CI, 1.04-1.08; p < 0.001).

Individualized autoregulation-guided cerebral perfusion pressure management may be a plausible alternative to fixed cerebral perfusion pressure threshold management in severe traumatic brain injury patients. Prospective randomized research will help define which autoregulation-guided method is beneficial, safe, and most practical 4).

Medicaments

Despite the incidence of these injuries and their substantial socioeconomic implications, no specific pharmacological intervention is available for clinical use.

see Progesterone for acute traumatic brain injury.

see 21-aminosteroids for severe traumatic brain injury.

Neuroprotection

see Neuroprotection in traumatic Brain Injury

see Decompressive craniectomy for severe traumatic brain injury.

Cell-based therapies

Cell-based therapies are currently being investigated in treating neurotrauma due to their ability to secrete neurotrophic factors and anti-inflammatory cytokines that can regulate the hostile milieu associated with chronic neuroinflammation found in TBI. In tandem, the stimulation and mobilization of endogenous stem/progenitor cells from the bone marrow through granulocyte colony stimulating factor (G-CSF) poses as an attractive therapeutic intervention for chronic TBI.

The potential of a combined therapy of human umbilical cord blood cells (hUCB) and G-CSF at the acute stage of TBI to counteract the progressive secondary effects of chronic TBI using the controlled cortical impact model.

Four different groups of adult Sprague Dawley rats were treated with saline alone, G-CSF+saline, hUCB+saline or hUCB+G-CSF, 7-days post CCI moderate TBI. Eight weeks after TBI, brains were harvested to analyze hippocampal cell loss, neuroinflammatory response, and neurogenesis by using immunohistochemical techniques. Results revealed that the rats exposed to TBI treated with saline exhibited widespread neuroinflammation, impaired endogenous neurogenesis in DG and SVZ, and severe hippocampal cell loss. hUCB monotherapy suppressed neuroinflammation, nearly normalized the neurogenesis, and reduced hippocampal cell loss compared to saline alone. G-CSF monotherapy produced partial and short-lived benefits characterized by low levels of neuroinflammation in striatum, DG, SVZ, and corpus callosum and fornix, a modest neurogenesis, and a moderate reduction of hippocampal cells loss. On the other hand, combined therapy of hUCB+G-CSF displayed synergistic effects that robustly dampened neuroinflammation, while enhancing endogenous neurogenesis and reducing hippocampal cell loss. Vigorous and long-lasting recovery of motor function accompanied the combined therapy, which was either moderately or short-lived in the monotherapy conditions. These results suggest that combined treatment rather than monotherapy appears optimal for abrogating histophalogical and motor impairments in chronic TBI 5).

Research

Research in traumatic brain injury (TBI) is challenging for several reasons; in particular, the heterogeneity between patients regarding causes, pathophysiology, treatment, and outcome. Advances in basic science have failed to translate into successful clinical treatments, and the evidence underpinning guideline recommendations is weak. Because clinical research has been hampered by non-standardised data collection, restricted multidisciplinary collaboration, and the lack of sensitivity of classification and efficacy analyses, multidisciplinary collaborations are now being fostered. Approaches to deal with heterogeneity have been developed by the IMPACT study group. These approaches can increase statistical power in clinical trials by up to 50% and are also relevant to other heterogeneous neurological diseases, such as stroke and subarachnoid haemorrhage. Rather than trying to limit heterogeneity, we might also be able to exploit it by analysing differences in treatment and outcome between countries and centres in comparative effectiveness research. This approach has great potential to advance care in patients with TBI 6).

Anticoagulation Resumption after traumatic brain injury

Anticoagulation Resumption after traumatic brain injury.

Thromboprophylaxis

The early administration of venous thromboembolism (VTE) chemoprophylaxis within 24 h after admission in patients with severe TBI did not increase the risk of intracranial bleeding progression 7).

Transcutaneous Vagus Nerve Stimulation for Severe Traumatic Brain Injury

see Transcutaneous Vagus Nerve Stimulation for Severe Traumatic Brain Injury.

References

1)

Marklund N, Bellander BM, Godbolt A, Levin H, McCrory P, Thelin EP. Treatments and rehabilitation in the acute and chronic state of traumatic brain injury. J Intern Med. 2019 Mar 18. doi: 10.1111/joim.12900. [Epub ahead of print] PubMed PMID: 30883980.
2)

Stocchetti N, Carbonara M, Citerio G, Ercole A, Skrifvars MB, Smielewski P, Zoerle T, Menon DK. Severe traumatic brain injury: targeted management in the intensive care unit. Lancet Neurol. 2017 Jun;16(6):452-464. doi: 10.1016/S1474-4422(17)30118-7. Review. PubMed PMID: 28504109.
3)

Prasanna KL, Mittal RS, Gandhi A. Neuroendocrine dysfunction in acute phase of moderate-to-severe traumatic brain injury: A prospective study. Brain Inj. 2015;29(3):336-342. PubMed PMID: 25671810.
4)

Donnelly J, Czosnyka M, Adams H, Robba C, Steiner LA, Cardim D, Cabella B, Liu X, Ercole A, Hutchinson PJ, Menon DK, Aries MJH, Smielewski P. Individualizing Thresholds of Cerebral Perfusion Pressure Using Estimated Limits of Autoregulation. Crit Care Med. 2017 Sep;45(9):1464-1471. doi: 10.1097/CCM.0000000000002575. PubMed PMID: 28816837.
5)

Acosta SA, Tajiri N, Shinozuka K, Ishikawa H, Sanberg PR, Sanchez-Ramos J, Song S, Kaneko Y, Borlongan CV. Combination therapy of human umbilical cord blood cells and granulocyte colony stimulating factor reduces histopathological and motor impairments in an experimental model of chronic traumatic brain injury. PLoS One. 2014 Mar 12;9(3):e90953. doi: 10.1371/journal.pone.0090953. eCollection 2014. PubMed PMID: 24621603.
6)

Maas AI, Murray GD, Roozenbeek B, Lingsma HF, Butcher I, McHugh GS, Weir J, Lu J, Steyerberg EW; International Mission on Prognosis Analysis of Clinical Trials in Traumatic Brain Injury (IMPACT) Study Group. Advancing care for traumatic brain injury: findings from the IMPACT studies and perspectives on future research. Lancet Neurol. 2013 Dec;12(12):1200-10. doi: 10.1016/S1474-4422(13)70234-5. Epub 2013 Oct 17. PubMed PMID: 24139680; PubMed Central PMCID: PMC3895622.
7)

Störmann P, Osinloye W, Freiman TM, Seifert V, Marzi I, Lustenberger T. Early Chemical Thromboprophylaxis Does not Increase the Risk of Intracranial Hematoma Progression in Patients with Isolated Severe Traumatic Brain Injury. World J Surg. 2019 Jul 2. doi: 10.1007/s00268-019-05072-1. [Epub ahead of print] PubMed PMID: 31267142.

Traumatic brain injury epidemiology

Traumatic brain injury epidemiology

In 2019, relevant articles and registries were identified via systematic review; study quality was higher in the high-income countries (HICs) than in the low- and middle-income countries (LMICs). Sixty-nine million (95% CI 64-74 million) individuals worldwide are estimated to sustain a TBI each year. The proportion of TBIs resulting from road traffic accidents was greatest in Africa and Southeast Asia (both 56%) and lowest in North America (25%). The incidence of RTA was similar in Southeast Asia (1.5% of the population per year) and Europe (1.2%). The overall incidence of TBI per 100,000 people was greatest in North America (1299 cases, 95% CI 650-1947) and Europe (1012 cases, 95% CI 911-1113) and least in Africa (801 cases, 95% CI 732-871) and the Eastern Mediterranean (897 cases, 95% CI 771-1023). The LMICs experience nearly 3 times more cases of TBI proportionally than HICs.

Sixty-nine million (95% CI 64-74 million) individuals are estimated to suffer TBI from all causes each year, with the Southeast Asian and Western Pacific regions experiencing the greatest overall burden of disease. Head injury following road traffic collision is more common in LMICs, and the proportion of TBIs secondary to road traffic collision is likewise greatest in these countries. Meanwhile, the estimated incidence of TBI is highest in regions with higher-quality data, specifically in North America and Europe 1).


Traumatic brain injury (TBI) is a critical public health and socio-economic problem throughout the world, making epidemiological monitoring of incidence, prevalence and outcome necessary.

Every 15 seconds someone suffers a traumatic brain injury (TBI) in the United States. TBI causes more deaths in males <35 years old than all other diseases combined, and it is estimated that 2% of the U.S. population lives with TBI-associated disability. Despite extensive research and success in animal studies, successful drug therapies have proved elusive in clinical trials 2).

It is one of leading causes of mortality and disability worldwide and is estimated to surpass many diseases by 2020 3) 4).

It is the leading cause of mortality and morbidity in children 5).

Nonaccidental head injury, as seen in domestic child abuse cases, is often associated with spine injury, and spinal subdural hematoma is the most frequent diagnosis. While spinal epidural hematomas are a rare occurrence, the incidence of spontaneous epidural hematomas occurring in nonaccidental head injury patients is even lower 6).

Epidemiology in China

Sun et al. conducted a nationally representative door-to-door survey in the general population across all age groups in 31 provinces in mainland China in 2013.

All participants were reviewed for a history of physician-diagnosed TBI by trained investigators using a structured questionnaire. TBI survivors were considered as prevalent cases at the prevalent time. The present study also examined the odds of TBI as a function of sex, age, and other demographical variables using logistic regression model. + Of 583,870 participants, 2,673 individuals had suffered from a TBI during their past life, yielding a weighted prevalence of being 442.4 (95% CI 342.2-542.6) per 100,000 person. The TBI prevalence increased with increasing age. The present study observed the multiadjusted ORs of TBI were 1.9 (95% CI 1.8-2.1) for the male, 1.9 (95% CI 1.2-3.1) for the farmers, 1.9 (95% CI 1.2-3.3) for the retiree or homemakers, 3.4 (95% CI 1.5-7.7), and 2.8 (95% CI 1.1-6.6) for those whose education were primary school and high school, respectively. The most common external cause was road traffic accidents among those who were aged 18-34 years old and those whose educational levels were middle school in both genders.

The results indicate TBI was substantially prevalent among Chinese population and underscore the need to develop national strategies to improve the safe education on road and traffic of TBI in rural residents and some subgroup population 7).

Epidemiology in the United States

The Centers for Disease Control and Prevention (CDC) estimate that more than 1.7 million each year in USA sustain TBI. Of these, approximately 1.4 million are treated and released from emergency centers, 275,000 are hospitalized, 80,000 suffer long-term disability and 52,000 die 8) ,and another 235,000 are hospitalized for non-fatal TBI 9).

Incidence of TBI in all industrialized countries is comparable to the U.S., with estimates ranging from 150 to more than 300 per 100,000

Annual incidence of approximately 250-600 patients per 100,000, and mortality of 17 cases per 100,000.

It is one of the most common causes of death in ordinary accidents, natural disasters, or warfare.

These injuries frequently occur outside, leaving injured individuals exposed to environmental temperature extremes before they are transported to a hospital.

Each year, approximately 100,000 patients require neurosurgical evacuation of an intracranial hematoma in the United States 10).

There are strong and demographically stable associations between TBI and substance use. These associations may not only increase the odds of injury but impair the quality of post injury recovery 11).

Epidemiology in India

The exact incidence is unavailable in India.

From August 2012 to May 2013 at Department of Neurosurgery, S.C.B. Medical College, Cuttack, Odisha, India. All the pertinent details from case records of hundred and forty-seven children <15 years with TBI were analyzed. Follow-up was done for 6 months at outpatients department.

Age wise, incidence and severity of TBI is more common in 10-15 years. Males outnumber females with a male: female ratio 2.19:1. Overall, road traffic accident (RTA) is the commonest mode of injury. Assault is not uncommon (7.48% cases). Falls is common in <5 years while RTA is common in 5-15 years. The extradural hematoma was the most common injury pattern; however, surgical consideration was maximal for fracture skull. Overall mortality was 7.48%. Diffuse axonal injury has the maximum individual potential for mortality. We noticed excellent recovery in 68.7%, disabilities in 17.68%, and persistent vegetative state in 5.45% cases.

TBI in children carries good outcome, if resuscitated and referred early to a neurotrauma center, and managed subsequently on an individualized basis with a well-organized team approach. Severe TBI in children has a poor outcome 12).

Epidemiology in Europe

Traumatic brain injury (TBI) is a common reason for presentation at the emergency department (ED) and hospital admission in Europe.

In total, 28 epidemiological studies on TBI from 16 European countries were identified in the literature. A great variation was found in case definitions and case ascertainment between studies. Falls and road traffic accidents (RTA) were the two most frequent causes of TBI, with falls being reported more frequently than RTA 13).

In 2006 it was difficult to reach a consensus on all epidemiological findings across the 23 published European studies because of critical differences in methods employed across the reports 14).

Spain

2015

A search was conducted in the PubMed electronic database using the terms: epidemiology, incidence, brain injur*, head injur* and Europe. Only articles published in English and reporting on data collected in Europe between 1990 and 2014 were included. In total, 28 epidemiological studies on TBI from 16 European countries were identified in the literature. A great variation was found in case definitions and case ascertainment between studies. Falls and road traffic accidents (RTA) were the two most frequent causes of TBI, with falls being reported more frequently than RTA. In most of the studies a peak TBI incidence was seen in the oldest age groups. In the meta-analysis, an overall incidence rate of 262 per 100,000 for admitted TBI was derived.

Interpretation of published epidemiologic studies is confounded by differences in inclusion criteria and case ascertainment. Nevertheless, changes in epidemiological patterns are found: falls are now the most common cause of TBI, most notably in elderly patients. Improvement of the quality of standardised data collection for TBI is mandatory for reliable monitoring of epidemiological trends and to inform appropriate targeting of prevention campaigns 15).

Romania

A coordinated strategy to evaluate this public health problem in Romania would first of all rely on a related advanced monitoring system, to provide precise information about the epidemiology, clinical and paraclinical data, but concerning the social and economic connected consequences, too 16).

References

1)

Dewan MC, Rattani A, Gupta S, Baticulon RE, Hung YC, Punchak M, Agrawal A, Adeleye AO, Shrime MG, Rubiano AM, Rosenfeld JV, Park KB. Estimating the global incidence of traumatic brain injury. J Neurosurg. 2018 Apr 1:1-18. doi: 10.3171/2017.10.JNS17352. [Epub ahead of print] PubMed PMID: 29701556.
2)

Maas, A. I. R., Menon, D. K., et al. (2012). “Re-orientation of clinical research in traumatic brain injury: report of an international workshop on comparative effectiveness research.” Journal of Neurotrauma 29(1): 32-46.
3)

Hyder AA, Wunderlich CA, Puvanachandra P, Gururaj G, Kobusingye OC. The impact of traumatic brain injuries: A global perspective. NeuroRehabilitation 2007;22:341-53. Back to cited text no. 1
4)

Lopez AD, Murray CC. The global burden of disease, 1990-2020. Nat Med 1998;4:1241-3.
5)

K. S. Quayle, D. M. Jaffe, N. Kuppermann et al., “Diagnostic testing for acute head injury in children: when are head computed tomography and skull radiographs indicated?” Pediatrics, vol. 99, no. 5, article e11, 1997.
6)

Rangwala SD, Birk DM, Tobin MK, Hahn YS, Nikas DC. Spontaneous Resolution of Spinal Epidural Hematoma Resulting from Domestic Child Abuse: Case Report. Pediatr Neurosurg. 2016 Sep 20. [Epub ahead of print] PubMed PMID: 27644085.
7)

Sun D, Jiang B, Ru X, Sun H, Fu J, Wu S, Wang L, Wang L, Zhang M, Liu B, Wang W; for the NESS-China investigators. Prevalence and Altered Causes of Traumatic Brain Injury in China: A Nationwide Survey in 2013. Neuroepidemiology. 2019 Dec 18:1-8. doi: 10.1159/000501911. [Epub ahead of print] PubMed PMID: 31851999.
8)

Faul M, Xu L, Wald MM & Coronado VG. (2010). Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations and Deaths 2002–2006. Centers for Disease Control and Prevention, National Center for Injury Prevention and Control
9)

Corrigan JD, Selassie AW, Orman JA. The epidemiology of traumatic brain injury. J Head Trauma Rehabil 2010; 25: 72–80.
10)

Feinberg M, Mai JC, Ecklund J. Neurosurgical Management in Traumatic Brain Injury. Semin Neurol. 2015 Feb;35(1):50-56. Epub 2015 Feb 25. PubMed PMID: 25714867.
11)

Ilie G, Mann RE, Hamilton H, Adlaf EM, Boak A, Asbridge M, Rehm J, Cusimano MD. Substance Use and Related Harms Among Adolescents With and Without Traumatic Brain Injury. J Head Trauma Rehabil. 2014 Nov 25. [Epub ahead of print] PubMed PMID: 25427256.
12)

Satapathy MC, Dash D, Mishra SS, Tripathy SR, Nath PC, Jena SP. Spectrum and outcome of traumatic brain injury in children <15 years: A tertiary level experience in India. Int J Crit Illn Inj Sci. 2016 Jan-Mar;6(1):16-20. PubMed PMID: 27051617.
13) , 15)

Peeters W, van den Brande R, Polinder S, Brazinova A, Steyerberg EW, Lingsma HF, Maas AI. Epidemiology of traumatic brain injury in Europe. Acta Neurochir (Wien). 2015 Oct;157(10):1683-96. doi: 10.1007/s00701-015-2512-7. Epub 2015 Aug 14. PubMed PMID: 26269030.
14)

Tagliaferri F, Compagnone C, Korsic M, Servadei F, Kraus J. A systematic review of brain injury epidemiology in Europe. Acta Neurochir (Wien). 2006 Mar;148(3):255-68; discussion 268. Review. PubMed PMID: 16311842.
16)

Popescu C, Anghelescu A, Daia C, Onose G. Actual data on epidemiological evolution and prevention endeavours regarding traumatic brain injury. J Med Life. 2015 Jul-Sep;8(3):272-7. Review. PubMed PMID: 26351526; PubMed Central PMCID: PMC4556905.

Severe traumatic brain injury outcome

Severe traumatic brain injury outcome

There has been a secular trend towards reduced incidence of severe traumatic brain injury in the first world, driven by public health interventions such as seatbelt legislation, helmet use, and workplace health and safety regulations. This has paralleled improved outcomes following TBI delivered in a large part by the widespread establishment of specialised neurointensive care 1).

Effect of trauma center designation in severe traumatic brain injury outcome

see Effect of trauma center designation in severe traumatic brain injury outcome


Mortality or severe disability affects the majority of patients after severe traumatic brain injury (TBI). Adherence to the brain trauma foundation severe traumatic brain injury guidelines has overall improved outcomes; however, traditional as well as novel interventions towards intracranial hypertension and secondary brain injury have come under scrutiny after series of negative randomized controlled trials. In fact, it would not be unfair to say there has been no single major breakthrough in the management of severe TBI in the last two decades. One plausible hypothesis for the aforementioned failures is that by the time treatment is initiated for neuroprotection, or physiologic optimization, irreversible brain injury has already set in. Lazaridis et al., and others, have developed predictive models based on machine learning from continuous time series of intracranial pressure and partial pressure of brain tissue oxygen. These models provide accurate predictions of physiologic crises events in a timely fashion, offering the opportunity for an earlier application of targeted interventions. In a article, Lazaridis et al., review the rationale for prediction, discuss available predictive models with examples, and offer suggestions for their future prospective testing in conjunction with preventive clinical algorithms 2).


Determining the prognostic significance of clinical factors for patients with severe head injury can lead to an improved understanding of the pathophysiology of head injury and to improvement in therapy. A technique known as the sequential Bayes method has been used previously for the purpose of prognosis. The application of this method assumes that prognostic factors are statistically independent. It is now known that they are not. Violation of the assumption of independence may produce errors in determining prognosis. As an alternative technique for predicting the outcome of patients with severe head injury, a logistic regression model is proposed. A preliminary evaluation of the method using data from 115 patients with head injury shows the feasibility of using early data to predict outcome accurately and of being able to rank input variables in order of their prognostc significance. 3).


A prospective and consecutive series of 225 patients with severe head injuries who were managed in a uniform way was analyzed to relate outcome to several clinical variables. Good recovery or moderate disability were achieved by 56% of the patients, 10% remained severely disabled or vegetative, and 34% died. Factors important in predicting a poor outcome included the presence of intracranial hematoma, increasing age, motor impairment, impaired or absent eye movements or pupillary light reflexes, early hypotension, hypoxemia or hypercarbia, and raised intracranial pressure over 20 mm Hg despite artificial ventilation. Most of these predictive factors were assessed on admission, but a subset of 158 patients was identified in whom coma was present on admission and was known to have persisted at least until the following day. Although the mortality in this subset (40%) was higher than in the total series, it was lower than in several comparable reported series of patients with severe head injury. Predictive correlations were equally strong in the entire series and in the subset of 158 patients with coma. A plea is made for inclusion in the definition of “severe head injury” of all patients who do not obey commands or utter recognizable words on admission to the hospital after early resuscitation 4).


Survival rate of isolated severe TBI patients who required an emergent neurosurgical intervention could be time dependent. These patients might benefit from expedited process (computed tomographic scan, neurosurgical consultation, etc.) to shorten the time to surgical intervention 5).

The impact of a moderate to severe brain injury can include:

Cognitive deficits including difficulties with:

Attention Concentration Distractibility Memory Speed of Processing Confusion Perseveration Impulsiveness Language Processing “Executive functions” Speech and Language

not understanding the spoken word (receptive aphasia) difficulty speaking and being understood (expressive aphasia) slurred speech speaking very fast or very slow problems reading problems writing Sensory

difficulties with interpretation of touch, temperature, movement, limb position and fine discrimination Perceptual

the integration or patterning of sensory impressions into psychologically meaningful data Vision

partial or total loss of vision weakness of eye muscles and double vision (diplopia) blurred vision problems judging distance involuntary eye movements (nystagmus) intolerance of light (photophobia) Hearing

decrease or loss of hearing ringing in the ears (tinnitus) increased sensitivity to sounds Smell

loss or diminished sense of smell (anosmia) Taste

loss or diminished sense of taste Seizures

the convulsions associated with epilepsy that can be several types and can involve disruption in consciousness, sensory perception, or motor movements Physical Changes

Physical paralysis/spasticity Chronic pain Control of bowel and bladder Sleep disorders Loss of stamina Appetite changes Regulation of body temperature Menstrual difficulties Social-Emotional

Dependent behaviors Emotional ability Lack of motivation Irritability Aggression Depression Disinhibition Denial/lack of awareness


Both single predictors from early clinical examination and multiple hospitalization variables/parameters can be used to determine the long-term prognosis of TBI. Predictive models like the IMPACT or CRASH prognosis calculator (based on large sample sizes) can predict mortality and unfavorable outcomes. Moreover, imaging techniques like MRI (Magnetic Resonance Imaging) can also predict consciousness recovery and mental recovery in severe TBI, while biomarkers associated with stress correlate with, and hence can be used to predict, severity and mortality. All predictors have limitations in clinical application. Further studies comparing different predictors and models are required to resolve limitations of current predictors 6).

References

1)

Khellaf A, Khan DZ, Helmy A. Recent advances in traumatic brain injury. J Neurol. 2019 Sep 28. doi: 10.1007/s00415-019-09541-4. [Epub ahead of print] PubMed PMID: 31563989.
2)

Lazaridis C, Rusin CG, Robertson CS. Secondary Brain Injury: Predicting and Preventing Insults. Neuropharmacology. 2018 Jun 6. pii: S0028-3908(18)30279-X. doi: 10.1016/j.neuropharm.2018.06.005. [Epub ahead of print] Review. PubMed PMID: 29885419.
3)

Stablein DM, Miller JD, Choi SC, Becker DP. Statistical methods for determining prognosis in severe head injury. Neurosurgery. 1980 Mar;6(3):243-8. PubMed PMID: 6770283.
4)

Miller JD, Butterworth JF, Gudeman SK, Faulkner JE, Choi SC, Selhorst JB, Harbison JW, Lutz HA, Young HF, Becker DP. Further experience in the management of severe head injury. J Neurosurg. 1981 Mar;54(3):289-99. PubMed PMID: 7463128.
5)

Matsushima K, Inaba K, Siboni S, Skiada D, Strumwasser AM, Magee GA, Sung GY, Benjaminm ER, Lam L, Demetriades D. Emergent operation for isolated severe traumatic brain injury: Does time matter? J Trauma Acute Care Surg. 2015 Aug 28. [Epub ahead of print] PubMed PMID: 26317818.
6)

Gao L, Wu X. Prediction of clinical outcome in severe traumatic brain injury. Front Biosci (Landmark Ed). 2015 Jan 1;20:763-771. PubMed PMID: 25553477.

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