Mild-to-Moderate Traumatic Brain Injury
Edit
This entry is adapted from the peer-reviewed paper 10.3390/neurolint14020038

Traumatic Brain Injury (TBI) is a major global public health problem. Neurological damage from TBI may be mild, moderate, or severe and occurs both immediately at the time of impact (primary injury) and continues to evolve afterwards (secondary injury). In mild (m)TBI, common symptoms are headaches, dizziness, and fatigue. Visual impairment is especially prevalent. Insomnia, attentional deficits and memory problems often occur. While symptoms resolve spontaneously in many, residual effects may linger for months or years in some mTBI patients. Optimally, the goal of any intervention is a return to baseline uninjured functioning with restoration of the ability to conduct daily activities.  

head injury prognosis traumatic brain injury visual pathways parietal lobe concussion rehabilitation brain imaging

1. Introduction

Traumatic brain injury (TBI) is an imminent global health challenge and the primary cause of trauma-related long-term or permanent disability worldwide [1]. In 2019, the CDC reported 61,000 deaths related to TBI [2]. With incidence rates of 50 million cases per year, TBI may be categorized as mild, moderate or severe [3]. Mild-to-moderate TBI accounts for about 90% of all TBIs while approximately 80% of TBI cases in the United States are classified as mild (mTBI) [4][5]. Severity and morbidity are disproportionately high among lower- and middle-income countries and the estimated global economic cost is 400 billion USD annually [6][7][8].
The assumption that mTBI has little consequence has been debunked as it may result in neurological symptoms and cognitive impairment with tangible impacts on quality of life and substantial demands on health services [9][10].

2. Basics of TBI

2.1. Detemining Severity

Manifestations of TBI occur after an external mechanical force is sustained by the patient in the area of the head, neck and/or face leading to a primary injury characterized by neuronal impairment [11]. The most commonly observed clinical features of mTBI are headache, dizziness, nausea and poor concentration [12]. More severe injuries can lead to aphasia, seizures, amnesia, behavioral abnormalities and, in the worst cases, coma [13]. These may manifest within seconds to minutes following TBI. The most widely used clinical assessment of TBI is the Glasgow Coma Scale (GCS) which classifies TBI as mild (14–15), moderate (9–13), or severe (3–8) [14][15]. The GCS is comprised of the eye opening, verbal, and motor subscales, which are combined to give a total GCS score. The GCS system has several shortcomings due to its ambiguity in diagnosing mild and moderate TBI. For instance, there is still persistent disagreement on whether a GCS of 13 should be treated as mild or moderate TBI [16]. Other notable challenges to the accurate diagnosis of TBI stem from inter-rater variability and a plurality of etiologies as well as a general disagreement in the literature over which of the many possible TBI symptoms should be used to determine disease severity [17]. Even after an accurate diagnosis, different patients with similar diagnoses on the GCS can present a multitude of outcomes due to underlying genetic factors, the type of injury, and the severity of the secondary injury that occurs due to the initiation of damaging biochemical cascades by the primary injury [18].

2.2. Initial Treatment

A large concern of TBI treatment relies on immediate therapeutic intervention to prevent secondary injury, as the primary injury cannot be undone. Secondary injury can present minutes to days after the initial insult due to neuro-inflammation, changes in cranial blood pressure, and the disruption of neurological homeostasis resulting in neuronal cell damage, apoptosis and death [19]. There is no pharmacological medication with proven efficacy for human TBI. Current treatments aim to prevent hypoxia, hypercapnia and hypotension and regulate cerebral perfusion pressure (CPP), ensuring that euvolemia is maintained and secondary injury is avoided [20][21].

2.3. Diagnostic Issues in mTBI

There is a lack of attention paid to mTBI since it is not regarded as an imminent medical emergency. This can result in the dismissal of patients from serious medical care and the failure to adequately characterize the severity of underlying neurological impairment. Additionally, many patients who have sustained mTBI injuries do not seek medical care, or are treated by healthcare providers lacking specific experience in this area. This is a pressing issue, since there exist a multitude of significant and persistent complications for mTBI patients such as impairments in cognition and motor function, psychiatric problems, and impaired neurological development in children [22]. Given that approximately 80–90% of TBIs are classified as mild, this neglects the lasting neurological implications of injuries for a large majority of TBI patients [23][24].
Public awareness surrounding the high incidence of mTBI has increased in recent years due to the publication of data surrounding high levels of mTBI complications in athletes and veterans, in particular [25]. Another subgroup with high rates of mTBI includes victims of abuse, who are a vulnerable and oftentimes neglected population. A greater emphasis on the treatment of mTBI and the management of its prolonged neurological consequences would have significant implications on quality of life for affected individuals [26][27].

3. Focal and Diffuse Injury

Traumatic brain injury results from either a blunt force directly striking the head in a closed or penetrating strike, or due to non-impact force. This initial strike results in a primary injury, which encompasses both direct brain damage caused by the sustained impact and the subsequent damage caused by the impairment of cerebral blood flow and alterations to homeostatic metabolism [28]. The type of primary injury sustained from the blunt or non-impact force usually fits into one of two broad categories: focal and diffuse injuries. Focal brain injury, often affecting the frontal and temporal lobes, results from the compression of brain tissue specifically at the site of impact due to collision forces acting on the skull and has clinical manifestations such as subdural and epidural hematoma and hemorrhagic contusions [29][30]. The temporal lobes are particularly vulnerable to the physical compression and vascular disruption that accompanies focal brain injury, perhaps because the bony covering is thinner relative to the bone over the frontal lobes. The frontal lobes also receive some cushioning from the air-filled sinuses. Since the temporal lobes harbor important memory-related structures, even mild contusions can lead to significant and enduring impairment [31]. Impacts to the frontal cortex can manifest as poor judgement and problem-solving abilities [32]. Focal TBI can disrupt the blood brain barrier (BBB), leading to cellular fluid extravasation into the extracellular space [33]. The cerebral blood flow may be altered, leading to hypo- or hyper-perfusion [28]. These homeostatic disruptions can cause brain tissue destruction, neuronal necrosis, and the formation of brain cavities due to glial cell reactivity [34]. Damage to the BBB is implicated in chronic inflammation after TBI, likely a result of microvasculopathy, which can lead to post-injury development of epilepsy and other neurological disorders [35].
Contrecoup brain injury is a specific subset of focal traumatic brain injury in which the major cerebral contusions occur on the side opposite from the site of blunt force impact. Mechanistically, this phenomenon can be explained by visualizing the brain, which at rest is encased in the skull and floating in the cerebrospinal fluid (CSF). When the head rapidly accelerates, and then suddenly decelerates, the brain is displaced in the denser CSF in relation to the skull and collides with the internal skull in the contrecoup location [36][37]. This is seen when the brain collides with the skull and then rebounds in the opposite direction (coup-contrecoup), causing additional brain injury across from the location of blunt force impact (Figure 1). Coup-contrecoup injuries can lead to widespread damage due to the additional site of injured tissue at a remote location in the brain, resulting in a broadened array of symptoms in patients. This has a particularly strong effect on visual symptoms of TBI, as accommodatively-based visual symptoms such as trouble focusing eyes, visual fatigue, and blurred vision are highly correlated with coup-contrecoup injury [38].
Neurolint 14 00038 g001 550
Figure 1. Coup contrecoup traumatic brain injury. The coup portion of the injury occurs when the movement of the head stops abruptly and the brain continues to move in the forward direction so that it hits the skull. The contrecoup portion further compounds the damage as the brain bounces off the skull and hits the side of the skull opposite the side of initial impact.
Diffuse brain damage generally occurs after rapid acceleration-deceleration of the head, and is associated with disorders of consciousness related to axonal and vascular injury as well as brain swelling [14]. Diffuse damage is often detected via CT scans, and a recent influx of magnetic resonance imaging (MRI) data due to advancements in imaging technology have suggested a relationship between the presence of diffuse axonal injury (DAI) and worse outcomes of TBI [39]. The location of axonal shearing or sustained focal lesions in DAI heavily affects patient outcome, with common locations including the corona radiata, corpus callosum, internal capsule, brainstem, and thalamus [40]. Many cases of fatal DAI contain three specific hallmark structural features: focal lesions in the corpus callosum, focal lesions in the rostral brain stem and diffuse axonal damage [41]. These features are difficult to identify in living patients, complicating not only the diagnosis of DAI but also the ease of studying less severe cases of DAI that do not result in death.

4. Brain Imaging Techniques in TBI

The most widely used brain imaging technologies for the diagnosis of TBI include standard CT and MRI scans. Standard noncontrast CT scans are preferentially employed for rapid and comparatively low-cost imaging results, especially in cases of critical moderate and severe TBI where immediate medical intervention may be required [42]. Repeated CT imaging is controversial, but has shown promise in improving patient outcome in several studies [43][44]. However, CT scans present several concerns pertaining to ionizing radiation exposure in vulnerable age groups, such as children and pregnant women [45][46][47]. Performing noncontrast CT scans also has significant limitations in TBI prognosis, including inaccurately displaying the severity of early traumatic contusions, limitations for detecting changes in intracranial pressure and cerebral edema, and difficulty in identifying diffuse traumatic injury [48].
The predictive value in determining prognosis is comparable for MRI and CT scans, with the added advantage of MRI of an increased sensitivity in detecting small contusions and hemorrhagic injury to axons [49][50]. The drawbacks of MRI in comparison to standard CT imaging include high cost, lower accessibility of MRI machinery, and longer duration of time to obtain results. CT is also superior in detecting skull fractures and CSF leak [51]. The most common acute and chronic finding on CT or MRI of the brain is a normal exam. Thus, the routine neuroradiological investigation of head trauma often performed in the emergency department is insensitive to the structural abnormalities that suggest a patient has undergone TBI. CT imaging usually appears normal when investigating subacute TBI (more than 7 days and less than 3 months after the primary injury) or chronic TBI (3 or more months after the primary injury) [52].
Several classifications centering on CT readings have been developed for risk stratification and prediction of mortality of TBI patients. These include Marshall, Rotterdam, Stockholm, Helsinki and NeuroImaging Radiological Interpretation System (NIRIS) scores [53][54][55][56][57][58] (Table 1).
Table 1. Summary of classifications systems based on imaging for risk stratification and prediction of mortality in TBI.
Table
Classification Scoring Key Features
Marshall (1992) [53] Diffuse Injury I to
Diffuse Injury VI		 Diffuse injury I—No visible intracranial pathology on CT.
Progresses up to Diffuse Injury VI with high or mixed
density lesion > 25 mL not surgically evacuated. Evaluates perimesencephalic cisterns, midline shift, and presence of a mass lesion.
Rotterdam (2006) [54] 1 to 6 4 scored elements: basal cistern compression status;
degree of midline shift; epidural hematomas,
intraventricular and/or subarachnoid hemorrhage.
Differentiates between types of mass lesions, recognizes more favorable prognosis for epidural hematomas.
Stockholm (2010) [55] Traumatic subarachnoid hemorrhage score
Range: (0 to 6)		 Builds on Marshall and Rotterdam. Adds separate
scoring for traumatic subarachnoid hemorrhage.
Magnitude of midline shift used as a continuous variable (not dichotomous) for prediction of favorable or
unfavorable outcome. Incorporates diffuse axonal injury.
Helsinki (2014) [56] −3 to 14 Refined to include type of mass lesion (subdural,
intracerebral or epidural hematoma. Intraventricular hemorrhage as a predictor of outcome. Includes
suprasellar cisterns status (normal, compressed,
obliterated).
NeuroImaging Radiological Interpretation System (NIRIS) (2018) [57] NIRIS 0
to NIRIS 4		 Score gives management guidance: NIRIS 0—patients typically discharged, NIRIS 1—follow-up neuroimaging and/or hospital admission, NIRIS 2—admission to an advanced care unit, NIRIS 3—neurosurgical intervention, NIRIS 4—high likelihood of fatal outcome from TBI.
The use of single photon emission computed tomography (SPECT) to detect abnormalities in regional cerebral blood perfusion (rCBF) allows for high resolution and detection of small perfusion differences that may aid in predicting the likelihood of recovery [59][60]. SPECT is a functional brain imaging tool that uses a gamma-emitting radionuclide that can cross the BBB to show regions of abnormal blood flow [61][62]. Performing a SPECT scan is a minimally invasive method of assessing regional cerebral blood flow, therefore providing useful information on the relative activity levels of different regions of the brain to help detect pathologically significant brain perfusion patterns [63][64][65]. The utility of SPECT comes into play particularly in cases where structural abnormalities are not found on CT. Irregularities in brain perfusion can be seen immediately after mTBI and can identify regions of both hypoperfusion and hyperemia as well as other tissue dysfunction local to sites of brain lesions, indicating BBB disruption [66].
Abnormalities in rCBF are most easily detected in moderate and severe cases. The detected abnormalities in rCBF are most commonly located in the frontal or parietal lobe for patients with traumatic brain disorder [67]. In approximately 50% of SPECT scans of TBI patients, abnormalities in the occipital lobe (the visual cortex) are also detected. Abnormalities in rCBF that are localized in the visual cortex manifest clinically in cortical visual impairment. Therefore, it is relevant to consider the visual findings in TBI for patients with mTBI [68].
Sequential SPECT scans can be used to track the clinical evolution of a TBI patient throughout the duration of treatment [67][69]. SPECT can be used as a marker for improvement. Normalizing blood flow over time (studies months or years apart) usually indicates clinical improvement. If a new drug is developed that may improve the long-term outcome of TBI patients, it would be very useful to have serial SPECT scans to help prove the drug is actually working. Imaging of the brain is critical in making a correct neurologic diagnosis. The limitations of the immediate head CT in the emergency room have been previously described. SPECT is not indicated in every case, but merits addition to the arsenal of tests as a companion to CT for evaluation of TBI patients.

5. Visual Symptoms of TBI

A significant percentage of patients with mTBI report visual symptoms. Among the most common of these is photophobia, a form of light sensitivity in which light exposure causes eye and head pain [70][71][72]. Photophobia and its associated migraine-like symptoms are major sources of functional impairment in TBI [73]. Other commonly reported visual symptoms of mTBI include disorders of extraocular movements, affecting saccadic movements and smooth pursuits. Patients that have experienced TBI exhibit latencies such as lagged smooth pursuit movements as well as position errors and reduced acceleration in saccadic movements [74]. Difficulties with reading in TBI patients are noteworthy, with documented abnormalities including increased fixations and regressions per 100 words, reduced reading rates, and lower comprehension and sophistication in reading level [75].

6. Visual Pathway, Parietal Lobes and Vision

Optic nerves from each eye transport visual impulses from retinal ganglion cells in the retina to the optic chiasm and then to higher visual processing centers in the brain. As a result of partial decussation at the optic chiasm, each optic tract contains the fibers from the ipsilateral temporal and contralateral nasal retina (Figure 2).
Neurolint 14 00038 g002 550
Figure 2. The visual pathway. The optic nerves from each eye partially cross at the optic chiasm so that fibers from the nasal half of each retina cross over to the contralateral optic tract. Fibers from the temporal portion of each retina remain ipsilateral. As a result, the left optic tract contains fibers originating from the left temporal retina, and the right nasal retina while the right optic tract contains fibers originating from the right temporal retina, and the left nasal retina.
The optic nerve and tracts can be damaged from transmitted forces during TBI, even when the impact is minor, and can result from either the primary or secondary injury. The mechanism of traumatic optic neuropathy is not fully understood, but may result from tension on the nerve or nerve compression and involve damage to the axons and/or reduction of the blood supply to the nerve [76][77][78]. The visual impairment from optic nerve damage in TBI generally occurs at the time of injury and may vary from a deficit in color vision to loss of visual acuity to sudden, complete visual loss [79][80]. Treatment is difficult and may be medical, with high dose systemic corticosteroids or surgical, with decompression of the optic canal, or a combination of surgery and corticosteroids. Observation is also a valid approach because spontaneous visual recovery is well-documented [81][82][83].
When evaluating the consequences of TBI on ophthalmologic function, a critical region of the brain to consider is the parietal cortex. The posterior parietal cortex is a central associative region of the brain and is located in the center of the brain behind the frontal lobes of the brain and in front of the occipital lobes [84]. This structural proximity lends itself to functional connections among the parietal cortex and the temporal visual area, the occipital visual area, and the prefrontal cortex [85]. The parietal lobes have great significance due to their involvement in sensorimotor integration, decision making, spatial navigation, and short term memory [86][87]. The parietal cortex encodes spatial coordinates and is engaged during the planning of reaching toward a target [88]. Surgery affecting the parietal lobes is associated with a risk of the loss of language and visual field deficits [89].

7. Conclusions

Large areas of the brain are involved in visual processing and this makes the visual system vulnerable to damage from mTBI. Early and thorough evaluation is important for detection of dysfunction and documentation of recovery or persistence of oculomotor, visual and other symptoms that may interfere with multiple aspects of everyday life. A pro-active approach to treatment involving a rehabilitation program may be preferable to the standard recommendation of rest after mTBI. Avoiding further head trauma is crucial and inter-disciplinary collaboration in research is needed to improve treatment options and maintain functional abilities.

Acknowledgement: Original art in figures by Samantha M. Steiner

References

  1. Iaccarino, C.; Carretta, A.; Nicolosi, F.; Morselli, C. Epidemiology of severe traumatic brain injury. J. Neurosurg. Sci. 2018, 62, 535–541.
  2. Centers for Disease Control and Prevention. National Center for Health Statistics: Mortality Data on CDC WONDER. Available online: https://wonder.cdc.gov/mcd.html (accessed on 20 April 2022).
  3. Savitsky, B.; Givon, A.; Rozenfeld, M.; Radomislensky, I.; Peleg, K. Traumatic brain injury: It is all about definition. Brain Inj. 2016, 30, 1194–1200.
  4. Dewan, M.C.; Rattani, A.; Gupta, S.; Baticulon, R.E.; Hung, Y.C.; Punchak, M.; Agrawal, A.; Adeleye, A.O.; Shrime, M.G.; Rubiano, A.M.; et al. Estimating the global incidence of traumatic brain injury. J. Neurosurg. 2019, 130, 1080–1097.
  5. Taylor, C.A.; Bell, J.M.; Breiding, M.J.; Xu, L. Traumatic brain injury–related emergency department visits, hospitalizations, and deaths—United States, 2007 and 2013. MMWR Surveill. Summ. 2017, 66, 1–16.
  6. Khellaf, A.; Khan, D.Z.; Helmy, A. Recent advances in traumatic brain injury. J. Neurol. 2019, 266, 2878–2889.
  7. Bonow, R.H.; Barber, J.; Temkin, N.R.; Videtta, W.; Rondina, C.; Petroni, G.; Lujan, S.; Alanis, V.; La Fuente, G.; Lavadenz, A.; et al. The outcome of severe traumatic brain injury in Latin America. World Neurosurg. 2018, 111, e82–e90.
  8. Rubiano, A.M.; Carney, N.; Chesnut, R.; Puyana, J.C. Global neurotrauma research challenges and opportunities. Nature 2015, 527, S193–S197.
  9. McAllister, T.W.; Flashman, L.A.; McDonald, B.C.; Saykin, A.J. Mechanisms of working memory dysfunction after mild and moderate TBI: Evidence from functional MRI and neurogenetics. J. Neurotrauma 2006, 23, 1450–1467.
  10. Cassidy, J.D.; Cancelliere, C.; Carroll, L.J.; Côté, P.; Hincapié, C.A.; Holm, L.W.; Hartvigsen, J.; Donovan, J.; Boussard, C.N.-D.; Kristman, V.L.; et al. Systematic review of self-reported prognosis in adults after mild traumatic brain injury: Results of the international collaboration on mild traumatic brain injury prognosis. Arch. Phys. Med. Rehabil. 2014, 95, S132–S151.
  11. Menon, D.K.; Schwab, K.; Wright, D.W.; Maas, A.I. Position statement: Definition of traumatic brain injury. Arch. Phys. Med. Rehabil. 2010, 91, 1637–1640.
  12. Feddermann-Demont, N.; Echemendia, R.J.; Schneider, K.J.; Solomon, G.S.; Hayden, K.A.; Turner, M.; Dvořák, J.; Straumann, D.; Tarnutzer, A.A. What domains of clinical function should be assessed after sport-related concussion? A systematic review. Br. J. Sports Med. 2017, 51, 903–918.
  13. Darshini, J.K.; Afsar, M.; Vandana, V.P.; Shukla, D.; Rajeswaran, J. The Triad of Cognition, Language, and Communication in Traumatic Brain Injury: A Correlational Study. J. Neurosci. Rural Pract. 2021, 12, 666–672.
  14. Capizzi, A.; Woo, J.; Verduzco-Gutierrez, M. Traumatic Brain Injury: An Overview of Epidemiology, Pathophysiology, and Medical Management. Med. Clin. N. Am. 2020, 104, 213–238.
  15. Teasdale, G.; Maas, A.; Lecky, F.; Manley, G.; Stocchetti, N.; Murray, G. The Glasgow coma scale at 40 years: Standing the test of time. Lancet Neurol. 2014, 13, 844–854.
  16. Mena, J.H.; Sanchez, A.I.; Rubiano, A.M.; Peitzman, A.B.; Sperry, J.L.; Gutierrez, M.I.; Puyana, J.C. Effect of the modified Glasgow Coma Scale score criteria for mild traumatic brain injury on mortality prediction: Comparing classic and modified Glasgow Coma Scale score model scores of 13. J. Trauma 2011, 71, 1185–1193.
  17. Chung, P.; Khan, F. Traumatic Brain Injury (TBI): Overview of Diagnosis and Treatment. J. Neurol. Neurophysiol. 2013, 5, 1.
  18. Davanzo, J.R.; Sieg, E.P.; Timmons, S.D. Management of Traumatic Brain Injury. Surg. Clin. N. Am. 2017, 97, 1237–1253.
  19. Abdelmalik, P.A.; Draghic, N.; Ling, G.S.F. Management of moderate and severe traumatic brain injury. Transfusion 2019, 59, 1529–1538.
  20. Taran, S.; Pelosi, P.; Robba, C. Optimizing oxygen delivery to the injured brain. Curr. Opin. Crit. Care 2022, 28, 145–156.
  21. Khan, R.; Alromaih, S.; Alshabanat, H.; Alshanqiti, N.; Aldhuwaihy, A.; Almohanna, S.A.; Alqasem, M.; Al-Dorzi, H. The Impact of Hyperoxia Treatment on Neurological Outcomes and Mortality in Moderate to Severe Traumatic Brain Injured Patients. J. Crit. Care Med. (Targu Mures) 2021, 7, 227–236.
  22. Laskowski, R.A.; Creed, J.A.; Raghupathi, R. Pathophysiology of Mild TBI: Implications for Altered Signaling Pathways. In Brain Neurotrauma: Molecular, Neuropsychological, and Rehabilitation Aspects; Kobeissy, F.H., Ed.; CRC Press/Taylor & Francis: Boca Raton, FL, USA, 2015.
  23. Skandsen, T.; Nilsen, T.L.; Einarsen, C.; Normann, I.; McDonagh, D.; Haberg, A.K.; Vik, A. Incidence of Mild Traumatic Brain Injury: A Prospective Hospital, Emergency Room and General Practitioner-Based Study. Front. Neurol. 2019, 10, 638.
  24. Forrest, R.H.; Henry, J.D.; McGarry, P.J.; Marshall, R.N. Mild traumatic brain injury in New Zealand: Factors influencing post-concussion symptom recovery time in a specialised concussion service. J. Prim. Health Care 2018, 10, 159–166.
  25. McCrory, P.; Meeuwisse, W.H.; Aubry, M.; Cantu, R.C.; Dvořák, J.; Echemendia, R.J.; Engebretsen, L.; Johnston, K.M.; Kutcher, J.S.; Raftery, M.; et al. Consensus statement on concussion in sport—The 4th International Conference on Concussion in Sport held in Zurich, November 2012. PM R 2013, 5, 255–279.
  26. Pavlovic, D.; Pekic, S.; Stojanovic, M.; Popovic, V. Traumatic brain injury: Neuropathological, neurocognitive and neurobehavioral sequelae. Pituitary 2019, 22, 270–282.
  27. Shepherd, D.; Landon, J.; Kalloor, M.; Barker-Collo, S.; Starkey, N.; Jones, K.; Ameratunga, S.; Theadom, A.; BIONIC Research Group. The association between health-related quality of life and noise or light sensitivity in survivors of a mild traumatic brain injury. Qual. Life Res. 2020, 29, 665–672.
  28. Werner, C.; Engelhard, K. Pathophysiology of traumatic brain injury. Br. J. Anaesth. 2007, 99, 4–9.
  29. Andriessen, T.M.; Jacobs, B.; Vos, P.E. Clinical characteristics and pathophysiological mechanisms of focal and diffuse traumatic brain injury. J. Cell. Mol. Med. 2010, 14, 2381–2392.
  30. McGinn, M.J.; Povlishock, J.T. Pathophysiology of Traumatic Brain Injury. Neurosurg. Clin. N. Am. 2016, 27, 397–407.
  31. Bigler, E.D. Anterior and middle cranial fossa in traumatic brain injury: Relevant neuroanatomy and neuropathology in the study of neuropsychological outcome. Neuropsychology 2007, 21, 515–531.
  32. Yue, J.K.; Winkler, E.A.; Puffer, R.C.; Deng, H.; Phelps, R.; Wagle, S.; Morrissey, M.R.; Rivera, E.J.; Runyon, S.J.; Vassar, M.J.; et al. The Track-Tbi Investigators Temporal lobe contusions on computed tomography are associated with impaired 6-month functional recovery after mild traumatic brain injury: A TRACK-TBI study. Neurol. Res. 2018, 40, 972–981.
  33. Cipolotti, L.; MacPherson, S.E.; Gharooni, S.; van-Harskamp, N.; Shallice, T.; Chan, E.; Nachev, P. Cognitive estimation: Performance of patients with focal frontal and posterior lesions. Neuropsychologia 2018, 115, 70–77.
  34. Korn, A.; Golan, H.; Melamed, I.; Pascual-Marqui, R.; Friedman, A. Focal cortical dysfunction and blood-brain barrier disruption in patients with Postconcussion syndrome. J. Clin. Neurophysiol. 2005, 22, 1–9.
  35. Bar-Klein, G.; Lublinsky, S.; Kamintsky, L.; Noyman, I.; Veksler, R.; Dalipaj, H.; Senatorov, V.V., Jr.; Swissa, E.; Rosenbach, D.; Elazary, N.; et al. Imaging blood-brain barrier dysfunction as a biomarker for epileptogenesis. Brain 2017, 140, 1692–1705.
  36. Drew, L.B.; Drew, W.E. The contrecoup-coup phenomenon: A new understanding of the mechanism of closed head injury. Neurocrit. Care 2004, 1, 385–390.
  37. Ratnaike, T.E.; Hastie, H.; Gregson, B.; Mitchell, P. The geometry of brain contusion: Relationship between site of contusion and direction of injury. Br. J. Neurosurg. 2011, 25, 410–413.
  38. Green, W.; Ciuffreda, K.J.; Thiagarajan, P.; Szymanowicz, D.; Ludlam, D.P.; Kapoor, N. Static and dynamic aspects of accommodation in mild traumatic brain injury: A review. Optometry 2010, 81, 129–136.
  39. Humble, S.S.; Wilson, L.D.; Wang, L.; Long, D.A.; Smith, M.A.; Siktberg, J.C.; Mirhoseini, M.F.; Bhatia, A.; Pruthi, S.; Day, M.A.; et al. Prognosis of diffuse axonal injury with traumatic brain injury. J. Trauma Acute Care Surg. 2018, 85, 155–159.
  40. Galgano, M.; Toshkezi, G.; Qiu, X.; Russel, T.; Chin, L.; Zhao, L.R. Traumatic Brain Injury: Current Treatment Strategies and Future Endeavors. Cell Transplant. 2017, 26, 1118–1130.
  41. Adams, J.H.; Graham, D.I.; Murray, L.S.; Scott, G. Diffuse Axonal Injury Due to Nonmissile Head Injury in Humans: An Analysis of 45 Cases. Ann. Neurol. 1982, 12, 557–563.
  42. Mutch, C.A.; Talbott, J.F.; Gean, A. Imaging Evaluation of Acute Traumatic Brain Injury. Neurosurg. Clin. N. Am. 2016, 27, 409–439.
  43. Lobato, R.D.; Alen, J.F.; Perez-Nuñez, A.; Alday, R.; Gómez, P.A.; Pascual, B.; Lagares, A.; Miranda, P.; Arrese, I.; Kaen, A. Utilidad de la TAC secuencial y la monitorización de la presión intracraneal para detectar nuevo efecto masa intracraneal en pacientes con traumatismo craneal grave y lesión inicial Tipo I-II . Neurocirugia 2005, 16, 217–234.
  44. Brown, C.V.; Zada, G.; Salim, A.; Inaba, K.; Kasotakis, G.; Hadjizacharia, P.; Demetriades, D.; Rhee, P. Indications for routine repeat head computed tomography (CT) stratified by severity of traumatic brain injury. J. Trauma 2007, 62, 1339–1344; discussion 1344–1345.
  45. Lindberg, D.M.; Stence, N.V.; Grubenhoff, J.A.; Lewis, T.; Mirsky, D.M.; Miller, A.L.; O’Neill, B.R.; Grice, K.; Mourani, P.M.; Runyan, D.K. Feasibility and Accuracy of Fast MRI Versus CT for Traumatic Brain Injury in Young Children. Pediatrics 2019, 144, e20190419.
  46. Wilson, T.T.; Merck, L.H.; Zonfrillo, M.R.; Movson, J.S.; Merck, D. Efficacy of Computed Tomography Utilization in the Assessment of Acute Traumatic Brain Injury in Adult and Pediatric Emergency Department Patients. R. I. Med. J. 2019, 102, 33–35.
  47. Darlan, D.; Prasetya, G.B.; Ismail, A.; Pradana, A.; Fauza, J.; Dariansyah, A.D.; Wardana, G.A.; Apriawan, T.; Bajamal, A.H. Algorithm of Traumatic Brain Injury in Pregnancy (Perspective on Neurosurgery). Asian J. Neurosurg. 2021, 16, 249–257.
  48. Smith, L.; Milliron, E.; Ho, M.L.; Hu, H.H.; Rusin, J.; Leonard, J.; Sribnick, E.A. Advanced neuroimaging in traumatic brain injury: An overview. Neurosurg. Focus 2019, 47, E17, Erratum in Neurosurg. Focus 2021, 50, E22.
  49. Chastain, C.A.; Oyoyo, U.E.; Zipperman, M.; Joo, E.; Ashwal, S.; Shutter, L.A.; Tong, K.A. Predicting outcomes of traumatic brain injury by imaging modality and injury distribution. J. Neurotrauma 2009, 26, 1183–1196.
  50. Audenaert, K.; Jansen, H.M.; Otte, A.; Peremans, K.; Vervaet, M.; Crombez, R.; de Ridder, L.; van Heeringen, C.; Thirot, J.; Dierckx, R.; et al. Imaging of mild traumatic brain injury using 57Co and 99mTc HMPAO SPECT as compared to other diagnostic procedures. Med. Sci. Monit. 2003, 9, MT112–MT117.
  51. Schweitzer, A.D.; Niogi, S.N.; Whitlow, C.T.; Tsiouris, A.J. Traumatic Brain Injury: Imaging Patterns and Complications. Radiographics 2019, 39, 1571–1595.
  52. Shetty, V.S.; Reis, M.N.; Aulino, J.M.; Berger, K.L.; Broder, J.; Choudhri, A.F.; Kendi, A.T.; Kessler, M.M.; Kirsch, C.F.; Luttrull, M.D.; et al. ACR Appropriateness Criteria Head Trauma. J. Am. Coll. Radiol. 2016, 13, 668–679.
  53. Marshall, L.F.; Marshall, S.B.; Klauber, M.R.; Van Berkum Clark, M.; Eisenberg, H.; Jane, J.A.; Luerssen, T.G.; Marmarou, A.; Foulkes, M.A. The diagnosis of head injury requires a classification based on computed axial tomography. J. Neurotrauma 1992, 9 (Suppl. S1), S287–S292.
  54. Maas, A.I.; Hukkelhoven, C.W.; Marshall, L.F.; Steyerberg, E.W. Prediction of outcome in traumatic brain injury with computed tomographic characteristics: A comparison between the computed tomographic classification and combinations of computed tomographic predictors. Neurosurgery 2006, 57, 1173–1182.
  55. Nelson, D.W.; Nyström, H.; MacCallum, R.M.; Thornquist, B.; Lilja, A.; Bellander, B.M.; Rudehill, A.; Wanecek, M.; Weitzberg, E. Extended analysis of early computed tomography scans of traumatic brain injured patients and relations to outcome. J. Neurotrauma 2010, 27, 51–64.
  56. Raj, R.; Siironen, J.; Skrifvars, M.B.; Hernesniemi, J.; Kivisaari, R. Predicting outcome in traumatic brain injury: Development of a novel computerized tomography classification system (Helsinki computerized tomography score). Neurosurgery 2014, 75, 632–646; discussion 646–647.
  57. Wintermark, M.; Li, Y.; Ding, V.Y.; Xu, Y.; Jiang, B.; Ball, R.L.; Zeineh, M.; Gean, A.; Sanelli, P. Neuroimaging Radiological Interpretation System for Acute Traumatic Brain Injury. J. Neurotrauma 2018, 35, 2665–2672.
  58. Khaki, D.; Hietanen, V.; Corell, A.; Hergès, H.O.; Ljungqvist, J. Selection of CT variables and prognostic models for outcome prediction in patients with traumatic brain injury. Scand. J. Trauma Resusc. Emerg. Med. 2021, 29, 94.
  59. Nedd, K.; Sfakianakis, G.; Ganz, W.; Uricchio, B.; Vernberg, D.; Villanueva, P.; Jabir, A.M.; Bartlett, J.; Keena, J. 99mTc-HMPAO SPECT of the brain in mild to moderate traumatic brain injury patients: Compared with CT—A prospective study. Brain Inj. 1993, 7, 469–479.
  60. Lin, A.P.; Liao, H.J.; Merugumala, S.K.; Prabhu, S.P.; Meehan, W.P., 3rd; Ross, B.D. Metabolic imaging of mild traumatic brain injury. Brain Imaging Behav. 2012, 6, 208–223.
  61. Raji, C.A.; Henderson, T.A. PET and Single-Photon Emission Computed Tomography in Brain Concussion. Neuroimaging Clin. N. Am. 2018, 28, 67–82.
  62. Goffin, K.; van Laere, K. Single-photon emission tomography. Handb. Clin. Neurol. 2016, 135, 241–250.
  63. Santra, A.; Kumar, R. Brain perfusion single photon emission computed tomography in major psychiatric disorders: From basics to clinical practice. Indian J. Nucl. Med. 2014, 29, 210–221.
  64. Pavel, D.; Jobe, T.; Devore-Best, S.; Davis, G.; Epstein, P.; Sinha, S.; Kohn, R.; Craita, I.; Liu, P.; Chang, Y. Viewing the functional consequences of traumatic brain injury by using brain SPECT. Brain Cogn. 2006, 60, 211–213.
  65. Gowda, N.K.; Agrawal, D.; Bal, C.; Chandrashekar, N.; Tripati, M.; Bandopadhyaya, G.P.; Malhotra, A.; Mahapatra, A.K. Technetium Tc-99m ethyl cysteinate dimer brain single-photon emission CT in mild traumatic brain injury: A prospective study. AJNR Am. J. Neuroradiol. 2006, 27, 447–451.
  66. Sakas, D.E.; Bullock, M.R.; Patterson, J.; Hadley, D.; Wyper, D.J.; Teasdale, G.M. Focal cerebral hyperemia after focal head injury in humans: A benign phenomenon? J. Neurosurg. 1995, 83, 277–284.
  67. Khalili, H.; Rakhsha, A.; Ghaedian, T.; Niakan, A.; Masoudi, N. Application of Brain Perfusion SPECT in the Evaluation of Response to Zolpidem Therapy in Consciousness Disorder Due to Traumatic Brain Injury. Indian J. Nucl. Med. 2020, 35, 315–320.
  68. Silverman, I.E.; Galetta, S.L.; Gray, L.G.; Moster, M.; Atlas, S.W.; Maurer, A.H.; Alavi, A. SPECT in patients with cortical visual loss. J. Nucl. Med. 1993, 34, 1447–1451.
  69. Laatsch, L.; Pavel, D.; Jobe, T.; Lin, Q.; Quintana, J.C. Incorporation of SPECT imaging in a longitudinal cognitive rehabilitation therapy programme. Brain Inj. 1999, 13, 555–570.
  70. Digre, K.B.; Brennan, K.C. Shedding light on photophobia. J. Neuroophthalmol. 2012, 32, 68–81.
  71. Merezhinskaya, N.; Mallia, R.K.; Park, D.; Millian-Morell, L.; Barker, F.M., 2nd. Photophobia Associated with Traumatic Brain Injury: A Systematic Review and Meta-analysis. Optom. Vis. Sci. 2021, 98, 891–900.
  72. Armstrong, R.A. Visual problems associated with traumatic brain injury. Clin. Exp. Optom. 2018, 101, 716–726.
  73. Mares, C.; Dagher, J.H.; Harissi-Dagher, M. Narrative Review of the Pathophysiology of Headaches and Photosensitivity in Mild Traumatic Brain Injury and Concussion. Can. J. Neurol. Sci. 2019, 46, 14–22.
  74. DiCesare, C.A.; Kiefer, A.W.; Nalepka, P.; Myer, G.D. Quantification and analysis of saccadic and smooth pursuit eye movements and fixations to detect oculomotor deficits. Behav. Res. Methods 2017, 49, 258–266.
  75. Reddy, A.; Mani, R.; Selvakumar, A.; Hussaindeen, J.R. Reading eye movements in traumatic brain injury. J. Optom. 2020, 13, 155–162.
  76. Li, Y.; Singman, E.; McCulley, T.; Wu, C.; Daphalapurkar, N. The Biomechanics of Indirect Traumatic Optic Neuropathy Using a Computational Head Model with a Biofidelic Orbit. Front. Neurol. 2020, 11, 346.
  77. Jacobs, S.M.; Van Stavern, G.P. Neuro-ophthalmic deficits after head trauma. Curr. Neurol. Neurosci. Rep. 2013, 13, 389.
  78. Rasiah, P.K.; Geier, B.; Jha, K.A.; Gangaraju, R. Visual deficits after traumatic brain injury. Histol. Histopathol. 2021, 36, 711–724.
  79. Ellis, M.J.; Ritchie, L.; Cordingley, D.; Essig, M.; Mansouri, B. Traumatic Optic Neuropathy: A Potentially Unrecognized Diagnosis after Sports-Related Concussion. Curr. Sports Med. Rep. 2016, 15, 27–32.
  80. Saliman, N.H.; Belli, A.; Blanch, R.J. Afferent Visual Manifestations of Traumatic Brain Injury. J. Neurotrauma 2021, 38, 2778–2789.
  81. Chen, H.H.; Lee, M.C.; Tsai, C.H.; Pan, C.H.; Lin, Y.T.; Chen, C.T. Surgical Decompression or Corticosteroid Treatment of Indirect Traumatic Optic Neuropathy: A Randomized Controlled Trial. Ann. Plast. Surg. 2020, 84, S80–S83.
  82. Yu-Wai-Man, P. Traumatic optic neuropathy-Clinical features and management issues. Taiwan J. Ophthalmol. 2015, 5, 3–8.
  83. Volpe, N.J.; Levin, L.A. How should patients with indirect traumatic optic neuropathy be treated? J. Neuroophthalmol. 2011, 31, 169–174.
  84. Whitlock, J.R. Posterior parietal cortex. Curr. Biol. 2017, 27, R691–R695.
  85. Caminiti, R.; Cafee, M.V.; Battaglia-Mayer, A.; Crowe, D.A.; Georgopoulos, A.P. Understanding the parietal lobe syndrome from a neurophysiological and evolutionary perspective. Eur. J. Neurosci. 2010, 31, 2320–2340.
  86. Hadjidimitrakis, K.; Bakola, S.; Wong, Y.T.; Hagan, M.A. Mixed Spatial and Movement Representations in the Primate Posterior Parietal Cortex. Front. Neural Circuits 2019, 13, 15.
  87. Medendorp, W.P.; Heed, T. State estimation in posterior parietal cortex: Distinct poles of environmental and bodily states. Prog. Neurobiol. 2019, 183, 101691.
  88. Baltaretu, B.R.; Monaco, S.; Velji-Ibrahim, J.; Luabeya, G.N.; Crawford, J.D. Parietal Cortex Integrates Saccade and Object Orientation Signals to Update Grasp Plans. J. Neurosci. 2020, 40, 4525–4535.
  89. Dziedzic, T.A.; Bala, A.; Marchel, A. Cortical and Subcortical Anatomy of the Parietal Lobe from the Neurosurgical Perspective. Front. Neurol. 2021, 12, 727055.
More
Related Content
Cognitive Assessment and Training in Extended Reality: Multimodal Systems, Clinical Utility, and Current Challenges Entry
Extended reality (XR) technologies—encompassing virtual reality (VR), augmented reality (AR), and mixed reality (MR)—are transforming cognitive assessment and training by offering immersive, interactive environments that simulate real-world tasks. XR enhances ecological validity while enabling real-time, multimodal data collection through tools such as galvanic skin response (GSR), electroencephalography (EEG), eye tracking (ET), hand tracking, and body tracking. This allows for a more comprehensive understanding of cognitive and emotional processes, as well as adaptive, personalized interventions for users. Despite these advancements, current XR applications often underutilize the full potential of multimodal integration, relying primarily on visual and auditory inputs. Challenges such as cybersickness, usability concerns, and accessibility barriers further limit the widespread adoption of XR tools in cognitive science and clinical practice. This review examines XR-based cognitive assessment and training, focusing on its advantages over traditional methods, including ecological validity, engagement, and adaptability. It also explores unresolved challenges such as system usability, cost, and the need for multimodal feedback integration. The review concludes by identifying opportunities for optimizing XR tools to improve cognitive evaluation and rehabilitation outcomes, particularly for diverse populations, including older adults and individuals with cognitive impairments.
Keywords: extended reality (XR); cognitive assessment; cognitive training; user experience; usability; acceptability; ecological validity; cybersickness; clinical utility; immersion
Neuropsychological Rehabilitation for Traumatic Brain Injury Video
Traumatic brain injury, or TBI, is a serious condition caused by external or internal factors, leading to cognitive, behavioral, physical, relational, and sensory challenges. The impact varies depending on the affected brain area and the severity of the injury. Numerous methods have been developed in neuropsychological rehabilitation to restore, compensate for, or substitute cognitive functions affected by TBI. But how effective are these methods? This video dives into the scientific literature to answer this question. Researchers analyzed over 5,000 studies from the SCOPUS and PUBMED databases, narrowing it down to 17 key articles. Among these, 11 were randomized or semi-randomized controlled trials, 5 were clinical studies, and 1 was a comparative study. The findings reveal that 58.82% of the studies used computerized rehabilitation methods, while 35.3% relied on traditional approaches, and 5.88% adopted holistic rehabilitation. Impressively, 90% of these methods showed significant efficacy. However, the success of neuropsychological rehabilitation depends on several factors, including the cause and phase of the TBI, the duration of the intervention, and the specific symptoms being treated. Rehabilitation must also be tailored to each patient’s unique context.
Keywords: acquired brain injury; traumatic brain injury; neuropsychological treatment; cognitive rehabilitation
Traumatic Brain Injury on Brain Region Entry
The following concerns and measures of neurotrauma are discussed here: It expands more on the protection role that the skull encompasses regarding the encephalon together with a detailed explanation of the effects of head injuries and their implications, which may include coma or death as a result of fractures or dysfunctions. The text gives descriptions of the incidence, especially in car-related accidents, and details about TBI such as the symptoms and the issues likely to occur as a result of the injury. The paper also draws attention to certain dangerous behaviors; such as; non-utilization of seat belts, driving when drunk, no helmet usage, and inadequate supervision to eliminate traumatic brain injury. Among the changes in management of the TBIs whether surgical or through medication, the text lastly highlights the fact that more emphasis has been placed on preventing this condition than on finding a cure for it.
Keywords: Concussions; Contusions; CT scans; Encephalon; Hematoma; MRI scans; Seizures; Stroke
A New Approach for Diagnosing Brainstem Infarction Using the Calling Method Video
This report proposes a new approach to assess dysarthria in patients with brainstem infarction by involving familiar individuals. Collaboration provides valuable insights compared to subjective traditional methods. A man in his 70s presented with resolved positional vertigo. Standard neurological tests showed no abnormalities, and inquiries with the patient’s friend did not reveal voice changes. While inquiring about voice changes with family, friends, and acquaintances is a common practice in clinical settings, our approach involved the patient calling out to his friend from a distance. Despite the physician detecting no abnormalities, the friend noticed a lower voice. Subsequent magnetic resonance imaging (MRI) confirmed brainstem infarction. Early and subtle symptoms of brainstem infarction pose a detection challenge and can lead to serious outcomes if overlooked. This report provides the first evidence that distance calling can detect subtle voice changes associated with brainstem infarction potentially overlooked by conventional neurological examinations, including inquiries with individuals familiar with the patient’s voice. Detecting brainstem infarction in emergency department cases is often missed, but conducting MRIs on every patient is not feasible. This simple method may identify patients overlooked by conventional screening who should undergo neuroimaging such as MRI. Further research is needed, and involving non-professionals in assessments could significantly advance the diagnostic process.
Keywords: brainstem infarction; dysarthria; stroke screenings; case report
When Surgery is Needed for Bone Fractures Entry
Discover when surgery is necessary for bone fractures, including key factors and treatment options for optimal recovery.
Keywords: imaging services for orthopedic injuries; diagnosing bone fractures through a CT scan
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Mild-to-Moderate Traumatic Brain Injury
Information
Subjects: Neurosciences
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Allison B. Reiss
,
Steven Rauchman
,
Jacqueline Albert
,
Aaron Pinkhasov
View Times: 982
Revisions: 4 times (View History)
Update Date: 15 Jun 2022
Table of Contents
Video Production Service
Feedback