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Open Access Review

Neurostimulation for Traumatic Brain Injury: Emerging Innovation

Michael Joseph Diaz 1, Kevin Thomas Root 1, Alice Beneke 1, Yordan Penev 1, Brandon Lucke-Wold 2,*

  1. College of Medicine, University of Florida, Gainesville, FL, USA

  2. Department of Neurosurgery, University of Florida, Gainesville, FL, USA

Correspondence: Brandon Lucke-Wold

Academic Editor: Severn B. Churn

Special Issue: Diagnosis, Prognosis, and Treatment of Traumatic Brain Injury

Received: October 07, 2022 | Accepted: February 27, 2023 | Published: March 06, 2023

OBM Neurobiology 2023, Volume 7, Issue 1, doi:10.21926/obm.neurobiol.2301161

Recommended citation: Diaz MJ, Root KT, Beneke A, Penev Y, Lucke-Wold B. Neurostimulation for Traumatic Brain Injury: Emerging Innovation. OBM Neurobiology 2023; 7(1): 161; doi:10.21926/obm.neurobiol.2301161.

© 2023 by the authors. This is an open access article distributed under the conditions of the Creative Commons by Attribution License, which permits unrestricted use, distribution, and reproduction in any medium or format, provided the original work is correctly cited.


Traumatic brain injury (TBI) is a significant source of brain deficit and death among neurosurgical patients, with limited prospects for functional recovery in the cases of moderate-to-severe injury. Until now, the relevant body of literature on TBI intervention has focused on first-line, invasive treatment options (namely craniectomy and hematoma evacuation) with underwhelming focus on non-invasive therapies following surgical stabilization. Recent advances in our understanding of the impaired brain have encouraged deeper investigation of neurostimulation strategies, owed largely to its demonstrated livening of damaged neural circuitry and capacity to stabilize erratic network activity. The objective of the present study is to provide a scoping review of new knowledge in neurostimulation published in the PubMed, Scopus, and Google Scholar databases from inception to November 2022. We critically assess and appraise the available data on primary neurostimulation delivery techniques, with marked emphasis on restorative opportunities for accessory neurostimulation in the interdisciplinary care of moderate-to-severe TBI (msTBI) patients. These data identify two primary future directions: 1) to relate obtained gain-of-function outcomes to hemodynamic and histological changes and 2) to develop a clearer understanding of neurostimulation efficacy, when combined with pharmacologic interventions or other modulatory techniques, for complex brain insult.


Traumatic brain injury; neurosurgical stimulation; rTMS; tLNS; tDCS; pharmaceutical management; interdisciplinary care

1. Introduction

Traumatic brain injury (TBI), or an acquired insult to the brain via an external force, is a major health and socioeconomic concern throughout the world with an estimated 10 million individuals affected by TBI annually [1,2]. In high income countries, TBI is largely a result of falls in older patients [3]. In younger patients in these countries, TBI is predominately due to traffic accidents. While preventative measures have been shown to decrease this source of injury, it continues to be a leading contributor to mortality and disability within this population [3,4]. Furthermore, TBI due to traffic accidents is also of significant concern in low-middle income countries. Current projections demonstrate the already high levels of mortality and morbidity are increasing in prevalence with the rapid adoption of motor vehicle transportation, signaling an international scale of the crisis [5]. The median age of onset of TBI is relatively low, even in high-income countries. Therefore, the ensuing fallout of TB is disproportionally costly to productive years lost, resulting in an outsized detriment to society [6]. In the USA alone, the financial impact is in excess of $60 billion dollars per annum with an estimated prevalence of 3.2 million citizens living with disability after a TBI associated hospitalization [7].

The pathophysiology of traumatic brain injury is multifactorial, including inflammation, oxidative stress, apoptosis, mitochondrial damage, shearing of white-matter tracks, focal contusions, and hematomas [8]. More, a diagnosis of traumatic brain injury encompasses a range of severities. Using the Glasgow Coma Scale (GSC, TBIs are classified as mild (14-15), moderate (9-13), and severe (3-8) [9,10]. In a systematic review, Buhangiar et. al. delineated the emerging effects of neuromodulation in TBI patients with an initial GCS of 13-15 and found neuromodulation had a positive effect on measured symptoms and neurophysiological functioning [11]. Consequently, the GCS may be of use when considering the relevance of neuromodulation in treatment, although more literature is needed to support such a claim. However, the proposed mechanism by which neuromodulation is theorized to influence such outcomes as discussed by Buhangiar et. al. is via adaptive neuroplasticity [11]. More precisely, neuromodulation can stimulate the cerebral cortex, inhibiting or activating neuronal cells. Such an effect has been evidenced to reorganize neural networks following traumatic brain injury and even improve cognitive dysfunction [12].

Considering the complex disease processes and varied severities, different forms of neurosurgical management of TBI are necessary and include operative and non-operative intervention. However, as surgical interventions are no longer the gold-standard of TBI management, nonoperative interventions such as neuromodulation are of increased relevance in the management of TBIs. Further, it is necessary to understand how this novel innovation may be combined with other, non-surgical management of TBIs such as pharmacological management [13,14,15]. Currently, there is a paucity of reviews summarizing the results of this neuromodulation in the context of current TBI management standards and practices. Thus, the objective of the current review is to discuss the current innovative techniques in neuromodulation, what the standard of pharmacological management of TBI is and how it can be accentuated by neuromodulation, and how best practice of TBI neuromodulation treatment may be within an interdisciplinary setting for increased effect.

2. Discussion

2.1 Novel Findings in Neurostimulation for Brain Injury

Several areas of intense focus in brain stimulation theory and practice have been identified: most notably in translingual neurostimulation and transcranial magnetic stimulation (Figure 1). Measured success in these domains primarily center on posturography analysis (e.g., Sensory Organization Test and dynamic gait index) and physiologic analysis (e.g., wavelet power analysis in electroencephalography).

Click to view original image

Figure 1 Images depicting targets of translingual neurostimulation and transcranial magnetic stimulation. (A) Translingual neurostimulation is achieved though neuroplastic changes. These changes are induced by facial and trigeminal nerve stimulation, excited by neural impulses to the pons Varolii and cerebellum. (B) During a rTMS session, an electromagnetic coil is placed against the scalp and a magnetic pulse is delivered to stimulate nerve cells in the brain. Figure created with BioRender.com.

2.1.1 Translingual Neurostimulation

Successful translingual neurostimulation (tLNS) is achieved by targeted stimulation of cranial nerves V and VII and represents a prime candidate for combination therapy of neurologic disease and stroke, inciting deserved interest in its clinical utility for traumatic brain injury [16,17]. In a 2019 double-blinded, randomized controlled trial investigating the efficacy of tLNS for improving mild-to-moderate TBI (mmTBI) outcomes, Tyler et al. first reported that tLNS administered over a 14-week period significantly improved related balance deficits from baseline (N = 44) (p < 0.0001) [18]. These findings corroborate even newer evidence validating tLNS for adjunct balance and gait rehabilitation, as measured by observable increases in Sensory Organization Test score and neuroplasticity, particularly for mmTBI patients with limited response to conventional physical therapy [19,20]. Moreover, available data indicates that tLNS may realistically provide clinical benefits beyond traditional therapeutic windows for TBI patients. A longitudinal case study detailing a retired Army Captain’s cognitive recovery reported that combined tLNS and physical therapy, delivered 14 years after the initial 2006 TBI event, yielded striking increases in basic attention (via P300 response analysis) and cognitive processing (via N400 response analysis) [21]. They additionally self-reported amelioration of ongoing symptoms related to the TBI event, indicating that incorporation of tLNS was commensurate with recognizable clinical benefit.

2.1.2 Repetitive Transcranial Magnetic Stimulation

Repetitive transcranial magnetic stimulation (rTMS) provides profound therapeutic benefit via unique delivery of focal to diffuse brain stimulation involving brief magnetic pulses generated from an iron-core coil. Previous research exploring rTMS protocols revealed its strength for treatment-resistant depression symptomology, lessening chronic orofacial pains, and obsessive-compulsive disorder, among several other ailments [22,23,24]. A hallmark characteristic of rTMS is its depth-focality tradeoff, which results in stimuli applied to non-targeted brain structures when probing deeper regions [25,26]. This feature seems to suggest that rTMS may prove highly efficacious in repairing dysfunctional neural networks (via activity-dependent modulation of synaptic plasticity), particularly in TBI patients with diffuse axonal injury. Supporting evidence reported by Wang et al. demonstrated that rTMS delivered to the left motor cortex significantly altered right cerebellar activity, which, in addition to specialized balance and coordination, plays established roles in verbal [27,28,29]. Pulse frequency too impacts clinical outcomes. At low frequency, rTMS enables cortical inhibition, perhaps by induced suppression of parvalbumin and calbindin, whereas high frequency rTMS (3-50 Hz) enables targeted excitation of the lesioned cortex, benefiting stroke patients, though the latter finding remains debated in the literature [30,31,32]. Moreover, emerging data purports that TMS can be safely delivered to infants with perinatal brain damage (N = 6) and in persons with co-occurring TBI and complex neuropsychiatric comorbidities [33,34,35]. Still, further research is needed to establish the safety and scoping efficacy of high-frequency rTMS in seizure-prone (or otherwise compromised) patient populations.

Other opportunities for functional recovery at the hands of electrical neuromodulation techniques have been described for a motley of conditions. For instance, a number of surfacing studies have explored the utility of deep brain stimulation for focal targeting of midbrain structures implicated in treatment-resistant depression [36,37,38], however sweeping conclusions remain ill-generalizable in the TBI patient population [39]. Hofer and Schwab further reviewed the therapeutic benefits afforded by electrical stimulation for spinal cord injury patients years after the initial injury event [40], owed to previously described activity-dependent restoration of residual brain and spinal cord networks [41].

2.2 Current Pharmacological Management

Seizures after TBI cause increased ICP and decreased cerebral perfusion [42]. Therefore, treatment with prophylactic anticonvulsant medications such as phenytoin are recommended to reduce the number of seizures in the first week following TBI; however, anticonvulsant medications do not prevent seizures after one week [43]. Many patients with TBI are placed on psychotropic medications following the TBI due to the presence of psychiatric problems, the most common being depression, bipolar disorder, generalized anxiety disorder, and substance abuse [44]. Beta blockers and mood-regulating epileptics can be administered as first-line treatments for agitation and aggression depending on comorbidities, while antidepressants, buspirone, neuroleptics, and benzodiazepines are second-line treatments [45]. SSRIs are considered the first-line treatment for TBI-related depression [46].

2.3 Emerging Pharmacological Management with Neurostimulation

At the time of writing, very limited research exists on the efficacy of combining pharmacological treatments of TBI with neurostimulation. Bender Pape et al. found that in post-TBI patients with disordered consciousness who had low probability of making a significant recovery, combining rTMI with amantadine improved neurobehavioral outcomes [47]. Auditory-language skills specifically were improved in patients who received rTMS prior to a combination therapy of rTMS and amantadine [48]. For psychiatric symptoms post-TBI, some research has looked into the use of rTMS after failed pharmacological management of symptoms. A systematic review conducted by Narapareddy and colleagues reported that while SSRIs, specifically sertraline, shows the best evidence for improving depression symptoms after TBI, rTMS might be effective for those patients that do not respond to pharmacological treatment [46]. Included patients took from 25 to 2000 mg/d of sertraline for time periods ranging from 3-30 weeks and were assessed by results on the Hamilton Depression Scale, Patient Health Questionnaire 9, and the Beack Depression Inventory. In patients that did not respond to pharmacological treatments of TBI depression, rTMS (Figure 1B) showed some immediate improvement in depression symptoms, but the long-term efficacy showed mixed results [46]. An independent case study revealed that high frequency DBS to the anterior limb of the internal capsule and nucleus accumbens at 100 Hz improved defects from a TBI on a patient with severe psychiatric symptoms who had showed no improvement using antipsychotic drugs [49]. Frequencies below 100 Hz to the nucleus accumbens improved auditory hallucinations in the patient, while high frequency stimulation to the anterior limb of the internal capsule improved emotional deficits [49]. While these two studies looked at rTMS after failed pharmacological treatment of depression symptoms, future research is needed to investigate the utility of combining pharmacological treatment with neurostimulation.

2.4 Neuromodulation in Interdisciplinary Care: Alternative Avenues

A growing body of evidence in TBI literature supports the application of interdisciplinary care models acutely as well as during the rehabilitative phase for achieving the most favorable patient outcomes. Frequent associations of the disease with comorbid diagnoses of a related etiology (i.e., accidental trauma, post-deployment conditions) such as post-traumatic stress disorder (PTSD) and major depressive disorder (MDD) require the simultaneous management of multiple clinical sequalae, often by different specialists (primary care, psychiatry, neurology, and others), in the same patient [50,51]. Beyond the management of comorbidities, addressing the complex pathophysiology of TBI alone has also been demonstrated to benefit from multidisciplinary care. As just one example, a quasi-experimental study of 56 TBI patients who were assigned to either multidisciplinary rehabilitation or single specialty care showed that patients who were cared for by multidisciplinary teams demonstrated significantly higher gains in independent living, cognitive and motor skills at the end of a 2-year rehabilitation period [52]. These findings have been consistent with the results of other experiments involving combinations of neuropsychologic and family, occupational as well as speech-language pathology therapy [53,54,55,56].

In this context, the application of neurostimulation needs to be considered alongside other therapeutic and rehabilitative approaches which are likely to be deployed concurrently for the holistic management of a patient with TBI. Recent advances in our understanding of TBI pathology and management have given rise to several new in-hospital TBI treatment innovations which likewise rely on interdisciplinary involvement. Alongside tLNS and rTMS, applications of transcranial direct current stimulation (tDCS), low-level laser therapy (LLLT), and transcranial doppler sonography (TDS), which were originally intended for medication-resistant depression, pain, spasticity, hand-eye coordination, gait, and speech and language pathologies are increasingly emerging as powerful complementary and/or alternative therapeutic modalities for TBI [57,58]. Among these, TDS (Figure 2A) provides particularly strong support for the synergistic effects of interdisciplinary collaboration as the development of this typically diagnostic method for therapeutic purposes in TBI is an apt example of convergent technological evolution with another emerging technique, focused ultrasound (FUS) (Figure 2B), which was first used in oncological surgery and later adapted to neurosurgery and TBI [59,60,61]. While most efforts around FUS are still centered validation of different adaptations of the technology to TBI in animal models, TDS therapy has already been demonstrated as clinically effective in humans [62,63,64,65,66]. It is conceivable that neurostimulatory approaches such as tLNS and rTMS will likewise benefit from technological integration with these new therapeutic alternatives in order to provide patient-centered care encompassing TBI as well as multiple comorbidities which may be present within the same individual. Despite this potential, a recent review by Marklund et al. reports that there is still a relative lack of robust trial data demonstrating the clinical efficacy of neurostimulation in the context of other simultaneous therapeutic approaches for TBI and/or comorbidities [67]. More research needs to be done to define the role and guide the development of neurostimulation as a standard of care tool within the toolbox of precise, patient-centered TBI care.

Click to view original image

Figure 2 Ultrasound applications in TBI. (A) transcranial doppler sonography in humans. (B) focused ultrasound adaptations from animal tumor models. Figure created with BioRender.com.

3. Concluding Remarks

Here we rigorously reviewed the current state of neurostimulation with due emphasis on its potential role in treatment of mild-to-severe TBI patients. Recent advances suggest that neurostimulation stands to immensely benefit our understanding and treatment of TBI and related neurological deficit. Notable data points in the field include the following: tLNS evidences unique neuromodulation benefits for stroke victims and widens the traditional therapeutic window; rTMS shows early signs of promise for treatment of diffuse axonal injury; the potential for pharmacologic co-intervention represents a gravely understudied area; alternative (namely non-electrical and non-magnetic) neuromodulation techniques remain promising, suggesting a role for co-administration possibilities. The present review is limited by the scarcity of available literature (at the time of writing) and inconsistent measured outcomes reporting. Still, the authors maintain that the body of evidence shared here provides meaningful insights into stimuli management for complex brain injury. Key advantages to this study are its focus on impactful discoveries in the neurostimulation arena for an understudied neurosurgical patient population, due reflection on prior landmark advancements, and the breadth of the literature search. These all represent salient points to clinicians and researchers alike. Future research should focus on bridging inconsistencies in measured outcomes and correlating realized motor improvements with histological results. Finally, we hope that the present review serves to inspire continued investigation of neurostimulation theory and practice towards the ultimate benefit of the TBI patient population.



Author Contributions

MJD – Conceptualization, Writing/Editing – Original Manuscript. KTR – Conceptualization, Writing/Editing – Original Manuscript. AB – Conceptualization, Writing/Editing – Original Manuscript. YP – Conceptualization, Writing/Editing – Original Manuscript. BLW – Conceptualization, Project Administration/Supervision.

Competing Interests

The authors have declared that no competing interests exist.


  1. Hyder AA, Wunderlich CA, Puvanachandra P, Gururaj G, Kobusingye OC. The impact of traumatic brain injuries: A global perspective. NeuroRehabilitation. 2007; 22: 341-353. [CrossRef]
  2. Capizzi A, Woo J, Verduzco-Gutierrez M. Traumatic brain injury: An overview of epidemiology, pathophysiology, and medical management. Med Clin. 2020; 104: 213-238. [CrossRef]
  3. Rusnak M, Janciak I, Majdan M, Wilbacher I, Mauritz W. Severe traumatic brain injury in Austria I: Introduction to the study. Wien Klin Wochenschr. 2007; 119: 23-28. [CrossRef]
  4. Maas AIR, Stocchetti N, Bullock R. Moderate and severe traumatic brain injury in adults. Lancet Neurol. 2008; 7: 728-741. [CrossRef]
  5. Dunne J, Quiñones-Ossa GA, Still EG, Suarez MN, González-Soto JA, Vera DS, et al. The epidemiology of traumatic brain injury due to traffic accidents in Latin America: A narrative review. J Neurosci Rural Pract. 2020; 11: 287-290. [CrossRef]
  6. Murray GD, Teasdale GM, Braakman R, Cohadon F, Dearden M, Iannotti F, et al. The European brain injury consortium survey of head injuries. Acta Neurochir. 1999; 141: 223-236. [CrossRef]
  7. Corrigan JD, Selassie AW, Orman JA. The epidemiology of traumatic brain injury. J Head Trauma Rehabil. 2010; 25: 72-80. [CrossRef]
  8. Shin SS, Dixon CE, Okonkwo DO, Richardson RM. Neurostimulation for traumatic brain injury. J Neurosurg. 2014; 121: 1219-1231. [CrossRef]
  9. Menon D, Harrison D. Prognostic modelling in traumatic brain injury. BMJ. 2008; 336: 397-398. [CrossRef]
  10. Finfer SR, Cohen J. Severe traumatic brain injury. Resuscitation. 2001; 48: 77-90. [CrossRef]
  11. Buhagiar F, Fitzgerald M, Bell J, Allanson F, Pestell C. Neuromodulation for mild traumatic brain injury rehabilitation: A systematic review. Front Hum Neurosci. 2020; 14: 598208. [CrossRef]
  12. Lu X, Bao X, Li J, Zhang G, Guan J, Gao Y, et al. High-frequency repetitive transcranial magnetic stimulation for treating moderate traumatic brain injury in rats: A pilot study. Exp Ther Med. 2017; 13: 2247-2254. [CrossRef]
  13. Carney N, Totten AM, O’reilly C, Ullman JS, Hawryluk GW, Bell MJ, et al. Guidelines for the management of severe traumatic brain injury, fourth edition. Neurosurgery. 2017; 80: 6-15. [CrossRef]
  14. Chesnut R, Videtta W, Vespa P, Le Roux P, Participants in the international multidisciplinary consensus conference on multimodality monitoring. Intracranial pressure monitoring: Fundamental considerations and rationale for monitoring. Neurocrit Care. 2014; 21: S64-S84. [CrossRef]
  15. Marshall LF, SMith RW, Rauscher LA, Shapiro HM. Mannitol dose requirements in brain-injured patients. J Neurosurg. 1978; 48: 169-172. [CrossRef]
  16. Tyler ME, Kaczmarek KA, Rust KL, Subbotin AM, Skinner KL, Danilov YP. Non-invasive neuromodulation to improve gait in chronic multiple sclerosis: A randomized double blind controlled pilot trial. J Neuroeng Rehabilitation. 2014; 11: 79. [CrossRef]
  17. Galea MP, Cofré Lizama LE, Bastani A, Panisset MG, Khan F. Cranial nerve non-invasive neuromodulation improves gait and balance in stroke survivors: A pilot randomised controlled trial. Brain Stimul. 2017; 10: 1133-1135. [CrossRef]
  18. Tyler M, Skinner K, Prabhakaran V, Kaczmarek K, Danilov Y. Translingual neurostimulation for the treatment of chronic symptoms due to mild-to-moderate traumatic brain injury. Arch Rehabil Res Clin Transl. 2019; 1: 100026. [CrossRef]
  19. Ptito A, Papa L, Gregory K, Folmer RL, Walker WC, Prabhakaran V, et al. A prospective, multicenter study to assess the safety and efficacy of translingual neurostimulation plus physical therapy for the treatment of a chronic balance deficit due to mild-to-moderate traumatic brain injury. Neuromodulation. 2021; 24: 1412-1421. [CrossRef]
  20. Hou J, Mohanty R, Chu D, Nair VA, Danilov Y, Kaczmarek KA, et al. Translingual neural stimulation affects resting-state functional connectivity in mild-moderate traumatic brain injury. J Neuroimaging. 2022; 32: 1193-1200. [CrossRef]
  21. Fickling SD, Greene T, Greene D, Frehlick Z, Campbell N, Etheridge T, et al. Brain vital signs detect cognitive improvements during combined physical therapy and neuromodulation in rehabilitation from severe traumatic brain injury: A case report. Front Hum Neurosci. 2020; 14: 347. [CrossRef]
  22. Gregory EC, Torres IJ, Blumberger DM, Downar J, Daskalakis ZJ, Vila-Rodriguez F. Repetitive transcranial magnetic stimulation shows longitudinal improvements in memory in patients with treatment-resistant depression. Neuromodulation. 2022; 25: 596-605. [CrossRef]
  23. Perera MP, Mallawaarachchi S, Miljevic A, Bailey NW, Herring SE, Fitzgerald PB. Repetitive transcranial magnetic stimulation for obsessive-compulsive disorder: A meta-analysis of randomized, sham-controlled trials. Biol Psychiatry Cogn Neurosci Neuroimaging. 2021; 6: 947-960. [CrossRef]
  24. Fricová J, Rokyta R. Transcranial neurostimulation (rTMS, tDCS) in the treatment of chronic orofacial pain. Neuromodulation Facial Pain. 2020; 35: 125-132. [CrossRef]
  25. Deng ZD, Lisanby SH, Peterchev AV. Electric field depth-focality tradeoff in transcranial magnetic stimulation: Simulation comparison of 50 coil designs. Brain Stimul. 2013; 6: 1-13. [CrossRef]
  26. Nurmi S, Karttunen J, Souza VH, Ilmoniemi RJ, Nieminen JO. Trade-off between stimulation focality and the number of coils in multi-locus transcranial magnetic stimulation. J Neural Eng. 2021; 18: 066003. [CrossRef]
  27. Park IS, Lee NJ, Kim TY, Park JH, Won YM, Jung YJ, et al. Volumetric analysis of cerebellum in short-track speed skating players. Cerebellum. 2012; 11: 925-930. [CrossRef]
  28. Stoodley CJ, Schmahmann JD. Evidence for topographic organization in the cerebellum of motor control versus cognitive and affective processing. Cortex. 2010; 46: 831-844. [CrossRef]
  29. Wang J, Deng XP, Wu YY, Li XL, Feng ZJ, Wang HX, et al. High-frequency rTMS of the motor cortex modulates cerebellar and widespread activity as revealed by SVM. Front Neurosci. 2020; 14: 186. [CrossRef]
  30. Castel-Lacanal E, Tarri M, Loubinoux I, Gasq D, de Boissezon X, Marque P, et al. Transcranial magnetic stimulation in brain injury. Ann Fr Anesth Reanim. 2014; 33: 83-87. [CrossRef]
  31. Funke K, Benali A. Modulation of cortical inhibition by rTMS-findings obtained from animal models. J Physiol. 2011; 589: 4423-4435. [CrossRef]
  32. de Jesus DR, de Souza Favalli GP, Hoppenbrouwers SS, Barr MS, Chen R, Fitzgerald PB, et al. Determining optimal rTMS parameters through changes in cortical inhibition. Clin Neurophysiol. 2014; 125: 755-762. [CrossRef]
  33. Oberman LM, Exley S, Philip NS, Siddiqi SH, Adamson MM, Brody DL. Use of repetitive transcranial magnetic stimulation in the treatment of neuropsychiatric and neurocognitive symptoms associated with concussion in military populations. J Head Trauma Rehabil. 2020; 35: 388-400. [CrossRef]
  34. Reti IM, Schwarz N, Bower A, Tibbs M, Rao V. Transcranial magnetic stimulation: A potential new treatment for depression associated with traumatic brain injury. Brain Inj. 2015; 29: 789-797. [CrossRef]
  35. Nemanich ST, Chen CY, Chen M, Zorn E, Mueller B, Peyton C, et al. Safety and feasibility of transcranial magnetic stimulation as an exploratory assessment of corticospinal connectivity in infants after perinatal brain injury: An observational study. Phys Ther. 2019; 99: 689-700. [CrossRef]
  36. Drobisz D, Damborská A. Deep brain stimulation targets for treating depression. Behav Brain Res. 2019; 359: 266-273. [CrossRef]
  37. Gadot R, Najera R, Hirani S, Anand A, Storch E, Goodman WK, et al. Efficacy of deep brain stimulation for treatment-resistant obsessive-compulsive disorder: Systematic review and meta-analysis. J Neurol Neurosurg Psychiatry. 2022; 93: 1166-1173. [CrossRef]
  38. Figee M, Riva-Posse P, Choi KS, Bederson L, Mayberg HS, Kopell BH. Deep brain stimulation for depression. Neurotherapeutics. 2022; 19: 1229-1245. [CrossRef]
  39. Haddad AR, Lythe V, Green AL. Deep brain stimulation for recovery of consciousness in minimally conscious patients after traumatic brain injury: A systematic review. Neuromodulation. 2019; 22: 373-379. [CrossRef]
  40. Hofer AS, Schwab ME. Enhancing rehabilitation and functional recovery after brain and spinal cord trauma with electrical neuromodulation. Curr Opin Neurol. 2019; 32: 828-835. [CrossRef]
  41. Samejima S, Henderson R, Pradarelli J, Mondello SE, Moritz CT. Activity-dependent plasticity and spinal cord stimulation for motor recovery following spinal cord injury. Exp Neurol. 2022; 357: 114178. [CrossRef]
  42. Dash HH, Chavali S. Management of traumatic brain injury patients. Korean J Anesthesiol. 2018; 71: 12-21. [CrossRef]
  43. Temkin NR, Dikmen SS, Wilensky AJ, Keihm J, Chabal S, Winn HR. A randomized, double-blind study of phenytoin for the prevention of post-traumatic seizures. N Engl J Med. 1990; 323: 497-502. [CrossRef]
  44. Vehviläinen J, Skrifvars MB, Reinikainen M, Bendel S, Marinkovic I, Ala-Kokko T, et al. Psychotropic medication use among patients with a traumatic brain injury treated in the intensive care unit: A multi-centre observational study. Acta Neurochir. 2021; 163: 2909-2917. [CrossRef]
  45. Luauté J, Plantier D, Wiart L, Tell L. Care management of the agitation or aggressiveness crisis in patients with TBI. Systematic review of the literature and practice recommendations. Ann Phys Rehabil Med. 2016; 59: 58-67. [CrossRef]
  46. Narapareddy BR, Narapareddy L, Lin A, Wigh S, Nanavati J, Dougherty III J, et al. Treatment of depression after traumatic brain injury: A systematic review focused on pharmacological and neuromodulatory interventions. Psychosomatics. 2020; 61: 481-497. [CrossRef]
  47. Bender Pape T, Bender Pape TL, Herrold AA, Livengood SL, Guernon A, Weaver JA, et al. A pilot trial examining the merits of combining amantadine and repetitive transcranial magnetic stimulation as an intervention for persons with disordered consciousness after TBI. J Head Trauma Rehabil. 2020; 35: 371-387. [CrossRef]
  48. Burgaleta C, Moreno T. Effect of β-lactams and aminoglycosides on human polymorphonuclear leucocytes. J Antimicrob Chemother. 1987; 20: 529-535. [CrossRef]
  49. Zhou B, Kuang W, Huang H, Zhu Y, Chen X, Li L, et al. Successful treatment of psychiatric symptoms after traumatic brain injury using deep brain stimulation to the anterior limb of internal capsule-nucleus accumbens. Clin Psychopharmacol Neurosci. 2020; 18: 636-640. [CrossRef]
  50. Wilk JE, Herrell RK, Wynn GH, Riviere LA, Hoge CW. Mild traumatic brain injury (concussion), posttraumatic stress disorder, and depression in US soldiers involved in combat deployments: Association with postdeployment symptoms. Psychosom Med. 2012; 74: 249-257. [CrossRef]
  51. Speicher SM, Walter KH, Chard KM. Interdisciplinary residential treatment of posttraumatic stress disorder and traumatic brain injury: Effects on symptom severity and occupational performance and satisfaction. Am J Occup Ther. 2014; 68: 412-421. [CrossRef]
  52. Gray JM. Traumatic brain injury. Arch Phys Med Rehabil. 1999; 80: 355-356. [CrossRef]
  53. Hardin KY, Kelly JP. The role of speech-language pathology in an interdisciplinary care model for persistent symptomatology of mild traumatic brain injury. Semin Speech Lang. 2019; 40: 65-78. [CrossRef]
  54. Powell JM, Rich TJ, Wise EK. Effectiveness of occupation-and activity-based interventions to improve everyday activities and social participation for people with traumatic brain injury: A systematic review. Am J Occup Ther. 2016; 70: 7003180040p1-7003180040p9. [CrossRef]
  55. Kreutzer JS, Marwitz JH, Sima AP, Mills A, Hsu NH, Lukow HR. Efficacy of the resilience and adjustment intervention after traumatic brain injury: A randomized controlled trial. Brain Inj. 2018; 32: 963-971. [CrossRef]
  56. Godwin EE, Kreutzer JS. Embracing a new path to emotional recovery: Adopting resilience theory in post-TBI psychotherapy. Brain Inj. 2013; 27: 637-639. [CrossRef]
  57. Demirtas-Tatlidede A, Vahabzadeh-Hagh AM, Bernabeu M, Tormos JM, Pascual-Leone A. Noninvasive brain stimulation in traumatic brain injury. J Head Trauma Rehabil. 2012; 27: 274-292. [CrossRef]
  58. Toccaceli G, Barbagallo G, Peschillo S. Low-intensity focused ultrasound for the treatment of brain diseases: Safety and feasibility. Theranostics. 2019; 9: 537-539. [CrossRef]
  59. Christian E, Yu C, Apuzzo ML. Focused ultrasound: Relevant history and prospects for the addition of mechanical energy to the neurosurgical armamentarium. World Neurosurg. 2014; 82: 354-365. [CrossRef]
  60. Wahab RA, Choi M, Liu Y, Krauthamer V, Zderic V, Myers MR. Mechanical bioeffects of pulsed high intensity focused ultrasound on a simple neural model. Med Phys. 2012; 39: 4274-4283. [CrossRef]
  61. Kennedy JE, Ter Haar GR, Cranston D. High intensity focused ultrasound: Surgery of the future? Br J Radiol. 2003; 76: 590-599. [CrossRef]
  62. Ract C, Le Moigno S, Bruder N, Vigué B. Transcranial Doppler ultrasound goal-directed therapy for the early management of severe traumatic brain injury. Intensive Care Med. 2007; 33: 645-651. [CrossRef]
  63. McCabe JT, Moratz C, Liu Y, Burton E, Morgan A, Budinich C, et al. Application of high-intensity focused ultrasound to the study of mild traumatic brain injury. Ultrasound Med Biol. 2014; 40: 965-978. [CrossRef]
  64. McCutcheon V, Park E, Liu E, Sobhebidari P, Tavakkoli J, Wen XY, et al. A novel model of traumatic brain injury in adult zebrafish demonstrates response to injury and treatment comparable with mammalian models. J Neurotrauma. 2017; 34: 1382-1393. [CrossRef]
  65. Yoon SH, Kwon SK, Park SR, Min BH. Effect of ultrasound treatment on brain edema in a traumatic brain injury model with the weight drop method. Pediatr Neurosurg. 2012; 48: 102-108. [CrossRef]
  66. Bouzat P, Oddo M, Payen JF. Transcranial Doppler after traumatic brain injury: Is there a role? Curr Opin Crit Care. 2014; 20: 153-160. [CrossRef]
  67. Marklund N, Bellander BM, Godbolt AK, Levin H, McCrory P, Thelin EP. Treatments and rehabilitation in the acute and chronic state of traumatic brain injury. J Intern Med. 2019; 285: 608-623. [CrossRef]
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