Brain Injuries, Traumatic Clinical Trial
Official title:
The Role of Hyperbaric Oxygen and Neuropsychological Therapy in Cognitive Function Following Traumatic Brain Injury
Verified date | July 2021 |
Source | Chang Gung Memorial Hospital |
Contact | n/a |
Is FDA regulated | No |
Health authority | |
Study type | Interventional |
Traumatic brain injury (TBI) caused by accidents is a very important public health problem in Taiwan. There are many people with brain damage and cognitive dysfunction caused by traumatic brain injury every year. Currently, there is no effective treatment for cognitive dysfunction caused by traumatic brain injury. Evidence from clinical studies in recent years suggests that hyperbaric oxygen therapy may be a treatment for repairing nerves after brain injury. Many studies have shown that oxidative stress and inflammatory responses play an important role in the pathogenesis of the central nervous system. In recent years, our research team has shown that oxidative stress and inflammatory response are significantly associated with the prognosis of patients with traumatic brain injury, cerebral hemorrhage, and stroke patients. More and more evidences also show that oxidative stress and inflammatory response play an important role in the neuropathological changes of mental cognitive sequelae after traumatic brain injury. This injury may be gradual from the time of head trauma. This process begins with the generation of oxidative stress and free radicals. When the cell repair and free radical scavenging system can not effectively overcome the excessive production of free radicals, an oxidative damage reaction will occur, causing a series of inflammatory cells and cytokines to be activated. Studies have also shown that when inhibiting those free radicals that produce oxidative stress, the neurological function and cognitive function of the head after trauma can be significantly improved. It is becoming widely acknowledged that the combined action of hyperoxia and hyperbaric pressure leads to significant improvement in tissue oxygenation while targeting both oxygenand pressure-sensitive genes, resulting in improved mitochondrial metabolism with anti-apoptotic and anti-inflammatory effects. The investigators published an article this year showing that hyperbaric oxygen therapy can improve the prognosis of patients with acute stroke and increase endothelial progenitor cells in the systemic circulation. The investigators plan to conduct this research project through hyperbaric oxygen therapy and neuropsychological therapy, and using scientific tests and neurocognitive function assessments. The investigators hope to answer the following questions: (1) Whether the treatment of hyperbaric oxygen can improve oxidative stress and inflammatory response after brain injury, and observe changes in biomarker concentration; (2) Whether hyperbaric oxygen therapy and neuropsychological therapy can improve cognitive function after brain injury; and (3) which biomarkers are factors that influence cognitive function prognosis.
Status | Terminated |
Enrollment | 10 |
Est. completion date | February 28, 2021 |
Est. primary completion date | February 28, 2021 |
Accepts healthy volunteers | Accepts Healthy Volunteers |
Gender | All |
Age group | 18 Years to 65 Years |
Eligibility | Inclusion Criteria: - Traumatic brain injury, mild and moderated. - Age between 18 and 65 years old Exclusion Criteria: 1. Penetrating injury, including gunshot injury 2. Combined with other major trauma which had unstable hemodynamics 3. Major systemic disease, such ESRD, liver cirrhosis, CHF, or a malignant disease 4. Evidence for alcoholism or any other addictive disorders, or known affective or other psychiatric disease or use of sedatives or neuroleptic medication 5. Known neurological disorders potentially affecting the central nervous system or severe recent life events that might have interfered with neuropsychological testing. |
Country | Name | City | State |
---|---|---|---|
Taiwan | Kaohsiung Chang Gung Memorial Hospital | Kaohsiung |
Lead Sponsor | Collaborator |
---|---|
Hung-Chen Wang |
Taiwan,
Ali A, Hall I, Blickwedel J, Hassiotis A. Behavioural and cognitive-behavioural interventions for outwardly-directed aggressive behaviour in people with intellectual disabilities. Cochrane Database Syst Rev. 2015 Apr 7;(4):CD003406. doi: 10.1002/14651858.CD003406.pub4. Review. — View Citation
Allerdings MD, Alfano DP. Neuropsychological correlates of impaired emotion recognition following traumatic brain injury. Brain Cogn. 2006 Mar;60(2):193-4. — View Citation
Awasthi D, Church DF, Torbati D, Carey ME, Pryor WA. Oxidative stress following traumatic brain injury in rats. Surg Neurol. 1997 Jun;47(6):575-81; discussion 581-2. — View Citation
Balabanov R, Goldman H, Murphy S, Pellizon G, Owen C, Rafols J, Dore-Duffy P. Endothelial cell activation following moderate traumatic brain injury. Neurol Res. 2001 Mar-Apr;23(2-3):175-82. — View Citation
Boussi-Gross R, Golan H, Fishlev G, Bechor Y, Volkov O, Bergan J, Friedman M, Hoofien D, Shlamkovitch N, Ben-Jacob E, Efrati S. Hyperbaric oxygen therapy can improve post concussion syndrome years after mild traumatic brain injury - randomized prospective trial. PLoS One. 2013 Nov 15;8(11):e79995. doi: 10.1371/journal.pone.0079995. eCollection 2013. — View Citation
Carson MJ, Thrash JC, Walter B. The cellular response in neuroinflammation: The role of leukocytes, microglia and astrocytes in neuronal death and survival. Clin Neurosci Res. 2006 Dec;6(5):237-245. — View Citation
Chen CY, Wu RW, Tsai NW, Lee MS, Lin WC, Hsu MC, Huang CC, Lai YR, Kung CT, Wang HC, Su YJ, Su CM, Hsiao SY, Cheng BC, Chiang YF, Lu CH. Increased circulating endothelial progenitor cells and improved short-term outcomes in acute non-cardioembolic stroke after hyperbaric oxygen therapy. J Transl Med. 2018 Sep 12;16(1):255. doi: 10.1186/s12967-018-1629-x. — View Citation
Chen Y, Nadi NS, Chavko M, Auker CR, McCarron RM. Microarray analysis of gene expression in rat cortical neurons exposed to hyperbaric air and oxygen. Neurochem Res. 2009 Jun;34(6):1047-56. doi: 10.1007/s11064-008-9873-8. Epub 2008 Nov 18. — View Citation
Chen Z, Ni P, Lin Y, Xiao H, Chen J, Qian G, Ye Y, Xu S, Wang J, Yang X. Visual pathway lesion and its development during hyperbaric oxygen treatment: a bold- fMRI and DTI study. J Magn Reson Imaging. 2010 May;31(5):1054-60. doi: 10.1002/jmri.22142. — View Citation
Efrati S, Fishlev G, Bechor Y, Volkov O, Bergan J, Kliakhandler K, Kamiager I, Gal N, Friedman M, Ben-Jacob E, Golan H. Hyperbaric oxygen induces late neuroplasticity in post stroke patients--randomized, prospective trial. PLoS One. 2013;8(1):e53716. doi: 10.1371/journal.pone.0053716. Epub 2013 Jan 15. — View Citation
Godman CA, Chheda KP, Hightower LE, Perdrizet G, Shin DG, Giardina C. Hyperbaric oxygen induces a cytoprotective and angiogenic response in human microvascular endothelial cells. Cell Stress Chaperones. 2010 Jul;15(4):431-42. doi: 10.1007/s12192-009-0159-0. Epub 2009 Dec 1. — View Citation
Harch PG. Hyperbaric oxygen therapy for post-concussion syndrome: contradictory conclusions from a study mischaracterized as sham-controlled. J Neurotrauma. 2013 Dec 1;30(23):1995-9. doi: 10.1089/neu.2012.2799. Epub 2013 Oct 11. — View Citation
Hart T, Brockway JA, Maiuro RD, Vaccaro M, Fann JR, Mellick D, Harrison-Felix C, Barber J, Temkin N. Anger Self-Management Training for Chronic Moderate to Severe Traumatic Brain Injury: Results of a Randomized Controlled Trial. J Head Trauma Rehabil. 2017 Sep/Oct;32(5):319-331. doi: 10.1097/HTR.0000000000000316. — View Citation
Huang L, Obenaus A. Hyperbaric oxygen therapy for traumatic brain injury. Med Gas Res. 2011 Sep 6;1(1):21. doi: 10.1186/2045-9912-1-21. — View Citation
Kadhim HJ, Duchateau J, Sébire G. Cytokines and brain injury: invited review. J Intensive Care Med. 2008 Jul-Aug;23(4):236-49. doi: 10.1177/0885066608318458. Epub 2008 May 25. Review. — View Citation
Kendall AC, Whatmore JL, Harries LW, Winyard PG, Eggleton P, Smerdon GR. Different oxygen treatment pressures alter inflammatory gene expression in human endothelial cells. Undersea Hyperb Med. 2013 Mar-Apr;40(2):115-23. — View Citation
Lehnardt S. Innate immunity and neuroinflammation in the CNS: the role of microglia in Toll-like receptor-mediated neuronal injury. Glia. 2010 Feb;58(3):253-63. doi: 10.1002/glia.20928. Review. — View Citation
Lenzlinger PM, Morganti-Kossmann MC, Laurer HL, McIntosh TK. The duality of the inflammatory response to traumatic brain injury. Mol Neurobiol. 2001 Aug-Dec;24(1-3):169-81. Review. — View Citation
Lin KC, Niu KC, Tsai KJ, Kuo JR, Wang LC, Chio CC, Chang CP. Attenuating inflammation but stimulating both angiogenesis and neurogenesis using hyperbaric oxygen in rats with traumatic brain injury. J Trauma Acute Care Surg. 2012 Mar;72(3):650-9. doi: 10.1097/TA.0b013e31823c575f. Erratum in: J Trauma Acute Care Surg. 2012 Jul;73(1):295-6. — View Citation
Lu J, Goh SJ, Tng PY, Deng YY, Ling EA, Moochhala S. Systemic inflammatory response following acute traumatic brain injury. Front Biosci (Landmark Ed). 2009 Jan 1;14:3795-813. Review. — View Citation
Maas AI, Stocchetti N, Bullock R. Moderate and severe traumatic brain injury in adults. Lancet Neurol. 2008 Aug;7(8):728-41. doi: 10.1016/S1474-4422(08)70164-9. Review. — View Citation
May M, Milders M, Downey B, Whyte M, Higgins V, Wojcik Z, Amin S, O'Rourke S. Social Behavior and Impairments in Social Cognition Following Traumatic Brain Injury. J Int Neuropsychol Soc. 2017 May;23(5):400-411. doi: 10.1017/S1355617717000182. Epub 2017 Apr 12. — View Citation
Milders M, Ietswaart M, Crawford JR, Currie D. Social behavior following traumatic brain injury and its association with emotion recognition, understanding of intentions, and cognitive flexibility. J Int Neuropsychol Soc. 2008 Mar;14(2):318-26. doi: 10.1017/S1355617708080351. Erratum in: J Int Neuropsychol Soc. 2008 May;14(3):508. — View Citation
Rhind SG, Crnko NT, Baker AJ, Morrison LJ, Shek PN, Scarpelini S, Rizoli SB. Prehospital resuscitation with hypertonic saline-dextran modulates inflammatory, coagulation and endothelial activation marker profiles in severe traumatic brain injured patients. J Neuroinflammation. 2010 Jan 18;7:5. doi: 10.1186/1742-2094-7-5. — View Citation
Schmidt OI, Leinhase I, Hasenboehler E, Morgan SJ, Stahel PF. [The relevance of the inflammatory response in the injured brain]. Orthopade. 2007 Mar;36(3):248, 250-8. Review. German. — View Citation
Sirois K, Tousignant B, Boucher N, Achim AM, Beauchamp MH, Bedell G, Massicotte E, Vera-Estay E, Jackson PL. The contribution of social cognition in predicting social participation following moderate and severe TBI in youth. Neuropsychol Rehabil. 2019 Oct;29(9):1383-1398. doi: 10.1080/09602011.2017.1413987. Epub 2017 Dec 18. — View Citation
Soriano SG, Piva S. Central nervous system inflammation. Eur J Anaesthesiol Suppl. 2008;42:154-9. doi: 10.1017/S0265021507003390. Review. — View Citation
Stein SC, Smith DH. Coagulopathy in traumatic brain injury. Neurocrit Care. 2004;1(4):479-88. Review. — View Citation
Tousignant B, Jackson PL, Massicotte E, Beauchamp MH, Achim AM, Vera-Estay E, Bedell G, Sirois K. Impact of traumatic brain injury on social cognition in adolescents and contribution of other higher order cognitive functions. Neuropsychol Rehabil. 2018 Apr;28(3):429-447. doi: 10.1080/09602011.2016.1158114. Epub 2016 Mar 10. — View Citation
Tyurin VA, Tyurina YY, Borisenko GG, Sokolova TV, Ritov VB, Quinn PJ, Rose M, Kochanek P, Graham SH, Kagan VE. Oxidative stress following traumatic brain injury in rats: quantitation of biomarkers and detection of free radical intermediates. J Neurochem. 2000 Nov;75(5):2178-89. — View Citation
Vlodavsky E, Palzur E, Soustiel JF. Hyperbaric oxygen therapy reduces neuroinflammation and expression of matrix metalloproteinase-9 in the rat model of traumatic brain injury. Neuropathol Appl Neurobiol. 2006 Feb;32(1):40-50. — View Citation
Wang HC, Lin YJ, Shih FY, Chang HW, Su YJ, Cheng BC, Su CM, Tsai NW, Chang YT, Kwan AL, Lu CH. The Role of Serial Oxidative Stress Levels in Acute Traumatic Brain Injury and as Predictors of Outcome. World Neurosurg. 2016 Mar;87:463-70. doi: 10.1016/j.wneu.2015.10.010. Epub 2015 Oct 23. — View Citation
Wang HC, Lin YJ, Tsai NW, Su BY, Kung CT, Chen WF, Kwan AL, Lu CH. Serial plasma deoxyribonucleic acid levels as predictors of outcome in acute traumatic brain injury. J Neurotrauma. 2014 Jun 1;31(11):1039-45. doi: 10.1089/neu.2013.3070. Epub 2014 Mar 31. — View Citation
Wang HC, Wang PM, Lin YJ, Kwan AL, Lin WC, Tsai NW, Cheng BC, Chang WN, Su BY, Kung CT, Lu CH. Serum adhesion molecules, outcome and neuro-psychological function in acute traumatic brain injury patients. Clin Chim Acta. 2013 Aug 23;423:122-9. doi: 10.1016/j.cca.2013.04.023. Epub 2013 Apr 30. — View Citation
Wang HC, Yang TM, Lin YJ, Chen WF, Ho JT, Lin YT, Kwan AL, Lu CH. Serial serum leukocyte apoptosis levels as predictors of outcome in acute traumatic brain injury. Biomed Res Int. 2014;2014:720870. doi: 10.1155/2014/720870. Epub 2014 Apr 17. — View Citation
Westerhof-Evers HJ, Visser-Keizer AC, Fasotti L, Schönherr MC, Vink M, van der Naalt J, Spikman JM. Effectiveness of a Treatment for Impairments in Social Cognition and Emotion Regulation (T-ScEmo) After Traumatic Brain Injury: A Randomized Controlled Trial. J Head Trauma Rehabil. 2017 Sep/Oct;32(5):296-307. doi: 10.1097/HTR.0000000000000332. — View Citation
Zhang JH, Lo T, Mychaskiw G, Colohan A. Mechanisms of hyperbaric oxygen and neuroprotection in stroke. Pathophysiology. 2005 Jul;12(1):63-77. — View Citation
Zhang X, Chen Y, Jenkins LW, Kochanek PM, Clark RS. Bench-to-bedside review: Apoptosis/programmed cell death triggered by traumatic brain injury. Crit Care. 2005 Feb;9(1):66-75. Epub 2004 Sep 3. Review. — View Citation
* Note: There are 38 references in all — Click here to view all references
Type | Measure | Description | Time frame | Safety issue |
---|---|---|---|---|
Primary | Neuropsychological testing- Wechsler Adult Intelligence scale-III (WAIS-III) | Subtests included the followings: Information with a measure of general knowledge, digit Span, vocabulary ability to define 35 words, arithmetic, comprehension, similarities, picture completion, picture arrangement, block design, digit symbol, and object assembly. The scores could further subscore into verbal comprehension, perceptual reasoning and working memory index. | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Primary | Neuropsychological testing- Cognitive Ability Screening Instrument (CASI) | includes tests of nine domains of cognitive function (attention, concentration, orientation, short and long-term memory, language ability, visual construction, word list generation, abstraction, and judgment), and the score ranges from 0 (worst) to 100 (best score). | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Primary | Neuropsychological testing- mini-mental state examination (MMSE) | The Mini-Mental State Examination (MMSE) test is a 30-point questionnaire. Any score greater than or equal to 24 points (out of 30) indicates a normal cognition. Below this, scores can indicate severe (=9 points), moderate (10-18 points) or mild (19-23 points) cognitive impairment. | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Primary | Neuropsychological testing- Short Form 36 questionnaire | The SF-36 taps eight health concepts: physical functioning, bodily pain, role limitations due to physical health problems, role limitations due to personal or emotional problems, emotional well-being, social functioning, energy/fatigue, and general health perceptions. Scoring the SF-36 is a two-step process. First, each item is scored on a 0 to 100 range so that the lowest and highest possible scores are set at 0 and 100, respectively. Scores represent the percentage of total possible score achieved. In step 2, items in the same scale are averaged together to create the 8 scale scores. | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Primary | Neuropsychological testing- The World Health Organization Quality of Life questionnaire (WHOQOL-BREF) | questionnaire is a 26-item questionnaire that evaluates 4 domains of quality of life (QoL), namely Physical, Psychological, Social Relationships and Environment | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Primary | Neuropsychological testing- Beck Depression Inventory | The BDI-II contains 21 questions, each answer being scored on a scale value of 0 to 3. Higher total scores indicate more severe depressive symptoms. The standardized cutoffs used here differ from the original as such: 0-13: minimal depression; 14-19: mild depression; 20-28: moderate depression; and 29-63: severe depression. | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Secondary | oxidative damage markers: Erythrocyte superoxide dismutase (SOD) activity | by a commercially available kit (Ransod, Randox Lab., Grumlin, UK) based on the method developed by McCord and Fridovich. The SOD activity is then measured by the degree of inhibition of this reaction. The assay will be carried out on washed red blood cells, by diluting the samples to give between 30 and 60% inhibition. Together with the kit, a standard is supplied, which is diluted to provide a range of standards and a calibration curve. A standard curve will be produced by plotting % inhibition for each standard against Log 10. The result will be multiplied by the appropriate dilution factor (100) and expressed in units/litre (U/L) of whole blood. | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Secondary | oxidative damage markers: Erythrocyte glutathione peroxidase (GPx) activity | Erythrocyte GPx activity will be measured using a commercially available kit (Ransel; Randox Lab, Crumlin, U.K.). The result obtained will be expressed in U/L of haemolysate and will be multiplied by the appropriate dilution factor to obtain the result in U/L of whole blood. | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Secondary | oxidative damage markers: serum malondialdehyde (MDA) content | Serum MDA will be measured using the thiobarbituric acid reactive substances (TBARS) assay. TBARS reagent (1 ml) will be added to a 0.5 ml aliquot of serum and heated for 20 minutes at 100°C. The antioxidant, butylated hydroxytoluene, will be added before heating the samples. After cooling on ice, samples will be centrifuged at 840 g for 15 mins and absorbance of the supernatant will be read at 532 nm. Blanks for each sample will be prepared and assessed in the same way to correct for the contribution of A532 to the sample. TBARS results will be expressed as MDA equivalents using 1,1,3,3-tetraethoxypropane. | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Secondary | oxidative damage markers: serum free thiol content | Plasma free thiols will be determined by directly reacting thiols with 5,5-dithiobis 2-nitrobenzoic acid (DTNB) to form 5-thio-2- nitrobenzoic acid (TNB). The amount of thiols in the sample will be calculated from the absorbance determined using extinction coefficient of TNB (A412 = 13,600 M-1cm-1). | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Secondary | Cytokines (IL-1ß) by Enzyme-linked immunosorbent assays | will be assayed in serum samples and quantified with a commercially available colorimetric ELISA. | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Secondary | Cytokines (IL-6) by Enzyme-linked immunosorbent assays | will be assayed in serum samples and quantified with a commercially available colorimetric ELISA. | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Secondary | Cytokines (IL-10) by Enzyme-linked immunosorbent assays | will be assayed in serum samples and quantified with a commercially available colorimetric ELISA. | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Secondary | Cytokines (TNF-a) by Enzyme-linked immunosorbent assays | will be assayed in serum samples and quantified with a commercially available colorimetric ELISA. | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Secondary | endothelium-leukocyte activation (ICAM-1) | will be assayed in serum samples and quantified with a commercially available colorimetric ELISA. | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Secondary | endothelium-leukocyte activation ( VCAM-1) | will be assayed in serum samples and quantified with a commercially available colorimetric ELISA. | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Secondary | endothelium-leukocyte activation (E-selectin) | will be assayed in serum samples and quantified with a commercially available colorimetric ELISA. | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Secondary | endothelium-leukocyte activation (L-selectin) | will be assayed in serum samples and quantified with a commercially available colorimetric ELISA. | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Secondary | neural inflammation markers (S-100) | by Enzyme-linked immunosorbent assays; The values of intra- and inter-assay coefficients were around 5%. Concentration is expressed as pg/ml | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Secondary | neural inflammation markers (tau protein) | by Enzyme-linked immunosorbent assays; The values of intra- and inter-assay coefficients were around 5%. Concentration is expressed as pg/ml | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Secondary | neural inflammation markers (MMP-2) | by Enzyme-linked immunosorbent assays; The values of intra- and inter-assay coefficients were around 5%. Concentration is expressed as ng/ml | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Secondary | neural inflammation markers (MMP-9) | by Enzyme-linked immunosorbent assays; The values of intra- and inter-assay coefficients were around 5%. Concentration is expressed as ng/ml | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. | |
Secondary | plasma cell-free DNA by Real-time quantative PCR | DNA will be extracted from 200µL plasma samples with use of a QIAamp Blood Kit (Qiagen) according to the "blood and body fluid protocol" as recommended by the manufacturer. Plasma DNA will be measured by a real-time quantitative PCR assay for the ß-globin gene and ND2 gene. The ß-globin gene is present in all nucleated cells of the body while ND2 gene is specific mitochondrial DNA. Expression of ß-globin and mtDNA will be measured by quantitative RT-PCR based on continuous measurements of Syber green fluorescent dye that binds to double stranded DNA generated during PCR and a specific primer pair for ß-globin-354F (5'-GTG CAC CTG ACT CCT GAG GAG A-3') and ß-globin-455R (5'-CCT TGA TAC CAA CCT GCC CAG-3') and ND2 (forward:5'-CAC AGA AGC TGC CAT CAA GTA -3'; reverse:5'-CCG GAG AGT ATA TTG TTG AAG AG -3'). | Change from baseline, at after 6 weeks of HBOT and at after 6 times of neuropsychological treatment. |
Status | Clinical Trial | Phase | |
---|---|---|---|
Recruiting |
NCT04111549 -
GOALS Cognitive Training Delivered to Aging Veterans in Person or Via Telehealth
|
N/A | |
Recruiting |
NCT05097261 -
Ketamine in Acute Brain Injury Patients.
|
Phase 4 | |
Completed |
NCT03504709 -
REsting and Stimulus-based Paradigms to Detect Organized NetworkS and Predict Emergence of Consciousness
|
||
Recruiting |
NCT03899532 -
Remote Ischemic Conditioning in Traumatic Brain Injury
|
N/A | |
Completed |
NCT05057377 -
Estimating Highest Capacity Performance During Evaluation of Walking for Individuals With Traumatic Brain Injury
|
||
Withdrawn |
NCT02776488 -
Exogenous Sodium Lactate Infusion in Traumatic Brain Injury (ELI-TBI)
|
Phase 2 | |
Completed |
NCT02426749 -
Treatment and Recovery Monitoring of Post TBI Symptoms
|
N/A | |
Completed |
NCT01339702 -
The EPIC Project: Impact of Implementing the EMS Traumatic Brain Injury Treatment Guidelines
|
||
Recruiting |
NCT05977270 -
The Effects of Lifebloom One on Physical Activity After Acquired Brain Injury
|
N/A | |
Recruiting |
NCT04666766 -
Detecting Traumatic Intracranial Hemorrhage With Microwaves and Biomarkers
|
N/A | |
Active, not recruiting |
NCT04559724 -
Gait Training Through a Novel Over-ground Wearable Robotic System in People With Pyramidal Hemisyndromes
|
N/A | |
Not yet recruiting |
NCT04515420 -
The Influence of Noradrenaline on Coagulation and Fibrinolysis in Severe Isolated Brain Injury
|
||
Not yet recruiting |
NCT05569993 -
Glutamine and Traumatic Brain Injury
|
Early Phase 1 | |
Recruiting |
NCT04331392 -
Online Memory Intervention for Individuals With Traumatic Brain Injury
|
N/A | |
Completed |
NCT03727737 -
Efficacy of Repetitive Transcranial Magnetic Stimulation for Improvement of Memory in Older Adults With TBI
|
N/A | |
Completed |
NCT03153397 -
Effect of Prebiotic Fiber- Enriched (scFOS) Enteral Feeding on the Microbiome in Neurological Injury Trauma Patients (PreFEED Microbiome Trial)
|
N/A | |
Completed |
NCT01336413 -
Neuroactive Steroids and Traumatic Brain Injury (TBI) in OEF/OIF Veterans
|
Phase 2 | |
Completed |
NCT02004080 -
CREACTIVE - Collaborative REsearch on ACute Traumatic Brain Injury in intensiVe Care Medicine in Europe
|
||
Completed |
NCT04957563 -
Clinical Utility of Olfactory Rehabilitation: Treatment for Pacients With Neurosensorial Anosmia
|
N/A | |
Completed |
NCT05179330 -
Visual Feedback in Lower Limb Rehabilitation
|
N/A |