Brain trauma remains to be a significant challenge for public health all across the globe. Around the world, it is the leading cause of disability and death, with middle and low income countries bearing the brunt of the illness load (1). The term "decompressive craniectomy" (DC) describe the process of bone flap removal by opening dura behind it in order to regulate the brain swelling which generates a high intracranial pressure (ICP) (2). Bifrontal craniectomy describes the process of bone flap removal for the extension of anterior cranial fossa floor to the coronal suture, and bilaterally to the floor of the middle cranial fossa. Unilateral craniectomy, also known as frontotemporoparietal craniectomy, describing the frontotemporoparietal bone flap removal. The operation requires either a large incision in the dura or a duraplasty in order to be successful (2). Decompressive craniectomy, often known as DC, is a surgery that is frequently used in neurosurgical practise and has been shown to be particularly helpful in the treatment of refractory intracranial hypertension. Because of this, there is much discussion and disagreement on the method that should be utilized, particularly in regard to how the opening dura mater should be handled. After the dura mater is exposed, there is no watertight duraplasty, and the exposed brain tissue is covered by the remaining open dura and Surgicel. This set of cases was published by Güresir et al (3) in 2011, and it introduced the idea of rapid-closure DC. Our goal was to carry out a prospective randomised controlled study in which we would compare two different surgical procedures for DC: including simple-closure (watertight duraplasty) and rapid-closure (without watertight duraplasty). A wide variety of surgical procedures, including craniectomy, dura opening, and duroplasty, have been documented in the medical literature. These procedures can be found in either the site or the extent of the craniectomy. Decompressions of the bony structures might be performed either unilaterally or bilaterally (4, 5), bifrontally (6, 7), subtemporally (8, 9), or circumferentially (10). In spite of this, unilateral hemicraniectomies and bifrontal craniectomies have emerged as the most popular forms of the procedure (11). After the removal of bones, it is considered essential to do a dura opening (8). In a study by Butensky et al, the frequency of CSF leak in the duraplasty group was 35% and 0% in the group without duraplasty. Clinical improvement in theduraplasty group was 79% and 82% in without duraplasty group (12). Results from a systematic review showed thst 243 out of 280 patients (86.7%) with duraplasty showed clinical improvement as compared to 143 out of 205 patients (69.7%) with put duraplasty (13).

The approval of an institutional review board (IRB) was acquired for a prospective randomized controlled experiment with a single center. All patients admitted to Neuro-trauma with a clinical indication for unilateral decompressive craniectomy with or without watertight duraplasty at Neurosurgery Bolan Medical College/Hospital Quetta, aged between 18 and 60 years. Consent was obtained from the patient's next of kin or legal guardian, as appropriate. After a clinical indication for unilateral DC, patients were randomized into two groups using numbered envelopes: those with watertight duraplasty and those without. In all cases, a large trauma flap was performed (i.e., a large inverted question mark beginning at the tragus and extending to the midline). According to the surgeon's preference, the skin, galea, and muscle layers were raised. Therefore, a wide craniotomy (at least 12 15 cm) was performed, and the temporal bone was removed until it was flush with the floor of the middle fossa. In group A, watertight duraplasty was performed with pericranium or an artificial graft (at the surgeon's discretion), whereas in group B, no watertight duraplasty was performed. The usual closure was then carried out. From the date of surgery until hospital discharge or death, patients were monitored daily by evaluators who were blind to the randomization (control or test group). Our primary outcome measure was the incidence of CSF leakage (CSF drainage through the surgical wound). After 7 days, CT scans of the head were performed to evaluate the presence of subgaleal fluid collections. The clinical improvement was evaluated as a secondary endpoint (analyzed using the Glasgow Outcome Scale [GOS]). Postoperative results in terms of CSF leakage and Clinical improvement (GOS) were recorded for both groups in accordance with the operational definition. Data was entered into SPSS version 23.0. Mean + SD are given for age and GCs. Frequency and percentages are given for gender, CSF leak and clinical improvement. Chi-square test was used to compare outcome in both groups. Data was stratified for age, gender, GCS at presentation, cause of trauma and duration since trauma to deal with effect modifiers. Post stratification chi-square test was applied. A p-value < 0.05 was taken as significant

A total of 144 cases of decompressive craniectomy with and without water tight duraplasty were compared for possible outcome. All cases were randomized into two groups having 72 cases in each group. In group A, all cases of water tight duraplasty were included while group B contained all cases of without water tight duraplasty having both genders respectively. In this study, in group A, 30.56% patients were between the ages of 18-30 years, 47.22% patients were between the ages of 31-40 years while 22.22% patients were between the ages of 41-60 years. On the other hand, in group B, 37.50% patients were between the ages of 18-30 years, 38.89% patients were between the ages of 31-40 years while 23.62% patients were between the ages of 41-60 years. The minimum age of the patient was 20 years while maximum age of the patient was 53 years. However, mean age of patients in group A was 34.28+7.80 years while in group B, mean age of the patient was 33.39+7.90 years. Regarding gender distribution, out of 144 patients 73.6% patients were male while remaining 26.4% patients were female. In group A 74.0% patients were male and 25.0% patients were female while in group B 72.2% patients were male and 27.8% patients were female respectively. Clinical improvement in patients with respect to cause of trauma. In group A, 40 patients from traffic accidents, 08 patients from assault and 20 patients from fall showed improvement. In group B, 38 patients from traffic accidents, 07 patients from assault and 17 patients from fall showed improvement. Collectively the total improvements were 62.5%. 37.5% patients showed less improvement. There was no significant difference between group A and group B in terms of clinical improvements (p = 0.544). According to the results of the independent sample t-test, there was not a significant difference between groups (p = 0.598) in terms of outcome as GOS score. In our study main focus was CSF leak. All patients were examined after seven days. In group A, total 6 (8.30%) patients showed complications while in group B total 2 (2.80%) patients showed complications. With regards to frequency of other complications, total 13 (18.1%) cases were reported for post surgery complications. Among them, most common being post operative CSF leak i.e. 8.3% for group A and 1.4% for group B followed by wound infections i.e. 2.8% and 1.4% respectively for group A and group B. Subgaleal collection was also noted in 1.4% in both groups. Results from (Table 1) showed no significant difference between group A and group B (p = 0.456). With regards to clinical improvement as GOS score, in group A, preoperative GOS score was 9.03 ± 0.79 while at the time of discharge mean GOS score was 13.60 ± 0.14 and at 3rd month follow up mean GOS score was 13.92±0.18. On the other hand, in group B, preoperative GOS score was 9.12±0.43 while at the time of discharge mean GOS score was 13.70±0.62 and at 3rd month follow up mean GOS score was 13.83±0.65 (Table 2). In Table 3 represents stratification of clinical improvement in patients with and without duraplasty with respect to age groups is presented. In group A, 40 patients of age <45 years and 08 patients of age >45 years showed improvement. In group B, 36 patients of age <45 years and 06 patients of age >45 years showed improvement. Results from Table 7 showed no significant difference between group A and group B (p >0.05). Stratification of CSF leak in patients with and without duraplasty with respect to age groups. In group A, 05 patients of age <45 years and 01 patients of age >45 years showed CSF leak. In group B, 02 patients of age <45 years and 00 patients of age >45 years showed CSF leak. Results from Table 3 showed no significant difference between group A and group B (p >0.05). Table 3 represents stratification of clinical improvement in patients with and without duraplasty with respect to gender. In group A, 32 male and 12 female patients showed improvement while in group B, 33 male and 09 female patients showed improvement Results from Table 9 showed no significant difference between group A and group B (p >0.05). CSF Leak in patients with and without duraplasty with respect to gender. In group A, 04 male and 02 female patients showed CSF Leak while in group B, 02 male and 01 female patients showed CSF Leak. Results from Table 3 showed no significant difference between group A and group B (p >0.05). Clinical improvement in patients with and without duraplasty with respect to GCS at presentation. In group A, 05 patients with GCS < 13 and 66 patients with GCS >13 showed improvement. In group B, 07 patients with GCS <13 and 63 patients with GCS >13 showed improvement. Results from Table 3 showed no significant difference between group A and group B (p >0.05). Table 3 represents stratification of CSF Leak in patients with and without duraplasty with respect to GCS at presentation. In group A, 02 patients with GCS <13 and 04 patients with GCS >13 showed CSF Leak. In group B, 01 patient with GCS <13 and 01 patients with GCS >13 CSF Leak. Results from Table 3 showed no significant difference between group A and group B (p >0.05). Table 3 represents stratification of clinical improvement in patients with and without duraplasty with respect to duration since trauma. In group A, 43 patients and in group B, 39 patients showed improvement in duration <12 hours. On other side, in group A, 07 patients and in group B, 08 patients showed improvement in duration >12 hours. Results from Table 3 showed no significant difference between group A and group B (p >0.05). Table 3 represents stratification of CSF Leak in patients with and without duraplasty with respect to duration since trauma. In group A, 02 patients and in group B, 01 patient showed CSF Leak in duration <12 hours. On other side, in group A, 04 patients and in group B, 01 patients showed CSF Leak in duration >12 hours. Results from Table 14 showed no significant difference between group A and group B (p >0.05). Clinical improvement in patients with and without duraplasty with respect to cause of trauma. In group A, 40 patients from traffic accidents, 08 patients from assault and 20 patients from fall showed improvement. In group A, 38 patients from traffic accidents, 07 patients from assault and 17 patients from fall showed improvement. Results from Table 3 showed no significant difference between group A and group B (p >0.05). Table 16 represents stratification of CSF leak in patients with and without duraplasty with respect to cause of trauma. In group A, 03 patients from traffic accidents, 02 patients from assault and 01 patient from fall showed CSF leak. In group A, 01 patient from traffic accidents, 01 patient from assault and 00 patients from fall showed CSF leak. Results from Table 3 showed no significant difference between group A and group B (p >0.05). Table No. 1 Age, Gender, Cause Of Trauma, Clinical Improvements As Gos Scale, Table No. 6 Complications After Seven Days Distribution Age (in Years) Group A Group B p-value No. of Patients (%) No. of Patients (%) Age Groups 18-30 22(30.56%) 27 (37.50%) 0.352 31-40 34 (47.22%) 28 (38.89%) 41-60 16 (22.22%) 17 (23.61%) Gender Gender Male 54 (75.0%) 52 (72.2%) 0.564 Female 18 (25.0%) 20 (27.8%) Cause of Trauma Cause of Trauma Traffic Accident 40 (55.55%) 38 (52.78%) 0.870 Assault 08 (11.11%) 07 (9.72%) Fall 20 (27.78%) 17(23.61%) Clinical improvement Clinical improvement Yes 48 (66.67%) 42 (58.33%) 0.544 No 24 (33.33%) 30 (41.67%) CSF LEAK CSF LEAK Yes 6 (8.30%) 2 (2.80%) 0.456 No 66 (91.67%) 70 (97.20%) Group A Age Mean+SD: 34.28 + 7.80 years Group B Age Mean+SD: 33.39 + 7.90 years Total Complications: 13 (18.1%). TABLE No. 2 Preoperative Improvements as GOS Score Mean GOS score p-value Group A Group B Follow up Preoperative 9.03 ± 0.79 9.12 ± 0.43 0.598 At time of Discharge 13.60 ± 0.14 13.70 ± 0.62 3rd Month 13.92 ± 0.18 13.83 ± 0.65 TABLE No. 3 Stratification of Clinical Improvement, CSF LEAK, Clinical Improvement, CSF LEAK, Clinical Improvement in Patients with and without Duraplasty With Respect To Age Groups, Gender Groups, GCS, CSF LEAK, Duration Since Trauma Category Group Improvement p –value Yes No Age < 45years Group A 40 20 0.567 Group B 36 28 Age > 45 years Group A 08 04 0.655 Group B 06 02 CSF LEAK Age < 45 years Group A 05 56 0.721 Group B 02 58 Age > 45 years Group A 01 10 0.872 Group B 00 12 Clinical Improvement Male Group A 32 18 0.823 Group B 33 17 Female Group A 12 06 0.887 Group B 09 13 CSF LEAK Age < 45 years Group A 05 56 0.721 Group B 02 58 Age > 45 years Group A 01 10 0.872 Group B 00 12 Clinical Improvement Male Group A 32 18 0.823 Group B 33 17 Female Group A 12 06 0.887 Group B 09 13 CSF LEAK Male Group A 04 46 0.589 Group B 01 55 Female Group A 02 20 0.798 Group B 01 15 GCS GCS < 13 Group A 05 00 0.662 Group B 07 01 GCS > 13 Group A 66 01 0.571 Group B 63 01 CSF LEAK GCS < 13 Group A 02 06 0.456 Group B 01 09 GCS > 13 Group A 04 60 0.339 Group B 01 61 Clinical Improvement Duration <12 hours Group A 43 17 0.234 Group B 39 18 Duration >12 hours Group A 07 05 0.331 Group B 08 07 CSF LEAK Duration <12 hours Group A 02 66 0.432 Group B 01 70 Duration >12 hours Group A 04 66 0.567 Group B 01 70 CLINICAL IMPROVEMEN Traffic Accidents Group A 40 01 0.786 Group B 38 02 Assault Group A 08 01 0.777 Group B 07 01 Fall Group A 20 03 0.792 Group B 17 06 CSF LEAK Traffic Accidents Group A 03 25 0.206 Group B 01 32 Assault Group A 02 28 0.147 Group B 01 27 Fall Group A 01 19 0.220 Group B 00 13

A brain injury that does not worsen over time as a result of a blow to the head is referred to as a TBI. In most cases, concussions are the result of a blow, bump, jolt, or a wound that penetrates the skull. It is estimated that between 54 and 60 million people experience TBIs every year, resulting in hospitalization or death. Low and middle income countries experience nearly three times as many cases of TBIs as high-income countries. It is the leading cause of death and disability on a global scale, and it has massive repercussions for economies around the world. TBI is a heterogeneous entity that reflects a range of brain injury processes in variable amounts. The gravity of (14). Since the dawn of time, the clinical severity of traumatic brain damage has been classified as mild (GCS 14-15), moderate (9-13), and severe (3-8) based on post-resuscitation Glasgow Coma Scale scores (16). In comparison of our results as reported in Table 1 in literature the age distribution of the 189 patients who participated in this research showed that 58.7% of them (n=111) were between the ages of 18 and 40, and that 41.3% of them (n=78) were between the ages of 41 and 60. It was determined that the average age was 36.57 years old. In comparison of our results as reported in Table 2 in literature, there were 116 male participants, which makes up 61.4% of the total, while there were only 73 female participants, which makes up 38.6%. In the current study, we discovered that the good outcome rate was 86.2% (n=163), the poor outcome rate was 13.8% (n=26), and complications occurred in 11.1% (57) (n=21) of patients who experienced DC with expansion duraplasty for severe head injury. Study was conducted on people who had undergone DC with expansion duraplasty. TBI was found to be a risk factor for not only PTSD, but also for other disorders, according to the findings of a private study that included 1084 people with TBI. According to estimates provided by the Centers for CDC, approx In the year 2000, there were 10,958 confirmed cases of TBI. This number reached a high of 344,030 in the year 2015. The mortality rate is approximately 3% of TBI severity, whereas it is more challenging to estimate the morbidity rate (17). Individually, however, the number of deaths that can be attributed to TBI has decreased over the same time period. This is most likely at least partially due to improved awareness, management, guidelines, and advance technologies in the treatment that are currently being used. It is also important to note that a certain percentage of TBIs are never treated by a medical professional; as a result, the overall rates of TBIs are probably underreported (15). The highest rates of TBI are seen in extremely young children aged 0 to 4 years, as well as in adolescents and young adults (15–24 y). A second incidence peak is seen among people older than 65 years of age. The majority of TBIs are caused by either falls or automobile accidents (16). An increasing number of people are living with significant disabilities that are directly related to their TBIs, which is a direct consequence of the overall rise in the number of TBIs. However, the rate of deaths that are caused by TBIs has decreased (17,19). TBI and the area of the brain that is damaged determine the symptoms that are experienced. People who have sustained injuries to the left side of their brain are more likely to remain unconscious for a longer period of time than those who have sustained injuries to the right side of their brain. The severity of the injury can also have an effect on the symptoms. After sustaining a mild TBI, the patient might remain conscious for a few seconds or minutes, or they might experience a momentary loss of consciousness. Headache, nausea, vomiting, lightheadedness, dizziness, balancing, sleepy eyes, ringing in the ears, exhaustion and abnormalities in sleep patterns are all signs of mild TBI. Some of the signs of a moderate or severe TBI include slurred speech, aphasia (difficulty finding the proper words), dysarthria, limb numbness, lack of coordination, disorientation, restlessness, or agitation. Other symptoms include a persistent headache, nausea or vomiting, seizures, inability to wake up, and dilatation. Continuing symptoms of moderate to severe traumatic brain damage often include changes in proper social behavior, social judgment deficiencies, and cognitive alterations, including issues with constant attention, speed and functioning. Alexithymia, impairment in recognizing, perceiving and processing emotions, is present in 60.9% of TBI patients. Irritability, combined with other symptoms such as persistent sobbing, inability to be comforted, lethargy, refusal to suckle and irritability, can be noticed in young children (20-25). Decompressive craniectomy, also known as DC, is a neurosurgical procedure that is performed frequently and is found to be effective in the cure of intracranial hypertension. In comparison of our results as reported in Table 3 in literature, in recent years, decompressive craniectomy, also known as DC, has become an increasingly common surgical procedure used to control intracranial hypertension in patients with TBI who have not responded favourably to medical treatment (26). Despite the fact that DC has the potential to save the lives of TBI patients, the procedure is linked to a number of potentially life-threatening complications (20,27). In comparison of our results as reported in Table 4 in literature, there is a more than 50% chance of complications with DC, despite the fact that it is an effective treatment for TBI. Age and the patient's initial neurologic state are both factors that can increase the likelihood of complications. Invasion of the orbital roof during the course of DC, proximity to the facial sinuses, and large contour abnormalities with corresponding large dead spaces are all factors that contribute to an increased risk of infection rate. There is a possibility that DC could result in complications such as a disorder of CSF leak, postoperative expansion, trephined syndrome infection. The emergency surgical procedure for DC may cause damage to the STA as well as a decrease in blood flow to the scalp flap, both of which may lead to necrosis of the tissue that is located in the surrounding area.(28-31) It is possible to contaminate the surgical field by opening the frontal sinus unintentionally, which is especially risky during a bifrontal craniectomy. Antibiotics given to patients during surgical procedures continue to bring the incidence of wound infections down to about 7 percent,(32-35) where they have remained for several years. In addition, the tight sealing provided by the dura prevents CSF leakage, which in turn helps to reduce wound complications brought on by CSF leakage. Headaches, irritability, dizziness, seizures, pain and particularly those related to large cranial defects, are among the clinical symptoms associated with this condition. There is a lack of understanding regarding the mechanism behind this syndrome; however, abnormal CSF flow, atmospheric pressure on the brain, and CBF disturbances have all been connected to it. Early cranioplasty, performed before the skin flap sinks, has the potential to alleviate the syndrome; however, because it raises the risk of infection, it is not recommended (36-37).

The findings from our investigation establish that decompressive craniectomy performed without watertight duraplasty demonstrates no association with elevated rates of adverse outcomes, encompassing cerebrospinal fluid leakage, subgaleal fluid accumulations, and infectious complications. Furthermore, our randomized controlled trial presents a comprehensive examination of decompressive craniectomy methodology, and our empirical findings furnish evidence-based guidance for selecting the most appropriate surgical approach for individual clinical scenarios.

1. Dewan MC, Rattani A, Gupta S, Baticulon RE, Hung Y-C, Punchak M, et al. Estimating the global incidence of traumatic brain injury. Journal of neurosurgery. 2018;130(4):1080-97. 2. Kolias AG, Viaroli E, Rubiano AM, Adams H, Khan T, Gupta D, et al. The current status of decompressive craniectomy in traumatic brain injury. Current trauma reports. 2018;4(4):326-32. 3. Güresir E, Vatter H, Schuss P, Oszvald A, Raabe A, Seifert V, et al. Rapid closure technique in decompressive craniectomy. Journal of neurosurgery. 2011;114(4):954-60. 4. Coplin WM, Cullen NK, Policherla PN, Vinas FC, Wilseck JM, Zafonte RD, et al. Safety and feasibility of craniectomy with duraplasty as the initial surgical intervention for severe traumatic brain injury. Journal of Trauma and Acute Care Surgery. 2001;50(6):1050-9. 5. Csókay A, Együd L, Nagy L, Pataki G. Vascular tunnel creation to improve the efficacy of decompressive craniotomy in post-traumatic cerebral edema and ischemic stroke. Surgical neurology. 2002;57(2):126-9. 6. Hutchinson P, Kirkpatrick P. Decompressive craniectomy in head injury. Current opinion in critical care. 2004;10(2):101-4. 7. Hutchinson P, Corteen E, Czosnyka M, Mendelow A, Menon D, Mitchell P, et al. Decompressive craniectomy in traumatic brain injury: the randomized multicenter RESCUEicp study (www. RESCUEicp. com). Brain edema XIII: Springer; 2006. p. 17-20. 8. Cushing H. The establishment of cerebral hernia as a decompressive measure for inaccessible brain tumors: with the description of intermuscular methods of making the bone defect in temporal and occipital regions. Surg Gynecol Obstet. 1905;1:297-314. 9. Gower DJ, Lee SK, McWhorter JM. Role of subtemporal decompression in severe closed head injury. Neurosurgery. 1988;23(4):417-22. 10. Clark K, Nash TM, Hutchison GC. The failure of circumferential craniotomy in acute traumatic cerebral swelling. Journal of neurosurgery. 1968;29(4):367-71. 11. Sahuquillo J. Decompressive craniectomy for the treatment of refractory high intracranial pressure in traumatic brain injury. Cochrane database of systematic reviews. 2006(1). 12. Butensky S, Rodgers S, Baron S, Schneider S, Mittler M. Comparison of surgical outcomes in patients with Chiari Type I malformation receiving posterior fossa decompression with and without duraplasty. Child's Nervous System. 2020;36(7):1399-405. 13. Tam SKP, Brodbelt A, Bolognese PA, Foroughi M. Posterior fossa decompression with duraplasty in Chiari malformation type 1: a systematic review and meta-analysis. Acta Neurochirurgica. 2021;163(1):229-38. 14. McAllister TW, Stein MB. Effects of psychological and biomechanical trauma on brain and behavior. Annals of the New York Academy of Sciences. 2010;1208(1):46-57. 15. Van Den Heuvel C, Thornton E, Vink R. Traumatic brain injury and Alzheimer's disease: a review. Progress in brain research. 2007;161:303-16. 16. Mayeux R, Ottman R, Maestre G, Ngai C, Tang M-X, Ginsberg H, et al. Synergistic effects of traumatic head injury and apolipoprotein-epsilon4 in patients with Alzheimer's disease. Neurology. 1995;45(3):555-7. 17. Levin HS, Shum D, Chan RC. Understanding traumatic brain injury: current research and future directions. 2014. 18. Galgano M, Toshkezi G, Qiu X, Russell T, Chin L, Zhao L-R. Traumatic brain injury: current treatment strategies and future endeavors. Cell transplantation. 2017;26(7):1118-30. 19. Smith M. Monitoring intracranial pressure in traumatic brain injury. Anesthesia & Analgesia. 2008;106(1):240-8. 20. Greenberg MS, Arredondo N. Handbook of neurosurgery: Thieme New York; 2001. 21. Mortazavi MM, Adeeb N, Griessenauer C, Sheikh H, Shahidi S, Tubbs R, et al. The ventricular system of the brain: a comprehensive review of its history, anatomy, histology, embryology, and surgical considerations. Child's Nervous System. 2014;30(1):19-35. 22. Woods SP, Kordovski VM, Tierney SM, Babicz MA. The neuropsychological aspects of performance-based Internet navigation skills: A brief review of an emerging literature. The Clinical Neuropsychologist. 2019;33(2):305-26. 23. Farrokh S, Cho S-M, Suarez JI. Fluids and hyperosmolar agents in neurocritical care: an update. Current opinion in critical care. 2019;25(2):105-9. 24. Snell DL, Martin R, Surgenor LJ, Siegert RJ, Hay-Smith EJC, Melzer TR, et al. Wrestling with uncertainty after mild traumatic brain injury: a mixed methods study. Disability and rehabilitation. 2020;42(14):1942-53. 25. Batty R, Francis A, Thomas N, Hopwood M, Ponsford J, Johnston L, et al. Executive dysfunction in psychosis following traumatic brain injury (PFTBI). Journal of clinical and experimental neuropsychology. 2015;37(9):917-30. 26. Miehl NJ. Shaken baby syndrome. Journal of forensic nursing. 2005;1(3):111-7. 27. Dang B, Chen W, He W, Chen G. Rehabilitation treatment and progress of traumatic brain injury dysfunction. Neural plasticity. 2017;2017. 28. Iftime-Nielsen SD, Christensen MS, Vingborg RJ, Sinkjær T, Roepstorff A, Grey MJ. Interaction of electrical stimulation and voluntary hand movement in SII and the cerebellum during simulated therapeutic functional electrical stimulation in healthy adults. Human Brain Mapping. 2012;33(1):40-9. 29. Makowski NS, Knutson JS, Chae J, Crago P, editors. Neuromuscular electrical stimulation to augment reach and hand opening after stroke. 2011 Annual International Conference of the IEEE Engineering in Medicine and Biology Society; 2011: IEEE. 30. Smith B, Sataloff RT. Choral pedagogy: Plural Publishing; 2013. 31. Moon JW, Hyun DK. Decompressive craniectomy in traumatic brain injury: a review article. Korean journal of neurotrauma. 2017;13(1):1. 32. Quinn T, Taylor J, Magarik J, Vought E, Kindy M, Ellegala D. Decompressive craniectomy. Acta Neurologica Scandinavica. 2011;123(4):239-44. 33. Aarabi B, Hesdorffer DC, Ahn ES, Aresco C, Scalea TM, Eisenberg HM. Outcome following decompressive craniectomy for malignant swelling due to severe head injury. Journal of neurosurgery. 2006;104(4):469-79. 34. Li X, von Holst H, Kleiven S. Decompressive craniectomy causes a significant strain increase in axonal fiber tracts. Journal of clinical neuroscience. 2013;20(4):509-13. 35. von Holst H, Li X, Kleiven S. Increased strain levels and water content in brain tissue after decompressive craniotomy. Acta neurochirurgica. 2012;154(9):1583-93. 36. Su T-M, Lan C-M, Lee T-H, Shih F-Y, Hsu S-W, Lu C-H. Posttraumatic cerebral infarction after decompressive craniectomy for traumatic brain injury: incidence, risk factors and outcome. Turk Neurosurg. 2017;23. 37. Kurland DB, Khaladj-Ghom A, Stokum JA, Carusillo B, Karimy JK, Gerzanich V, et al. Complications associated with decompressive craniectomy: a systematic review. Neurocritical care. 2015;23(2):292-304.