injury

Update: Spine injury

Spine injury

Controversies

At this moment there is persistent controversy within the spinal trauma community, which can be grouped under 6 headings:
First of all there is still no unanimity on the role and timing of medical and surgical interventions for patients with associated neurologic injury.
Type and timing of surgical intervention in multiply injured patients.
In some common injury types like odontoid fractures and thoracolumbar burst fracture, there is wide variation in practice between operative versus nonoperative management without clear reasons.
The role of different surgical approaches and techniques in certain injury types are not clarified yet.
Methods of nonoperative management and care of elderly patients with concurrent complex disorders are also areas where there is no consensus1).

Types

Spinal cord injury
Whiplash-associated disorders
Pediatric spine injury
Cervical spine injury
Thoracolumbar spine fracture
Sacral fracture
Osteoporotic vertebral fracture
Spinal gunshot wound
Penetrating neck trauma…

Traumatic spine injuries are often transferred to regional tertiary trauma centers from OSH and subsequently discharged from the trauma center’s emergency department (ED) suggesting secondary overtriage of such injuries.
A study to investigate interfacility transfers with spine injuries found high rate of secondary overtriage of neurologically intact patients with isolated spine injuries. Potential solutions include increasing spine coverage in community EDs, increasing direct communication between the OSH and spine specialist at the tertiary center, and utilization of teleradiology 2).

Complications

Hydrocephalus is a rare complication of traumatic spine injury. A literature review reflects the rare occurrence with cervical spine injury.
Dragojlovic et al present a case of traumatic injury to the lumbar spine from a gunshot wound, which caused communicating hydrocephalus. The patient sustained a gunshot wound to the lumbar spine and had an L4-5 laminectomy with exploration and removal of foreign bodies. At the time of surgery, the patient was found to have dense subarachnoid hemorrhage in the spinal column. He subsequently had intermittent headaches and altered mental status that resolved without intervention. The headaches worsened, so a computed tomography scan of the brain was obtained, which revealed hydrocephalus. A ventriculoperitoneal shunt was placed, and subsequent computed tomography scan of the brain showed reduced ventricle size. The patient returned to rehabilitation with complete resolution of hydrocephalus symptoms. Intrathecal hemorrhage with subsequent obstruction or decreased absorption of cerebrospinal fluid at the distal spinal cord was thought to lead to communicating hydrocephalus in this case of lumbar penetrating trauma. In patients with a history of hemorrhagic, traumatic spinal injury who subsequently experience headaches or altered mental status, hydrocephalus should be included in the differential diagnosis and adequately investigated 3).

Assessment

ATLS® algorithm and spine trauma assessment. In Step „A“ cervical spine (C-Spine) protection is indispensable. Every unconscious patient is stabilized by stiff-neck. Patients with signs of chest injury in step „B” and abdominal injury in step „C“, especially retroperitoneal are highly suspicious for thoracic (T-) and/or (L-) lumbar spine injury. Normal motor exam and reflexes do not rule out significant spine injury in the comatose patient. Abnormal neurologic exam is a sign for substantial spinal column injury including spinal cord injury (SCI). Log roll in step „E” is important to assess the dorsum of the cervical to the sacral spine and to look out for any signs of bruising, open wounds, tender points and to palpate the paravertebral tissue and posterior processus in search for distraction injury. Spine precautions should only be discontinued when patients gain back consciousness and are alert to communicate sufficiently on spinal discomfort or neurologic sensations before the spine is cleared 4).
Data on all patients with traumatic spine injuries admitted to the Alfred Hospital, Melbourne between May 1, 2009, and January 1, 2011, were collected:
There were 965 patients with traumatic spine injuries with 2,333 spine trauma levels. The general cohort showed a trimodal age distribution, male-to-female ratio of 2:2, motor vehicle accidents as the primary spine trauma mechanism, 47.7% patients with severe polytrauma as graded using the Injury Severity Score (ISS), 17.3% with traumatic brain injury (TBI), the majority of patients with one spine injury level, 7% neurological deficit rate, 12.8% spine trauma operative rate, and 5.2% mortality rate. Variables with statistical significance trending toward mortality were the elderly, motor vehicle occupants, severe ISS, TBI, C1-2 dissociations, and American Spinal Injury Association (ASIA) A, B, and C neurological grades. Variables with statistical significance trending toward the elderly were females; low falls; one spine injury level; type 2 odontoid fractures; subaxial cervical spine distraction injuries; ASIA A, B, and C neurological grades; and patients without neurological deficits. Of the general cohort, 50.3% of spine trauma survivors were discharged home, and 48.1% were discharged to rehabilitation facilities. This study provides baseline spine trauma epidemiological data. The trimodal age distribution of patients with traumatic spine injuries calls for further studies and intervention targeted toward the 46- to 55-year age group as this group represents the main providers of financial and social security. The study’s unique feature of delineating variables with statistical significance trending toward both mortality and the elderly also provides useful data to guide future research studies, benchmarking, public health policy, and efficient resource allocation for the management of spine trauma 5).

Outcome

There is no universally accepted outcome instrument available that is specifically designed or validated for spinal trauma patients, contributing to controversies related to the optimal treatment and evaluation of many types of spinal injuries. Therefore, the AOSpine Knowledge Forum Trauma aims to develop such an instrument using the International Classification of Functioning Disability and Health (ICF) as its basis.
Experts from the 5 AOSpine International world regions were asked to give their opinion on the relevance of a compilation of 143 ICF categories for spinal trauma patients on a 3-point scale: “not relevant,” “probably relevant,” or “definitely relevant.” The responses were analyzed using frequency analysis. Possible differences in responses between the 5 world regions were analyzed with the Fisher exact test and descriptive statistics.
Of the 895 invited AOSpine International members, 150 (16.8%) participated in this study. A total of 13 (9.1%) ICF categories were identified as definitely relevant by more than 80% of the participants. Most of these categories were related to the ICF component “activities and participation” (n = 8), followed by “body functions” (n = 4), and “body structures” (n = 1). Only some minor regional differences were observed in the pattern of answers.
More than 80% of an international group of health care professionals experienced in the clinical care of adult spinal trauma patients indicated 13 of 143 ICF categories as definitely relevant to measure outcomes after spinal trauma. This study creates an evidence base to define a core set of ICF categories for outcome measurement in adult spinal trauma patients 6).
Early independent risk factors predictive of suboptimal physical health status identified in a level 1 trauma center in polytrauma patients with spine injuries were tachycardia, hyperglycemia, multiple chronic medical comorbidities, and thoracic spine injuries. Early spine trauma risk factors were shown not to predict suboptimal mental health status outcomes 7).

References

1)

Oner C, Rajasekaran S, Chapman JR, Fehlings MG, Vaccaro AR, Schroeder GD, Sadiqi S, Harrop J. Spine Trauma-What Are the Current Controversies? J Orthop Trauma. 2017 Sep;31 Suppl 4:S1-S6. doi: 10.1097/BOT.0000000000000950. PubMed PMID: 28816869.
2)

Bible JE, Kadakia RJ, Kay HF, Zhang CE, Casimir GE, Devin CJ. How often are interfacility transfers of spine injury patients truly necessary? Spine J. 2014 Apr 14. pii: S1529-9430(14)00379-9. doi: 10.1016/j.spinee.2014.01.065. [Epub ahead of print] PubMed PMID: 24743061.
3)

Dragojlovic N, Stampas A, Kitagawa RS, Schmitt KM, Donovan W. Communicating Hydrocephalus Due to Traumatic Lumbar Spine Injury: Case Report and Literature Review. Am J Phys Med Rehabil. 2016 Jun 17. [Epub ahead of print] PubMed PMID: 27323322.
4)

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2660300/figure/F1/
5)

Tee JW, Chan CH, Fitzgerald MC, Liew SM, Rosenfeld JV. Epidemiological trends of spine trauma: an Australian level 1 trauma centre study. Global Spine J. 2013 Jun;3(2):75-84. doi: 10.1055/s-0033-1337124. Epub 2013 Mar 19. PubMed PMID: 24436855; PubMed Central PMCID: PMC3854579.
6)

Oner FC, Sadiqi S, Lehr AM, Aarabi B, Dunn RN, Dvorak MF, Fehlings MG, Kandziora F, Post MW, Rajasekaran S, Vialle L, Vaccaro AR. Toward Developing a Specific Outcome Instrument for Spine Trauma: An Empirical Cross-sectional Multicenter ICF-Based Study by AOSpine Knowledge Forum Trauma. Spine (Phila Pa 1976). 2015 Sep 1;40(17):1371-1379. PubMed PMID: 26323025.
7)

Tee JW, Chan CH, Gruen RL, Fitzgerald MC, Liew SM, Cameron PA, Rosenfeld JV.Early predictors of health-related quality of life outcomes in polytrauma patients with spine injuries: a level 1 trauma center study. Global Spine J. 2014 Feb;4(1):21-32. doi: 10.1055/s-0033-1358617. Epub 2013 Nov 6. PubMed PMID: 24494178.

Update: Spinal cord injury treatment

Spinal cord injury treatment

Substantial heterogeneity in the patient population, their presentation and underlying pathophysiology has sparked debates along the care spectrum from initial assessment to definitive treatment.
In seeking a cure, these patients often undergo treatments that lack scientific and methodological rigor.
Ahuja et al. reviews spinal cord injury (SCI) management followed by a discussion of the salient controversies in the field. Current care practices modeled on the American Association of Neurological Surgeons/Congress of Neurological Surgeons joint section guidelines are highlighted including key recommendations regarding immobilization, avoidance of hypotension, early International Standards for Neurological Classification of SCI examination and intensive care unit treatment. From a diagnostic perspective, the evolving roles of CT, MRI, and leading-edge microstructural MRI techniques are discussed with descriptions of the relevant clinical literature for each. Controversies in management relevant to clinicians including the timing of surgical decompression, methylprednisolone administration, blood pressure augmentation, intraoperative electrophysiological monitoring, and the role of surgery in central cord syndrome and pediatric SCI are also covered in detail. Finally, the article concludes with a reflection on clinical trial design tailored to the heterogeneous population of individuals with SCI 1).

Cell therapy

see Spinal cord injury stem cell therapy.

Perfusion

Increased spinal cord perfusion and blood pressure goals have been recommended for spinal cord injury (SCI).
Treatment consists of restoration of CSF flow, typically via arachnoidolysis and syrinx decompression Research into treatments for spinal cord injuries includes controlled hypothermia and stem cells, though many treatments have not been studied thoroughly and very little new research has been implemented in standard care.
Treatment of spinal cord injuries starts with restraining the spine and controlling inflammation to prevent further damage. The actual treatment can vary widely depending on the location and extent of the injury.
Acute spinal cord injury (SCI) is commonly treated by elevating the mean arterial pressure (MAP). Other potential interventions include cerebrospinal fluid drainage (CSFD).
Both MAP elevation alone and CSFD alone led to only short-term improvement of SCBF. The combination of MAP elevation and CSFD significantly and sustainably improved SCBF and spinal cord perfusion pressure. Although laser Doppler flowmetry can provide flow measurements to a tissue depth of only 1.5 mm, these results may represent pattern of blood flow changes in the entire spinal cord after injury 2).
Lumbar cerebrospinal fluid drainage after spinal cord injury, as used in the pig study by Martirosyan et al would reduce intrathecal pressure at the injury site only if the spinal cord is not compressed against the surrounding dura. Unfortunately, in most patients with severe spinal cord injury, the spinal cord is compressed against the surrounding dura; therefore, drainage of cerebrospinal fluid from the lumbar region will not reduce intrathecal pressure at the injury site 3).
Unfortunately, no data correlate the severity of spinal cord injury, the degree of spinal cord swelling, and persistent CSF flow across an injured segment in the human spinal cord. The physiological observations in animals and humans alike indicate that CSF drainage and induced hypertension warrant further investigation as a potential treatment for acute spinal cord injury 4).

Rehabilitation

In many cases, spinal cord injuries require substantial physical therapy and rehabilitation, especially if the patient’s injury interferes with activities of daily life.

Pharmacological Therapy

Despite a degree of theoretical progress, there is a lack of effective drugs that are able to improve the motor function of patients following spinal cord injury (SCI) 5) 6) 7) 8).
see Methylprednisolone for Spinal cord injury.
Dexamethasone acetate (DA) produces neuroprotective effects by inhibiting lipid peroxidation and inflammation by reducing cytokine release and expression. However, its clinical application is limited by its hydrophobicity, low biocompatibility and numerous side effects when using large dosage. Therefore, improving DA’s water solubility, biocompatibility and reducing its side effects are important goals that will improve its clinical utility. The objective of this study is to use a biodegradable polymer as the delivery vehicle for DA to achieve the synergism between inhibiting lipid peroxidation and inflammation effects of the hydrophobic-loaded drugs and the amphipathic delivery vehicle. Wang et al., successfully prepared DA-loaded polymeric micelles (DA/MPEG-PCL micelles) with monodispersed and approximately 25 nm in diameter, and released DA over an extended period in vitro. Additionally, in the hemisection spinal cord injury (SCI) model, DA micelles were more effective in promoting hindlimb functional recover, reducing glial scar and cyst formation in injured site, decreasing neuron lose and promoting axon regeneration. Therefore, data suggest that DA/MPEG-PCL micelles have the potential to be applied clinically in SCI therapy 9).

Surgery

After traumatic spinal cord injury (TSCI), laminectomy does not improve intraspinal pressure (ISP), spinal cord perfusion pressure (SCPP) or the vascular pressure reactivity index (sPRx) at the injury site sufficiently because of dural compression.
21 patients with acute, severe TSCI had realignment of the fracture and surgical fixation; 11 had laminectomy (laminectomy group) and 10 had laminectomy and duroplasty (laminectomy + duroplasty group). Primary outcomes were MRI evidence of spinal cord decompression (increase in intradural space, cerebrospinal fluid around the injured cord) and spinal cord physiology (ISP, SCPP, sPRx). The laminectomy and laminectomy + duroplasty groups were well matched. Compared with the laminectomy group, the laminectomy + duroplasty group had greater increase in intradural space at the injury site and more effective decompression of the injured cord. In the laminectomy + duroplasty group, ISP was lower, SCPP higher and sPRx lower, i.e. improved vascular pressure reactivity, compared with the laminectomy group. Duroplasty caused cerebrospinal fluid leak that settled with lumbar drain in one patient and pseudomeningocele that resolved in five patients. We conclude that, after TSCI, laminectomy + duroplasty improves spinal cord radiological and physiological parameters more effectively than laminectomy 10).

References

1)

Ahuja CS, Schroeder GD, Vaccaro AR, Fehlings MG. Spinal Cord Injury-What Are the Controversies? J Orthop Trauma. 2017 Sep;31 Suppl 4:S7-S13. doi: 10.1097/BOT.0000000000000943. PubMed PMID: 28816870.
2)

Martirosyan NL, Kalani MY, Bichard WD, Baaj AA, Gonzalez LF, Preul MC, Theodore N. Cerebrospinal fluid drainage and induced hypertension improve spinal cord perfusion after acute spinal cord injury in pigs. Neurosurgery. 2015 Apr;76(4):461-9. doi: 10.1227/NEU.0000000000000638. PubMed PMID: 25621979.
3)

Papadopoulos MC. Letter: Intrathecal Pressure After Spinal Cord Injury. Neurosurgery. 2015 Sep;77(3):E500. doi: 10.1227/NEU.0000000000000862. PubMed PMID: 26110999.
4)

Martirosyan NL, Kalani MY, Theodore N. In Reply: Intrathecal Pressure After Spinal Cord Injury. Neurosurgery. 2015 Sep;77(3):E500-1. doi: 10.1227/NEU.0000000000000857. PubMed PMID: 26111000.
5)

Hu R, Zhou J, Luo C, et al. Glial scar and neuroregeneration: Histological, functional, and magnetic resonance imaging analysis in chronic spinal cord injury. J Neurosurg Spine. 2010;13:169–180. doi: 10.3171/2010.3.SPINE09190.
6)

Macias CA, Rosengart MR, Puyana JC, et al. The effects of trauma center care, admission volume, and surgical volume on paralysis after traumatic spinal cord injury. Ann Surg. 2009;249:10–17. doi: 10.1097/SLA.0b013e31818a1505.
7)

Samantaray S, Sribnick EA, Das A, et al. Neuroprotective efficacy of estrogen in experimental spinal cord injury in rats. Ann NY Acad Sci. 2010;1199:90–94. doi: 10.1111/j.1749-6632.2009.05357.x.
8)

Fu ES, Tummala RP. Neuroprotection in brain and spinal cord trauma. Curr Opin Anaesthesiol. 2005;18:181–187. doi: 10.1097/01.aco.0000162838.56344.88.
9)

Wang Y, Wu M, Gu L, Li X, He J, Zhou L, Tong A, Shi J, Zhu H, Xu J, Guo G. Effective improvement of the neuroprotective activity after spinal cord injury by synergistic effect of glucocorticoid with biodegradable amphipathic nanomicelles. Drug Deliv. 2017 Nov;24(1):391-401. doi: 10.1080/10717544.2016.1256003. PubMed PMID: 28165815.
10)

Phang I, Werndle MC, Saadoun S, Varsos GV, Czosnyka M, Zoumprouli A, Papadopoulos MC. Expansion Duroplasty Improves Intraspinal Pressure, Spinal Cord Perfusion Pressure and Vascular Pressure Reactivity Index in Patients with Traumatic Spinal Cord Injury. J Neurotrauma. 2015 Feb 23. [Epub ahead of print] PubMed PMID: 25705999.

Update: AOSpine subaxial cervical spine injury classification system

AOSpine subaxial cervical spine injury classification system

See: aospine_subaxial_cervical_spine_injury_classification_system.pdf

This project describes a morphology-based subaxial cervical spine injury classification system. Using the same approach as the AOSpine Thoracolumbar Classification System, the goal was to develop a comprehensive yet simple classification system with high intra- and interobserver reliability to be used for clinical and research purposes.
A subaxial cervical spine injury classification system was developed using a consensus process among clinical experts. All investigators were required to successfully grade 10 cases to demonstrate comprehension of the system before grading 30 additional cases on two occasions, 1 month apart. Kappa coefficients (κ) were calculated for intraobserver and interobserver reliability.
The classification system is based on three injury morphology types similar to the TL system: compression injuries (A), tension band injuries (B), and translational injuries (C), with additional descriptions for facet injuries, as well as patient-specific modifiers and neurologic status. Intraobserver and interobserver reliability was substantial for all injury subtypes (κ = 0.75 and 0.64, respectively).
The AOSpine subaxial cervical spine injury classification system demonstrated substantial reliability in this initial assessment, and could be a valuable tool for communication, patient care and for research purposes 1).

The AOSpine subaxial cervical spine injury classification system (using the four main injury types or at the sub-types level) allows a significantly better agreement than the Allen and Ferguson classification of subaxial cervical spine injury. The A&F scheme does not allow reliable communication between medical professionals 2).

see also Subaxial Injury Classification (SLIC).

Case series

2017

Aarabi et al. analyzed the relevant clinical, imaging, management, and American Spinal Injury Association (ASIA) impairment scale (AIS) grade conversion of 92 AIS grades A-C patients with cervical spine injury. We correlated morphology class with age, injury severity score (ISS), follow-up ASIA motor score (AMS), intramedullary lesion length (IMLL), and AIS grade conversion at 6 months after injury.
The mean age of patients was 39.3 years, 83 were men, and 69 were injured during an automobile accident or after a fall. The AOSpine class was A4 in 8, B2 in 5, B2A4 in 16, B3 in 19, and C in 44 patients. The mean ISS was 29.7 and AMS was 17.1. AIS grade was A in 48, B in 25, and C in 19 patients. Mean IMLL on postoperative magnetic resonance imaging was 72 mm: A4 = 68.1; B2A4 = 86.5; B2 = 59.3; B3 = 46.8; and C = 79.9. At a mean follow-up of 6 months, the mean AMS was 39.6. Compared to patients with class B3 injuries, those with class C injuries were significantly younger (P < 0.0001), had longer IMLL (P < 0.002), and were less likely to have AIS grade conversion to a better grade (P < 0.02).
The AOSpine subaxial cervical spine injury classification system successfully predicted injury severity (longer IMLL) and chances of neurologic recovery (AIS grade conversion) across different class subtypes 3).

2016

Silva et al., evaluated the new classification
Patients with subaxial cervical spine trauma (SCST) treated at the authors’ institution according to the Subaxial Cervical Spine Injury Classification system were included. Five different blinded researchers classified patients’ injuries according to the new AOSpine system using CT imaging at 2 different times (4-week interval between each assessment). Reliability was assessed using the kappa index (κ), while validity was inferred by comparing the classification obtained with the treatment performed.
Fifty-one patients were included: 31 underwent surgical treatment, and 20 were managed nonsurgically. Intraobserver agreement for subgroups ranged from 0.61 to 0.93, and interobserver agreement was 0.51 (first assessment) and 0.6 (second assessment). Intraobserver agreement for groups ranged from 0.66 to 0.95, and interobserver agreement was 0.52 (first assessment) and 0.63 (second assessment). The kappa index in all evaluations was 0.67 for Type A, 0.08 for Type B, and 0.68 for Type C injuries, and for the facet modifier it was 0.33 (F1), 0.4 (F2), 0.56 (F3), and 0.75 (F4). Complete agreement for all components was attained in 25 cases (49%) (19 Type A and 6 Type C), and for subgroups it was attained in 22 cases (43.1%) (16 Type A0 and 6 Type C). Type A0 injuries were treated conservatively or surgically according to their neurological status and ligamentous status. Type C injuries were treated surgically in almost all cases, except one.
While the general reliability of the newer AOSpine system for SCST was acceptable for group classification, significant limitations were identified for subgroups. Type B injuries were rarely diagnosed, and only mild (Type A0) and extreme severe (Type C) injuries had a high rate of interobserver agreement. Facet modifiers and intermediate injury patterns require better descriptions to improve their low agreement in cases of SCST 4).

References

1)

Vaccaro AR, Koerner JD, Radcliff KE, Oner FC, Reinhold M, Schnake KJ, Kandziora F, Fehlings MG, Dvorak MF, Aarabi B, Rajasekaran S, Schroeder GD, Kepler CK, Vialle LR. AOSpine subaxial cervical spine injury classification system. Eur Spine J. 2016 Jul;25(7):2173-84. doi: 10.1007/s00586-015-3831-3. Epub 2015 Feb 26. PubMed PMID: 25716661.
2)

Urrutia J, Zamora T, Campos M, Yurac R, Palma J, Mobarec S, Prada C. A comparative agreement evaluation of two subaxial cervical spine injury classification systems: the AOSpine and the Allen and Ferguson schemes. Eur Spine J. 2016 Jul;25(7):2185-92. doi: 10.1007/s00586-016-4498-0. Epub 2016 Mar 5. PubMed PMID: 26945747.
3)

Aarabi B, Oner C, Vaccaro AR, Schroeder GD, Akhtar-Danesh N. Application of AOSpine Subaxial Cervical Spine Injury Classification in Simple and Complex Cases. J Orthop Trauma. 2017 Sep;31 Suppl 4:S24-S32. doi: 10.1097/BOT.0000000000000944. PubMed PMID: 28816872.
4)

Silva OT, Sabba MF, Lira HI, Ghizoni E, Tedeschi H, Patel AA, Joaquim AF. Evaluation of the reliability and validity of the newer AOSpine subaxial cervical injury classification (C-3 to C-7). J Neurosurg Spine. 2016 Sep;25(3):303-8. doi: 10.3171/2016.2.SPINE151039. Epub 2016 Apr 22. PubMed PMID: 27104288.

A Different Perspective After Brain Injury: A Tilted Point of View (After Brain Injury: Survivor Stories)

A Different Perspective After Brain Injury: A Tilted Point of View (After Brain Injury: Survivor Stories)
By Christopher Yeoh

A Different Perspective After Brain Injury: A Tilted Point of View (After Brain Injury: Survivor Stories)

List Price: $170.00
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Whilst preparing for his travel adventures into a world he had yet to explore, Christopher Yeoh was involved in a road traffic accident and experienced something few others would be “privileged” to witness. Eight days in a coma, more than a year in and out of hospital and a gradual re-introduction to the world of work.
A Different Perspective After Brain Injury: A Tilted Point of View is written entirely by the survivor, providing an unusually introspective and critical personal account of life following a serious blow to the head. It charts the initial insult, early rehabilitation, development of understanding, the return of emotion, moments of triumph and regression into depression, the exercise of reframing how a brain injury is perceived and a return to work. It also describes the mental adjustments of awareness and acceptance alongside the physical recovery process.
Readily accessible to the general public, this book will also be of particular interest to professionals involved in the care of people who have had significant brain injuries, brain injury survivors, their families and friends and also those who fund and organise health and social care. This unique author account will provide a degree of understanding of what living with a hidden disability is really like.

Product Details

  • Published on: 2017-06-20
  • Original language: English
  • Binding: Hardcover
  • 154 pages

Editorial Reviews

Review
‘This very engaging book, written by a high functioning survivor of a traumatic brain injury, gives an introspective and critical account of what it actually feels like to suffer a brain injury and ‘come through the other side’. Christopher Yeoh integrates his phenomenological experience of brain injury with science, literature, autobiography, and philosophy, resulting in an extremely readable account of his experience. It provides a real ‘insider’s view’ of brain injury not possible to capture in a purely academic textbook. For this reason, the book will be of huge importance not only to the individuals and their families affected by brain injury, but also the clinicians involved in their care and rehabilitation.’ Rudi Coetzer, Consultant Neuropsychologist, North Wales Brain Injury Service, Betsi Cadwaladr UHB NHS Wales and Senior Lecturer in Clinical Neuropsychology, School of Psychology, Bangor University.
‘Christopher’s poignant narrative of his recovery and rehabilitation shows how personal characteristics and social resources interact to overcome the serious aftermath of severe traumatic brain injury. This is a balanced and insightful account of loss, challenge and triumph. He writes with humility and humour, whilst never masking the devastation the injury caused for him and his loved ones. Many inspiring books are written by survivors; A Different Perspective After Brain Injury will strike a chord with people grappling with changes to self in the context of ANY major life change. This is also an invaluable resource for clinicians, researchers and educators who seek a deeper understanding of the experience of brain injury.’ – Professor Tamara Ownsworth, School of Applied Psychology, Griffith University, Australia
About the Author
Christopher Yeoh is a holder of an LLB and LLM from the London School of Economics. He continues to practice securities law as a solicitor of England and Wales at a major global law firm.
After his adventure he now runs a multi award winning food and travel blog at quieteating.com and is a featured photographer in the Telegraph and Sunday Times newspapers. His photos have also been featured in brochures by the luxury travel company, Audley Travel.
As an action man he was previously an avid triathlete and a national award winning karateka. Now he prefers a slower pace of life by writing and irritating people with his camera.
Life after brain injury is not something less but just something different.

Book: Traumatic Brain Injury Rehabilitation, An Issue of Physical Medicine and Rehabilitation Clinics of North America, 1e (The Clinics: Orthopedics)

Traumatic Brain Injury Rehabilitation, An Issue of Physical Medicine and Rehabilitation Clinics of North America, 1e (The Clinics: Orthopedics)
By Blessen C Eapen MD, David X. Cifu MD

Traumatic Brain Injury Rehabilitation, An Issue of Physical Medicine and Rehabilitation Clinics of North America, 1e (The Clinics: Orthopedics)

List Price:$98.99
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This issue will focus on traumatic brain injury and will include articles on the following: Pathophysiology of TBI; Acute Management of Moderate-Severe TBI; Disorder of Consciousness; Rehabilitation of Moderate-Severe TBI; Acute Diagnosis and Management of Concussion; Rehabilitation of Persistent Symptoms after Concussion Chronic Traumatic Encephalopathy; Unique Aspect of TBI in the Military and Veteran; and many more!

Product Details

  • Published on: 2017-05-31
  • Original language: English
  • Dimensions: 8.27″ h x .87″ w x 5.91″ l,
  • Binding: Hardcover

Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition

see Severe traumatic brain injury guidelines.

The scope and purpose of the Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. is 2-fold: to synthesize the available evidence and to translate it into recommendations. This document provides recommendations only when there is evidence to support them. As such, they do not constitute a complete protocol for clinical use.
The intention is that these recommendations be used by others to develop treatment protocols, which necessarily need to incorporate consensus and clinical judgment in areas where current evidence is lacking or insufficient.
Carney et al. think it is important to have evidence-based recommendations to clarify what aspects of practice currently can and cannot be supported by evidence, to encourage use of evidence-based treatments that exist, and to encourage creativity in treatment and research in areas where evidence does not exist. The communities of neurosurgery and neurointensive care have been early pioneers and supporters of evidence based medicine and plan to continue in this endeavor. The complete guideline document, which summarizes and evaluates the literature for each topic, and supplemental appendices (A-I) are available online at https://www.braintrauma.org/coma/guidelines 1).
4th edition
Free article of Neurosurgery
1) Carney N, Totten AM, OʼReilly C, Ullman JS, Hawryluk GW, Bell MJ, Bratton SL, Chesnut R, Harris OA, Kissoon N, Rubiano AM, Shutter L, Tasker RC, Vavilala MS, Wilberger J, Wright DW, Ghajar J. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery. 2016 Sep 20. [Epub ahead of print] PubMed PMID: 27654000.

Update: Spinal cord injury stem cell therapy

At present, Spinal cord injury stem cell therapy is a therapeutic promise in this field of research 1) 2) 3) 4) 5) 6) 7) 8) 9) but still subject to many uncertainties, with significant confusion due to the disparity of protocols, selection of subjects, cell type, dose and routes of administration used. In experimental studies, it is noteworthy that the functional recovery of paraplegic animals after mesenchymal stem cell (MSC) transplantation starts before tissue regeneration occurs to allow the passage of ascending and descending axons. Therefore, it is obvious that after MSC transplantation into injured central nervous system (CNS) must exist various repair processes, including the release of neurotrophic factors by the transplanted stem cells, or the activation of endogenous processes, including the release of neurotrophic factors by the transplanted stem cells, or the activation of endogenous mechanisms of the spinal cord, able to partially restore neurological functions previously abolished 10) 11) 12) 13) 14)15) 16) 17) 18).

Unflammation and toxins released by damaged cells at the site of a spinal injury often cause further harm to surrounding cells. Researchers are developing treatments that reduce inflammation and soak up toxins and free radicals to minimise additional damage.
Spinal cord injuries often damage neurons and the supporting cells that wrap & insulate neurons. Damaging the supporting cells can cause otherwise functional neurons to die. Researchers are studying how stem cells might be used to replace neurons and their supporting cells to greatly improve a patient’s chances for recovering function.

As a potentially unlimited autologous cell source, patient induced pluripotent stem cells (iPSCs) provide great capability for tissue regeneration, particularly in spinal cord injury (SCI). However, despite significant progress made in translation of iPSC-derived neural stem cells to clinical settings, a few hurdles remain. Among them, non-invasive approach to obtain source cells in a timely manner, safer integration-free delivery of reprogramming factors, and purification of NSCs before transplantation are top priorities to overcome.
Liu et al., developed a safe and cost-effective pipeline to generate clinically relevant NSCs. They first isolated cells from patients’ urine and reprogrammed them into iPSCs by non-integrating Sendai virus vectors, and carried out experiments on neural differentiation. NSCs were purified by A2B5, an antibody specifically recognizing a glycoganglioside on the cell surface of neural lineage cells, via fluorescence activated cell sorting. Upon further in vitro induction, NSCs were able to give rise to neurons, oligodendrocytes and astrocytes. To test the functionality of the A2B5+ NSCs, they grafted them into the contused mouse thoracic spinal cord. Eight weeks after transplantation, the grafted cells survived, integrated into the injured spinal cord, and differentiated into neurons and glia.
The specific focus on cell source, reprogramming, differentiation and purification method purposely addresses timing and safety issues of transplantation to SCI models. It is Liu et al., belief that this work takes one step closer on using human iPSC derivatives to SCI clinical settings 19).

1) Syková E, Homola A, Mazanec R, Lachmann H, Konrádová SL, Kobylka P, et al. Autologous bone marrow transplantation in patients with subacute and chronic spinal cord injury. Cell Transplant 2006;15:675–87.
2) Yoon SH, Shim YS, Park YH, Chung JK, Nam JH, Kim MO, et al. Complete spinal cord injury treatment using autologous bone marrow cell transplantation and bone marrow stimulation with granulocyte macrophage-colony stimulating factor: phase I/II clinical trial. Stem Cells 2007;25:2066–73.
3) Deda H, Inci MC, Kürekçi AE, Kayihan K, Ozgün E, Ustünsoy GE, et al. Treatment of chronic spinal cord injured patients with autologous bone marrow-derived hematopoietic stem cell transplantation: 1-year follow-up. Cytotherapy 2008;10:565–74.
4) Saito F, Nakatani T, Iwase M, Maeda Y, Hirakawa A, Murao Y, et al. Spinal cord injury treatment with intrathecal autologous bone marrow stromal cell transplantation: the first clinical trial case report. J Trauma 2008;64:53–9.
5) Pal R, Venkataramana NK, Bansai A, Balaraju S, Jan M, Chandra R, et al. Ex vivo-expanded autologous bone marrowderived mesenchymal stromal cells in human spinal cord injury/paraplegia: a pilot clinical study. Cytotherapy 2009;11:897–911.
6) Park JH, Kim DY, Sung I, Choi GH, Jeon MH, Kim KK, et al. Long-term results of spinal cord injury therapy using mesenchymal stem cells derived from bone marrow in humans. Neurosurgery 2012;70:1238–47.
7) Saito F, Nakatani T, Iwase M, Maeda Y, Murao Y, Suzuki Y, et al. Administration of cultured autologous bone marrow stromal cells into cerebrospinal fluid in spinal injury patients: a pilot study. Restor Neurol Neurosci 2012;30:127–36.
8) Jiang PC, Xiong WP, Wang G, Ma C, Yao WQ, Kendell SF, et al. A clinical trial report of autologous bone marrow-derived mesenchymal stem cell transplantation in patients with spinal cord injury. Exp Ther Med 2013;6:140–6.
9) Mendonça MVP, Larocca TF, Souza BS, de Freitas Souza BS, Villarreal CF, Silva LF, et al. Safety and neurological assessments after autologous transplantation of bone marrow mesenchymal stem cells in subjects with chronic spinal cord injury. Stem Cell Res Ther 2014;5:126
10) Zurita M, Vaquero J. Functional recovery in chronic paraplegia after bone marrow stromal cells transplantation. Neuroreport 2004;15:1105–8.
11) Zurita M, Vaquero J. Bone marrow stromal cells can achieve cure of chronic paraplegic rats: functional and morphological outcome one year after transplantation. Neurosci Lett 2006;402:51–6.
12) Vaquero J, Zurita M, Oya S, Santos M. Cell therapy using bone marrow stromal cells in chronic paraplegic rats: systemic or local administration? Neurosci Lett 2006;398:129–34.
13) Zurita M, Vaquero J, Bonilla C, Santos M, De Haro J, Oya S, et al. Functional recovery of chronic paraplegic pigs after autologous transplantation of bone marrow stromal cells. Transplantation 2008;86:845–53.
14) Vaquero J, Zurita M. Bone marrow stromal cells for spinal cord repair: a challenge for contemporary neurobiology. Histol Histopathol 2009;24:107–16.
15) Bonilla C, Zurita M, Otero L, Aguayo C, Vaquero J. Delayed intralesional transplantation of bone marrow stromal cells increases endogenous neurogenesis and promotes functional improvement after severe traumatic brain injury. Brain Inj 2009;23:760–9.
16) Vaquero J, Zurita M. Functional recovery after severe CNS trauma: current perspectives for cell therapy with bone marrow stromal cells. Prog Neurobiol 2011;93:341–9.
17) Otero L, Zurita M, Bonilla C, Aguayo C, Vela A, Rico MA, et al. Late transplantation of allogeneic bone marrow stromal cells improves neurological deficits subsequent to intracerebral hemorrhage. Cytotherapy 2011;13:562–71.
18) Otero L, Zurita M, Bonilla C, Aguayo C, Rico MA, Rodriguez A, et al. Allogeneic bone marrow stromal cell transplantation after cerebral hemorrhage achieves cell transdifferentiation and modulates endogenous neurogenesis. Cytotherapy 2012;14: 34–44.
19) Liu Y, Zheng Y, Li S, Xue H, Schmitt K, Hergenroeder GW, Wu J, Zhang Y, Kim DH, Cao Q. Human neural progenitors derived from integration-free iPSCs for SCI therapy. Stem Cell Res. 2017 Jan 5;19:55-64. doi: 10.1016/j.scr.2017.01.004. [Epub ahead of print] PubMed PMID: 28073086.

Progesterone for acute traumatic brain injury

Progesterone is a naturally produced hormone that has well-defined pharmacokinetics, is widely available, inexpensive, and has steroidal, neuroactive and neurosteroidal actions in the central nervous system. It is, therefore, a potential candidate for treating traumatic brain injury (TBI] patients. However, uncertainty exists regarding the efficacy of this treatment.

Systematic reviews

2016

Ma et al., updated the searches of the following databases: the Cochrane Injuries Group’s Specialised Register (30 September 2016), the Cochrane Central Register of Controlled Trials (CENTRAL; Issue 9, 2016), MEDLINE (Ovid; 1950 to 30 September 2016), Embase (Ovid; 1980 to 30 September 2016), Web of Science Core Collection: Conference Proceedings Citation Index-Science (CPCI-S; 1990 to 30 September 2016); and trials registries: Clinicaltrials.gov (30 September 2016) and the World Health Organization (WHO) International Clinical Trials Registry Platform (30 September 2016).
They included randomised controlled trials (RCTs) of progesterone versus no progesterone (or placebo) for the treatment of people with acute TBI.
Two review authors screened search results independently to identify potentially relevant studies for inclusion. Independently, two review authors selected trials that met the inclusion criteria from the results of the screened searches, with no disagreement.
They included five RCTs in the review, with a total of 2392 participants. We assessed one trial to be at low risk of bias; two at unclear risk of bias (in one multicentred trial the possibility of centre effects was unclear, whilst the other trial was stopped early), and two at high risk of bias, due to issues with blinding and selective reporting of outcome data.All included studies reported the effects of progesterone on mortality and disability. Low quality evidence revealed no evidence of a difference in overall mortality between the progesterone group and placebo group (RR 0.91, 95% CI 0.65 to 1.28, I² = 62%; 5 studies, 2392 participants, 2376 pooled for analysis). Using the GRADE criteria, we assessed the quality of the evidence as low, due to the substantial inconsistency across studies.There was also no evidence of a difference in disability (unfavourable outcomes as assessed by the Glasgow Outcome Score) between the progesterone group and placebo group (RR 0.98, 95% CI 0.89 to 1.06, I² = 37%; 4 studies; 2336 participants, 2260 pooled for analysis). We assessed the quality of this evidence to be moderate, due to inconsistency across studies.Data were not available for meta-analysis for the outcomes of mean intracranial pressure, blood pressure, body temperature or adverse events. However, data from three studies showed no difference in mean intracranial pressure between the groups. Data from another study showed no evidence of a difference in blood pressure or body temperature between the progesterone and placebo groups, although there was evidence that intravenous progesterone infusion increased the frequency of phlebitis (882 participants). There was no evidence of a difference in the rate of other adverse events between progesterone treatment and placebo in the other three studies that reported on adverse events.
This updated review did not find evidence that progesterone could reduce mortality or disability in patients with TBI. However, concerns regarding inconsistency (heterogeneity among participants and the intervention used) across included studies reduce our confidence in these results.There is no evidence from the available data that progesterone therapy results in more adverse events than placebo, aside from evidence from a single study of an increase in phlebitis (in the case of intravascular progesterone).There were not enough data on the effects of progesterone therapy for our other outcomes of interest (intracranial pressure, blood pressure, body temperature) for us to be able to draw firm conclusions.Future trials would benefit from a more precise classification of TBI and attempts to optimise progesterone dosage and scheduling 1).

2012

Ma et al., searched: the Cochrane Injuries Group’s Specialised Register (13 July 2012), Cochrane Central Register of Controlled Trials (CENTRAL) (Issue 7, 2012), MEDLINE (Ovid) (1950 to August week 1, 2012), EMBASE (Ovid) (1980 to week 32 2012), LILACS (12 August 2012), Zetoc (13 July 2012), Clinicaltrials.gov (12 August 2012), Controlled-trials.com (12 August 2012). SELECTION CRITERIA: We included published and unpublished randomised controlled trials (RCTs) of progesterone versus no progesterone (or placebo) for the treatment of people with acute TBI. DATA COLLECTION AND ANALYSIS: Two review authors independently screened search results to identify the full texts of potentially relevant studies for inclusion. From the results of the screened searches two review authors independently selected trials meeting the inclusion criteria, with no disagreement. MAIN RESULTS: Three studies were included with a total of 315 people. Two included studies were of high methodological quality, with low risk of bias in allocation concealment, blinding and incomplete outcome data. One study did not use blinding and had unclear risk of bias in allocation concealment and incomplete outcome data. All three studies reported the effects of progesterone on mortality. The pooled risk ratio (RR) for mortality at end of follow-up was 0.61, 95% confidence interval (CI) 0.40 to 0.93. Three studies measured disability and found the RR of death or severe disability in patients treated with progesterone to be 0.77, 95% CI 0.62 to 0.96. Data from two studies showed no difference in mean intracranial pressure or the rate of adverse and serious adverse events among people in either group. One study presented blood pressure and temperature data, and there were no differences between the people in the progesterone or control groups. There was no substantial evidence for the presence of heterogeneity.
Current clinical evidence from three small RCTs indicates progesterone may improve the neurologic outcome of patients suffering TBI. This evidence is still insufficient and further multicentre randomised controlled trials are required 2).

2011

Junpeng et al., searched: the Cochrane Injuries Group’s Specialised Register (to April 2010), Cochrane Central Register of Controlled Trials 2010, Issue 1 (The Cochrane Library), MEDLINE (Ovid) (1950 to April week 1 2010), EMBASE (Ovid) (1980 to week 14 2010), LILACS (to 17 April 2010 ), Zetoc (to 21 April 2010), Clinicaltrials.gov (17 April 2010 ), Controlled-trials.com (17 April 2010).
They included published and unpublished randomised controlled trials (RCTs) of progesterone versus no progesterone (or placebo) for the treatment of acute TBI.
Two authors independently screened search results to identify the full texts of potentially relevant studies for inclusion. From the results of the screened searches two authors independently selected trials meeting the inclusion criteria, with no disagreement.
Three studies were included with 315 patients. All three studies reported the effects of progesterone on mortality. The pooled relative risk (RR) for mortality at end of follow-up is 0.61, 95% confidence interval (CI) 0.40 to 0.93. Three studies measured disability and found the RR of death or severe disability in patients treated with progesterone was 0.77, 95% confidence interval (CI) 0.62 to 0.96. Two studies presented data on intracranial pressure and adverse events. One study presented blood pressure and temperature data. There was no substantial evidence for the presence of heterogeneity.
Current clinical evidence from three small RCTs indicates progesterone may improve the neurologic outcome of patients suffering TBI. This evidence is still insufficient and further multicentre randomised controlled trials are required 3).

Progesterone has been associated with robust positive effects in animal models of traumatic brain injury (TBI) and with clinical benefits in two phase 2 randomized controlled trials. Skolnick et al, investigated the efficacy and safety of progesterone in a large, prospective, phase 3 randomized controlled trial.
A multinational placebo controlled study, in which 1195 patients, 16 to 70 years of age, with severe traumatic brain injury TBI (Glasgow Coma Scale score, ≤8 (on a scale of 3 to 15, with lower scores indicating a reduced level of consciousness and at least one reactive pupil) were randomly assigned to receive progesterone or placebo. Dosing began within 8 hours after injury and continued for 120 hours. The primary efficacy end point was the Glasgow Outcome Scale score at 6 months after the injury.
Proportional-odds analysis with covariate adjustment showed no treatment effect of progesterone as compared with placebo (odds ratio, 0.96; confidence interval, 0.77 to 1.18). The proportion of patients with a favorable outcome on the Glasgow Outcome Scale (good recovery or moderate disability) was 50.4% with progesterone, as compared with 50.5% with placebo. Mortality was similar in the two groups. No relevant safety differences were noted between progesterone and placebo.
Primary and secondary efficacy analyses showed no clinical benefit of progesterone in patients with severe TBI. These data stand in contrast to the robust preclinical data and results of early single-center trials that provided the impetus to initiate phase 3 trials. (Funded by BHR Pharma; SYNAPSE ClinicalTrials.gov number, NCT01143064 .) 4).
There was no significant difference between the progesterone group and the placebo group in the proportion of patients with a favorable outcome (relative benefit of progesterone, 0.95; 95% confidence interval [CI], 0.85 to 1.06; P=0.35). Phlebitis or thrombophlebitis was more frequent in the progesterone group than in the placebo group (relative risk, 3.03; CI, 1.96 to 4.66). There were no significant differences in the other prespecified safety outcomes. Conclusions This clinical trial did not show a benefit of progesterone over placebo in the improvement of outcomes in patients with acute TBI. (Funded by the National Institute of Neurological Disorders and Stroke and others; PROTECT III ClinicalTrials.gov number, NCT00822900 .) 5).

There is significant theoretical evidence for the potential role of estrogen and progesterone use in altering the pathogenesis of SAH. Nevertheless, this has received mixed reviews in both case controlled studies and cohort analysis within the literature 6)

1) Ma J, Huang S, Qin S, You C, Zeng Y. Progesterone for acute traumatic brain injury. Cochrane Database Syst Rev. 2016 Dec 22;12:CD008409. doi: 10.1002/14651858.CD008409.pub4. [Epub ahead of print] Review. PubMed PMID: 28005271.
2) Ma J, Huang S, Qin S, You C. Progesterone for acute traumatic brain injury. Cochrane Database Syst Rev. 2012 Oct 17;10:CD008409. doi: 10.1002/14651858.CD008409.pub3. Review. PubMed PMID: 23076947.
3) Junpeng M, Huang S, Qin S. Progesterone for acute traumatic brain injury. Cochrane Database Syst Rev. 2011 Jan 19;(1):CD008409. doi: 10.1002/14651858.CD008409.pub2. Review. Update in: Cochrane Database Syst Rev. 2012;10:CD008409. PubMed PMID: 21249708.
4) Skolnick BE, Maas AI, Narayan RK, van der Hoop RG, MacAllister T, Ward JD, Nelson NR, Stocchetti N; the SYNAPSE Trial Investigators. A Clinical Trial of Progesterone for Severe Traumatic Brain Injury. N Engl J Med. 2014 Dec 10. [Epub ahead of print] PubMed PMID: 25493978.
5) Wright DW, Yeatts SD, Silbergleit R, Palesch YY, Hertzberg VS, Frankel M, Goldstein FC, Caveney AF, Howlett-Smith H, Bengelink EM, Manley GT, Merck LH, Janis LS, Barsan WG; the NETT Investigators. Very Early Administration of Progesterone for Acute Traumatic Brain Injury. N Engl J Med. 2014 Dec 10. [Epub ahead of print] PubMed PMID: 25493974.
6) Young AM, Karri SK, Ogilvy CS. Exploring the use of estrogen & progesterone replacement therapy in subarachnoid hemorrhage. Curr Drug Saf. 2012 Jul;7(3):202-6. Review. PubMed PMID: 22950381.

Book: New Therapeutics for Traumatic Brain Injury: Prevention of Secondary Brain Damage and Enhancement of Repair and Regeneration

New Therapeutics for Traumatic Brain Injury: Prevention of Secondary Brain Damage and Enhancement of Repair and Regeneration

New Therapeutics for Traumatic Brain Injury: Prevention of Secondary Brain Damage and Enhancement of Repair and Regeneration

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New Therapeutics for Traumatic Brain Injury: Prevention of Secondary Brain Damage and Enhancement of Repair and Regeneration explores traumatic brain injury (TBI), a major cause of death and disability throughout the world. The delayed nature of the secondary injury phase suggests that there is a therapeutic window for pharmacological interventions or other approaches to prevent progressive tissue damage and improve functional outcomes. It is now apparent that therapeutic interventions should entail both protective and repair/regeneration strategies depending on the phase of brain injury.
This book describes emerging experimental strategies for the treatment of TBI, including new anti-inflammatory or anti-apoptotic therapeutics that limit brain damage, and novel or repurposed drugs that enhance repair or regeneration of the brain after injury.

  • Comprehensive overview of basic approaches and translational development of new therapies for TBI
  • Edited by a prominent TBI researcher that includes contributions by leading global researchers in the field
  • Presents a great resource for researchers and practitioners to learn more about the many evolving preclinical studies and clinical trials currently underway, and the challenges of bringing translational studies in TBI to the clinic

Product Details

  • Published on: 2016-10-25
  • Original language: English
  • Dimensions: 9.00″ h x 6.00″ w x .75″ l,
  • Binding: Hardcover
  • 352 pages

Editorial Reviews

About the Author
Kim A. Heidenreich is Professor of Pharmacology and Neuroscience at the University of Colorado School of Medicine. She also serves on the Keystone Scientific Advisory Board and is Chief Scientific Advisor for the American Traumatic Brain Injury Association. Dr. Heidenreich has been conducting neuroscience research for over 30 years with continual funding in the area of neurotrophic factors, mechanisms of neuronal cell death, and recently, traumatic brain injury (TBI). Her laboratory has identified a number of protein kinase signaling pathways that trigger or prevent neuronal cell death in response to neuronal insults and neurotrophic factors, respectively. She has examined the ways in which key proapoptotic and antiapoptotic protein kinases regulate cytoplasmic, mitochondrial, and nuclear targets to control neuronal apoptosis and autophagy. Her recent studies have focused on preventing secondary brain damage after a TBI. She has recently discovered that leukotrienes, potent inflammatory lipid mediators normally absent in brain, are produced by a transcellular mechanism involving infiltrating neutrophils after TBI. Blockade of leukotriene production using 5-lipoxgenase (FLAP) inhibitors prevents edema, cell death, and cognitive deficits after TBI. These findings have important implications for treating human TBI and suggest that development of FLAP inhibitors for use in TBI is feasible for both intervention and prevention. Toward this goal, Dr. Heidenreich is currently developing FLAP inhibitors with improved CNS properties and novel delivery methods for these drugs in TBI.
As a strong advocate of Neuroscience research, Dr. Heidenreich has previously served as chair of the membership committee of the UC Denver Neuroscience Program and as President of the Rocky Mountain Neuroscience Research Group, a Colorado chapter of the Society of Neuroscience. She has mentored many pre- and post-doctoral scientists, as well as junior physician scientists, in her laboratory. She also has served as mentor for the NIH Building Research Achievement in Neuroscience (BRAiN) Training Program and was the recipient of the 2006 Dean’s Mentoring Award at her institution. Dr. Heidenreich has served on numerous study sections reviewing grants for the NIH, DOD, VA and small research granting agencies. Recently, she has been invited to speak at numerous national and international TBI conferences including the Annual Traumatic Brain Injury Conference in Washington, D.C. and the C4CT Concussion Awareness Summits, the last one held Pre-superbowl 2014 at the United Nations. She has been a recipient of research support from the State of Colorado Brain Injury Program for the past five years. Dr. Heidenreich received her undergraduate degree in Biology from Westminster College in 1974 and her Ph.D. in Physiology/Biophysics from the University of Vermont in 1979.