Category Archives: Neurotraumatología

New Book:Traumatic Brain Injury, Part I, Volume 127: Handbook of Clinical Neurology

Traumatic Brain Injury, Part I, Volume 127: Handbook of Clinical Neurology (Series Editors: Aminoff, Boller and Swaab)Traumatic Brain Injury, Part I, Volume 127: Handbook of Clinical Neurology (Series Editors: Aminoff, Boller and Swaab)

Price:$232.63

ADD TO SHOPPING CART

The Handbook of Clinical Neurology volume on traumatic brain injury (TBI) provides the reader with an updated review of emerging approaches to traumatic brain injury (TBI) research, clinical management and rehabilitation of the traumatic brain injury patient. Chapters in this volume range from epidemiology and pathological mechanisms of injury, and neuroprotection to long-term outcomes with a strong emphasis on current neurobiological approaches to describing the consequences and mechanisms of recovery from TBI. The book presents contemporary investigations on blast injury and chronic traumatic encephalopathy, making this state-of-the-art volume a must have for clinicians and researchers concerned with the clinical management, or investigation, of TBI.

  • Internationally renowned scientists describe cutting edge research on the neurobiological response to traumatic brain injury, including descriptions of potential biomarkers and indicators of potential targets for treatments to reduce the impact of the injury
  • Explores cellular and molecular mechanisms as well as genetic predictors of outcome
  • Offers coverage of various diagnostic tools – CT, MRI, DDTI, fMRI, EEG, resting functional imaging, and more
  • State-of-the-art traumatic brain injury management and treatment principles are presented for both civilian and military care

Product Details

  • Binding: Hardcover
  • 490 pages

Editorial Reviews

About the Author

Jordan Grafman, PhD, is director of Brain Injury Research at the Rehabilitation Institute of Chicago. Before joining RIC, Dr. Grafman was director of the Traumatic Brain Injury Research at Kessler Foundation. His investigation of brain function and behavior contributes to advances in medicine, rehabilitation, and psychology, and informs ethics, law, philosophy, and health policy. His study of the human prefrontal cortex and cognitive neuroplasticity incorporates neuroimaging and genetics, an approach that is expanding our knowledge of the impact of traumatic brain injury, as well as other diseases that impair brain function, such as stroke, multiple sclerosis and degenerative diseases. Dr. Grafman aims to translate his research into more effective, targeted rehabilitation to achieve the best outcomes for people with cognitive disabilities. Dr. Grafman’s background includes 30 years of experience in brain injury research. He has studied brain function in dementia, depression, and degenerative neurological diseases, as well as TBI. He has authored more than 300 research publications, co-editor of the journal Cortex, and provides peer review for numerous specialty journals. At the National Institutes of Health, he served as chief of the Cognitive Neuroscience Section at the National Institute of Neurological Disorders and Stroke. While in the US Air Force, he served at Walter Reed Army Medical Center as neuropsychology chief of the Vietnam Head Injury Project, a long-term study of more than 500 soldiers with serious injuries of the head and brain. He is the leading expert on the long-term effects of penetrating brain injuries in military personnel. His expertise includes the scope of challenges faced during recovery, including behavioral changes like aggression, late sequelae such as seizures, and the impact on TBI on family life and employment, and legal implications. He is an elected fellow of the American Psychological Association and the New York Academy of Sciences. Dr. Grafman is the recipient of many prestigious awards including the Department of Defense Meritorious Service Award, the National Institutes of Health Award of Merit, 2010 National Institutes of Health Director’s Award, and the Humboldt Reserach Award. He is a frequent speaker at national and international conferences. His expert opinion is often sought by national media on issues related to brain function and behavior, cognitive rehabilitation, and policy and legal issues related to brain-behavior research.

Update: Chronic traumatic encephalopathy

Chronic traumatic encephalopathy

J.Sales-Llopis

Neurosurgery Department, University General Hospital of Alicante, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Alicante, Spain

“Chronic traumatic encephalopathy” (CTE) is described as a slowly progressive neurodegenerative diseasebelieved to result from multiple concussions.

The damaging neurological effects of sports-related repetitive head trauma were described by Harrison S. Martland in 1928 1). His clinical description of ‘punch drunk syndrome’ in a group of former boxers has been extended to include a complex neuropathological and clinical diagnosis known today as Chronic Traumatic Encephalopathy (CTE).

The more generic designation, chronic traumatic encephalopathy (CTE), has been employed since the mid-1900s and has been used in recent years to describe a neurodegenerative disease found not just in boxers but in American football players, other contact sport athletes, military veterans, and others with histories of repetitive brain trauma, including concussions and subconcussive trauma 2).

This has prompted renewed interest and controversy regarding the potential for long-term neurodegenerative changes to occur after concussive and even sub-concussive repetitive or blast wave associated head trauma 3) 4).

In recent years, there has been tremendous media attention regarding CTE, primarily because of the deaths of high profile American football players who were found to have CTE upon neuropathological examination. However, the study of CTE remains in its infancy 5).

Epidemiology

Thus far CTE research has been limited to selective case reports. There are no published systematic studies incorporating both sport and non-sport related head trauma populations. Based on this lack of data, it is currently impossible to determine the incidence of new cases occurring within contact sport. Additionally, overall prevalence of CTE amongst all cases of head trauma cannot be determined at this time. Finally, due to the fragmented data collected in case reports, no conclusions can be drawn about potential risk factors for developing CTE in contact sports 6).

To date, all pathologically confirmed CTE cases have had a history of head trauma; however, the reported degree of severity, frequency of blows to the head, and documentation of prior concussion is highly variable 7).

Of 153 pathologically confirmed cases of CTE represents the most current and most complete number of confirmed CTE cases in the medical literature. The final number of CTE cases was determined after accounting for 113 duplicate reported cases. Duplicate cases accounted for 43% of all cases of CTE identified in the medical literature by this review. Although Maroon et al. acknowledge the occasional need for re-evaluating former CTE cases in order to further understand CTE findings presented to date, the high rate of re-reporting cases often without explicit notation of previous documentation has led to an erroneous, inflated impression of the number of CTE cases reported. The 153 CTE cases described in the review also include four unique cases of CTE found in media reports which were substantiated by cross confirmation from multiple sources including quotes from CTE investigators.

Of the 153 unique pathologically confirmed cases of CTE, six major mTBI subgroups were identified: former boxers, former football players, former hockey players, former military veterans, former professional wrestlers, and other miscellaneous causes of head trauma. Former boxers and football players made up the majority of all cases (86.2%). This observation is consistent with the long standing history of CTE research in the sport of boxing and the recent focus on former football players 8).

Pathophysiology

Traditionally, concussions were considered benign events and although most people recover fully, about 10% develop a post-concussive syndrome with persisting neurological, cognitive and neuropsychiatric symptoms. CTE was once thought to be unique to boxers, but it has now been observed in many different athletes having suffered multiple concussions as well as in military personal after repeated blast injuries. Much remains unknown about the development of CTE but its pathological substrate is usually tau protein, similar to that seen in Alzheimer’s disease (AD) and frontotemporal lobar degeneration (FTLD).

There is an urgent need for understanding the relationship between concussion and the development of CTE as it may provide a window into the development of a proteinopathy and thus new avenues for treatment 9).

Chronic traumatic encephalopathy is characterized by a unique pattern of accumulation of hyperphosphorylated tau in neurons and astrocytes. The tau abnormalities begin focally and perivascularly at the depths of the cerebral sulci, spread to the superficial layers of the adjacent cortex, and eventually become widespread throughout the medial temporal lobes, diencephalon, and brainstem. Abnormalities in 43 kDa TAR DNA-binding protein are also found in most cases of CTE. To date, CTE can only be diagnosed by postmortem neuropathological examination, although there are many ongoing research studies examining imaging techniques and biomarkers that might prove to have diagnostic utility. Currently, the incidence and prevalence of CTE are unknown, although great strides are being made to better understand the clinical symptoms and signs of CTE. Further research is critically needed to better identify the genetic and environmental risk factors for CTE as well as potential rehabilitation and therapeutic strategies 10).

Neuropathology

Although it shares certain histopathological findings with Alzheimer disease, chronic traumatic encephalopathy has a more specific presentation (hyperphosphorylated tau protein deposited as neurofibrillary tangles, associated with neuropil threads and sometimes with beta-amyloid plaques).

The neuropathological findings in a animal model of repetitive mTBI resemble some of the histopathological hallmarks of CTE, including increased astrogliosis, microglial activation, and hyperphosphorylated tau protein accumulation 11).

Clinical features

Its clinical presentation is insidious; patients show mild cognitive and emotional symptoms before progressing to parkinsonian motor signs and finally dementia.

The clinical features of CTE are often progressive, leading to dramatic changes in mood, behavior, and cognition, frequently resulting in debilitating dementia 12).

Diagnosis

Several recent reviews have focused on the various neuropathological findings and the clinical criteria used for the diagnosis of CTE and have drawn attention to the confusion and inconsistency of the diagnosis of CTE 13) 14).

Results from new experimental diagnostic tools are promising, but these tools are not yet available.

Differential diagnosis

Chronic postconcussion syndrome, and chronic neurocognitive impairment 15).

Management

The mainstay of managing this disease is prevention and early detection of its first symptoms.

The inhibition of monoacylglycerol lipase (MAGL), the key enzyme that metabolizes the endocannabinoid 2-arachidonoylglycerol (2-AG) in the brain, significantly reduced CTE-like neuropathologic changes in a mouse model of repetitive mild closed head injury (rmCHI). Inhibition of 2-AG metabolism promoted neurologic recovery following rmCHI and reduced proinflammatory cytokines, astroglial reactivity, expression of amyloid precursor protein and the enzymes that make Aβ, as well as formation of Aβ. Importantly, neurodegeneration, TDP-43 protein aggregation, and tau phosphorylation, which are the neuropathologic hallmarks of CTE, were significantly suppressed by MAGL inactivation. Furthermore, alterations in expression of glutamate receptor subunits and impairments in basal synaptic transmission, long-term synaptic plasticity, and spatial learning and memory were recovered by inhibition of 2-AG metabolism in animals exposed to rmCHI. The results suggest that MAGL inhibition, which boosts 2-AG and reduces 2-AG metabolites prostaglandins in the brain, may lead to a new therapy for CTE 16).

1) Martland HS (1928) Punch Drunk. JAMA 91: 1103–1107.
2) Montenigro PH, Baugh CM, Daneshvar DH, Mez J, Budson AE, Au R, Katz DI, Cantu RC, Stern RA. Clinical subtypes of chronic traumatic encephalopathy: literature review and proposed research diagnostic criteria for traumatic encephalopathy syndrome. Alzheimers Res Ther. 2014 Sep 24;6(5):68. doi: 10.1186/s13195-014-0068-z. eCollection 2014. Review. PubMed PMID: 25580160; PubMed Central PMCID: PMC4288217.
3) McKee AC, Stern RA, Nowinski CJ, Stein TD, Alvarez VE, et al. (2013) The spectrum of disease in chronic traumatic encephalopathy. Brain 136: 43–64 doi: 10.1093/brain/aws30723208308
4) Omalu B, Bailes J, Hamilton RL, Kamboh MI, Hammers J, et al. (2011) Emerging histomorphologic phenotypes of chronic traumatic encephalopathy in American athletes. Neurosurgery 69: 173–183 doi: 10.1227/NEU.0b013e318212bc7b21358359
5) Riley DO, Robbins CA, Cantu RC, Stern RA. Chronic traumatic encephalopathy: Contributions from the Boston University Center for the Study of Traumatic Encephalopathy. Brain Inj. 2015;29(2):154-63. doi: 10.3109/02699052.2014.965215. PubMed PMID: 25587744.
6) McCrory P (2013) Consensus Statement on Concussion in Sport: The 4th International Conference on Concussion in Sport Held in Zurich (November 2012). Br J Sports Med 47: 250–258 doi: 10.1136/bjsports-2013-09231323479479
7) McKee AC, Cantu RC, Nowinski CJ, Hedley-Whyte ET, Gavett BE, et al. (2009) Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury. J Neuropathol Exp Neurol 68: 709–735 doi: 10.1097/NEN.0b013e3181a9d50319535999
8) Maroon JC, Winkelman R, Bost J, Amos A, Mathyssek C, Miele V. Chronic traumatic encephalopathy in contact sports: a systematic review of all reported pathological cases. PLoS One. 2015 Feb 11;10(2):e0117338. doi: 10.1371/journal.pone.0117338. eCollection 2015. PubMed PMID: 25671598; PubMed Central PMCID: PMC4324991.
9) Tartaglia MC, Hazrati LN, Davis KD, Green RE, Wennberg R, Mikulis D, Ezerins LJ, Keightley M, Tator C. Chronic traumatic encephalopathy and other neurodegenerative proteinopathies. Front Hum Neurosci. 2014 Jan 31;8:30. doi: 10.3389/fnhum.2014.00030. eCollection 2014. PubMed PMID: 24550810; PubMed Central PMCID: PMC3907709.
10) Kiernan PT, Montenigro PH, Solomon TM, McKee AC. Chronic Traumatic Encephalopathy: A Neurodegenerative Consequence of Repetitive Traumatic Brain Injury. Semin Neurol. 2015 Feb;35(1):20-28. Epub 2015 Feb 25. PubMed PMID: 25714864.
11) Petraglia AL, Plog BA, Dayawansa S, Dashnaw ML, Czerniecka K, Walker CT, Chen M, Hyrien O, Iliff JJ, Deane R, Huang JH, Nedergaard M. The pathophysiology underlying repetitive mild traumatic brain injury in a novel mouse model of chronic traumatic encephalopathy. Surg Neurol Int. 2014 Dec 23;5:184. doi: 10.4103/2152-7806.147566. eCollection 2014. PubMed PMID: 25593768; PubMed Central PMCID: PMC4287910.
12) Montenigro PH, Corp DT, Stein TD, Cantu RC, Stern RA. Chronic Traumatic Encephalopathy: Historical Origins and Current Perspective. Annu Rev Clin Psychol. 2015 Jan 12. [Epub ahead of print] PubMed PMID: 25581233.
13) Smith DH, Johnson VE, Stewart W (2013) Chronic neuropathologies of single and repetitive TBI: substrates of dementia? Nat Rev Neurol 9:211–221 doi: 10.1038/nrneurol.2013.2923458973
14) Gardner A, Iverson GL, McCrory P (2013) Chronic traumatic encephalopathy in sport: a systematic review. Br J Sports Med 48: 84–90 doi:10.1136/bjsports-2013-09264623803602
15) Jordan BD. Chronic traumatic encephalopathy and other long-term sequelae. Continuum (Minneap Minn). 2014 Dec;20(6 Sports Neurology):1588-604. doi: 10.1212/01.CON.0000458972.94013.e1. PubMed PMID: 25470162.
16) Zhang J, Teng Z, Song Y, Hu M, Chen C. Inhibition of monoacylglycerol lipase prevents chronic traumatic encephalopathy-like neuropathology in a mouse model of repetitive mild closed head injury. J Cereb Blood Flow Metab. 2014 Dec 10. doi: 10.1038/jcbfm.2014.216. [Epub ahead of print] PubMed PMID: 25492114.

New Book:Brain Neurotrauma: Molecular, Neuropsychological, and Rehabilitation Aspects (Frontiers in Neuroengineering Series)

Brain Neurotrauma: Molecular, Neuropsychological, and Rehabilitation Aspects (Frontiers in Neuroengineering Series)

Brain Neurotrauma: Molecular, Neuropsychological, and Rehabilitation Aspects (Frontiers in Neuroengineering Series)

List Price:$229.95

ADD TO SHOPPING CART

Every year, an estimated 1.7 million Americans sustain brain injury. Long-term disabilities impact nearly half of moderate brain injury survivors and nearly 50,000 of these cases result in death.

Over the last decade, the field of neurotrauma has witnessed significant advances, especially at the molecular, cellular, and behavioral levels. This progress is largely due to the introduction of novel techniques, as well as the development of new animal models of central nervous system (CNS) injury.

Brain Neurotrauma: Molecular, Neuropsychological, and Rehabilitation Aspects provides a comprehensive and up-to-date account on the latest developments in the area of neurotrauma, including brain injury pathophysiology, biomarker research, experimental models of CNS injury, diagnostic methods, and neurotherapeutic interventions as well as neurorehabilitation strategies in the field of neurotraum research.

The book includes several sections on neurotrauma mechanisms, biomarker discovery, neurocognitive/neurobehavioral deficits, and neurorehabilitation and treatment approaches. In addition, a section is devoted to models of mild CNS injury, including blast and sport-related injuries.

This book, with its diverse coherent content, is a valuable and comprehensive reference for individuals interested in the diverse and heterogeneous aspects of CNS pathology and/or rehabilitation needs.


Product Details

  • Original language: English
  • Number of items: 1
  • Dimensions: 10.98″ h x .0″ w x 8.50″ l, .0 pounds
  • Binding: Hardcover
  • 725 pages

Editorial Reviews

Review

“As traumatic brain injury is now well recognized as a world health issue, this text is timely and well deserving in terms of a review or our current understanding of several topics related to traumatic brain injury and recovery of function. [It] is a “must read” for all investigators interested in the field as this text will cover the current advancements in scientific technology, clinical care and, most importantly, the undeniable value of translational research.”
—David A. Hovda, PhD, Director, UCLA Brain Injury Research Center

“[An] appealing package of knowledge in the mechanisms, epidemiology, psychology, pathology, diagnosis, treatment and rehabilitation of traumatic brain injuries.”
—Mårten Risling MD, PhD, Professor, Department of Neuroscience, Karolinska Institutet

“Broad in its scope and coverage, [the book] is sure to be an outstanding resource for anyone interested in the pathophysiology or treatment of military or civilian head trauma.”
—Gregory Elder, MD, Research Professor, Psychiatry, Icahn School of Medicine at Mount Sinai

About the Author

Firas Hosni Kobeissy is an assistant professor in the Department of Psychiatry of the University of Florida McKnight Brain Institute and serves as the associate scientific director of the Center for Neuroproteomics and Biomarkers Research. He earned his PhD from the University of Florida and has published in the field of brain injury biomarkers, neuroproteomics, and neurosystems biology. Dr. Kobeissy’s current research overlaps the fields of neuroscience and psychiatry with a focus on drug abuse neurotoxicity and traumatic brain injury neuroproteomics. He has published more than 70 peer-reviewed papers, reviews, and book chapters as well as co-edited three books. He has also co-authored five U.S. patents. Dr. Kobeissy serves as an editorial member on several journals related to proteomics, neuroscience, and brain injury and has been a member on several study sections of brain injury and stroke.

Stuart W. Hoffman is the scientific program manager of the brain injury portfolio in the rehabilitation research and development service at the U.S. Department of Veteran Affairs (VA) The portfolio is focused on promoting translational research that improves outcomes in veterans living with the chronic effects of stroke, traumatic brain injury, and its co-morbidities. He also represents VA/ORD on TBI research. In this role, he is the co-chair of the government steering committee for the VA/DoD Chronic Effects of Neurotrauma Consortium, as well as a member of several advisory boards for VA research centers, and serves on the congressionally mandated Traumatic Brain Injury Advisory Committee for the Veterans Health Administration. He received his doctoral degree in behavioral and molecular neuroscience at Rutgers University.

Concussion Inc.: The End of Football As We Know It

Concussion Inc.: The End of Football As We Know It

By Irvin Muchnick

Concussion Inc.: The End of Football As We Know It

List Price:$19.95
ADD TO SHOPPING CART

Product Description

Inside the controversial and newsworthy issue of concussions in American football — Muchnick’s trademark no-holds-barred investigation reveals the corruption and scandals in real time

Traumatic brain injury in football is not incidental, but an inevitable and central aspect of the sport. Starting in high school, through college, and into the NFL, young players face repeated head trauma, and those sustained injuries create lifelong cognitive and functional difficulties.

Muchnick’s Concussion Inc. blog exposed the decades-long cover-up of scientific research into sports concussions and the ongoing denial to radically reform football in North America. This compilation from Muchnick’s no-holds-barred investigative website reveals the complete head injury story as it developed, from the doctor who played fast and loose with the facts about the efficacy of the state-mandated concussion management system for high school football players, to highly touted solutions that are more self-serving cottage industry than of any genuine benefit.

Known for extensive reporting on the tragic story of the Chris Benoit murder-suicide, Muchnick turns his investigative analysis to traumatic brain injury and probes deep into the corporate, government, and media corruption that has enabled the $10-billion-a-year National Football League to trigger a public health crisis.


Product Details

  • Dimensions: 9.00″ h x 6.00″ w x 1.00″ l, .0 pounds
  • Binding: Paperback
  • 300 pages

Editorial Reviews

About the Author

Irvin Muchnick: Irvin Muchnick is the author of Wrestling Babylon: Piledriving Tales of Drugs, Sex, Death, and Scandal and Chris & Nancy: The True Story of the Benoit Murder-Suicide and Pro Wrestling’s Cocktail of Death, and a co-author of Benoit: Wrestling with the Horror that Destroyed a Family and Crippled a Sport. He lives in Berkeley, California.

Predicting Recurrence after Chronic Subdural Haematoma Drainage

Recurrence of chronic subdural haematomas (CSDHs) after surgical drainage is a significant problem with rates up to 20%. This study focuses on determining factors predictive of haematoma recurrence and presents a scoring system stratifying recurrence risk for individual patients. Methods : Between the years 2005 and 2009, 331 consecutive patients with CSDHs treated with surgery were included in this study. Univariate and multivariate analyses were performed searching for risk factors of increased post-operative haematoma volume and haematoma recurrence requiring repeat drainage. Results: We found a 12% reoperation rate. CSDH septation (seen on computed tomogram scan) was found to be an independent risk factor for recurrence requiring reoperation (p=0.04). Larger post-operative subdural haematoma volume was also significantly associated with requiring a second drainage procedure (p<0.001). Independent risk factors of larger post-operative haematoma volume included septations within a CSDH (p<0.01), increased pre-operative haematoma volume (p<0.01), and a greater amount of parenchymal atrophy (p=0.04). A simple scoring system for quantifying recurrence risk was created and validated based on patient age (< or ≥80 years), haematoma volume (< or ≥160cc), and presence of septations within the subdural collection (yes or no). Conclusion: Septations within CSDHs are associated with larger post-operative residual haematoma collections requiring repeat drainage. When septations are clearly visible within a CSDH, craniotomy might be more suitable as a primary procedure as it allows greater access to a septated subdural collection. Our proposed scoring system combining haematoma volume, age, and presence of septations might be useful in identifying patients at higher risk for recurrence1

  1. Jack A, O’Kelly C, McDougall C, Max Findlay J. Predicting Recurrence after Chronic Subdural Haematoma Drainage. Can J Neurol Sci. 2015 Jan 5:1-6. [Epub ahead of print] PubMed PMID: 25557536. []