Tbi powerpoint for class 2

2,642 views

Published on

Published in: Education, Health & Medicine
0 Comments
2 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total views
2,642
On SlideShare
0
From Embeds
0
Number of Embeds
2
Actions
Shares
0
Downloads
82
Comments
0
Likes
2
Embeds 0
No embeds

No notes for slide
  • Diffuse axonal injuries are very common, especially after motor vehicle accidents that involve angular acceleration and shearing stress/injury of axons. The signature neuropathology is axonal swellings, called retraction balls, best depicted with amyloid precursor protein immunocytochemistry (top). Structural brain imaging (MRI, bottom) can detect microhemorrhages in the form of black hemosiderin deposits (red arrow) and diffuse or local brain atrophy.
  • Tbi powerpoint for class 2

    1. 1. Blast-related TBI and Psychopharmacological Treatment Gerd R. Naydock, MSS, LSW Philadelphia College of Osteopathic Medicine
    2. 2. Traumatic Brain Injury• Generally defined as a physiologically significant disruption of brain functioning subsequent to the application of external forces, including acceleration/deceleration forces which cause damage to brain structures.• American Congress of Rehabilitation Medicine, 1993
    3. 3. Blast –related TBIs in OEF/OIF Veterans• Increased frequency of blast-related TBI compared to previous military conflicts.• Use of Improvised Explosive Devices (IEDs) and Rocket-Propelled Grenades (RPGs) by enemy combatants.• TBI s account for one-fourth of the medical evacuations in Iraq and Afghanistan.• Improved equipment and post-trauma medical treatment enhance survivability.
    4. 4. Types of Blast Injuries• Primary – Occur as rapid changes in atmospheric pressure force rotational acceleration of the brain within the cranium.• Secondary – Occurs from fast-moving ballistic objects which as a result of an explosion strike and often penetrate skull.• Tertiary – Individuals are picked up and thrown by the blast.
    5. 5. Rotational Acceleration
    6. 6. Rocket-Propelled Grenades
    7. 7. Video – Blast Injuries• http://www.youtube.com/watch?feature= player_detailpage&v=4JAHBKe_RAU
    8. 8. Mild TBI• Mild traumatic brain injury is defined as a loss or alteration of consciousness < 30 minutes, post- traumatic amnesia < 24 hours, focal neurologic deficits that may or may not be transient, and/or Glasgow Coma Score (GCS) of 13-15.• By definition, a mild traumatic brain injury typically involves symptoms of brain damage but no sign of damage based on a neurological exam.• Controversy over whether primary blast injuries damage brain. Animal models suggest they do.
    9. 9. Mild TBI - Symptoms• Headache, dizziness, insomnia, impaired memory and/or lowered tolerance for noise and light. In most cases of mTBI the patient returns to their previous level of function within 3 to 6 months• 10-15% of patients may go on to develop chronic post-concussive symptoms.
    10. 10. Chronic Post-Concussive Symptoms• These symptoms can be grouped into three categories: somatic (headache, tinnitus, vertigo, insomnia, etc.), cogn itive (memory, attention and concentration difficulties and emotional/behavioral (irritability, depression, anxiety, behavioral dyscontrol).
    11. 11. Comorbid Psychiatric Disorders• Patients who have experienced mTBI are also at increased risk for psychiatric disorders compared to the general population, including depression and PTSD.
    12. 12. Video – Mild TBI - Magnetoencephalography• http://www.youtube.com/watch?v=uhlANIGA JXA
    13. 13. Neurobiological Changes after TBI• The principal neurobiological consequences of TBI are: – cortical contusions (mostly in severe TBI) • results in a loss of function served by that area – white matter lesions • results in interruption of information processing between cortical areas – diffuse axonal injury • results in slowed and inefficient information processing • disproportionately affects glutamatergic and cholinergic projections – results in problems with attention, memory, and various aspects of frontally-mediated cognition (ie, working memory, executive function) • may affect serotonergic systems • dysfunction in these systems may secondarily affect the efficiency of function in dopaminergic or noradrenergic systems
    14. 14. Diffuse Axonal Injuries• Damage to the pathways (axons) that connect the different areas of the brain. This occurs when there is twisting and turning of the brain tissue secondary to unrestricted head movement at the time of blast.• Affects white matter of the cerebrum, corpus callosum, deep gray matter, internal capsule, upper brainstem and the cortico-meullary (gray- white matter) junctions of cerebral cortex.
    15. 15. Diffuse Axonal Injuries• Damage to rats’ axonal cytoskeleton results in loss of their elasticity and impaired transport and accumulation of axonal transport proteins within axonal swellings.• Axonal swellings are caused by damage to sodium and calcium ion channels and can lead to dysfunction of the mitochondria.
    16. 16. Secondary Neurological Injury• With the progression of time, axons can become disconnected within the white matter of the brain which will lead to chronic neurological impairment for the individual affected.
    17. 17. Diffusion Tensor Imaging
    18. 18. Secondary & Tertiary Blast Injuries• Responsible for the majority of macroscopic, focal, brain injuries.• Include, cerebral contusions, edema and hematomas.• Significant axonal damage when compressed within brainstem. Leads to coma.
    19. 19. Symptoms of Secondary and Tertiary Blast Injuries• Cranial Nerve Dysfunction – opthalmopareses, olfactory and gustatory problems, dysphagia and vestibulopathy.• Psychomotor – Involuntary movements, spastisity, tremors and dyspraxia.
    20. 20. Symptoms of Secondary & Tertiary Blast Injuries• Cognitive – gross memory loss and orientation.• Behavioral – Agitation, aggression and other inappropriate and extreme bxs which stem from disinihibition. Usually caused by damage in the hippocampus, prefrontal cortex, frontolimbic pathways. Abnormal serotonergic modulation contributes to this.
    21. 21. Cognition• Cognitive Impairments constitute the most common chronic sequelae of blast-related TBI.• Cognitive functioning is highly dopamine dependent and TBI is usually associated with decreased dopaminergic activities in the striatum, large areas of the cerebral cortex to include the caudate nucleus and mediofrontal cortex.
    22. 22. Cognition• Many neurotransmitters are involved in the regulation of cognition• Several neurotransmitters are particularly relevant to the regulation of frontal and frontotemporal structures involved in cognition: – dopamine – norepinephrine – serotonin – acetylcholine – glutamate gamma-aminobutyric acid (GABA)
    23. 23. Psychopharmacology• At present, there are no FDA approved treatments for cognitive, emotional, or behavioral impairment due to TBI• Pharmacotherapies are generally modeled after those for patients with phenomenologically similar but etiologically distinct disorders (i.e., attention-deficit hyperactivity disorder, Alzheimer’s disease, etc.).
    24. 24. Psychopharmacology Issues• Medication approaches generally take three broad approaches: – amelioration of psychiatric complications – amelioration of specific somatic symptoms (e.g., headache, dizziness, sleep disturbances) – augmentation of cognition
    25. 25. Approach to Cognitive Deficits• Main target domains: – Memory • Particularly working memory – Attention – Executive Functions
    26. 26. Dopamine Agonists• A variety of agonists have been shown effective in animal models and are used clinically: – Methylphenidate (most widely studied) (stimulant) – Amantadine ( >pre- & post-synaptic dopamine in striatum) (non-stimulant) – Bromocriptine (presynaptic D2 agonist) (non- stimulant)
    27. 27. Cholinergic Augmentation• Multiple studies demonstrate that cholinergic augmentation, generally using one of several cholinesterase inhibitors (e.g., physostigmine, donepezil) can improve arousal, processing speed, and sustained attention/vigilance even in the late post-injury period (>1 year) in some TBI survivors• Hypocholinergic activity results in learning and memory impairments and decreased arousal.
    28. 28. Acetylcholine PathwaysFC = Frontal cortexPC = Parietal cortexOC = Occipital cortexH = Hippocampus M TM = Medial septal nucleus and diagonal band of BrocaT = Diagonal band of Broca projecting into the olfactory tubercleB = Nucleus basalis of Meynert
    29. 29. Aggression & TBI• Acute phase: 35% - 96% of patients exhibit agitated behaviors – 89 patients assessed during the first six months after TBI, aggressive behavior found in 33.7% of TBI patients, compared to 11.5% of patients with multiple trauma but without TBI (Tateno et al)• Recovery phase: 31% - 71% of patients with severe TBI and 5% - 70% of patients with mild TBI are agitated or irritable• Irritability increases with more TBI’s
    30. 30. Aggression & TBI• Reactive: Triggered by modest or trivial stimuli• Nonreflective: Usually does not involve premeditation or planning• Nonpurposeful: Aggression serves no obvious long-term aims or goals• Explosive: Buildup is NOT gradual• Periodic: Brief outbursts of rage and aggression, punctuated by long periods of relative calm• Ego-dystonic: After outbursts, patients are upset, concerned, and/or embarrassed, as opposed to blaming others or justifying behavior
    31. 31. Neuropathology of Aggression• Hypothalamus Orchestrates neuroendocrine response to sympathetic arousal Monitors internal status• Limbic system Amygdala Activates and/or suppresses hypothalamus Input from neocortex Temporal cortex Associated with aggression on both ictal and interictal status• Frontal neocortex Modulates limbic and hypothalamic activity Associated with social and judgment aspects of aggression
    32. 32. Beta Blockers• Increases in norepinephrine, dopamine and acetylcholine also increase violent behaviors in animal models.• Propranalol, pindolol etc. serve as antagonists and block the action of epinephrine and norepinephrine on beta 1 and beta 2 andrenergic receptors exerting effects on the locus coerulus – primary norandrenergic system in CNS.
    33. 33. Apathy• Believed to be caused by cholinergic dysfunction in the frontal lobe, particularly the nucleus basalis, anterior cingulated gyrus as well as subregions of the basal ganglia.• Dysfunction of these pathways is linked to < ability to discern emotional significance to environmental stimuli.• MAO B inhibitors raise dopamine levels in the striatal cortex. (Rasagaline & Selegiline)
    34. 34. Why Target Apathy?
    35. 35. References• Adams, J.H., Graham, D.I., Murray, L.S., and Scott, G. (1982). Diffuse axonal injury due to nonmissile head injury in humans: an analysis of 45 cases. The Annals of Neurology, 12, 557-563. doi:10.1002/ana.410120610• Adams, J.H., Graham, D.I., and Gennarelli, T.A. (1983). Head injury in man and experimental animals: neuropathology. Acta Neurochirurgica Supplementum (Wien), 32, 15-30.• American Congress of Rehabilitation Medicine: Definition of mild traumatic brain injury. Journal of Head Trauma Rehabilitation, 1993; 8(3): 86-87. doi:10.1097/00001199-199309000-00010• Bailly, D., Vignau, J., Racadot, N., Beuscart, R., Servant, D., and Parquet, P.J. (1993). Platelet serotonin levels in alcoholic patients: changes related to physiological and pathological factors. Psychiatry Research, 47(1), 57-88. doi:10.1016/0165-1781(93)90055-L Belanger, H.G., Kretzmer, T., Yoash-Gantz, R., Pickett, T., and Tupler, L.A. (2009). Cognitive sequelae of blast-related versus other mechanisms of brain trauma. Journal of the International Neuropsychological Society, 15, 1- 8. doi:10.1017/S1355617708090036• Cernak, I., Savic, J., Malicevic, Z., Zunic, G., Radosevic, P., Ivanovic, I., and Davidovic, L. (1996) Involvement of the central nervous system in the response of general pulmonary blast injury. Journal of Trauma, 40, S100-104. doi:10.1097/00005373-199603001-00023• Cernak, I.; Wang, Z.; Jiang, J.; Bian, X.; Savic, J. (2001). Cognitive deficits following blast injury induced neurotrauma. Brain Injury, 15 (7), 593–612. doi:10.1080/02699050119009• Chew, E., and ZaFonte, R.D. (2009). Pharmacological management of neurobehavioral disorders following traumatic brain injury: A state of the art review. Journal of Rehabilitation Research & Development, 46(6), 851-878. doi:10.1682/JRRD.2008.09.0120
    36. 36. References• Christman, C.W., Grady, M.S., Walker, S.A., Holloway, K.I., and Povlischock, J.T. (1994). Ultrastructural studies of diffuse axonal injury in humans. Journal of Neurotrauma, 11, 173-186. doi:10.1089/neu.1994.11.173• DePalma, R.G., Burris, D.G., Champion, H.R. et al. (2005). Blast injuries. New England Journal of Medicine, 352, 1335-1342 doi:10.1056/NEJMra042083• Eichelman, B. (1987). Neurochemical and psychopharmacologic aspects of aggressive behavior. In H.Y. Meltzer (Ed.), Psychopharmacology: The third generation of progress (pp. 697-704). New York: Raven Press.• Elliott, F.A. (1977). Propranalol for the control of belligerent behavior following acute brain damage. The Annals of Neurology, 1(5), 489-491. doi:10.1002/ana.410010516• French, L.M., and Parkinson, G.W. (2008). Assessing and treating veterans with traumatic brain injury. Journal of Clinical Psychology, 64, 1004-1013. doi:10.1002/jclp.20514• Galarneau, M.R., Woodruff, S.I., Dye, J.L., Mohrle, C.R., and Wade, A.L. (2008). Traumatic brain injury during Operation Iraqi Freedom: findings from the United States Navy – Marine Corps Combat Trauma Registry. Journal of Neurosurgery, 108, 950-957. doi:10.3171/JNS/2008/108/5/0950 Gennarelli, T.A. (1993). Mechanisms of brain injury. Journal of Emergency Medicine, 11(Suppl 1), 5-11.• Grafman, J., Schwab, K., Warden, D., Pridgen, A., Brown, H.R., and Salazar, A.M. (2006). Frontal lobe injuries, violence, and aggression: a report of the Vietnam Head Injury Study. Neurology, 46(5), 1231-1238.• Graham, D.I., McLellan, D., Adams, J.H., Doyle, D., Kerr, A., and Murray, L.S. (1983) The neuropathology of the vegetative state and severe disability after non-missile head injury. Acta Neurochirurgica Supplementum (Wien), 32, 65-67.
    37. 37. References• Griffin, S.L., van Reekum, R., and Masanic, C. (2003). A review of cholinergic agents in the treatment of neurobehavioral disorders following traumatic brain injury. Journal of Neuropsychiatry and Clinical Neurosciences, 15, 17-26. doi:10.1176/appi.neuropsych.15.1.17• Gualtieri, C.T., Chandler, M., Coons, T.B., and Brown, L.T. (1989). Amantadine: a new clinical profile for traumatic brain injury. Clinical Neuropharmacology, 12(4), 258-270. doi:10.1097/00002826-198908000-00003• Gualtieri, C.T., and Evans, R.W. (1988). Stimulant treatment for neurobehavioral sequelae of traumatic brain injury. Brain Injury, 2(4), 273-290. doi:10.3109/02699058809150898• Gutierrez-Cadavid J.E. (2005) Imaging of head trauma. In Latchaw, R.E., Kucharczyk, J., & Moseley, M.E. (Eds.), Imaging of the Nervous System. (pp. 869-904) Philadelphia: Elsevier Mosby. Guy, R.J., Glover, M.A., and Cripps, N.P. (2000) Primary blast injury: pathophysiology and implications for treatment. Part III: Injury to the central nervous system and the limbs. Journal of the Royal Naval Medical Service, 86(1), 27-31.• Hall, G.F., Lee, V.M. (1995). Neurofilament sidearm proteolysis is a prominent early effect of axotomy in lamprey giant central neurons. Journal of Comparative Neurology, 1, 38-49. doi:10.1002/cne.903530106• Hoge, C.W., McGurk, D., Thomas, J.L., Cox, A.L., Engel, C.C., and Castro, C.A. (2008). Mild traumatic brain injury in U.S. Soldiers returning from Iraq. New England Journal of Medicine, 358, 453-463. doi:10.1056/NEJMoa072972• Hornyak, J.E., Nelson, V.S., and Hurvitz, E.A. (1997). The use of methylphenidate in paediatric traumatic brain injury. Pediatric Rehabilitation, 1(1), 15-17.
    38. 38. References• Hurley, R.A., McGowan, J.C., Arfanakis, K., and Taber, K.H. (2004). Traumatic axonal injury: novel insights into evolution and identification. Journal of Neuropsychiatry and Clinical Neurosciences, 16(1), 1-7. doi:10.1176/appi.neuropsych.16.1.1• Iwata, A., Chen, X.H., McIntosh, T.K., Browne, K.D., and Smith, D.H. (2002) Long-term accumulation of amyloid-beta in axons following brain trauma without persistent upregulation of amyloid precursor protein genes. Journal of Neuropathology and Experimental Neurology, 61, 1056-1068.• Kaelin, D.L., Cifu, D.X., and Matthies, B. (1996). Methylphenidate effect on attention deficit on acutely brain-injured adult. Archives of Physical and Medical Rehabilitation, 77(1), 6-9. doi:10.1016/S0003-9993(96)90211-7• Kant, R., Duffy, J.D., and Pivovarnik, A. (1998). Prevalence of apathy following brain injury. Brain Injury, 12, 87-92. doi: 10.1080/026990598122908• Kim, Y.H., Ko, M.H., Na, S.Y and Park, S.H. (2006). Effects of a single dose methylphenidate on cognitive performance in patients with traumatic brain injury: a double-blind, placebo-controlled study. Clinical Rehabilitation, 20(1), 24-30. doi:10.1191/0269215506cr927oa• Kocsis, J.D. and Tessler, A.D. (2009). Pathology of brain-related injury. Journal of Rehabilitation & Development, 46, 667-672. doi:10.1682/JRRD.2008.08.0100• Lee, H., Kim, S.W., Kim, J.M., Shin, I.S., Yang, S.J., and Yoon, J.S. (2005). Comparing effects of methylphenidate, sertraline, and placebo on neuropsychiatric sequelae in patients with traumatic brain injury. Human Psychopharmacology, 20(2), 97-104. doi:10.1002/hup.668• Lee, H.B., Lyketsos, C., Rao, V. (2003). Pharmacological management of the psychiatric aspects of traumatic brain injury. International Review of Psychiatry, 15(4), 359-370. doi:10.1080/09540260310001606746
    39. 39. References• Levin H.S., Wilde E., Troyanskaya, M., Petersen, N.J., Scheibel, R., Newsome, M., Radaideh, M., Wu, T., Yallampalli, R., Chu, Z., and Li, X. (2010). Diffusion tensor imaging of mild to moderate blast-related traumatic brain injury and its sequelae. Journal of Neurotrauma, 27(4), 683-694. doi:10.1089/neu.2009.1073 London, E.D., Ernst, M., Grant, S., Bonson, K., and Weinstein, A. (2000). Orbitofrontal cortex and human drug abuse: functional imaging. Cerebral Cortex, 10(3), 334-342.• Mahalik, D.M., Carmel, P.W., Greenberg, J.P., Malofsky, W., Brown, J.A., Heary, R.F., Marks, D., Zampella, E., Hodosh, R., and von der Schmidt, E. 3rd. (1998) Psychopharmacologic treatment of acquired attention disorders in children with brain injury. Pediatric Neurosurgery, 29(3), 121-126. doi:10.1159/000028705• Maxwell, W.L., Kosanlavit, R., McCreath, B.J., Reid, O., and Graham, D.I. (1999). Axonal Cytoskeletal Responses to Nondisruptive Axonal Injury and the Short-Term Effects of Posttraumatic Hypothermia Journal of Neurotrauma, 16(12), 1225-1234. doi:10.1089/neu.1999.16.1225• Mayorga, M.A. (1997). The pathology of primary blast overpressure injury. Toxicology, 121, 17-28. doi:10.1016/S0300-483X(97)03652-4• McDowell, S., Whyte, J., and Esposito, M. (1998). Differential effect of a dopaminergic agonist on prefrontal function in traumatic brain injury patients. Brain, 121(part 6), 1155-1164. doi:10.1093/brain/121.6.1155• McLeod, A.D. (2004). Shell shock, Gordon Holmes and the Great War. Journal of the Royal Society of Medicine, 97(2), 86-89. doi:10.1258/jrsm.97.2.86• Meythaler, J.M., Peduzzi, J.D., Eleftheriou, E., and Novack, T.A. (2001). Current concepts: diffuse axonal injury-associated traumatic brain injury. Archives of Physical and Medical Rehabilitation, 10, 1461-1471. doi:10.1053/apmr.2001.25137
    40. 40. References• Morey, C.E., Cilo, M., Berry, J., and Cusick, C. (2003). The effect of Aricept in persons with persistent memory disorders following traumatic brain injury: a pilot study. Brain Injury, 17(9), 809-815. doi:10.1080/0269905031000088586• Mott, F.W. (1916). The effects of high explosives upon the central nervous system. Lancet, 1, 441-449.• Moyer, K.E. (1976). The Psychobiology of Aggression. New York: Harper & Row.• Moutaouakil, F., El Otmani, H., Fadel, H., and Slassi, I. (2007). Severe apathy following head injury: improvement with selegiline treatment. Neurochirurgie., 55(6), 551-4• Newburn, G. and Newburn, D. (2005). Selegiline in the management of apathy following traumatic brain injury. Brain Injury, 19(2), 149-154. doi:10.1080/02699050410001719989• Okie, S. (2005). Traumatic brain injury in the war zone. New England Journal of Medicine, 352, 2043-2047. doi:10.1056/NEJMp058102• Owens, B.D., Kragh, J.F., Jr., Wenke, J.C., Macaitis, J., Wade, C.E., and Holcomb, J.B. (2008). Combat wounds in Operation Iraqi Freedom and Operation Enduring Freedom. Journal of Trauma, 64, 295-299. doi:10.1097/TA.0b013e318163b875• Paré, N., Rabin, L.A., Fogel, J., and Pepin, M. (2009). Mild Traumatic Brain Injury and Its Sequelae: Progression of Divided Attention Deficits. Neuropsychological Rehabilitation 19, 110-137. doi:10.1080/09602010802106486• Passler, M.A., and Riggs, R.V. (2001). Positive outcomes in traumatic brain injury – vegetative state: Patients treated with bromocriptine. Archives of Physical and Medical Rehabilitation, 82(3), 311-315. doi:10.1053/apmr.2001.20831• Paul, R.H., Brickman, A.M., Navia, B. (2005). Apathy is associated with volume of the nucleus accumbens in patients infected with HIV. Journal of Neuropsychiatry and Clinical Neurosciences 17:167–171.
    41. 41. References• Pierce, J.E., Smith, D.H., Trojanowski, J.Q., and McIntosh, T.K. (1998). Enduring cognitive, neurobehavioral and histopathological changes persist for up to one year following severe experimental brain injury in rats. Neuroscience, 87, 359-369. doi:10.1016/S0306-4522(98)00142-0• Posmantur, R., Kampfl, A., Siman, R., Liu, J., Zhao, X., Clifton, G.L., and Hayes, R.L. (1997). A caplain inhibitor attenuates cortical cytoskeletal protein loss after experimental traumatic brain injury in the rat. Neuroscience, 3, 875-888. doi:10.1016/S0306-4522(96)00483-6• Povlischock, J.T., and Katz, D.I. (2005). Update of neuropathology and neurological recovery after traumatic brain injury. Journal of Head Trauma Rehabilitation, 20(1), 76-94. doi:10.1097/00001199-200501000- 00008• Rao, V., and Lyketsos, C. (2000). Neuropsychiatric sequelae of traumatic brain injury. Psychosomatics, 41(2), 95-103. doi:10.1176/appi.psy.41.2.95• Rapoport, M.J., McCullagh, S., Shammi, P., and Feinstein, A. (2005). Cognitive impairment associated with major depression following mild and moderate traumatic brain injury. Journal of Clinical Neuropsychiatry and Clinical Neurosciences, 17(1), 61-65. doi:10.1176/appi.neuropsych.17.1.61• Roth, R.M., Flashman, L.A., Saykin, A.J., McAllister, T.W., and Vidaver, R. (2004). Apathy in schizophrenia: Reduced frontal volume and neuropsychological deficits American Journal of Psychiatry, 161(1), 157-159. doi:10.1176/appi.ajp.161.1.157 Schneiderman, A.I., Braver, E.R., and Kang, H.K. (2008). Understanding sequelae of injury mechanisms and mild traumatic brain injury incurred during the conflicts in Iraq and Afghanistan: persistent postconcussive symptoms and post-traumatic stress disorder. American Journal of Epidemiology, 167, 1446-1452. doi:10.1093/aje/kwn068• Silver, J.M., McAllister, T.W., and Arciniegas, D. (2009). Depression and cognitive complaints following
    42. 42. References• mild traumatic brain injury. American Journal of Psychiatry, 166(6). 653-661.• Silver, J.M., Yudofsky, S.C., Slater, J.A., Gold, R.K., Stryer, B.L., Williams, D.T., Wolland, H., and Endicott, J. (1999). Propranalol treatment of chronically hospitalized aggressive patients. Journal of Neuropsychiatry and Clinical Neurosciences, 11(3), 328-335. Smith, D.H., Meaney, D.F., and Shull, W.H. (2003). Diffuse axonal injury in head trauma. Journal of Head Trauma Rehabilitation, 18(4), 307-316. doi:10.1097/00001199-200307000-00003• Tenovuo, O. (2005). Central acetylcholinesterase inhibitors in the treatment of chronic traumatic brain injury: clinical experience in 111 patients. Progress in Neuro- Psychopharmacology and Biological Psychiatry, 29(1), 61- 67. doi:10.1016/j.pnpbp.2004.10.006• Terrio, H., Brenner, L.A., Ivins, B.J., Cho, J.M., Helmick, K., Schwalb, K., Scally, K., Bretthauer, R., and Warden, D. (2009) Traumatic brain injury screening; preliminary findings in a US Army Brigade Combat Team. Journal of Head Trauma Rehabilitation, 24, 14-23. doi:10.1097/HTR.0b013e31819581d8• Valzelli, L. (1981). Psychopharmacology of aggression: an overview. International Pharmacopsychiatry, 16(1), 39-48.• Waldron-Perrine, B., Hanks, R.A., and Perrine, S.A. (2008). Pharmacotherapy for postacute traumatic brain injury: a literature review for guidance in psychological practice. Rehabilitation Psychology, 53(4), 426-444. doi:10.1037/a0013530
    43. 43. References• Warden, D.L., Gordon, B. McAllister, T.W., Silver, J.M., Barth, J.T., Bruns, J., Drake, A., Gentry, T., Jagoda, A., Katz, D.I., Kraus, J., Labbate, L.A., Ryan, L.M., Sparling, M.B., Walters, B., Whyte, J., Zapata, A., and Zitnay, G. (2006). Guidelines for pharmacologic treatment of neurobehavioral sequelae of traumatic brain injury. Journal of Neurotrauma, 23(10), 1468-1501. doi:10.1089/neu.2006.23.1468• Warden, D. (2006). Military TBI during the Iraq and Afghanistan wars. Journal of Head Trauma Rehabilitation, 21, 398-402. doi:10.1097/00001199-200609000-00004• Whyte, J., Hart, T., Vaccaro, M., Grieb-Neff, P., Risser, A., Polansky, M., and Coslett, H.B. (2004) Effects of methylphenidate on attention deficits after traumatic brain injury: A multidimensional, randomized, controlled trial. American Journal of Physical and Medical Rehabilitation, 83(6), 401-420. doi:10.1097/01.PHM.0000128789.75375.D3• Whyte, J., Hart, T., Schuster, K., Fleming, M., Polansky, M., and Coslett, H.B. (1997). Effects of methylphenidate on attentional function after traumatic brain injury. A randomized placebo-controlled trial. American Journal of Physical and Medical Rehabilitation, 76(6), 440-450. doi:10.1097/00002060-199711000-00002.• Wightman, J.M., Gladish, S.L., (2001). Explosions and blasts injuries. Annals of Emergency Medicine, 37, 664-678. doi:10.1067/mem.2001.114906• Writer, B.W., and Schillerstrom, J.E. (2009). Psychopharmacological treatment for cognitive impairment in survivors of traumatic brain injury: a critical review. Journal of Neuropsychiatry and Clinical Neurosciences, 21(4), 362-370. doi:10.1176/appi.neuropsych.21.4.362
    44. 44. References• Zasler, N.D. (1999). Posttraumatic tension pneumocephalus. Journal of Head Trauma Rehabilitation, 14(1), 81-84. doi:10.1097/00001199-199902000-00009• Zhang, L., Plotkin, R.C., Wang, G., Sandel, M.E., and Lee, S. (2004). Cholinergic augmentation with donepezel enhances recovery in short-term memory and sustained attention after traumatic brain injury. Archives of Physical and Medical Rehabilitation, 85(7), 1050-1055. doi:10.1016/j.apmr.2003.10.014

    ×