Traumatic brain injury


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  • International brain injury association
  • a child’s brain is in an almost constant state of development
  • post-traumatic amnesia (PTA), and loss of consciousness (LOC) Department of Defense and Department of Veterans Affairs 
  • Damage may occur directly under the site of impact, or it may occur on the side opposite the impact (coup and contrecoup injury, respectively). When a moving object impacts the stationary head, coup injuries are typical,while contrecoup injuries are usually produced when the moving head strikes a stationary object
  • Epidural--arterial bleeding,quick onset, less common Subdural-- venous bleeding
  • Pupilary dilatation- serious
  • Areas involved in social behavior, emotion regulation, olfaction, and decision-making, hence the common social/emotional and judgment deficits
  • difficulty identifying feelings and distinguishing between feelings and the bodily sensations of emotional arousal difficulty describing feelings to other people constricted imaginal processes, as evidenced by a scarcity of fantasies
  • The possibility that there may be a statistical link between Alzheimer’s disease and earlier head trauma remains intriguing. This could be explained by increased β-amyloid deposition in the cortex in the wake of trauma (see above). An alternative explanation is that the reduced neuronal reserve brought about by the head injury brings forward the clinical presentation of dementia in those patients who would have developed a dementia anyway, regardless of the head injury.
  • Phineas Gage. his personality changes: from being a responsible and socially well-adapted man, Gage became negligent, irreverent and profane, unable to take responsibility
  • lack of insight into the injury and its effects
  • During the post-traumatic delirium some patients pass through an excitable and overactive phase
  • Low levels of serotonin
  • Traumatic brain injury

    1. 1. Traumatic brain injuryDr. Syed Faheem ShamsMD (Part III) studentDept. of PsychiatryBSMMU
    2. 2. ObjectivesTraumatic brain injury-What? Epidemiology? Cause andeffect?Types? When to give attention?Why we need to know?
    3. 3. Brain InjuriesBrain InjuriesCongenital brain injuryPre-birth During birthAcquired Brain InjuryAfter birth processTraumatic Brain Injury(external physical force)Non-traumaticBrain InjuryClosed HeadInjuryOpen HeadInjury
    4. 4. What is a TBI?What is a TBI?Sudden damage to the brain due to anSudden damage to the brain due to anexternal forceexternal force
    5. 5. Two types of TBITwo types of TBIOPEN-HEAD INJURY(penetrating)Example:• Skull fracture thatpenetrates the brain• Gunshot woundCLOSED-HEAD INJURY(non penetrating)when the head forcefullywhen the head forcefullycollides with anothercollides with anotherobjectobjectExample:• Coup-Contra Coup• Diffuse axonal injury
    6. 6. ICD-10 S 06- Intracranial injuryS06.0 ConcussionCommotio cerebriS06.1 Traumatic cerebral oedemaS06.2 Diffuse brain injuryCerebralcontusion NOSlaceration NOSTraumatic compression of brain NOSS06.3 Focal brain injuryFocal:cerebral:contusionlacerationtraumatic intracerebral haemorrhageS06.4 Epidural haemorrhageExtradural haemorrhage (traumatic)S06.5 Traumatic subdural haemorrhageS06.6 Traumatic subarachnoid haemorrhageS06.7 Intracranial injury with prolonged comaS06.8 Other intracranial injuriesTraumatic haemorrhage:cerebellarintracranial NOSS06.9 Intracranial injury, unspecifiedBrain injury NOS
    7. 7. Brain Injury FactsWorldwide• Brain injury is the leading cause of deathand disability• Traumatic brain injury is the leading causeof seizure disorders• The global incidence rate of TBI isestimated at 200/100 000 people per year
    8. 8. Brain Injury Facts(contd.)United States Europe01 million hospitaladmissions per yearIn the south of Europe, themain cause --trafficaccidentsIn the north of Europe, themajor causes- falls,mainly related to alcoholuse (Tagliaferri et al 2006) million Treated andreleasedfrom hospital80,000 Some TBI-relateddisability50,000 dieMales>females15-24 years
    9. 9. EpidemiologyEpidemiologyPercentage of Average Annual TBI-related emergency department visits,Percentage of Average Annual TBI-related emergency department visits,hospitalizations, and deaths, by External Cause, United States, 1995-2001hospitalizations, and deaths, by External Cause, United States, 1995-2001Falls, 28%Motor Vehicle-Traffic, 20%StruckBy/Against, 19%Assault, 11%Unknown,9%Other, 7%Pedal Cycle(non MV), 3%Suicide, 1%Other Transport,2%
    10. 10. The greatest number of TBIs occur in people aged15–24TBI rates are higher in malesOccupational Therapy and Physical Dysfunction: Principles, Skills and Practice.Edinburgh: Churchill Livingstone. pp. 395–96
    11. 11. TBI in children can beTBI in children can beespecially devastatingespecially devastating
    12. 12. Brain Rates of DevelopmentBrain Rates of DevelopmentP-OCTF-TP-OCF-T P-OTCF-T5 DistinctPeriods ofMaturationP - O parietal/occipitalC central(limbic &brainstem)T temporalF - T frontal/temporal
    13. 13. Severity of traumatic braininjuryGCS PTA LOCMild 13-15 <1 day 0-30 minModerate 9-12 >1- 14 days >30 min–6 hrsSevere 3-8 >14 days >6 hrsLishman’s Organic psychiatry, 4thedition
    14. 14. In severe diffuse traumatic injury:PTA (weeks) = 0.4 × LOC (days) + 3.6Katz and Alexander (1994)
    15. 15. Brain ConcussionBrain Concussion• Impaired function• No structural damage• Extreme variance in severity– LOC• Diffuse
    16. 16. CONCUSSION vs CONTUSIONCONCUSSION• Temporary loss ofneurologic functionwith no structuraldamage lasting for afew seconds to fewminutesCONTUSION• More severe injury inwhich the brain isbruised, with possiblesurface hemorrhage• Unconscious for morethan a few seconds orminutes• Picture is somewhatsimilar to that ofshock
    17. 17. Coup Contra-Coup InjuryCoup Contra-Coup Injury
    18. 18. Epidural haemorrhage Subdural haemorrhage
    19. 19. Subarachnoid haemorrhage
    20. 20. ManagementManagementThe acute management of severeThe acute management of severetraumatic brain injury:traumatic brain injury:– 1. Protect the airway & oxygenation– 2. Ventilate to normocapnia– 3. Correct hypovolaemia & hypotension– 4. CT Scan when appropriate– 5. Neurosurgery if indicated– 6. Intensive Care for further monitoring andmanagement
    21. 21. Significant Head InjuriesSignificant Head InjuriesSigns of increased ICP---Signs of increased ICP---–Visual difficultiesVisual difficulties–VomitingVomiting–DyspneaDyspnea– BradycardiaBradycardia
    22. 22. How Brain Injuries treated?How Brain Injuries treated?
    23. 23. Interesting findingsThe most common areas to have focallesions in non-penetrating traumatic braininjury are the orbitofrontal cortex and theanterior temporal lobes"Frontal lobe dysfunction following closed head injury. A review of the literature". Journal of Nervous & MentalDisorders 178 (5): 282–291. "Deformation of the human brain induced by mild acceleration". Journal ofNeurotrauma 22 (8): 845–856."Frontal-subcortical circuits and human behavior".Archives of Neurology 50 (8): 873–880."TASIT: A new clinical tool for assessing social perception after traumatic brain injury". Journal of Head TraumaRehabilitation 18 (3): 219–238.
    24. 24. Interesting findings (contd.)• Alexithymia, a deficiency in identifying,understanding, processing, and describingemotions occurs in 60.9% of individualswith TBIAlexithymia and emotional empathy following traumatic brain injury". J Clin ExpNeuropsychol 32 (3): 259–67.
    25. 25. Is head injury a risk fordementia??β-amyloid protein have been found toaccumulate in about 30% of patients afterTBI and may form plaques(Roberts et al. 1994; Ikonomovic et al. 2004)However, some groups have failed to findelevated Aβ after head injury(Adle-Biassette et al. 1996; Macfarlane et al. 1999)
    27. 27. Adolf Meyer published comprehensivecase reports about patients whopresented behavior disturbances afterhead injuries and proposed a set ofdisorders called “traumatic insanities”,which included consciousness alterations,psychosis, and neurological symptoms (Neylan 2000)
    28. 28. Post-traumatic delirium (post-traumaticconfusional state) and post-traumaticamnesiaPost-traumatic delirium (confusional state)shows much variation, depending on theseverity of the injury and its complications
    29. 29. Post-traumatic deliriumApathetic Restless, Irritability Florid delirious statesWithdrawalFear, persecutory beliefs, and perplexity are commonDisorientation for time and place is marked at first
    30. 30. Post-traumatic delirium (contd.)As the confusional state improves,confabulations come to dominate, almostalways accompanied by lack of insight anddisorientationAssociated with misinterpretation ofsurroundings and misidentification of people. Itis not unusual for patients to believe that staff orother patients on the ward are familiar to themHallucinatory experiences may be troublesome;visual hallucinations are most evident
    31. 31. Post-traumatic agitationPatient may be abusive, aggressive,sexually disinhibitedOccurs in about 10% of patients withsevere brain injury (Brooke et al. 1992)Last a few daysAgitated behavior is associated withfrontotemporal injury and doubles the riskof later emotional sequelae (van der Naalt et al.2000).
    32. 32. Post-traumatic amnesiaIt ends at the time from which the patientcan later give a clear and consecutiveaccount of what was happening aroundhimPeriod of unconsciousness + Post-traumatic delirium
    33. 33. Post-traumatic amnesia (contd.)A study of orientation during PTA showedthat the usual sequence of recovery wasfor person place time (Levin 1990).
    34. 34. Summary of findings fordepression after TBIIncidence 15.3%–33%Kim et al 2007 Prevalence 18.5%–61%Kim et al 2007 Abnormalities on CTLevin et al 2005 Lower bilateralhippocampal volumeJorge et al 2007   Volume reduction of the leftprefrontal grey matterJorge et al 2004UnemploymentSeel et al 2003; Dikmen et al 2004; Jorge et al 2004 Lower economic status;aggression; anxietyDikmen et al 2004 
    35. 35. Why depression?Rupture of neural circuits involving theprefrontal cortex, amygdala,hippocampus, basal ganglia, andthalamus may be related to thedevelopment of depression due TBI. (Jorge and Starkstein 2005)The hippocampus is an anatomic regionvulnerable to TBI (Campbell and MacQueen 2004)
    36. 36. Treatment of depression in TBICitalopram and sertraline (Turnes-Stokes and MacWalter 2005).Citalopram (Rapoport et al 2008).The use of fluoxetine, paroxetine,venlafaxin, minalcipran, amitryptiline,desipramine, bupropio presentedgenerally positive results (Alderfer et al 2005;Warden et al 2006).
    37. 37. Caution with TCAsAnticholinergic effects of TCAs canexacerbate cognitive impairment.
    38. 38. Summary of findings for Maniaafter TBIIncidence 9%Jorge et al 1999Prevalence 4.2%van Reekum et al 2000 Higher rates for menvan Reekum et al 1996 Lesions in the temporal basal polesJorge et al 1993b; Murai and Fujimoto 2003 
    39. 39. Treatment of Mania in TBIValproic acid and lithium, while casereports pointed out the usefulness ofquetiapine, carbamazepine, clonidine, andelectroconvulsive therapy(Warden et al 2006; Oster et al 2007)
    40. 40. Summary of findings forPsychosis after TBIIncidence 0.1%–9.8%David and Prince 2007 Prevalence 0.7%van Reekum et al 2000  Damage in frontal and temporal lobesAchte 1969; Sachdev et al 2001; Fujii and Ahmed 2002a Predominance of positive symptomsSachdev et al 2001 Persecutory (56%), reference (22%), control(22%), and grandiosity (20%).Fujii and Ahmed (2001)
    41. 41. Treatment of Psychosis in TBITypical antipsychotics haveanticholinergic, hypotensive, or sedativeeffects, or a strong dopaminergicantagonism are potentially able to worsenthe already existent deficits for TBIsurvivors.(Feeney et al 1982; Goldstein 1993)
    42. 42. Summary of findings for OCDafter TBIPrevalence 1.6%–15%Hibbard et al 1998; Deb et al 1999 Oribitofrontal cortex, cingulate cortex and caudatenucleus damageBerthier et al 2001; Bilgic et al 2004; Ogai et al 2005 Obsessive slowness; compulsive exercisespractice; aggressionBerthier et al 2001
    43. 43. Summary of findings for PTSDafter TBIIncidence 11.3%–24%Bryant and Harvey 1998; Bombardier et al 1999 Prevalence 3%–27.1%Bryant et al 2000; Glaesser et al 2004 Impaired quality of life and social function; chronicpainBryant et al 1999 Posttraumatic amnesia as a protective factorSbordone and Liter 1995; Glaesser et al 2004; Gil et al 2005 
    44. 44. Summary of findings forPersonality change after TBIApathy Prevalence 34.5% after severe TBIPelegrín-Valero et al 2001 Younger age; more severe TBIKant et al 1998 Affective lability Prevalence 5%–32.7%Zeilig et al 1996; Pelegrín-Valero et al 2001 Frontal lobe damage; aggression; anxietyRobinson et al 1993Aggression Prevalence 16.4%–33.7%Pelegrín-Valero et al 2001; Tateno et al 2003 
    45. 45. Predictors of poor outcome• “ Poor response to psychiatric medications• “ Failure in behavioral programs requiringmemory and problem-solving• “ Social network failure: divorce, separation• Failure at work• “Persistence of chronic pain and headachesymptoms• “Lack of support system
    46. 46. OUTCOME In Severe BraininjuryGood recovery 25-30%Moderate disability 15-20%Sever disability 15%Vegetative stat 5%Death 30-35%
    47. 47. Thank you all !!