traumatic brain injury

Click here to load reader

Post on 02-Jan-2016




5 download

Embed Size (px)


Traumatic Brain Injury. Dayna Ryan, PT, DPT Winter 2012. TRAUMATIC BRAIN INJURY. Lesion: Brain ~ 5 million persons living with TBI ~$60 billion in the United States in 2000. TBI INCIDENCE (March 2010 CDC data). ~ 80% of TBI treated & released. - PowerPoint PPT Presentation


  • Traumatic Brain InjuryDayna Ryan, PT, DPTWinter 2012

  • TRAUMATIC BRAIN INJURY Lesion: Brain ~ 5 million persons living with TBI ~$60 billion in the United States in 2000

  • TBI INCIDENCE (March 2010 CDC data)~ 1. 7 million TBI occur in the US annually TBI rates among individuals younger than 65 y. o.Male : Females = 1.4 : 1

  • TBI INCIDENCE BY AGE (March 2010 CDC data)Highest incidence among ages0-4 (children), 15-19 (teens), 65+ (elderly)~ 90% ER visits by children aged 0-14 y. o.Highest rates of TBI-related hospitalizations & deaths occur in adults aged > 75 y. o.

  • CAUSE OF TBI(March 2010 CDC data)Falls are #1 cause of TBI among all age groupsHighest rates of fall-related TBI in children 0-4 y.o. & adults > 75 y.o. Highest rates of motor vehicle & assault-related TBI among adults aged 20-24 y.o.Alcohol involved in >50% of cases

  • RISK FACTORSYoung (average age of TBI = 29 y. o.)MaleRisk taking behaviors (age 15-24 y. o.)Low income inner city dwellersSubstance abuse (50% hospitalizations by TBI due to alcohol intoxication)Availability of firearmPrevious TBI (e.g. sports-related concussions)Old age (more susceptible to tearing of blood vessels, declines in cerebrovascular circulation, slower reaction time, movements & gait)

  • CLASSIFICATION OF TBI (BY MECHANISM)Openmeninges have been breached, brain is exposedClosedno skull fracture or laceration of the braincoup-contrecoupPrimary injury at impact2nd injury at the opposite sideBlastBlast wave from explosion hits the bodyAir-filled organ or brain surrounded by fluid are particularly at risks of blast injuries

  • Coup-Countercoup Injury

  • CLASSIFICATION OF TBI - BY TYPES OF INJURIESPrimary vs. Secondary (Biomolecular response to injury)Primary = direct injury to the brainSecondary = damage after the traumatic event, caused by brain hypotension, hypoxia, or herniation Focal vs. Diffuse or a Combination of the TwoFocal = localized trauma (gun shot) Diffuse = trauma over a large area (swelling)

  • CLINICAL CLASSIFICATION OF TBI- BY SEVERITY OF DAMAGE Mild (i.e. concussion): ~ 75% of TBI *ModerateSevere Classification Criteria & Prognosis

    (* Centers for Disease Control and Prevention (CDC), National Center for Injury Prevention and Control. Report to Congress on mild traumatic brain injury in the United States: steps to prevent a serious public health problem. Atlanta (GA): Centers for Disease Control and Prevention; 2003. )

  • SPECIFIC INJURIES Concussion (= mild TBI)Diffuse axonal injuryContusionSkull fractureIntracerebral hematomaSubdural hematomaEpidural hematomaSubarachnoid hemorrhage

  • COMMON SYMPTOMSheadachedizzinessirritabilitydecreased memory &concentrationdepression/anxietyfatiguesleep disturbancepainTHESE SYMPTOMS ARE ALSO COMMONIN THE GENERAL POPULATION AND AMONG CHRONIC PAIN PATIENTSPatient: MILD T.B.I. (Concussion)

  • CONCUSSION (MILD TBI)Most common head injuryAlteration of consciousness & memoryNon-penetrating (non-opened) injuryCT or MRI usually normalGood prognosisCumulative effects of repeated concussioncan cause chronic dementia50-100% mortality rate in second impact syndrome seen in athletesa 2nd TBI while the 1st is NOT yet resolved

  • Post-Concussion SyndromeCharacterized by: dizziness, disorientation, nausea, headache, fatigueAlso see decreased control of emotions and personality changesAttention deficit usually present

    **If concussion lasts >2 minutes, patient should be kept under observation

  • DIFFUSE AXON INJURY (DAI)Severe and fatal head injuriesWidespread axonal damageAs a result of shear and tensile forces within the brainComa and decerebrate posturingPoor prognosisCT or MRI usually unremarkable

  • CONTUSIONCoup-countercoup injuriesCan involve a small (mild) or large (severe) areaMost common in the frontal & temporal lobes Lesion often enlarge during the first week after injuries

  • HEMORRHAGEIntracerebral hematomaSubdural hematomaSubarachnoid hemorrhageEpidural hematoma

  • Intracerebral hematomaIn brain parenchymahematoma may enlarge during the first few days after injury

    Subdural hematomaBeneath the duraAcute or chronic (>2 wk) Laceration of bridgingcortical veins during sudden head decelerationA feature of shaken baby syndrome

  • Subarachnoid hemorrhagePoor prognosis if bleeding into ventricular systemNeed to r/o aneurysm

  • Epidural hematomaIn epidural spaceBetween dura mater & skullAcute bleedingCommon in temporal bone fracture

  • Severe TBIAssess severity of brain injuryAcute surgical care: expanding mass lesion from increasing ICPAddress life-threatening injuries (ABC airway, breathing, circulation)Prevent complicationsPreventative Rehab interventions


    Altered Level of ConsciousnessCognitive & Behavioral DeficitsCranial Nerve DamagesMotor DeficitsSensory Deficits

  • Altered Level of ConsciousnessReduction in response to stimuliDue to diffuse bilateral cerebral hemispheric damage or a lesion in the brainstemArousal is associated with wakefulness and depends on an intact reticular formation and upper brainstemComa rarely last > 4 wksComa is used to determine current status and prognosis

  • Altered Level of Consciousness Coma: state of unresponsiveness; not opening eyesPersistent vegetative state or stupor: no evident cerebral cortical function; eye opening with sleep-wake cyclesObtundity: decreased interest in the environment; slowed responses to stimulation; sleep more than normal; drowsiness between sleep statesLethargy: severe drowsiness; aroused by moderate stimuli & then drift back to sleepConfusion: disorientation, bewilderment, and difficulty following commandsClouding: inattention & reduced wakefulness

  • COGNITIVE IMPAIRMENTDifficulties in:Attention, concentrationLearning, memoryAbstract thinking, information processingProblem solvingInitiation, executive functionsInaccurate perception (leaning)

    Deficits often remain despite a full return of consciousness

  • MEMORY DEFICITS IN TBIRetrograde amnesiaLoss of memory of events immediately preceding the injury

    Post-traumatic amnesia (PTA) (impaired anterograde memory) (50 first dates)Unable to recall events that occur after the injuryInability to form new memoryNo carryover or tasks requiring memory / learningDuration of PTA indicates the severity of injury

  • BEHAVIORAL IMPAIRMENTMood disturbances including depression and anxietySymptoms depending on brain area involvedInappropriate, excessive social behaviorsInappropriate sexual behaviorsIrritability; rage; refuse to cooperateEuphoria; involuntary laughing or cryingApathy; indifferenceMotor, sensory, verbal perserveration

  • CRANIAL NERVE DAMAGEUsually occur following focal damage in the brainstem or herniationDisturbances in CN functione.g. gaze and tracking deficits, diplopia, ptosis, facial sensory deficits, absent corneal reflex, hearing & vestibular dysfunction, cardiac irregularities, dysphagia, loss of gag reflexCN dysfunction reflects level of lesionNormal pupillary reflex (to light) indicates a lesion rostral to the midbrain

  • MOTOR DEFICITSUsually flaccid at onsetIncreased tone, spasticity and rigidity develop gradually Decortical posturingHyperactive UE flexorsHyperactive LE extensors Decerebrate posturingHyperactive UE & LE extensors

  • A. Decerebrate posturingseen in cerebral hemisphere/white matter, internal capsule and thalamic lesionsB. Decortical posturing seen with midbrain lesions/compression; also with cerebellar and posteria fossa lesions

  • MOTOR DEFICITSMonoplegia, hemiplegiaAbnormal reflexes (e.g. palmar grasp & Babinski reflex)Abnormal balance reactionsCerebellar and BG dysfunction: e.g. ataxia, dysmetria, tremor, bradykinesia

    SENSORY DEFICITSSomatosensory dysfunction is determined by the brain area involved

  • COMPLICATIONS Increased intracranial pressure (ICP) Heterotoptic ossification: osteoclast destroy bone, so increase od Ca in blood, form boney spurs at joint. DVT Spasticity / Contracture Decubitus ulcer (tuberosity) Seizure

  • INCREASED INTRACRANIAL PRESSURE (ICP)Secondary complications develop over hours or days after the primary injuryCause: swelling, fluid build-up in the brain & hematomasIncreased ICP compresses the brain within the rigid skullSerious, life-threatening ICP monitoring:Medications Fluid managementDecompressive craniectomy Lynda Yang

  • Cycle of Primary and Secondary InjuryCerebral Perfusion Pressure = Mean Arterial Pressure - Intracranial Pressure

  • Abnormal bone growth around a joint Most commonly in hips, elbows, shoulders and kneesOnset 4-12 wk after injuryDiagnostic testX-rayBone scan with increased uptakeElevation of alkaline phospataseSymptoms and signsloss of ROM, tenderness, palpable mass, redness, swelling, pain with movement


  • DIAGNOSIS OF TBIHistory Clinical examImagingFunctional capacity

  • Magnitude of injuryAltered consciousness and memorywitnessedself-reportDuration of coma correlates with severity of injuryHISTORY

  • CLINICAL EXAMEvidence of trauma Glasgow Coma ScaleRanchos Los Amigos Cognitive ScalePost-traumatic amnesia

  • GLASGOW COMA SCALEEYE OPENINGSCOREspontaneousE4 to speechE3to painE2noneE1

  • GLASGOW COMA SCALEVERBAL RESPONSE SCOREappropriate V5confused, disoriented V4inappropriate words V3unintelligible V2none V1


View more