traumatic brain injury

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

GENERAL SYMPTOMS & SIGNS

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 http://www-personal.umich.edu/~chronis/ICP.html

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

HETEROTOPIC OSSIFICATION

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

GLASGOW COMA SCALEMOTOR RESPONSE SCOREFollows comm