Traumatic Brain Injury
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Traumatic Brain Injury
Dayna Ryan, PT, DPTWinter 2012
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TRAUMATIC BRAIN INJURY
• Lesion: Brain
• ~ 5 million persons living with TBI
• ~$60 billion in the United States in 2000
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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
~ 80% of TBI treated & released
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TBI INCIDENCE BY AGE (March 2010 CDC data)
Highest incidence among ages 0-4 (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.
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CAUSE OF TBI(March 2010 CDC data)
Falls are #1 cause of TBI among all age groups Highest 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
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RISK FACTORS Young (average age of TBI = 29 y. o.) Male Risk taking behaviors (age 15-24 y. o.) Low income inner city dwellers Substance abuse (50% hospitalizations by TBI due
to alcohol intoxication) Availability of firearm Previous TBI (e.g. sports-related concussions) Old age (more susceptible to tearing of blood
vessels, declines in cerebrovascular circulation, slower reaction time, movements & gait)
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CLASSIFICATION OF TBI (BY MECHANISM)
Open meninges have been breached, brain is exposed
Closed no skull fracture or laceration of the brain coup-contrecoup
Primary injury at impact2nd injury at the opposite side
Blast Blast wave from explosion hits the body Air-filled organ or brain surrounded by fluid are
particularly at risks of blast injuries
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Coup-Countercoup Injury
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CLASSIFICATION OF TBI- BY TYPES OF INJURIES
• Primary vs. Secondary (Biomolecular response to injury)– Primary = direct injury to the brain– Secondary = damage after the traumatic
event, caused by brain hypotension, hypoxia, or herniation
• Focal vs. Diffuse or a Combination of the Two– Focal = localized trauma (gun shot) – Diffuse = trauma over a large area (swelling)
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CLINICAL CLASSIFICATION OF TBI- BY SEVERITY OF DAMAGE
Mild (i.e. concussion): ~ 75% of TBI * Moderate Severe Classification Criteria & Prognosis
Types
Loss of Consciousness
(LOC)
Glasgow Coma Scale
Memory Loss
Prognosis
Mild
(Concussion)
< 30 min 13-15 < 24 hr Good Most recover
completely
Moderate
> 30 min < 24 hr
8-12 > 24 hr < 7 days
Good Learn to manage
problems resulting from TBI
Severe
> 24 hr <8 > 7 days
Most impossible to recover completely
Physical and/or cognitive disability
(* 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. )
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SPECIFIC INJURIES
Concussion (= mild TBI) Diffuse axonal injury Contusion Skull fracture Intracerebral hematoma Subdural hematoma Epidural hematoma Subarachnoid hemorrhage
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COMMON SYMPTOMS headache dizziness irritability decreased memory
&concentration
depression/anxiety fatigue sleep disturbance pain
THESE SYMPTOMS ARE ALSO COMMONIN THE GENERAL POPULATION AND AMONG
CHRONIC PAIN PATIENTS
Patient: MILD T.B.I. (Concussion)
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CONCUSSION (MILD TBI) Most common head injury Alteration of consciousness & memory Non-penetrating (non-opened) injury CT or MRI usually normal Good prognosis Cumulative effects of repeated concussion
can cause chronic dementia 50-100% mortality rate in second impact
syndrome seen in athletes a 2nd TBI while the 1st is NOT yet resolved
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Post-Concussion Syndrome Characterized by: dizziness,
disorientation, nausea, headache, fatigue
Also see decreased control of emotions and personality changes
Attention deficit usually present
**If concussion lasts >2 minutes, patient should be kept under observation
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DIFFUSE AXON INJURY (DAI) Severe and fatal head injuries Widespread axonal damage As a result of shear and tensile forces within
the brain Coma and decerebrate posturing Poor prognosis CT or MRI usually unremarkable
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CONTUSION Coup-countercoup injuries Can involve a small (mild) or large (severe)
area Most common in the frontal & temporal lobes Lesion often enlarge during the first week
after injuries
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HEMORRHAGE• Intracerebral hematoma• Subdural hematoma• Subarachnoid hemorrhage• Epidural hematoma
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• Intracerebral hematoma– In brain parenchyma– hematoma may enlarge during
the first few days after injury
• Subdural hematoma– Beneath the dura– Acute or chronic (>2 wk) – Laceration of bridging
cortical veins during sudden head deceleration
– A feature of shaken baby syndrome
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• Subarachnoid hemorrhage– Poor prognosis if bleeding
into ventricular system– Need to r/o aneurysm
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• Epidural hematoma– In epidural space– Between dura mater & skull– Acute bleeding– Common in temporal bone fracture
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Severe TBI Assess severity of brain injury Acute surgical care: expanding mass
lesion from increasing ICP Address life-threatening injuries (ABC
– airway, breathing, circulation) Prevent complications Preventative Rehab interventions
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GENERAL SYMPTOMS & SIGNS
Altered Level of Consciousness Cognitive & Behavioral Deficits Cranial Nerve Damages Motor Deficits Sensory Deficits
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Altered Level of Consciousness Reduction in response to stimuli Due to diffuse bilateral cerebral hemispheric
damage or a lesion in the brainstem Arousal is associated with wakefulness and
depends on an intact reticular formation and upper brainstem
Coma rarely last > 4 wks Coma is used to determine current status and
prognosis
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Altered Level of Consciousness
Coma: state of unresponsiveness; not opening eyes Persistent vegetative state or stupor: no evident
cerebral cortical function; eye opening with sleep-wake cycles
Obtundity: decreased interest in the environment; slowed responses to stimulation; sleep more than normal; drowsiness between sleep states
Lethargy: severe drowsiness; aroused by moderate stimuli & then drift back to sleep
Confusion: disorientation, bewilderment, and difficulty following commands
Clouding: inattention & reduced wakefulness
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COGNITIVE IMPAIRMENT Difficulties in:
Attention, concentration Learning, memory Abstract thinking, information processing Problem solving Initiation, executive functions Inaccurate perception (leaning)
Deficits often remain despite a full return of consciousness
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MEMORY DEFICITS IN TBI Retrograde amnesia
Loss 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 injury Inability to form new memory No carryover or tasks requiring memory / learning Duration of PTA indicates the severity of injury
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BEHAVIORAL IMPAIRMENT Mood disturbances including depression and
anxiety Symptoms depending on brain area involved
Inappropriate, excessive social behaviors Inappropriate sexual behaviors Irritability; rage; refuse to cooperate Euphoria; involuntary laughing or crying Apathy; indifference Motor, sensory, verbal perserveration
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CRANIAL NERVE DAMAGE Usually occur following focal damage in the
brainstem or herniation Disturbances in CN function
e.g. gaze and tracking deficits, diplopia, ptosis, facial sensory deficits, absent corneal reflex, hearing & vestibular dysfunction, cardiac irregularities, dysphagia, loss of gag reflex
CN dysfunction reflects level of lesion Normal pupillary reflex (to light) indicates a
lesion rostral to the midbrain
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MOTOR DEFICITS
Usually flaccid at onset Increased tone, spasticity and rigidity develop
gradually Decortical posturing
Hyperactive UE flexors Hyperactive LE extensors
Decerebrate posturing Hyperactive UE & LE extensors
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A. Decerebrate posturing seen in cerebral hemisphere/white matter, internal
capsule and thalamic lesions B. Decortical posturing
seen with midbrain lesions/compression; also with cerebellar and posteria fossa lesions
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MOTOR DEFICITS Monoplegia, hemiplegia Abnormal reflexes (e.g. palmar grasp & Babinski
reflex) Abnormal balance reactions Cerebellar and BG dysfunction: e.g. ataxia,
dysmetria, tremor, bradykinesia
SENSORY DEFICITS Somatosensory dysfunction is determined by the
brain area involved
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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
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INCREASED INTRACRANIAL PRESSURE (ICP)
Secondary complications develop over hours or days after the primary injury
Cause: swelling, fluid build-up in the brain & hematomas
Increased ICP compresses the brain within the rigid skull
Serious, life-threatening ICP monitoring:
Medications Fluid management Decompressive craniectomy
Lynda Yang http://www-personal.umich.edu/~chronis/ICP.html
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Cycle of Primary and Secondary Injury
Cerebral Perfusion Pressure = Mean Arterial Pressure - Intracranial Pressure
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• Abnormal bone growth around a joint • Most commonly in hips, elbows, shoulders
and knees• Onset 4-12 wk after injury• Diagnostic test
– X-ray– Bone scan with increased uptake– Elevation of alkaline phospatase
• Symptoms and signs– loss of ROM, tenderness, palpable mass,
redness, swelling, pain with movement
HETEROTOPIC OSSIFICATION
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DIAGNOSIS OF TBI
• History • Clinical exam• Imaging• Functional capacity
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• Magnitude of injury• Altered consciousness and memory
– witnessed– self-report
• Duration of coma correlates with severity of injury
HISTORY
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CLINICAL EXAM
• Evidence of trauma • Glasgow Coma Scale• Ranchos Los Amigos Cognitive Scale• Post-traumatic amnesia
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GLASGOW COMA SCALE
EYE OPENING SCORE spontaneous E4 to speech E3 to pain E2 none E1
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GLASGOW COMA SCALE
VERBAL RESPONSE SCORE appropriate V5 confused, disoriented V4 inappropriate words V3 unintelligible V2 none V1
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GLASGOW COMA SCALE MOTOR RESPONSE SCORE
Follows commands M6 Localized (to pain) M5 Generalized (to pain) M4 Decorticate posturing (flexion) M3 Decerebrate posturing (extension) M2 None M1
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GLASGOW COMA SCALE
Most accurate early in course >12 = Mild 9-12 = Moderate <8 for longer than 6 hours = severe
3 = Dead
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RANCHO LOS AMIGOS COGNITIVE SCALE
I. no response
II. generalized
response
III. localized
response
IV. confused, agitated
V. confused, inappropriate
VI. confused, appropriate
VII. automatic, appropriate
VIII. purposeful, appropriate
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Diagnostic Imaging
CT MRI DTI SPECT PET
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Computed Tomography Anatomic
Bone & brain tissue Can see damage to gray matter
1st line of imaging studies Rapid (< 1 min for whole brain) Less costly Accessible (even with monitor, life-support equipment,
or combative patient)
Best for skull fx, hemorrhage vs. edema, & intracerebral hemorrhage
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Computed Tomography
Abnormal findings in ~ 18% of patients without neurologic deficits
Severity of findings correlates with outcome Not sensitive enough in detecting mild TBI
(concussion) May underestimate non-hemorrhagic lesion May not show non-hemorrhagic parenchymal
(neurons and glial cell) injuries
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M.R.I. Anatomic Most sensitive 24-48 hours after injury Higher resolution than CT Better for hemorrhagic contusions (after first 24
hours) More sensitive than CT to diffuse axon injury Scans > 6 months post-injury correlate with outcome Disadvantage compared to CT
Duration of scan time, more costly Not for combative patients
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Diffusion Tensor Imaging Neuroimaging that builds on MRI technology Study movement of fluid in the brain Detect damage in the white matter (axons) Axons are colored according to orientation
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Single Photon Emission Computed Tomography (S.P.E.C.T.)
Injection of a small amount of short-lived radioactive particles into the blood
Image of regional blood flow More sensitive than MRI Limited value in acute stage Abnormal in many patients with normal
neurologic exam, CT, and MRI Poor image resolution Not readily available
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Positron Emission Tomography Study metabolic activity and function Used in mild TBI
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NEUROPSYCHOLOGICAL TESTING Standardized measure to assess
Memory Concentration Attention Motor control Processing / Decision making
Use testing findings to Plan and implement treatment Monitor progress Return to work
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ACUTE TBI MEDICAL AND SURGICAL MANAGEMENT Surgery (e.g. for hemorrhage; reduce ICP) Monitor intracranial pressure (ICP) Cerebral vasoconstrictive agents to decrease
cerebral blood volume Mannitol Barbiturates Etomidate Proprofol
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SUBACUTE AND CRHONIC TBI MEDICAL AND SURGICAL MANAGEMENT Spasticity medications
Bacolfen Diazepam Dantrolene
Seizure control Depakote
Depression Non-tricyclic antidepressants
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CONDITONS PREDICTING POOR PROGNOSIS IN TBI
Loss of pupillary light reflexes Oculomotor deficits Significant damage to brainstem Midline shift of brain structures Acute hemispheric swelling with extra-cerebral
hematoma Multiple small hemorrhages Skull is fractured Subarachnoid hemorrhage Diffuse axon injury Rigidity persists Epilepsy develops within first 7 days of injury Long duration of post-traumatic amnesia
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FUNCTIONAL CONSIDERATIONS
If with NG tube is in place Head of bed > 30º to avoid aspiration
If chest tubes are in place Drainage tube should be kept below level of chest
at all times
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PRECAUTIONS AND CONTRAINDICATIONS
In presence of increased intracranial pressure Pulmonary PT (percussion and vibration) may be
contraindicated
Hetertopic ossification developed 4-12 weeks following TBI Palpable tenderness and mass by a joint from
abnormal bone growth Can decrease ROM