traumatic brain injury

Traumatic Brain Injury

Dayna 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

~ 80% of TBI treated & released

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.

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

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)

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

Coup-Countercoup Injury

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)

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. )

SPECIFIC INJURIES

Concussion (= mild TBI) Diffuse axonal injury Contusion Skull fracture Intracerebral hematoma Subdural hematoma Epidural hematoma Subarachnoid hemorrhage

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)

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

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

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

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

HEMORRHAGE• Intracerebral hematoma• Subdural hematoma• Subarachnoid hemorrhage• Epidural hematoma

• 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

• Subarachnoid hemorrhage– Poor prognosis if bleeding

into ventricular system– Need to r/o aneurysm

• Epidural hematoma– In epidural space– Between dura mater & skull– Acute bleeding– Common in temporal bone fracture

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

GENERAL SYMPTOMS & SIGNS

Altered Level of Consciousness Cognitive & Behavioral Deficits Cranial Nerve Damages Motor Deficits Sensory Deficits

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

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

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

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

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

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

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

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

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

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 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

Cycle of Primary and Secondary Injury

Cerebral Perfusion Pressure = Mean Arterial Pressure - Intracranial Pressure

• 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

DIAGNOSIS OF TBI

• History • Clinical exam• Imaging• Functional capacity

• Magnitude of injury• Altered consciousness and memory

– witnessed– self-report

• Duration of coma correlates with severity of injury

HISTORY

CLINICAL EXAM

• Evidence of trauma • Glasgow Coma Scale• Ranchos Los Amigos Cognitive Scale• Post-traumatic amnesia

GLASGOW COMA SCALE

EYE OPENING SCORE spontaneous E4 to speech E3 to pain E2 none E1

GLASGOW COMA SCALE

VERBAL RESPONSE SCORE appropriate V5 confused, disoriented V4 inappropriate words V3 unintelligible V2 none V1

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

GLASGOW COMA SCALE

Most accurate early in course >12 = Mild 9-12 = Moderate <8 for longer than 6 hours = severe

3 = Dead

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

Diagnostic Imaging

CT MRI DTI SPECT PET

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

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

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

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

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

Positron Emission Tomography Study metabolic activity and function Used in mild TBI

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

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

SUBACUTE AND CRHONIC TBI MEDICAL AND SURGICAL MANAGEMENT Spasticity medications

Bacolfen Diazepam Dantrolene

Seizure control Depakote

Depression Non-tricyclic antidepressants

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

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

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