Mild Traumatic Brain Injury: Current Diagnosis and Management

Kathleen R. Bell, MD

Department of Rehabilitation Medicine

University of Washington

May 6, 2004

Overview

Why do we care about mild TBI? TBI overview and spectrum Mild traumatic brain injury

– Mechanism of injury– Presentation– Dilemmas in diagnosis and definition– Medical issues and management

Mild Traumatic Brain Injury

Why do we care?

What is concussion?

Mild Traumatic Brain Injury (MTBI) Defined by symptoms (1 or more)

– Any period of observed or self-reported Transient confusion, disorientation or impaired

consciousness Dysfunction of memory around the time of the injury Loss of consciousness lasting less than 30 minutes

Observed signs of neurological or neuropsychological problem– Seizures right afterwards– Young children – irritability, lethargy, vomiting– Symptoms like headache, dizziness, irritability,

fatigue or poor concentration soon after injury

Traumatic Brain Injury

1. Incidence - 500,000 admitted cases per year estimated 1.5 million sustain non-fatal brain injury

never admitted 2. Severity - 80% mild TBI, remaining 20% 3. Gender - male preponderance in more severe TBI,

possible female preponderance in mild TBI 4. Age - young adults 15-24 years (infants, children,

elderly); wider ranger for mild

How often does it happen?

Centers for Disease Control estimates:– 1.5 million people a year have a TBI– About 75% of these are mild (like concussions)– Don’t really know how many because:

No one keeps track outside of hospitals Lots of concussions aren’t reported to anyone

Etiology of TBI

1. No study has specifically focussed on mild TBI

2. Leading Cause - MVA approx. 28-50% 3. Falls 20-30% (infants, children, elderly) 4. Assaults 9-10% 5. Sports and recreational - 10-20%

Costs of TBI

For TBI associated with hospitalization and rehabilitation: $37 billion dollars in direct and indirect costs

For mild TBI: ?

Mechanisms of Severe TBI Penetrating (hi velocity, more damage) Closed/Moderate-Severe

High velocity translational (inferior frontal and temporal lobes)

High velocity rotational (shearing at grey-white interface)

Blunt Force skull fracture contusion at point of impact contrecoup injury (fall)

– Space occupying lesions epidural hematomas 6% - good recovery subdural hematomas 24% intracerebral hemorrhage/intraventricular hemorrhage temporal lobe contusion/bleed - transtentorial herniation

– Basilar skull fractures infection, CSF leaks

Secondary Brain Injury– altered cerebral blood flow– hypotension (relationship to ICP and CPP)– release of neurotoxic compounds

cellular inflammatory response cytokines calcium influx oxygen free radicals

What Happens in Mild TBI?

Because full recovery often occurs, must be temporary neuronal dysfunction rather than cell death– Ionic shifts– Altered metabolism– Impaired connectivity– Changes in neurotransmission

Acute Metabolic/Ionic Changes

Disruption of neuronal membranes and axonal stretching– Increase in extracellular potassium– Release of excitatory amino acid (EAA) glutamate

Increases kainate, NMDA, D-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA)

– Increases extracellular potassium and so on

“Spreading depression”

This cascade results in neuronal depression May be the cause of early loss of

consciousness, amnesia, and other cognitive dysvunction

Manning the pumps

To head off further ionic fluxes:– Activation of membrane pumps

Increase in glucose use– Results in glycolysis

Glyocolysis and poor mitochondrial function– Results in increased lactate production

Results in neuronal dysfunction: acidosis, membrane damage, altered blood brain barrier permeability, and edema

Further disruptions

Cerebral blood flow usually matches up to glucose metabolism– BUT after a percussion injury to the brain, the

cerebral blood flow drops– Now have a mismatch in supply (blood) and

demand (increased neuronal metabolism)

Other Ion Malfunctions

Calcium accumulation in the cells because of EAA

Calcium gums up the mitochondria, impairing energy production in the cerebral cortex and the hippocampus

Global decreases in cerebral glucose metabolism lasting 2-4 weeks after injury (present regardless of severity of injury)

Still more problems

Reduced intracellular magnesium levels (correlated with neurologic deficits)– Results in reduced glyocolytic and oxidative

energy production, disordered membrane function, and decreased protein synthesis

– Higher flux of calcium

Mechanical axonal disruption

Stretching of axons can occur immediately and axonal disconnection can persist for days or weeks– Blocks neuronal transmission by treakdown of the

microtubules

Neurotransmitter alterations

Postconcussive alterations in– Glutamatergic (NMDA) systems– Adrenergic systems– Cholinergic systems

Impaired long-term potentiation (NMDA dependent) in hippocampus

Changes in choline acetyltransferase activity and loss of forebrain cholinergic neurons – learning and memory

Other Mechanisms of Mild TBI

Acceleration-deceleration mechanism– Mild diffuse axonal injury without shear

“strain” to neural tissue - affecting intra-axonal neurofilament organization

– Focal contusions in white matter– Labyrinth injury– Subtle changes in blood-brain barrier inducing

neurotransmitter release

Diagnostic dilemma

Defining the lower and upper limits of mild TBI

Insensitivity of GCS to mild injury Ineffectiveness of imaging studies for

detecting mild injury Reporting of PTA highly unreliable (even

reporting LOC!)

Mild Traumatic Brain Injury

ACRM Brain Injury Special Interest Group:– Any period of LOC <30 minutes and GCS of 13-15 after this

period of LOC– Any loss of memory for events immediately before or after

the accident, with PTA of <24 hours– Any alteration in mental state at the time of the accident– Focal neurological deficit(s) that may or may not be

transient

DSM-IV Post-concussional disorder

1. LOC > 5 minutes 2. PTA > 12 hours 3. New onset of seizures or marked worsening of

pre-existing seizure disorder occurring in the first 6 months

4. Rec: abnormal neuropsychological exam 5. Persisting symptoms

AAN Practice Parameter Sports Concussion

Grade 1: Transient confusion, no LOC, resolution in <15 minutes

Grade 2: Transient confusion, no LOC, lasts >15 minutes

Grade 3: Any LOC, brief or prolonged

Sports-Related Concussion

(Cantu) Grade I - no LOC, PTA <30 minutes Grade 2 - LOC <5 min Grade 3 - LOC >5 min, PTA >24 hrs

Scales of Severity of TBI

I. Confusion Normal consciousness, no amnesia

II. Confusion Normal consciousness, PTA

III. Confusion Normal consciousness, PTA, RGA

IV. Coma (paralytic) Level III: Normal consciousness, PTA, RGA

V. Coma Vegetative state or death

VI. Death

Glasgow Coma Scale

Eyes Open Spontaneously 4 To verbal command 3 To pain 2 No response 1 Best motor response

To verbal command

Obeys 6

To painful stimulus

Localizes pain 5

Flexion-withdrawal 4 Flexion-abnormal 3 Extension 2 No response 1 Best verbal response

Oriented, converses 5

Disoriented, converses 4 Inappropriate 3 Incomprehensible sounds 2 No response 1

Severe 3-8

Moderate 9-12

Mild 13-15

What the heck is Post-Concussion Syndrome?

Constellation of symptoms:– Headache, sleep disturbance, dizziness/vertigo,

nausea, fatigue, oversensitivity to noise/light, attention/concentration problems, decreased memory, irritability, anxiety, depression, emotional lability

Physical complaints

Headache - usually mixed Neck pain - often associated with HA Tinnitus Dizziness - BPPV vs. central vs. possible

other otologic problems Fatigue/drowsiness

Cognitive Sequelae

Memory difficulties (consolidation and retrieval

Diminished attention and concentration (especially divided and alternating attn)

Slowed information processing Decreased cognitive endurance and

judgment

Behavioral/affective sequelae

Depression Loss of emotional

control Anxiety Irritability Sleep disturbances

Sexual disturbances Hypochondriacal

concern Hypersensitivity to

noise Photophobia

Duration of symptoms in Mild TBI

Most report resolution of symptoms within the first 3 months after injury

Perhaps 12% of all have symptoms persisting into one year

Does persistence reflect interplay of organic and psychologic factors?

Diagnostic dilemma

– No strict rule ins/outs for the diagnosis of mild TBI– Head CT, MRI, SPECT - none are entirely reliable

for diagnosis Presence of lesions on CT/MRI indicate a “complicated”

mild TBI PET scans can measure metabolic derangements but

no difference between those with a LOC and those without

– Abnormalities require about 10 days to resolve

Diagnostic dilemma

Neuropsychological testing– No consensus on which tests to use– Impairments generally resolve 3-6 months– Must be paired with an interview to avoid “faking”

results– Heavily dependent on the diagnostic

interpretation of the examiner PASAT, Wechsler Memory Scale

Contribution from Sports Medicine

Observed concussions– Disturbances in mental function measured

immediately after concussion can determine the severity of injury

– Players with a LOC (brief) do not recover to baseline in 15 minute but did within 48 hours (small study 91 participants, Kelly)

Catastrophic outcomes

1. Really not a mild injury 2. Unrecognized posttraumatic depression 3. Premorbid psychiatric condition is

organized around the mild TBI as a focal event

4. Signs of a “functional” event

Cerebral reserve

Effects of cumulative brain injuries (dementia pugilistica)

Persons with lower initial “reserve” for other reasons

Premorbid psychiatric coditions

Doctor/Attorney dilemma

Role of litigation– conflicting studies

comparison of 2 groups, one with and one without litigation: equivalent cognitive performance, similar family reports

Canadian study 2000: amending tort law regarding MVA resulted in significant decrease of claims for mild TBI

“Compensation neurosis”

Rehabilitation of Mild TBI

Most cases: reassurance Persistent symptoms

– reassurance, education, support, and regular monitoring

– teaching effective coping– cognitive remediation

Medical management: avoid prolonged passive treatments, reconditioning

“I don’t know what it is, but there’s something out there, Mr. Jones.”

Bob Dylan