Download Mild Traumatic Brain Injury

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-methyl4-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.
II.
III.
IV.
V.
VI.
Confusion
Normal consciousness, no
amnesia
Confusion
Normal consciousness, PTA
Confusion
Normal consciousness, PTA, RGA
Coma (paralytic)
Level III: Normal
consciousness, PTA, RGA
Coma
Vegetative state or death
Death
Glasgow Coma Scale
Eyes
Open
Best
motor
response
To verbal
command
To painful
stimulus
Best
verbal
response
Severe 3-8
Moderate 9-12
Mild
13-15
Spontaneously
To verbal command
To pain
No response
Obeys
4
3
2
1
6
Localizes pain
5
Flexion-withdrawal
Flexion-abnormal
Extension
No response
Oriented, converses
4
3
2
1
5
Disoriented, converses
Inappropriate
Incomprehensible sounds
No response
4
3
2
1
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