Download Brain Injury - Dr. John Lavelle

Brain Injury
John M. Lavelle, MS4 OMM Fellow
Midwestern University
Chicago College of Osteopathic Medicine
The Brain
Homunculi
Sensory
Lat
Motor
Med
Med
Lat
Left Hemisphere
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Understanding and use of language (listening,
reading, speaking and writing)
Memory for spoken and written messages
Detailed analysis of information
Controls the right side of the body
Right Hemisphere
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Judging the position of things in space
Knowing body position
Understanding and remembering things we do and
see
Putting bits of information together to make an entire
picture
Controls the left side of the body
Corpus Callosum
Functions


Connects right and left
hemisphere to allow for
communication between the
hemispheres.
Forms roof of the lateral and
third ventricles.
Dysfunctions

Damage to the Corpus
Callosum may result in
"Split Brain" syndrome.
Frontal Lobe
PREFRONTAL CORTEX SYSTEM – executive control
Dysfunctions
Functions
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attention span
perseverance
planning
judgment
impulse control
organization
self-monitoring and supervision
problem solving
critical thinking
forward thinking
learning from experience and
mistakes
ability to feel and express
emotions
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Loss of spontaneity in interacting
with others.
Loss of flexibility in thinking.
Persistence of a single thought
(Perseveration).
Inability to focus on task
(Attending).
Mood changes (Emotionally
Labile).
Changes in social behavior.
Changes in personality.
Difficulty with problem solving.
Inablility to express language
(Broca's Aphasia).
Frontal Lobe
Functions
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
Motor – responsible for
making movements
Premotor – selects
movements, selection and
direction of motor
sequences
Dysfunctions

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Loss of simple movement of
various body parts
(Paralysis).
Inability to plan a sequence
of complex movements
needed to complete multistepped tasks, such as
making coffee
(Sequencing).
Parietal Lobe
Functions
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Processes sensory information
Localize touch, pressure, pain, and temperature on the opposite side of the body
side
Spatial processing
Visual guidance of hands, fingers, eyes, and limbs, head
Responsive to eye movements
Visual motor guidance for reaching and grabbing objects
Tactile recognition
Information on limb position
Localize objects around us
Directing movement in space
Detecting stimuli in space
Distinguishing left from right
Parietal Lobe
Dominant Parietal Lobe
Dysfunctions
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finger agnosia (can’t tell position
of finger with eyes closed)
agraphia (trouble writing)
R-L confusion
acalculia
dyslexia
errors in grammar
apraxia
inability to copy movements or
make gestures
Non-dominant Parietal
Lobe Dysfunctions
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neglect of left side (such as in
drawing a clock, left side of
drawing a person, left side of
words, shaving)
unaware anything is wrong or a
problem is present
constructional apraxia (impaired
at combining blocks to build a
design or doing puzzles)
impaired copying, paper cutting,
spatial relations, drawing maps,
dressing)
Occipital Lobe
Functions

Vision
Dysfunctions
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Defects in vision (Visual Field Cuts).
Difficulty with locating objects in
environment.
Difficulty with identifying colors
(Color Agnosia).
Production of hallucinations
Visual illusions - inaccurately seeing
objects.
Word blindness - inability to
recognize words.
Difficulty in recognizing drawn
objects.
Inability to recognize the movement
of an object (Movement Agnosia).
Difficulties with reading and writing.
Dominant Temporal Lobe
Functions
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Perception of words
Process language related sounds
Sequential analysis
Increased blood flow during
speech perception
Process details, individual units
Intermediate term memory
Long term memory
Auditory learning
Dysfunctions
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Decreased verbal memory (words,
lists, stories)
Difficulty placing words or pictures
into discreet categories
(Catagorization).
Trouble understanding the context of
words (Wernicke's Aphasia)
Aggression, internally or externally
driven
Dark or violent thoughts
Sensitivity to slights, mild paranoia
Word finding problems
Auditory processing problems
Reading difficulties
Emotional instability
Non-dominant Temporal Lobe
Functions
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Perception of melodies
Pitch/prosody
Social cues
Reading facial expression
Increased blood flow during tonal
memory
Decoding vocal intonation
Rhythm
Visual learning
Dysfunctions
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Difficulty recognizing facial
expression (Prosopagnosia).
Difficulty decoding vocal
intonation
Social skill struggles
Trouble processing music
Poor visual imagery
Decreased selective attention to
visual input
Decreased recall of nonverbal
items – shapes, faces, tunes
Cerebellum
Functions
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Coordination of voluntary
movement
Balance and equilibrium
Some memory for reflex motor
acts.
Dysfunctions
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Loss of ability to coordinate fine
movements (dysmetria).
Loss of ability to walk (ataxia).
Inability to reach out and grab
objects.
Intention Tremor.
Dizziness (Vertigo).
Slurred Speech (Scanning
Speech).
Inability to make rapid
movements (dysdiadocokinesia).
Brainstem
Functions
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Breathing
Heart Rate
Swallowing
Reflexes to seeing and hearing
(Startle Response).
Controls sweating, blood
pressure, digestion, temperature
(Autonomic Nervous System).
Affects level of alertness.
Ability to sleep.
Sense of balance (Vestibular
Function).
Dysfunctions
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Decreased vital capacity in
breathing, important for speech.
Swallowing food and water
(Dysphagia).
Difficulty with
organization/perception of the
environment.
Problems with balance and
movement.
Dizziness and nausea (Vertigo).
Sleeping difficulties (Insomnia,
sleep apnea).
Limbic System
Parts
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Amygdala: involved in emotion,
learning and memory. It is part of
a system that processes
"reflexive" emotions like fear and
anxiety.
Cingulate gyrus: processing
conscious emotional experience.
Fornix: connects the hippocampus
to other parts of the limbic
system.
Hippocampus: plays a significant
role in the formation of long-term
memories.
Functions
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stores emotional memories
modulates motivation
controls appetite and sleep cycles
promotes bonding
directly processes the sense of
smell
modulates libido
Limbic System
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Dysfunctions
moodiness, irritability, clinical depression
decreased or increased sexual responsiveness
increased negative thinking
perceive events in a negative way
decreased motivation
flood of negative emotions
appetite and sleep problems
social isolation
Basal Ganglia
Striatum & Globus Pallidus (caudate and putamen)
Functions
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Initiation and direction of
voluntary movement.
Postural Balance
Emotional motor expression
(smiling, frowning, laughing, crying)
Dysfunctions
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Tremor-at-rest
Dyskinesia with hypertonia
Parkinson’s disease (Loss of
dopamine)
Dyskinesia with hypotonia
Chorea
Athetosis
Hemiballism (Subthalamic
nucleus)
Thalamus
Thalamus
Sensory Function
 Visual input in the lateral geniculate nucleus (LGN) - lesions result in hemianopia.
 Auditory input in the medial geniculate nucleus (MGN) - Unilateral lesions have
little effect on hearing; auditory information ascends bilaterally.
 Somatosensory input for position, vibration, pain and temperature in the VPL and
VPM nuclei - Lesions cause loss of all sensation on one side of the body. Some
patients experience abnormally painful sensations on the anesthetic side - Thalamic
Pain syndrome
Motor function
 Interruption of the cerebellar input to VA and VL cause ataxia
 Interruption of basal ganglia input VA and VL cause akinesia.
Cognitive function
 Arousal: bilateral lesions affecting the intralaminar thalamic nuclei cause
unresponsiveness, but the eyes remain open - called coma vigil or akinetic mutism.
 Memory: Lesions affecting medial thalamic structures cause amnesia.
 Aphasia, neglect and visuospatial dysfunction
Hypothalamus
Functions
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Homeostasis: body temperature,
BP, circadian rhythm
Endocrine function of pituitary:
FSH, LH, ACTH, TSH, Pr, GH,
oxytocin, ADH
Anterior Hypothalamus:
parasympathetic activity
Posterior Hypothalamus:
sympathetic activity ("Fight" or
Flight", stress response.
Behavioral patterns: Physical
expression of behavior.
Feeding center.
Pleasure center.
Dysfunctions
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Hormone imbalances
Inability to control temperature
Uncontrolled BP
Diabetes Insipidus (DI)
SIADH
Emotional abnormalities
Decreased libido
Excessive thirst
Horner’s syndrome
Internal Capsule
Functions

Motor tracts.
Dysfunctions

Contralateral plegia
(Paralysis of the opposite
side of the body)
Brain Injury
Causes

Diffuse Axonal Injury (DAI): caused by strong rotational forces of the
head, such as with a car accident. The unmoving brain lags behind the
movement of the skull, causing brain structures to tear. There is extensive
tearing of axons throughout the brain which can disrupt the brains regular
communication and chemical processes.

Anoxic brain injury: when the brain does not receive any oxygen.

Hypoxic brain injury: when the brain receives some, but not enough
oxygen.
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Hematomas: swelling or mass of blood in the brain caused by a break in a
blood vessel. i.e: epidural/subdural/subarachnoid or intracerebral
hemmorrhage
Brain Injury
Causes

Laceration: or tearing of the brain, usually from a
skull fracture or gunshot wound, results in rupture of
large blood vessels with bleeding into the brain and
subarachnoid space. This can result in hematomas,
edema and increased intracranial pressure.

Contusion: a visible bruise (bleeding) on the brain.

Coup-contrecoup injury: contusions that are both at
the site of the impact and on the complete opposite
side of the brain.
DC-ML System
STT System
SENSORY
ASSOCIATION
CORTEX
PRIMARY
SENSORY
CORTEX
PRIMARY
SENSORY
CORTEX
VPM
VPM
SENSORY
ASSOCIATION
CORTEX
WIDESPREAD
CORTEX
INTRALAMINAR
THALAMIC
NUCLEI
VPL
VPL
STT
SUP. COLL.
PAG
MES
V
CHIEF
V
SpTT
SPINAL
V
RETICULAR
FORMATION
SRTT
TST
NC
NG
NG
FAST PAIN &
TEMP.
ALS
2nd order axons
decussate 1-2 spinal
segments above their
entry level
Reflex pathway to ventral horn of cervical spinal cord
LEFT
NC
UE
DRGs
DORSAL
HORN
OF
SPINAL
CORD
LE
UE
DRGs
LE
SLOW PAIN &
TEMP.
REFLEX ACTIVITY
RIGHT
CST System
LEFT
PMC
6
SMA
RIGHT
S-I
PMA
3,1,2 5,7
M-I
4
Int. Capsule
Post. Limb
Crus
Cerebri
Within
Basilar
Pons
CST
Pyramid
Pyramidal
Decussation
LCST
+
ACST
awc
+
-
Sensory
Information
DORSAL HORN
OF SPINAL CORD
VENTRAL
HORN OF
SPINAL CORD
All muscles, but
primarily distal
muscles of
extremities
Primarily axial muscles
MOTOR UMNs
CORTEX
CEREBRAL
CORTEX
SENSORY
CORTEX
BASAL
GANGLIA
contra
signs
DIENCEPHALON
THALAMUS
III
CEREBELLUM
ipsi signs
CN
LMNs
MIDBRAIN
IV
CST
contralateral
projection
V
PONS
VI
VII
ML
PPRF
hearing, equilibrium VIII
IX
X
XI
STT
MEDULLA
XII
DC-ML
SPINAL CORD
LMNs
STT
Upper Motor Neurons
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Paresis (generalized)
Increased DTRs
Increased muscle tone
Spasticity
Babinski sign present
Clonus may be present
Disuse atrophy
Guidelines for Medication
Usage After TBI
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Define the problem as objectively and specifically as
possible.
Use medicines that have some proven efficacy; don’t
just use “something” (e.g. Neurontin).
Develop clear cut goals and metrics to assist in
determining when to stop treatment.
Begin low but get to a therapeutic dosing before
abandoning usage.
Be alert to side effects and undesired effects.
Alterations in Cognition and
Behavior After TBI
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Hypoarousal
Hypoattention
Memory Deficits
Depression
Delirium
Agitation
Factors Affecting Cognitive and
Behavioral Function After TBI
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Effects of the TBI
Medical Instability
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Infection
Metabolic Disturbances
Hormonal/NeuroEndocrine Disturbances
Hypoxia
Sleep-Wake Disturbances
Pain
Seizures
Factors Affecting Cognitive and
Behavioral Function After TBI
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Medications
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Cognitive-Impairing Medications
Central Acting Antihypertensives (Clonidine)
 Central Acting Antispasmodics (Tizanidine)
 GI Agents (H2 Blockers, Reglan)
 Pain Medications (Narcotics, ? NSAID’s)
 Sedatives (Benzodiazepines, Sleep Aids)
 Anticonvulsants (Phenytoin, Carbamazepine, Phenobarbital)

Factors Affecting Cognitive and
Behavioral Function After TBI
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Cognitive-Improving Medications
Stimulants [Methylphenidate, Dextramphetamine]
 Amantadine [Symmetrel]
 Bromocriptine [Parlodel]
 Selective Serotoninergic Re-Uptake Inhibitors [Prozac, Zoloft,
Paxil,Celexa]
 Combination Antidepressants [Wellbutrin]
 ? Levodopa-Carbidopa [Sinemet]
 ? Anti-Alzheimer's Agents [Aricept, Exelon]

Coma Intervention
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Directed Multisensory Stimulation (DMS)
demonstrated superior (increased
responsiveness, improved RLAS, improved
GCS) versus Non-Directed Stimulation (NDS)
in RLAS II patients
Hall:Brain Injury 1992:6:435-45
Coma Intervention

Comatose receiving greater therapy intensity (by
60%) demonstrated a 31% decrease in length of
stay.
Blackerby:Brain Injury 1989;4:167-73
Cognitive Interventions: Hypoarousal

No reliable data to support the efficacy of
pharmacologic intervention in the comatose
(RLAS I) or vegetative (RLAS II) patient. All
you get is a very “alert”-looking comatose or
vegetative patient.

Small trials do support use of
neurostimulants (Amantadine 150 mg bid) in
“emerging” patients (RLAS III).
Kaelin: Arch Phys Med Rehabil 1996;77:6-9
Cognitive Interventions: Hypoattention
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Neurostimulants have been demonstrated to
improve attention (and +/- function) in
responsive patients (RLAS IV-VIII) .
Methylphenidate has the most clinically
demonstrated efficacy for individuals who have
progressed out of coma.
Dosing 5-30 mg q 7am and 12 pm.
Kaelin: Arch Phys Med Rehabil 1996;77:6-9
Methylphenidate (Ritalin)

Modes of Action

Release of Dopamine from reserpine sensitive presynaptic pool
Braestrup: J Pharm. Pharmacol. 1977, 29: 463 - 470.

Inhibition of Dopamine uptake
Ferris,Tang: J of Pharmacol. Exp. Ther. 1979, 210: 422 - 428.

Inhibition of Monoamine Oxidase
Szporny, Gorog: Biochem. Pharmacol. 1961, 8: 263 - 268.
Methylphenidate (Ritalin)

Pharmacokinetics
Peak serum levels are reached within 2 hours (Half life = 24 hrs)
 Both a wide inter-individual and intra-individual variability
in serum concentrations exist
 MPH levels are not different in responders and nonresponders

Gualtieri, CT, et al. J of Amer Acad of Child Psych 1982, 21(1): 19-26.
Selective Serotonin Re-Uptake
Inhibitors (SSRI’s)
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Prozac, Zoloft, Paxil, Celexa
Inhibit CNS reuptake of Serotonin
Activating antidepressants, however somnolence present
w/ Paxil at doses >20 mg/day
Increase dosage q 4-6 weeks
If treating depression, need to commit to 12 month
course (or increase recurrence)
Bromocriptine (Parlodel)
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Dopamine receptor agonist
Adjunctive treatment for Parkinson’s disease
Suggested for low level patients, however limited proven efficacy
Dosage: 2.5-15 mg/day in 2 doses
Increase dosage weekly
High incidence of N/V and Headaches with increasing dosages.
Amantadine (Symmetrel)
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Potentiates Dopamine (mechanism unclear)
Adjunctive treatment for Parkinson’s disease (tremor)
Dosage: 100-400mg/day in bid dosing (elevated seizure
risk above 300 mg/day)
Increase dosage weekly
Hallucinations dose limiting side effect.
Probable efficacy in RLAS III patients.
Other Antidepressants
[Effexor, Wellbutrin]

Effexor and Wellbutrin inhibit Serotonin, NE, and Dopamine
reuptake = Activating agents

Effexor Dosage: 75-225 mg/day in 2-3 doses (Occasional
HTN side effects)

Wellbutrin Dosage: 200-450 mg/day in 3 doses (May have
worsening effects on agitation)
Levodopa-Carbidopa [Sinemet]
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Increases cerebral dopamine
Suggested for low level patients, however limited proven
efficacy
Side effects can include dyskinesias and cognitive changes
Dosage: 400-1600 mg Levodopa/day in 2-3 doses
(tablets contain either 100 or 200 mg Levodopa)
Anti-Alzheimer's Agents
[Aricept, Exelon]
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Reversible cholinesterase inhibitors = increases cerebral
acetylcholine
Effective in improving memory in individuals with
Alzheimer’s disease
Limited research suggests efficacy in TBI patients
Extremely expensive, occasional GI side effects
Treatment Algorithm:
Hypoarousal/Hypoattention

Day 1
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Define pathology -> CT/MRI, Mechanism of Injury, Secondary BI
Assess function: DRS, FIM, RLAS (limited efficacy in RLAS I-III)
Assess medical status -> Infections, Oxygenation, Metabolics, Fluid Status, Seizures
Remove medications -> H2 blockers, narcotics, central acting anti-HTN/GI,
Benzodiazepines, Sleepers
Day 1-4
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
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Stabilize/Improve medical status
Assess/Improve sleep-wake cycle: Trazadone, Ambien
Assess behavior: ABS, Therapy attendance/participation, Attention to Task
Treatment Algorithm:
Hypoarousal/Hypoattention

Day 5-10
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Initiate Methylphenidate 5 mg q 7 am and 12 pm, increase 5-10 mg/day to 60 mg
maximum
Monitor behavior and sleep-wake cycle
Day 10-20
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If Methylphenidate effective, continue at lowest effective dose for 2-3 weeks, then wean
off in 2-4 days
If Methylphenidate ineffective by 30 mg/day, then initiate wean and begin new agent.
Recommend: SSRI’s may be appropriate if mild but limited response to Ritalin ( if
depression is suspected, then Ritalin only effective 4-6 weeks and will need SSRA for
3 months minimum).
Cognitive Interventions: Agitation

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Agitation occurs in >50% of all TBI patients (RLAS
IV), however delirium, seizures, pain, hypoxia can
also manifest with agitation.
True TBI agitation should be treated with
environmental and behavioral interventions.
Pharmacologic treatment should only be
implemented in specific behaviors are identified and
goals established.
Agitation is defined as an Agitated Behavior Scale
score > 21
Cognitive Interventions: Agitation

Etiologies
Environmental
 Pain
 Seizure activity
 Delirium (meds, hypoxia, metabolic)
 Inadequate sleep/wake hygiene
… or TBI-related confusion

Cognitive Interventions: Agitation

Treatment

Assess for correctable
etiology
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Sleep/Wake Charting
Medical Management
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Behavioral
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establish desired behavior
positive reinforcement
shaping
structured therapy
Agitated Behavior Scale


Assess pattern of agitation
Documentation
Evaluate effectiveness of
intervention
Physical Restraint
Pharmacologic

ABS > 28
Agitation: Medications

Day 1-3 Use prn for ABS >28



Ativan
Risperidone
Day 4+
 Schedule agents if persistent ABS > 28
Aggression - Beta-Blockers (Propranolol)
 Restlessness - AED’s (Tegretol, VPA)
 Emotional lability - TCA’s (Nortriptyline)


Wean agent when ABS <21 for 3 days.
Cifu: J NeuroRehabil 1995;5:245-254
Post-Traumatic Seizures:
Background


TBI-related seizures account for 20% of symptomatic
epilepsy. Hauser: Epilepsia 1991:32;429-45
PTS accounts for 5% of all cases of epilepsy.
Hauser: Epilepsia 1991:32;429-45

Late PTS is present in 4-7% all TBI, nearly 20% rehab
TBI, and 35-50% penetrating TBI patients.
Yablon: Arch PM&R 1993:74;983-1001

EEG has no predictive value for PTS.
Yablon: Arch PM&R 1993:74;983-1001
Prophylaxis for PTS



73% reduction in early PTS and 50% reduction in 1
year PTS in individuals given phenytoin for 1 week
post-TBI.
No proven benefits to giving prophylaxis >7 days postTBI.
Temkin:N Engl J Med 1990:323;497-502
No benefit to use of up to 1 month VPA.
Temkin: J NeuroSurg 1999:91;593-600

AANS and AAPM&R recommend 7 days of either
PTH or CBZ post-TBI.
Prophylaxis for PTS

Do not treat seizure in first 24 hours post-TBI longer
than initial 7 days, unless status epilepticus.

Seizures in the first week should be treated (1 year)
unless there is a non-TBI cause evident (infection,
hypoxia, metabolic, hydrocephalus).

Seizures after 1 week must be treated for at least 1 year.
GI Ulcer Prophylaxis


Use of H2-Blockers has been demonstrated to
decrease ICU-related stress ulceration of the GI
tract in specific patient populations (e.g., burns).
No specific information in patients with TBI,
with or w/o PEG/J tubes.
GI Ulcer Prophylaxis



Newer H2-Blockers, while expensive, have
limited CNS effects.
High risk patients (h/o PUD, h/o GERD,
comatose, > 65 years old) are appropriate for
prophylaxis while in ICU.
No clear indication for all TBI patients in ICU.
Spasticity Management

Treatment should be initiated if the spasticity is
limiting function, ROM, or is causing pain.

Potential side effects of treatment must be
weighed against potential benefits.
Spasticity Management:
Third Line

Systemic medications are effective, but often
have systemic side effects:
Hepatotoxicity (Baclofen, Dantrium)
 Generalized weakness (Dantrium)
 Lethargy (Zanaflex, Baclofen, Valium)
 Hypotension (Zanaflex)
 Addiction (Valium)
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Spasticity Management:
Third Line
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Dantrolene Sodium (Dantrium)
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Acts peripheral by blocking release of Ca++ from the ttubules of the sarcoplasmic reticulum.
Hepatotoxicity is not uncommon.
May cause generalized weakness.
No central effects.
Most often used in Brain Injury and CVA.
Start 25 mg qid -> Max 100 mg qid.
Spasticity Management:
Third Line

Tizanidine (Zanaflex)
Central acting alpha-blocker.
 Often causes hypotension.
 May cause lethargy.
 very gradual dose increase.
 Most often used in SCI.
 Start 1 mg tid -> Max 8 mg tid.

Spasticity Management:
Fourth Line

Phenol (1-10% Aqueous Solution)
Direct neurocidal agent, effect lasts for 3-6 months
(until nerve regenerates). Works immediately.
 Eliminates spasticity in specific nerve distribution or
muscle.
 Nerve/muscle motor point (where nerve innervates)
must be isolated electrically.
 Inexpensive.

Spasticity Management:
Fourth Line

Botulinum Toxin (Botox, NeuroTox)
Neurotoxin that prevents the release of acetylcholine
(Ach) from presynaptic vacuoles at the
neuromuscular junction.
 Produces paralysis of the muscle for 2-4 months.
 Maximal effects take 2 weeks.
 Expensive.

Spasticity Management:
Fourth Line
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Focal blockade needs to be combined with a
structured stretching/bracing program.
Focal blockade often reveals underlying
connective tissue contractures.
If they are “soft”, they can be improved with
stretching.
 If they are hard, surgical intervention is indicated.

Guidelines for Medication
Usage After TBI
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Define the problem as objectively and specifically as
possible.
Use medicines that have some proven efficacy; don’t
just use “something” (e.g. Neurontin).
Develop clear cut goals and metrics to assist in
determining when to stop treatment.
Begin low but get to a therapeutic dosing before
abandoning usage.
Be alert to side effects and undesired effects.
Thank You!
References
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Moore, K.L; Agur, A.M. Essential Clinical Anatomy. Lippincott
Williams&Wilkins, 2002 Baltimore, MD.
Nolte, J; The Human Brain: An Introduction to Its Functional Anatomy,
Mosby, 2002 New York, New York.
Zasler, ND, Katz, DI, Zafonte, RD; Brain Injury Medicine, Demos Medical
Publishing, 2007, New York, New York.
www.brainanatomy.net
www.neuroskills.com
www.uptodate.com