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S The Rural Veterans Health Access Program presents: Dr. Amy Murphy Certified Brain Injury Specialist Behavioral Health Issues related to all levels of TBI

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The Rural Veterans Health Access

Program presents:

Dr. Amy Murphy Certified

Brain Injury Specialist

Behavioral Health Issues

related to all levels of TBI

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DISCLOSURE

Purpose:

The purpose of the Traumatic Brain Injury – Medical Management of Behavioral Health Issues related to TBI webinar is to enable health care providers to better understand, identify, and treat traumatic brain injury-related behavioral health issues with new onset or existing conditions, and to develop medical management plans to improve care.

Criteria for Successful Completion:

Participants will attend the entire webinar and complete an evaluation form.

Upon completion, a CE certificate for 1.16 contact hours will be awarded.

Conflict of Interest:

There is no conflict of interest for any program planner or presenter involved with this activity.

NOTE:

This nursing CE activity is being jointly provided by the Alaska Nurses Association (AaNA), Alaska AHEC, and the State of Alaska Division of Public Health Rural Veterans Health Access Program.

Rural Veterans Health Access

Program

The Rural Veterans Health Access Program (RVHAP) is part of the Health Planning and Systems Development

Section, Division of Public Health,

Alaska Department of Health and Social Services

The RVHAP is funded by HRSA Office of Rural Health Policy: Grant number H3GRH26369

• The Rural Veterans Health Access Program (RVHAP)

deploys telehealth connectivity in selected remote SE rural

communities with no or limited health care services to

provide a Telehealth care network for behavioral health

and primary care.

• The Rural Veterans Health Access Program also provides

training to behavioral and medical health professionals on

the delivery of telehealth services using TH technology for

Behavioral Health and Primary Care related to Traumatic

Brain Injury

• Traumatic Brain Injury is one of RVHAP’s

priorities for the primary group served,

Veterans and their caregivers as well as

other rural community members with TBI

and their families and caregivers

• Provides Traumatic Brain Injury

Assessment and Treatment training to

RVHAP agencies and community health

providers including the VA and other

military health practitioners.

Tenakee SpringsOne of the remote rural Southeast Alaska communities served

by the Rural Veterans Health Access Program

http://dhss.alaska.gov/dph/HealthPlanning/Pages/veterans/default.aspx

For more information on the RVHAP or this webinar

contact the Program Director:

Susan Maley, MPH, Ph.D. [email protected], 907-

269-2084

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Medical Management

of Behavioral Health Issues

related to all levels of TBI

Amy L. Murphy, DO

Brain Injury Medicine

Physical Medicine and Rehabilitation

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Psychological Manifestations After Brain Injury:

Objectives

• Definitions

• Assessment

• Symptoms

• Treatment

• Discussion and Questions

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DefinitionsNational Brain Injury Association

TBI is an insult to the brain, not of a congenital or

degenerative nature, that may produce a diminished or

altered state of consciousness which results in impairment

of cognitive abilities or physical functioning. It can also

result in the disturbance of cognitive abilities or physical

functioning. These impairments may be either temporary

or permanent and cause partial or total functional

disability or psychosocial impairment.

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Definitions

Mild TBI

Traumatic head injury with ANY of the following:

LOC: < 30 min

GCS of 13-15

PTA: < 24 H

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Definitions

Moderate TBI

Traumatic head injury with ANY of the following:

LOC: >30 min but <24H

GCS of 9-12

PTA: > 24 H but <1 week

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Definitions

Severe TBI

Traumatic head injury with ANY of the following:

LOC: > 24 hours

GCS 8 or less

PTA: >1 week

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NOTE!!!

Psychological Manifestations

• Can occur with all levels of TBI

• Some symptoms are more common with severe

injury but not golden rule

• Symptoms after TBI require more thought for

underlying process

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Assessment• Symptoms commonly misunderstood and mismanaged

• Common scenarios post brain injury

• Complete new onset of symptoms

• Worsening of traits, now requiring treatment

• Well managed symptoms now no longer managed

• Complete shift/resolution of previous symptoms

• Treatment paradigms that are not congruent with TBI

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Assessment• Complete history- especially risk factors, previous

behavioral health and brain injury

• Full exam- both neurologic and mental status

exam

• Overview of laboratory studies, prior radiologic

studies- especially brain

• Cognitive function

• Co-morbid physical/neurologic symptoms

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Symptoms• Aggression: usually occurs after PTA as

patient is regaining awareness• Aggressive behavior greater concern than agitation

• More difficult to treat

• Long-term

• Safety for patient, family, staff

• Agitation: acute phase of recovery/PTA

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Symptoms• Mood- looking at prominent symptoms

• Depressive symptoms

• Anxiety symptoms (panic attacks)

• Mania/Bipolar symptoms

• PTSD/stress response symptoms

• Hallucinations

• Unsafe behaviors/impulsivity

• Lack of insight

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Symptoms• Personality Disorders

• Substance Abuse• Frequency

• Self medicating

• Psychosocial issues/stressors• Financial, home, family

• Legal issues/stressors• Charges pending

• Competency

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Other Considerations• Metabolic

• Alcohol/drug withdrawal/toxicity

• Infection/systemic process

• Seizure disorder

• Endocrine dysfunction

• Cognition

• Headache

• Sleep

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Treatment• Look for any medications/substance abuse that

worsen symptoms

• Look for physical issues that cover multiple

domains and treat first:• Sleep

• Seizures

• Migraines

• Delirium versus agitation

• Endocrine- especially testosterone

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Treatment• Cognition first, unless mood is

overwhelming

• Then cognition second unless completely

assured

• Mood disorders after head injury respond

differently than primary mood disorders

• Hallucinations- think NOT typical psychosis

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Treatment• Non-pharmacologic management should be used as much

as possible!

• Environment- adequate exposure to sunlight, reduced noise and distractions at night.

• Ensure that activating medications are reduced or given early

• Education staff and family

• Neurofeedback, EMDR, supportive counseling, neuropsychology

• If environmental and behavioral interventions are maximized and need for pharmacologic intervention is necessary, use medications that can cross cover multiple symptoms

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Treatment

Seizures

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Medication Chemistry Pharmaco

dynamics

Kinetics US/EU Side Effects

Levetiracetam Selectively prevents

hyper-

synchronization of

epileptiform burst

firing

Hydrolysis

primarily, urine

excretion

Half life 6-8 hours US- not approved

for mono-therapy,

adjunct for general

or partial seizures

Depression,

aggression,

somnolence,

asthenia, headache

Divalproex

sodium/ valproic

acid

Increases GABA,

may inhibit

glutamate/NMDA

receptor mediated

excitation

Metabolized liver,

CYP 450 2A6, 2B6,

2C9 substrate, 2C9

inhibitor

Half life 9-16 hours US- partial and

absence seizures,

migraine

prophylaxis and

bipolar disorder

Hepatotoxicity,

pancreatitis,

SIADH,

pancytopenia,

Stevens-Johnson

syndrome,

somnolence,

dyspepsia, diarrhea,

weight gain, hair

loss, dizziness,

teratogenicity

Lamotrigine Inhibits voltage-

dependent sodium

channels,

decreasing

presynaptic

glutamate and

aspartate release

Liver metabolism,

UGT 1A4 and 2B7

substrate, may

induce own

metabolism as

mono-therapy

Half life 25 hours US- partial and

generalized

seizures, bipolar

disorder,

Steven Johnsons

syndrome, toxic

epidermal

necrolysis, nausea,

vomiting, dizziness,

somnolence, ataxia,

headache

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Medication Chemistry Pharmaco

dynamics

Kinetics US Side Effects

Phenytoin Modulates neuronal

voltage-dependent

sodium and calcium

channels

Liver metabolism,

CYP 450 2C9

primary, 2C19

substrate, 2B6, 2C9,

2C19 and 3A4

inducer

Half life 22 hours US- status

epilepticus, seizure

disorder, seizure

prophylaxis

Cardiovascular risk

with rapid infusion,

ventricular

fibrillation, severe

hypotension,

hepatotoxicity,

nausea, vomiting,

rash, ataxia,

confusion

Carbamazepine Reduces post-

tetanic potentiation,

decreasing seizure

spread, exact

mechanism of

action in trigeminal

neuralgia and

bipolar disorder

unknown

Liver metabolism,

CYP 450 3A4

substrate, 1A2, 2B6,

2C9 and 3A4

inducer. Also

induces own

metabolism with

active metabolite,

urine excretion

Half life variable

due to

autoinduction

US- seizure

disorder, trigeminal

neuralgia, bipolar

disorder,

Fatal dermatologic

reactions including

toxic epidermal

necrolysis, Stevens

Johnsons with

increased risk for

HLA B1502 allele,

arrhythmias,

syncope, dizziness,

drowsiness, blurred

vision,

hyponatremia,

increase AST and

ALT

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Treatment

Headaches

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Treatment

Cognition

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Treatment

Agitation/Aggression

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Medication Chemistry Pharmaco

dynamics

Kinetics US/EU Side Effects

Haloperidol Dopamine

antagonist, D2

blocker

Metabolized liver,

CYP 450 2D6

primary, 3A4

substrate, 2D6

inhibitor

Half-life 21-24

hours

US- psychosis and

acute agitation,

Increased mortality

in elderly patients,

sedation,

extrapyramidal

side effects, tardive

dyskinesia,

neuroleptic

malignant

syndrome, QT

prolongation

Ziprasidone Dopamine D2

antagonist,

serotonin 5-HT2A

antagonist

Metabolized liver,

CYP 450 3A4

substrate

Half-life 7 hours US- schizophrenia,

bipolar disorder,

schizophrenia

associated

agitation

Same as

haloperidol plus

hyperglycemia and

serotonin

syndrome

Risperidone D2 antagonist, 5-

HT2 antagonist

Metabolized liver,

CYP 450 2D6

substrate

Half-life 20 hours

PO, 3-6 days IM

US- schizophrenia,

bipolar,dementia

associated

aggression

Same as

haloperidol plus

hyperglycemia,

priapism

Quetiapine Antagonizes D2

and 5-HT2

receptors

Metabolized liver

CYP 450 3A4

substrate

Half life 6-7 hours,

7-12 for ER

US- schizophrenia

and bipolar

disorder,

Same as

risperidone

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Medication Chemistry Pharmaco

dynamics

Kinetics US Side Effects

Propranolol Non-selective beta-1

and beta-2

adrenergic receptor

antagonist

Liver metabolized,

CYP 450 1A2,

2C19, 2D6 substrate

Half life 3-5 hours,

8-11 hours with

extended release

US- hypertension,

arrhythmias,

migraine

prophylaxis,

essential tremor

Myocardial

infarction and

ventricular

arrhythmia with

abrupt withdrawal,

CHF, bradycardia,

heart block, fatigue,

dizziness,

depression

Lorazepam Binds to

benzodiazepine

(BZD) receptors,

enhances GABA

effects

Metabolized liver

CYP 450

Half life 14 hours US- anxiety,

insomnia, status

epilepticus,

Respiratory

depression, apnea,

withdrawal seizures,

hypotension,

suicidality

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Treatment

Mood

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Medication Chemistry Pharmaco

dynamics

Kinetics US Side Effects

Lorazepam Binds to benzodiazepine (BZD)

receptors, enhances GABA effects

Metabolized

liver CYP 450

Half life 14

hours

US- anxiety,

insomnia, status

epilepticus,

Respiratory

depression,

apnea,

withdrawal

seizures,

hypotension,

suicidality

Tizanidine Binds to central

alpha-2

adrenergic

receptors,

increasing

presynaptic

motor neuron

inhibition,

centrally acting

muscle relaxant

Liver

metabolism,

CYP 450 1A2

substrate

Half life 2.5

hours

US- spasticity, Hepatotoxicity,

bradycardia,

hypotension,

syncope,

rebound

hypertension if

sudden

withdrawal,

xerostomia,

somnolence

Buspirone Unknown. High

affinity for

serotonin 5-

HT1A,

moderate

dopamine D2,

known to

modulate other

receptors, no

BZD

Liver

metabolism,

CYP 450 3A4

substrate

Half life 2-3

hours

US- generalized

anxiety disorder,

anxiety

disorders/sympt

oms

Dizziness,

insomnia,

lightheadedness,

nausea, tinnitus

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Summary• Behavioral symptoms are common after all levels

of brain injury

• Understanding the root of the problem is key!

• Treatment goals

• Physical/underlying issues first

• Maximize therapies and environment

• Education for family/staff

• Maximize medications for covering multiple areas

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References• Watanabe, T.K. et al. Systematic Review of Interventions for Post-traumatic Headache. PM R.

4, 129-140. (2012).

• Hou, L. et al. Risk Factors Associated with Sleep Disturbance following Traumatic Brain Injury: Clinical Findings and Questionnaire Based Study. PLoS One. 8(10), e76087. (2013)

• Giacino J, Whyte J, Bagiella E et al. Placebo-Controlled Trial of Amantadine for Severe Traumatic Brain Injury. N Eng J Med. 366(9), 819-826 (2012).

• Jha A, Weintraub A, Allshouse A et al. A Randomized Trial of Modafinil for the Treatment of Fatigue and Excessive Daytime Sleepiness in Individuals with Chronic Traumatic Brain Injury. J Head Trauma Rehabil. 23(1), 52-63 (2008).

• McNett M, Sarver W, Wilczewski P. The prevalence, treatment and outcomes of agitation among patients with brain injury admitted to acute care units. Brain Inj. 26(9), 1155-1162 (2012).

• Ferguson PL, Smith GM, Wannamaker BB et al. A population-based study of risk of epilepsy after hospitalization for traumatic brain injury. Epilepsia. 51(5), 891-898 (2010).

• Fountain N. Choosing Among Antiepileptic Drugs. Continuum Lifelong Learning Neurol. 16(3), 121-135 (2010).

• Tatum W. Antiepileptic Drugs: Adverse Effects and Drug Interactions. Continuum Lifelong Learning Neurol. 16(3), 136-158 (2010).

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References• Perna R. Brain Injury: Benzodiazepines, Antipsychotics, and Functional Recovery. J

Head Trauma Rehabil. 21(1), 82-84 (2006).• Mysiw WJ, Bogner J, Corrigan J et al. The impact of acute care medications on

rehabilitation outcome after traumatic brain injury. Brain Injury. 20(9), 905-911 (2006).

• Willmott C, Ponsford J. Efficacy of methylphenidate in the rehabilitation of attention following traumatic brain injury: a randomised, crossover, double blind, placebo controlled inpatient trial. J Neurol Neurosurg Psychiatry. 80, 552-557 (2009).

• Erickson JC, Neely ET, Theeler BJ. Posttraumatic Headache. Continuum Lifelong Learning Neurol. 16(6), 55-78 (2010).

• Rizzoli P. Acute and Preventive Treatment of Migraine. Continuum Lifelong Learning Neurol. 18(4), 764-782 (2012).

• Kaniecki R. Tension-type headache. Continuum Lifelong Learning Neurol. 18(4), 823-834 (2012).

• Wagner A, McCullough E, Niyonkuru C et al. Acute Serum Hormone Levels: Characterization and Prognosis after Severe Traumatic Brain Injury. J Neurotrauma. 28, 871-888 (2011).