Session IV - Brain Injury and Substance Abuse

4/21/2016
TBI and the Problem of Substance Abuse
TBI and the Problem of Substance Abuse
Frank R. Sparadeo, Ph.D.
Clinical Neuropsychologist
211 Quaker Lance
West Warwick, R.I. 02893
401‐398‐7681
[email protected]
Drug Effect
The Process of Learning
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38 years
Supervised over 2000 detox’s
Evaluated over 5,000 TBI cases
Evaluated over 2,000 cases of combined TBI and Substance Abuse
• Treated over 1,000 people with TBI/SA
• Currently working with TBI survivors experiencing pseudo‐addiction and pain
Set Points of Drug Self Administration
OD
Nodding
High
Pain relief
Relaxation
Pinned pupils
Comfortable
Drug desire
Craving
Restlessness
Bone Aches
Chills
Nausea
Sweats
Cramps
Diarrhea
Vomiting
Off
Ah
Ah
On
On
On
Withdrawal
Incidence of Cognitive Impairment
• 30‐80% of persons entering addictions treatment have been found to show mild to severe neuropsychological deficits (Martin et al., 1986; Meek et al., 1989; O’Malley et al., 1992; Spencer, Wilde & Sander, 2014).
Impact of Cognitive Impairment
• Neuropsychological deficits contribute to the inattention, distractibility and apparent lack of motivation early in treatment.
• Understanding the cognitive weaknesses and strengths is useful for clinical decision making and in providing clinicians with realistic expectations about treatment goals.
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Cognitive Aspects of Sobriety
Prevalence of Substance Abuse
• Staying sober or drug free requires a number of “executive” functions:
• Substance abuse is more prevalent among persons with disabilities than society in general
• Post injury alcohol use declines initially and eventually (two years post injury) increases to pre‐injury levels or greater
– Self‐monitoring/self‐guidance
– Use of knowledge to guide behavior
– Impulse Control
– Learning from negative feedback
– Reflection/Empathy
TBI 101
TBI 101
• The CDC defines traumatic brain injury (TBI) as an injury to the head that involves at lest one of the following: 1.) decreased level of consciousness, 2.) amnesia, 3.) skull fracture, or 4.) objective neurological or neuropsychological abnormality or diagnosed intracranial lesion.
TBI 101
TBI 101
• 1.7 million people sustain a TBI annually
• 80,000 to 90,000 persons have new onset disability each year due to TBI
• 5.3 million Americans are living with disability due to TBI
• Falls and MVA’s are the two most common causes of injury with males overall showing higher rates of TBI than females.
• TBI ranges from mild to severe
• TBI results in some disturbance in cognitive, behavioral, emotional and/or physical functioning.
• These effects may be transient, long‐lasting, or permanent.
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TBI 101
• Uncomplicated mild TBI (mTBI) usually improves over a period of days to weeks in the majority of patients, with no indication of permanent impairment by three months post‐injury.
• Evidence indicates that incomplete recovery from mTBI may be associated with or complicated by pre‐existing or comorbid psychiatric, medical, psychosocial or litigation factors in some cases.
TBI 101
• Additional evidence indicates that repeated mTBI and complicated mTBI may also place individuals at risk for prolonged or atypical recovery course.
TBI 101
TBI 101
• Secondary Injury
– Delayed edema
– Hydrocephalus
– Drug interactions
– Organ failure
– Seizure activity
TBI 101
• Typically, TBI is seen as a diffuse injury to the brain
• Initial symptoms can and usually include: Loss of consciousness, significant chemical changes in the brain, blood pressure changes, changes in intracerebral pressure.
• Neurosurgery may be necessary for many reasons
• The use of steroids is common to reduce edema
• Coma and persistent vegetative states can occur. The longer they persist the less likely the patient will recover without disability.
TBI
 Focal deficits can occur
 This occurs in the presence of a specific focal lesion usually due
to intraparenchymal bleeding in a specific area of the brain.
 The interaction of the cognitive deficits and the physical
disability needs to be considered when planning rehabilitation
and long-term goals.
 A patient with a focal lesion in the right parietal lobe will
display anosognosia (inability to appreciate his own illness).
An organic denial syndrome. Such patients have difficulty
understanding the purpose of various treatments and
procedures.
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Substance Abuse
Substance Abuse
 Estimates indicate that 18.9 million adults in the
 Cannabis is classified as a Schedule I substance
U.S. were diagnosed with substance abuse or
dependence in 2011, or approximately 8% of the
adult population
 Approximately 23.5 million Americans age 12 and
older required intervention for substance use.
 It is projected that disability caused by substance use
disorders will surpass that caused by any other
physical disease worldwide by 2020.
making it comparable to drugs such as heroin with
respect to legal penalties for use, possession and
distribution.
 In 1969 84% of Americans were against legalization
of marijuana and 12% in favor of it.
 In 2011 46% of Americans are against legalization
and 50% in favor of legalization.
Substance Abuse
Substance Abuse
 Diagnosed when it is determined that substance use
 A major distinction between substance dependence
had led to significant recurrent negative
consequences in one or more of four domains over
the same 12-month period. These domains include:
legal, interpersonal, work/school, hazardous
behaviors.
 Substance dependence is diagnosed when substance
use persists despite leading to three or more
recurrent negative cognitive, behavioral or
physiological consequences over a 12-month period.
and substance abuse is the compulsive use of the
substances with an inability to control their use,
despite realization that use causes negative
consequences.
ASAM New Definition of Addiction
Addiction is a primary, chronic disease of brain
reward, motivation, memory, and related circuitry.
Dysfunction in these circuits leads to characteristic
biological psychological social and spiritual
manifestations. This is reflected in an individual
pathologically pursuing reward and/or relief by
substance use and other behaviors.
August 15,2011
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Factors Contributing to Vulnerability to Develop a Specific
Addiction
use of the drug of abuse essential (100%)
Genetic
(25‐50%)
Environmental
(very high)
• DNA
• SNPs
• other polymorphisms
• prenatal
• postnatal
• contemporary
• cues
• comorbidity
• mRNA levels
• peptides
• proteomics
Drug‐Induced Effects
(very high)
Kreek et al., 2000
• neurochemistry
• behaviors
Reward System
 REWARD, COMFORT, AND PLEASURE from
ordinary activities; and a degree of calming to fight
off unwanted stress. However, your genetics and
environment greatly affect this cascade; and
unfortunately, some of our genes come with
variations called polymorphisms. Polymorphisms
change the way the gene expresses itself. Most
people will call this a predisposition. These
polymorphism’s can alter their intended genetic
function.
The Human Genome
• In the human genome, there are ~3 billion bases (nucleotides) • In humans, there are estimated to be ~30,000 genes (many but not all identified and annotated)
• Each gene is a sequence of bases or nucleotides
Kreek (Rockefeller University) & Hassin
(Columbia P&S), 2004
Single Nucleotide Polymorphisms (SNPs) in Genes:
Definitions
 SNP — a single
nucleotide
polymorphism, that is,
one nucleotide or base of
any base pair
 Allelic Frequency:
<1% low or rare
1–5% intermediate
>5% high, frequent
Kreek (Rockefeller University) & Hassin
(Columbia P&S), 2004
The Brain Reward Cascade
All Roads Lead to Dopamine
 DA is used to signal novel and motivationally
relevant environmental events.
Gene Targets in
the
Brain Reward
Cascade
 DA is also important for the motivation and
reinforcement of actions. Drugs that interfere with
DA transmission interfere with reinforcement
learning, while manipulations that enhance DA
transmission, such as brain stimulation and
addictive drugs, often act as reinforcers.
 DA transmission is crucial for creating a state of
motivation to seek rewards.
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>1/3 OF THE Total US Population Carries the DRD2 A1
(Over 100,000,000 people)
50%ofAfricanAmericanscarrytheDRD2A1gene
58%ofHispanicscarrytheDRD2A1gene
72%ofAsianscarrytheDRD2A1gene
85%ofNativeAmericanscarrytheDRD2A1gene
Reward Deficiency Syndrome
 Carriers of the DRD2 A1allele
 at birth have a 74% chance of
becoming addicted to many
Reward Deficiency Behaviors
 Carriers of the DRD3 are
particularly sensitive to Cocaine
effects .
 Carriers of the G allele of the mu –opiate receptor
have a very high risk for heroin seeking behavior.
 With low function of the opiate receptor this will
 There is evidence that these carriers
are at greater risk for all RDS
behaviors including opioids and
nicotine.
result in too much activity of the neurotransmitter
GABA which will prevent dopamine release from the
neurons in the reward site of the brain (accumbens) .
 The result is increased cravings for drugs and food.
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 Carriers of the 3R allele of the MAO –A gene
 Carriers of the 181 allele of GABAB3 gene
have an altered function of GABA
transmission leading to an augmented
anxiety trait.
 Carriers of this Allele may be prone to
alcoholism to reduce the anxiety level.
 Carriers have an inability to cope with
stress.
have increased metabolism of dopamine in the
cell at the energy producing mitochondria.
 Having this allele causes an increased breakdown
of dopamine in the cell resulting in reduced
dopamine in the storage sites and as such lower
amounts of dopamine are released to combat
stress as only one example.
 All RDS behaviors are at risk with this allele.
“Go” and “Stop” Switches
 The area of the brain that encourages a human (or
 Carriers of the COMT-G allele are at
high risk for all RDS behaviors because
this allele causes an enhanced
catabolism of dopamine in the synapse
after being released from the neuron at
the reward site of the brain.
“Go” and “Stop”
any mammal) to perform or repeat an action that
promotes survival is called the
survival/reinforcement circuit. Its normal function
is to reinforce an action that promotes survival (e.g.
eating, drinking, having sex). It is also the part of
the brain most affected by psychoactive drugs.
 Technically, this circuit is referred to as the
mesolimbic dopaminergic reward pathway which is
located in the old brain.
Role of the Pre-Frontal Cortical Regions in Drug Addiction
 This survival/reinforcement circuit, located in the old
 Pre-frontal cortical areas work in tandem with striatal
brain, acts as a “go” or “more” switch. At the heart of the
circuit is the Nucleus Accumbens Septi (NAc).
 The Ventral Tegmental Area, lateral hypothalamus and
amygdala also play important roles.
 The control circuit, located mostly in the new brain, acts as
a “stop” switch and is driven by the left orbital prefrontal
cortex. The stop switch works in conjunction with the
fasciculus retroflexus and the lateral habenula, which
connect and communicate from the “Stop” switch to the
“go” switch.
regions via corticostriatal networks that are modulated by
DA
 These include the dorsolateral PFC, which is involved in
higher cognitive operations and decision-making; the OFC,
which is involved in salience attribution and goal-directed
behaviors; and the anterior cingulate cortex, involved in
inhibitory control and awareness in addicted subjects could
underlie the enhanced incentive motivational value of drugs
and the user’s loss of control over drug intake.
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Memory, Psychoactive Drugs and Euphoric Recall
 When people use psychoactive drugs, memories of the
experience are imprinted on the brain: where they got the
drug, the reason they used it, and what feelings (emotional
and physical) resulted.
 The stronger the drug, the more rapid the growth and
proliferation of memory “footprints” (dendritic spines) and
therefore the more deeply imprinted the memory.
 The earlier in life a person begins using drugs or practices
addictive behaviors, the longer and stronger the memories
remain in the brain and the more likely the brain is to use
the information from those memories to deal with events
later in life.
Old Brain – New Brain
 The old brain responds to internal changes and
memories as well as to sensory inputs from external
influences.
 When a person uses a psychoactive drug, most often
it is the old brain that remembers the experience and
how it felt.
Old Brain – New Brain
 The new brain (neocortex) processes informaiton
from the old brain, from different areas of the new
brain, and from the senses via the peripheral nervous
system.
 The new brain allows us to speak, reason, create,
remember, make decisions and then act. The old
brain simply reacts.
Old Brain – New Brain Distinction
 The old brain consists of: brainstem, cerebellum and
mesocortex (mid brain), which contain the limbic
system (the emotional center).
 Regulating physiological functions of the body.
 Experiencing basic emotions and cravings (e.g.
anger, fear, hunger, thirst, lust, pain and pleasure).
 Imprinting survival memories (e.g. that green plant
tastes good, this bad odor signifies danger)
Old Brain – New Brain
 The old brain is the senior partner and the new brain
is the young upstart.
 Whenever the two brains are challenged by a crisis
such as fear or anger, there is an automatic tendency
to revert to the more established old-brain function.
 And because the craving to use a psychoactive drug
almost always resides in the old brain, the desire for
the pleasure, pain relief and excitement that drugs
promise can be very powerful.
Old Brain – New Brain
 Craving can override the new brain’s rational arguments of
“too expensive” or “bad consequences” or “there’s a
midterm tomorrow so don’t party tonight.”
 The old brain acts four or five times more rapidly than the
new brain, so an action is usually well under way before
common sense kicks in.
 During intentional abstinence from a drug cravings are
evoked by memory and emotions and a virtual tug of war
between the old brain and the new brain occurs. There is a
conscious desire to remain drug-free but the old brain seeks
to resume drug use, mistaking the craving as a survival
need.
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Old Brain – New Brain
 The old brain and the new brain carry out their
functions by creating, storing and utilizing
memories. Even emotions and cravings depend on
memories. Some memories are stored on a
conscious level (explicit memory) and some are
stored on an unconscious level (implicit memory).
 Storage, activation, and use of memories are at the
heart of the obsession to use drugs, which is one-half
of the addictive process.
OFC
 The OFC has been shown to participate in outcomes
related to primary reinforcers in both nonhuman and
human studies. These neurons encode details
concerning the sensory properties of rewards, such
as visual, olfactory and gustatory aspects, and the
size or timing of past or future rewards, as well as the
magnitude of more abstract rewards and penalties.
OFC and ACC
 Impaired self-control in addicted people is believed to
reflect disrupted prefrontal regulation of striatal regions.
The level of impairment is influenced by the emotional
state (negative mood increases impairment) and the
context (exposure to unexpected cues can also impair it).
 Damage to the OFC also interferes with the inhibition of
responding to formerly rewarding cues that are no longer
reinforcing, thus favoring the emergence of perseverative
behaviors even when these are no longer reinforcing
Development
 As humans develop they continue to learn to integrate the
drives of the old brain and the common sense of the new
brain. Some people, however, lose some of this ability due
to genetic learning abnormalities, a chaotic or abusive
childhood, brain injury, the use of psychoactive drugs and
the practice of compulsive behaviors.
 Psychoactive drugs subvert the survival mechanism from
common sense integration of the new and old brains,
resulting in the irrational behavior of addiction, which
relies on the “wants” of the old brain rather than the
rational “needs” of the new brain.
OFC and ACC
 Impairments of the OFC and ACC are associated
with compulsive behaviors and impulsivity, and it
has also been postulated that impaired modulation
of these regions by DA might underlie the
compulsive and impulsive aspects of drug-taking and
abuse.
 Impaired self-control plays a fundamental role in
drug-taking behaviors in addiction. Successful selfregulation functions require top-down control from
the PFC to the striatal and limbic regions involved
with rewards and emotions.
OFC and ACC
 Thus, dysregulated activity of the OFC could underlie
both the impulsive choices for immediate rewards
and compulsive drug taking when the drug-induced
DA increases may be profoundly attenuated in
addicted people. This loss of control might continue
even when drug-taking has become less rewarding or
when adverse consequences far outweigh the
psychological or physiological benefits of drugtaking.
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Substance Abuse and TBI
Substance Abuse and TBI
 History of TBI is frequent among individuals receiving
 There is strong evidence that intoxication at the time of
treatment for alcohol and substance use disorders
 The relationship between alcohol abuse and TBI is complex
and probably circular
 Adolescents who drink regularly were twice as likely to
sustain a TBI compared with adolescents who had never
used alcohol.
 Initial alcohol-related TBI sustained after age 12 were
associated with a four-fold increased risk of repeat TBI by
age 34
injury is related to acute complications, longer hospital
stays, and poorer discharge status.
 Alcohol abuse prior to TBI has consistently been found to
mediate outcome from TBI.
 Corrigan (1995) documented that a history of substance
abuse is related to a wide range of outcomes, including
higher mortality rates, poorer neuropsychological
functioning, increased chance of repeated injury, late
deterioration and worse functional outcome.
Substance Abuse and TBI
Substance Abuse and TBI
 Intoxication and a history of premorbid alcohol use
 Pre-injury history of alcohol abuse also appears to
are related to worsening injury severity indicators
and early medical outcomes.
 Patient’s with +BALs on hospital admission have
lower levels of consciousness when admitted, longer
duration of coma, and longer lengths of
hospitalization.
 Post-traumatic amnesia and loss of consciousness
were significantly longer in groups of patients with
pre-injury alcohol abuse.
exacerbate the effects of TBI on brain structure and
function.
 TBI patients with a history of alcohol abuse
demonstrated greater volumes of intracranial
hemorrhage.
 TBI patients with a history of alcohol abuse also have
more pronounced local brain atrophy over time
compared to non-drinkers.
Substance Abuse and TBI
 TBI sustained in people with a history of alcohol
intoxication at the time of the injury demonstrated worse
cognitive outcomes than those with negative toxicology
screens, with particular difficulty on tests of verbal
intelligence, verbal memory and attention and
concentration.
 Harmful or hazardous alcohol use in the 12 months prior to
TBI was associated with poorer verbal learning and
memory and slowed processing speed.
 Previous alcohol abuse increases the risk for development
of mood disorders following TBI
Mechanisms of Behavior Change
 Current evidence-based treatments for alcohol and
drug-use disorders vary in theoretical foundations,
approaches and presumed mechanisms of action.
 Yet, it remains a conundrum that these treatments
are often equally effective across clients who differ
substantially in neurocognitive impairment and
other distinguishing features such as age, disorder
severity, and co-occurring psychopathology
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Mechanisms of Behavior Change
 Several putative mechanisms of behavior change in
Mechanisms of Behavior Change
 Key Question: Do the direct effects of
addiction treatments that have received relatively
consistent support for enhancing treatment success
include the clients motivation for behavioral change,
the alliance between the treatment provider and the
client, the client’s perceived self-efficacy to resist
urges to use alcohol/drugs, and social support
networks that support and encourage abstinence
goals.
alcohol/drugs on the brain, or neurocognitive
problems due to co-occurring TBI, and metabolic
and nutritional disturbances have down-stream
effects on addiction treatment processes and thereby
alter substance-use-related treatment outcomes,
and/or psychosocial adaptation more generally?
Mechanisms of Behavior Change
Mechanisms of Behavior Change
 Some of the most potentially disruptive effects of
 Deficits in prospective memory functioning may
psychoactive substances on the brain are that they
compromise the structure and function of the
prefrontal cortex, which results in substantial
impairment to central executive control and
inhibitory functions.
 Memory impairment is also prevalent in addiction
populations. This includes prospective memory
functioning, which refers to the memory needed to
plan and carry out future actions and involves
integrated memory and executive functions.
contribute to problems encountered in everyday
living both during and after addiction treatment
 Thus, neuropsychological impairment may
contribute to the failure to regulate drinking and
drug-taking behaviors in the moment, thereby
escalating the risk for relapse, and over the long term
may contribute to the maintenance of substance-use
behaviors, even in the face of severe, negative
consequences of such use.
Mechanisms of Behavior Change
 Clinically, neuropsychological impairments have
been associated with reduced treatment retention
and compliance, self-efficacy to resist urges to use
alcohol/drugs, coping-skill development and other
prognostic indicators of addiction treatment
outcomes.
 In a large study of alcohol-use-disordered clients,
impairment led to less treatment compliance and
lower self-efficacy to resist urges to use alcohol,
which in turn predicted less successful outcomes
following treatment.
Mechanism of Behavior Change
 In addition, in both alcohol- and drug-use-disordered
clients, neuropsychological impairment interacted with
self-efficacy to resist urges to use, such that a relatively
higher level of self-efficacy was a less robust indicator of
successful substance use outcomes in impaired clients
compared to those without neuropsychological impairment.
 This finding suggests that mechanisms of behavior change,
such as perceptions of self-efficacy to resist urges to use
alcohol and drugs, operate differently, or are perceived or
reported less accurately in impaired clients.
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Recap: Scope of the problem of
TBI and Substance Abuse
Mechanisms of Behavior Change
 Greater involvement in A.A. has been observed in impaired
compared to unimpaired clients, suggesting that social
support for abstinence might be particularly useful to
bolster treatment effectiveness in cognitively impaired
clients.
 More severe executive and verbal impairment at treatment
entry predicted better substance-use outcomes in
outpatients who had frequent contact with a social network
that supported abstinence, while impairment predicted
poorer substance-use outcomes in clients with more severe
alcohol-use histories who had frequent contact with a social
network that encourage drinking.
 20% to 30% of persons with TBI show alcohol intox-
ication at hospitalization, minimal data on other drugs.
 50% to 60% of adolescents and adults in acute
rehabilitation have prior histories of substance abuse.
 Indices of brain structure and function suggest an
additive effect of substance abuse and TBI.
 Substance abuse is associated with unemployment,
living alone, criminal activity, lower subjective wellbeing.
 Need for assistance controlling use going unmet.
Neuropsychological Considerations
SPECIFIC DRUGS
Alcohol
 Vulnerable brain structures
 Neocortex (especially the frontal lobes)
 Limbic system (especially the hippocampus and
hypothalamus)
 Cerebellum
Alcohol
Alcohol
 Decreased neuron density in the frontal cortex
 Comorbid conditions:
 15-23% of cortical neurons are selectively lost from the frontal
Malnutrition, diseases of the liver and the cardiovascular
system
 Head injury, encephalopathy
 Psychiatric conditions and the use of medicines and other
drugs
 Cognitive deficits
 Impaired reasoning
 Impaired Learning (poor semantic encoding)
 Impaired Visuoperceptual processing
association cortex following chronic alcohol consumption
 After four weeks of abstinence there is a partial reversal of brain
shrinkage and some recovery of metabolic functions in the frontal
lobes and cerebellum
 Frontal lobe blood flow continues to increase with abstinence
returning to normal levels within four years
 Relapse leads to resumption of shrinkage, continued declines in
metabolism and cognitive function and evidence of neuronal cell
damage.

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Wenicke’s Encephalopathy
Benzodiazepines
 Interact with a specific binding site in the CNS—Gamma-
aminobutyric acid (GABA) receptor complex
 GABA is the dominant inhibitory neurotransmitter of the
CNS and is the most wide spread neurotransmitter released
at 30% of all synapses and helps to shape, integrate and
refine the information conveyed by excitatory
neurotransmission
 GABA tends to act like a “brake” on the brain, with too
much transmission causing the individual to become
drowsy and sedated, and too little making the individual
become anxious and over excited.
Benzodiazepines
 Tolerance to the various actions of
benzodiazepines does not develop at the same rate.
For example, tolerance to the hypnotic effects can
develop rapidly while tolerance to the anxiolytic
effects tends to develop more slowly
 Discontinuance should occur gradually
 Discontinuance syndrome: rebound, recurrence
and withdrawal
Benzodiazepines
 Areas of long-term impairment
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Verbal Memory
Psychomotor speed
Speed of processing
Motor control/performance
Working memory
Visuospatial
General Intelligence
Attention/Concentration
Nonverbal memory
Problem-solving
Verbal reasoning
Benzodiazepines
 Neuropsychological impact
 Across 12 areas of cognitive assessment all long-term Benzo
users were impaired while using (Barker et al., 2004)
 All 12 areas improved with withdrawal
 11 areas of cognitive assessment were impaired as compared to
normal controls 6 months after withdrawal
Cocaine
 Heavy use of cocaine is associated with alterations
of neurotransmitter systems in humans.
 These alterations can manifest as abnormalities in
regional cerebral blood flow and cerebral glucose
metabolism in the prefrontal cortex and in other
limbic areas, which in turn provide the substrates
for neurobehavioral effects (depression,
compulsive behavior, cognitive deficits)
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Cocaine
Brain and Cocaine
 Neuropsychological Sequelae
 Greater errors of commission on sustained attention tasks
 Attentional response speed is impaired
 Vigilance impairments
 Verbal learning/memory—shallow learning curves
 Poor immediate and delayed recall
 Poor working memory
 Poor response inhibition
 Cognitive switching impairments
Cocaine and CVA
Cocaine and Brain Hemorrhage
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Cocaine
Cocaine
 Cocaine-induced neurological abnormalities such as
 Prefrontal brain regions, including the OFC, ACC,
atrophy and/or cell death as a results of ischemic
events, can also manifest as neuropsychological
impairment.
 Vulnerable brain areas include: Orbitofrontal cortex,
anterior cingulate cortex, the dorsolateral prefrontal
cortex, amygdala, putamen and cerebellum.
DLPFC and amygdala are activated during
intoxication, craving and binging and deactivated
during withdrawal.
 These same brain areas are also involved in critical
behaviors such as decision-making, control and
inhibition of inappropriate responses, conflict
monitoring and evaluation of the saliency of a
stimuli or reward.
Cocaine
Cocaine
 Based upon this brain-behavior relationship, Goldstein &
Volkow (2002) have proposed that cocaine addiction is a
syndrome of impaired response inhibition and salience
attribution. This model conceptualizes addiction as a
dysregulation of cognitive and emotional processes that
results in overvaluing of drug reinforcers, the undervaluing
of alternative reinforcers and difficulty with the inhibitory
cognitive control that culminates as an inability to abstain
from drug taking.
Cocaine
 Neurocognitive deficits associated with cocaine use
appear to be dose-related and persistent for at least 6
months of abstinence. Heavy cocaine use = 4
gms/wk.
 Deficits in executive function, spatial processing,
memory, concentration and motor function.
 Based on this logic, the heavy use of cocaine,
because of repeated ischemic events due to its
vasoconstrictive properties, might have caused a
state comparable to what is observed with lacunar
infarcts in the white matter of the brain. This
might in turn, cause neurological states akin to
deconnection syndromes between regions within
cerebral hemispheres.
Cocaine and Alcohol
 Many heavy cocaine users also use other substances,
including alcohol.
 Most studies have found that the interaction of cocaine
and alcohol is associated with greater neuropsychological
impairment.
 The cognitive domains most affected were short- and
long-term memory and visuomotor functions
 Neuroimaging studies demonstrate additional reductions
in rCBF are observed when alcohol and cocaine were used
 The mechanism is the formation of the highly toxic
substance cocaethylene.
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Methamphetamine
Methamphetamine (cell loss)
 Methamphetamine use produces long-lasting and negative
changes in brain structure and function.
 Meth use is associated with an increased risk for
experiencing intracrainal hemorrhage
 Meth use is associated with an increased risk for CVA for
the following reasons: increased bp, vasculitis, toxic effects
on the cerebral vasculature and cardiac abnormalities.
 In a recent study 19/21 meth using subjects had
cardiomyopathy.
92
Methamphetamine
Frequency of Impairment by Neuropsychological
Domain
 Neuropsychological deficits are demonstrated for
at least 1 year after cessation.
 Frontal activation is reduced (fMRI)
 Impaired learning and memory
 Impaired fluency
 Impaired psychomotor speed
 Impaired processing speed during decision making
Opioids
 Reduced dopamine and serotonin activity in
the striatum
 A decrease in neurofilament (NF-L) proteins
in the frontal cortex. These proteins are
thought to be involved in axonal transport and
neuronal morphology, suggesting that
decreases in NF-L may be associated with
functional impairment, particularly executive
functions and other functions associated with
the frontal cortex.
Opioids
 Hypoperfusion in several brain areas including the
frontal and parietal lobes.
 Hypoperfusion in abstinent (4 months) abusers
 Psychiatric comorbidity moderated these findings
such that hypoperfusion in the right frontal and
left temporal lobes occurred with depression and
in the right frontal lobe only in those with
antisocial personality disorder
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Opioids
Opioids
 Methadone Maintenance Patients performed worse
 Mintzer & Stitzer (2002) found MMP to be impaired
than normal controls on tests of psychomotor
performance, information processing, attention,
short-term memory, long-term memory and
problem-solving. Difficult to generalize from this
study since 67% reported a history of head injury
(Darke et al. 2000)
on psychomotor speed, working memory, decisionmaking and meta-memory.
 A separate study in which the MMP group was
divided into smokers and nonsmokers found that the
MMP smokers were more impaired than controls
and MMPI nonsmokers.
3,4-methylenedioxymethamphetamine
 MDMA is a compound with properties common




to both the central stimulants and the
hallucinogens.
Difficulty to predict the behavioral effects of
MDMA
Usually taken intermittently
Not as reinforcing as cocaine or meth
Does not produce frank hallucinations
MDMA
 A pronounced MDMA-induced denervation
has been visualized throughout the neocortex,
striatum and thalamus, while lesser damage in
the hippocampus, hypothalamus and basal
forebrain (5HT)
 MDMA depletes 5-HT.
 Neuropsychological deficits in
attention/concentration, learning/memory,
motor/psychomotor speed and executive
functioning.
Cannabis
 During 2003 in the U.S. alone, 97 million people
over the age of 12 reported using cannabis.
 Cannabis use in the US is most prevalent among
adolescents and young adults between the ages of 15
and 29.
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Cannabis
 Cannabis use produces a wide range of acute effects,
including changes in mood, mental status, and
perception as well as promotes physiological
alterations (e.g. analgesia, neuroprotection and
decreased intraocular pressure, body temperature,
inflammation, and neuronal excitability).
 Acute subjective sensations commonly include
sedation/relaxation, euphoria, depersonalization,
happiness/laughter and increased sensory
perception or subtle perceptual distortions.
Cannabis
 Cannabis research increased dramatically following
the discovery of the cannabinoid receptor CB1.
 The CB receptors are in the family of G-protein-
coupled receptors. Such proteins are involved in
second messenger signaling, and modulate chemical
reactions inside cells.
 The highest concentration of CB receptors are in the
basal ganglia, cerebellum, hippocampus and
amygdala.
Cannabis
 Naturally occurring ligands in the brain:


Arachidonic acid (an essential fatty acid found in cell
membranes and the brain)
Anandimide
Cannabis
 Acute intoxication is associated with hypotension,
paranoid thinking, anxiety, panic attacks,
unpleasant feelings of depersonalization, and
undesirable hallucinations.
Cannabis
 Less frequent adverse reactions include: anxiety,
depression, paranoia, panic symptoms, panic
reactions or psychotic symptoms.
 These less frequent adverse reactions are most often
experienced by naïve users.
Cannabis
 Neurocognitive Effects of cannabis:
 Acute Effects
Working memory difficulty
Learning and recent memory (immediate recall)
 Sustained Attention
 Reduced motivation



Residual Effects


Minimal
Mostly apply to heavy and recent users. After 4 weeks no
disadvantage.
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Cannabis
Over-The-Counter High
 Neuropsychological Sequelae
 0-6 hours after use
Deficits in psychomotor coordination
Deficits in selective and sustained attention
 Deficits in speed of information processing
 Deficits in learning and memory
 Deficits in inhibition and executive functions


Ether
 There are a number of OTC drugs that when used
improperly can create euphoria at a similar level as
illicit drugs of abuse.
Ether (Diethyl Ether)
 Diethyl Ether, more commonly just called Ether, is
mainly used medically, as an anesthetic. However, it
also has a long history of recreational use. In the late
nineteenth century, it was used regularly in Ireland,
Russia, France, Norway, the United States
and elsewhere. The effect of ether was similar to
alcohol, but it was cheaper, and allowed someone to
sober up quicker, making it popular among those
who didn’t have much money.
Robitussin
Robitussin (Dextromethorphan)
 Recreationally, DXM can have very powerful
effects, ranging from euphoria, elevated mood,
dissociation, dream-like states, and increased
awareness. Some other effects which may or may
not be considered good, depending on the person,
include disorientation, confusion, altered
perception of time, decreased sexual functioning,
and hallucinations. Higher doses can greatly
impair memory, language and judgment. Using
this drug is often referred to as “robo-tripping”.
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Unisom
Unisom (Doyxlamine)
 Teenagers will abuse Doxylamine for its
hallucinogenic properties, but it also makes them
agitated and confused. It actually doesn’t sound
exactly like a very fun high, but people try all kinds of
stupid things. In large doses, it can be quite
dangerous, resulting in prolonged agitation, seizures,
and the occasional coma.
Tramadol
Tramadol (opiate receptor agonist)
 Tramadol enjoys a very unique legal status. While it
is considered a prescription drug, it is not federally
scheduled, and has only been scheduled in a few US
states. What this means is that, while one is
supposed to have a prescription to purchase
Tramadol, it is perfectly legal to posses the drug
without a prescription in most of the United States.
Kava
Kava
 Kava is an herb that comes from the Pacific Islands,
where the islanders have been using it medicinally
for a very long time. Kava has recently developed
some popularity in the Western world, where it is
still very legal to buy and use. While low-tomoderate doses of Kava give one a sense of euphoria,
relaxation, or general well-being, higher doses can
cause hallucinations. It is also believed by scientists
that chronic use can cause yellow skin discoloration,
drowsiness, ataxia, liver damage, and malnutrition,
none of which sound very fun at all.
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Kratom
Kratom (Mitragyna Speciosa)
 Kratom, referred to in scientific literature as Mitragyna
Speciosa, is a plant native to Southeast Asia. This plant is
from the same family as coffee, and is often used
medicinally to relieve pain. However, it has gained recent
popularity in the United States for its psychoactive
properties. It is currently unregulated, and can easily be
bought at online or at certain “herbal supplement” stores.
The powder or leaves are usually ingested in a tea-like
preparation, or smoked; sometimes it is also ingested
orally. A few grams of this substance can give someone a
high for two to three hours. While it was originally used
medicinally, it has been banned in its native Thailand,
due to the abuse of the plant. Watch out, this plant is
considered highly addictive.
Benadryl
Benadryl (Diphenhydramine)
 Diphenhydramine usually goes by the trade name
Benadryl; it is marketed to deal mainly
with allergies, but is also often used as a sedative
when people are having trouble sleeping. It has
some popularity among recreational drug users, due
to its affect as a deliriant. When recreational users
take a high dose, they can expect such symptoms as
drowsiness, fatigue, disturbed coordination,
dizziness, blurred vision, confusion, and
hallucinations, which are somehow considered
positive things by recreational users.
Dramamine
Dramamine
 Dimenhydrinate is a drug that most of you probably
know as Dramamine, and is mainly used to combat
motion sickness. It is also a deliriant, and is popular
among recreational drug users for the audio and
visual hallucinations that it provides in high doses.
Setting it apart from its cousin Diphenhydramine, it
is reported to also have a euphoric effect, along with
the hallucinations. It is not only abused by
recreational users, but also by psychiatric patients,
though in their case it is for self-treating anxiety and
the like, not for recreation.
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Benedrex
Benedrex (Propylhexedrine)
 Propylhexedrine is the active drug in a nasal spray
called Benzedrex, and it originally replaced
amphetamine sulfate as the active ingredient years
back due to abuse. Unfortunately, Propylhexedrine is
also capable of abuse. Recreational users have been
known to use some sort of extraction process to gain
crystals from it, and it has hence earned the
nickname “stove top speed,” due to the effect that it
has on people.
Afrin
Afrin (Oxymetazoline)
 Oxymetazoline is a drug used in a widely-used
commercial nasal spray called Afrin. It does not have
a particularly strong high, and is instead more likely
to cause psychosis in those who use it, some of whom
have reported recurring hallucinations. What makes
this drug noteworthy is just how addicting it is.
Doctors have found that those hooked on it simply
cannot function without the drug.
4 Quadrant Model of Service Provision
High
Severity
Quadrant III
Collaboration in the
Substance Abuse
System
Integrated Treatment
of Traumatic Brain Injury and
Substance Abuse
Low
Severity
Quadrant IV
Integrated Treatment
in the Community
Quadrant I
Quadrant II
Acute Medical Settings
and Primary Care
Collaboration in
Rehabilitation Programs
& Services
Acquired Brain Injury
High
Severity
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4 Quadrant Model of Service Provision
High
Severity
Quadrant IV
Quadrant III
Collaboration in the
Substance Abuse
System
Integrated Treatment
in the Community
Low
Severity
Case Management to change the
environment and
organize the team
Substance abuse treatment
to establish new attitudes,
beliefs and skills
Integrated
Programs
Collaborative Care
Quadrant I
Quadrant II
Acute Medical Settings
and Primary Care
Collaboration in
Rehabilitation Programs
& Services
Screening & Referral
Integrated Treatment of TBI and SA
Therapeutic
Alliance(s)
Collaborative Care
Rehabilitation to
improve functional
abilities
Acquired Brain Injury
High
Severity
Integrated Treatment of TBI and SA
Integrated Treatment of TBI and SA
 Unique challenge for persons with TBI:

Establishing a therapeutic alliance is more difficult
with clients who are ego-centric, or otherwise lack
insight into others’ thoughts and feelings.

Professionals will need greater commitment to and
experience with this population, as well as flexibility
engaging them in treatment.
Programmatic options: specialized caseloads, smaller
caseloads, greater counselor freedom to customize
procedures, consistency in personnel from engagement
through treatment completion.
Therapeutic
Alliance

Integrated Treatment of TBI and SA
Integrated Treatment of TBI and SA
 Unique challenge for persons with TBI:
Therapeutic

Having multiple therapeutic alliances can lead to
inconsistencies, if not confusion.

Professionals need to communicate with each
other, optimally with the client included.

Programmatic options: joint treatment planning
and progress review and agency flexibility in allowing
staff participation with “ad hoc” teams.
Alliance(s)
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Integrated Treatment of TBI and SA
Substance abuse treatment
to establish new attitudes,
beliefs and skills
Integrated Treatment of TBI and SA
 Unique challenge for persons with TBI:

Substance abuse services are not cognitively and
attitudinally accessible.

Substance abuse providers need to be able to identify
and treat clients with unique learning or communication
styles; be able to appreciate both neurobehavioral and
motivational sources of behavior; and understand the
unique presentation of traumatic brain injury.

Programmatic options: in-service and pre-service
training, staff sharing, reduce barriers to consultation,
allow more flexibility in program structure.
Therapeutic
Alliance(s)
Rehabilitation to improve
functional abilities
Integrated Treatment of TBI and SA
 Unique challenge for persons with TBI:

Rehabilitation professionals have biased views
and, thus, expectations about persons with substance
use disorders.

Rehabilitation professionals need current and
accurate information about the nature and extent of
addictions, as well as their treatment. They need to
increase their knowledge and comfort level so that they
can address these issues and clients more objectively.

Programmatic options: in-service and pre-service
training, staff sharing, reduce barriers to consultation.
Integrated Treatment of TBI and SA
 Unique challenge for persons with TBI:

Case management requires the time to develop a
strong therapeutic relationship and address multiple
access and resource needs, while taking responsibility for
the coordination of all the providers involved.

Case managers need smaller caseloads, the capability to
engage via outreach, and longer allowable lengths of stay.
Changing the environment requires knowledge of health,
behavioral health, social service and vocational systems, as
well as cooperation from these provider communities.

Programmatic options: skilled staff, specialized
caseloads, smaller caseloads, flexibility structuring treatment.
Integrated Treatment of TBI and SA
Case Management to change the
environment and
organize the team
Substance abuse treatment
to establish new attitudes,
beliefs and skills
Therapeutic
Alliance(s)
Rehabilitation to
improve functional
abilities
Integrated Treatment of TBI and SA
Case Management to change the
environment and
organize the team
Substance abuse treatment
to establish new attitudes,
beliefs and skills
Therapeutic
Alliance(s)
Rehabilitation to
improve functional
abilities
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The Population
Making Services More Responsive
• Initiate cross-training, facilitate consultation and
explore staff-sharing options.
• Promote staff participation in “ad hoc” teams.
• Take advantage of specialized caseloads.
• Allow smaller caseloads and maximize consistency of
 Four Groups
 Actively Using and Uninterested in Treatment
 Impulsively Using and Interested in Changing
 Regularly Using and Interested in Changing
 Not using and fearful of relapse
personnel throughout treatment.
• Provide case management services that can engage and
be effective with this population.
• Attract the most skilled staff to the most demanding
roles, and empower them.
The Population
 Demographics
 Mostly males between the ages of 18 & 50.
 Most were substance users prior to TBI
 Most have ongoing emotional disability
 Most have executive function impairment and/or memory
impairment
 Most have slowed information processing
Substance Abuse Assessment
 Assessing substance abuse
 History taking
 Medical Issues
 Specifics regarding substance use
 Understanding the implications of specific drugs (e.g. MDMA).
 Understanding the circumstances of use
Neuropsychological Assessment
 Assessing Neuropsychological Status
 Slowed Processing Speed
 Decreased Attention Span/Immediate recall
 Word Finding Difficulty
 Retrieval Difficulty
 Executive Function Difficulty
Lessons Learned
 Taking Neuropsychological status into account when
planning treatment


Cognitive demands of treatment
Cognitive demands of living sober/drug free
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Lessons Learned
Lessons Learned
 Slowed processing = increased stress and
demand in voc. Rehab
 Word finding difficulty = decreased elaboration
 Poor retrieval = loss of didactic information
 Executive difficulty = poor self-cueing,
difficulty with reflection, empathy and planning
 Executive difficulty = poor impulse control,
failure to learn from negative experience, poor
guidance.
 Assessing Readiness for Change
 Process of Change Model
 Formal Assessment
 Change Ladders
Psychological Assessment
 Assessing Emotional Status
 Diagnostic Interview
 Formal testing
Personality Assessment Inventory
Detailed Assessment of Posttraumatic Stress
 BDI
 BAI


Initiating Treatment
 Counseling
 Over 100 models of counseling
 MET/CBT
 Modifications are necessary
Lessons Learned
 Intervention
 Shaped by the Assessment results
 Counseling Principles
Genuineness
Empathy
 Avoid Arguments
 Point out discrepancies
 Reduce barriers
 Provide choice


Lessons Learned
 Making Modifications
 Formal Treatment approaches must be understood well
enough that modifications can be made.
 Even Self-Help approaches may need modifications
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Psychotherapy and Cognitive Impairment
Initiating Treatment
 The combination of diffuse deficits (e.g. slow
 The first step is to identify the sensory-perceptual,
processing) and focal cognitive deficits (e.g.
impaired verbal attention) requires flexibility
throughout the psychotherapy process.
 The scope and nature of psychological services for
the TBI/SA patient should stem from continual
appraisal, understanding and responsiveness on
the part of the therapist
attentional, linguistic, memory and reasoning or
planning deficits that could prevent the delivery of
effective psychological treatment.
 These deficits represent the most basic level of
potential obstacles for the therapist.
 The integration of cognitive rehabilitation may be
critical
Modifications
 For successful psychological intervention, a patient
must be able to attend to and understand verbal
material or therapeutic dialogue as it unfolds within
a session
 Strategies to assist a patient in staying focused may
be needed
Modifications
 At the outset of each session, the therapist should
present a limited number of topics or themes to be
covered in the session; providing a patient with a
written list of these topics strengthens this strategy.
 The patient will find it easier to retain the topical
thread of a discussion if the therapist avoids long,
complex sentences and dialogue
Modifications
 Early in treatment, the therapist should establish a
contract or predefined set of rules for refocusing the
discussion if a session becomes derailed due to the
patient’s inattention or decreased self-monitoring
 The therapist and the patient should agree on a
prompt or cue phrase, such as “Let’s get back on
track,” to regain focus
Modifications
 The patient’s risk of becoming lost also can be
reduced if the therapist pauses frequently while
presenting therapeutic material or during
dialogue to allow the patient to mentally review
the previous 5 min of the session.
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Modifications
 It is difficult to achieve a cumulative effect if memory
deficits prohibit a patient from retaining the
conclusions, insights or context of even a single
session.
 Three aspects of memory dysfunction are germane to
the success of psychotherapeutic intervention:
working memory, long-term memory and metamemory
Modifications
 Meta-memory: self-monitoring of one’s own
Modifications
 Working Memory: the limited, temporary store
where new information is held while it is
manipulated in a meaningful way to solve a current
problem.
 Long-term memory: Memories formed over a longer
period of time from minutes to days or longer
Modifications
 Working Memory
 Frequently rehearsing verbal information
 Grouping similar psychotherapeutic topics or goals
 Regulate the rate at which verbal information is presented
memory (e.g. remembering to remember)
Modifications
 Long-term Memory
 Instruct the patient in ways to use symbolism
 Teach the client ways to generate visual images
 Use of mnemonic strategies
Modifications
 Meta-memory
 Help the patient to recognize and monitor his/her own
limitations. Such an awareness motivates the patient to
learn and use compensatory strategies and devices, the
most critical of which is the memory notebook.
 The memory notebook fosters organization and provides
a method for rehearsal of treatment information. Can be
coupled with an alarm device found on a digital
wristwatch.
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Modifications
Modifications
 In view of the highly verbal nature of psychotherapy
 Language deficits derived from right hemisphere
for substance abuse language deficits can seriously
diminish its effectiveness.
damage can be overlooked but are critical since
nonverbal aspects of language contribute
significantly to overall comprehension.


Direct consultation with a speech/language specialist can be
very helpful.
Journaling can be helpful for patients with motor based
language difficulty
Modifications
 Patients manifesting deficits in motivation, initiation
of behavior, abstract reasoning, insight, planning,
problem solving or impulse control can present the
most challenging situations.

Structure, goal, and action-based therapeutic strategies are
necessary.
Modifications
 When motivation for treatment is compromised by
decreased awareness or insight that a problem
exists, the use of video technology makes abstract
issues of therapy more salient for the patient.

Videotaping group setting reveals issues related to social
interaction that a TBI survivor might not have recognized
just from the subtle reactions of people in natural social
situations
Modifications
 The significance of current behavioral problems
should be emphasized to help the patient see the
importance of productive therapeutic work.

Discussing the impact of negative behaviors on family
members or a significant other can increase the patient’s
motivation for treatment.
Modifications
 Modeling of desired behavior is important
 Combining modeling and videotape technology
shows objective and salient examples of behaviors
to be targeted for treatment
 Additional structuring and rule setting within the
context of therapy may be required for patients
who have sustained orbital frontal damage and
therefore, experience increased impulsivity and
reduced self-regulatory capacities.
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Modifications
Modifications
 Awareness and Denial
 Diminished insight and awareness of self are common
sequelae of TBI and other neurological illnesses
 Three levels of awareness are: Information, Implication and
Integration
 Information Level
 Problems perceiving information about their disorders and can
even be completely unaware of any impairment (anosagnosia)
 Difficulty understanding medical information and material
related to the diagnosed condition also is classified as reduced
awareness at the information level
Modifications
Modifications
 Implication Level
 When patient’s perceive information but are incapable of
appreciating the implications or long-term consequences
of their conditions, deficits, or life situations.
 Integration Level
 Patient accurately perceives their condition and are
aware of the implications but are unable to absorb
emotionally the gravity or meaning of their situation.
Defense mechanisms such as denial may appear when
deficits of awareness occur at the integration level.
Model
Concent.
Impairment
Memory
Impairment
Executive
Impairment
MET
Summarize
Verbal Cues
Nonverbal
Cues
Familiarization, notes,
audio tape,
rehearsal,
homework
Role rever.
Paper/pen
problem
solving
Coaching
 To effectively treat an individual with a
neurological condition that affects self-awareness
it is critical to clarify the etiology of the awareness
deficit.
 Interventions will vary
Pain, Addiction and TBI
 Complex population
 The issues related to substance abuse and TBI treatment are similar for
behavioral pain management
 Addiction related to pain management may be better perceived as
“pseudo-addiction” in most cases
 Is chronic pain a type of brain injury?


CBT
Repeat info
Nonverbal &
verbal
cueing
Verbatim
written
materials
Homework
Videotape,
role playing,
in vivo
practice



Peri-aquaductal gray
Insular
Prefrontal cortex
Thalamus
Parietal Lobes
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Pain and Brain
Pain and Addiction
 30-50% of chronic pain patients experience cognitive
impairment
 fMRI studies indicate 30% reduction of cell volume
in the parietal lobes of chronic pain patients
 Specialized programs for people with both chronic
pain and addiction are currently being developed
 Interesting new treatments for chronic pain are
being developed that is responding to neuromatrix
theory of chronic pain (e.g. Scrambler Therapy)
References
 Allen & Woods, Eds (2014). Neuropsychological aspects of substance
use disorders. Oxford University Press
 Corrigan, J., Smith-Knapp, K. & Granger, C. (1998). Outcomes in the
first five years after traumatic brain injury. Archives of Physical
Medicine and Rehabilitation, 79, 298-305.
 Sparadeo, F. & Gill, D. (1989). Effects of prior alcohol use on head
injury recovery. Journal of Head Trauma Rehabilitation.
 Sparadeo, F. and Barth, J. & Stout, C. (1992). Addiction and traumatic
brain injury. In C.E Stout, J.L. Levitt & D.H. Ruben (Eds.), Handbook
for assessing and treating addictive disorders (pp. 237-251). New
York: Greenwood Press.
 Sparadeo, F. and D’Amato, S. (2014). Scrambler Therapy: Effective
use of artificial neurons in the treatment of chronic neuropathic pain.
Journal of Nurse Life Care Planning, 14, (4). 14-27. New York.
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