MedicineLakex

Microsoft powerpoint - substance abuse and tbi bianh.pptx [read-only]

TBI and the Problem of Substance Abuse Set Points of Drug Self Administration

– Impulse Control – Reflection/Empathy mTBI and complicated mTBI may also place  • Secondary Injury – Delayed edema– Hydrocephalus– Drug interactions– Organ failure– Seizure activity  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

 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 making it comparable to drugs such as heroin with dependence in 2011, or approximately 8% of the respect to legal penalties for use, possession and  Approximately 23.5 million Americans age 12 and  In 1969 84% of Americans were against legalization older required intervention for substance use.
of marijuana and 12% in favor of it.
 It is projected that disability caused by substance use  In 2011 46% of Americans are against legalization disorders will surpass that caused by any other and 50% in favor of legalization.
physical disease worldwide by 2020.
 Diagnosed when it is determined that substance use  A major distinction between substance dependence had led to significant recurrent negative and substance abuse is the compulsive use of the consequences in one or more of four domains over substances with an inability to control their use, the same 12-month period. These domains include: despite realization that use causes negative legal, interpersonal, work/school, hazardous  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.
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.

Factors Contributing to Vulnerability to Develop a Specific Kreek (Rockefeller University) & Hassin
(Columbia P&S), 2004
Single Nucleotide Polymorphisms (SNPs) in Genes:  REWARD, COMFORT, AND PLEASURE from
ordinary activities; and a degree of calming to fight  SNP — a single off unwanted stress. However, your genetics and
polymorphism, that is, environment greatly affect this cascade; and
one nucleotide or base of unfortunately, some of our genes come with variations called polymorphisms. Polymorphisms  Allelic Frequency: change the way the gene expresses itself. Most people will call this a predisposition. These 1–5% intermediate polymorphism's can alter their intended genetic >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.
 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.

>1/3 OF THE Total US Population Carries the DRD2 A1 (Over 100,000,000 people)
50% of African Americans carry the DRD2 A1 gene
58% of Hispanics carry the DRD2 A1 gene
72% of Asians carry the DRD2 A1 gene
85% of Native Americans carry the DRD2 A1 gene
 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  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 result in too much activity of the neurotransmitter are at greater risk for all RDS GABA which will prevent dopamine release from the neurons in the reward site of the brain (accumbens) .
behaviors including opioids and nicotine.  The result is increased cravings for drugs and food.  Carriers of the 3R allele of the MAO –A gene  Carriers of the 181 allele of GABAB3 gene have increased metabolism of dopamine in the have an altered function of GABA cell at the energy producing mitochondria. transmission leading to an augmented anxiety trait.  Having this allele causes an increased breakdown of dopamine in the cell resulting in reduced  Carriers of this Allele may be prone to dopamine in the storage sites and as such lower alcoholism to reduce the anxiety level. amounts of dopamine are released to combat stress as only one example.  Carriers have an inability to cope with  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 any mammal) to perform or repeat an action that high risk for all RDS behaviors because promotes survival is called the survival/reinforcement circuit. Its normal function this allele causes an enhanced is to reinforce an action that promotes survival (e.g. catabolism of dopamine in the synapse eating, drinking, having sex). It is also the part of after being released from the neuron at the brain most affected by psychoactive drugs.
the reward site of the brain.  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 regions via corticostriatal networks that are modulated by circuit is the Nucleus Accumbens Septi (NAc).
 The Ventral Tegmental Area, lateral hypothalamus and  These include the dorsolateral PFC, which is involved in amygdala also play important roles.
higher cognitive operations and decision-making; the OFC,  The control circuit, located mostly in the new brain, acts as which is involved in salience attribution and goal-directed a "stop" switch and is driven by the left orbital prefrontal behaviors; and the anterior cingulate cortex, involved in cortex. The stop switch works in conjunction with the inhibitory control and awareness in addicted subjects could fasciculus retroflexus and the lateral habenula, which underlie the enhanced incentive motivational value of drugs connect and communicate from the "Stop" switch to the and the user's loss of control over drug intake.
"go" switch.
Memory, Psychoactive Drugs and Euphoric Recall Old Brain – New Brain Distinction  When people use psychoactive drugs, memories of the  The old brain consists of: brainstem, cerebellum and experience are imprinted on the brain: where they got the mesocortex (mid brain), which contain the limbic drug, the reason they used it, and what feelings (emotional system (the emotional center).
and physical) resulted.
 Regulating physiological functions of the body.
 The stronger the drug, the more rapid the growth and proliferation of memory "footprints" (dendritic spines) and  Experiencing basic emotions and cravings (e.g. therefore the more deeply imprinted the memory.
anger, fear, hunger, thirst, lust, pain and pleasure).
 The earlier in life a person begins using drugs or practices  Imprinting survival memories (e.g. that green plant addictive behaviors, the longer and stronger the memories tastes good, this bad odor signifies danger) 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 Old Brain – New Brain  The old brain responds to internal changes and  The old brain is the senior partner and the new brain memories as well as to sensory inputs from external is the young upstart.
 Whenever the two brains are challenged by a crisis  When a person uses a psychoactive drug, most often such as fear or anger, there is an automatic tendency it is the old brain that remembers the experience and to revert to the more established old-brain function.
how it felt.
 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 Old Brain – New Brain  The new brain (neocortex) processes informaiton  Craving can override the new brain's rational arguments of from the old brain, from different areas of the new "too expensive" or "bad consequences" or "there's a brain, and from the senses via the peripheral nervous 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  The new brain allows us to speak, reason, create, common sense kicks in.
remember, make decisions and then act. The old  During intentional abstinence from a drug cravings are brain simply reacts.
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.
Old Brain – New Brain  The old brain and the new brain carry out their  As humans develop they continue to learn to integrate the functions by creating, storing and utilizing drives of the old brain and the common sense of the new memories. Even emotions and cravings depend on brain. Some people, however, lose some of this ability due memories. Some memories are stored on a to genetic learning abnormalities, a chaotic or abusive childhood, brain injury, the use of psychoactive drugs and conscious level (explicit memory) and some are the practice of compulsive behaviors.
stored on an unconscious level (implicit memory).
 Psychoactive drugs subvert the survival mechanism from  Storage, activation, and use of memories are at the common sense integration of the new and old brains, heart of the obsession to use drugs, which is one-half resulting in the irrational behavior of addiction, which of the addictive process.
relies on the "wants" of the old brain rather than the rational "needs" of the new brain.
 The OFC has been shown to participate in outcomes  Impairments of the OFC and ACC are associated related to primary reinforcers in both nonhuman and with compulsive behaviors and impulsivity, and it human studies. These neurons encode details has also been postulated that impaired modulation concerning the sensory properties of rewards, such of these regions by DA might underlie the as visual, olfactory and gustatory aspects, and the compulsive and impulsive aspects of drug-taking and size or timing of past or future rewards, as well as the magnitude of more abstract rewards and penalties.
 Impaired self-control plays a fundamental role in drug-taking behaviors in addiction. Successful self-regulation functions require top-down control from the PFC to the striatal and limbic regions involved with rewards and emotions.
 Impaired self-control in addicted people is believed to  Thus, dysregulated activity of the OFC could underlie reflect disrupted prefrontal regulation of striatal regions. both the impulsive choices for immediate rewards The level of impairment is influenced by the emotional and compulsive drug taking when the drug-induced state (negative mood increases impairment) and the DA increases may be profoundly attenuated in context (exposure to unexpected cues can also impair it).
addicted people. This loss of control might continue  Damage to the OFC also interferes with the inhibition of even when drug-taking has become less rewarding or responding to formerly rewarding cues that are no longer reinforcing, thus favoring the emergence of perseverative when adverse consequences far outweigh the behaviors even when these are no longer reinforcing psychological or physiological benefits of drug-taking.
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 injury is related to acute complications, longer hospital  The relationship between alcohol abuse and TBI is complex stays, and poorer discharge status.
and probably circular  Alcohol abuse prior to TBI has consistently been found to  Adolescents who drink regularly were twice as likely to mediate outcome from TBI. sustain a TBI compared with adolescents who had never  Corrigan (1995) documented that a history of substance used alcohol.
abuse is related to a wide range of outcomes, including  Initial alcohol-related TBI sustained after age 12 were higher mortality rates, poorer neuropsychological associated with a four-fold increased risk of repeat TBI by 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 exacerbate the effects of TBI on brain structure and and early medical outcomes.
 Patient's with +BALs on hospital admission have  TBI patients with a history of alcohol abuse lower levels of consciousness when admitted, longer demonstrated greater volumes of intracranial duration of coma, and longer lengths of  TBI patients with a history of alcohol abuse also have  Post-traumatic amnesia and loss of consciousness more pronounced local brain atrophy over time were significantly longer in groups of patients with compared to non-drinkers. pre-injury alcohol abuse.
Substance Abuse and TBI Mechanisms of Behavior Change  TBI sustained in people with a history of alcohol  Current evidence-based treatments for alcohol and intoxication at the time of the injury demonstrated worse drug-use disorders vary in theoretical foundations, cognitive outcomes than those with negative toxicology approaches and presumed mechanisms of action.
screens, with particular difficulty on tests of verbal intelligence, verbal memory and attention and  Yet, it remains a conundrum that these treatments are often equally effective across clients who differ  Harmful or hazardous alcohol use in the 12 months prior to substantially in neurocognitive impairment and TBI was associated with poorer verbal learning and other distinguishing features such as age, disorder memory and slowed processing speed.
severity, and co-occurring psychopathology  Previous alcohol abuse increases the risk for development of mood disorders following TBI Mechanisms of Behavior Change Mechanisms of Behavior Change  Several putative mechanisms of behavior change in  Key Question: Do the direct effects of
addiction treatments that have received relatively alcohol/drugs on the brain, or neurocognitive consistent support for enhancing treatment success problems due to co-occurring TBI, and metabolic include the clients motivation for behavioral change, and nutritional disturbances have down-stream the alliance between the treatment provider and the effects on addiction treatment processes and thereby client, the client's perceived self-efficacy to resist alter substance-use-related treatment outcomes, urges to use alcohol/drugs, and social support and/or psychosocial adaptation more generally? networks that support and encourage abstinence goals.
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 contribute to problems encountered in everyday compromise the structure and function of the living both during and after addiction treatment prefrontal cortex, which results in substantial  Thus, neuropsychological impairment may impairment to central executive control and contribute to the failure to regulate drinking and drug-taking behaviors in the moment, thereby  Memory impairment is also prevalent in addiction escalating the risk for relapse, and over the long term populations. This includes prospective memory may contribute to the maintenance of substance-use functioning, which refers to the memory needed to behaviors, even in the face of severe, negative plan and carry out future actions and involves consequences of such use.
integrated memory and executive functions.
Mechanisms of Behavior Change Mechanism of Behavior Change  Clinically, neuropsychological impairments have  In addition, in both alcohol- and drug-use-disordered been associated with reduced treatment retention clients, neuropsychological impairment interacted with and compliance, self-efficacy to resist urges to use self-efficacy to resist urges to use, such that a relatively alcohol/drugs, coping-skill development and other higher level of self-efficacy was a less robust indicator of successful substance use outcomes in impaired clients prognostic indicators of addiction treatment compared to those without neuropsychological impairment.
 This finding suggests that mechanisms of behavior change,  In a large study of alcohol-use-disordered clients, such as perceptions of self-efficacy to resist urges to use impairment led to less treatment compliance and alcohol and drugs, operate differently, or are perceived or lower self-efficacy to resist urges to use alcohol, reported less accurately in impaired clients.
which in turn predicted less successful outcomes following treatment.
Recap: Scope of the problem of Mechanisms of Behavior Change TBI and Substance Abuse  Greater involvement in A.A. has been observed in impaired compared to unimpaired clients, suggesting that social  20% to 30% of persons with TBI show alcohol intox- support for abstinence might be particularly useful to ication at hospitalization, minimal data on other drugs.
bolster treatment effectiveness in cognitively impaired  50% to 60% of adolescents and adults in acute rehabilitation have prior histories of substance abuse.
 More severe executive and verbal impairment at treatment entry predicted better substance-use outcomes in  Indices of brain structure and function suggest an outpatients who had frequent contact with a social network additive effect of substance abuse and TBI.
that supported abstinence, while impairment predicted  Substance abuse is associated with unemployment, poorer substance-use outcomes in clients with more severe living alone, criminal activity, lower subjective well- alcohol-use histories who had frequent contact with a social network that encourage drinking.
 Need for assistance controlling use going unmet.
 Vulnerable brain structures  Neocortex (especially the frontal lobes)  Limbic system (especially the hippocampus and  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 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  Head injury, encephalopathy lobes and cerebellum  Psychiatric conditions and the use of medicines and other  Frontal lobe blood flow continues to increase with abstinence returning to normal levels within four years  Cognitive deficits  Relapse leads to resumption of shrinkage, continued declines in metabolism and cognitive function and evidence of neuronal cell  Impaired reasoning  Impaired Learning (poor semantic encoding)  Impaired Visuoperceptual processing Wenicke's Encephalopathy  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.
 Tolerance to the various actions of  Neuropsychological impact benzodiazepines does not develop at the same rate.  Across 12 areas of cognitive assessment all long-term Benzo For example, tolerance to the hypnotic effects can users were impaired while using (Barker et al., 2004) develop rapidly while tolerance to the anxiolytic  All 12 areas improved with withdrawal effects tends to develop more slowly  11 areas of cognitive assessment were impaired as compared to normal controls 6 months after withdrawal  Discontinuance should occur gradually  Discontinuance syndrome: rebound, recurrence  Areas of long-term impairment  Heavy use of cocaine is associated with alterations  Verbal Memory of neurotransmitter systems in humans.
 Psychomotor speed  Speed of processing  These alterations can manifest as abnormalities in  Motor control/performance regional cerebral blood flow and cerebral glucose  Working memory metabolism in the prefrontal cortex and in other limbic areas, which in turn provide the substrates  General Intelligence for neurobehavioral effects (depression, compulsive behavior, cognitive deficits)  Nonverbal memory  Problem-solving  Verbal reasoning 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 Brain Hemorrhage  Cocaine-induced neurological abnormalities such as  Prefrontal brain regions, including the OFC, ACC, atrophy and/or cell death as a results of ischemic DLPFC and amygdala are activated during events, can also manifest as neuropsychological intoxication, craving and binging and deactivated during withdrawal.
 Vulnerable brain areas include: Orbitofrontal cortex,  These same brain areas are also involved in critical anterior cingulate cortex, the dorsolateral prefrontal behaviors such as decision-making, control and cortex, amygdala, putamen and cerebellum.
inhibition of inappropriate responses, conflict monitoring and evaluation of the saliency of a stimuli or reward.
 Based upon this brain-behavior relationship, Goldstein &  Based on this logic, the heavy use of cocaine, Volkow (2002) have proposed that cocaine addiction is a because of repeated ischemic events due to its syndrome of impaired response inhibition and salience vasoconstrictive properties, might have caused a attribution. This model conceptualizes addiction as a dysregulation of cognitive and emotional processes that state comparable to what is observed with lacunar results in overvaluing of drug reinforcers, the undervaluing infarcts in the white matter of the brain. This of alternative reinforcers and difficulty with the inhibitory might in turn, cause neurological states akin to cognitive control that culminates as an inability to abstain deconnection syndromes between regions within from drug taking.
Cocaine and Alcohol  Neurocognitive deficits associated with cocaine use  Many heavy cocaine users also use other substances, appear to be dose-related and persistent for at least 6 including alcohol.
months of abstinence. Heavy cocaine use = 4  Most studies have found that the interaction of cocaine and alcohol is associated with greater neuropsychological impairment.
 Deficits in executive function, spatial processing, memory, concentration and motor function.
 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 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 Frequency of Impairment by Neuropsychological  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  Reduced dopamine and serotonin activity in  Hypoperfusion in several brain areas including the frontal and parietal lobes.
 A decrease in neurofilament (NF-L) proteins  Hypoperfusion in abstinent (4 months) abusers in the frontal cortex. These proteins are thought to be involved in axonal transport and  Psychiatric comorbidity moderated these findings neuronal morphology, suggesting that such that hypoperfusion in the right frontal and decreases in NF-L may be associated with left temporal lobes occurred with depression and functional impairment, particularly executive in the right frontal lobe only in those with functions and other functions associated with antisocial personality disorder the frontal cortex.
 Methadone Maintenance Patients performed worse  Mintzer & Stitzer (2002) found MMP to be impaired than normal controls on tests of psychomotor on psychomotor speed, working memory, decision- performance, information processing, attention, making and meta-memory.
short-term memory, long-term memory and  A separate study in which the MMP group was problem-solving. Difficult to generalize from this divided into smokers and nonsmokers found that the study since 67% reported a history of head injury MMP smokers were more impaired than controls (Darke et al. 2000) and MMPI nonsmokers.
 MDMA is a compound with properties common  A pronounced MDMA-induced denervation to both the central stimulants and the has been visualized throughout the neocortex, striatum and thalamus, while lesser damage in  Difficulty to predict the behavioral effects of the hippocampus, hypothalamus and basal  Usually taken intermittently  MDMA depletes 5-HT.
 Not as reinforcing as cocaine or meth  Neuropsychological deficits in  Does not produce frank hallucinations attention/concentration, learning/memory, motor/psychomotor speed and executive functioning.
 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.
 Cannabis use produces a wide range of acute effects,  Cannabis research increased dramatically following including changes in mood, mental status, and the discovery of the cannabinoid receptor CB1. perception as well as promotes physiological  The CB receptors are in the family of G-protein- alterations (e.g. analgesia, neuroprotection and coupled receptors. Such proteins are involved in decreased intraocular pressure, body temperature, second messenger signaling, and modulate chemical inflammation, and neuronal excitability).
reactions inside cells.
 Acute subjective sensations commonly include  The highest concentration of CB receptors are in the sedation/relaxation, euphoria, depersonalization, basal ganglia, cerebellum, hippocampus and happiness/laughter and increased sensory perception or subtle perceptual distortions.
 Naturally occurring ligands in the brain:  Acute intoxication is associated with hypotension, paranoid thinking, anxiety, panic attacks,  Arachidonic acid (an essential fatty acid found in cell unpleasant feelings of depersonalization, and membranes and the brain)  Less frequent adverse reactions include: anxiety,  Neurocognitive Effects of cannabis: depression, paranoia, panic symptoms, panic  Acute Effects reactions or psychotic symptoms.
 Working memory difficulty  These less frequent adverse reactions are most often  Learning and recent memory (immediate recall) experienced by naïve users.
 Sustained Attention  Reduced motivation  Residual Effects  Mostly apply to heavy and recent users. After 4 weeks no  Neuropsychological Sequelae  0-6 hours after use  Deficits in psychomotor coordination  There are a number of OTC drugs that when used  Deficits in selective and sustained attention improperly can create euphoria at a similar level as  Deficits in speed of information processing illicit drugs of abuse.
 Deficits in learning and memory  Deficits in inhibition and executive functions 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.
 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".
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 (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 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-to- moderate 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.
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.
 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.
 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.
 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 (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 Quadrant III
Quadrant IV
Collaboration in the Integrated Treatment Integrated Treatment of Traumatic Brain Injury and Quadrant I
Quadrant II
Acute Medical Settings Collaboration in Rehabilitation Programs Acquired Brain Injury 4 Quadrant Model of Service Provision Integrated Treatment of TBI and SA Case Management to change the Quadrant III
Quadrant IV
Collaboration in the Integrated Treatment organize the team Substance abuse treatment to establish new attitudes, Integrated
Collaborative Care beliefs and skills Quadrant I
Quadrant II
Acute Medical Settings Collaboration in Rehabilitation Programs Screening & Referral Collaborative Care Rehabilitation toimprove functionalabilities Acquired Brain Injury 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.
Integrated Treatment of TBI and SA Integrated Treatment of TBI and SA  Unique challenge for persons with TBI: 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. Integrated Treatment of TBI and SA Integrated Treatment of TBI and SA  Unique challenge for persons with TBI: Substance abuse treatment to establish new attitudes, Substance abuse services are not cognitively and
beliefs and skills 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.
Rehabilitation to improve functional abilities Programmatic options: in-service and pre-service training, staff sharing, reduce barriers to consultation, allow more flexibility in program structure. Integrated Treatment of TBI and SA Integrated Treatment of TBI and SA Case Management to change the environment and  Unique challenge for persons with TBI: organize the team Substance abuse treatment Rehabilitation professionals have biased views
to establish new attitudes, and, thus, expectations about persons with substance
beliefs and skills 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.
Rehabilitation toimprove functionalabilities Programmatic options: in-service and pre-service training, staff sharing, reduce barriers to consultation. Integrated Treatment of TBI and SA Integrated Treatment of TBI and SA Case Management to change the  Unique challenge for persons with TBI: Case management requires the time to develop a
organize the team Substance abuse treatment strong therapeutic relationship and address multiple
to establish new attitudes, access and resource needs, while taking responsibility for
beliefs and skills 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.
Rehabilitation toimprove functional Programmatic options: skilled staff, specialized caseloads, smaller caseloads, flexibility structuring treatment. Making Services More Responsive • Initiate cross-training, facilitate consultation and explore staff-sharing options.
• Promote staff participation in "ad hoc" teams.
 Actively Using and Uninterested in Treatment  Impulsively Using and Interested in Changing • Take advantage of specialized caseloads.
 Regularly Using and Interested in Changing • Allow smaller caseloads and maximize consistency of  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.
Substance Abuse Assessment  Assessing substance abuse  Mostly males between the ages of 18 & 50.
 History taking  Most were substance users prior to TBI  Medical Issues  Most have ongoing emotional disability  Specifics regarding substance use  Most have executive function impairment and/or memory  Understanding the implications of specific drugs (e.g. MDMA).
 Understanding the circumstances of use  Most have slowed information processing  Assessing Neuropsychological Status  Taking Neuropsychological status into account when  Slowed Processing Speed planning treatment  Decreased Attention Span/Immediate recall  Cognitive demands of treatment  Word Finding Difficulty  Cognitive demands of living sober/drug free  Retrieval Difficulty  Executive Function Difficulty  Slowed processing = increased stress and demand in voc. Rehab  Assessing Readiness for Change  Word finding difficulty = decreased elaboration  Process of Change Model  Poor retrieval = loss of didactic information  Formal Assessment  Executive difficulty = poor self-cueing,  Change Ladders difficulty with reflection, empathy and planning  Executive difficulty = poor impulse control, failure to learn from negative experience, poor guidance.
Psychological Assessment  Assessing Emotional Status  Diagnostic Interview  Shaped by the Assessment results  Counseling Principles  Formal testing  Personality Assessment Inventory  Detailed Assessment of Posttraumatic Stress  Avoid Arguments  Point out discrepancies  Reduce barriers  Provide choice Initiating Treatment  Making Modifications  Formal Treatment approaches must be understood well  Over 100 models of counseling enough that modifications can be made.
 Even Self-Help approaches may need modifications  Modifications are necessary 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. attentional, linguistic, memory and reasoning or impaired verbal attention) requires flexibility planning deficits that could prevent the delivery of throughout the psychotherapy process.
effective psychological treatment.
 The scope and nature of psychological services for  These deficits represent the most basic level of the TBI/SA patient should stem from continual potential obstacles for the therapist.
appraisal, understanding and responsiveness on  The integration of cognitive rehabilitation may be the part of the therapist  For successful psychological intervention, a patient  Early in treatment, the therapist should establish a must be able to attend to and understand verbal contract or predefined set of rules for refocusing the material or therapeutic dialogue as it unfolds within 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  Strategies to assist a patient in staying focused may prompt or cue phrase, such as "Let's get back on track," to regain focus  At the outset of each session, the therapist should  The patient's risk of becoming lost also can be present a limited number of topics or themes to be reduced if the therapist pauses frequently while covered in the session; providing a patient with a presenting therapeutic material or during written list of these topics strengthens this strategy.
dialogue to allow the patient to mentally review  The patient will find it easier to retain the topical the previous 5 min of the session.
thread of a discussion if the therapist avoids long, complex sentences and dialogue  It is difficult to achieve a cumulative effect if memory  Working Memory: the limited, temporary store deficits prohibit a patient from retaining the where new information is held while it is conclusions, insights or context of even a single manipulated in a meaningful way to solve a current  Three aspects of memory dysfunction are germane to the success of psychotherapeutic intervention:  Long-term memory: Memories formed over a longer working memory, long-term memory and meta- period of time from minutes to days or longer  Working Memory  Frequently rehearsing verbal information  Grouping similar psychotherapeutic topics or goals  Meta-memory: self-monitoring of one's own  Regulate the rate at which verbal information is presented memory (e.g. remembering to remember)  Long-term Memory  Instruct the patient in ways to use symbolism  Help the patient to recognize and monitor his/her own  Teach the client ways to generate visual images limitations. Such an awareness motivates the patient to  Use of mnemonic strategies 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.
 In view of the highly verbal nature of psychotherapy  Language deficits derived from right hemisphere for substance abuse language deficits can seriously damage can be overlooked but are critical since diminish its effectiveness.
nonverbal aspects of language contribute  Direct consultation with a speech/language specialist can be significantly to overall comprehension.
very helpful.
 Journaling can be helpful for patients with motor based language difficulty  Patients manifesting deficits in motivation, initiation  The significance of current behavioral problems of behavior, abstract reasoning, insight, planning, should be emphasized to help the patient see the problem solving or impulse control can present the importance of productive therapeutic work.
most challenging situations.
 Discussing the impact of negative behaviors on family  Structure, goal, and action-based therapeutic strategies are members or a significant other can increase the patient's motivation for treatment.
 When motivation for treatment is compromised by  Modeling of desired behavior is important decreased awareness or insight that a problem  Combining modeling and videotape technology exists, the use of video technology makes abstract shows objective and salient examples of behaviors issues of therapy more salient for the patient.
to be targeted for treatment  Videotaping group setting reveals issues related to social  Additional structuring and rule setting within the interaction that a TBI survivor might not have recognized context of therapy may be required for patients just from the subtle reactions of people in natural social situations who have sustained orbital frontal damage and therefore, experience increased impulsivity and reduced self-regulatory capacities.
 Awareness and Denial  Information Level  Diminished insight and awareness of self are common  Problems perceiving information about their disorders and can sequelae of TBI and other neurological illnesses even be completely unaware of any impairment (anosagnosia)  Three levels of awareness are: Information, Implication and  Difficulty understanding medical information and material related to the diagnosed condition also is classified as reduced awareness at the information level  Implication Level  To effectively treat an individual with a  When patient's perceive information but are incapable of neurological condition that affects self-awareness appreciating the implications or long-term consequences of their conditions, deficits, or life situations.
it is critical to clarify the etiology of the awareness  Integration Level  Patient accurately perceives their condition and are  Interventions will vary 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.
Concent.
Pain, Addiction and TBI Impairment Impairment Impairment
 Complex population  The issues related to substance abuse and TBI treatment are similar for Verbal Cues tion, notes, 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?  Peri-aquaductal gray  Prefrontal cortex Nonverbal & written  Parietal Lobes Pain and Brain
Pain and Addiction  30-50% of chronic pain patients experience cognitive  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 neuromatrixtheory of chronic pain (e.g. Scrambler Therapy)  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.

Source: http://www.bianh.org/pdf/SubstanceAbuseTBI.pdf