How Advances in Neuro-Science Impact the Way we

Conceptualize and Deliver Treatment

Presenter: Dr. Felix A. OrtizLicensed Clinical Neuropsychologist

FADAA Annual Conference, Orlando FL.August 14, 2009

How Advances in Neuro-Science Impact the Way we Conceptualize

and Deliver Treatment• Identify brain damages associated with

neurotoxic substances and advances in the field

• Identify cognitive rehabilitation principles• Conceptualization and Treatment

applications of cognitive rehabilitation principles

EQUIFINALITY• Definition: Developmental psychopathology

principle that a behavior or disorder may have several different causes.

• “…the concept that a particular disorder may arise from multiple and different paths, is particularly appropriate for substance disorders”.

• Just as there are many reasons for a fever, there may be number of reasons for depression.

Durand and Barlow, 2006

Neurotoxic

• Difficulties:1. diffused vs. focal 2. recently systematically studied3. emphasis on neurotoxic properties of

these compounds, i.e. cocaine, heroin and others, is reasonably new

Hartman 2000,1995

Neurotoxic cont.: principles of neurotoxic damage

• “The influence of neurotoxic substances on behavior is the end result of biochemical, structural and functional interaction on the human organism.”(Spencer, 1990).

• Direct: i.e. damage to the neuron, indirect damage, i.e. lungs.

• Damage maybe silent/subclinical Hartman 1995

Neurotoxic cont.: principles of neurotoxic damage

• Neurotoxic damage varies based on substance and exposure; i.e. intranasal, I.V., or smoked

• Damage conceived in syndromes

Hartman 1995

Cocaine as a neurotoxicant: Neurochemical effects:

• Lipid-soluble penetrating BBB. • Interacts with dopaminergic circuits, (stimulates

production and blocks reuptake). Precipitates depression-depletion cycles, depletion in thyroid axis (partially related psychological cocaine induced depression and drug induced hypothyroidism

• Blocks norepinephrine reuptake Hartman 1995

Cocaine as a neurotoxicant: neurophysiological effects

• Powerful CNS stimulant: massive adrenergic discharge “fight or flight”. Increase in alpha waves in frontal and temporal structures and increase in beta in frontal and central region.

• Seizures of tonic-clonic type: “kindling”= outward spread of electrical activity from the limbic system.

Hartman 1995

Cocaine as a neurotoxicant: Chronic effects

• Marked reduced alpha power in frontal and temporal regions.

• Cerebral atrophy: decreased cerebral blood flow (CBF) mode; IV and inhaled

• Hypoprofusion in frontal, periventricular and/or temporal areas; impairment in attention concentration and new learning mode; smoked

• Ischemic and hemorragic stroke mode; smokedHartman 1995

Cocaine use and comorbidity• Anhedonia, anxiety, anergia, paranoia,

depression and bipolar mood disorder.• Anxiety, phobias, ADHD, APD, depression

and alcoholism tend to precede. • Changes may persist for months and

years.

NIDA: Research Monograph 163

Conceptual relationships between brain damage and

cocaine/stimulant abuse

Brain Damage:Habenula

Fasciculus retroflexusVTA

Raphe Hippocampus

Prefrontal Cortex

Cocaine/Stimulant Abuse

Brain Trauma

Genetic Errors

PTSD

Environmental Toxins

Developmental Errors

Neurophysiology of Cocaine Use

• Prefrontal cortex• Temporal regions• Parietal regions • Periventricular

Neurophysiological interface of depression and cocaine neurotoxicity

• Hippocampal-Pituitary-Adrenal Axis• Dopaminergic circuits• Noredrenergic circuits

Research Design• Correlational Design• Hypothesis:

- Positive correlation between the severity of cocaine (PAI DRG) use and depressive symptoms (PAI DEP) r=.*50 r²=28%

- Positive correlation between cocaine severity (PAI DRG) and neurobehavioral deficits (MAQ COG)

- Positive correlation between depressive symptoms (PAI DEP) and neurobehavioral deficits (MAQ COG) r= .*54 r²=30%

Participants

• 72 hrs of supervised abstinence, ARF• Cocaine (crack) use only• No prior neurological history• No prior mental health history• No prior

Participants cont.

• 50 participants completed all three questionnaires

• Ethnic breakdown – 17 European-American 34%– 29 African-American 58%– 3 Latino 6%– 1 Asian-American 3%

Participants cont.

• Educational background- Average educational level 11.7- Range 8th to 3 years of college

• Substance use history - 26 (52%) participants reported daily use - 25.6 years old average onset of substance use- 32 (64%) were between 32 and 42 years old- 38 (76%) reported between four to 13 years of substance use

Psychometric Tools

• Personality Assessment Inventory– Depression (DEP)– Drug (DRG)

• Maryland Addictions Questionnaire– Cognitive (COG)

• State/Trait Depression Adjective Check List (ST-DACL) form 1

Results• A moderately strong positive correlation

between the severity of cocaine (PAI DRG) use and depressive symptoms (PAI DEP) r=.*50r²=28%

• Not statistically significant, clinically significant association between cocaine severity (PAI DRG) and neurobehavioral deficits (MAQ COG)

• Positive correlation between depressive symptoms (PAI DEP) and neurobehavioral deficits (MAQ COG) r= .*54 r²=30%

Traditional challenges• The substance abuse field was conceived,

influenced and shape by individuals in recovery.

• Limited formal training and education in the topics for professionals in the field.

• Emphasis in linear models, conceptualization, assessment and treatment.1. “Denial”2. “Don’t want it”3. “Have not hit bottom”4. “Not ready”

Traditional challenges; cont.

• Neurosciences and other sciences recently included in the picture.

• Emphasis in behaviors. • Gap between research and clinical

practice.

Depression Associated with Cocaine Use:

Neuropsychological Considerations

Integrative Model

• Bio-psycho-social• Durand & Barlow

Exposure To

substance

DrugUse

Psychological influence

Psychosocialstressors

Drug Abuse

Drug Dependence

Biological Influences

Cognitive Remediation: based on Luria’s model

• Principle of differential restoration and functional system, (what higher cerebral processes are intact and which are not).

• Principle of teaching through systems of information processing not affected.

• Extended program of restorative activity: breakdown task to simpler series of articulated routines.

• Constant signalization of the defect and effect of the actions.

Rosenthal, Griffith, Bond and Miller (1990)

Gorski’s Model

• PAW• Internal and external cues• Use of building blocks/steps in treatment• Emphasis on understanding of effects• Emphasis on process• Emphasis the learning from the

experience

Self Help Groups

• These programs tend to emphasize: sameness, predictability, consistency, and simplicity.

• Emphasize what works, repetition, gradual increase level of difficulty– Keep it simple– Just for today– This shall pass

• Emphasize complete abstinence

Bibliography • Carlson, N.R., Physiology of Behavior, Fifth Edition, Allyn & Bacon,

Paramount Publishing, 1994 • Durand, V.M. Barlow, D.H., Essential of Abnormal Psychology, Fourth

Edition, Thomson and Wadsworth, United States, 2006 • Hartman, D.E.; Neuropsychological Toxicology: Identification and

Assessment of Human Neurotoxic Syndromes, Second Edition, Plenum Press, New York and London,1995

• Herman, J., Stimmel, B., The Neurobiology of Cocaine Addiction, Haworth Medical Press, 1996

• National Institute on Drug Abuse, Research Monograph Series 163,Neurotoxicity and Neuropathology Associated with Cocaine Abuse, p. 1-16

• Ortiz Pedraza, F.A., Depressive Symptomatology Associated with Crack Cocaine: Neuropsychological considerations, 2001

• Rosenthal, M., Griffith, E.R., Bond, M.R., Miller, J.D., Rehabilitation of the Adult and Child with Traumatic Brain Injury, Second Edition F.A. Davis Company Philadelphia, 1990

• Strub, R.L., Black, F.W., Neurobehavioral Disorders: A Clinical Approach, F.A. Davis Company Philadelphia, 1992