Psychiatric Disorders

·         SIG-E-CAPS: sleep changes (increase during day or decreased sleep at night, Interest (loss of), Guilt (worthless), Energy (lack of), Cognition/Concentration (reduced/difficulty), Appetite (weight loss), Psychomotor (agitation- anxiety, retardations- lethargic), Suicide (Ideation/Preoccupation); RISKS FOR SUICIDE- male, living alone, EtOH, comorbid physical illnesses

b.      Age of onset: mid-teens to late 20s

2. Diagnostic Studies

a. Psychological testing not useful to diagnose MDD.

b. No laboratory findings/imaging useful since it’s state dependent

(seasons); consider Low T4 once on somatic tx’s (antidepressants, lithium, sleep deprivation, ECT)

c. Dexamethasone Suppression Test: little use as clinical marker for MDD.  However, in some depressed patients, this allowed researchers to predict or monitor long-term tx outcome.  Ie) DST+ patients RESPONDED FAVORABLY to ANTICDEPPRESSANTS or ECT

d. Corticotropin-Releasing Hormone Test: In those depressed patientsàBLUNTED ACTH response noted

e. Sleep Electroencephalogram “EEG”- MOST DEPRESSED PATIENTS HAVE INSOMNIA. Results: shortened REM latency, shift of slow-wave sleep (stages 3 and 4), increased REM density during first few hours of sleep.  MAY BE NORMAL after ACUTE MDD episode.  Great for differentiating b/w Delirium vs. Depression vs. Dementia

f. Brain Imaging– Possible decreased PFCortex (left), blood flow and metabolism.  Basal ganglia abnormalities?

3. Diagnosis

a. 5+ of the following symptoms present during a 2-week period with at least one of the symptoms either (1) depressed mood or (2) loss of interest or pleasure:

Depressed mood, Markedly diminished interest/pleasure, significant weight loss when not dieting or weight gain or increase/decrease in appetite, Insomnia/hypersomnia, Psychomotor agitation or retardation, Fatigue or loss of energy, feelings of worthlessness/excessive/inappropriate guilt, diminished ability to think/concentrate/indecisiveness, recurrent thoughts of death/suicide

b. Symptoms don’t meet criteria for a mixed episode

c. Symptoms cause stress/impairment in social, occupational, or other important areas of fxning.

d. Symptoms not related to substance abuse (physiological effects) or medical condition (hypothyroidism)

e. Symptoms not accounted for by: bereavement (symptoms persist >2 months)

f. Differential Diagnosis: Bipolar disorder, Schizoaffective Disorder

Make sure: 1) illness not d/t substance abuse or medical condition 2) illness not part of mixed episode and 3) symptoms aren’t accounted for by bereavement

4. Health Maintenance

a. No association between Social Class or Menopause and MDD

b. High risk in families w/ h/o depression or alcoholism

c. Less common in African Americans

d. May be preceded by: recent negative life events, personalities

(insecure, worried, introverted, stress sensitive, obsessive, unassertive, dependent), early childhood trauma (significant loss, environment- disruptive/hostile/negative), postpartum, and relative lack of interpersonal relationships

e. More common in adolescent and adult females, More common overall in age group 25-44 y/o

5. Clinical Intervention

a. Electroconvulsive Therapy (ECT)- most effective in most severely depressed patients.  Less useful in those who have concurrent mental/medical dz or in tx of depression that was refractory to meds.

b. When refractory to general medications.. try Lithium carbonate, thyroid hormone (T3).

c. Phototherapy: especially for those w/ Seasonal Affective D/O

6. Clinical Therapeutics

a. FIRST LINE Selective Serotonin Reuptake Inhibitors– “Citalopram- Celexa, Escitalopram- Lexapro, Fluoxetine- Prozac, Fluoxamine- Luvox, Paroxetine- Paxil, Sertraline- Zoloft” (NOTE: Fluoxetine has quickest half life of 3-6 days) meaning also higher risk of getting Antidepressant Discontinuation Syndrome if d/c’d ABRUPTLY.  (should taper over 6-8 weeks); AE: GI disturbances, Anorgasmic OR

Selective Dual-Action Reuptake Inhibitors (aka SNRIs)– Inhibits reuptake of 5HT + NE; “Duloxetine- Cymbalta, Venlafaxine- Effexor”

Mixed Action Antidepressants/”Atypical”– Inhibits NT reuptake and blocks NT receptors- “Atomoxetine- Strattera, Bupropion- Wellbutrin, Mirtazapine- Remeron, Nefazadone- Serzone, Trazodone (tetracyclic amines– Desyrel”

b. SECOND LINE

Tricyclic Antidepressants (TCAs)- Tertiary Amines: “Amitriptyline- Elavil, Doxepin- Sinequan, Imipramine- Tofranil”, Secondary Amines: “Amoxepine-Asendin, Despiramine- Norpramin, Maprotiline- Ludiomil, Nortriptyline- Pamelor, Protriptyline- Vivactil”

TCAs used in OCD- clomipramine, Enuresis- imipramine, psychotic depression- amoxapine, reducing craving in cocaine w/drawal- desipramine

ACCUMULATION OF HISTAMINE AND ACETYLCHOLINE CAUSES HIGH ADVERSE EFFECTS vs. SSRIs or DUAL ACTION AGENTS

Adverse rxns w/ TCAs (anticholinergic effects): dry mouth, constipation, confusion, heat stroke

c. THIRD LINE

Monoamine Oxidase Inhibitors (MAOIs)- “Phenelzine- Nardil, Tranylcypromine- Parnate, Selegiline- Elderyl”; (monoamines = dopamine, serotonin, NE)

MUST NOT EAT TYRAMINE RICH FOODS (Cheese/Deli meats/Smoked meats or fish/Red wine/Beer/Soy sauce) and BEWARE OF OTHER CNS INTERXNS

d.      Overall ADVERSE EFFECTS (esp if used w/ mood stabilizer): Increased agitation, suicidality, serotonin syndrome, sometimes Akathisia and other extrapyramidal symptoms (dystonias) especially in withdrawal states

d.      Stimulants: dextroamphetamine and methylphenidate

7. Scientific Concepts

a. Dysfunction of Serotonin, Norepinephrine, and Dopamine Neurotransmitters

b. MAO and COMT degrades 5HT

c. MAO and COMT and NA reuptake transporter degrades Noradrenaline

d. TCAs binds to monoamine reuptake transporters to prevent reuptake and degradation of 5HT and NA

b.      Duration of episode: before 1960 = 7-13 months; after 1960= 2-4 months

c.       Recovery: 5-10% don’t recover

d.      Mortality and Suicide: 10-15% of patients with bipolar I disorder COMPLETES SUICIDE

e.      Fluctuation between periods of deep, prolonged and profound depression and excessively elevated or irritable mood known as mania

f.        2 Types: Bipolar I and Bipolar II

2.       Diagnostic Studies

a.       Psychological Testing: Not involved in Bipolar Diagnosis

* “Dickstein and Leibenluft” Cambridge Neuropsychological Test Automated Battery (CANTAB) shows difficulties in attentional set shifting and visuospatial memory in pediatric bipolar disorder.  Children with bipolar and anxiety d/o’s misinterpreted sad/happy/fearful child faces s angry vs. healthy children.

b.      No lab findings are diagnostic

c.       Neuroimaging- preliminary.  MRI suggest white matter hyperintensities in cortical and subcortical brain regions and smaller amygdalar size.

3.       Diagnosis

a.       Manic Episode: Abnormal and persistently elevated/expansive/irritable mood for 1+ week (or any duration if hospitalized)

* During the disturbance, must have 3+ of following symptoms

-Inflated self-esteem or grandiosity

-Decreased need for sleep (ie- feels rested after 3 hours of sleep)

-More talkative than usual or pressure to keep talking

-Flight of ideas or subjective experience that thoughts are racing

-Distractibility

-Increase in goal-directed activity or psychomotor agitation

-Excessive involvement in pleasurable activities with high potential for painful consequences (unrestrained buying sprees)

-Symptoms doesn’t meet criteria for a Mixed Episode

b.      Hypomanic Episode: Persistently elevated, expansive, or irritable mood lasting 4+ days clearly different from nondepressed mood

* Same as above (Manic Episode)

* Episode associated with an unequivocal change in fxning that is uncharacteristic of the person when not symptomatic

* Disturbance in mood/fxning is noticeable by others

* Not severe enough to cause marked impairment in social or occupational fxning or to necessitate hospitalization; NO PSYCHOTIC FEATURES

* SYMPTOMS NOT D/T SUBSTANCE ABUSE OR MEDICAL CONDITION

c.       MIXED EPISODE = Criteria met both for Manic Episode and Major Depressive Episode nearly EVERY DAY during at least 1 week period

* MARKED IMPAIRMENT NOTED IN FXNING

* NOT D/T SUBSTANCE ABUSE NOR GENERAL MEDICAL CONDITION

d.      BIPOLAR I-

* Currently/recently in a Manic Episode

* Previously at least 1 MDD, Manic Episode, or Mixed Episode

* Mood episodes in the first 2 criteria aren’t better accounted for by Schizoaffective Disorder and not superimposed on Schizophrenia, Schizophreniform D/O, Delusional D/O, or Psychotic D/O NOS

e.      BIPOLAR II

* Presence (H/O) 1+ Major Depressive Episodes

* Presence (H/O) 1+ Hypo(mild) manic Episode

* NEVER has there been a MANIC episode NOR a MIXED episode

* Mood episodes in the first 2 criteria aren’t better accounted for by Schizoaffective D/O and are not superimposed on Schizophrenia, Schizophreniform D/O, Delusional D/O, or Psychotic D/O NOS

* Symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

f.        Differential Diagnosis: ADHD, schizophrenia, pervasive developmental disorder, child abuse, seizure disorders or other medical condition, substance abuse (steroids, amphetamines, cocaine)

4.       Health Maintenance

a.       Correlation b/w genetics and neuroimaging findings and Bipolar disorder; ie) stressful family environment and abuse associated w/ earlier onset, if 1 twin has Bipolar D/O most likely the other twin has it too

b.      High rates in children of coexisting ADHD and anxiety D/O

c.       In everyone else, comorbid disorders include: ADHD, ODD, Conduct D/O, Anxiety D/O, Substance-use D/O, and pervasive developmental D/O

5.       Clinical Intervention

a.       Psychotherapy: CBT may be effective in 8-18 y/o’s with BP

·         Reward-based CBT with interpersonal psychotherapy; “empathetic validation”

b.      Psychoeducation: teaching parents and teachers about symptoms, course, and tx of BP

c.       Family focused therapy (FFT): addresses concerns of adolescents with BP and builds resources to manage stress and lower expressed emotion w/in family

d.      ECT (electroconvulsive therapy)

e.      Omega-3 fatty acids: FDA approved 3g/day in adults

6.       Clinical Therapeutics

a.       For BP1, Manic or mixed Episode without psychosis: Mood stabilizer +Atypical Antipsychotic

* First line = Mood Stabilizers (if non psychotic mania): Lithium, Divalproex (Depakote/Valproic Acid), and Carbamazepine OR Atypical Antipsychotics (yields a quicker response in patient): Olanzapine, Quetiapine, and Risperidone

* If only mild to moderate improvementàadd another agent to augment results (most likely another: mood stabilizer or atypical antipsychotic)

* If still no optimal resultsàdo monotherapy with another agent

b.      For bipolar depression: Lithium(prophylactic drug)/Depakote/Atypical Antipsychotics/Lamotrigine OR Traditional Mood stabilizers + Atypical Antipsychotics + SSRIs/Bupropion

c.       Note: since most children and adolescents with BP also have comorbid d/o’s like ADHD, tx should be directed to comorbid d/o’s

d.      ADVERSE EFFECTS OF MEDS: All meds for BP-Weight gain (leading to DM, Hyperlipidemia, and elevation of LFTs), Valproate (Black box warning- PANCREATITIS), Lithium (Hypothyroidism, weight gain, changes in renal fxn)

e.      No studies for BP II tx in children and adolescents

7.       Scientific Concepts

a.       N-acetyl-aspartate, choline, myoinositol, and creatinine/phosphocreatinine affected in fronto-striatal region, cingulated cortex, DLPFC, and other areas of brain

b.      Pediatric BP- small amygdala size, decrease in hippocampal volume, white matter hyperintensities in cortical and subcortical brain regions, smaller parietal and temporal lobe cortical gray matter, reduced gray matter volume in dorsolateral prefrontal cortex, larger basal ganglia, increase in putamen size, increased left thalamus

b.      Hypomania can be triggered by interpersonal stressors or by losses.

2.       Diagnostic Studies

a.       Psychological Testing of no use

b.      Laboratory tests of no use

c.       Neuroimaging of no use

3.       Diagnosis

a.       At least 2 year (1 yr in children and adolescents) duration of symptoms milder than those in MDD or Manic episodes

b.      Differential diagnoses: Shizoaffective d/o, schizophrenia, schizophreniform d/o, delusional d/o, psychotic d/o NOS.  (Adjustment disorder, medication-induced, schizophrenia, partial complex seizures, panic d/o’s, anxiety d/o’s, thyroid dysfxn, malignancies/tumors, strokes)

4.       Health Maintenance

a.       There is a link between 1^st relatives having MDD and BPI/II in patients w/ cyclothymic d/o

5.       Clinical Intervention– NONE OF VALUE

6.       Clinical Therapeutics

a.       Lithium for hypomanic cycles

b.      Bupropion/MAOIs/low dose SSRIs + Lithium/other mood stabilizersà for if patient’s depression was treated w/ TCA solely resulting in rapid cycling

c.       ADVERSE EFFECTS: sleep disorders

7.       Scientific Concepts

a.       Begins early in life

2.       Diagnostic Studies

a.       Psychological Testing- Minnesota Multiphasic Personality Inventory

·         Can help ID suidical risk and degree of depression

b.      Neuropsychological testing- no impairments found unless they have depression or other d/o’s

c.       Laboratory findings- elevated cortisol levels in response to stress (not specific to adjustment d/o), decrease in delta sleep

d.      Neuroimaging- If refractory to treatment, may image to get DDx

·         May be able to reveal epilepsy

·         MRI- may reveal Hallervorden-Spatz disease (eye of tiger)

3.       Diagnosis

a.       Emotional or behavioral symptoms occurring as a reaction to identifiable stressors occurring w/in 3 months of onset of stressor

b.      These symptoms result in significant impairment of social/occupational fxning OR marked distress more than normal is noted

c.       Doesn’t meet another Axis I specific d/o nor an exacerbation of Axis I/II d/o

d.      Symptoms don’t persist for more than add’l 6 months (ie- 9 months?)

4.       Health Maintenance

a.       M/C in adolescents when compared to adults

b.      Adjustment d/o’s appear more often in indvls who are at risk for otherpsych d/o’s

c.       Risk factors: prior stress exposure, stressful early childhood experiences, and h/o mood/eating d/o, families who are divorced/not united, families who move constantly (ie- military), immigrant populations, prison populations

d.      Little genetic link

e.      Link w/ Type A personalities

5.       Clinical Intervention

a.       Behavioral- CBT, Interpersonal, family or supportive psychotherapy

b.      Nontraditional- Relaxation techniques, yoga, and massage

6.       Clinical Therapeutics

a.       FIRST LINE: Antidepressant (ie: sertraline- SSRI)

b.      SECOND LINE: Hypnotics- Zolpidem “Ambien” (ONLY if patient has no h/o EtOH abuse) OR Anxiolytics- Clonazepam (Benzo)

c.       Herbal Preparations: St. John’s Worts?

7.       Scientific Concepts

a.       Neurobiological characteristics (ie- elevated corticosteroids blood levels in response to stress) have been associated w/ Adjustment d/o’s just as it has been associated w/ PTSD

b.      Similar to MDD except without the depressive symptoms

2.       Diagnostic Studies

a.       Neuroimaging: GAD associated w/ asymmetric increases in N-acetylaspartate-creatinine ratio showing “neuronal viability” in right dorsolateral prefrontal cortex.

3.       Diagnosis

a.       Excessive anxiety and worry occurring many days for at least 6 months

b.      Person finds it difficult to control the worry

c.       Anxiety and worry are associated w/ 3+ of the following symptoms (in children, only 1 item required):

·         Restlessness/feeling on edge

·         Easily fatigued

·         Difficulty concentration/mind going blank

·         Irritability

·         Muscle tension

·         Sleep disturbance

d.      Disturbance isn’t due to substance abuse nor medication use, nor a medical condition or another mood or psychotic D/O

e.      Differential Diagnosis: MDD, Panic D/O, OCD, Separation anxiety D/O, Anorexia nervosa, Somatization D/O, Hypochondriasis, PTSD, other medical illnesses (cardiac, endocrinologic, neoplastic, pulmonary, neurologic)

4.       Health Maintenance

a.       Slightly more common in women; usually is chronic

b.      High rates of comorbidity w/ Major Depression

c.       Genetical link: twins, heritable

d.      GAD is more common to present in a medical office vs. a psychiatric office

5.       Clinical Intervention

a.       Behavioral therapy- deep muscle relaxation to desensitize

b.      Other therapies- marital, family, occupational

c.       No psychological testing nor laboratory studies that prove helpful

d.      Neuroimaging: abnormalities in limbic, paralimbic, and sensory association regions.

6.       Clinical Therapeutics

a.       Treat underlying causes

·         FIRST LINE- Buspirone (Serotonin1A Receptor Partial Agonist)- no abuse potential, no motor/memory/concentration impairments; ADVERSE EFFECTS: anxiety/nervousness, h/a, nausea

·         SECOND LINE- Imipramine(TCA); ADVERSE EFFECTS: anticholinergic/ Venlafaxine(SNRI); ADVERSE EFFECTS: sexual dysfxn, w/drawal rxns, anxiety/nervousness, diarrhea

·         Benzos- reduces symptoms; not curative, slow to moderate dosages.  After a few weeks, this should be reduced and eventually d/c’d due to risk of abuse esp in those w/ EtOH abuse hx; ADVERSE EFFECTS: daytime sedation, ataxia, accident proneness, H/A’s, memory problems, paradoxical excitement or anxiety.

7.       Scientific Concepts

a.       Abnormalities in fxning of these 3 areas- 1) Gamma Amino Butyric Acid (GABA) receptor/Benzodiazepine Receptor/Chloride Channel Complex; meds are benzos that interxct w/ GABA receptors, 2) Noradrenergic Nucleus locus coeruleus and related brain stem nuclei; meds are TCAs that activate noradrenergic receptors, and 3)Serotonin system (raphe nuclei and their projections); meds are SSRIs or Buspirone that interact with serotonergic activity

b.      May occur in people who have repeated hospital/ER visits since each panic attack they may think that they are getting a “heart attack or stroke”

c.       The feeling that an attack is reduced in “safe places”- home or with “safe people”- spouse or parent in the event a panic attack occurs

2.       Diagnostic Studies

a.       Labs: Patients with this have greater anxiety responses to the inhalation of enhanced CO₂ mixtures vs. Patients w/o Panic D/O

b.      Neuroimaging: Emerging evidence that 5HT1A receptor binding is REDUCED

3.       Diagnosis

a.       Both 1) recurrent, unexpected panic attacks AND 2) at least 1 of attacks has been followed by 1+ month of: persistent concern about having add’l attacks, worrying about implications of attack or consequences, or significant change in behavior related to attacks

b.      Presence or absence of agoraphobia

c.       Panic attacks are not due to the direct physiological effects of a substance or a general medical condition

d.      Aren’t better accounted for by another mental d/o

e.      PANIC ATTACK: 4+ of the following start starts abruptly and peaks w/in 10 minutes

·         Palpitations/pounding heart/accelerated heart rate

·         Sweating

·         Trembling or shaking

·         Sensations of shortness of breath or smothering

·         Feeling of choking

·         CP or discomfort

·         Nausea or abdominal distress

·         Feeling dizzy, unsteady, lightheaded, or faint

·         Derealization or depersonalization

·         Fear of losing control or going crazy

·         Fear of dying

·         Paresthesias (numbness/tingling)

·         Chills or hot flashes

f.        DDX: OCD, specific and social phobias, PTSD, MDD, Psychotic D/O’s, and personality D/O’s; DIFFERENCE IS- SPONTANEOUS PANIC ATTACKS = PANIC D/O. OTHER MEDICAL DDX: Paroxysmal atrial tachycardia, pulmonary embolus, seizure d/o, Meniere’s dz, TIA, carcinoid syndrome, Cushing dz, hyperthyroidism, true hypoglycemia, pheochromocytoma

4.       Health Maintenance

a.       Mid twenties is median age

b.      More common in females than males

c.       Strongest familial link

5.       Clinical Intervention

a.       CBT: Cognitive Behavioral Psychotherapy (“Interoceptive exposure”- spinning in place, hyperventilating voluntarily, ingesting large amounts of caffeine) can be used to reduce both agoraphobic avoidance, while recognizing and correcting catastrophic thoughts to avoid panic attacks themselves

6.       Clinical Therapeutics

a.       Treatment of choice: Psychotherapy- Behavioral or CBT

b.      For severely ill patients: can use Meds (TCAs- Imipramine, MAOI- Phenelzine, SSRI- Paroxetine, Sertraline, Benzos- Alprazolam, Clonazepam, SNRI- Venlafaxine) in combo w/ Psychotherapy

·         +Agoraphobia

·         +MDD or Personality D/O

·         Suicidal ideation

·         Patient preference

7.       Scientific Concepts

a.       Comorbid depression worsens outcome of panic disorder and increases rate of suicide

2.       Diagnostic Studies

3.       Diagnosis

a.       1) Person was exposed to a traumatic event in which they experienced/witness/confronted with events involving actual/threatened death/serious injury or threat to self/others + 2) Person’s response involved intense fear/helplessness/horror; (Note: in children, this may be expressed instead by disorganized or agitated behavior)

b.      Reexperience occurs resulting in recollections of event, including images, thou

4.       Health Maintenance

5.       Clinical Intervention

6.       Clinical Therapeutics

7.       Scientific Concepts

A1. NEEDS 6+ OF THE FOLLOWING for at least 6 months-Fails to give close attention to details or makes careless mistakes in schoolwork, work, or other activities; Often has difficulty sustaining attention in tasks or play activities; doesn’t seem to listen when spoke to directly and doesn’t follow thru on instructions, failing to finish chores or duties; often loses necessary things; easily distracted; forgetful in daily activities OR

 -Hyperactivity (some age<7y/o):

A2. NEEDS 6+ OF THE FOLLOWING for at least 6 months- fidgets with hands or feet or squirms in seat, leaves seat in classroom, runs or climbs excessively inappropriately (restlessness), Difficulty playing or engaging in leisure activities quietly, often talks excessively, often “on the go” or acts as if “driven by a motor”

                  -Impulsivity (some age<7y/o):

Blurts out answers before questions have been completed, can’t wait his turn, interrupts or intrudes on others

b. Some hyperactive-impulsive or inattentive symptoms that caused impairment were present before age 7 y/o

c. Some impairment from symptoms is present in 2+ settings

d. There must be clear evidence of clinically significant impairment in social, academic, or occupational functioning

e. The symptoms don’t occur exclusively during the course of a Pervasive Developmental D/O, Schizophrenia, or other Psychotic D/O, and not better accounted for by another mental D/O.

2. Diagnostic Studies

     a. Rating Scales: Available for all age groups and can monitor and assess home, academia, and occupational performance; “Likert ratings”

b. Psychological Testing: May be helpful in narrowing the DDx and IDing comorbid learning difficulties

c. Labs- not indicated unless h/o seizures, neurodevelopmental regression, or localizing neurologic signs or if medical d/o suspected

-Neuroimaging: CT or MRI: structural brain abnormalities of smaller volumes of frontal cortex, cerebellum, and subcortical structures.  Dysfxn of frontosubcortical pathway since those w/ ADHD have pathways rich in catecholamines so body naturally increases reuptake of NE and DA.

3. Diagnosis via DSM IV

a. Attention-Deficit/Hyperactivity D/O, Combined Type: A1 +A1 for past 6 months

b. Attention-Deficit/Hyperactivity D/O, Predominantly Inattentive Type: A1 for past 6 months

c. Attention-Deficit/Hyeractivity D/O, Predominantly Hyperactive-Impulsive Type: A2 for past 6 months

d. Differential Diagnosis: Oppositional Defiant Disorder (negativistic, hostile and defiant behavior), Conduct D/O (severe d/o of habitual rule breaking w/ aggression/destruction/lying/stealing/trancy; strong predictor of substance abuse), Mood D/O (higher rates of depression in those w/ ADHD), childhood anxiety d/o’s, cognitive performance and learning disabilities, ADHD +Tics, Sbstance-Use D/Os

4. Health Maintenance

a. Association w/ Morbidity and Disability in children, adolescents, and adults

b. Those w/ ADHD in youth are at risk for developing other psych difficulties in childhood, adolescence, and adulthood including delinquency, mood, anxiety, and substance-use disorder.

c. Risk Factors: food additives/diet, lead contamination, cigarette and EtOH exposure, maternal smoking during pregnancy, and low-birth weight, psychosocial adversity (family conflicts).

5. Clinical Intervention (non-pharmacological)

a. Psychotherapy (school consultation, classroom aide, 8-week summer tx program, 35 sessions parent management training)

6. Clinical Therapeutics (note: transdermal patch bypasses 1^st pass effect)

a. 1^st line: Stimulants release intrasynaptic catecholamines/inhibits presynaptic reuptake to release catecholamines(Methylphenidate– Ritalin/Concerta, Dimethylphenidate– Focalin, Dextroamphetamine– Dexadrin, Lisdexamfetamine– Vyvanse, Mixed amphetamine salts– Adderall)

b. 2^nd line: Atomoxetine- Strattera (NE reuptake Inhibitors)

c. 3^rd line: Tricyclic Anti-depressants

d. 4^th line: Antihypertensives- Clonidine (Catapress), Guanfacine (Tenex)

e. Other: Antinarcoleptic- Modafinil

7. Scientific Concepts (not enough norepi nor dopamine)

a. Dysregulation of Noradrenergic and Dopaminergic neurons in brain

-Norphinephrine in frontal cortex mediates attention, concentration, working memory, and information processing

-Dopamine in prefrontal cortex mediates focus, vigilance, acquisition, and perception

-Drugs that elevate synaptic norepi and/or dopamine transmission in brain cortex have greatest impact on ADHD symptoms