Goals for Today

The Medication-Maltreatment Collision: After the workshop, participants will be able to: Psychopharmacology and Neurobiology for Play Therapists (1) Have an understanding of brain development and functioning as they relate to affect, behavior, and play therapy.

(2) Differentiate the complexities of brain functioning in non-maltreated and Franc Hudspeth, PhD, NCC, LPC-S, RPh, RPT-S, ACS, CPC, DDP-1 maltreated children and adolescents. Associate Dean, Southern New Hampshire University (3) Identify different medications and their mechanisms of action. Editor, International Journal of Play Therapy [email protected] (4) Understand the interaction of neurobiology, medication, and maltreatment, and playtherapytraining.com play therapy.

(5) Discern how medication side effects may impair play therapy process and how to utilize play therapy techniques to compensate for medication side effects. New York Association for Play Therapy March 23, 2019 (6) Develop an individualized, play therapy treatment plan for medicated, dysregulated children and adolescent

1 Brain Complexities Nervous System

2 Nervous System (cont) Endocrine System

Sympathetic NS The Endocrine System is Arouses the body’s slow (fight-or-flight) chemical communication system. Communication is Parasympathetic carried out through NS hormones synthesized Calms by a set of glands. (rest and digest)

3 The Basic Brain Brainstem

Self-regulation, Vision and Sensory motor Hearing, problem solving, perception perception, & language, goal setting, & spatial abilities memory, & The Thalamus [THAL-uh-muss] is Reticular Formation is a nerve social cognition social the brains sensory switchboard, network in the brainstem that plays emotional located on top of the brainstem. It an important role in controlling function directs messages to the sensory areas arousal. in the cortex and transmits replies to the cerebellum and medulla.

4 The Limbic System Cerebellum

The Limbic System is a doughnut-shaped system of neural structures at the border The “little brain” of the brainstem and attached to the rear of cerebrum, associated the brainstem. It helps with emotions such as coordinate voluntary fear, aggression and movements and drives for food and sex. balance. It includes the hippocampus, amygdala, and hypothalamus.

The Hypothalamus lies below (hypo) the thalamus. It directs The Amygdala [ah-MIG- several maintenance dah-la] consists of two lima activities like eating, bean-sized neural clusters drinking, body linked to the emotions of temperature, and fear and anger. control of emotions. It helps govern the endocrine system via the pituitary gland.

6 The Cerebral Cortex Functions of the Cortex

The intricate fabric of interconnected neural cells that The Motor Cortex is the area at the rear of the covers the cerebral hemispheres. It is the body’s ultimate control and information processing center. frontal lobes that control voluntary movements. The Sensory Cortex (parietal cortex) receives information from skin surface and sense organs.

7 Brain Changes Brain Changes (cont)

At birth, most neurons the brain will have are present Overproduction of neurons and connections among (approx. 100 billion neurons) neurons By age 2 years, brain is 80% of adult size Selective reduction of neurons and connections among What keeps growing? neurons Other brain cells (glia) Waves of intense branching and connecting followed by New neuron connections reduction in neurons approx. 1000 trillion connections by age 3 yrs. Before birth through 3-years-old Again at 11- or 12-years-old

8 Brain Changes (cont) Brain Changes (cont)

Anatomical studies of brain development show Myelin & Age Changes Occipital lobes show earliest pruning Frontal and Temporal lobes show growth of neural Speed of connection and conductivity connections longer than other areas of the brain… Begins at birth, rapidly increases to 2-years old through 3 years old Continues to increase more slowly through 30-years- Frontal and Temporal lobes show pruning of old connections longer than other areas of the brain

Greatest change between 2 years and 5 years

9 Brain Changes and Important Brain Changes - Critical Events (Toga & Mazziotta, 2000) Developments Brain areas with longest periods of organization related to… self-regulation, problem-solving, language/communication Social bonding Most vigorous growth, pruning, connecting, and activity occurs between 1-1/2 years through 3 or 4 years old. May be one of the most important periods for developing self-regulation, problem-solving, social- emotional, and language/communication behaviors.

10 Impacting Brain Development Brain Areas and Anatomical Development Genes form neurons, connections among major brain regions. • Brainstem (0-1)--Regulation of arousal, sleep, and fear Environment and experience refines the • Diencephalon (1-3)--Integration of sensory input and fine connections; enhancing some connections motor skills while eliminating others. • Limbic System (3-8)--Emotional states and emotional Brain development is activity-dependent regulation, social language, interpretation of non-verbals Every experience excites some neural circuits and • Cortical Areas (8-adult)--Abstract cognitive functioning, leaves others alone. integration of socio-emotional information Neural circuits used over and over strengthen, those that are not used are dropped resulting in *Brain stem and Diencephalon are harder to change if poorly pruning. developed. Medication ?????????????????

11 Source: Australian Childhood Foundation, 2010, Making Space for Learning: Trauma Informed Practice in Schools, pp 21.

12 Polyvagal Theory Polyvagal Theory

The more primitive branch elicits • The vagus nerve is a component of the autonomic nervous immobilization behaviors (e.g., feigning death), system • Originates in the medulla whereas the more evolved branch is linked to • Two (2) branches social communication and self-soothing • Associated with a different adaptive behavioral strategy behaviors. • Inhibitory in nature via the parasympathetic nervous system • The vagal system is in opposition to the sympathetic-adrenal system, which is involved in mobilization behaviors

13 Normal Development and Regulation Polyvagal Theory Dorsal branch Consider: • unmylenated The Individual • primal survival strategies Attachments • freezing Ventral branch Relationships • Mylenated Culture • A sophisticated system of behavioral and affective Environment responses to an increasingly complex environment Genetics • Regulates of the sympathetic “fight or flight” Produces Functional & Regulated Affect/Behavior • Social Communication, Calming, Self-soothing • Can inhibit or disinhibit the limbic system

Adaptive Functioning (Shore, 2001, 2009) The Right Brain

The right brain, according to Schore (2000 and 2009b) is comprised of a • lateral tegmental circuitry, which controls negative emotions, avoidance mechanisms, and passive coping • a ventral tegmental circuitry, which controls positive emotions, approach mechanisms, and active coping

Order of Activation The Ventral System

• The autonomic nervous system, providing sensory information; Schore (2000, 2009b) states, when • amygdala, which generates fight, flight, attachment is disrupted or fails to occur (i.e., and freeze responses; lacks appropriate stimulation), it is the ventral tegmental circuitry that is impacted • cingulate, which interprets social cues; by dysfunctional patterns of relating; hence, • orbitofrontal cortex, which provides the approach process is disrupted and executive control. avoidance process goes unaffected.

Whats Functional? Neurobiology and Attachment 3 Types of Self-Regulation • Secure Attachment- a person capable of • Emotional Self-Regulation--between self emotional self-regulation and has the ability and caregiver (self & other). to cope with stress • Behavioral Self-Regulation--the ability to • Secure Attachment in Neurobiological initiate/inhibit behavior appropriate to Formation: healthy, consistent, and complete context. development of the orbitofrontal cortex, • Sensory Modulation--the ability to ventromedial prefrontal cortex, and regulate ones reactivity (responsiveness) connections in to subcortical regions of the to sensory input. brain.

17 Okay, So Let’s Consider Dysfunction and Attachment Neurobiology Process Dysregulation?

External Input/ Events In Life

Audio, Visual, Tactile Posterior Cortex The Dysregulated Brain Has a Mind of Its Own!!!!!!

Internal Input Whats Leads to Dysfunction? Dopaminergic (DA), Seratonergic (5HT), Nuclei in the Subcortical reticular •Abnormal Development Noradenergic (NE) formation • Attachment Disturbances

Prefrontal Cortex • Direct Physical Brain Trauma

Executive Control Center for Arousal

18 Right Brain Development: Affect Regulation (Schore, Abnormal Development and Dysregulation 2001)

Consider: • Amygdala inhibition by orbitofrontal The Individual regions Attachments Relationships • Amygdala hijacking – fight response Culture • Hippocampus memory systems and Environment Autonomic Nervous System (ANS) Genetics • Consequences of Trauma Produces Dysfunctional & Dysregulated Affect/Behavior – Poor affect regulation

19 The Neurochemical Origins of Disruptive Traumatic Brain Injury Behaviors Childhood illnesses (high fevers, meningitis) • Those related to dopamine [DA] and aggression, irritability, hyperactivity, and problems with attention

and motivation; Accidents or Physical Abuse • Those related to norepinephrine [NE] and negative emotions and withdrawal; ???? Medications ?????? • Those related to serotonin [5HT] and impulsivity. • A fourth category, gamma-aminobutyric acid [GABA], is not usually responsible for disruptive behaviors, but may be involved in regulating these behaviors.

20 Disruptive Behaviors, Neurotransmitters, and Disruptive Behaviors, Neurotransmitters, and Brain Regions Brain Regions (cont) • Emotional regulation is connected to the limbic system and prefrontal cortex (Wise, 2004) and is facilitated by DA and • Impulsivity is connected to the dorsolateral prefrontal cortex, NE pathways. orbitofrontal cortex, and anterior cingulate cortex (Adinoff et al., 2003; Royall et al., 2002) and is facilitated by DA and 5HT (Dagher & Robbins, 2009). • Motivation is connected to the striatum and prefrontal cortex (Aarts, van Holstein, & Cools, 2011) and is facilitated by DA pathways. • Finally, the previously mentioned neurotransmitters are excitatory in nature, while GABA is inhibitory in nature and connected to all levels of the central nervous system (Levy & • Attention and hyperactivity are connected to the lateral Degnan, 2012). prefrontal cortex, dorsal anterior cingulate cortex, caudate, & putamen (Bush, Valera, & Seidman, 2005) and are facilitated by DA and NE pathways.

21 TRAUMA Two Conditions Lead to Traumatization: Trauma Defined Negative life events that cause multiple psychological responses from victims • • TYPE I Overwhelming Fear – Victims who have experienced a single traumatic event • Inescapable • TYPE II – Victims of repeated, chronic trauma, such as emotional, physical and sexual abuse

Terr (1990, 1994) - theorizes that dissociation is not as pre- valent a defense in single trauma because trauma is not expected However, in repeated and chronic trauma, dissociation becomes the defense needed for survival.

22 Abuse Trauma Relationship Trauma Simple vs Complex Trauma (Acts of Commission) (Acts of Omission) Simple Trauma Complex Trauma • Threats of harm to self &/ • Neglect Non-interpersonal Interpersonal or others • Abandonment Limited Exposure Multiple Exposures: • Physical abuse/violence • Loss Short Duration different trauma types • Sexual abuse • Repeated Separations Onset typically at later Longer Duration • Witnessing Domestic • Bullying developmental stage Onset at early stage of Violence Family Support development Situational Brain Lack of family support Dysregualtion Brain Dysregulation Secure attachment Insecure Attachment

Neurobiological Changes in Children with PTSD DeBellis et al. (Cont’d) (DeBellis et al., 1999)

• Abused children excreted greater amounts of cortisol and • Study: University of Pittsburgh, took MRI catecholamines than non-abused kids

scans of the brains of 44 children with • Abused children had 7-8% less cerebral volumes (impairing histories of abuse and diagnoses of PTSD memory, dysregulating arousal) and compared them with 61 healthy • Neurons enlarge with age and axons thicken. Between the ages of 5 and 18 years, the process of coating the neurons in the controls who had not experienced abuse. central nervous system with a myelin sheath is most influential in determining brain size The average age of the subjects was 12 years • In the PTSD children, the corpus callosum did not grow with age compared with controls, which may be due to a failure of myelination.

24 The Prefrontal Cortex The Prefrontal Cortex (PFC)

• • Connected with the amygdala and exerts inhibitory Allows “executive control” – or at least control over stress responses and emotional guidance – over more primitive brain reactivity; goals, reason, controls habits structures • Middle region is critical to relational • Prefrontal cortex actually shrinks with PTSD; functioning, empathy, connecting children/adolescents/young adults don’t have developed PFC • Helps us with:

– Being able to focus • Successful SSRI treatment restored PFC activation – Memory and reason patterns – Self-awareness, reflection, emotions, impulses

25 Other Neurobiological Responses Areas of Impairment During trauma chemical changes in the body increase the brain’s release of painkilling hormones - “Freeze-numbing responses may serve the function of allowing organisms to not ‘consciously experience’ or to not remember situations of • Physical biology of the individual overwhelming stress” van der Kolk, 1994, p. 257. • Attachment to others* Trauma may be stored: • Affect Regulation* Body sensations Movements • Dissociation* Feelings • Behavior Management Images • Sounds Cognitive Processing • Self-Concept*

High Arousal (Fear) = Impaired Prefrontal Cortex * Key Elements in Developmentally Stress chemicals disable the mid cortex and limbic brain takes over Appropriate, Neurobiologically-Informed Treatment

26 Startle Physiological Hypervigilenc Foreshortened hyperarousal e Psychomotor future Nightmares agitation Hopelessnesss DISSOCIATIVE SYMPTOMS Generalized Intrusive anxiety Panic memories Decreased attacks Flashbacks concentration Insomnia Somatization Amnesia Substance abuse • Re-experiencing the Trauma Eating disorders Decreased Numbing interest • Avoidance Self-destructive behavior

Irritability Identity • Psychic Numbing disturbance • Depression Depression Trauma Depersonalization Derealization • Difficulty Concentrating • Hypervigilance Anxiety Disorder Major Depression • Panic PTSD Borderline Personality

Bremner & Marmer, 1998

27 Dissociation False Connections

State-dependent learning - ability to take in information, store it, and remember it under certain external and internal conditions The brain makes associations between sensory signals that Dissociation - partitions off the information from co-occur in any given moment in time. This capacity allows us everyday experiences to Events remains outside of awareness survive but it also makes us vulnerable to false associations. Situation occurs that is similar (may not seem to be to others) to the trauma Triggers symptoms of PTSD or DID These false associations impact children in a number of ways. They can cause a traumatized child to jump at a loud sound or Personalities in DID - separate learning states - environment lash out at a raised voice, either of which may not be triggers that state - personality emerges that contains the threatening information that matches the context. at all but increase arousal based upon memories of abuse.

28 Other Risks Associated with Complex The ACE Study (Anda et al., 2005; CDC, Trauma 1998-2010; Edwards et al., 2005) Adverse childhood experiences are the most basic cause of health risk behaviors, morbidity, disability, mortality, and

healthcare costs • At higher risk for re-victimization • Lifelong risk of interpersonal Traumatic events----Prolonged alarm reaction-----Altered neural systems Attachment Problems Altered cardiovascular regulation Behavioral impulsivity Treatment Should Focus on Attachment and Attachment Security Increased anxiety Increased startle response Sleep abnormalities

29 CDC (1998-2010)

30 As the number of ACEs increases so does the risk for ACE the following Old New • Emotional abuse • Emotional abuse • Alcoholism and alcohol abuse • Risk for intimate partner violence • • Physical abuse Physical abuse • Chronic obstructive pulmonary • Multiple sexual partners • Sexual abuse disease • Sexually transmitted diseases • Sexual abuse • Physical neglect • Depression • Smoking • Physical neglect • Emotional neglect • Fetal death • Suicide attempts • Emotional neglect • Household mental illness • Health-related quality of life • • Property victimization Unintended pregnancies • Mother treated violently (nonsibling) • Illicit drug use • Early initiation of smoking • Household substance • Peer victimization • Ischemic heart disease • Early initiation of sexual activity abuse (nonsibling) • Liver disease • Adolescent pregnancy • Exposure to community • Household mental illness violence • Poor work performance • Risk for sexual violence • Incarcerated household • Socioeconomic status • Financial stress • Poor academic achievement member • Someone close had a bad accident or illness • Parental separation or • Below-average grades divorce • Parents always arguing • No good friends (at time of interview)

31 Stress, the Brain, & the Body

• Stress is the set of changes in the body and the brain that are set into motion when there are threats to physical or psychological

• Under threat, the limbic system engages and the frontal lobes disengage. When safety returns, the limbic chemical reaction stops and the frontal lobes re- engage.

(van der Kolk, B., 2005)

WHEN STRESS ---BECOMES---TRAUMA

Stress becomes trauma when the intensity of the frightening events becomes unmanageable to the point of threatening physical and psychological integrity (Lieberman et al., 2008)

33 Early Childhood Disturbances from Trauma and Risk (ACE Study) The Continuum

Regulatory disturbances Attachment Disturbance PTSD Oppositional Defiant Disorder ADHD, Bipolar Disorder Conduct Disorder Oppositional Defiant ADHD Conduct Disorder Anxiety and Depression Personality Disorder Attachment disturbances Developmental delays

34 Neurotransmitters What’s The Point? Categorized into three major groups:

We Now Have a Neurobiological Maze, Which (1) amino acids (glutamic acid, GABA, & glycine) is Difficult to Solve? (2) peptides (vasopressin, somatostatin, & neurotensin)

And (3) monoamines (norepinephrine NA, dopamine DA & serotonin 5-HT) plus acetylcholine (ACh).

Medications Can Simplify the Maze or Workhorse neurotransmitters of the brain are glutamic Complicate Maze! acid (glutamate) and GABA.

35 Neurotransmitters & Function Neurotransmitter (Excitation vs. Inhibition) Acetylcholine - voluntary movement of the muscles, learning, & memory EXCITATORY INHIBITORY Norepinephrine – alertness, wakefulness, & arousal Acetylcholine GABA Dopamine - voluntary movement, emotional arousal, & learning, attention Aspartate Glycine Serotonin - memory, emotions, wakefulness, sleep, hunger, & Dopamine temperature regulation Histamine GABA (gamma aminobutyric acid) - motor behavior & mood Norepinephrine Glutamate - memory Epinephrine Glycine - spinal reflexes & motor behavior Glutamate Neuromodulators - sensory transmission-especially pain Serotonin

36 Dopamine (DA) Serotonin (5-HT)

Dopamine is transmitted via The principal centers for three major pathways. The first serotonergic neurons are the extends from the substantia nigra rostral and caudal raphe to the caudate nucleus-putamen nuclei. From the rostral raphe (neostriatum) and is concerned nuclei axons ascend to the with sensory stimuli and movement. The second pathway cerebral cortex, limbic projects from the ventral regions and specifically to the tegmentum to the mesolimbic basal ganglia. Serotonergic forebrain and is thought to be nuclei in the brain stem give associated with cognitive, reward rise to descending axons, and emotional behavior. The some of which terminate in third pathway, known as the the medulla, while others tubero-infundibular system, is descend the spinal cord. concerned with neuronal control of the hypothalmic-pituatory endocrine system.

37 Norepinephrine (NE) Gamma-aminobutyric acid (GABA)

Many regions of the brain are GABA is the main inhibitory supplied by the neurotransmitter in the central noradrenergic systems. The principal centers for nervous system (CNS). noradrenergic neurons are the GABAergic inhibition is seen at locus coeruleus and the caudal all levels of the CNS, including raphe nuclei. The ascending the hypothalamus, hippocampus, nerves of the locus coeruleus cerebral cortex and cerebellar project to the frontal cortex, cortex. As well as the large well- thalamus, hypothalamus and established GABA pathways, limbic system. Noradrenaline GABA interneurons are is also transmitted from the abundant in the brain, with 50% locus coeruleus to the cerebellum. Nerves projecting of the inhibitory synapses in the from the caudal raphe nuclei brain being GABA mediated. ascend to the amygdala and descend to the midbrain.

38 Glutamate Acetylcholine (Ach) There are three Acetylcholine In the normal brain the prominent pathways in the CNS. (a) The glutamatergic pathways are: the Pons to thalamus and cortex, cortico-cortical pathways; the (b) Magnocellular forebrain pathways between the thalamus and nucleus to cortex, & (c) the cortex; and the extrapyramidal Septohippocampal. In the pathway (the projections between central nervous system, ACh the cortex and striatum). Other has a variety of effects as a glutamate projections exist between neuromodulator upon the cortex, substantia nigra, plasticity, arousal and reward. subthalmic nucleus and pallidum. Glutamate-containing neuronal ACh has an important role in terminals are ubiquitous in the the enhancement of sensory central nervous system and their perceptions when we wake up importance in mental activity and and in sustaining attention. neurotransmission is considerable. ACh has also been shown to promote REM sleep

39 Transmission Research, Use, & Age

>6 months –diazepam (Valium), chlorpromazine (Thorazine) >2 yrs –Valproate (Depakene), lamotrigine (Lamictal) (for seizures) >3 yrs – hydroxyzine (Atarax), dextroamphetamine (Dexedrine) >5yrs- imipramine (Tofranil) (for enuresis) >5 yrs –risperidone (Risperdal), autistic disorder with irritability >6 yrs – atomxetine (Strattera), methylphenidate (Ritalin), sertraline (Zoloft)

40 Several Neurotransmitters Are Involved in Research, Use, & Age (cont) Regulating Mood

>7yrs- fluoxetine (Prozac) Norepinephrine Serotonin >8yrs- fluvoxamine (Luvox) Anxiety >10 yrs –risperidone, bipolar mania Irritability Energy Impulsivity >13 yrs-risperidone, Schizophrenia Interest >12 yrs old – thiothixene (Navane), molindone (Moban), Mood, emotion, perphenazine (Trilafon), Clonidine (Catapres), Lithium, cognitive function Sex Appetite lorazepam (Ativan), amitryptilline (Elavil) Motivation Aggression Unspecified – thioridazine (Mellaril), trifluoperazine (Stelazine), carbamazepine (Tegretol) Drive

Dopamine

Stahl SM. Essential Psychopharmacology: Neuroscientific Basis and Practical Applications. 2nd ed. Cambridge, UK: Cambridge University Press; 2000:152.

41 Gamma-aminobutyric acid (GABA) Antianxiety Agents GABA is the main inhibitory neurotransmitter in the central nervous system (CNS). GABA receptors GABAergic inhibition is seen at all levels of the CNS, including Valium (diazepam) the hypothalamus, hippocampus, cerebral cortex and cerebellar Ativan (lorazepam) cortex. As well as the large well- Klonopin (clonazepam) established GABA pathways, GABA interneurons are Xanax (alprazolam) abundant in the brain, with 50% of the inhibitory synapses in the brain being GABA mediated.

42 Antianxiety Agents (cont) Serotonin (5-HT) The principal centers for serotonergic neurons are the Valium/Ativan/Klonopin/Xanax rostral and caudal raphe nuclei. From the rostral raphe Clumsiness nuclei axons ascend to the cerebral cortex, limbic Sleepiness regions and specifically to the Dizziness basal ganglia. Serotonergic nuclei in the brain stem give Irritability rise to descending axons, some of which terminate in Unsteadiness the medulla, while others Confusion descend the spinal cord. Problems with memory

43 Antianxiety Agents (cont) Antianxiety Agents (cont)

5HT Receptors 5HT Buspar (buspirone) Buspar Confusion, Dizziness, Disinhibition, Drowsiness MISC (MOA unknown) MISC Atarax (hydroxizine HCl) Atarax/Vistaril Vistaril (hydroxizine pamoate) Cognitive Impairments, Sedation, Blurred Vision

44 Norepinephrine (NE) Serotonin (5-HT) Many regions of the brain are supplied by the The principal centers for noradrenergic systems. The serotonergic neurons are the principal centers for rostral and caudal raphe noradrenergic neurons are the nuclei. From the rostral raphe locus coeruleus and the caudal nuclei axons ascend to the raphe nuclei. The ascending cerebral cortex, limbic nerves of the locus coeruleus regions and specifically to the project to the frontal cortex, basal ganglia. Serotonergic thalamus, hypothalamus and limbic system. Noradrenaline nuclei in the brain stem give is also transmitted from the rise to descending axons, locus coeruleus to the some of which terminate in cerebellum. Nerves projecting the medulla, while others from the caudal raphe nuclei descend the spinal cord. ascend to the amygdala and descend to the midbrain.

45 Antidepressants Antidepressants (cont)

TCA (NE and/or 5HT reuptake presynaptic) TCA Elavil (amitriptyline) Elavil/Tofranil/Pamelor Asendin (amoxapine) Anafranil (clomipramine) Fatigue Norpramin (desipramine) Drowsiness/Insomnia Sinequan (doxepin) Tofranil (imipramine) Mild Tremors Pamelor/Aventyl (nortriptyline) Nightmares Vivactil (protriptyline) Restlessness Surmontil (trimipramine) Confusion

46 Serotonin (5-HT) Antidepressants (cont) The principal centers for serotonergic neurons are the rostral and caudal raphe SSRI (selective seratonin reuptake inhibitors) nuclei. From the rostral raphe nuclei axons ascend to the cerebral cortex, limbic Celexa (citalopram) regions and specifically to the Lexapro (escitalopram) basal ganglia. Serotonergic nuclei in the brain stem give Prozac/Sarafem (fluoxetine) rise to descending axons, some of which terminate in Paxil (paroxetine) the medulla, while others Zoloft (sertraline) descend the spinal cord. Luvox (fluvoxamine) Viibryd (vilazodone) Trintellix (vortioxetine)

47 Antidepressants (cont) Antidepressants (cont)

SSRI MAOI (monoamine oxidase inhibitors) Celexa/Prozac/Paxil/Zoloft/Lexapro/Viibryd Agitation Nardil (phenelzine) Nervousness Parnate (tranylcypromine) Fatigue Marplan (isocarbozide) Sleep Problems Vertigo Sexual Side Effects

48 Norepinephrine (NE) Antidepressants (cont) Many regions of the brain are supplied by the noradrenergic systems. The MAOI principal centers for noradrenergic neurons are the Nardil/Parnate/Marplan locus coeruleus and the caudal raphe nuclei. The ascending nerves of the locus coeruleus project to the frontal cortex, Dizziness thalamus, hypothalamus and limbic system. Noradrenaline Headache is also transmitted from the locus coeruleus to the Sleep Problems cerebellum. Nerves projecting from the caudal raphe nuclei ascend to the amygdala and descend to the midbrain.

49 Antidepressants (cont) Serotonin (5-HT) SNRI

The principal centers for Effexor (venlafaxine) serotonergic neurons are the rostral and caudal raphe Cymbalta (duloxetine) nuclei. From the rostral raphe Pristiq (desvenlafaxine) nuclei axons ascend to the cerebral cortex, limbic Fetzima (levomilnacipran) regions and specifically to the Savella (milnacipran) basal ganglia. Serotonergic nuclei in the brain stem give MISC (MOA unclear) rise to descending axons, some of which terminate in the medulla, while others Desyrel (trazodone) Oleptro (trazodone hcl) descend the spinal cord. Wellbutrin/Zyban (bupropion) Remeron (mirtazepine) Serzone (nefazodone)

50 Antidepressants (cont) ,

MISC Intake Desyrel/Wellbutrin/Effexor/Serzone/Cymbalta/ Pristiq/Remeron Gathering Information

Agitation Drowsiness Sleep Disturbance Initial Treatment Plan Strange Dreams Increased Blood Pressure

51 Gathering Information Intake

Past medications: List, in chronological order, all psychotropic medications The Initial Play Therapy Session the individual took in the past. If the list is long, print it separately and bring it to your appointment.

Observation: Medication Symptoms/Impact Age Medication Name Dose Comments Behavioral Changes ______Cognitive Changes ______Emotional Changes ______

52 Medication/Behavioral/Cognitive/Emotional/Developmental Intake Time Line

Current medications: List, in chronological order, all psychotropic medications the individual is currently taking. Don’t forget about over-the counter medications.

Age Medication Name Dose Comments ______

53 The Initial Treatment Plan Medication Side Effect Goals/Objectives Interventions

• How will you address medication side effect(s) as part of the therapeutic process?

• Can you link a skill/activity/technique to a side effect and reduce its impact on therapy?

• What can you do to accomplish side effect reduction as well as therapeutic progress?

54 Addressing Medication Side Effects in the Treatment Plan Left and Right Brain

4 Presentation Types, Each Requires Something Different LEFT BRAIN FUNCTIONS RIGHT BRAIN FUNCTIONS uses logic uses feeling The Warm Up detail oriented "big picture" oriented facts rule imagination rules words and language symbols and images The Cool Down present and past present and future math and science philosophy & religion can comprehend can "get it" (i.e. meaning) The Warm Up-Cool Down knowing believes acknowledges appreciates order/pattern perception spatial perception knows object name knows object function The Cool Down-Cool Down reality based fantasy based forms strategies presents possibilities practical impetuous safe risk taking

55 Working with Lethargy in Play Therapy Working with Lethargy in Play Therapy (cont)

If you have an outdoor space: Slow Down Consider the benefits of fresh air and natural sunlight Experiential Activities Walks

Arts and Crafts Hop Scotch

Swinging

56 Dopamine (DA) Antipsychotics Dopamine is transmitted via three major pathways. The first extends from the substantia nigra Phenothiazine Derv. (DA receptor antagonist) to the caudate nucleus-putamen (neostriatum) and is concerned with sensory stimuli and Thorazine (Chlorpromazine) movement. The second pathway projects from the ventral Prolixin (fluphenazine) tegmentum to the mesolimbic forebrain and is thought to be Serentil (mesoridazine) associated with cognitive, reward and emotional behavior. The Trilafon (perphenazine) third pathway, known as the Compazine (prochlorperazine) tubero-infundibular system, is concerned with neuronal control Stelazine (trifluoperazine) of the hypothalmic-pituatory endocrine system. Mellaril (thioridazine)

57 Antipsychotics (cont) Antipsychotics (cont)

Phenothiazine derv. Phenylbutylpiperadine derv.

Thorazine/Stelazine/Mellaril Haldol (haloperidol) Orap (pimozide) Akathisia Akinesia Sleepiness Cognitive Blunting Stiffness

58 Dopamine (DA) Antipsychotics (cont) Dopamine is transmitted via three major pathways. The first Phenylbutylpiperadine derv. extends from the substantia nigra to the caudate nucleus-putamen (neostriatum) and is concerned with sensory stimuli and Haldol/Orap movement. The second pathway projects from the ventral tegmentum to the mesolimbic Akathisia forebrain and is thought to be associated with cognitive, reward Akinesia and emotional behavior. The Blurred Vision third pathway, known as the tubero-infundibular system, is Sleepiness concerned with neuronal control of the hypothalmic-pituatory Cognitive Blunting endocrine system.

59 Serotonin (5-HT) Glutamate

The principal centers for In the normal brain the prominent serotonergic neurons are the glutamatergic pathways are: the rostral and caudal raphe cortico-cortical pathways; the nuclei. From the rostral raphe pathways between the thalamus and nuclei axons ascend to the the cortex; and the extrapyramidal cerebral cortex, limbic pathway (the projections between regions and specifically to the the cortex and striatum). Other basal ganglia. Serotonergic glutamate projections exist between the cortex, substantia nigra, nuclei in the brain stem give subthalmic nucleus and pallidum. rise to descending axons, Glutamate-containing neuronal some of which terminate in terminals are ubiquitous in the the medulla, while others central nervous system and their descend the spinal cord. importance in mental activity and neurotransmission is considerable.

60 Acetylcholine (Ach) There are three Acetylcholine pathways in the CNS. (a) The Pons to thalamus and cortex, (b) Magnocellular forebrain nucleus to cortex, & (c) Septohippocampal. In the central nervous system, ACh has a variety of effects as a neuromodulator upon plasticity, arousal and reward. ACh has an important role in the enhancement of sensory perceptions when we wake up and in sustaining attention. ACh has also been shown to promote REM sleep

61 Antipsychotics (cont) Antipsychotics (cont) Dibenzapine derv.

Dibenzapine derv. Loxitane/Zyprexa/Seroquel

Loxitane (loxapine) Sedation Cognitive Blunting Zyprexa (olanzapine) Seroquel (quetiapine) Benzisoxazole derv. Risperdal Benzisoxazole derv. Drowsiness, Dizziness, Cognitive Blunting, Movement Disorders Risperdal (risperidone) Invega (paliperidone)

62 Antipsychotics (cont) Dihydroindolones Antipsychotics (cont) Geodone (ziprasidone) Moban (molindone) Dihydroindolones Geodone/Moban Sleepiness Quinolinone Confusion Abilify (aripiprazole) Quinolinone Abilify Benzoisothiazol derv. Confusion Benzoisothiazol derivatives Latuda (lurasidone) Latuda (lurasidone) Drowsiness Piperidinyl-Benzisoxazole An internal restless or jittery feeling (akathisia) Fanapt (Iloperidone) Movement or muscle disorders Insomnia MISC Dibenzo-oxepino Pyrroles Lithium Saphris (asenapine) Tremors

MISC Eskalith/Lithobid (lithium)

63 Working With Cognitive Cloudiness in Working With Cognitive Cloudiness in Play Therapy Play Therapy (cont)

Slow Down Simple Games (still require an attempt to focus)

Consider the benefits of “fresh air and natural Matching Games sunlight” Card Games

64 Working With Cognitive Cloudiness in Working With Emotional Blunting in Play Therapy (cont) Play Therapy Rhythm Puzzles Music Mazes

Dance Guessing Games

Bibliotherapy Hangman

65 Working With Emotional Blunting in Working With Emotional Blunting in Play Therapy (cont) Play Therapy (cont) Emotions Tic Tac Toe Art—Guided or Abstract Emotions Identification Jokes Emotion Cards—identification and act out Cartoons Facial Expressions

66 Working with Coordination Difficulties in Play Therapy Gross Motor Skills

Involve the following in Play Therapy: Practice Crafts Use Rhythm Finger Paints

Hula Hoops Increase speed/intensity

67 Gross Motor Skills (cont) Fine Motor Skills

Involve the following in Play Therapy: Involve the following in Play Therapy:

Things that can be manipulated, stacked, etc. but Things that can be manipulated, stacked, etc. but are larger. are smaller.

Legos Pick up Sticks Blocks Tiddlywinks Dominos The game Operation Marbles Ring Toss Games Jenga Fishing Games

68 Fine Motor Skills (cont) Other Things

Crafts which include: Consult or get to know an Occupational Therapist Beads Macaroni/Shaped Pasta

69 Dopamine (DA) CNS Stimulants Dopamine is transmitted via three major pathways. The first extends from the substantia nigra Analeptic to the caudate nucleus-putamen (neostriatum) and is concerned Provigil (modafinil) with sensory stimuli and movement. The second pathway Amphetamines projects from the ventral tegmentum to the mesolimbic Dexedrine (dextroamphetamine) forebrain and is thought to be associated with cognitive, reward Desoxyn (methamphetamine) and emotional behavior. The Adderall (amphetamine mixture) third pathway, known as the tubero-infundibular system, is Vyvanse (lisdexamfetamine) concerned with neuronal control of the hypothalmic-pituatory endocrine system.

70 CNS Stimulants (cont) CNS Stimulants (cont)

Analeptic Non-Amphetamines Provigil Irritability Amphetamines Ritalin/Concerta/Metadate/Methylin (methylphenidate) Adderall/Dexedrine/Desoxyn/Vyvanse Cylert (pemoline) Agitation/Aggression Sleep Problems Focalin (dexmethylphenidate) Nervousness Daytrana (methylphenidate)---Patch Restlessness Adderall more likely to create some mood lability and irritability than the other stimulant medications.

71 CNS Stimulants (cont) Norepinephrine (NE) Non-Amphetamines Many regions of the brain are supplied by the Ritalin/Concerta/Daytrana/Metadate/Methylin noradrenergic systems. The Sleep Problems principal centers for Nervousness noradrenergic neurons are the Agitation/Aggression locus coeruleus and the caudal raphe nuclei. The ascending Cylert nerves of the locus coeruleus project to the frontal cortex, Insomnia thalamus, hypothalamus and Depression limbic system. Noradrenaline Irritability is also transmitted from the locus coeruleus to the Focalin cerebellum. Nerves projecting from the caudal raphe nuclei Nervousness ascend to the amygdala and Sleep Problems descend to the midbrain.

72 MISC ADHD Medications MISC ADHD Medications (cont)

Strattera (atomoxetine) potent inhibitor of presynaptic Strattera NE transporter

Fatigue Sleep Disturbance

73 Working with Agitation/Aggression in Working with Agitation/Aggresion in Play Therapy Play Therapy (cont)

Sandtray or Sand Play Consider the benefits of “fresh and Natural sun light”

Rhythm Clay Therapy (Paul White) Music Natural Sounds Bibliotherapy

74 Gamma-aminobutyric acid (GABA) Sedative/Hypnotics GABA is the main inhibitory neurotransmitter in the central nervous system (CNS). (GABA) GABAergic inhibition is seen at all levels of the CNS, including Newer the hypothalamus, hippocampus, Ambien (zolpidem) cerebral cortex and cerebellar cortex. As well as the large well- ProSom (estazolam) established GABA pathways, Lunesta (eszopiclone) GABA interneurons are abundant in the brain, with 50% Sonata (zaleplon) of the inhibitory synapses in the brain being GABA mediated. Older Halcion (triazolam) Restoril (temazepam)

75 Sedative/Hypnotics (cont) Sedative/Hypnotics (cont)

GABA Melatonin

Ambien/Prosom/Lunesta/Sonata/Halcion/Restoril Rozerem (ramelteon)

Fatigue Fatigue Clumsiness Clumsiness

76 Gamma-aminobutyric acid (GABA) Anticonvulsants/Psychiatric Uses GABA is the main inhibitory neurotransmitter in the central nervous system (CNS). Tegretol/Carbatrol (carbamazepine) GABAergic inhibition is seen at all levels of the CNS, including Trileptal (oxcarbazepine) the hypothalamus, hippocampus, Neurontin (gabapentin) cerebral cortex and cerebellar cortex. As well as the large well- Topamax (topiramate) established GABA pathways, GABA interneurons are Depakote/Depakene (valproic acid) abundant in the brain, with 50% of the inhibitory synapses in the Lamictal (lamotrigine) brain being GABA mediated. Gabitril (tiagabine)

77 Anticonvulsants/Psychiatric Uses Acetylcholine (Ach) (cont) There are three Acetylcholine pathways in the CNS. (a) The Pons to thalamus and cortex, (b) Magnocellular forebrain Tegretol/Carbatrol nucleus to cortex, & (c) Dizziness, Drowsiness, Blurred Vision Septohippocampal. In the central nervous system, ACh Trileptal/Neurontin/Topamax/Lamictal has a variety of effects as a neuromodulator upon Fatigue, Dizziness, Nervousness plasticity, arousal and reward. Depakote/Depakene ACh has an important role in the enhancement of sensory Drowsiness, Lethargy perceptions when we wake up and in sustaining attention. Gabitril ACh has also been shown to Fatigue, dizziness, unstable walking, seizures promote REM sleep

78 Antiparkinsons/Psychiatric Uses MISC MISC MISC/Psychiatric Uses

Cogentin (bentropine) Benadryl (diphenhyramine)—with older Artane (trihexyphenidyl) Antipsychotics Inversine (mecamylamine)---Tourette’s No major negative effects Revia (naltrexone)---Severe Behavioral Disorder in MR, Pervasive Developmental Disorders

79 Norepinephrine (NE) MISC MISC MISC Psychiatric Uses (cont) Many regions of the brain are supplied by the noradrenergic systems. The Benadryl principal centers for noradrenergic neurons are the Sedation, Cognitive Impairments locus coeruleus and the caudal raphe nuclei. The ascending nerves of the locus coeruleus project to the frontal cortex, thalamus, hypothalamus and limbic system. Noradrenaline is also transmitted from the locus coeruleus to the cerebellum. Nerves projecting from the caudal raphe nuclei ascend to the amygdala and descend to the midbrain.

80 MISC MISC MISC/Psychiatric Uses Antihypetensives

Inderal (propranolol)---IED, PTSD Inderal (propranolol) Catapres (clonidine)—ADHD, Conduct Disorder, Drowsiness, Hypotension Tourette’s Tenex/Intuniv (guanfacine)---ADHD, Tourette’s Catapres (clonidine) Sedation, Drowsiness, Depression, Irritability, Irritability, Tiredness, Hypotension Hypotension

Tenex/Intuniv (guanfacine) Irritability, Tiredness, Hypotension

81 Items We Should All Have: They Games We Should All Have: They Accomplish Multiple Tasks Accomplish Multiple Tasks

Jenga Cards Pick-up-Sticks Marbles Connect 4 Jacks Tic Tac Toe Dominos Operation Clay Chutes and Ladders Sand

82 Conclusion References Aarts, E., van Holstein, M., & Cools, R. (2011). Striatal dopamine and the interference between motivation and cognition. Frontiers in Psychology, 2(163), 1-11. Remember: Adinoff, B., Devous, M. D. Sr., Cooper, D. B., Best, S. E., Chandler, P., Harris, T.,… Cullum, C. M. (2003). Resting regional cerebral blood flow and gambling task The goal is to go slow and be supportive. performance in cocaine-dependent subjects and healthy comparison subjects. American Journal of Psychiatry, 160(10), 1892-1892. Allow the child to push past the side effect. Anda, R. F., Felitti, V. J., Walker J., Whitfield, C. L., Bremner, J. D., Perry, B. D., Dube S. R., & Giles, W. H. (2006). The enduring effects of abuse and related adverse When stimulated the brain/body can experiences in childhood: A convergence of evidence from neurobiology and overcome/compensate for medication side epidemiology. European Archives of Psychiatry and Clinical Neurosciences, 56(3), 174–86. effects. Bremner, J. D., & Marmer, C. R. (Eds.). (1998). Trauma, memory, and dissociation. Washington, DC: American Psychiatric Press. Brown, R. T., Carpenter, L. A., & Simerly, E. (2005). Mental health medications for Children: A primer. New York: The Guilford Press.

83 References (cont) References (cont)

Bush, G., Valera, E. M., & Seidman, L. J. (2005). Functional neuroimaging of attention- Lanius, R. A., Bluhm, R. L., & Frewen, P. A. (2011). How understanding the deficit/hyperactivity disorder: A review and suggested future directions. Biological neurobiology of complex post-traumatic stress disorder can inform clinical Psychiatry, 57(11), 1273–1284. practice. A social cognitive and affective neuroscience approach. Acta Psychiatrica Scandinavica, 124(5), 331-348. Centers for Disease Control and Prevention. (2012). Retrieved on August 11, 2012 from Lieberman, A., & Van Horn, P. (2008). Psychotherapy with infants and young http://www.cdc.gov/ace/images/ace_pyramid_home.jpg children: Repairing the effects of stress and trauma on early attachment. New Colton, D. L., & Sheridan, S. M. (1998). Conjoint behavioral consultation and social York, NY. The Guilford Press skills Nestler, E. J., Hyman, S. E., & Malenka, R. C. (2001). Molecular training: Enhancing the play behaviors of boys with attention deficit hyperactivity neuropharmacology: A foundation for clinical neuroscience. New York: McGraw-Hill. disorder. Journal of Educational and Psychological Consultation, 9(1), 3-28. Perry, B. D. (2008). Child maltreatment: A neurodevelopmental perspective on the Dagher, A., & Robbins, T. W. (2009). Personality, addiction, dopamine: Insights from role Parkinsons disease. Neuron, 61(4), 502-510. of trauma and neglect in psychopathology. In T. Beauchaine & S. P. Hinshaw, Child De Bellis, M. D., Baum, A. S., Birmaher, B., Keshavan, M. S., Eccard, C. H., Boring, A. M.,… and adolescent psychopathology (pp. 93-129). Hoboken, NJ: John Wiley & Sons Ryan, N. D. (1999). Developmental traumatology part I: Biological stress systems. Preston, J. D., O'Neal. J., & Talaga, M.C. (2010). Child and adolescent Biological Psychiatry, 45, 1259–1270. psychopharmacology made simple (2nd ed.) . Oakland, CA: New Harbinger Edwards, V. J., Anda, R. F., Dube, S. R., Dong, M., Chapman, D. F., & Felitti, V. J. Publications, Inc. (2005). The wide-ranging health consequences of adverse childhood experiences. In K. Robbins, T. W., & Everitt, B. J. (1995). The cognitive neurosciences. Cambridge, MA: Kendall-Tackett & S. Giacomoni (Eds.) Victimization of children and youth: Patterns MIT Press. of abuse, response strategies, Kingston, NJ: Civic Research Institute.

84 References (cont) References (cont) Royall, D. R., Lauterbach, E. C., Cummings, J. F., Reeves, A., Rummans, T. A., Seale, H. A. (2006). The trauma symptomology of peer abused children. Kaufer, D. I.,…Coffey, C. E. (2002). Executive control function: A review of Dissertation Abstracts International, 3246046. its promise and challenges for clinical research. Journal of Neuropsychiatry Sinacola, R. S., & Peter-Strickland, T. (2011). Basic psychopharmacology for and Clinical Neurosciences, 14(4), 377-405. counselors and psychotherapists (2nd ed.). Upper Saddle River, NJ: Pearson Schore, A. N. (2001), The effects of early relational trauma on right brain Higher Education, Inc. development, affect regulation, and infant mental health. Infant Mental Health Terr, L. (1990). Too scared to cry: Psychic trauma in childhood. New York, NY: Journal, 22(1-2), 201-269. doi:10.1002/1097 Harper & Row. 0355(200101/04)22:1<201::AID-IMHJ8>3.0.CO;2-9 Terr, L. (1994). Unchained memories: True stories of traumatic memories, lost and found. New York, NY: Basic Books. Schore, A. N. (2005). Right-brain affect regulation: An essential mechanism of Toga, A. W., & Mazziotta, J. C. (2000). Brain mapping: The systems: San Diego, development, trauma, dissociation, and psychotherapy. In centers, D., CA: Academic Press. Solomon, M., & Siegel, D. (Eds.), The healing power of emotion: Integrating Willis, D. W. (March 23, 2007). Early brain development: Relational healing relationships, body and mind. A dialogue among scientists and clinicians (pp. from risk. Paper presented at the Substance Use and Brain Development 112-144). New York: WW Norton. Conference, Eugene, OR. Schore, A. N. (2009). Relational trauma and the developing right brain. Annals of the New York Academy of Sciences, 1159(1), 189-2003. doi:10.1111/j.1749 6632.2009.04474.

85 References (cont) Basic Psychopharmacology Wilson, S. N (2005). The meanings of medication. American Journal of for Psychotherapy, 59(1), 19-29. Wise, R. A. (2004). Dopamine, learning, and motivation. Nature Reviews: Mental Health Practitioners Neuroscience, 5, 483-494. van der Kolk, B. A., Roth, S., Pelcovitz, D., Sunday, S., & Spinazzola, J. (2005). Disorders of extreme stress: The empirical foundation of complex adaptation to trauma. Journal of Traumatic Stress, 18(5) 389-399. van der Kolk, B. A. (2003). The neurobiology of childhood trauma and abuse. Child and Adolescent Psychiatric Clinics of North American, 12, 293-317.

86 Resources Recommended videos: Agency for Healthcare Research and Quality (AHRQ), https://www.ahrq.gov/ Medicating Kids—Frontline (2001) • The Medicated Child—Frontline—(2008) http://childtrauma.org/ The Secret Life of the Brain—PBS (2002) • http://www.traumacenter.org/index.php Generation Meds—ABC World News—Diane Sawyer—(2011) —Over Medication of Children in Foster Care

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