Neurobiology of autism

Neurobiology of autism
By:Christopher Gillberg, MD, PhD
Professor of Child and Adolescent Psychiatry
University of Göteborg (Queen Silvia´s Hospital)
University of London (St George´s Hospital Medical School)


Autism spectrum disorders: neurobiology

* Overview
* Acquired brain lesions
* Genetics
* Where in the brain is autism?
* Psychosocial interactions
* Intervention implications
* Outcome implications
* The future

Overview
* At least four clinical presentations of autism (autism/autistic spectrum disorder)
* Autistic disorder (Kanner syndrome)
* Asperger’s disorder (Asperger syndrome)
* Childhood disintegrative disorder (Heller syndrome)
* PDD NOS (atypical autism, other autistic-like condition, other autism spectrum disorder)
* Prevalence much higher than believed in the past: ASD in 1% of population, AD in 0.2%
* Associated with learning disability 15% (80% in autistic disorder/AD)
* Associated with epilepsy 5-10% (35% in AD)
* Medical disorder in 5% (25% in AD)
* Skewed male:female ratio 2-4:1
* High rate of visual, hearing and motor impairments (including at birth)
* Sibling rate raised; identical twin conocordance rate much raised in classic autism

”Acquired” brain lesions
* Tuberous sclerosis, Fragile X syndrome, Partial tetrasomy 15, Down syndrome, XYY, XO, Hypomelanosis of Ito, Rett complex variants, Angelman syndrome, Williams syndrome, CHARGE association, Smith-Magenis syndrome, Smith-Lemli-Opitz syndrome, 22q11 deletion, Silver-Russell syndrome, Fetal alcohol syndrome, Retinopathy of prematurity, Thalidomide embryopathy, Moebius syndrome, Herpes and rubella infection
* Known medical disorders 25% in autistic disorder ”proper” (unselected samples) and 2-5% in Asperger syndrome
* These are either genetic in their own right, affect autism susceptibility gene areas, or cause brain lesions through direct/indirect insults
* High rate of pre- and perinatal risk factors
* Tuberous sclerosis
o 3-9% of all autism cases, more common in those with epilepsy
o chromosome 16p involved in one variant (autism susceptibility genetic area? ADHD susceptibility genetic area)
o dopamine genes on chromosome 9 affected in other TS variant
o autism likely if TS lesions in temporofrontal regions and if there are many lesions

* Herpes encephalitis
o affects temporofrontal areas more often than other brain structures
o can lead to classic symptoms of autism even in previously unaffected individuals who are 14 and 31 years of age
* Thalidomide embryopathy
o 5% of all have (classic) autism
o Brainstem lesions
o Day 20-24 postconceptionally

Genetics
* Sibs affected in 3%: core syndrome
* Sibs affected in 10-20%: spectrum disorder
* Identical twins affected in 60-90%
* Non-identical twins affected in 0-3%
* All of these findings refer to probands with autism proper, not spectrum disorders
* First-degree relatives increased rates of affective disorders (depression, bipolar), social phobia, obsessive-compulsive phenomena, and ”broader phenotype symptoms”, ADHD?, Tourette syndrome?
* First-degree relatives also show possibly increased rates of learning disorders including MR, dyslexia and SLI
* Genes on certain chromosomes (e.g. 2, 6, 7, 16, 18, 22, and X) may be important (genome scan studies of sib-pairs)
* Clinical findings in particular syndromes such as partial tetrasomy 15 (15q), Angelman (15q), tuberous sclerosis (9q, 16p), fragile X (X), Rett syndrome (X), Turner syndrome (X)

* Neuroligin genes on X-chromosome mutated in some cases
o (Jamain, Bourgeron, Gillberg et al 2003. Laumonnier et al 2004)
* Neuroligin genes on other chromosomes, including chromosome 17
o (Jamain et al 2003)
* Other neurodevelopmental genes according to microarray study
o (Larsson, Dahl, Gillberg et al 2003)

Where in the brain is autism?

* Clinical finding: macrocephalus common
o (Bayley et al 1997, Gillberg & deSouza 2002)
* Acquired brain lesions implicate temporal, frontal, fronto-temporal and bilateral dysfunction in core syndrome; right or left dysfunction in spectrum disorder
o (Gillberg & Coleman 2000)
* Autopsy data suggest: amygdala, pons and cerebellum
o (Bauman 1988)
* Brainstem damage suggested by
o Thalidomide
+ (Strömland, Gillberg et al 1994)
o Moebius syndrome association
+ (Gillberg & Steffenburg 1997)
o CHARGE association
+ Johansson et al 2004
o Auditory brainstem responses
+ (Rosenhall, Gillberg et al 2003)
o Decrease in/lack of postrotatory nystagmus
+ (Ornitz, Ritvo 1967)
o Aberrant muscle tone and concomitant squint
+ (Gillberg & Coleman 2000)
* Cerebellar dysfunction suggested by
o Autopsy studies
+ (Bauman et al 1992, Bayley et al 1999, Oldfors, Gillberg et al 2000, Weidenheim, Rapin, Gillberg et al 2001)
o Imaging studies
+ (Courchesne 1988)
o Relationship to ataxia
+ (Åhsgren, Gillberg et al 2003)
* Frontotemporal brain dysfunction suggested by
o Autopsy studies
o Functional imaging studies
o Neuropsychological studies
o Combined neuropsychological-neuroimaging studies
o Clinical picture
* Neuropsychological studies show
o Metarepresentation problems
o Central coherence problems
o Non-verbal learning disability in AS
o Verbal learning disability in AD
o Executive function deficits
o Procedural (complex) learning deficits
o Superior fact learning
o Aberrant reading of facial expression

* At least four biological variants of autism?
o Early brainstem/cerebellar associated with severe secondary problems
o Midtrimester bitemporal lobe damage
o Uni- or bilateral frontotemporal dysfunction in high-functioning cases
o Multi-damage autism

* Likely that several functional neural loops are implicated and that all impinge on neurocognitive/social cognitive functions that are crucially (but possibly not specifically) impaired in autism

Where in the brain is autism?
* Dopamine
o (Gillberg et al 1987)
* Serotonin (in LD also)
o (Coleman 1976)
* Noradrenaline dysfunction
o (Gillberg et al 1987)
* Neuroligins
o (Jamain et al 2003)
* GFA-protein
o (Ahlsén et al 1993)
* Gangliosides
o (Nordin et al 1998)
* Endorphines
o (Gillberg et al 1985)
* Immune system
o (Plioplys 1989)
* Glycine, GABA, Ach, glutamate?

Psychopharmacology of autism
* Only dopamine antagonists (neuroleptics) have been convincingly shown to affect core symptoms of autism
o (van Buitelaar 2000)
* SRIs?
* Antiepileptics??
* Peptides?? And peptide-targeted drugs

The pathogenetic chain
* Genetic or environmental insult
* Damage or neurochemical dysfunction
* Neurocognitive and social cognitive functions restricted (metarepresentations, central coherence, executive functions, procedural learning, )
* The ”syndrome” (or, sometimes, the ”arbitrary” symptom constellation) of autism
* The dyad of social impairment plus the monad of restricted behaviour pattern as a common comorbidity? (rather than the triad?)

Psychosocial interactions
* Not associated with social class
* Not associated with psychosocial disadvantage; however, “pseudoautism” described in children exposed to extreme psychosocial deprivation
* Temporally restricted major improvement in good psychoeducational setting
* Immigration links? Indirect link with genetic factors?
* Abnormal child triggers unusual interactions
* Some parents have autism spectrum disorders themselves
* Anxiety, violent behaviours, self-injury and hyperactivity reduced in autism-know-how-millieu

Implications for treatment
* All people are individuals first and foremost; at least as true in autism as in “neurotypicality”
* People WITH autism; not autistic people!
* Change attitudes
* Respect for people in the autism spectrum
* Focus on changing environment and
* Foster adaptive skills
* If known underlying disorder: treat this (and be aware of syndrome-specific symptoms such as gaze avoidance in fragile X)
* If epilepsy: treat this (however, there are major caveats here)
* If hearing, vision, or motor impaired: treat this
* Psychoeducational measures
* Symptomatic biological treatments
* No medication for majority
* Atypical neuroleptics, antiepileptics, SSRIs, stimulants, lithium (and other drugs) for some
* Diets??
* Physical exercise!!
* “Sensory awareness” environment (reduce noise, certain sounds, smell etc.)
* Concrete, visual (not always), straight-forward
* Minimize ambiguities and symbolic interpretation

Outcome
* Very variable
* Better with early diagnosis
* Majority probably live to be old, but increased mortality in subgroup
* Basic problems remain, albeit modified
* High rate of secondary psychiatric problems (personality disorder, affective, social, catatonia)

Outcome
* Better but also very restricted in Asperger syndrome
+ Cederlund et al 2004
* If autism and no language at age 7, classic autism in adulthood
* If autism and no language at age 3, some classic, some Asperger in adulthood
* If autism and some language at age 3, most will be Asperger in adulthood


The future
* Specific knowledge (including genetic) and treatment for subgroups (new diagnostic criteria)
* Symptomatic treatments
* Psychoeducation
* Acceptance and attitude change!
* People with autism, not autists or autistic people! Cannot be stressed enough
* Respect!

Neurobiology of autism .ppt

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Eating and Sleeping Disorders

Eating and Sleeping Disorders

Eating Disorders
* 13.4% of girls and 7.1% of boys engage in disordered eating patterns.
* Paradox: As emphasis on thinness is increasing, so is the problem of obesity.
* 7 million women and 1 million men in the U.S. suffer from eating disorders.
* 15% of young women have “substantially disordered” eating attitudes and behaviors.

Factors Associated with Disordered Eating Patterns
* Being overweight
* Low self-esteem
* Depression
* Substance use
* Suicidal ideation
* More prevalent among females
* Least likely among African American females

Eating Disorders
Prevalence of Weight Concerns of Youth in Grades 5-12

Eating Disorders Anorexia Nervosa
* Anorexia Nervosa: Eating disorder characterized by:
o Refusal to maintain a body weight above the minimum normal weight for a person’s age and height.
o Intense fear of becoming obese that does not diminish with weight loss.
o Body image distortion
o In females, absence of at least 3 consecutive menstrual cycles otherwise expected to occur.
Anorexia Nervosa
* Subtypes:
o Restricting: Lose weight through dieting or exercising.
o Binge-Eating/Purging: Lose weight through use of self-induced vomiting, laxatives, or diuretics.
* Physical complications:
o Cardiac arrhythmia, low blood pressure, slow heart rate, weakened heart muscle
o Lethargy, dry skin, brittle hair, swollen parotid glands, hypothermia
o Males: Osteoporosis, substance use disorder, antisocial personality disorder
* Associated characteristics:
o Obsessive-compulsive behaviors and thoughts about food
* Associated characteristics:
o Personality disorders/characteristics:
+ Restricting: introversion, conformity, perfectionism, rigidity
+ Binge eating/purging: Extroverted, histrionic, emotionally volatile, impulse control problems, substance abuse

* Course and outcome: Highly variable
o Usually begins in adolescence
o Better outcome for binge-eating/purging
o More severe is associated with constricted/ overcontrolled profile
o ~ 44% recover completely, ~28% show some weight gain but remain underweight, poor outcome for ~ 24%
o Death: 5-20%, primarily from cardiac arrest or suicide


Eating Disorders Bulimia Nervosa
* Bulimia Nervosa: Eating disorder characterized by:
o Recurrent episodes of binge eating (rapid consumption of large quantities of food) at least twice a week for 3 months, during which the person loses control over eating and uses vomiting, laxatives, and excess exercise to control weight.
o More psychopathology than non-bulimics: Greater external locus of control, lower self-esteem and sense of personal effectiveness, negative self-image, although most are within normal weight range.

* More prevalent than anorexia
o Up to 3% of women suffer from bulimia, another 10% report some symptoms
o ~10% of bulimics are male
* Physical complications:
o Effects of vomiting: Erosion of tooth enamel, dehydration, swollen parotid glands, low potassium (can weaken heart and cause arrhythmia and cardiac arrest)
o Binge eating may cause stomach ruptures
o Gastrointestinal disturbances

* Related to:
o Coping responses to stress
o Mood disorders, especially seasonal affective disorder
o Also shares characteristics of borderline personality

* Course and outcome:
o Generally begins late adolescence/early adulthood
o Mixed, but better course than for anorexia
o Some bulimics continue to show disturbed eating patterns, low self-esteem, depressive disorder, but most recover either fully or partially.
o Poorer prognosis with associated history of substance use and longer duration before treatment.

Eating Disorders Binge-Eating Disorder (BED)
* Diagnostic category “provided for further study” in DSM-IV-TR:
o Binge Eating Disorder: Involves a large consumption of food over a short period of time at least twice weekly for 6 months
o Unlike bulimia, does not involve use of extreme behavioral attempts of vomiting, fasting, or excessive exercise as compensation for binge eating.
o Diagnosis: History of binge-eating episodes at least 2 days/week for 6 months
* Prevalence:
o Prevalence: 0.7-4% of population
o Females are 1.5 times as likely as males to have the disorder.
o Prevalent among white, African American, and American Indian women (possibly 10%), although white women are more likely to be seen for the disorder.

* Associated characteristics/risk factors:
o Overweight with history of weight fluctuation
o Prevalence: 2-5%
o Adverse childhood experiences, parental depression, vulnerability to obesity, repeated negative comments re weight and body
o Binges preceded by poor mood, low alertness, feelings of poor eating control, cravings for sweets.
o Complications: High blood pressure, high cholesterol, diabetes, and depression
* Comorbid features:
o Major depressive disorder
o Obsessive-compulsive personality disorder
o Avoidant personality disorder
* Course and outcome:
o Begins in late adolescence/early adulthood
o Positive course compared with other eating disorders: Most recover within 5 years
o Weight remains high (over time, ~1/3 meet criteria for obesity)

Eating Disorders Eating Disorder Not Otherwise Specified
* Eating Disorder Not Otherwise Specified: Eating disorders not meeting criteria for anorexia or bulimia nervosa:
o Individuals with binge-eating disorder
o Female who meets criteria for anorexia but has regular menses
o Individual who has lost significant weight but is in normal weight range

Eating Disorders Hyperphagia
* Hyperphagia: Excessive hunger and overly large amounts of food ingestion.
Eating Disorders Rumination
* Rumination: An eating disorder characterized by having the contents of the stomach drawn back up into the mouth, chewed for a second time, and swallowed again. This regurgitation appears effortless, may be preceded by a belching sensation, and typically does not involve retching or nausea. In rumination, the regurgitant does not taste sour or bitter. The behavior must exist for at least 1 month, with evidence of normal functioning prior to onset.

Eating Disorders Pica
* Pica: An appetite for non-foods (e.g., coal, soil, chalk, paper etc.) or an abnormal appetite for some things that may be considered foods, such as food ingredients (e.g., flour, raw potato, starch). In order for these actions to be considered pica, they must persist for more than one month, at an age where eating dirt, clay, etc., is considered developmentally inappropriate.
* Geophagia: Eating of dirt or clay.

Do You Have an Eating Disorder?

Overview of Major Risk Factors for Eating Disorders

Hunger and Satiety
* Ig Nobel awards celebrate the sillier side of science
* The Ig Nobel for nutrition went to a concept that sounds like a restaurant marketing ploy: a bottomless bowl of soup.
* Cornell University professor Brian Wansink used bowls rigged with tubes that slowly and imperceptibly refilled them with creamy tomato soup to see if test subjects ate more than they would with a regular bowl.
* "We found that people eating from the refillable soup bowls ended up eating 73 percent more soup, but they never rated themselves as any more full," said Wansink, a professor of consumer behavior and applied economics. "They thought 'How can I be full when the bowl has so much left in it?' "
* His conclusion: "We as Americans judge satiety with our eyes, not with our stomachs.“
* CNN.Com 10-7-07
* Societal influences:
o Mass media portray ideal female body as 5’7” 110 lbs; actual average is 5’4” 162 lbs
o Sociocultural demand for thinness
o Peer influences
o Criticisms by family members about weight
o Dating

* Body dissatisfaction:
o Males see their bodies as smaller than what they believe is preferred; females see their bodies as larger than what they believe is preferred
o Most dissatisfaction parallels low self-esteem
* Certain predisposition and characteristics lead some people to interpret images of thinness as evidence of their own inadequacy.
* Exposure to ultra-thin ideal by media can lead to:
o Internalization of that image and eating patterns intended to bring about that ideal
o Negative affect, which triggers dieting
o Social comparison, which leads to disordered eating to meet external standards of comparison.

* Top figure
o Body image ratings of women who score high on measure of distorted eating behaviors.
* Bottom Figure
o Body image ratings of women who score low on measure of distorted eating behaviors.

Route to Eating Disorders Eating Disorders
Etiology
* Family and peer influences
o Psychodynamic (for anorexia):
+ Fear of maturation:
# Growing up and separating from family
# Developing own identity
# Fulfills unconscious desire to remain a child
o Family systems: Problematic family communication patterns result in anorexia
o Socialization agents (peers and family)
o Relationship problems and role models

Eating Disorders
Etiology
* Cultural factors:
o Culture-bound (Western cultures) and other societies influenced by Western culture.
o Many African Americans seem insulated from thinness standard, but equally as likely to have binge-eating disorder.
o Internalization of U.S. societal values regarding attractiveness affects self-esteem and body dissatisfaction.
Differences in Body Image and Weight Concerns Among African American and White Females

Eating Disorders Other Etiological Factors
* Personality characteristics and negative emotional moods
* Sexual abuse
* Low self-esteem and feelings of helplessness
* Passivity, dependence, nonassertivness
* Anorexia: Perfectionism, obedience, academic and athletic success, model children
* Bulimia: Perfectionism, seasonal affective disorder
* Genetic factors: First-degree relatives

Eating Disorders Treatment
* Prevention programs:
o Goals of school-based intervention program:
+ Develop positive attitude toward one’s body
+ Become aware of societal messages re being female
+ Develop healthier eating/exercise habits
+ Increase comfort in expressing feelings
+ Develop healthy strategies to deal with stress
+ Increase assertiveness skills
o Teach females to examine consequences of gender messages
o Institutional awareness of the problem is critical
* Anorexia nervosa:
o Inpatient/outpatient depends on weight and health of individual
o Initial goal: Restore weight with psychological support
+ Nutritional/physical rehabilitation
+ Identify/understand dysfunctional attitudes
+ Improve interpersonal/social functioning
+ Address comorbid psychopathology/psychological conflicts

* Anorexia nervosa:
o Family therapy: Parents involved in meal planning, reduce criticism (understanding seriousness of anorexia), negotiate new relationship patterns, move toward separation and individuation.

* Bulimia nervosa:
o Identify conditions contributing to purging
o Identify physical conditions resulting from purging
o Normalize eating pattern and eliminate binge-purge cycle
* Bulimia nervosa:
o Cognitive-behavioral therapy and use of antidepressants:
+ Encourage eating 3 or more balanced meals a day
+ Reduce rigid food rules and body image concerns
+ Develop cognitive and behavioral strategies

* Binge-Eating Disorder
o Similar to treatments for bulimia with fewer physical complications
o Because most are overweight, therapy programs try to help individual lose weight
o Three phases:
+ Determine underlying cognitive factors
+ Use cognitive strategies to change distorted beliefs about eating
+ Relapse prevention strategies


Primary Sleep Disorders
* Most adults require 8 hours of sleep to function optimally.
* Insufficient sleep results in lapses in attention, vigilance, and deterioration of performance.
* Five stages of sleep:
o Stage 1 (5%): Transition from wakefulness to sleep
o Stage 2 sleep (50%)
o Stages 3-4 (10-20%): Deepest level
o Rapid eye movement (REM-20-25%): Dream sleep

Primary Sleep Disorders Dyssomnias
* Most problems are either inability to initiate or maintain sleep at night or excessive daytime sleepiness.
* Dyssomnias: Difficulties in getting to sleep, maintaining sleep, or complaints of excessive sleepiness during the day.


Primary Sleep Disorders Primary Insomnia
* Primary Insomnia: Characterized by difficulty getting to sleep, maintaining sleep, or having nonrestorative sleep for at least one month, causing clinically significant distress in social, occupational, or other areas of functioning.
o Causative factors: caffeine, alcohol, heavy meals, exercising 2 hours before bedtime, stress, intrusive/ uncontrollable cognitive activity, altered sleep habits
o Highest rate: 52% of older adults
* Many people with primary insomnia have undiagnosed sleep Apnea or Restless Leg Syndrome.
* RLS (which is also sometimes referred to as Jimmy Legs, spare legs or "the kicks") may be described as uncontrollable urges to move the limbs in order to stop uncomfortable, painful or odd sensations in the body, most commonly in the legs. Moving the affected body part eliminates the sensation, providing temporary relief. The sensations and need to move may return immediately after ceasing movement, or at a later time. RLS may start at any age, including early childhood, and is a progressive disease for a certain percentage of sufferers, although it has been known for the symptoms to disappear permanently in some sufferers.


Primary Sleep Disorders Primary Hypersomnia
* Primary Hypersomnia: Characterized by excessive daytime sleepiness or prolonged nighttime sleep for at least one month, causing significant distress or impairment in social, occupational, or other important areas of functioning.
o Compelling need to nap during the day that provides no relief from sleepiness.
o Results in problems with driving, work performance, or social functioning.

Primary Sleep Disorders Narcolepsy
* Narcolepsy: Characterized by overwhelming need for daytime sleep even when adequate sleep occurs at night; daily for at least 3 months, together with at least 2 of the following:
o Irresistible drowsiness/falling asleep without warning
o Cataplexy
o Sleep paralysis during wakefulness
o Hypnogogic hallucinations before falling asleep

Primary Sleep Disorders Breathing-Related Sleep Disorder

* Breathing-Related Sleep Disorder: Excessive sleepiness caused by sleep disruption through abnormalities of breathing during sleep
o Obstructive Sleep Apnea: Upper-airway obstruction during sleep
+ Undiagnosed in ~75% of treatable cases
+ Disruptive snoring, breathing pauses, gasping, excessive daytime sleepiness
+ Obstruction of airway prevents breathing during sleep
o Central sleep apnea syndrome
o Central alveolar hypoventilation syndrome

Primary Sleep Disorders Circadian Rhythm Sleep Disorder
* Circadian Rhythm Sleep Disorder: Pattern of recurrent sleep disruption caused by disruption of the biological sleep-wake cycle or mismatch between internal “clock” for sleeping and waking and environmental demands.
o Jet lag, shift work
o Associated with major disasters (e.g., Exxon Valdez oil spill)


Primary Sleep Disorders Dyssomnias Not Otherwise Specified

* Dyssomnias Not Otherwise Specified: Do not meet criteria for specific dyssomnia, but produce significant impairment:
o Insomnia caused by environmental factors
o Excessive sleepiness caused by sleep deprivation
o Restless leg syndrome
o Periodic limb movement disorder


Primary Sleep Disorders Parasomnias
* Parasomnias: Activation of physiological systems at inappropriate times during the sleep-wake cycle.
* Generally involve activation of the autonomic nervous system, including cognitive processes during sleep or sleep-wake transitions.

Primary Sleep Disorders Parasomnias
* Nightmare disorder: Nightmares several times/week during REM sleep.
o 3% of preschoolers and school-aged children
* Sleep Terror Disorder: Vivid nightmares during first third of deep sleep (non-REM); child screams with terror, is not fully aroused, and does not remember what happened.
o ~6% of children, disappears in adolescence
o In adults age 20-30 it has a chronic course
* Sleepwalking Disorder: Motor activity ranging from sitting up to getting out of bed and walking about while still asleep.
o ~2% of school-aged children sleepwalk at least a few nights a week
o Up to 30% of children sleepwalk at least once
o 1-5% of children have sleepwalking disorder
o Tends to disappear in adolescence; in adults it will have a chronic waxing/waning course.

* Parasomnias Not Otherwise Specified:
o REM sleep behavior disorder: Violent motor behavior during REM sleep
o Sleep paralysis/inability to move during transition from wakefulness and sleep


Primary Sleep Disorders Etiology and Treatment of Dyssomnias
* Etiology: Subclinical anxiety and depression, environmental changes, health and behavioral habits; for some etiology is unknown but may include:
o Cognitions or intrusive, uncontrollable thoughts
o Personality and psychological adjustment problems
o Lifestyle factors
o Nocturnal activities that interfere with sleep
* Treatment for specific disorders:
o Excessive sleepiness (narcolepsy or hypersomnia): Stimulants, though more success with hypersomnia than narcolepsy.
o Insomnia: Sleep pills, which tend to become ineffective over the long-term.
o Sleep apnea: Avoid medications, alcohol and other substances; lose weight if overweight; sleep on side rather than back; pressure mask during sleep may also help with moderate and severe apnea.

* Treatment for RLS and PLMD: Behavioral treatment, medications for RLS
* Treatment for sleep disorders generally:
o Relaxation/focusing procedures
o Changing mental state prior to bedtime
o Slow deep breaths
o Eliminate distractions
o Avoid daytime naps, caffeine late in day, heavy meals/exercise/alcohol/nicotine 2 hours before bedtime.


Eating and Sleeping Disorders.ppt

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Eating Disorders, Obesity & Sleep Disorders

Eating Disorders, Obesity & Sleep Disorders

Eating Disorders
* Characterized by severe disturbances in eating behavior
* Types of eating disorders:
o Anorexia Nervosa (peak onset – 14-18 yrs)
o Bulimia Nervosa (peak onset – late adolescence to early adulthood)
o Binge-eating Disorder (unknown)

Anorexia Nervosa
* Essential features:
o Refusal to maintain a minimally normal body weight (for height and age)
o Intensely afraid of gaining weight
o Exhibit a severe disturbance in perception of shape/size of one’s body
o Absence of at least 3 consecutive menstrual periods
* Self-esteem highly dependent on shape/size
* Refusal to maintain minimal body weight:
o Generally weigh less than 85% of the normal body weight
* Weight loss is usually a result of:
o Reduction of food
o Purging (vomiting, laxatives)
o Excessive exercise regimes
* Intensely afraid of gaining weight:
o Fear of becoming fat is not alleviated by weight loss
o Weight loss is seen as an impressive achievement and a sign of self-discipline
o Weight gain is viewed as failure of self-control
* Distorted view of body weight and shape
o Some feel overweight all over, no matter how thin they become
+ Others feel that a particular part of the body is “too fat”
o Some demonstrate excessive weighing
+ Measure body parts
+ Use mirrors to check body parts for fat
* Resulting physiological problems:
o Constipation, impaired renal functioning
o Cold intolerance  lanugo
o Emaciation, yellowing of the skin, dry skin
o Tend to lose 20-25% of body weight, some lose up to 35%;
o Cardiovascular/heart problems, amenorrhea, osteoporosis & death

Bulimia Nervosa

* Essential features:
o Binge eating
o Inappropriate compensatory methods to prevent weight gain
o Binge eating and compensatory behaviors must occur, on average, at least 2x/wk for 3 months
o Perception of self is excessively influenced by one’s body shape and weight.
* Binge eating:
o Eating an amount of food that is definitely larger than most individuals would eat under similar circumstances
+ Binges can last up to 2 hours
o Could occur in one setting or as a continuation of eating

* Food consumed typically includes sweet, high-caloric foods
* Usually ashamed of the eating problem
o Attempt to hide their symptoms

* Binge eating usually occurs in secrecy, or as inconspicuously as possible:
o Binges may be planned in advance
o Usually characterized by rapid consumption
o Eating continues until person is uncomfortably, even painfully full
o The individual experiences a sense of a lack of control during the binge-eating episode

* Recurrent use of inappropriate compensatory behaviors:
o 80-90% of binge eaters who seek treatment report self-induced vomiting  relief from discomfort/fear of gaining weight  eventually can vomit at will
o Others use laxatives, diuretics and enemas
* Compensatory behaviors (cont.)
o Individuals with bulimia may fast for a day or more to compensate for binges
o They may compensate by exercising excessively

* Similar to Anorexia Nervosa in that the individual:
o Has a fear of gaining weight
o Has a desire to lose weight
o Are dissatisfied with their bodies

* Different from Anorexia Nervosa in that:
o Individuals with Bulimia recognize their behavior is not normal
+ People with Anorexia Nervosa don’t
o Despite behaviors, weight is usually normal
+ People with anorexia become very thin
o Individuals with Bulimia are more likely to seek and respond to treatment.

* Resulting physiological problems:
o Skin irritations (esp. around mouth and fingers due to contact with stomach acid)
o Tooth decay and cavities
o Damaged taste receptors
o Abdominal pain, bowel problems
o Digestive disorders
o Possible cessation of menstruation

Theoretical Perspectives: Anorexia and Bulimia Nervosa

* Sociocultural factors:
o http://www.youtube.com/watch?v=knEIM16NuPg
o http://www.youtube.com/watch?v=I0u0wWOMIsE&feature=related
o Social learning theory:
o Purging is a negative reinforcer; it alleviates the fear of gaining weight
* Cognitive theory:
o Behaviors are a result of irrational thoughts

* Family factors
o Tend to be dysfunctional
+ Critical, less nurturing, overprotective
+ Mother tends to feel daughter is unattractive and needs to lose weight
o Identified patient
* History of childhood physical/sexual abuse
o Especially with bulimia

* Biological factors:
o Low serotonin levels may prompt binge eating in people with bulimia, esp. carbohydrate cravings
o Genetics
+ Eating disorders tend to run in families

Binge Eating Disorder
* Essential features:
o Binge eating without purging or compensatory behaviors
o Must average at least 2 episodes/week for 6 months or longer
o Impaired control over eating
o Experience significant distress due to the eating behavior
* Impaired control over eating:
o Eating rapidly
o Eating until painfully full
o Eating large amounts when not hungry
* Significant distress
o Eating alone out of embarrassment
o Feeling disgust, guilt or depressed after the eating episode
o Concern over how episodes will affect body size/shape

* Associated features:
o Some episodes are triggered by depression or anxiety
+ Others report no specific trigger, though report the behavior initially relieves tension
o Some report a dissociative quality during the episodes
o Most are overweight & were yo-yo dieters.

Obesity: A Chronic Medical Disease
* Weighing 20% above the recommended weight
* Americans eat 815 billion calories daily
o That’s 200 billion more than is necessary to maintain their weight
o Those extra calories would sustain a country of 80 million people
* Potential Causes
o High set-point
o Genetics
o Hypothalamus
o Coping technique
o Clock-watchers
o Addiction
o Eat too much + inactivity

Sleep Disorders
* Dyssomnias:
o Disorders in which a person has difficulty getting to sleep, staying asleep or sleeping too much
* Characterized by a disturbance in the:
o Amount of sleep
o Quality of sleep
o Or the timing of sleep
* Dyssomnia disorders include:
o Primary Insomnia
o Primary Hypersomnia
o Narcolepsy
o Breathing-Related Sleep Disorder
o Circadian Rhythm Sleep Disorder

Primary Insomnia
* Essential features:
o Difficulty falling asleep, staying asleep, or awakening too early that lasts at least one month (some report nonrestorative sleep)
o Causes distress or impairment in social, occupational or other important areas of functioning
* Some facts:
o As much as 30% of the population suffers from this; 9-15% have chronic bouts; nearly everyone has bouts at some point
o Primarily affects middle-age and older pop.; affects more females than males
* Most probable cause of insomnia – stress
o Person goes to bed  thinks about the days events or problems in life  mind races  can’t get to sleep  think about the fact s/he can’t get to sleep causes bodily arousal and more anxiousness  makes it even less likely s/he will get to sleep

* Question
o What should you do if you don’t fall asleep within about 20 minutes of getting in bed?

Primary Hypersomnia

* Essential feature:
* Excessive sleepiness for at least 1 month
o Prolonged sleep episodes
o Daytime sleep episodes which occur almost daily
o Must be severe enough to cause distress or impairment in social, occupational or other important areas of functioning

Primary Hypersomnia
* Duration of major sleep episodes range from 8-12 hours
o Often followed by difficulty awakening
* Excessive sleep during normal waking hours takes the form of
o Intentional naps
o Inadvertent episodes of sleep
* Daytime naps
o Are relatively long (lasting an hour or more)
o Are not refreshing
o Do not lead to heightened alertness
* Unintentional sleep episodes occur in low-stimulation and low-activity situations
o Such as?
* Hypersomnia can lead to distress and dysfunction:
o Difficulty in meeting morning obligations
o Unintentional daytime sleep episodes can be dangerous and embarrassing
o Low level of alertness can lead to poor efficiency, poor concentration, and poor memory

Narcolepsy
* Essential features:
o Repeated irresistible attacks of refreshing sleep
o Cataplexy and/or
o Intrusion of REM sleep between wakefulness and periods of sleep
* For diagnostic purposes, the sleep attacks must occur daily over a period of at least 3 months

* Repeated irresistible attacks of refreshing sleep:
o Sleep is irresistible; results in unintended sleep in inappropriate places
o Sleep episodes usually last 10-20 minutes, but can last up to an hour
o Individuals typically have 2-6 daily episodes
+ some attempt to control sleepiness by taking naps

* Cataplexy: Loss of muscle tone during episodes (usually lasts only seconds):
o Can be subtle or dramatic
o Person is fully conscious/alert during episode
o Occurs in approx. 70% of cases
+ Often develops years after onset
+ Triggered by strong emotions

* Approx. 20-40% experience intense dreamlike imagery:
o Hypnagogic hallucinations – just prior to falling asleep
o Hypnopompic hallucinations – just after awakening
o Most hallucinations are visual and incorporate elements of one’s environment

* Approximately 30-50% of individuals with narcolepsy experience sleep paralysis:
o Occurs just on falling asleep or awakening
o Individual is awake but unable to move or speak
+ Some feel like they can’t breathe
o Hallucinations and paralysis can occur simultaneously
+ Typically lasts seconds–minutes, ends abruptly

Narcolepsy

* Causes:
o Unknown
o May be genetic – higher degree of incidence among biological relatives
o May be partly due to a loss of certain brain cells in hypothalamus
+ Produce sleep-regulating chemical

Breathing-Related Sleep Disorder
* Essential feature:
o Sleep disruption, leading to excessive sleepiness or insomnia, that is due to abnormalities of ventilation during sleep
o Daytime sleepiness is the most frequently reported complaint

* Obstructive sleep apnea syndrome
o Temporary cessation of breathing during sleep
+ Seems to be a result of blocked upper air passages, causing breathing to stop temp.
# Enlargement of soft tissue may cause airways to narrow
+ May also be the result of structural deformities
+ Cessation of breathing lasts from 15-90 seconds
+ Individual may wake up as many as 500x/night
o Individual may wake up gasping for air, making a loud snorting sound, and go back to sleep
+ Individual is usually not aware of these interruptions of sleep
o Approx. 20 million Americans suffer from this disorder; men are 2x as like as women to suffer from it; usually occurs in overweight people

* Things that may help:
o Dieting
o Surgery (tonsils and adenoids)
o Dental appliances which reposition the tongue
o Ventilating machines

Circadian Rhythm Sleep Disorder
* Essential features:
o Disruption of normal sleep wake pattern
o Must be severe enough to cause severe distress or impairment of social, occupational or other important functioning
o Result of jet lag, working swing shifts, etc

Parasomnias
* Sleep disorders characterized by abnormal behavior or physiological events that occur in association with:
o Sleep
o Specific sleep stages or
o Sleep-wake transitions
* Usually complain of unusual behavior during sleep

Parasomnias

* Parasomnias include:
o Nightmare Disorder
o Sleep Terror Disorder
o Sleepwalking Disorder

Nightmare Disorder

* Essential Feature:
o Repeated occurrence of frightening dreams that lead to awakenings from sleep
o Must result in significant distress or result in social or occupational dysfunction

* Nightmares defined:
o A lengthy, elaborate dream sequence that is highly anxiety provoking or terrifying
* Dream content:
o Usually focuses on imminent danger to the individual
+ Sometimes the danger is more subtle, as involving personal failure or embarrassment

* Nightmares may replicate a real life traumatic experience a person had
o But not usually
* Individuals are alert upon wakening
o Can describe the dream in detail
* Occur almost exclusively during REM sleep
* Believed to be caused by stress

* Upon awakening, the individual experiences a lingering sense of anxiety or fear  difficulty returning to sleep
* Some individuals avoid sleeping, resulting in
o Excessive sleepiness
o Poor concentration, irritability
o Depression/anxiety

Sleep Terror Disorder
* Def: repeated abrupt awakenings from NREM sleep accompanied by:
o Intense physiological arousal
o Feelings of panic
* Often occurs during times of stress
* Most frequently occurs in children (up to 6%); rare in adults (<1%)
* Typical experience (lasts 1-10 minutes):
o Wake up in a state of panic, screaming
+ Body is in full physiological arousal
o Child may thrash about while still sleeping
o If awakened, the child is usually confused and incoherent
+ Soon fall back into deep sleep

Sleep Terror Disorder

o Children do not remember the incident in the morning; more terrifying to the parent
o Sleepwalking and sleep-talking may accompany sleep terror disorder
* Typically outgrown by adolescence
o Though some cases last into adulthood
* Cause is unknown
o But it is thought to be associated with stress

Sleepwalking Disorder

* Essential features:
o Arising from bed and walking about while asleep
* During episodes, the person has
o Reduced alertness/responsiveness
o A blank stare
o Is unresponsive to communication with others or efforts to wake them

Sleepwalking Disorder

* Individual typically has little recall of the incident upon awakening
* For diagnosis, the sleepwalking must cause severe distress or impairment of social or occupational functioning

* Sleepwalking episodes can include a variety of behaviors:
o May sit up in bed, look around, pick at blankets
o May walk into closets, out of the room, down stairs and even out of a building
o Some use the bathroom, eat or talk
o On occasion, some run from a perceived threat
o Some have operated machinery

* Particularly during childhood, sleepwalking can include inappropriate behavior
o E.g. Urinating in a closet
* Individuals often wake up in another place
o Or with evidence they performed some activity
* Most episodes last minutes to half an hour
* Cause: Unknown
o Genetics and environment may be involved

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Sleep and Sleep Disorders

Sleep and Sleep Disorders
The Science of Sleep
By:Robert Averbuch, MD
Assistant Professor of Psychiatry

Lecture Outline

* Physiology of Normal Sleep
o Non-REM
o REM
o Normal patterns of sleep
* Sleep Disorders
o Dyssomnias
o Parasomnias

Physiology of Normal Sleep

2 Phases: REM and Non-REM Sleep

Non-REM Sleep

* 4 stages of progressively deeper sleep
* Normal muscle tone
* Associated with increased 5HT (serotonin)
* Decreased autonomic activity:
o Lower BP, Pulse, respirations slow

Stage One
* Brief transition between wakefulness and sleep (accounts for only 5% of sleep time)
Stage Two
* Light sleep
* Accounts for 50% of total sleep time
* ElectroEncephaloGram (EEG) shows some characteristic findings…

EEG in Stage 2
Stages 3,4

* Most restful, restorative stages of sleep
* Aka: Delta wave sleep/ slow wave sleep
* Greatest proportion is in the first 1/3 to 1/2 of night

NREM Sleep: Theories of its purpose…

* The decrease in metabolic demand on the brain during NREM allows glycogen stores to replenish
* Allows for consolidation of memories and learning

REM (dreamland)

* 10-20 min. cycles consisting of:
o Rapid Eye Movements
o ElectroEncepahaloGram shows fast activity very similar to wakeful EEG pattern
o Suppression of peripheral muscle tone
o Penile Tumescence
o Often increased autonomic tone- ie, increased blood pressure, resp, heart rate

REM (dreamland)

* Where dreaming occurs
* REM is marked by increased cholinergic activity
o Thus REM-supression seen with anti-cholinergic drugs (ex. some antidepressants)

Normal Sleep Pattern
* Sleep cycles between NREM and REM approx. 4-5 times/night
* Cycles last approx. 90min
* REM duration and frequency increase thru night
* Proportion of slow wave sleep (stages 3,4) decreases thru night

Normal Sleep Parameters
* Sleep Onset Latency- the time it takes one to fall asleep, averages 10-20min
* REM Latency- time between sleep onset and the first REM period, averages 90-120min

Normal Sleep Distribution
* REM sleep accounts for approximately 25% of total sleep time
* Non-REM sleep accounts for 75% of sleep time, with 25% of that spent in Stages 3,4 (most restful portion)

Sleep Onset
* Mediated by increased Serotonergic activity in the Dorsal Raphe Nuclei of the Pons
o Dampens activity in the ascending reticular activating system (RAS), inducing sleep
* Dopamine has opposite effect- promotes wakefulness

Age-Related Changes

* Decreases in dreaming, total sleep time, REM, and slow-wave (deep sleep)
* Increases in early morning awakening, fragmentation, daytime napping, and phase advancement-
o Ie, earlier to bed, and awaken earlier

“Measuring” Sleep
Polysomnography

The Polysomnogram

* EEG, ECG
* EOG (oculogram)
* Chin EMG (myelogram)
* Ant. Tibialis EMG
* Pulse Oxymeter
* Blood Pressure

Sleep Disorders
Sleep Disorders- 2 Divisions

* Dyssomnias- disorders of quality, timing, or amount of sleep (quantity)
* Parasomnias- abnormal behaviors associated with sleep or sleep-wake transition, that often produce arousals

Dyssomnias
* Primary Insomnia
* Narcolepsy
* Sleep Apnea
* Circadian Rhythm Sleep Disorder (jet lag, et al.)
* Restless Legs Syndrome (RLS)
* Medical/Substance related insomnia

Primary Insomnia
* “Primary”, meaning no underlying medical cause
* Onset often with stressor or disruption to sleep schedule or environment
* Results from poor sleep hygiene, along with classical conditioning-
o Faulty learning/association of sleep environment with state of arousal

INSOMNIA- an epidemic?
* Definition: “Subjective” experience of poor sleep quality or quantity that adversely affects daily functioning
* Extremely common complaint in general practice
* 30-40% adults have occasional poor sleep
* 15-20% adults have chronic insomnia

Consequences of Insomnia
* Depression
* Irritability
* Decreased cognitive functioning
* Decreased productivity
* Injuries and accidents

Narcolepsy
* A dyssomnia characterized by poor sleep quality (restless, fragmented) and dysfunction in the transitions between sleep and wakefulness
* Presents with Excessive Daytime Sedation (EDS)

Narcolepsy Tetrad

* Classic tetrad of associated findings:
o 1. Sleep attacks
o 2. Cataplexy
o 3. Sleep paralysis
o 4. Sleep hallucinations

1. Sleep Attacks
* Most common symptom of the tetrad
* Brief (10-20min) “power-naps”- refreshing and restful
* Average 10-20/wk

2. Cataplexy
* Sudden loss of muscle tone (rarely full body paralysis) caused by intrusion of REM activity into daytime wakefulness
* Triggered by heightened emotion
* Average duration: 30 seconds
* No loss of consciousness

3. Sleep Paralysis
* Brief paralysis upon waking
* Remain alert with full eye movements Can occur in the absence of Narcolepsy (ie, normal variant)

4. Sleep Hallucinations
* Hypnogogic hallucinations- occur during transition into sleep
* Hynopompic hallucinations- occur upon awakening from sleep
* Can occur in the absence of Narcolepsy (ie, normal variant)

Narcolepsy: Etiology
* CNS lesions: brain trauma, stroke, tumor, Multiple Sclerosis
* Familial/idiopathic: onset in adolescence or young adulthood

Sleep Apnea
* Dyssomnia characterized by poor sleep quality due to frequent awakenings (apneas)
* Apneas last sec-minutes- produce brief arousal
* Presents with excessive daytime sedation- EDS

Sleep Apnea: Two Types
* Obstructive Sleep Apnea: most common
* Central Sleep Apnea

Obstructive Sleep Apnea
* Classic- obese, middle-aged male with thick neck or enlarged tonsils
* Apneas- brief gasps…silence, followed by loud “resuscitative” snores, and sometimes body movements (restless)
* Usually unaware of snoring, arousals…but sleep partner is aware

Central Sleep Apnea
* Apneas- episodic cessation of central ventilation drive
o Thus snoring is less common
* More in elderly, with underlying CNS lesions- ex. tumor, stroke

Sleep Apnea: Consequences
* Depression
* Anxiety
* Morning headaches
* Cognitive dysfunction
* Hypertension

Restless Legs Syndrome
* Paresthesias and/or dysesthesias in the legs, relieved by movements
* Usually occur in transition from wakefulness to sleep

RLS Causes
* Peripheral neuropathies
* Peripheral vascular disease
* Medication side effects
* Anemia
* Pregnancy
* Renal failure

Circadian Rhythm Disorders
* Delayed Sleep Phase Syndrome
* Jet Lag
* Accelerated Sleep Phase Syndrome
* Shift Work Sleep Disorder

Insomnia from Medical Conditions
* Reflux (GERD)
* Nocturia
* Peripheral neuropathies
* Breathing problems- Asthma, COPD
* Heart Disease/Failure
* Pain conditions

Psychiatric Causes of Insomnia
* Depression
* Anxiety
* Psychosis
* Substance intoxication/withdrawal

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Children and Adolescents with Bipolar Disorder

Children and Adolescents with Bipolar Disorder
By: Boris Birmaher MD
Department of Child Psychiatry
Western Psychiatric Institute and Clinic
University of Pittsburgh Medical Center

Do children and adolescents have Bipolar Disorder (BP)?
Bipolar Disorder in Youth
Clinical Manifestations
Bipolar Disorder – Classical Clinical Manifestations
DSM-IV Manic episode
DSM-IV Hypomanic episode
Bipolar Disorder Clinical Manifestations
DSM-IV Major depression episode
Subtypes of Bipolar Disorder
Bipolar I disorder
o Manic
o Depressed
o Mixed
o Rapid cycling
o Psychotic

Bipolar II disorder (hypomania and MDD episodes)
Cyclothymic disorder (hypomania and mild depressions)
Bipolar Not Otherwise Specified (NOS)
Difficulties Diagnosing Pediatric Bipolar Disorder
Developmental Manifestations of Manic Symptoms in Children
To clarify the diagnosis:
Retrospective Studies of Adults with BP-I
Frequent Prodromal Features Before Onset of BP-I
WPIC Child Mood & Anxiety Disorder Outpatient Clinic
Hamilton Depression Scores
Child & Adolescent Bipolar Services (CABS)
Course and Outcome of Bipolar Youth (COBY)
Demographics (COBY) (Cont’)
COBY Subjects – Lifetime Presence of Psychiatric Diagnoses
Prepubertal Bipolar Disorder
In General, BP in youth can presented as:
* Typical phenotype (DSM Bipolar I and II)
o Many have frequent episodes and mixed bipolar episodes
* Typical phenotype but for a short time (DSM-IV BP NOS or rapid cycling)
o Many have frequent episodes and mixed episodes
* Broad phenotype (DSM-IV BP NOS or rapid cycling)
Clinical Manifestations - Questions?
In addition to different subtypes of BP disorder, severity of symptoms, and rapid changes in symptomatology it is difficult to diagnose BP in children because:

1) Coexisting disorders
2) Overlap in symptoms with other disorders
Bipolar Disorder - Comorbidity
Bipolar Disorder - Differential Diagnoses
Diagnostic Overlap between Mania & ADHD
DSM-IV Criteria
Hyperactivity / goal-directed activity
DSM-IV Criteria
Distractibility
Inflated self-esteem / grandiosity Commonly associated
Epidemiology
BP-I Natural Course Multicenter
Pilot Study
BPD-I Natural Course
Course and Outcome of Bipolar Youth (COBY)
Diagnosis at Intake:
Bipolar Disorder - Natural Course
Natural Course General Conclusions
Sequela
Bipolar Disorder - Sequela
Pediatric Bipolar Disorder - WPIC Mood & Anxiety D/O Outpatients
Pediatric Bipolar Disorder Oregon Study
Predictors of Bipolar Disorder
Bipolar Disorder- Family Studies
Children of Parents with BP
NIMH-Bipolar Offspring Study (BIOS)
Bipolar Offspring Study (BIOS) Instruments
BIOS - SAMPLE
BIOS - Demographics – Offspring Preliminary Analyses
BIOS- Probands
Lifetime Disorders
BIOS- Offspring of BP parents-Lifetime Disorders- Definite/Probable
Any Substance/alcohol
Offspring of BP vs. Controls-CBCL Scores
Treatment
Bipolar Disorder - Psychoeducation
Pharmacological Treatment
Divalproex Treatment for Bipolar Disorder
Lithium for Adolescents with Acute Mania
Side Effects/Laboratory Tests Prior and During Psychopharmacological Treatment
Check for presence of “side effects” prior to starting treatment
Bipolar Depression - Treatment
Psychosocial Treatments
Family-Focused Treatment of Bipolar Disorder
Family-Focused Treatment for Adolescent Bipolar Patients
Interpersonal and Social Rhythms Therapy (IPSRT)
Bipolar Disorder – Treatment Other Considerations
Bipolar Disorder- Conclusions

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Depression: A Brief Overview of the Disorder in Childhood

Depression: A Brief Overview of the Disorder in Childhood
By: James H. Johnson, Ph.D., ABPP
University of Florida

Case Examples
Childhood Depression:
History
Acceptance of Depression as a Child Disorder
Child Depression Lite
DSM IV CRITERIA: Major Depressive Episode
Major Depressive Episode
Major Depressive Disorder
Anxiety Versus Depression
Childhood Depression:
Prevalence
Comorbidity
Prognosis: Initial Recovery
Prognosis: Recurrence
Etiology: Conceptual Models of Depression
Psychoanalytic Views
The Role of Life Stress
Specific Life Stressors
Cognitive/Behavioral Views
Examples of Cognitive Distortions
Cognitive/Behavioral Views
Behavioral Views
Learned Helplessness and Depression
Learned Helplessness
Cognitive/Behavioral Views: Child Research Findings
Research Findings
Biological Perspectives
Genetic Factors
Other Biological Findings
Treatment of Childhood Depression
Interpersonal Therapy
Cognitive Behavior Therapy
Psychotropic Medications
Combination Therapies
Treatment: Final Comments

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Mood Disorder

Mood Disorder
* Depressive disorders
Major depressive disorder (MDD)
Dysthymic disorder
* Biopolar Disorder
* Mood disorder due to a medical condition
* Substance-induced mood disorder

Psychopathology of Mood Disorders - Depression
* Not diagnosed or misdiagnosed - a lot
* Prevalence - 9-20% in general population
* Female - 10-20%; male - 5-12% (life time)
* Recurrence rate - 50% - 80%
* Seeking professional help - 16-23%
* Suicide rate

Assessment
* History of onset
* Comorbid substance - alcohol, med.
* Physical examination - senile, meta. dis.
* Non mood psychiatric disorders
* Stress level, coping & social support
* Presence and/or level of suicidal ideation
* Others - measurement scales, biological measures (cortisol, hormone, sleep pattern)

Measures of Depression (I)
Measures of Depression (II)
Diagnosis Criteria for Depression
Dysthymic Disorder
Diagnosis Criteria for Major Depression
Etiology of Depression
Genetic theory
Cultural, age, gender considerations
Depression in Children
Predisposing factors in Children and adolescents
Depression in Women
Depression in Men
Depression and the Elderly
Predictors for elderly suicide
Diagnostic Evaluation
Treatment of Depression
Nursing Diagnoses related to Mood Disorders
Assessment for Suicidal behavior
Suicide Prevention
Interventions
Interventions (II)
Monitor the side-effect of antidepressant
* Energy & motivation↑ -suicide tendency ↑
* Drug-drug & food-drug interactions
* Toxicity of the medications
* TCAs – drowsiness, agitation, tachycardia
* MAOIs – dizziness, fatigue, vertigo
* SSRIs – nausea, vomiting, tremor
* Lithium – diarrhea, muscle weakness, atxia; lag time 7-10 days
Biopolar Disorders
Young & Biopolar
Checklist for the Bioplar Child
Criteria for Bipolar Disorders - Manic episode
Manic Genius
Tendencies of Manic Patients
Etiology of Bipolar Disorders
Intervention - Bipolar Disorders
Interventions for suicidal pts
Self-help
Family and friends can help
Where to get help

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Bipolar Disorder in DSM-IV

Bipolar Disorder in DSM-IV
* Bipolar I disorder: manic episode(s)
or mixed episode(s) plus MDE(s)
* Bipolar II disorder: major depressive episode(s) plus hypomanic episode(s)
* Cyclothymia: hypomanic symptoms
plus depressive symptoms

Bipolar Disorders: DSM-IV Nosology
Criteria
Mania
Hypomania
Major depression
Mixed state
BPD I
BPD II
Manic Episode: Diagnostic Criteria
Manic Episode: Differential Diagnoses
Hypomanic episode
Mixed episode
History of treatment for depression
Differential diagnosis
* Physical
* Psychological
Mixed Episode: Diagnostic Criteria
Characteristics BPD I BPD II
Ethnic/racial differential
Gender differential M = F F›M (?)
Bipolar Disorders: Epidemiology
Characteristics BPD I BPD II
Bipolar Disorders: Epidemiology
Epidemiology
Diagnostic Dilemmas:
Unipolar Versus Bipolar
Unipolar
Etiology
Heritability
ADOPTION STUDIES
Cognitive Deficits
* Working memory
* Sustained attention
* Abstract reasoning
* Visuomotor skills
* Verbal memory
* Verbal fluency
* Cognitive flexibility
* General cognitive functioning
Potential Explanations for Cognitive Deficits
* Iatrogenic or Alcohol use
* Temporary functional changes
* Degenerative brain changes
* Permanent structural lesions
* Permanent functional alterations of neural networks underlying affect and cognition

Alcohol Use
Iatrogenic
Temporal Functional Deficits
Summary

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Psychiatric disorders

Psychiatric disorders
By: * Peter Liddle * Chris Rorden

Disorders of Mind & Brain
* Mind and brain are two sides of one coin; disorders of the mind are disorders of the brain.
* Particular clusters of symptoms (syndromes) tend to occur together in various different mental illnesses
* The ways in which symptoms cluster together tells us something about the structure of the human mind and brain

Anatomy of psychiatric disorders
* Contemporary psychiatry implicates neurotransmitters rather than anatomy.
o Schizophrenia :: dopamine
o Depression :: serotonin
* To some degree, this may reflect the popular treatments – neurotransmitters specific to brain regions.

Major symptom clusters
* Reality distortion
* Disorganization
* Psychomotor poverty
* Psychomotor excitation
* Depression
* Euphoria
* Anxiety

Reality distortion

* Mismatch between representation of reality in individual’s mind and representation supported by objective evidence
* Hallucinations and delusions
* Hallucination: perception with quality of a sensory perception but nor derived form stimulation of a sense organ
* Delusion: fixed belief derived by erroneous inference or unjustified assumption that cannot be accounted for by culture or religion

Delusions
* Delusions usually false but the key issue is lack of rational grounds and fixity.
* Ability to engage in logical deduction about other issues is usually intact; certain ideas seem exempted from the need for logic.
* Non-psychotic distortions of reality (eg in OCD or in non-psychotic depression) reflect biased thinking but are less resistant to debate

Psychotic Reality Distortion
* Can occur in schizophrenia, mania, psychotic depression, brain injury or degeneration
* Themes: persecution; alien control, religion, grandiosity, guilt
* Influenced by culture, but some themes are common across cultures

Reality distortion in schizophrenia
* Characteristic forms (but not present in every case)
* Less specific but common forms:

Affective psychosis
* Mood disorder with psychotic features is diagnosed if psychotic illness is dominated by mood symptoms unless there is reality distortion without substantial mood symptoms for at least two weeks
* Delusions and hallucinations are usually mood congruent (eg guilt, worthlessness, critical voices with depressed mood; grandiose delusions and self-reinforcing halluciations in mania)
* Reality distortion shows similar response to antipsychotic medication irrespective of diagnosis

Neuropsychological correlates of reality distortion
* Reality Distortion can occur in absence of general defect in reasoning.
* Defective internal monitoring of self-generated mental activity (Frith & Done 1989; Mlakar et al, 1994)
* Jumping to conclusions – the bead test (Huq et al, 1988)
* Patients with persecutory delusions tend to attribute negative outcomes to external causes (Bentall, 1994)

Regional cerebral activity and reality distortion
Neurochemistry and pharmacology of reality distortion
Pharmacology of reality distortion
Hypothesis for generation of reality distortion
Disorganization syndrome
Neuropsychological correlates of disorganization
Regional cerebral activity and disorganization
Psychomotor poverty and excitation
Neuropsychological correlates of psychomotor poverty
Psychomotor poverty and brain structure
Neurochemistry & pharmacology of psychomotor poverty
Neurochemistry & pharmacology of psychomotor excitation
Depression & Elation
Mood disorders
Neuropsychological correlates of depression
Brain structure and mood disorders
Regional cerebral activity and depression
Regional cerebral activity associated with elation
Regional cerebral metabolism in bipolar disorder
Neurochemistry and pharmacology of mood disorders
Bipolar affective disorder
Anxiety
Regional cerebral activity associated with anxiety
Pharmacology of anxiety
Concepts of schizophrenia
Reality distortion
Characteristic time course
ICD 10 diagnostic criteria
Aetiology : predisposing factors
Brain structure in schizophrenia
Cognitive deficits in schizophrenia
Pharmacology
Bipolar mood disorder
Genetics
Aetiology of bipolar disorder
Ventricular enlargement
Anatomy of bipolar disorder
Pharmacology of bipolar disorder
Psychopathy
Aetiology of psychopathy
Cognition and information processing in psychopathy

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Rett’s Disorder

Rett’s Disorder
By:By: Natalie Sten

An Overview of Rett Syndrome for Professionals
Possibly the leading cause of mental retardation and neurodevelopmental impairment in females.

After this seminar you will be able to:

* List the warning signs and symptoms of Rett Syndrome.
* Describe how to cope with children with Rett Syndrome and what the most important aspects of treatment are.
* State how school dynamics can play a critical role in the development of children with Rett Syndrome.

GLOSSARY
* Rett Syndrome (RS): A neurodevelopmental disorder that is classified as a pervasive developmental disorder
* Pervasive Development Disorders (PDD): Refers to a group of five disorders characterized by delays in the development of multiple basic functions including socialization and communication.
* Apraxia: A neurological disorder characterized by loss of the ability to execute or carry out learned purposeful movements, despite having the desire and the physical ability to perform the movements.
* Respite Care: The provision of short-term, temporary relief to those who are caring for family members who might otherwise require permanent placement in a facility outside the home.

What is diagnostic criteria for Rett Syndrome?
* Diagnostic Criteria for 299.80 Rett's Disorder
All of the following:
o apparently normal prenatal and perinatal development
o apparently normal psychomotor development through the first 5 months after birth
o normal head circumference at birth
o deceleration of head growth between ages 5 and 48 months
o loss of previously acquired purposeful hand skills between 5 and 30 months with the subsequent development of stereotyped hand movements (e.g., hand-wringing or hand washing)
o loss of social engagement early in the course ( although often social interaction develops later)
o appearance of poorly coordinated gait or trunk movements
o severely impaired expressive and receptive language development with severe psychomotor retardation

RS is Associated with PDDs or Autistic Spectrum Disorder
* Autism, also called autistic disorder, is a complex developmental disability that appears in early childhood, usually before age 3.
* Autism prevents children and adolescents from interacting normally with other people and affects almost every aspect of their social and psychological development.

How is Rett Syndrome Associated with Autism?
* Girls with RS often have autistic-like characteristics (speech & emotional contact impairment/ repetitive hand gestures) at an early age but differences begin to occur as the child continues to grow.

* The critical difference is the gene mutation that is defining of RS. However, females meeting criteria for RS do not meet the symptoms for autism.

Symptoms seen in RS that are NOT seen in Autism are:
* Deceleration of the rate of head growth
* Loss of purposeful hand skills
* Mobility or the irregular breathing patterns
* Repertoire of purposeless hand stereotypes
* Children with RS almost always prefer people to objects
* Children with RS often enjoy affection

Who is affected by RS?
Warning Signs and Symptoms:
There are 4 stages in the child’s development:
* Stage 1: Early Onset (6-18 months)
* Stage 2: Rapid Destructive (1-4 yrs old)
* Stage 3: Plateau (2-10 yrs. old)
* Stage 4: Late Motor Deterioration (Usually after age 10)

Do biological factors play a role?
Rett Syndrome:
Is a neurodevelopmental disorder that is quite rare. It causes a genetic mutation, linked to the X chromosome, which affects the production of a vital protein that controls brain development.
School dynamics associated with students with RS:
* A secure emotional environment is the first, most important aspect of a teaching environment so that children feel safe.
* Children with RS could be placed in a variety of classrooms from special education units to full inclusion according to their own individual needs and abilities.
* Structured, stimulating, restrictive-free classroom environments with direction and organization are necessary.
Interventions must be created based on the individualized needs of the child!

What can families do?
Stimulating environments at home:
Can you think of some emotionally motivating movements that could occur automatically?
It’s the Law in Pennsylvania

How you can help:
Parents and professionals can expect difficulties. What can help you cope?
* Talk about it.
* Be gentle with yourself.
* Learn how to ask for help.
* Trust your instincts.
* Learn to let go and to accept what can’t be changed.
TREATMENT
Therapies Include:
* Aquatic Rehabilitation
* Hydrotherapy
* Love Therapy
* Music Therapy
* Physical Therapy
* Therapist's Role
* Behaviors
* Hippotherapy
* Motor Development
* Occupational Therapy
* Speech Therapy

Where to go for more info?
1) International Rett Syndrome Association www.rettsyndrome.org
2) NIH/National Institute of Neurological Disorders and Stroke
www.ninds.nih.gov
3) National Institute of Child Health and Human Development (NICHD)
www.nichd.nih.gov
References

Rett’s Disorder.ppt

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Evidence-based Treatment of Psychotic Depression

Evidence-based Treatment of Psychotic Depression
By:Gregory W. Dalack, MD

The Practice of EBM

Step 1: Asking an answerable question
Step 2: Tracking down the best evidence to answer that question
Step 3: Critically appraise the evidence for validity, size of the effect, and utility of the findings
Step 4: Incorporate the clinical appraisal into our clinical expertise and patient’s individual issues
Step 5: Evaluate and improve steps 1-4 with each new opportunity to apply these principles


Brief case history
Asking answerable clinical questions (CEBM- Oxford)
An answerable clinical question

For patients with psychotic depression...
...is antidepressant treatment alone...
...when compared to antidepressant plus antipsychotic treatment…
...result in greater improvement of depressive/psychotic symptoms?

Search Treatment of Psychotic Depression

Electronic Books
Classic Study
The pharmacological treatment of delusional depression
Search Treatment of Psychotic Depression
Relative Risk: the ratio in the treated group to the risk in the control group (TG/CG)
Conclusions

Evidence-based Treatment of Psychotic Depression.ppt

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Combined Pharmacotherapy and Psychotherapy for Anxiety Disorders

Combined Pharmacotherapy and Psychotherapy for Anxiety Disorders: Is Efficacy Enhanced?
An Evidenced-Based Approach
By: Heide Klumpp, Ph.D.


Components of Evidence-Based Treatment include:
Chambless and Hollon (1998)
Comparison with a no-treatment control group, alternative treatment group, or placebo in a randomized control trial or equivalent time-samples design


Study must have been conducted with:

a) Treatment manual
b) Population, treated for specified problems
c) Reliable/valid outcome assessment measures
d) Appropriate data analysis

Clinical scenario

Family hx
Clinical questions:
Does she meet DSM-IV criteria for Social Phobia?
What’s your Evidenced-Based Treatment plan?
2) Psychotherapy (e.g., cognitive-behavioral treatment)?
3) Combined therapy?

Rationale for combined therapy:

Sources for evidence regarding combined therapy
Results consisted of:
Articles comparing treatment approaches
+ Provides details of research methods and analysis
- Difficult to compare results across different studies

Meta-analytic studies
Literature reviews
Efficacy of combined pharmacotherapy and psychotherapy for Social Phobia
Primary outcome measure:
Clinician rated: Clinic Global Impression Inventory-Social Phobia Scale (CGII-SPS)
Patient rated: CGII-SPS

Response defined as:

1) Overall severity score at final visit in the “no menta
Pharmacotherapy:
Exposure therapy:
Outcome after 24 weeks of treatment
Conclusions:
Points to consider:
Recruitment: two outpatient programs at medical centers
Response primarily via Clinical Global Impressions Improvement (CGII):
Pharmacotherapy: Double-blind administration
Cognitive-behavioral treatment:
Points to consider:
Recruitment: 133 participants from Cognitive behavioral treatment program at an Anxiety Disorders Clinic at a hospital
Pre Post Pre Post
Conclusion:
Points to consider:
Summary
Questions regarding clinical scenario

Combined Pharmacotherapy and Psychotherapy for Anxiety Disorders.ppt

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Delirium, Dementias, and Related Disorders

Delirium, Dementias, and Related Disorders

Key Concepts
* Cognition
o System of interrelated abilities, such as perception, reasoning, judgment, intuition and memory
o Allows one to be aware of oneself
* Memory
o Facet of cognition, retaining and recalling past experiences
* Delirium
o Acute cognitive impairment caused by medical condition
* Dementia
o Chronic, cognitive impairment
o Differentiated by cause, not symptoms

Delirium Clinical Course
* Disturbance in consciousness and a change in cognition
* Develops over a short period of time
* Usually reversible if underlying cause identified
* Serious, should be treated as an emergency

Delirium Diagnostic Criteria
* Impairment in consciousness - key diagnostic criteria
* Children - can be related to medications or fever
* Elderly - most common in this group, often mistaken as dementia

Delirium Epidemiology & Risk Factors
* Prevalence rates from 10-30% of patients
* In nursing homes, prevalence reaching 60% of those older than the age of 75 years
* Occurs in 30% of hospitalized cancer patients
* 30-40% of those hospitalized with AIDS
* Higher for women than men
* Common in elderly, post-surgical patients

Delirium Etiology
Variety of brain alterations
o Imbalance of neurotransmitter
o Raised plasma cortisol level
o Involvement of white matter
Types

* Due to General Medical Condition
* Substance-Induced
* Substance-Intoxication
* Substance-Withdrawal
* Multiple Etiologies

Medications
Physiological
* Fluid/kidney
o Dehydration, Hypocalcemia, Hypokalemia, Abnormal sodium, Low serum albumin, Elevated BUN, Elevated creatinine, Azotemia, Proteinuria, CRD
* Cardiac/Respiratory
o Hypotension, CVD, CHF, AA, Elevated PT, Low hematocrit, Respiratory insufficiency, Noncardiac thoracic surgery
LABS

* BUN
* Creatinine Clearance
* Serum Albumin
* Hyponatremia
* Hypocalcemia
* Hypokalemia
* Elevated PT

Physiological
* Metabolism/Temperature
* Age, gender

PhysiologicalInfection and Trauma
o Symptomatic infection
o Urinary tract infection
o Respiratory infection
o Elevated WBC
o Emergency Admission
o Fracture
o Falls
o Orthopedic surgery
o Combination illnesses
Physiological
* More than 4 medications
* Drugs with anticholinergic or CNS effects
* Hypoxia/Ischemia
Interdisciplinary Treatment & Priorities
Nursing Management Biologic Domain Assessment
Nursing Management Pharmacologic Assessment
Delirium: Biologic Domain Nursing Diagnosis
Delirium Biologic Nursing Interventions
Delirium Psychological Domain Assessment
Delirium: Psychologic Domain Nursing Diagnosis
Delirium Psychological Nursing Interventions
Delirium Social Domain Assessment
Delirium: Social Domain Nursing Diagnosis
Delirium Social Nursing Interventions
Evaluation Delirium Dementia
Dementia Alzheimer’s Type
Personality changes
Language difficulties
Dementia/Alzheimers Progression
Diagnosis of AD
Epidemiology
Risk Factors
Etiology
Interdisciplinary Treatment
Priority Care Issues
Family Response to AD
Nursing Management Biologic Domain Assessment
Dementia: Biologic Domain Nursing Diagnosis
Dementia Biologic Nursing Interventions
Pharmacologic Interventions
Dementia Psychological Domain Assessment
Dementia: Psychological Domain Nursing Diagnosis
Dementia Psychological Nursing Interventions
Dementia Psychological Nursing Interventions
Dementia Psychological Nursing Interventions
Dementia Social Domain Assessment & Nursing Diagnosis
Dementia Social Nursing Interventions
Family Interventions
Other Dementias
Amnestic Disorder

Delirium, Dementias, and Related Disorders.ppt

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Geropsychiatry: Delirium and Dementia

Geropsychiatry: Delirium and Dementia
By:Robert Averbuch, MD
Assistant Professor, Department of Psychiatry

Disorders of Cognition
* DSM-IV devotes an entire section to a subset of “organic” disorders that primarily affect cognition: “Delirium, Dementia, and Amnestic and other Cognitive Disorders”
What is “organic”?
* Previous differentiation between mental disorders with a clear “physical or biological” etiology (Organic) and those without (“Functional” or “Primary”)
* Falsely implied that Functional (or primary) disorders have no underlying pathophysiological basis
* Primary mental disorder- not due to a GMC or substance
Disorders of Cognition
* Delirium-disturbance in consciousness and cognition that develops rapidly
* Dementia- multiple cognitive deficits that include memory disturbance
* Amnestic Disorder- primarily memory impairment
Delirium: defined

* Disturbance of consciousness (awareness of the environment) and attention,
* PLUS…
o Changes in cognition (ie, “thinking”-memory, orientation, language, etc) OR
o Perceptual disturbances
The Course of Delirium
Delirium: Associated Features
* Disturbance in sleep-wake cycle
* Easily distracted by irrelevant stimuli
* Changes in activity level
o Restlessness, hyperactivity
o Picking at clothes, getting out of bed
o OR hypoactivity (lethargy)
* Emotional disturbances- mood lability, anger, irritability, euphoria, apathy
* Speech or language disturbances
* Perceptual abnormalities- common:
o Illusions, hallucinations, delusions
* Neurological deficits/dysfunction

What Are the Causes?
* DIRECT: Brain pathology: head injury, seizures (during and after), strokes, infections
* INDIRECT: Systemic Illness: electrolyte abnormalities, dehydration, uremia, hepatic encephalopathy, cardiovascular compromise
* Sensory deprivation
* After surgery (post-operative state)- ie. “ICU Psychosis”
* Side effects of medications or toxins or with abused recreational drugs:
Treating Delirium
* Considered a Medical Emergency
* Supportive care in an ICU setting
* Safety- close monitoring
* Remove offending agent, treat underlying cause
Dementia
Hallmark is Memory Impairment
Dementia- defined
Details: Aphasia
Disturbances in Executive Functioning
Associated Features
More associated features
Course of Dementia
What causes Dementia?
More causes:
Alzheimer’s Dementia of the Alzheimer’s Type (DAT)
Vascular Dementia
Aka Multi-Infarct Dementia
Treatment of Dementia
Medications

Geropsychiatry: Delirium and Dementia.ppt

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Delirium in the Elderly: Evaluation and Management

Delirium in the Elderly: Evaluation and Management
By:M. Andrew Greganti, MD

Outline of Discussion
* Case Presentation
* Characteristics of Delirium
* Etiology/Pathogenesis
* Risk Factors
* Prevalence
* Clinical Presentation
* Diagnosis
* Evaluation
* Prevention and Treatment
Case Presentation
Hospital Course
Post Hospital Course
Characteristics of Delirium
Other Characteristics
Etiology
Pathogenesis
How common is delirium?
Risk Factors
Other Risk Factors
Prodrome
Clinical Presentation
Diagnosis
Differential Diagnosis
Prognosis
Evaluation
Preventive Measures Perioperatively
Treatment
Treatment of “Yelling Out”
Summary of Key Points

Delirium in the Elderly: Evaluation and Management.ppt

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Delirium in the Elderly

Delirium in the Elderly
By:Bree Johnston MD MPH
UCSF Division of Geriatrics

Case Study
Atypical Presentations
Learning Objectives
* Recognize that delirium is a common presentation of disease in the elderly
* Recognize that delirium is associated with adverse outcomes
* Know how to distinguish between delirium and other diagnoses (dementia, depression)
* Identify risk factors for delirium and strategies for risk reduction
* Discuss management strategies, recognizing the limitations of current data
Definition
* “an acute disorder of attention and cognition” (de lira “off the path”)
* Standard definition not use until 1980 with publication of DSM III
* Other terms used include organic brain syndrome, metabolic encephelopathy, toxic psychosis, acute mental status change, exogenous psychosis, sundowning
Pathophysiology
Delirium Risk Factors
* Age
* Cognitive impairment
* Male gender
* Severe illness
* Hip fracture
* Fever or hypothermia
* Hypotension
* Malnutrition
* High number of meds
* Sensory impairment
* Psychoactive medications
* Use of lines and restraints
* Metabolic disorders:
* Depression
* Alcoholism
* Pain

Delirium Risk Model
Baseline Risk Group
Precipitating Factor Group
Surgical Prediction Rule
Clinical Prediction Rule for Post-surgical Delirium
Differential Diagnosis
* CNS pathology
* Dementia, particularly frontal lobe
* Other Psychiatric disorders
o Psychosis
* Depression: 41% misdiagnosed as depression Farrell Arch Intern Med 1995
o Bipolar disorder
* Aconvulsive status epilepticus
* Akathisia
* Overall, 32-67% missed or misdiagnosed

Diagnosis
Diagnostic Tools
Delirium versus Dementia
Medications and Delirium
Searching for the cause
103 treatment and 111 controls
Intervention: Surgery as soon as possible & geriatric evaluation pre and post op vs usual care
Outcomes Treatment Control
Possible Benefit From:
* Preoperative psychiatric assessment followed by nursing reorienation (33% vs 14%)
* Postoperative reorienation (87% vs 6%)
* Preoperative education about delirium (78% vs. 59%)
* Pre and post operative psychiatric intervention (13% vs 0)
Can Interventions Prevent Delirium?
Intervention Protocol
* Cognition Orientation, activities
* Sleep Bedtime drink, massage, music, noise reduction
* Immobility Ambulation, exercises
* Vision Visual aids and adaptive equipment
* Hearing Portable amplifiers, cerumen disimpaction
* Dehydration BUN, volume repletion
Preventing Delirium post Hip fracture
* Protocols for:
o Fluid/electrolytes
o Pain treatment
o Eliminating unnecessary medications
o Bowel/bladder function
o Nutrition
o Mobilization
o CNS oxygenation
o Prevention of complications (MI, PE, UTI, pneumonia)
o Environmental stimuli
o Treatment of agitated delirium
Delirium in Hip fracture
Severe delirium, cumulative incidence
Delirium, cumulative incidence
Delirium at discharge
Interventions that May Help
Drug therapy
Drug Therapy of Delirium
Neuroleptics
Use of Haloperidol
Atypical neuroleptics
Benzodiazepines
Other agents
Delirium in the ICU
Sedation in the ICU
Prevention is the Best Medicine

Delirium in the Elderly.ppt

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Alcoholic Hepatitis and Delirium Tremens

Alcoholic Hepatitis and Delirium Tremens

Normal liver
Fatty Liver
Alcoholic Hepatitis
Cirrhosis
Acute Alcoholic Hepatitis
Symptoms include
How to assess severe acute alcoholic hepatitis
Management of Alcoholic Hepatitis
TNF and Alcoholic Hepatitis
Management of Alcoholic Hepatits
Delirium Tremens
Treatment
Selecting patients for alcohol withdrawal outpaitent treatment
* Indications: Alchohol dependence with evidence of tolerance and withdrawal
* Contraindications:
o Coexisting acute or chronic illness requiring inpatient treatment
o Current severe withdrawal with DTs
o No possibility for follow up
o Pregnancy
o Seizure disorder or risk of withdrawal seizure
o Suicide risk
* Relative contraindications
o Benzo dependance
o h/o unsuccessful outpatient detozification
o Age>40 years
o Drinking >100g ethanol daily
o Elevated MCV
o Elevated BUN
o Cirrhosis
o Random blood alcohol >200mg/dl
References
Alcoholic Hepatitis and Delirium Tremens.ppt

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Management of Sedation and Delirium in Ventilated ICU Patients

Management of Sedation and Delirium in Ventilated ICU Patients
By:Gabriel Tsao
Stanford University, School of Medicine

Introduction
Presentation Outline
* Sedation in the ICU
o Drug overview
o Sedation assessment
o Drug selection
* Delirium in the ICU
o Incidence and mortality
o Delirium assessment
o Management of delirium

Sedation in Ventilated Patients
* Mechanical ventilation is uncomfortable and anxiety provoking
* Sedation is often necessary for comfort and airway, line, foley, nursing protection
* >85% of ventilated patients receive sedation

Commonly Used Sedatives
Central alpha-agonists
Dexmedetomidine
Fentanyl
Assessing Sedation
Selection of sedative agent
Sedation Use Recommendations
Sedation Interruption
Sedative Dependence
Presentation Outline
* Sedation in the ICU
o Drug overview
o Sedation assessment
o Drug selection
* Delirium in the ICU
o Incidence and mortality
o Delirium assessment
o Management of delirium
Delirium highly prevalent in ICU
Delirium in ventilated patients
Overview of Delirium
Subtypes of Delirium
Assessing Delirium
Pathophysiology Poorly Understood
Treatment of Hyperactive and Mixed Delirium
Other Treatments for Hyperactive/Mixed Delirium
Treatment of Hypoactive Delirium

Management of Sedation and Delirium in Ventilated ICU Patients.ppt

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