what every clinician needs to know about grief ...€¦ · pleasure and joy in being alive . 16 ....
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A L A N A I G L E W I C Z , M D
A I G L E W I C Z @ U C S D . E D U
A S S I S T A N T C L I N I C A L P R O F E S S O R
U N I V E R S I T Y C A L I F O R N I A , S A N D I E G O
&
V A S A N D I E G O H E A L T H C A R E S Y S T E M
WHAT EVERY CLINICIAN NEEDS TO KNOW ABOUT GRIEF,
BEREAVEMENT AND DEPRESSION
Ms. B
Ms. B, a 75 year old woman who comes for an evaluation because she is not getting past her intense grief over her deceased husband who died suddenly following a myocardial infarction 4 years ago. Although she thinks about her husband daily, she avoids looking at pictures, visiting the grave-site or even going to places they used to enjoy together to try to ward off the intense bouts of misery these reminders provoke. Ms. B is tearful, recalling how wonderful her husband was, that he was her soul-mate, and he loved her in a way no one else ever did.
Ms. B (2)
Ms. B has been ruminating over thoughts about how and why her husband did not really need to die. Her husband had seen his doctor a week before he died and she is plagued by angry thoughts about the doctors who did not diagnose the impending heart attack. She cannot get the idea out of her mind that his doctor could have suspected that her husband had blocked arteries and done something to save him.
She often neglects to take her hypertension medication knowing this could be dangerous and endorses that she wishes to leave death to chance. She has come close to taking an overdose of her hypertension medication but it is against her religion to take one’s own life. Religion used to be source of comfort, but she no longer attends church regularly or finds companionship or support from the church community. Ms. B maintains that no one can help her because no one can bring her husband back.
Ms B’s physician is puzzled. Ms B is tearful and sad, but does not meet criteria for MDD. The physician wonders if this could be normal grief . It has been a long time since Jim died, but knows that everyone grieves in their own way.
Ms B (3)
What is the nature of grief? When does it end? Should grief be treated? When?
What is complicated grief? Should it be treated? Can it be treated? How?
When and how should “depressed” bereaved people
be treated?
Questions to Ponder
Outline
Terminology Grief and Bereavement Acute Integrated
Complicated Grief Suicide Bereavement Distinguishing Grief from Depression Bereavement Related Depression
Loss and Grief
Loss is universal and often the most painful of human experiences
In both our personal and professional lives, we will face meaningful losses regularly
For every person who dies, an average of five - six loved ones are left behind
Grief is the response to loss
Terminology
Grief: constellation of feelings, behaviors, cognitions, and changes in function associated with loss of any kind
Bereavement: Grief specifically tied to the death of a “meaningful” other DSM-III,IV – depressive syndrome within 2 months of death
Mourning: Behavioral , social and cultural rituals of grief
Complicated Grief (aka, prolonged acute, unresolved, traumatic grief): Prolonged, intense grief requiring intervention Persistent difficulty accepting the death; recurrent pangs of intense grief;
preoccupation with thoughts and images of the deceased; avoidance of reminders of the loss; and difficulty adjusting to life without the deceased
WHAT IS THE NATURE OF GRIEF?
Erich Fromm
A Universal Reaction
To spare oneself from grief at all costs can be achieved only at the price of total detachment, which excludes the ability to experience happiness
Grief is Painful
“The loss of a loved person is one of the most intensely painful experiences any human being can suffer. Nothing but the return of the lost person can bring true comfort; should what we provide fall short of that it is felt almost as an insult.”
John Bowlby Loss pp 7-8
1980
Grief: 2 Forms
Acute Integrated
1. The transition is instinctive 2. It usually begins within months 3. Integrated grief is life long
ACUTE GRIEF
Acute Grief Contains a Mix of Emotions
Unpleasant emotions Sadness Anxiety (e.g., about how the
person will manage) Guilt (e.g., about not doing
enough and about surviving) Anger (e.g., about others not
doing or caring enough) Shame (e.g., about sense
of vulnerability and uncontrollable emotionality)
Pleasant emotions Enjoyment in recalling happy
times Amusing anecdotes Pride in honoring the
deceased Warmth in recollecting
closeness Relief from burden Pleasure and joy in being alive
16
Healing after Grief: From Acute to Integrated Grief
Acute grief may last most of the day, most days for up to 6 months, and then recurs transiently
Grief does not fully remit and can periodically surge, as in “difficult times” of the year (holidays, anniversaries, stress, other losses)
Grief usually moves from a place where it dominates a person’s mind to reside more comfortably in the person’s heart.
INTEGRATED GRIEF
Integrated Grief
Enduring sorrow and longing, along with memories of the deceased become assimilated into the life and mind of a bereaved person Usually present by about 6 months after a death Evolves over time
Characteristic features Acceptance of the death Interest and engagement in ongoing life A mix of emotions related to the deceased with positive
emotions usually dominant Thoughts and memories of the deceased accessible but not
preoccupying
19
George And Gracie
“I visit my dear Gracie weekly. I leave fresh flowers and tell her about my week. I tell her about the kids; I tell her what I’m doing. And you know what? Not once has she answered back. I know she’s listening and that’s very reassuring.”
Helping Bereaved
Dos Direct expression of sympathy Acknowledgement that the
clinician does not know exactly what the bereaved person is going through
Talking about the deceased, saying his/her name
Inquiring about the circumstances of the death
Encourage expression of feelings
3 “Hs”: hush, hug and hang out
Don’ts Be casual or passive (“call me
when you want to talk” or “let me know what I can do”)
Imply death for the best or acceptable
Convey the bereaved person is strong and will/should get over it
Avoid discussion of the death or the person who died
Prigerson and Jacobs,2001; Rene Tietsworth, 11/05/04
“A trouble shared is a trouble halved”
Considerations for Clinicians
Crying
Condolence cards
Funeral/memorial attendance
Complicated Grief
Characteristics Consequences Continued difficulty
accepting the death beyond 6 months
Persistent strong yearning Anger and bitterness Preoccupation and/or Excessive avoidance Futility about the value of
ongoing life and relationships
Ongoing pain and suffering Impaired functioning and
disability Increased risk for cancer,
cardiac disease, hypertension, substance abuse
Co-morbid depression Elevated rate of suicidal
ideation and attempts
Failure to Progress from Acute to Integrated Grief
Tends to persist endlessly without treatment
BA SED ON A SIM PLE PRINCIPLE:
A CUTE GRIEF WILL PROG RESS INSTINCTIVELY TO INTEG RA TION IF
COMPLICA TIONS A RE A DDRESSED A ND THE NA TURAL MOURNING
PROCESS IS SUPPORTED
Complicated Grief Treatment
CGT: A Targeted Treatment
Integrates interpersonal psychotherapy, prolonged
exposure, motivational and cognitive behavioral treatment
strategies
Based on a model of coping with grief that posits
contemporaneous oscillating attention to loss-focused work
and life-focused work
Loss
Life
CGT
IPT
PE
MI
CBT
Strategies Procedures
Address complicating thoughts, feelings and behaviors
Establish a rhythm of oscillation between confrontation and comfort
Attend to dual processes of reflection upon the death (loss-focus) and re-envisioning the future (restoration-focus)
Grief monitoring Psychoeducation Imaginal and situational
revisiting exercises Memories and pictures Imaginal conversation with
the person who died Involving significant other Attention to self care, core
values and meaningful future plans
Complicated Grief Treatment (Cont.)
CGT Produced Better Results Than Standard IPT
0%
10%
20%
30%
40%
50%
60%
70%
INTENT-TO TREAT COMPLETERS
51%
66%
28% 32%
CGT IPT
chi-square=7.56, df=1, p =0.006 chi-square=5.07, df=1, p <0.024
NNT: Completers: 3 ITT: 4
Shear et al JAMA 293:2601 2005
% B
ette
r or
ver
y m
uch
bett
er
Do Medications Play a Role?
59.00%
42.00% 40.00%
19.00%
38%
0.00%
10.00%
20.00%
30.00%
40.00%
50.00%
60.00%
CGT IPT Escitalopram
With antidepressant Without antidepressant
Simon et al, 2009
Outcome With And Without Antidepressant Medication
HEALING EMOTIONS AFTER LOSS (HEAL) 4 Sites:Columbia (Shear), MGH (Simon), Pittsburgh (Reynolds) , San Diego (Zisook)
Baseline Assessment
CIT/CM N=125
PBO/CM
N=125
CIT + CGT
N=125
PBO+ CGT
N=125
Post-Treatment
Assessment
16 weeks
Referrals: Ilanit T. Young (858) 552-7598 ityoung@vapop.ucsd.edu
6 months
Back to Ms. B: Should She Be Offered Treatment For Her Grief?
She does not meet criteria for major depression She has not accepted her husband’s death She continues to yearn and long for him and remains
preoccupied with thoughts and memories of Jim She has little evidence of interest in ongoing life or other
people Anger, bitterness and guilt guide most of her thoughts There is no evidence of healing or of integrated grief; rather
it is as though Jim died very recently Ms B meets criteria for complicated grief She SHOULD be treated.
SUICIDE BEREAVEMENT
“WHEN A PATIENT SUICIDES, THE PROBLEM CAN NO LONGER BE SEEN
ONLY AS AN INDIVIDUAL AND FAMILY TRAGEDY, TO BE BORNE IN SECRECY
AND STIGMA. SUICIDE IS EVERYBODY’S BUSINESS.”
- - T H E P S Y C H O L O G I C A L S O C I E T Y O F L O N D O N , P O L I C Y D O C U M E N T O N S U I C I D E , S E C T . 9 . 2 .
Gaffney et al, Death Studies, 2009
When a Patient Suicides
An occupational risk “There are 2 kinds of psychiatrists: those who have lost a
patient to suicide and those who will.”
>50% of psychiatrists have lost at least one patient to suicide Many more than once
Our responses are human responses
Impact of Patient Suicide on Residents/Physicians
• Shame – “I am stupid or lazy” • Doubt – “I am in the wrong career” • Guilt – “Shoulda, woulda, coulda, if” • Rejection, abandonment, anger, relief • Other stress, trauma and loss symptoms
Common reactions
• Depression • ASD and/or PTSD • Complicated Grief
Less common reactions
Important Issues
Death happens – MDD can be a fatal disease Notifying risk management, service chiefs, training directors Notifying and talking to family Funerals Condolence cards Permission to grieve Self care Support from program/colleagues Debriefing M&Ms
Professional help
DISTINGUISHING GRIEF FROM DEPRESSION
Distinguishing Grief from Depression
Quantitatively similar Sadness Anhedonia Guilt Suicidality
Qualitatively different Both can be intensely painful Yet, fundamentally different constructs
Grief Major Depressive Episode
Positive emotions intermixed with sadness
Loss of pleasure related to longing for the deceased loved one
Guilt or remorse is focused on letting the person down
Wish to die is related to longing for reunion
Sad mood is pervasive Loss of interest and
pleasure is pervasive Guilt is related to feeling
worthless or like a bad person
Suicidal thinking is related to a feeling of not deserving to live
Distinguishing Grief from Depression
Distinguishing Grief from Depression
When in doubt consider Time Severity Past and family history
Time since death is not the distinguishing
characteristic
Not either/or, but potentially both
Is Depression Occurring After the Death of a Loved-One Depression?
WHEN IS DEPRESSION NOT DEPRESSION?
Consider the case of Mr. A
Mr. A is 73-year-old male whose wife of 50 years died 5 weeks previously. He has no appetite, has lost 8 lbs in the past month, consistently awakens at 4 a.m, “can’t think straight,” and no longer takes any takes pleasure in customary activities. He denies feelings of guilt or worthlessness. Although he denies suicide intent, he confides that he wishes to join his dearly departed wife. When discussing his wife, he shows moderate psychomotor agitation and spends most days mindlessly sitting in front of his television.
Questions Arising From Mr. A
If Mr. A. meets all symptom and duration criteria for MDD, but falls within “2 month” period of DSM-IV bereavement exclusion, what should you diagnose? Do you try to “normalize” the experience for Mr. A. (“Anybody in
your position would feel as you do”) & advise against medical treatment?
Or
Do you formulate this as “clinical depression” and recommend psychotherapy and/or an antidepressant?
The Relationship Between Bereavement and Depression Remains Controversial
Many believe that “depression” is a normal consequence of bereavement MDD shouldn’t be diagnosed MDD shouldn't be treated
May interfere with grief DSM vs. ICD
Does the data support this belief? No: depression following bereavement is: Common Persistent Poor outcome Responds to treatment
The “Fallacy of Misplaced Empathy” (Ronald Pies, MD)
MDD Following Bereavement Is Common: Overall Rates MDE Following Bereavement Higher Than
Expected For At Least 2 Years
0
5
10
15
20
25
2 months 13 months 25 months
Percentage with MDD Risk factors Past and family MDD Death by suicide Lack of treatment
Greatest risk for MDE 13 months is MDE 2 months
Married Controls (4% MDD)
aZisook and Shuchter, 1993 bZisook et al, 1997
Summary of 24 Longitudinal Studies
Bereavement related MDD is about equally prevalent in children, adults and older adults
In controlled studies, rates of MDD consistently greater in recently bereaved than non-bereaved controls
Bereavement-related MDD is persistent over time
• In panel studies beginning pre-bereavement, rates of MDE and dysphoria already higher in soon to be widowed than those who will remain married
• Pre-bereavement MDE and dysphoria predict post-bereavement BRD • Dysphoria and MDE are highest in months after death, decrease over time, but remain
elevated, compared to non-bereaved, for 1-3 years
Consequences, including dysfunction, disability, changes in sleep architecture, immune impairment and suicidal ideation, are similar to MDD
Bereavement-related MDD responds to antidepressant treatment
Zisook and Kendler, 2007; Zisook et al, 2008
Does Bereavement-Related Major Depression Differ from Major Depression Associated with Other Forms of Stressful
Events? BRD (N=82) SLERD (N=224) Significance
Demographics
Age at index episode 35.1 ± 7.4 33.0 ± 8.2 0.04
Gender (% female) 72.0 56.3 0.01
DSM-IV Exclusion Criteria (%)
Duration > 2 months 32.9 43.3 0.12
Psychomotor retardation 39.0 41.1 0.64
Suicidal ideation 14.6 22.8 0.21
Severe work impairment 17.1 14.9 0.77
Meets Criteria for “Uncomplicated Loss” 28.1 24.6 0.53
Treatment Seeking For Index Episode (%) 26.8 36.2 0.05
Kendler, Myers and Zisook, AJP, 2009
No difference in duration of episodes, age at first episode, number of previous episodes, likelihood of subsequent episodes, co-morbid anxiety or substance-use disorders or risk of lifetime MDD in co-twin
What are the Implications for DSM-V?
Findings - BRD is: similar to other types of MDD often associated with pain and considerable suffering as often associated with those features of MDD the DSM says are more
characteristic of MDD than of “normal” grief as other, non-bereavement related depression
highly comorbid with a number of Axis I conditions known to be associated with MD
genetically influenced tends to be chronic and recurrent and responds to antidepressant treatment
Conclusion: “To continue the bereavement exclusion in DSM-V would be to provide license to bereaved individuals, their families and health care providers to continue ignoring signs and symptoms of a potentially debilitating, life-threatening, yet treatable disorder”.
Kendler, Myers and Zisook et al, 2009
Treatment of Bereavement-Related MDD
“Give sorrow words: the grief that does not speak whispers the o’er-fraught heart, and bids it break”.
Shakespeare, Macbeth
“Your tale is very sad, Ben. I’m almost sorry I took an anti-depressant.”
Treatment of Bereavement Related MDE
No RTCs of Psychotherapy 5 open studies antidepressant medication Jacobs et al, 1987 Pasternak et al, 1991 Zisook et al, 2001 Oakley et al, 2002 Hensley et al, 2006
1 Placebo controlled study – Reynolds et al, 1999
Bereavement Related MDE Medication Study Conclusions
• depression does • depression responds to standard treatment • grief responds in kind
Treating depression does not interfere with
grief
MDE associated with bereavement responds to treatment like other,
nonbereavement-related MDE
Role of psychotherapy not yet clear
Summary Acute grief is painful and disruptive – but usually evolves into less painful “integrated” grief • Grief is not a medical condition • Acute and integrated grief do not require professional treatment
Acute grief can become “prolonged” (i.e., “complicated grief”)and/or be accompanied by MDD
• Complicated grief and bereavement related major depression can be identified and should be treated
“In the depth of winter, I finally learned that within me there lay an invincible summer”.
Albert Camus
Cognitive Behavioral Therapy with Older Adults Steven R. Thorp, Ph.D.
VA San Diego Healthcare System Center of Excellence for Stress and Mental Health
University of California, San Diego
Outline
Older Adulthood and Mental Health
Cognitive-Behavioral Therapy Mood Disorders in Older Adults
Anxiety Disorders in Older Adults
Assessment Guidelines
Treatment Guidelines
Barriers to Mental Health Services for Older Adults
Older patients’ reluctance to seek psychiatric treatment; medication noncompliance1 Under-treatment by primary care physicians; General medicine physicians provide up to half of all outpatient mental health care2, but they often fail to prescribe adequate pharmacotherapy or refer for mental health specialty care3 Ageism in assessment (especially neglecting to ask questions about psychological problems, especially childhood problems and early traumatic events) and treatment (Freud called adults over 50 “ineducable”)4
1Bortz & O’Brien, 1997; 2Regier et al., 1993; 3Rogers et al., 1993; 4Freud, 1905
Treatment Preferences
Among older medical patients, 79% said they would use any psychological services However, 72% preferred to talk with their primary care provider, while 46% said they would speak to a mental health worker or nurse about their problems Only 34% said they would attend “group therapy,” but 68% said they would attend “psychoeducational classes”
Areán et al., 2002
CBT
Cognitive-Behavioral Therapy (CBT) is the most studied (and often shown to be the most successful) psychotherapy in a variety of populations1
CBT is a very general term (psychotherapies that address “thoughts” and “behaviors”), but it requires certain elements
1Barlow (2001)
Characteristics of CBT
Brief & time-limited Involves client-therapist collaboration Structured, with active and directive therapist Views thoughts as hypotheses to be questioned and tested Present focused and problem focused Involves homework Can be done in individual, group, couples, or family formats Adapted from National Association of Cognitive-Behavior Therapists (2003)
Hallmarks of CBT Sessions
Choosing specific goals to target within a specific number of sessions (often 12-20, 50-90 minutes) Setting an agenda for each session Addressing problematic thoughts and behaviors, and noting how they influence mood and progress toward goals Review of session Assigning homework to be done between sessions
The Basic Theory Underlying CBT
Feelings
Behaviors Thoughts
Common CBT Techniques
Behavioral activation and scheduling activities Cognitive restructuring Cognitive rehearsal Exposure Role playing
CBT and Pharmacotherapy
Medications for older adults sometimes work well, but complications include:
sensitivity to side effects
dosing “window” issues
potential for harmful interactions with other medications
potential for addiction and falls
comorbid medical and neurological disorders
costs of lifetime use
CBT and Pharmacotherapy
CBT has yielded effects sizes as large or larger than pharmacotherapy or other forms of psychotherapy1, and patients are less likely to relapse (vs. medications)2
CBT + medications generally superior to medications alone for older adults3
1APA, 2000; 2Hollon et al., 2002; 3Areán & Cook, 2002
Mood Disorders
In Older Adults Depression
Depression and Axis II
Bipolar Disorder
Depression in Older Adults
Depression is the most common emotional disorder in older adults (15% in community, higher in ill populations)1,2 and there is a poor prognosis for untreated depression in the elderly3
It is important for primary care physicians to detect psychiatric issues and address them (by treatment or referral)
1Bortz & O’Brien, 1997; 2Reynolds & Kupfer, 1999; 3Burvill et al., 1986
CBT for Depression
CBT for geriatric depression has been studied by different investigators, using diagnostic interviews, treatment manuals, supervision of therapists, and control conditions1
Among older patients studied over a 10-year period, 75% showed clear improvement or full remission after 15-20 outpatient sessions of CBT, though 30-40 sessions worked best for those with more chronic or complex problems2
1Areán & Cook, 2002; 2 Gallagher et al.; 1987
Efficacy of CBT and Depression
Social Problem Solving Therapy (a type of CBT) works well for treating depression in older adults1
From RCTs of older adults, CBT appears to be superior to usual care and no treatment for MDD and depressive symptoms, with maintenance of gains for up to 3 years2
CBT in group format also works well for older adults with depression3
1Areán et al., 1993; 2Areán & Cook, 2002; 3Gallagher-Thompson et al., 1990
Depression and Axis II
Although clinical lore suggests that Axis II disorders “burn out” in late life, 13% of community-dwelling older adults have personality disorders (PDs)1 and PDs often occur with geriatric depression2
Older patients with MDD have higher rates of PDs than those with other Axis I (or no Axis I) disorders3
Among older adults with depression, one-third had a PD, and those with PD were less likely to benefit from short-term psychotherapy4
1Sidelitz, 2001; 2Thorp & Lynch, 2005; 3 Bizzini, 1998; 4Thompson, Gallagher, & Czirr, 1988
Dialectical Behavior Therapy
Dialectical Behavior Therapy (DBT) is a CBT that integrates mindfulness skills; designed to treat borderline personality disorder1
Study 1 (34 depressed older adults): 47% in medication only group had depression in remission at posttreatment; 71% of those in medication plus DBT skills groups were in remission at posttreatment2
Study 2 (35 medication resistant, depressed plus PD patients): After treatment, 50% in med group were in remission for depression and 71% of the DBT plus med group were in remission; the latter group had lower interpersonal sensitivity and aggression scores2
1Linehan, 1993; 2Lynch et al., 2007
Bipolar Disorder
Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD)
Participants with Bipolar I or II disorder and depression randomized to one of 4 arms:
Collaborative care: n=130 or
Three types of intensive psychotherapy (n=163): CBT
Family-Focused Therapy
Interpersonal and Social Rhythm Therapy
Miklowitz, 2007
STEP-BD Study Results
No differences among the 3 intensive psychotherapies
Intensive psychotherapies yielded significantly higher year-end recovery rates and shorter times to recovery than patients in collaborative care
Miklowitz, 2007
Anxiety Disorders
In Older Adults
CBT does not appear to reduce anxiety for older adults as well as it does for younger adults1
Acceptance and Commitment Therapy (ACT) integrates mindfulness as well as traditional CBT methods. We found no dropouts from ACT in a preliminary trial and it reduces anxiety, but it did not work as well as in younger adults2
1Wolitzky-Taylor et al. (2010); 2 Wetherell et al. (2010)
Meta-Analysis of Behavioral Treatments
We1 screened 300 studies and compared effect sizes from 19 clinical trials (with sample size of at least 5) of behavioral treatments for geriatric anxiety (CBT alone, CBT with Relaxation Training, or RT alone)
Mostly Generalized Anxiety Disorder and Panic Disorder, with some Social Anxiety, Simple Phobias, and unspecified anxiety symptoms
No studies of Obsessive-Compulsive Disorder or Posttraumatic Stress Disorder (PTSD)
Treatments were more effective than wait lists or active controls; comparable to effects in the general population
1Thorp et al, 2009
Meta-Analysis of Behavioral Treatments, cont.
Surprise finding: CBT did not appear to add anything beyond RT alone, and one could argue that RT is easier to teach and administer Interpret with caution, given different sample characteristics and control conditions
1Thorp et al, 2009
Psychotherapy with Older Adults with PTSD
No controlled trials of psychotherapy for PTSD in older adults1 Only 7 peer-reviewed empirical studies of older adults with PTSD, and the modal (most common) sample size is 1 Exposure therapies are most studied in general population, but concerns about older adults being too frail or not being able to “handle” exposure therapies2
1Thorp et al, 2009; 2Hyer & Woods, 1998
Exposure Therapy for Older Veterans with PTSD
Thorp, S. R., Stein, M. B., Jeste, D. V., Patterson, T. L., & Wetherell, J. L. (2012). Prolonged exposure therapy for older veterans with posttraumatic stress disorder: Pilot study. American Journal of Geriatric Psychiatry, 20, 276-280.
Pilot Study
Pilot study of older male veterans with PTSD from military traumas
Objectives: Determine feasibility of recruitment, assessment, and the treatment protocol
Design: Pre/post (“open label”) trial of Prolonged Exposure (PE) therapy (n = 11), with a comparison to a separate Treatment as Usual (TAU) sample from the same clinic (n = 53)
Subjects
Comparison of Groups
PE TAU
Variable % Mean
(SD)
% Mean
(SD) Age 63.1 (7.1) 61.9 (5.3)
Education (years) 14.0 (1.6) 14.1 (1.9)
Married 50 51
Caucasian 88 60
Time Since Trauma 39 years 40 years
Prolonged Exposure Therapy (PE)
PE is a manualized treatment for PTSD1, and it is the most well validated type of psychotherapy for PTSD2 Protocol: Six weeks of 90-minute individual sessions for imaginal exposure (talking aloud, in detail, about worst traumatic event) plus weekly homework (in vivo exposure; engaging in feared but safe activities)
1Foa, Hembree, & Rothbaum, 2008; 2Bradley et al., 2005
PE Theory
PTSD symptoms remit by 3-4 months after traumatic events for most individuals Individuals who develop chronic PTSD tend to avoid people, places, and things (e.g., objects, sounds, thoughts, feelings) linked to the trauma and have unhelpful thoughts Treatment: Planned, extended contact with feared memories and situations will decrease the physiological response over time, making PTSD symptoms less intense
1Foa, Hembree, & Rothbaum, 2007
Results
Clinician-Rated PTSD (CAPS)
0
10
20
30
40
50
60
70
80
90
100
PE TAU
PrePost
*p<.05, Wilcoxon Matched Pairs Signed Ranks Test
CAPS ≥ 60 indicates clinically
significant PTSD
* *
Cohen’s d = 1.7 Cohen’s d = 0.5
Thorp et al., 2012, AJGP
Conclusions from Pilot
Early indications that older veterans can be recruited, that exposure therapy is well tolerated, and that exposure can reduce PTSD symptoms
Results should be interpreted with caution, given the small sample size, but the data suggest that exposure therapy may be promising for older male veterans with PTSD
PE vs. Relaxation in Older Veterans
VA Career Development Award (Thorp, PI): Five-year randomized clinical trial: PE vs. Relaxation Training for Older Adults (age 60 and older) with PTSD Independent clinical assessments with follow-up assessments every 6 months during study Testing to examine cognitive functioning as a potential predictor of treatment outcome Final data from 87 veterans will be collected this year
Risk of Dementia Among Veterans
There is a link between PTSD and dementia1
Researchers followed 181,000 veterans over six years, including more than 53,000 with PTSD
Those with PTSD were more than twice as likely to develop dementia
1Yaffe et al., 2010
Risk of Dementia Among Veterans
A meta-analysis of cognitive functioning in older adults with PTSD found that trauma exposure is linked to worse performance on learning tasks and PTSD is linked to poorer memory1
1Schuitevoerder et al., in press, Journal of Anxiety Disorders
Cognitive Impairment and Psychotherapy
Depression
For older adults with depression, cognitive strategies worked well for mild dementia, behavioral strategies worked best for more advanced cognitive impairment1
1Teri & Gallagher-Thompson (1991)
PTSD
In study of 145 sexual assault survivors with PTSD, older women in exposure therapy and younger women in cognitive therapy had best outcomes (authors posit this is due to “long standing cognitions” in older group)1
Among veterans with PTSD, those with poor verbal memory and narrative encoding deficits were less likely to be responsive to CBT (differences not due to IQ, attention, PTSD severity, depression, time since trauma, or substance misuse)2
1Rizvi, Vogt, & Resick, 2009; 2Wild & Gur, 2008
Residential Treatment (CPT) of PTSD in Veterans with
Comorbid TBI
Chard et al. (2010)
PTSD
Sev
erity
(CA
PS)
Residential Treatment (CPT) of PTSD in Veterans with
Comorbid TBI
0
10
20
30
40
50
60
70
80
90
100
Mild TBI (n = 28) Moderate-Severe TBI (n = 14)
Baseline Post-Treatment
Chard et al. (2011)
PTSD
Sev
erity
(CA
PS)
Treatment Response by Age
We examined data from a recent psychotherapy trial to see if there were differences in PTSD pre- and post-treatment between veterans aged 60 and older (n = 60) and younger (n =139) veterans
PTSD Severity C
APS
Each *p<.05
Assessment Guidelines
Assessment
Assess: Physical exam
History of work, relationships, disorders
Traumatic event, if applicable
Social support
Cognitive status
ADLs (e.g., grooming, shopping, cooking, med management)
Thorp & Lynch, 2005; Weintraub & Ruskin, 1999
Assessment, cont.
Older adults may report problems with appetite, sleep, or cognitive problems rather than mood problems1,2; they may resist “airing dirty laundry”
It is often helpful to begin assessments by inquiring about more somatic issues and then inquire about anything that may be causing them stress
1APA, 2000; 2Reynolds & Kupfer, 1999
Assessment, cont.
Vision problems are more common in older adults – these problems can lower cognitive testing scores1 and macular degeneration can mimic visual hallucinations)2
Try to print in larger, high contrast font (e.g., 16 point bold) More than half of adults aged 70 or older have hearing problems, so may need to speak louder than normal; assess history of hearing treatments, and consider hearing problems in group therapy setting
1Lezak, 1995; 2Holroyd et al., 1992
Assessment, cont.
Consider stigma: “How much do you do X behavior (or feel X feeling)” vs. “Do you ever do (or feel) X?” (especially about violent, sexual, or illegal activities)
Recommend the use of several measures and lower cutoffs
Use observation and collateral reports (family, friends, caregivers) in addition to self-report
Thorp & Lynch, 2005; Weintraub & Ruskin, 1999
Treatment Guidelines
Language Guidelines
Avoid slang and jargon in speech with older adults (unless they use it)
Avoid terms overly linked to “mental problems” (e.g., feeling “down” vs. “depressed”) or sound like psychobabble or “new age” treatments (“working with your inner child”)
“Classes” vs. “Group Therapy”
Instead of, “Would you like help with your mental problem?” Or “Will you go to a psychotherapist or psychoanalyst?” , try “How would you feel about talking to someone about this common problem?”
Thorp & Lynch, 2005; Weintraub & Ruskin, 1999
Treatment Guidelines
Professional, more conservative dress
Use proper name and title (both ways)
More time for presentation and review
Repeat often and give written instructions, calendars, or other visual aids
Record sessions for clients to review
Areán, 2003; Massey, 1997; Thompson, 1996; Thorp & Lynch, 2005
Treatment Guidelines, cont.
Couples and family interventions/support
Visual and other modes of learning
Metaphors for psychotherapy, such as “exercising”, “tracking blood sugar”, or “getting shots”)
Provide more practical assistance and concrete recommendations
Take breaks as needed; perhaps extend length of sessions or duration of treatment
Natural Advantages of CBT for Older Adults
Includes psychoeducation about disorders and treatment (to reduce stigma and normalize problems)
Strong relationship between therapist and client and collaborative agenda
Measureable goals
Continual reviews of new information and practice in and out of session
Areán, 2003; Massey, 1997; Thorp & Lynch, 2005
Summary and Future Directions
There is a growing need for mental health treatment for older adults Older patients are often willing to utilize CBT and may benefit from CBT alone or in conjunction with pharmacotherapy Presentation and language can encourage older adults to initiate and maintain CBT Assessment and treatment should be multi-modal and multi-faceted
Summary and Future Directions
CBT is effective in improving symptoms and psychosocial outcomes in depression, with less evidence for bipolar disorder and anxiety disorders
Newer CBT interventions include mindfulness and acceptance strategies in addition to more traditional CBT strategies that target changes in thoughts and behaviors
Summary and Future Directions
Cognitive remediation or training may be an appropriate intervention for older adults with PTSD and cognitive deficits
Compensatory cognitive training has shown positive effects on cognition and functional capacity in severe mental illness, even among older clients1,2
1Twamley et al., 2011; 2Twamley et al., in press
Thank You!
From Symptoms to Circuits in From Symptoms to Circuits in y py pPsychopharmacology: Imaging Psychopharmacology: Imaging
Brain Circuits and Applying Brain Circuits and Applying PharmacogenomicsPharmacogenomics in Modern in Modern
Clinical PracticeClinical Practice
Stephen M. Stahl MD PhDUniversity of California San DiegoUniversity of California San Diego
andUniversity of Cambridge, UK
1
DisclosuresType Company
Consultant Advent; Alkermes; Arena;AstraZeneca; BioMarin; BoehringerIngelheim; Bristol-Myers Squibb; CeNeRx;Cypress; Lilly; Forest;Ingelheim; Bristol Myers Squibb; CeNeRx;Cypress; Lilly; Forest; GenOmind, Janssen; Jazz; Labopharm; Lundbeck; Merck; Neuronetics; Novartis; Ono; Orexigen; Otsuka; Pamlab; Pfizer; Rexahn; Roche; Royalty; Servier; Shire; Solvay; Sunovion; V lValeant
Grant/Research Support
AstraZeneca,Cenerex,Lilly,Forest,GenOmind,Merck,Neuronetics,PamLab,Pfizer,Roche,Servier,Shire,Sunovion, Torrent
Speaker’s Bureau
Arbor Scientia,Astra Zeneca,Lilly,Forest,J & J,Merck, N i Ed ti I tit t Pfi S i d S iBureau Neuroscience Education Institute,Pfizer,Servier and Sunovion
Shareholder Neuroscience Education Institute
Obj tiObj ti•• To discuss modern formulations for the role of genetics inTo discuss modern formulations for the role of genetics in
ObjectivesObjectivesTo discuss modern formulations for the role of genetics in To discuss modern formulations for the role of genetics in psychiatric disorders, i.e. “nature”psychiatric disorders, i.e. “nature”
•• To show that environmental stress also converges on the To show that environmental stress also converges on the expression of genes, via epigenetic mechanisms, i.e., expression of genes, via epigenetic mechanisms, i.e., “nurture “nurture
T d t t h 21T d t t h 21stst t t l h ltht t l h lth•• To demonstrate how a 21To demonstrate how a 21stst century mental health century mental health professional puts this all together to make diagnoses and professional puts this all together to make diagnoses and to select psychopharmacologic treatments to select psychopharmacologic treatments p y p gp y p g
Psychiatric DisordersPsychiatric Disorders
• Psychiatric disorders are categorical collections of y gsymptoms chosen by a committee of experts
• Psychiatric disorders are revised periodically by the DSM (Diagnostic and Statistical Manual of the American Psychiatric Association)
Ps chiatric disorders are descripti e and reliable b t not• Psychiatric disorders are descriptive and reliable but not predictive of treatment response nor linked to neurobiology
• Psychiatric disorders are not diseases
Symptoms and Psychiatric DisordersSymptoms and Psychiatric Disorders
Symptoms and Psychiatric DisordersSymptoms and Psychiatric Disorders
• Each psychiatric disorder is likely to represent many diseases (maybe hundreds)
• Psychiatric symptoms correlate somewhat with lf ti i b i i itmalfunctioning brain circuits
• Psychiatric disorders do not correlate well with genotype biosignatures or brain circuitsgenotype, biosignatures or brain circuits
• Thus, the current diagnostic strategy is to attempt to link symptom domains that cut across psychiatric disorderssymptom domains that cut across psychiatric disorders first to inefficient information processing in specific brain circuits and eventually to genes regulating those circuits
orde
r
rder
DH
D
essi
ve d
iso
xiet
y di
sor
goric
al/A
D
maj
or d
epre
raliz
ed a
n
DS
M c
ateg
egor
ical
/m
rical
/gen
er D
DS
M c
ate
SM
cat
egor
RDoC dimensional/cognitive symptoms
DS RDoC dimensional/cognitive symptoms
RDoC dimensional/arousal/regulatory symptoms
Psychiatric Symptoms are Dimensional, Cutting Across Many Psychiatric DisordersAcross Many Psychiatric Disorders
Five Symptom Domains across psychiatric conditions searching for their underlying circuits and genes g y g g
(Research Domain Criteria RDoC of NIMH)
Social Processes Social Processes
• social cognition and social behaviors
Cognitive Systems Cognitive Systems
• attention, perception, working memory
Positive Valence Systemsy
• reward, appetitive behaviors
Negative Valence Systems
• depression, defeat, loss
Arousal-regulatory
• activity, sleep, rhythms
Circuits and SymptomsCircuits and SymptomsCircuits and SymptomsCircuits and Symptoms
What is the topographical distribution of What is the topographical distribution of f ti d th f t ti if ti d th f t ti ifunction and thus of symptom generation in function and thus of symptom generation in
the brain?the brain?
Overlap of MDD and Anxiety Disorders
fatigue
concentration
fatiguepsychomotor
sleepguilt/
worthlessness
dep’dmood Interest/
pleasurephobic
avoidance
panic attacks
anxietyworry
suicidalityappetite/weightirritability muscle
tension
compul-sions
avoidance
major depressivedisorderanxiety
disorders
14-1
positive symptoms negative
symptoms
schizophreniaaffective
symptoms cognitiveaggressivesymptoms
symptoms
9-5
Match Each Symptom to HypotheticallyMalfunctioning Brain Circuits
mesocortical/prefrontal cortexmesolimbic
positive symptoms
negative t
nucleus accumbensreward circuits
affective
symptoms symptoms
aggressiveaffectivesymptoms cognitive
symptoms
aggressivesymptoms
dorsolateralprefrontal cortex
amygdalaorbito-
ventromedialprefrontal cortex
9-12
amygdalaorbitofrontal cortex
ADHD: Deconstruct the Syndrome into DSM-V Diagnostic Symptoms
ADHD
inattentive symptoms
selectiveattention
sustained attentionproblem solving
hyperactive impulsive ypsymptoms
psymptoms
17-1
dorsal ACC DLPFC
selectiveattention
sustained attentionproblem solving
impulsive symptoms
hyperactive symptoms
prefrontal motor
orbitalfrontal
17-2
motor cortex
frontal cortex
Psychiatric “Stress” TestingPsychiatric “Stress” Testing
Putting a load on a brain circuit and becoming Putting a load on a brain circuit and becoming a CNSa CNS--I (Central Nervous System Investigator)I (Central Nervous System Investigator)a CNSa CNS I (Central Nervous System Investigator)I (Central Nervous System Investigator)
Cortical pyramidal neurons and neurotransmitters: more is not always bettery
onal
mid
al n
euro
nctio
ning
receptor stimulation
pyra
m fu
receptor stimulation
7-26
N-Back Test
ti lstimulus
response
0-back 1 4 2 3
1-back none 1 4 2
8-8
Hypothetical CSTC Loop for Executive FunctionsDLPFC Striatum Thalamus DLPFC
7-17
The Stroop Task
right answer = “red”
Blue
Red
wrong answer = “blue”
Red
Orange
RedRed
Green
Green
8-14
Dorsal ACC Bottom of Striatum Thalamus ACC
Hypothetical CSTC Loop for Attention
7-18
Processing Fearful Faces
“match the emotion”
8-11
Subgenual ACC Nucleus Accumbens Thalamus Cortex
Hypothetical CSTC Loop for “Emotions”
7-19
Hypothetical CSTC Loop for Impulsivity/Compulsivity
OFC B tt f C d t Th l OFCOFC Bottom of Caudate Thalamus OFC
7-20
Genes and Psychiatric DisordersGenes and Psychiatric Disorders
Classical Theory: Genes Cause Mental Illness
hypothetical mental illness geneg
abnormal gene product causes
neuronal malfunction
mental illness
6-2
mental illness
Symptom Endophenotype Model: Genes Cause Psychiatric Symptoms, Behaviors,
Personalities and Temperamentshypothetical gene for
a symptom,b h i lit
Personalities and Temperaments
behavior, personality ortemperament
abnormal gene causesneuronal malfunction
b lhi t i
6-3
abnormal behavior
psychiatricsymptom personality temperament
Hypothetical Gene for Subtle Molecular Abnormalities
neuro-d l t
hypothetical gene for
btl
developmentserotonin
transportera subtle
molecularabnormality
axonal and dendritic protein
synthesis and internaland internal
transport
signalsignal transduction
pathway
synaptic plasticity
6-4
y p p ymachinery
enzymes for monoamine degradation
Genes and Psychiatric Disorders
• There is no known gene for any psychiatric disorder, nor isThere is no known gene for any psychiatric disorder, nor is there ever expected to be one found
• Genes do not code for psychiatric disorders
• Genes do not code for psychiatric symptoms
• Genes code for proteins and epigenetic regulators, many p p g g , yof which regulate the efficiency of information processing in brain circuits, which can be visualized with neuroimaging techniquestechniques
• Thus, psychiatric research is attempting to link circuits upstream to treatment response and downstream toupstream to treatment response and downstream to regulatory genes
Hypothetical Path from Gene to Behavior
genotype
subtle molecular abnormality
abnormal informationprocessing
(biological endophenotype)
behavior with complexfunctional interactions
and emergent phenomena( )
6-5
(symptom endophenotype)
Hypothetical Path from Genes via Molecules, Circuits andInformation Processing to Symptoms, Syndromes, and Mental Illnesses
risk gene 1 risk gene 2 risk gene 3
altered alteredaltered enzymefor monoamine
degradation
alteredsynapticplasticity
machinery
altereddevelopmentin prefrontal
cortex
biological biological A B
overactivationnormalbaselineg
endophenotypeg
endophenotypeA Bbaseline
hypoactivation
tisymptom symptomh t
6-6
executive dysfunction delusionssymptom
endophenotypesymptom
endophenotypeschizophrenia
phenotype
N t N t ?N t N t ?Nature or Nurture?Nature or Nurture?
Genes or the Environment?Genes or the Environment?Genes or the Environment?Genes or the Environment?
Genetics or Genetics or EpigeneticsEpigenetics??
Model of “Diabolical Learning”
A B C
tibiological
endophenotype X Y Z
time
inadequate or no
treatmentunprovoked,
decompensation with either overactivation or circuit breakdown
treatment
symptomendophenotype
orphenotype psychiatric symptom of a psychiatric
disorder( d b i i d d
8-6A
(e.g., drug abuse, pain, panic, depressed mood, insomnia)
Model of “Diabolical Learning”
A B C
timebiological
endophenotype X Y Z
time
inadequate or no
treatment
decompensation and circuit breakdown worsening
treatment
symptomendophenotype
orphenotype symptoms worsen
or relapse
8-6B
Model of “Diabolical Learning”
A B C
biological endophenotype X Y Z
further plastic changes in circuitry that facilitate maladaptive information
processing, which is difficult to reversep g,
symptomendophenotype
orphenotype new symptoms
or treatment resistance
8-6C
Normal Functioning of a Circuit:Normal Activation Under Stress
normal genes
bad childhood divorce
virus org
life events
virus or toxin
overactivationnormal overactivationnormalbaselinehypoactivation
circuit
normal activation
6-7normal phenotype
Genetically Biased Circuit but No Symptoms:able to compensate for genetically inefficient
information processing by overactivationrisk gene
divorceinformation processing by overactivation
single life event stressor
“biased” circuit
overactivationnormalbaseline
overactivation
baselinehypoactivation
inefficient informationprocessing
6-8
normal phenotype
Stress-Diathesis Model of Psychiatric Symptoms:too many genetic biases combined with too many stressors results in
psychiatric symptoms
risk gene
risk gene
risk
risk gene bad childhood divorce
virus or
psychiatric symptoms
ggene
multiple life events
virus or toxin
“biased” diathesis stress overactivation
normalb licircuit
hypoactivation unsuccessful
baselinehypoactivation
hypoactivationwith
malfunction
unsuccessfulcompensation
6-9psychiatric symptoms
Stress-Diathesis Model Part 1: no risk gene, normal function
mild stressor severe stressor
no stressor normal function normal functionno stressor normal function normal function
6-10
Stress-Diathesis Model Part 2: one risk gene, normal function
mild stressor severe stressorrisk gene
normal function normal functionno stressor normal function normal function no stressor
6-11
Stress-Diathesis Model Part 3: two risk genes, slowing of function but compensation and no breakdown
mild stressor severe stressorrisk gene 1 risk
gene 2gene 2
normal function normal functionno stressor normal function normal function no stressor
6-12
Stress-Diathesis Model Part 4: multiple risk genes, slowing of function with mild stressor, but decompensation and breakdown with severe stressorbut decompensation and breakdown with severe stressor
mild stressor severe stressorrisk gene
1
risk gene 2
risk gene 3
risk gene 3
1
slowing of function breakdownno stressor slowing of function breakdownno stressor
6-13
Hypothetical Path Linking Circuits to Symptom Domains and to Biomarkers
symptom domain
DSM syndrome clinical subtype/treatment response
abnormal informationprocessing (neuroimaging)
y p
gene expression
molecular abnormality (biomarker signature)
gene expression
epigenetic genetic
Genetics and Psychiatric TreatmentsGenetics and Psychiatric Treatments
Genes and Psychiatric TreatmentsGenes and Psychiatric Treatments
• Markers for psychotropic drug metabolism are well established (pharmacokinetics)
• Low drug levels and lack of efficacy
• High drug levels and side effects
• Pharmacodynamics
• Unmet need for predictors of responses to specific h t i dpsychotropic drugs
Pathways of genetic variability can lead to an adverse drug reaction or to an inadequate response g q p
Genetic Polymorphisms
Pharmacokinetic Pharmacodynamic
Ab ti ExcretionImmune System
ReceptorsAbsorption Excretion Receptors
Distribution Metabolism EnzymesIon Channels
Adapted from Pirmohamed, M. et al. Genetic susceptibility to adverse drug reactions. Trends in Pharmacological Sciences 22, 298-305.
Genes and Side Effects of Psychotropic Drugs
• Most psychotropic drug labels already contain references to genetic markers that recommend dosereferences to genetic markers that recommend dose adjustments to mitigate side effects or drug interactions
• However these are not commonly usedHowever, these are not commonly used• Expensive/reimbursement
• Availability, delayAvailability, delay
• Not current standard of care/best practices
• If anything, phenotyping with therapeutic drug levels is more common than genotyping
• Most side effects are nuisances (nausea, insomnia, sedation) rather than dangerous (agranulocytosissedation) rather than dangerous (agranulocytosis, tardive dyskinesia), so current practice is trial and error, not genotyping
Safety/tolerability Genomic Markers Biomarkers That May Require Dose Adjustments or at Risk for Drug Interactions
Antidepressant Enzymes responsible for biotransformation
Tricyclics (demethylation) CYP2C19, CYP1A2, CYP3A4
Fluoxetine CYP2D6, CYP2C9, CYP2C19, CYP3A4
Paroxetine CYP2D6, CYP3A4,
Fluvoxamine CYP1A2, CYP2D6
Sertraline CYP2C9, CYP2C19, CYP2D6, CYP3A4
Cit l CYP2C19 CYP2D6 CYP3A4Citalopram CYP2C19, CYP2D6, CYP3A4
Escitalopram CYP2C19, CYP2D6, CYP3A4
Venlafaxine CYP2D6, CYP3A4
Duloxetine CYP2D6, CYP1A2
Mirtazapine CYP2D6, CYP1A2, CYP3A4
Trazadone CYP3A4Trazadone CYP3A4
Buproprion CYP2B6
Genes and Therapeutic Response to Psychotropic Drugsy p g
• No current psychotropic drug is labeled with reference t ti k th t li k d t h thto genetic markers that are linked to whether an individual is more likely to respond/not respond
• Trial and error is the current practice• Trial and error is the current practice
• However, there is a premium on early response in depression, as the longer it takes to find an effectivedepression, as the longer it takes to find an effective treatment, the less likely it is to work and to keep working
S d C l iS d C l iSummary and ConclusionsSummary and Conclusions
•• Genes bestow risk for mental illness, and many genes Genes bestow risk for mental illness, and many genes must “conspire” in order to produce risk for the majormust “conspire” in order to produce risk for the majormust conspire in order to produce risk for the major must conspire in order to produce risk for the major mental mental disordersdisorders
•• Environmental stressors converge upon the expression of Environmental stressors converge upon the expression of g p pg p pgenes, and via epigenetic mechanisms, cause the good or genes, and via epigenetic mechanisms, cause the good or bad expression of normal genes, i.e., “nurturebad expression of normal genes, i.e., “nurture””
S dS d C l i (2)C l i (2) AA 2121stst centurycentury mental health professional putsmental health professional puts this allthis all
Summary and Summary and Conclusions (2)Conclusions (2)A A 2121 century century mental health professional puts mental health professional puts this all this all together together byby
FirstFirst, constructing a , constructing a diagnosisdiagnosisss , co s uc g a, co s uc g a d ag os sd ag os s
ThenThen, deconstructing the diagnosis into its component , deconstructing the diagnosis into its component symptomssymptomsy py p
NextNext, matching each symptom with its hypothetically , matching each symptom with its hypothetically malfunctioning brain malfunctioning brain circuitcircuitgg
FinallyFinally, selecting treatments that change neurotransmitters , selecting treatments that change neurotransmitters in that circuit to improve the efficiency of information in that in that circuit to improve the efficiency of information in that p yp ycircuit and thus reduce circuit and thus reduce symptomssymptoms
Special Issues in the Long Term Care Patient with Neurobehavioral
Disorders John W. Daly MD Clinical Professor
UCSD Geriatric Medicine Medical Director SOCARE
Number of persons over 65 in US
0
10
20
30
40
50
60
70
1900 1920 1940 1960 1980 2000 2020
Year
Mill
ions Over 85
Over 65
Percent of community elderly living alone
0
10
20
30
40
50
60
65-74 75-84 85+
malefemale
Prevalence of at least 1 ADL or IADL difficulty among older individuals in the community
0
10
20
30
40
50
60
65-69 70-74 75-79 80-84 85+
malefemale
Nursing home use increases with age
0
5
10
15
20
25
65-74 75-84 85+
malefemale
Psychiatric illness in nursing home
• May affect as much as 80 to 90 % of nursing home population
• Most common illness is dementia, affecting 50 to 75% – Rover, German et al 1990 – Parmalee, et al 1992
Long term care environments
• Skilled nursing Care • Custodial nursing care • Residential care for the elderly **
– Assisted living – Board and care (I’m bored and they don’t care)
• Residential Care for dementia ** – ** not covered by Medicare, Medical, Medicaid
Short stay
1-6 months
Long stay
6 months or more
Hospice
Terminal
illness
Rehab
and
Sub-acute care
Primary
Cognitive
impaired
Primary Physical impaired
Both
All long term care patients
Special features of long term care
• Patient population • Co-morbid conditions • Medical information • Poly-pharmacy • Resource availability
The patient in long term care
• Dependant for ADL’s • Impaired mobility • Sensory impairment • Impaired communication • Impaired cognition
Long term care admission
Impaired mobility Behavioral or
cognitive disorder
ADL dependence
Lack of caregiver support Incontinence
Factors leading to long term care placement
Pain
Long term care
Acute care hospital
Home
Other long term care facility
Other: ER, APS
Sources of LTC admission
Dangerous combinations
• Impaired mobility and incontinence = – Falls and fractures
• Cognitive and motor impairment = – Dehydration, malnutrition, falls and fractures
• Sensory and cognitive impairment = – Falls, fractures, depression, delusions and
agitation
Co-morbidity in LTC
• Previously diagnosed conditions • Previously undiagnosed conditions • Previously misdiagnosed conditions • New conditions developing after admission
to LTC
Co-morbidity in patients with psychiatric illness
• Chart review of admissions to the Senior Behavioral Medicine unit at UCSD ( an inpatient Geriatric Psychiatry facility) revealed that 40% of all admissions had previously unrecognized and untreated medical conditions.
Dr. John’s first rule in evaluation of the LTC patient
Do not assume that the list of diagnosis on the admission H & P is
complete or even accurate
Barriers to accurate medical information
• Patient unable to provide history
• Incomplete medical records in LTC facilities
• Family with limited or erroneous understanding of the history
• Many providers and sub-specialty fragmentation of the history
• Doctor shopping and “shopping list” medical records
Adverse drug reactions (ADRs) in the elderly
• 10% to 17% of acute geriatric admissions are for ADRs
• In Outpatients – 18% 0f elderly outpatients suffer ADRs – 35% of high risk (i.e. those taking 5 or more
medications) suffer ADRs
Classes of drugs that contribute to delirium
• Analgesics &
Hypnotics • Psychotropics • Anticholinergics • Antiparkinsonian • Antihistamines
• Antihypertensives Cardiovascular agents
• Hypoglycemics • Steroids • Antimicrobials • Others/ idiosyncratic
This image cannot currently be displayed.
Physician measures to evaluate drug appropriateness
• Strive to confirm the diagnosis • Evaluate thoroughly to identify conditions:
– That could benefit from therapy – Be adversely affected by drug therapy – Influence the efficacy of drug therapy
• Manage medical conditions without drugs if possible, but remember advanced age in itself should never be considered a contraindication to potential beneficial therapy
General recommendations
• Simplify drug regimen • Evaluate need for each drug taken • With new drug start low, go slow • Use a few drugs well, rather than many
drugs poorly • Titrate based on response • Close attention to adverse reactions
The risk of Adverse drug reactions are much higher in patients with
dementia • We just don’t know how much higher • Adverse drug reactions can contribute to all
of the complications of advanced dementia
The cognitively impaired patient in LTC
Dementia or delirium?
Delirium and mortality
• 6 month mortality of elderly patients admitted to post acute care facility – With delirium: 25.0% – With sub-syndrome delirium: 18.3% – Without delirium: 5.7%
• (Marcantonio et al. JAGS #6,June 2005:963-9)
Causes of delirium
• Metabolic • Infection • Cardiovascular • Cerebral vascular • Pulmonary Disease • Drugs / intoxication • Anemia • Trauma
• Fecal impaction • Urinary retention • Acute psychosis • Altered or impaired
sensory input • Hypo or hyperthermia
Classes of drugs that contribute to delirium
• Analgesics &
Hypnotics • Psychotropics • Anticholinergics • Antiparkinsonian • Antihistamines
• Antihypertensives Cardiovascular agents
• Hypoglycemics • Steroids • Antimicrobials • Others
This image cannot currently be displayed.
The Medical History
• Existing and past medical illness may manifest as an apparent cognitive decline
• The presence of cognitive impairment may mask the symptoms of other underlying medical conditions
The Clinical Management of Moderate and Severe Dementia
Late stage dementia care guidelines
• Few clinical studies and there is little that is evidence based to guide clinical care.
• There are no well established guidelines • Recommendations must rely on the
observations and experiences of “seasoned” clinicians (experts in the field)
Complications of late stage dementia
• Behavioral disturbance • Gait disorder and falls • Weight loss and cachexia • Co-morbid chronic illness • New onset acute medical illness
Falls and Late Stage Dementia
• Individuals with dementia have an increased risk for falls and fractures – Fracture rate 3 X greater in AD than age and sex
adjusted general population – Buchner and Larson, JAMA 257:11, 1987
• Many variables are involved in the risk for falling in dementia patients – Co-existing illness, adverse drug reactions, gender,
dementia stage & type, gait apraxia, environment
Co-existing conditions contributing to gait disorder in dementia
• Adverse drug reaction • Orthopedic abnormalities • Muscle wasting and weakness • Cerebellar, basal ganglion or vestibular
deficits • Peripheral neuropathy • Peripheral vascular disease
Common chronic conditions that increase fall risk
• Hypertension • Atrial Fibrillation • Congestive heart failure • Diabetes • Urinary incontinence
Drugs that contribute to fall risk
• Diuretics • Antihypertensives • Antiarrhythmics • Antipsychotics • Antidepressants • Benzodiazepams • Hypoglycemic agents • Drug-drug interactions
• Cholinesterase inhibitors? (bradycardia)
• Anticonvulsants • Anticholinergics • Hypnotics • Antihistamines • Opiates • Others (idiosyncratic)
Weight loss and dementia
Progressive weight loss is one of the hallmarks of end-stage dementia
Advanced dementia and weight loss
• Accelerated weight loss is common in advanced dementia • There is a loss of skeletal muscle mass and decreased fat
free mass • Association between low body weight and atrophy of
mesial cortex • There is no compelling evidence for a hyper-metabolic
syndrome in dementia • Decreased active energy expenditure is associated with
decreased energy intake – Review by Poehlman and Dvorak Am J Clin Nutr 2000:71 (suppl)
Strategies to ameliorate weight loss in dementia
• Eliminate unnecessary or appetite suppressing medications (poly-pharmacy)
• Energy dense foods • Assisted feeding • Increase physical activity
– Increase of energy expenditure leads to increase of energy intake
– May help decrease sarcopenia
Drugs that can contribute to weight loss
• Statins • Cholinesterase
inhibitors • Antibiotics • Opiates • NSAIDs • Digoxin
• Sedatives and hypnotics
• Antidepressants – SSRIs – Amitriptyline
• Anticholinergics • Antipsychotics
So what about tube feedings in dementia patients
• Review of the evidence showed no evidence of benefit for patients with dementia – No benefit for: survival, pneumonia, pressure sores, or
function – Finucane et al. JAMA 1999:282(14)
• Worse outcomes for dementia patients – Mortality 54%/1 month 90%/1 yr dementia – VS 28%/1 month 63% /1yr non dementia
– Sanders et al. Amer Jour Gastroenterology 2000: 95(6)
Agitation and aggressiveness in late stage dementia
• Are common and have a significant adverse impact on care
• Most frequent reason for failure of care at home or for transfer from care facility to inpatient geriatric psychiatry unit
• Have numerous biologic and environmental triggers.
Antipsychotics and dementia
• Are commonly used to treat symptoms of psychosis and agitation in dementia
• Do not have FDA approval for use in dementia
• Recent review of the clinical trial evidence has questioned the efficacy and safety of these medications
The FDA and atypical antipsychotics
• Public health advisory for the use of all atypical antipsychotic medications in elderly patients with dementia – Data suggests an increased mortality mostly
from cardiac events or infections (pneumonia) – http://www.fda.gov/cder/drug/advisory/antipsy
chotics.htm
PRN medications in RCFE
• Every prescription and non-prescription PRN medication for which the licensee provides assistance must have a prescription including: – Specific symptoms which indicate need – Exact dosage – Minimum # of hours between doses – Maximum # of doses in 24 hour period
PRN medications rule 1
• If the resident’s physician has stated in writing that the resident is able to determine and communicate need for a prescription or non-prescription PRN medication, facility staff shall be permitted to administer
PRN medications rule 2
• If the resident’s physician has stated in writing that the resident is unable to determine his/her need for PRN med but can communicate symptoms staff may administer
PRN medications rule 3
• IF the resident is unable to determine need for a PRN med, and is unable to clearly communicate symptoms – Facility staff shall contact the resident’s physician prior
to each dose, describe the symptoms and receive direction to assist
– Date and time of each contact with physician and the directions shall be documented
– The date and time, dose and resident’s response shall be documented
PRN the take home message
• In general in a frail elderly individual with impairment of cognition and/or communication PRN medications are to be avoided!
• The preferred approach to symptom management is scheduled medication, with observation and documentation of target symptoms and/or potential medication side effects and regular schedule reevaluation (such as behavior or symptom mapping)
Problems with PRN medication use
• Inconsistent dosing – Variations with changes in staff (weekend and
night shift) • Overuse/ underuse • With brief episodic behaviors medication
frequently given after behavior has subsided • Decreased use of non pharmacological
measures
Medical conditions that cause or contribute to agitation in dementia
• Adverse drug reaction • Sensory impairment • Metabolic disorders • Infections • Dyspnea • Anemia
• Fecal impaction • Urinary retention • Pain
– Muscle-skeletal – Inflammatory – Visceral – Neuropathic
Pain is Special
• Can present as agitation, aggressiveness, depression, apathy or functional decline
• Difficult to recognize in a patient with impaired ability to communicate
• Advanced dementia may alter perception of pain • Presence of agitation or aggression may result in
an incomplete exam and failure to identify the source of pain
Dementia features that may contribute to agitation
• Agnosia: – Misperceptions and misinterpretation of the
environment can cause fear response • Aphasia:
– Inability to communicate or understand leads to frustration response
• Apraxia: – Difficulty with common automatic daily tasks also
causes frustration and anger
Environmental triggers to agitation and aggression
• Noisy, chaotic or confusing environment • New environment or situation • Confinement or restraint • Staff or caregiver response
– Attempts to restrain or confine patient – Confrontational approach – Loud, threatening or angry voice – Facial expressions
Non-drug interventions for agitation
• Redirection away from focus of agitation – Engagement in conversation or activity – Walk with me , talk with me – Avoid confrontation – Be flexible, creative and innovative
• Behavior mapping – To identify triggers and patterns of agitation
• Quiet rooms – Music, mood lighting, comfy chair
The “General”
• A retired military man with advanced dementia living in Alzheimer’s care community. He is non-verbal with gait apraxia and is mobile with a wheelchair. He feeds himself with assistance and responds non-verbally with the staff.
The General: a change in scene
• He has been relatively stable with slow progressive decline at the community.
• His baseline behavior is that he constantly hums to himself and smiles when addressed.
• Because his wife is suffering from a terminal illness he is moved to a facility closer to her.
The General’s return 6 month’s later
• The original care center is notified by his children that they are bringing him back and that he is dying. His wife has died from her illness.
• On admission is apathetic, withdrawn, unable to feed himself and has pneumonia
• He Is NOT Humming
A case of over reaction to the symptoms
• The new facility had interpreted his constant humming as a target symptom of agitation.
• On his transfer back he was on an atypical antipsychotic, an anticonvulsant and a benzodiazepam.
• These medications were discontinued, he was given an oral antibiotic and in 2 weeks was humming, eating and smiling.
A pragmatic approach to behavioral symptoms in late stage dementia
• Evaluate thoroughly for underlying cause or trigger for behavior
• Focus on those symptoms that place the patient or others at risk
• Do not treat trivial or annoyance behaviors • Try non-drug interventions first, and
educate staff or caregiver
Dementia and chronic illness
• Diabetes • Hypertension • Congestive heart failure • Prostate disease
Diabetes
• With dementia progression, weight loss and poor oral intake there is an increased risk for hypoglycemia
• Glycemic control may need to be loosened
• The patient with hyperglycemia and poor fluid intake is at increased risk for dehydration and hyper-osmolality syndrome
• But not too loose
Hypertension
• Increased risk for orthostatic hypotension and falls, especially if antipsychotic or antidepressant is started
• Diuretics may increase risk for dehydration, orthostatic hypotension and falls
• Combination of beta blocker and cholinesterase inhibitor may cause significant bradycardia
CHF and dementia
• Agitation is a common first symptom of CHF decompensation
• Diuretics and poor fluid intake can cause dehydration
• Increased risk for hypotension with dementia progression
Prostate disease and dementia
• Urinary retention commonly presents as increased agitation.
• Many antidepressants and antipsychotics increase the risk of urinary retention
• Increased risk for urinary tract infections
A case of impaired communication
• 85 y/o male with moderate dementia that presented initially as primary progressive aphasia
• Pt developed increased agitation and pacing at home, psychiatrist consulted and trazodone started for agitation.
• Agitation worsened and risperidone added • Pt experienced functional decline, more agitated,
urinating in inappropriate places (potted plants)
The problem and the solution
• Patient admitted to Senior Behavioral Health Unit • Physical exam: markedly distended bladder • Foley catheter placed and 2 liters of urine obtained • Agitation resolved. Medications discontinued. Pt
discharged with Urology follow-up
Special considerations in LTC
• Safety versus autonomy • Quality of life, comfort care, hospice care • Hospitalization, emergency room use • Competence, capacity, and dignity
Advanced Directives and Long Term Care
• Resuscitation status, power of attorney and decision making capacity are assessed and documented at time of admission
• For individuals who are a “do not resuscitate” status a pre-hospital DNR form must be completed and displayed in the chart
POLST
• Used in most RCFE facilities • Addresses the patient preferences for
resuscitation status, IV fluid or feeding tube use, antibiotic use and hospitalization
• Provides easy to access guidance for decision making by covering physicians
Dementia and hospice care
• Dementia is a progressive neurodegenerative condition that is invariably fatal
• The end stage of dementia is often a protracted course of functional impairment, and significant suffering
• Hospice and palliative care services are often underutilized for dementia patients
Barriers to hospice care for dementia
• Difficulty in predicting the course of end stage disease: “six month prognosis”
• Misconception that “one does not die of dementia” (7th leading cause of death in US)
• Physician lack of awareness of hospice services for dementia
Hospice care and dementia
• Is appropriate, but is underutilized • Needs different criteria for implementation • Perhaps palliative care should be started
sooner in late stage dementia given the course of protracted decline
• There is a need for more research into appropriate modalities to alleviate suffering in late stage dementia
Summary: the harsh reality
• Until there is a treatment that alters the progression of Alzheimer’s Disease and other dementias there will be an increasing number of late stage cases
• Very little evidence based guidance exists for appropriate treatment standards and practice
• There has been a failure of health care policy agencies at all levels to develop a strategic plan to address the growing need for care
Sleep Disorders in the Older Adult
Sonia Ancoli-Israel, Ph.D.
Professor Emeritus of Psychiatry and Medicine, UCSD
Director, Gillin Sleep & Chronomedicine Research Center
Director of Education, UCSD Sleep Medicine Center
VA Center of Excellence for Stress and Mental Health (CESAMH)
Sonia Ancoli-Israel Disclosures
Consultant/Scientific Advisory Board: Astra Zeneca, Ferring Pharmaceuticals Inc.,
GlaxoSmithKline, Hypnocore, Johnson & Johnson, Merck, NeuroVigil, Inc., OrphagenPharmaceuticals, Pfizer, Philips, Purdue PharmaLP, sanofi-aventis,
Reported Hours Slept Older vs. Younger American Adults
2003 NSF Sleep in America Poll
Changes in Sleep with Age
Meta-analytic review of 65 sleep studies in healthy persons3557 total subjects aged 5-102 years
Most age-related sleep changes occur in early and mid-years of human life span
In healthy older adults:Sleep remains relatively constant from age 60 to
mid-90sExcept for SE which decreases
Ohayon MM et al. Sleep. 2004, 27:1255-1273.
Rec
ordi
ng T
ime
(%)
Slow Wave Sleep
0
5
10
15
20
25
16-25 26-35 36-50 51-60 61-70 71-83
Van Cauter E et al. JAMA. 2000;284:861-868.
Changes with Age: Sleep Efficiency
Age
100
90
80
70
6010 20 30 40 50 60 70
MenWomen
Modified from Ohayon et al. Sleep 2004, 27:1255-1273
Sleep disturbance and cognition in older women (n=2932 women, mean age 83.5 years)
Objectively measured (5-days actigraphy) disturbed sleep was consistently related to poorer cognition,
Blackwell, Yaffe, Ancoli-Israel et al, J Gerontol: MED SCI, 2006, 61A(4):405–410
MMSE<26 Trails B >278s P-value
SE<70% 1.61
(95% CI 1.20–2.16)
1.96
(95% CI 1.43–2.67)
<0.05
Higher sleep latency (30m)
1.23
(95% CI 1.13–1.33)
1.13
(95% CI 1.04–1.24)
<0.05
Higher WASO (30m)
1.15
(95% CI 1.06–1.23)
1.24
(95% CI 1.15–1.34)
<0.05
All analyses adjusted for age, race, depression, education, body mass index, health status, history of stroke, history of hypertension, functional status, smoking, alcohol use, caffeine, antidepressant use, and physical activity.
Sleep disturbance and depression in older men (MrOS sleep study; n=3051)
Paudel et al, J Am Geriatr Soc. 2008 Jul;56(7):1228-35
Normal)
(n=2310)
Depressive symptoms
(n=537)
Depression
(n=204)
P-value
Subjective (PSQI)
Pittsburgh Sleep Quality Index >5
1.0
(referent)
2.06
(95% CI 1.67-2.55)
3.68
(95% CI 2.54-5.33)
<0.001
Objective (5-days actigraphy)
Sleep latency >1 hour 1.0
(referent)
1.40 (1.03-1.90) 1.68 (1.08-2.61) 0.006
All analyses adjusted for age, clinic site, race, body mass index, living alone, alcohol intake, smoking status, cognitive impairment, physical activity, certain medical conditions, education, self-reported health status, IADL impairments, and use of antidepressants, benzodiazepines and non-benzodiazepine anxiolytic/hypnotics.
Depressive symptoms have a strong, graded association with subjective sleep disturbances and are moderately associated with objectively measured prolonged sleep latency
Summary of Study of Osteoporotic Fractures Study Results (n= 3,022)
A 30-40% increased risk of subsequent falls associated in older women withTST< 7 hours / nightSE 65%
An increased mortality risk in older women with TST< 5 hours / nightSE 65%>2 hour naps
After adjusting for race, age, BMI, medical conditions, depression, cognitive function, exercise, IADL, use of anti-depressant or benzodiazepine
Stone,K.L., Ewing,S.K., Lui,L.Y., Ensrud,K.E., Ancoli-Israel,S.,et al. JAGS 54:1177-1183, 2006; Stone,K.L., Ancoli-Israel,S., Blackwell,T., et al. Arch. Intern. Med. :168(16):1768-1775:2008
Consequences of Disturbed Sleep
Difficulty sustaining attention
Decreased physical function
Slowed response time
Difficulty with memory
Decreased performance
May all be misinterpreted as dementia
Ancoli-Israel S, Roth T. Sleep. 1999;22(suppl 2):S347-S353; Ancoli-Israel, 2000, Sleep, 23 (suppl), S23 - S30.
Insomnia Complaints Prevalence Within Elderly (n=9282)
Perc
ent
Foley, et al., Sleep, 1995, 18:425-432
Chronic sleep disturbances primarily associated with indications of poor health (depressed mood, respiratory symptoms, fair to poor health, and physical disability).
Incidence of Insomnia in the Elderly
Of the 2000 survivors with chronic insomnia at baseline, about 50% had no symptoms at follow-upImproved self-perceived health associated with
discontinuation of insomnia symptoms
Foley et al concluded:“…these data do not support a model of incident
insomnia caused by the aging process per se.”
Foley D et al. Sleep. 1999;22:S366-372.
Factors Affecting Ability to Sleep in the Elderly
Medical illness
Medications/polypharmacy
Circadian rhythm disturbances
Primary sleep disorders
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. Washington, DC: American Psychiatric Association; 2000:597-661.
Many Medical Conditions Disturb Sleep
Hauri PJ. Clin Chest Med. 1998;19:157-168; Ancoli-Israel, 2000, Sleep, 23 (suppl), S23 - S30
Headaches
Neurodegenerative Processes
Arthritic Pain
CAD/ CHFGI changes (GERD, Dyspepsia)
Benign prostatic hypertrophy & Nocturia
Orofacial Pain/ TMJ
Peripheral Neuropathy with Pain
COPD
Psychiatric disorders
Sleep Problems and Multiple Medical Conditions
Foley, Ancoli-Israel, Bitz, Walsh, J Psychosom Res. 2004, 56(5):497-502.
Medications and Substances Associated with Insomnia
AlcoholAcute useWithdrawal
Caffeine
Nicotine
AntidepressantsSSRISNRI, atypical
Corticosteroids
DecongestantsPhenylpropanolaminePseudoephedrine
β agonists, theophylline derivatives
β antagonists
Statins
Stimulants
Dopamine agonists
Any drug that crosses the blood brain barrier and affects a
neurotransmitter system may be associated with
insomnia
SSRI = Selective Serotonin Reuptake Inhibitor; SNRI = Serotonin and Norepinephrine Reuptake Inhibitor; Schweitzer, PPSM.
Hauri PJ. Insomnia. Clin Chest Med. 1998;19:157-168. A Special Report: Sleep Disturbance. Boston, MA: Harvard Medical School Health Publications Group; 1999.
Sleepy Go to bed
Wake up
Wake up
Sleepy–Go to bed
Sleepy–Go to bed
Wake up
18.00 21.00 24.00 3.00 6.00 9.00 12.00
Advanced phase
Standard phase
Delayed phase
Circadian Sleep Phases
Modified from Ancoli-Israel, All I Want is a Good Night’s Sleep, 1996.Modified from Ancoli-Israel, All I Want is a Good Night’s Sleep, 1996.
Time of Day
SDB Prevalence According to AgeMrOs (n=2911; age 76y)
26.4% had RDI>15; 60% had RDI>5 SHHS definitions for hypopnea
The prevalence of RDI>15 increased with increasing age quartile (p=0.005) SDB prevalence increased with
increasing age, from 22.8% (95% confidence interval (CI)519.7–26.2%) for those <72y to 30.1% (95% CI526.9–33.3%) for those >80y
The prevalence of RDI>5 did not increase with increasing age quartile (p=0.68)
Age
Mehra R et al. JAGS 55:1356–1364, 2007
Older women with SDB have an increased risk of developing cognitive impairment – Prospective Study
Compared with women without SDB (n=193), women with SDB (n=105; 35.2%) were more likely to develop MCI or dementia (31.1% [n=60] vs 44.8% [n=47]; adjusted OR, 1.85; 95% CI, 1.11-3.08)
Elevated SaO2 (>15 events/hour) and high % of TST (>7%) with apnea or hypopnea were associated with risk of developing MCI (AOR, 1.71 [95% CI, 1.04-2.83]) or dementia (AOR, 2.04 [95% CI, 1.10-3.78])
Measures of sleep fragmentation (arousal index and wake after sleep onset) or sleep duration (total sleep time) were not associated with risk of cognitive impairment
Yaffe, K et al. JAMA. 2011;306(6):613-619
SDB+EDS = Mortality Risk
Gooneratne NS; et al Sleep disordered breathing with excessive daytime sleepiness is a risk factor for mortality in older adults. SLEEP 2011;34(4):435-442.
The presence of SDB is an important risk factor for mortality from EDS in older adults. In the presence of SDB at AHI≥20, EDS was associated with an increased all-cause mortality risk in older adults, even when adjusting for other significant risk factors, such as prolonged sleep duration. In older patients who had SDB without EDS, or EDS without SDB, there was no increased all-cause mortality rate.
Treating Apnea in Alzheimer’s Disease
Patients with AD do show high amounts of SDB
Patients with AD can tolerate CPAPAverage number of hours (5 h) worn did
not differ from clinic patients
CPAP improved Reduced AHI, EDS; deepened sleep, improved
some aspects of cognitive function
Continued use of CPAP over six months slowed the cognitive deterioration and improved mood
Ancoli-Israel,S., et al JAGS. 2008, 56:2076-81; Cooke et al. J Clinical Sleep Medicine, 2009, 5(4): 305-309; Ayalon et al. AJGP 2006 14(2):176-80; Chong et al JAGS 2006 54(5):777-81
When to Treat Sleep Apnea in the Elderly?
The bottom line is that if the sleep apnea is associated with clinical symptoms, then it should be treated, regardless of the age of the patient.Excessive daytime sleepinessHypertensionCognitive dysfunctionNocturiaCardiac disease High levels of sleep-disordered breathing
Ancoli-Israel, Sleep Med Rev. 2007 Apr;11(2):83-5.
Treatment for OSA
CPAP/BiPAP
Weight loss
Body position
Oral appliances
Surgery
RBD Case ExampleA 60-year old surgeon began to punch and kick his wife and jump out of bed during nightmares of being attacked “by criminals, terrorists, and monsters who always tried to kill me.” Work-related stress was the presumed cause of his sleep disturbance, but the violent behaviors intensified despite retirement 3 years later. He sustained several head lacerations, and his wife once had a severe headache for 2 days after receiving an accidental blow to the ear. The proper diagnosis was established after 11 years. A prodrome of excessive limb and body jerking during sleep had been present for at least 33 years.
Principles and Practice of Sleep Medicine, 1994
Pharmacologic Treatment of RBDNeurological exam
Pharmacological TreatmentClonazepam* – effective in ~90% of patients0.25-0.5mg at bedtimeTolerance generally does not developDiscontinuation = immediate relapseMechanism of action unknown
Melatonin*One hour before bedtimestarting at 6mg; increasing to 12-15 mg
Behavioral treatment*off-label
Restless Legs Syndrome
Restless Legs Syndrome Feelings of “creepy/crawling”
sensations in legs Relieved only with movement Diagnosis made on history:
“When you try to relax in the evening or sleep at night, do you ever have unpleasant, restless feelings in your legs that can be relieved by walking or movement?”
Prevalence of RLS by Age
Age Group, Range in Years
Perc
ent w
ith R
LS
Ohayon MM and Roth T. J Psychosom Res. 2002;53:547-554. Phillips B et al. Arch Intern Med. 2000;160:2137-2141.Berger K et al. Arch Intern Med. 2000;164:196-202.Rothdach AJ et al. Neurology. 2000;54:1064-1068.Lavigne GJ and Montplaisir JY. Sleep. 1994;17:739-743.Ulfberg J et al. Mov Disord. 2001;16:1159-1163.
Ohayon MM and Roth T. J Psychosom Res. 2002;53:547-554. Phillips B et al. Arch Intern Med. 2000;160:2137-2141.Berger K et al. Arch Intern Med. 2000;164:196-202.Rothdach AJ et al. Neurology. 2000;54:1064-1068.Lavigne GJ and Montplaisir JY. Sleep. 1994;17:739-743.Ulfberg J et al. Mov Disord. 2001;16:1159-1163.
Treatment for RLS/PLMSDopamine Agonists
ropinirole (Requip) 0.5-4 mg Can be safely titrated up to 4 mg po 2 hours before bedtime
pramipexole (Mirapex) 0.125-.5 mgUsually 0.5 to 0.75 mg po 2 hours before bedtime is enough to
control RLS or PLMD
gabapentin enacarbil (Horizant) Extended-Release Tablets 600mg approved for moderate-severe RLS 600 mg once daily taken with food at about 5 PM; doubling dose
does gets no additional benefit compared with the 600-mg dose, but caused an increase in adverse reactions
levodopa/carbidopa (Sinemet) 25/100 *
Hening et al. Sleep. 2004;27:560-583; Littner et al. Sleep. 2004;27:557-559.
* off-label
Behavioral and Cognitive Therapies
Behavioral and cognitive-behavioral therapies (CBTs) have demonstrated efficacy in RCTs.
Found to be as effective as prescription medications are for brief treatment of chronic insomnia.
Moreover, there are indications that the beneficial effects of CBT, in contrast to those produced by medications, may last well beyond the termination of treatment.
There is no evidence that such treatment produces adverse effects, but thus far, there has been little, if any, study of this possibility.
NIH State of the Science Conference Statement Manifestations and Management of Chronic Insomnia in Adults. Sleep 28(9): 1049-1057, 2005
Behavioral and Pharmacologic Therapy Combined - Wake Time
Morin CM, et al. JAMA. 1999;281:991-999.
Placebo(n=20)
*CBT = cognitive behavioral therapy: stimulus control, sleep restriction, sleep hygiene, and cognitive therapy
Randomized, Controlled Trial: 78 Men and Women, Mean Age 65
CBT*(n= 18)
Temazepam(n=20)
Combined(n=20)
Min
utes
Pharmacological Treatment
There are currently ten medications approved by the FDA for treatment of insomnia. benzodiazepines e.g., estazolam, flurazepam, quazepam, temazepam, and
triazolam the more recently introduced agents that act as benzodiazepine
receptors but have a nonbenzodiazepine structure (BzRAs)e.g., zaleplon, zolpidem, eszopiclone, etc
Melatonin agonist ramelteon
Histamine antagonist doxepin
Choosing A Pharmacologic TherapyDo you have difficulty initiating or maintaining sleep (or both)?
How many hours can you devote to sleep or inactivity, after taking the medication?
Agent Initiates Sleep
Maintains Sleep
Sleep with limited opportunity
Required Inactivity
Eszopiclone (Lunesta) √ √ 8+ hours
Zaleplon (Sonata) √ √ 4 hours
Zolpidem (Ambien) √ 7-8 hours
Zolpidem MR (Ambien CR) √ √ 7-8 hours
Zolpidem sublingual (Edluar) √ 7-8 hours
Zolpidem oral spray (Zolpimist) √ 7-8 hours
Zolpidem sublinqual (Intermezzo) √ √ 4 hours
Ramelteon (Rozerem) √ -
Doxepin (Silenor) √ -
BzRAs - Conclusions from the NIH State-of-the-Science Insomnia Conference 2005
Results from clinical trials indicate that these agents are efficacious in the short-term management of insomnia
The frequency and severity of these adverse effects are much lower in the newer benzodiazepine receptor agonistsmost likely because these agents have shorter half-
lives.
NIH State of the Science Conference Statement Manifestations and Management of Chronic Insomnia in Adults. Sleep 28(9): 1049-1057, 2005
Anti-depressants
Trazodone has been shown to be effective for two weeks
Another antidepressant, doxepin, has been found to have beneficial effects on sleep for up to 4 weeks for individuals with insomnia.
Data on other antidepressants (e.g., amitriptyline and mirtazepine) in individuals with chronic insomnia are lacking.
All antidepressants have potentially significant adverse effects, raising concerns about the risk–benefit ratio.
NIH State of the Science Conference Statement Manifestations and Management of Chronic Insomnia in Adults. Sleep 28(9): 1049-1057, 2005
Other Sedating Medications
A number of other sedating medications have been used in the treatment of insomnia. barbiturates (e.g., phenobarbital) antipsychotics (e.g., quetiapine and olanzepine).
Studies demonstrating the usefulness of these medications for either short- or long-term management of insomnia are lacking.
Furthermore, all of these agents have significant risks, and thus their use in the treatment of chronic insomnia cannot be recommended.
NIH State of the Science Conference Statement Manifestations and Management of Chronic Insomnia in Adults. Sleep 28(9): 1049-1057, 2005
OTC Antihistamines (H1 Receptor Antagonists)
Antihistamines (H1 receptor antagonists, such as diphenhydramine) are the most commonly used OTC treatments for chronic insomnia,
there is no systematic evidence for efficacysignificant concerns about risks of these
medications.
NIH State of the Science Conference Statement Manifestations and Management of Chronic Insomnia in Adults. Sleep 28(9): 1049-1057, 2005
Diphenhydramine and other antihistamines(H1-Receptor Antagonists)
Adverse EffectsSedation, grogginessDry mouth, blurred
vision, urinary retentionPsychomotor
impairment, dizziness, incoordinationDeliriumRenal failure
Advantages Available OTC Low cost Perceived as “safer than sleeping pills”
DisadvantagesHypnotic dose not well definedTolerance within a week
Tips for Older Adults
Exercise
Limit naps to 1 per day for <30 minutes
Take a walk to increase light exposure
Check medications
Avoid alcohol, caffeine, nicotine
Limit liquids
Keep regular hoursAncoli-Israel, S. Geriatrics, 1997, 52:20-30
Summary of Key Points – The Bottom Line
1. It is not aging per se that results in poor sleep but rather all the things that go along with aging.
2. Whether or not need changes, the ability to sleep does change with age.
3. Poor sleep in the older adult is most often associated with medical and psychiatric illness, medication, circadian rhythm changes and primary sleep disorders.
4. No matter the age of the patient, sleep disorders should be treated if they are interfering with quality of life or if there is a medical risk associated with it.
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