Neuro-Psychiatry Module: Psychopathology Martina Wiwie S. Nasrun, MD, PhD.
UPDATE IN PSYCHIATRY Robert K. Schneider, MD James L. Levenson, MD Departments of Psychiatry and...
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UPDATE IN PSYCHIATRY
Robert K. Schneider, MD
James L. Levenson, MD
Departments of Psychiatry and Medicine
The Medical College of Virginia at
the Virginia Commonwealth University
Richmond, Virginia
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Annals: October 1999
Annals: March 2001
Annals: February 2002
Previous Updates
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TOPICS COVERED –
• Mood Disorders
• Anxiety Disorders
• Medical-Psychiatric Interface
• Cognitive Disorders
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MOOD DISORDERS
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sertraline
Prozac
paroxetine
Celexa
fluoxetinePaxil
Zoloftcitalopram
Which SSRI is works best?
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SSRIs Compared in Primary CareKroenke, JAMA 2001;286:2947
• Many claims of differences in efficacy
• ARTIST: – A Randomized Trial Investigating SSRI Treatment
• Aim: – Compare the effectiveness of 3 SSRIs in
depressed primary care patients.
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SSRIs in Primary Care
• Methods– RCT of paroxetine, fluoxetine and sertraline
– 573 patients, in 2 primary care consortiums
• Main Findings– No statistical differences between the 3 SSRIs
in any of the outcomes.
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0%
20%
40%
60%
80%
100%
Recovery Rate 84% 81% 77%
Completers 43% 41% 50%
Sertraline Paroxetine Fluoxetine
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SSRIs in Primary Care
• Limitations– Therapy based on MD perception
– 74% met diagnostic criteria for major depression at baseline
– Low power for small differences
– No placebo control
– Mostly female (80%) and white (80%)
– No citalopram
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Impact on clinical practice
• Efficacy not a basis for choosing SSRI
• Consider instead:– Comorbidities
– Half-life
– Side effects
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Which came first, the depression or the erectile dysfuction?
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Erectile Dysfunction and DepressionSeidman, Am J Psych 2001;158:1623
• Depression and erectile dysfunction occur often together in men, but the causal relationship is unclear.
• Aim: – Evaluate sildenafil in men with erectile
dysfunction and mild depression
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Erectile Dysfunction and Depression
• Methods– RCT, double bind, placebo controlled
– Mild depression only
• Main Findings– All measures of sexual function improved
significantly more in the sildenafil group (p<.001).
– Treatment-responders (48/66 given sildenafil, 10/70 given placebo) had significant improvements in depression symptoms and quality of life compared to nonresponders
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Erectile Dysfunction and Depression
• Limitations– ? generalizable to patients with major
depression or taking psychotropic medications
– 12 week trial
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Impact on clinical practice
• Treating physical symptoms in patients with minor depression relieves depressive symptoms.– Erectile dysfunction
– Insomnia
– Pain
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Is St. John’s wort an effective antidepresant?
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St. John’s WortShelton, JAMA 2001; 285:1978
• Background:– Many controlled trials of St. John’s wort claim
efficacy for the treatment of depression, but they are methodologically flawed.
• Aim:– To compare the efficacy and safety of St.
John’s wort vs. placebo in major depression
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St. John’s Wort
• Methods– RCT, double-blind, placebo-controlled
– 200 patients received either St. John’s wort or placebo for 8 weeks.
• Main Findings– No significant differences in any outcome
measures between the two groups
– St. John’s wort: 1% discontinued due to adverse effects
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St. John’s Wort
• Limitations– Subjects had chronic depression (average
over 2 years)
– Subjects from tertiary care clinics
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Impact on clinical practice
• St. Johns wort probably safe in minor depression
• Caution with interactions with other drugs – warfarin, cyclosporine, theophylline, digoxin,
protease inhibitors, anticonvulsants, oral contraceptives, triptans, SSRIs
• Not a good choice for severe depression
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Is estrogen an antidepressant in menopausal women?
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Estradiol for depression Novaes Soares, Arch Gen Psych 2001;58:529
• Depressive and somatic symptoms are common in women entering menopause.
• Studies of ERT for mood symptoms are complex and have shown mixed results. – Estrogen preparation: oral vs. transdermal
– Longitudinal measurements of estradial
– Endocrine confirmation of perimenopause: FSH
– Measurement of mood symptoms
– Placebo control difficult
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Estradiol for depression
• Aim– Assess efficacy of transdermal ERT for treating
depression in perimenopausal women.
• Methods– RCT, double-blind, placebo-controlled
– FSH > 25 IU/L
– Depressive disorder (i.e. major depression, dysthymia or minor depression)
– 17β-estradiol (100μg) transdermal patches or placebo for 12 weeks and 4 week washout.
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Estradiol for depression
Main Findings– Remission of depressive symptoms in 68% vs. 20%
(P=0.001)
– no significant differences in response per type of depressive disorder
– 50% reduction in menopausal symptoms was seen in 68% vs. 28% (P=0.005).
Limitations– Small, short study in specialty clinic
– No progesterone
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MADRSDepression
BKMIPerimenopausal
Symptoms
0
5
10
15
20
25
30
Baseline Week 4 Week 8 Week 12 Week 16
Estradiol
Placebo
0
5
10
15
20
25
Baseline Week 4 Week 8 Week 12 Week 16
Estradiol
Placebo
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Impact on clinical practice
• Treatment with transdermal estrogen patches is effective for depressive symptoms in some perimenopausal women.
• This represents a good first step in treatment of the depressed perimenopausal women
• If symptoms persist or worsen, then consider the addition of an antidepressant
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How often do depressed patients turn out to be bipolar?
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Conversion from unipolar to bipolar depression Goldberg, Am J Psychiatry 2001;158:1265
• Background– Underdiagnosis of bipolar disorder
– 20% of Major Depression may be bipolar
– Prescription of antidepressants without mood stabilizers may precipitate a switch to mania
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Unipolar to bipolar depression
• Aim– In patients presenting with depression,
what are the odds they will turn out to really be bipolar?
• Methods– Young (mean 23 years), hospitalized
patients with depression
– Followed prospectively for 15 years
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Unipolar to bipolar depression • Main Findings
– 41% developed either hypomania or mania (26% hypomania, 15% mania).
– 80% of the 10 patients who were initially psychotic developed hypomania (4/10) or mania (4/10).
– 34% of the non-psychotically depressed eventually became either manic or hypomanic
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What’s the differnece between mania and hypomania? • Mania (Bipolar I):
– At least 7 days of racing thoughts, sleeplessness, grandiosity and sometimes psychosis
• Hypomania (Bipolar II)– At least 4 days of racing thoughts,
irritability, and sleeplessness
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5-5 Stahl S M, Essential Psychopharmacology (2000)
DEPRESSION
NORMAL MOOD
MANIA
HYPOMANIA
MIXED EPISODE
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Unipolar to bipolar depression
• Limitations– Started in the early 1980s
• psychiatric hospitalization differs
• treatments differ
– Psychiatric inpatients
– Naturalistic study and not a treatment intervention
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Impact on clinical practice
• Younger patients with depression especially with psychotic features may be at a particularly high risk for conversion to bipolar depression.
• Remember that antidepressants may precipitate switch to mania.
• “Side Effects” to antidepressants may represent hypomania or mania
• Screen for mania/hypomania BEFORE starting an antidepressant
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How good is the care given for depression and anxiety disorders?
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Quality of Care for Depression and Anxiety Disorders Young, Arch Gen Psych 2001;58:55
• Depressive and anxiety disorders are common, and cause substantial disability.
• Medications and psychotherapies have empirically demonstrated efficacy
• BUT many patients do not receive adequate treatment
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Quality of Care
• Aim– To estimate the rate of appropriate treatment
of anxiety and depressive disorders
– Measure effects of insurance, provider type, and demographics
• Methods– One year of data, from the National
Comorbidity Survey (1997-98)
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Quality of Care One year, adults, major anxiety or depression
• Main Findings:– 83% saw a health care provider
– 30% received some appropriate treatment
– Most only saw PCP’s; 19% received appropriate care.
– 90% visiting MH professionals received appropriate care.
– Insurance status affected whether the individual saw a provider, but had no effect on whether appropriate care was received.
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Quality of CareOne year, adults, major anxiety or depression
• Main Findings:– Appropriate treatment was less likely for
• men
• blacks
• the less educated
• those <30 or >59 years old
– When a psychiatric medication was used, it was at an appropriate dose and duration in about 75% of the individuals.
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Quality of Care
• Main Findings:– For patients seeing PCPs, those who received
poor quality care were less likely to report that…
• their mental health problems were evaluated
• psychiatric drugs were recommended
• referral to a mental health specialist was made
– Patients who received poor quality care were less likely to view themselves as needing mental health care (31.4% vs. 70%)
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Impact on clinical practice• Limitations
– Self report data, response rates
• Conclusions– Most adults with depression or anxiety disorders did
not receive appropriate treatment, though they saw health care providers
– When given, psychiatric medications were usually given at appropriate dosage and duration.
– The current barriers to appropriate treatment lie in recognition, diagnosis, referral, and acceptance by patients.
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ANXIETY DISORDERS
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What are the psychiatric consequences of a terrorist disaster?
“The most severe incident of terrorism ever experienced on American
soil.”
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Psychiatric Disorders Among Survivors of the Oklahoma City Bombing North, JAMA 1999; 282:755
• Sometimes difficult to distinguish normal from pathological reactions
• Aim– Assess the psychiatric impact on adult survivors
directly exposed to the bomb blast.
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Oklahoma City Bombing• Methods
– Single diagnostic interview
• Main Findings– 87% reported injuries
– Predisaster (lifetime) prevalence vs postdisaster prevalence:
• PTSD [15% vs. 34%]
• Major Depression [12.6% vs. 22.5%]
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Oklahoma City Bombing
• Main Findings:– Postdisaster, 74% of PTSD and 56% of
major depression was new.
– Conversely, 71% of those with no predisaster psychiatric diagnosis remained without a postdisaster diagnosis
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Oklahoma City Bombing
• Main Findings:– Over 80% of the survivors had intrusive
reexperiences or hyperarousal symptoms.
– Only 34% of survivors had all three criteria (including avoidance) for PTSD.
– Avoidance/numbing criterion was 100% sensitive for detecting PTSD.
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Oklahoma City Bombing
• Limitations– Retrospective; direct exposure only
• Conclusions– PTSD and Major Depression were the major
psychiatric disorders
– Hyperarousal and reexperiences common
– Avoidance/numbing screens for full PTSD
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Impact on clinical practice• Health predicts health
• Terror trauma uncommon,
sudden death of a loved one is not
• PTSD is very treatable– Medications
– Psychotherapy
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What’s the best initial drug treatment for panic disorder?
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Early Coadministration of Benzodiazepines and SSRIs Goddard, Arch Gen Psych 2001;58:681
• SSRIs are indicated for all anxiety disorders
• But response to SSRIs is delayed
• Psychiatrists often start benzodiazepines with SSRIs, but few controlled trials
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Short vs. Longer Acting Benzodiazepines• Short acting benzodiazepine (alprazolam) seems
like a good choice (rapid onset of action) – BUT is bad (rebound anxiety, euphoria, difficult to taper)
• Clonazepam is a intermediate half-life benzodiazepine with a slower onset of action– Early symptom reduction without euphoria
– Easily tapered
– Also, few active metabolites
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Early Benzodiazepinesand SSRIs • Aim
– Test the efficacy of early coadministration of clonazepam and sertraline in panic disorder
• Methods– 12 week, RCT
– Open-label sertraline
– Blinded to clonazepam 0.5mg TID or placebo
– Three week clonazepam taper at week 4
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Early Benzodiazepinesand SSRIs• Main Findings:
– Response rates:• Week one (41% vs. 4%)
• Week three (63% vs. 32%)
– At end of trial, both groups’ response rates were over 70%.
– No differences in secondary measures between groups (i.e. drop out rates, adverse reactions).
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Early Benzodiazepinesand SSRIs• Limitations
– Small group size
– 100 mg of sertraline may be more than needed
– May titrate slower
• Conclusions– Rapid stabilization of panic disorder can be
achieved with early coadministration of sertraline and clonazepam
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Impact on clinical practice
• Panic disorder is common in the primary care setting.
• A common practice used by psychiatrists that could easily be used by non-psychiatrists in the early treatment of panic disorder.
• Intermediate-acting benzos have advantages over short-acting ones
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MEDICAL-PSYCHIATRIC
INTERFACE
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Can medication-induced depression be prevented?
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Interferon and Treatment of Depression Musselman, N Engl J Med 2001; 344:961
• Background– Depression is the most frequent adverse effect
leading to discontinuation of interferon
– Interferons are important in the treatment of: hepatitis C, multiple sclerosis, and malignancies
– Antidepressants effective in treating interferon-induced depression
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Interferon and Depression
• Aim– Will pretreatment with antidepressants reduce
depressive symptoms following interferon?
• Methods– RCT, placebo controlled
– 2 week pretreatment with paroxetine before interferon alpha for malignant melanoma
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Interferon and Depression
• Major findings: – Major depression (paroxetine vs. placebo):
11% vs. 45%
– Severe depression led to discontinuation of interferon (paroxetine vs. placebo):
5% vs. 35%
– In the placebo group, if major depression,
then 78% discontinued interferon
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Interferon and Depression
• Conclusions– Pretreatment with paroxetine appears
effective in preventing depression induced by interferon alfa in malignant melanoma
• Limitations– Generalizable to other interferons and
diseases?
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Impact on clinical practice• Vital drugs may cause depression
e.g.interferons, steroids, betablockers, isotretinoin
• When it is not possible to substitute an alternative medication, then:– try treating the drug-induced depression with
antidepressants
– consider prevention before administering the drug
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What’s the risk of sudden cardiac death with antipsychotics?
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Antipsychotics and QTc Prolongation Ray, Arch Gen Psych 2001;58:1161
• Background– Case reports have linked antipsychotic drugs with:
QTc prolongation, torsades de pointes, and sudden deaths
– “Black box” warnings regarding these risks added to PDR for the older antipsychotics thioridazine and mesoridazine
– Sertindole (new antipsychotic), was not registered in the U.S. because it caused QTc prolongation and sudden
death
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Antipsychotics and QTc
• Aim:
To determine the risk of sudden cardiac death in antipsychotic users.
• Methods:
Retrospective cohort study of Tennessee Medicaid enrollees
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Antipsychotics and QTc
• Main Findings:Corrected Risk Ratios:
– Moderate-dose antipsychotic use vs. nonuse: 2.39
– Low-dose antipsychotic use vs. nonuse: 1.30
– Moderate-dose antipsychotic use vs. nonuse in patients with severe cardiovascular disease : 3.53
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Antipsychotics and QTc • Limitations
– Cannot determine causality
– Era before atypical antipsychotics
– Smoking and obesity not controlled for
– Sudden Death may be first symptom of CAD
• Conclusions– Relative and absolute increases in the risk of
sudden death in patients taking moderate doses of antipsychotics
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Impact on clinical practice
• If prescribing an antipsychotic, take a careful history for syncope or family history of sudden death
• Patients at high risk should have pretreatment EKG and receive antipsychotics not shown to increase QTc
(olanzapine, risperidone, quetiapine)
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Does group therapy prolong life in metastatic breast cancer?
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Group Therapy and Breast CancerGoodwin, N Engl J Med. 2001;345:1719
• Background
Group therapy has been reported to provide benefits for metastatic breast cancer, including improvement in mood, pain control, and in some but not all studies, survival.
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Group Rx and Breast Cancer
• Aim– To assess whether group therapy influences
survival, mood, and pain in women with metastatic breast cancer
• Methods– Multi-center randomized trial of supportive-
expressive group therapy
– Group therapy consisted of weekly 90-minute sessions for at least one year
– All received routine care
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Group Rx and Breast Cancer
• Main Findings:– Greater improvements in psychological symptoms and
pain control (p=0.04) in the intervention group
– These benefits occurred in those women who were more distressed at baseline.
– Did not prolong survival compared to routine care alone (17.9 vs. 17.6 months)
• Limitations– Only 9% of eligible women were randomly assigned
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Impact on clinical practice• Conclusions
– Many support groups are available
– Some women do not want to participate
– But increased survival is “proven” so they may feel obligated to join
– Patient can be reassured that groups improve pain control and mood but do not prolong survival
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COGNITIVE DISORDERS
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Does cognitive function decline after CABG?
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Cognition after CABG Newman, N Eng J Med 2001;344:395
• Background– Perioperative cognitive decline after CABG
appears to be greatest at discharge.
– Cognition gradually improves for most patients over next 6 months.
– But a significant number (10-30%) continue to
decline
• Aim– To prospectively assess cognitive functioning
before and after CABG for five years
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Cognition after CABG• Methods
– Neurocognitive testing was performed before surgery, at discharge, 6 weeks, 6 months and 5 years after CABG
• Main Findings– Incidence of cognitive decline:
• 53% at discharge
• 36% at six weeks
• 24% at six months
• 42% at five years
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Cognition after CABG
• Main Findings (cont)– Most returned to baseline functioning
within 6 months.
– However, at 5 years, the patients with cognitive decline at discharge had a marked decline from their baseline functioning (P<0.001); the patients without cognitive decline at discharge did not.
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Cognition after CABG• Limitations
– Selective attrition may underestimate cognitive decline
• One third of sample not available for long term followup were more likely to have had complex disease
– Some cognitive decline due to illness not CABG
• Conclusions– Patients with cognitive decline immediately after
elective CABG are at increased risk for long-term cognitive decline
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Impact on clinical practice• Prior to elective CABG, the potential for
cognitive decline should be discussed :– Cognitive decline is common
– Most improve over the first six months
– But a significant number will have impairment at five years post-operatively
– This is one quality of life factor among others• Especially important in the elderly
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Is there a quick way to screen for dementia?
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Mini Cog: New, Easy-to-use Screening Test for Dementia Scanlan, Int J Geriatr Psych 2001;16:216 Borson, Int J Geriatr Psych 2000;15:1021
Background
• Screening for cognitive disorders has usually been with the Mini Mental Status Exam (MMSE). – Hard to remember and time consuming.
– Research tool NOT a screening tool
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Mini Cog Screen for Dementia
• Background (cont)The Mini-Cog has just:
the 3-item recall from the MMSE
the Clock Drawing Test (CDT)Requests the subject to fill in the numbers on a predrawn circle and then add the hands for a designated time.
• Aim– To evaluate the Mini-Cog at case-finding for
cognitively impaired adults.
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Mini Cog Screen for Dementia
• Methods– Community dwelling subjects, seen at a
university memory clinic
– Completed the MMSE, CASI (Cognitive Abilities Screening Instrument), and the Mini-Cog.
– Expert raters performed the MMSE and CASI and “naïve” raters performed the Mini-Cog.
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Mini Cog Screen for Dementia
SENSITIVITY SPECIFICITY
MMSE 91% 92%
CASI 92% 96%
MINI-COG 99% 93%
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Mini Cog Screen for Dementia
• Main Findings– Concordance between naïve and trained raters
was >98% for normal, moderately and severely impaired clock drawings.
– Concordance dropped to 60% in mildly impaired clock drawings
• But assuming naive raters would score mildly impaired clocks as normal
• Then the Mini-Cog sensitivity and specificity changed little (97% and 95%).
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Mini Cog Screen for Dementia
• Conclusions– The Mini-Cog is a time-efficient, sensitive and specific
tool that effectively identifies patients with probable dementia, even by naïve raters.
• Limitations– Conducted in a university memory clinic
– The population screened by an internist would have a lower incidence of dementia, increasing false positives and lowering specificity.
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Impact on clinical practice• The Mini-Cog provides an effective first-stage
screening tool for detecting dementia.
• Trained staff (naïve raters) could easily perform this in an office setting.
• Combining this first-stage screening with a second stage caregiver brief interview probably represents an efficient and effective system for screening for cognitive impairment in the elderly.
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