ECT/MEDICAL COMORBIDITY
| GOLD-STANDARD ELECTROCONVULSIVE THERAPY— Michael A. Taylor, MD, Adjunct Clinical Professor
of Psychiatry, University of Michigan Medical School, Ann Arbor
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| Introduction: historically, camphor oil used to induce seizures in mentally ill; electroconvulsive therapy (ECT)
to induce seizure introduced in 1938; currently, ECT not widely available in United States (<10% of psychiatrists
perform it), and usually thought of as last resort after medication trials exhausted; prototypical ECT practitioner
male, >45 yr of age, and international medical graduate (IMG) who learned about ECT >10 yr ago in
another country; in United States, no requirements for residents to train in ECT, and ECT competence certification
not required; ECT often classed with alternative treatments, eg, biofeedback and phototherapy
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| Maximizing ECT efficacy: “one size does not fit all”; dosing and stimulus parameters must be individualized;
treatments must be monitored by electroencephalography (EEG) and patient restimulated if induced seizure
inadequate; bilateral electrode placement preferred to unilateral
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 | Terminology: “dose” measured in millicoulombs (mC); energy needed to achieve mC dose measured in joules
(J); resistance (also called impedance) is obstacle that energy must overcome to deliver mC dose; only 2 machines
available in United States; Thymatron delivers maximum dose of 504 mC; MECTA delivers maximum
dose of 576 mC
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| Individualized dosing: “active ingredient” grand mal electrical seizure achieved by overcoming patient’s seizure
threshold; seizure threshold increases with age; half-age dose-calculation method—divide patient’s age by 2
and multiply machine’s maximum capacity by that percentage (eg, if patient 70 yr of age, divide 70 by 2 [=35]
and multiply machine’s maximum capacity by 35%); titration dose-calculation method—start at very low
dose (eg, 5%-10% of machine’s maximum capacity) and stimulate at successively higher doses until seizure
achieved (seizure threshold); that dose then “multiplied by another number, depending on what else is being
done”
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| Cognitive side effects: electricity from power source takes form of continuous sine wave; ECT machines convert
that into brief pulses punctuated by brief rest periods, which minimizes cognitive problems; having pulses at
narrow widths and low frequencies makes less work for machine (fewer joules) and reduces cognitive side effects;
the longer the stimulus duration, the better (6 to 8 sec typical)
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| Unilateral ECT or bilateral? controversial; bilateral—electrodes placed on either frontotemporal area; electricity
passes through midbrain, producing centrencephalic generalized seizure; unilateral always given initially
on right side of head (to avoid area that controls verbal functioning on left side of frontotemporal region), with 1
electrode in right frontotemporal position and other in galea position, producing right cerebral hemisphere seizure
that generalizes to rest of brain; found to reduce anterograde and retrograde amnesia; however, when patients
asked to recall details about tester, those who received bilateral ECT recalled details as well as controls,
whereas those who received unilateral ECT forgot more details, presumably because visuospatial functioning
concentrated in right hemisphere; whether ECT unilateral or bilateral, memory loss temporary, resolving within
≈1 yr; problems with unilateral ECT—to be equivalent to bilateral, must be given at very high doses, which
minimizes cognitive advantage; because of machine limitations, calculated high dose not available for some patients;
high doses cannot be sustained throughout treatment course; when given at seizure threshold, unilateral
ECT no better than placebo
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| EEG monitoring of ECT: essential in determining whether seizure occurred; in studies, when practitioner tried
to determine whether seizure had occurred by observing patient, “there were too many false positives” (ie, occurrence
of seizure cannot be determined accurately by observing patient); especially worrisome in unilateral
ECT, in which 25% of practitioners said patient was having seizure when he or she was not; EEG also necessary
to determine that seizure has ended before patient leaves treatment room; in some patients, especially
younger ones, electrical seizure can continue for up to several minutes after motor seizure has ended; possible
for some patients to go into status epilepticus, and EEG can help determine that
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| Determining efficacy of EEG: morphology of EEG tracing indicates quality of seizure; duration of seizure irrelevant;
recruitment is time from electrical stimulation to when patient achieves full grand mal seizure with high
amplitude and hypersynchronous activity; the shorter the recruitment and the denser the global power (high-
amplitude period), the better; best seizure ends abruptly into electrical quiet; important to obtain preanesthesia
EEG so change in tracing due to anesthesia not mistaken for seizure
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| Bottom line: remission rates higher when seizures consistently meet above criteria
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| MANAGEMENT OF CO-OCCURRING PSYCHIATRIC AND MEDICAL CONDITIONS —Curley L. Bonds,
MD, Chair, Department of Psychiatry, Charles R. Drew University School of Medicine and Science; Associate
Clinical Professor of Psychiatry, Neuropsychiatric Institute, University of California, Los Angeles
|
| Introduction: depression more common with certain medical illnesses, including cardiovascular disease and
HIV infection; major depression associated with 4-fold increase in risk for mortality during first 6 mo after myocardial
infarction (MI); mental stress can trigger decreased blood flow to heart
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| Depression and heart disease: platelet aggregation and reactivity and blood clotting affected by depression;
beat-to-beat variability decreased in depressed individuals; depression associated with decreased compliance
with exercise, diet, and medications
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| Sertraline Antidepressant Heart Attack Randomized Trial (SADHART): results suggest sertraline safe
and effective treatment for recurrent depression in patients with recent MI or unstable angina and without other
life-threatening medical conditions; study not powerful enough to show whether treating depression decreased
morbidity and mortality, “but there seemed to be a trend in that direction”
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| Blacks and heart disease: after MI, blacks less likely than whites to receive certain interventions; more likely to
have diabetes and hypertension, to delay seeking care, and to refuse angioplasty; black women—rate of death
after MI 34% higher than in white women; physical recovery slower than in white women; less likely to have
used hormone replacement therapy
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| More on depression and heart disease: depression associated with increased risk for coronary artery disease
(CAD) in men and women; also known to increase CAD-related mortality in men but not in women; patients
with depression and MI have altered autogenic tone (increased sympathetic activity and decreased parasympathetic
activity)
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| Platelet factor 4 and β-thromboglobulin: plasma levels elevated in depressed patients with ischemic heart disease
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| Cardiac autogenic tone: derangements may lead to ventricular tachycardia and fibrillation and sudden death
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| Cultural considerations: some studies suggest that blacks respond better to tricyclic antidepressants (TCAs) than
to other antidepressants; however, increased side effects of TCAs occur in blacks, and may be result of slower
metabolism; blacks have lower rates of major depression, dysthymia, and panic disorder than whites, and
higher rates of phobic disorders; speaker suggests lower rate of depression is because symptoms of depression
and ischemic heart disease (eg, fatigue and insomnia) overlap, and patients reluctant to report symptoms because
they believe myth that depression is “normal” reaction to CAD
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| Hostility and MI: hostility stress-related condition that has been linked to increased mortality rate; no standardized
scale for measuring hostility, but studies show higher hostility ratings predict higher risk for MI and death;
patients with high hostility ratings ≈25% more likely to have restenosis of coronary arteries after percutaneous
transluminal coronary angioplasty (PTCA) than patients with low hostility ratings
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| Cardiovascular effects of antidepressants: TCAs—increase heart rate; cause orthostatic hypotension; slow
cardiac conduction; increase risk for sudden cardiac death; may reduce metabolism by 50% in black patients;
have anticholinergic, antiadrenergic, and quinidine-like effects; selective serotonin reuptake inhibitors (SSRIs)—
most extensively studied antidepressants in cardiac population; decrease platelet aggregation; no effect on heart
rate variability or on QT segment variability (eg, bradycardia); studies exist for fluoxetine, paroxetine, and sertraline;
drugs with high protein binding (eg, SSRIs) may require adjustment of warfarin (Coumadin) levels; warfarin
levels should be followed closely
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| Depression and HIV infection: depression among most common psychiatric disorders observed in HIV-positive
patients; ≈50% of HIV-positive patients screen positive for psychiatric disorder; 33% screen positive for
major depressive disorder during previous year; depressive symptoms may have adverse effect on immune
function (studies suggest CD cells less healthy in patients with depression); in one study, chronic non-bereavement-related
depressed mood predicted decline in CD4+ cell counts across 5-yr span in HIV-positive
homosexual men; prevalence of depression higher among HIV-positive women than in those who are HIV
negative; clinical studies suggest higher mortality among HIV-positive men and women with depression than
among those without depression
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| Neuropsychiatric complications of HIV infection: incidence of delirium lower with newer treatments for
HIV infection but still occurs; patients with HIV infection, especially those with end-stage disease, at increased
risk for dementia; risk factors for dementia include patient not taking antiviral medications, having high viral
load, being of older age, having anemia, using illicit drugs, and being female
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| Treatment of HIV/AIDS-associated conditions: can place patients at risk for depression; certain antiviral
medications known to cause suicidal ideation and to alter cognition; other medications can be neuroprotective
(neuroprotective agents given to patients with Alzheimer’s disease may be helpful in patients with HIV infection);
literature suggests psychostimulants may improve appetite and mood and help patients function better; judicious
doses of testosterone shown to improve mood and appetite, and may help to increase muscle mass; use
antidepressants aggressively
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| Cardiac disease and obesity: people who have 10% weight gain by 20 yr of age have 50% increased risk for
having cardiac disease later; those who have 10% weight gain by 20 yr of age and who smoke have 300% increased
risk; unfortunately, obesity and smoking common in people with schizophrenia, and newer antipsychotic
medications often have weight gain as side effect; modifiable risk factors for cardiac disease in people
with schizophrenia include obesity, dyslipidemia, diabetes, hypertension, and smoking; nonmodifiable risk factors
include sex, family history or personal history of cardiovascular disease, and age; if newer antipsychotic
medications must be used, clinician must be more aggressive in helping patients control their weight
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| Somatization and depression: people from ethnic minorities more likely than whites to report physical
symptoms of depression (eg, sleep disturbance, indigestion, headache, muscle aches and pains) rather than
emotional aspects; challenging to diagnose depression in people with medical illness and physical complaints
such as headache, backache, joint pain, and abdominal pain
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| Approaching the depressed patient: use medical model (ie, brain as organ); distinguish clinical depression from
routine melancholia or sadness; emphasize improvements in neurovegetative function
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| Endicott substitution criteria: proposes that somatic symptoms in medically ill are substituted by nonsomatic
alternatives; eg, change in weight and appetite substituted by tearfulness and depressed mood;
method can be used to identify psychologic symptoms of depression that indicate presence of major depressive
disorder in elderly patients with medical illness
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Suggested Reading
Allison DB et al: The distribution of body mass index among individuals with and without schizophrenia. J Clin
Psychiatry 60:215, 1999; Benbow SMet al: Electroconvulsive therapy clinics in the United Kingdom should routinely
monitor electroencephalographic seizures. J ECT 19:217, 2003; Fink M et al: Catatonia in autistic spectrum
disorders: a medical treatment algorithm. Int Rev Neurobiol 72:233, 2006; Girish K et al: Seizure threshold
in ECT: effect of stimulus pulse frequency. J ECT 19:133, 2003; Hermann RC et al: Characteristics of psychiatrists
who perform ECT. Am J Psychiatry 155:889, 1998; Hermann RC et al: Diagnoses of patients treated with
ECT: a comparison of evidence-based standards with reported use. Psychiatr Serv 50:1059, 1999; Krystal AD,
Coffey CE: Neuropsychiatric considerations in the use of electroconvulsive therapy. J Neuropsychiatry Clin Neurosci
9:283, 1997; Laghrissi-Thode F et al: Elevated platelet factor 4 and beta-thromboglobulin plasma levels
in depressed patients with ischemic heart disease. Biol Psychiatry 42:290, 1997; Luber B et al: Quantitative EEG
during seizures induced by electroconvulsive therapy: relations to treatment modality and clinical features. II. Topographic
analyses. J ECT 16:229, 2000; Mayur PM et al: Motor-seizure monitoring during electroconvulsive
therapy. Br J Psychiatry 174:270, 1999; Nobler MS et al: Quantitative EEG during seizures induced by electroconvulsive
therapy: relations to treatment modality and clinical features. I. Global analyses. J ECT 16:211, 2000;
Owen JE et al: Psychiatric evaluations of heart-transplant candidates: predicting posttransplant hospitalizations,
rejection episodes, and survival. Psychosomatics 47:213, 2006; Perera TD et al: Seizure expression during electroconvulsive
therapy: relationships with clinical outcome and cognitive side effects. Neuropsychopharmacology
29:813, 2004; Prudic J et al: Effectiveness of electroconvulsive therapy in community settings. Biol Psychiatry
55:301, 2004; Prudic J et al: Electroconvulsive therapy practices in the community. Psychol Med 31:929, 2001;
Scott AI, Cull RE: Unilateral, prolonged, nonconvulsive cerebral seizure activity in ECT. J ECT 17:292, 2001;
Swartz CM, Manly DT: Efficiency of the stimulus characteristics of ECT. Am J Psychiatry 157:1504, 2000;
Taylor MA, Fink M: Catatonia in psychiatric classification: a home of its own. Am J Psychiatry 160:1233,
2003; Taylor MA: Use of suprathreshold electroconvulsive therapy. Arch Gen Psychiatry 58:607, 2001.
Educational Objectives
| The goal of this program is to educate the clinician about electroconvulsive therapy (ECT) and the management of
concomitant psychiatric and medical conditions. After hearing and assimilating this program, the clinician will be
better able to:
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| 1. Select patients who might benefit from ECT.
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| 2. Maximize the efficacy of ECT.
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| 3. Monitor the quality of ECT-induced seizures through electroencephalography.
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| 4. Discuss the relationship between certain medical illnesses and depression.
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| 5. Treat depression that occurs concurrently with medical illness.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty members to disclose
relevant financial relationships within the past 12 months that might create any personal conflicts of interest.
Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and
not a proprietary business or commercial interest. For this issue, Dr. Bonds disclosed that he is on the Speakers’
Bureaus for Abbott Laboratories and Pfizer, Inc.
Acknowledgements
Dr. Taylor was recorded at Mood Disorders Update and Current Issues in Electroconvulsive Therapy and Neuromodulation,
held November 9-10, 2006, in Ann Arbor, MI, and sponsored by the University of Michigan Medical
School, the Michigan Psychiatric Society, and the Depression and Bi-Polar Alliance. Dr. Bonds was recorded at 2006
Behavioral Health Symposium, held October 6, 2006, in Industry Hills, CA, and sponsored by Kaiser Permanente.
The Audio-Digest Foundation thanks the speakers and the sponsors for their cooperation in the production of this program.
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