User login
7 psychopharm myths debunked
As a psychopharmacology consultant, I often encounter bits of received wisdom that do not square with results of controlled studies. Although all these “myths” contain a grain of truth, their uncritical acceptance can be a barrier to effective care.
1 Dual-acting antidepressants are more effective than serotonergic agents.
Although some serotonin/norepinephrine reuptake inhibitors may be modestly more effective than some selective serotonin reuptake inhibitors (SSRIs), no randomized studies show that one class of antidepressants is clearly superior to another. The overall difference in remission rates between venlafaxine and SSRIs—about 6% favoring venlafaxine—is not robust.1
2 Lithium is not as effective as divalproex for treating rapid-cycling bipolar disorder.
Rapid-cycling bipolar disorder can indicate reduced drug responsiveness, but lithium should not be disregarded. The relapse rate into any mood episode among rapid cyclers is not significantly different among patients maintained on lithium vs valproate,2 though concomitant antidepressant treatment complicates some studies.
3 Psychotropics with short elimination half-lives need to be administered 2 or more times a day.
This statement may be true for some patients taking short-acting benzodiazepines for panic disorder or psychostimulants for attention- deficit/hyperactivity disorder. However, no randomized, head-to-head studies show that antidepressants or antipsychotics with half-lives 3 Antipsychotic effects probably persist at dopamine-2 receptors even at trough blood levels.
4 Tardive dyskinesia (TD) is not a problem with atypical antipsychotics.
Atypical or second-generation antipsychotics (SGAs) are associated with TD rates approximately one-tenth to one-half that of first-generation antipsychotics. But TD can occur with atypicals, particularly in very old and very young patients. Some data indicate TD rates >10% in African-American children taking SGAs.4
5 Stimulants should never be combined with a monoamine oxidase inhibitor (MAOI) because a dangerous hypertensive reaction is likely.
No controlled studies or case reports show that carefully adding a psychostimulant—such as methylphenidate, 5 to 10 mg/d—to an MAOI leads to serious hypertensive or other life-threatening reactions.5 Nevertheless, a careful risk-benefit assessment and close monitoring are indicated when prescribing this combination.
6 Antidepressants are effective and necessary in maintenance treatment of bipolar disorder.
Most recent studies find little benefit from adjunctive antidepressants in maintenance treatment of bipolar disorder.6 Although most stabilized bipolar patients don’t need an antidepressant, some may experience depressive relapse when adjunctive antidepressants are discontinued.
7 Co-administered mood stabilizers prevent antidepressant-induced ‘switching’ into bipolar mania.
It is not clear that mood stabilizers as a class provide reliable protection against antidepressant-induced switching, though lithium may offer more protection than anticonvulsants.7 Even if switching is not caused by antidepressants,6 irritability, insomnia, and cycle acceleration may occur in susceptible patients.
1. Nemeroff CB, Entsuah R, Benattia I, et al. Comprehensive analysis of remission (COMPARE) with venlafaxine versus SSRIs. Biol Psychiatry 2008;63(4):424-34.
2. Calabrese JR, Rapport DJ, Youngstrom EA, et al. New data on the use of lithium, divalproate, and lamotrigine in rapid cycling bipolar disorder. Eur Psychiatry 2005;20:92-5.
3. Chengappa KN, Parepally H, Brar JS, et al. A random-assignment, double-blind, clinical trial of once- vs twice-daily administration of quetiapine fumarate in patients with schizophrenia or schizoaffective disorder: a pilot study. Can J Psychiatry 2003;48:187-94..
4. Wonodi I, Reeves G, Carmichael D, et al. Tardive dyskinesia in children treated with atypical antipsychotic medications. Mov Disord 2007;22(12):1777-82.
5. Feinberg SS. Combining stimulants with monoamine oxidase inhibitors: a review of uses and one possible additional indication. J Clin Psychiatry 2004;65:1520-4.
6. Sachs GS, Nierenberg AA, Calabrese JR, et al. Effectiveness of adjunctive antidepressant treatment for bipolar depression. N Engl J Med 2007;26:356:1711-22.
7. Henry C, Sorbara F, Lacoste J, et al. Antidepressant-induced mania in bipolar patients: identification of risk factors. J Clin Psychiatry 2001;62:249-55.
Dr. Pies is professor of psychiatry, SUNY Upstate Medical Center, Syracuse, and clinical professor of psychiatry, Tufts University School of Medicine, Boston.
As a psychopharmacology consultant, I often encounter bits of received wisdom that do not square with results of controlled studies. Although all these “myths” contain a grain of truth, their uncritical acceptance can be a barrier to effective care.
1 Dual-acting antidepressants are more effective than serotonergic agents.
Although some serotonin/norepinephrine reuptake inhibitors may be modestly more effective than some selective serotonin reuptake inhibitors (SSRIs), no randomized studies show that one class of antidepressants is clearly superior to another. The overall difference in remission rates between venlafaxine and SSRIs—about 6% favoring venlafaxine—is not robust.1
2 Lithium is not as effective as divalproex for treating rapid-cycling bipolar disorder.
Rapid-cycling bipolar disorder can indicate reduced drug responsiveness, but lithium should not be disregarded. The relapse rate into any mood episode among rapid cyclers is not significantly different among patients maintained on lithium vs valproate,2 though concomitant antidepressant treatment complicates some studies.
3 Psychotropics with short elimination half-lives need to be administered 2 or more times a day.
This statement may be true for some patients taking short-acting benzodiazepines for panic disorder or psychostimulants for attention- deficit/hyperactivity disorder. However, no randomized, head-to-head studies show that antidepressants or antipsychotics with half-lives 3 Antipsychotic effects probably persist at dopamine-2 receptors even at trough blood levels.
4 Tardive dyskinesia (TD) is not a problem with atypical antipsychotics.
Atypical or second-generation antipsychotics (SGAs) are associated with TD rates approximately one-tenth to one-half that of first-generation antipsychotics. But TD can occur with atypicals, particularly in very old and very young patients. Some data indicate TD rates >10% in African-American children taking SGAs.4
5 Stimulants should never be combined with a monoamine oxidase inhibitor (MAOI) because a dangerous hypertensive reaction is likely.
No controlled studies or case reports show that carefully adding a psychostimulant—such as methylphenidate, 5 to 10 mg/d—to an MAOI leads to serious hypertensive or other life-threatening reactions.5 Nevertheless, a careful risk-benefit assessment and close monitoring are indicated when prescribing this combination.
6 Antidepressants are effective and necessary in maintenance treatment of bipolar disorder.
Most recent studies find little benefit from adjunctive antidepressants in maintenance treatment of bipolar disorder.6 Although most stabilized bipolar patients don’t need an antidepressant, some may experience depressive relapse when adjunctive antidepressants are discontinued.
7 Co-administered mood stabilizers prevent antidepressant-induced ‘switching’ into bipolar mania.
It is not clear that mood stabilizers as a class provide reliable protection against antidepressant-induced switching, though lithium may offer more protection than anticonvulsants.7 Even if switching is not caused by antidepressants,6 irritability, insomnia, and cycle acceleration may occur in susceptible patients.
As a psychopharmacology consultant, I often encounter bits of received wisdom that do not square with results of controlled studies. Although all these “myths” contain a grain of truth, their uncritical acceptance can be a barrier to effective care.
1 Dual-acting antidepressants are more effective than serotonergic agents.
Although some serotonin/norepinephrine reuptake inhibitors may be modestly more effective than some selective serotonin reuptake inhibitors (SSRIs), no randomized studies show that one class of antidepressants is clearly superior to another. The overall difference in remission rates between venlafaxine and SSRIs—about 6% favoring venlafaxine—is not robust.1
2 Lithium is not as effective as divalproex for treating rapid-cycling bipolar disorder.
Rapid-cycling bipolar disorder can indicate reduced drug responsiveness, but lithium should not be disregarded. The relapse rate into any mood episode among rapid cyclers is not significantly different among patients maintained on lithium vs valproate,2 though concomitant antidepressant treatment complicates some studies.
3 Psychotropics with short elimination half-lives need to be administered 2 or more times a day.
This statement may be true for some patients taking short-acting benzodiazepines for panic disorder or psychostimulants for attention- deficit/hyperactivity disorder. However, no randomized, head-to-head studies show that antidepressants or antipsychotics with half-lives 3 Antipsychotic effects probably persist at dopamine-2 receptors even at trough blood levels.
4 Tardive dyskinesia (TD) is not a problem with atypical antipsychotics.
Atypical or second-generation antipsychotics (SGAs) are associated with TD rates approximately one-tenth to one-half that of first-generation antipsychotics. But TD can occur with atypicals, particularly in very old and very young patients. Some data indicate TD rates >10% in African-American children taking SGAs.4
5 Stimulants should never be combined with a monoamine oxidase inhibitor (MAOI) because a dangerous hypertensive reaction is likely.
No controlled studies or case reports show that carefully adding a psychostimulant—such as methylphenidate, 5 to 10 mg/d—to an MAOI leads to serious hypertensive or other life-threatening reactions.5 Nevertheless, a careful risk-benefit assessment and close monitoring are indicated when prescribing this combination.
6 Antidepressants are effective and necessary in maintenance treatment of bipolar disorder.
Most recent studies find little benefit from adjunctive antidepressants in maintenance treatment of bipolar disorder.6 Although most stabilized bipolar patients don’t need an antidepressant, some may experience depressive relapse when adjunctive antidepressants are discontinued.
7 Co-administered mood stabilizers prevent antidepressant-induced ‘switching’ into bipolar mania.
It is not clear that mood stabilizers as a class provide reliable protection against antidepressant-induced switching, though lithium may offer more protection than anticonvulsants.7 Even if switching is not caused by antidepressants,6 irritability, insomnia, and cycle acceleration may occur in susceptible patients.
1. Nemeroff CB, Entsuah R, Benattia I, et al. Comprehensive analysis of remission (COMPARE) with venlafaxine versus SSRIs. Biol Psychiatry 2008;63(4):424-34.
2. Calabrese JR, Rapport DJ, Youngstrom EA, et al. New data on the use of lithium, divalproate, and lamotrigine in rapid cycling bipolar disorder. Eur Psychiatry 2005;20:92-5.
3. Chengappa KN, Parepally H, Brar JS, et al. A random-assignment, double-blind, clinical trial of once- vs twice-daily administration of quetiapine fumarate in patients with schizophrenia or schizoaffective disorder: a pilot study. Can J Psychiatry 2003;48:187-94..
4. Wonodi I, Reeves G, Carmichael D, et al. Tardive dyskinesia in children treated with atypical antipsychotic medications. Mov Disord 2007;22(12):1777-82.
5. Feinberg SS. Combining stimulants with monoamine oxidase inhibitors: a review of uses and one possible additional indication. J Clin Psychiatry 2004;65:1520-4.
6. Sachs GS, Nierenberg AA, Calabrese JR, et al. Effectiveness of adjunctive antidepressant treatment for bipolar depression. N Engl J Med 2007;26:356:1711-22.
7. Henry C, Sorbara F, Lacoste J, et al. Antidepressant-induced mania in bipolar patients: identification of risk factors. J Clin Psychiatry 2001;62:249-55.
Dr. Pies is professor of psychiatry, SUNY Upstate Medical Center, Syracuse, and clinical professor of psychiatry, Tufts University School of Medicine, Boston.
1. Nemeroff CB, Entsuah R, Benattia I, et al. Comprehensive analysis of remission (COMPARE) with venlafaxine versus SSRIs. Biol Psychiatry 2008;63(4):424-34.
2. Calabrese JR, Rapport DJ, Youngstrom EA, et al. New data on the use of lithium, divalproate, and lamotrigine in rapid cycling bipolar disorder. Eur Psychiatry 2005;20:92-5.
3. Chengappa KN, Parepally H, Brar JS, et al. A random-assignment, double-blind, clinical trial of once- vs twice-daily administration of quetiapine fumarate in patients with schizophrenia or schizoaffective disorder: a pilot study. Can J Psychiatry 2003;48:187-94..
4. Wonodi I, Reeves G, Carmichael D, et al. Tardive dyskinesia in children treated with atypical antipsychotic medications. Mov Disord 2007;22(12):1777-82.
5. Feinberg SS. Combining stimulants with monoamine oxidase inhibitors: a review of uses and one possible additional indication. J Clin Psychiatry 2004;65:1520-4.
6. Sachs GS, Nierenberg AA, Calabrese JR, et al. Effectiveness of adjunctive antidepressant treatment for bipolar depression. N Engl J Med 2007;26:356:1711-22.
7. Henry C, Sorbara F, Lacoste J, et al. Antidepressant-induced mania in bipolar patients: identification of risk factors. J Clin Psychiatry 2001;62:249-55.
Dr. Pies is professor of psychiatry, SUNY Upstate Medical Center, Syracuse, and clinical professor of psychiatry, Tufts University School of Medicine, Boston.
How long to wait for an antidepressant to ‘work’
Prevailing wisdom says it takes 3 to 4 weeks for an antidepressant to show clinical effect. Historically, patients who improve in the first 2 weeks have been labeled “placebo responders.”1 Several recent studies, however, demonstrate a real, drug-based response in many patients as early as the first week of treatment, depending on the medication (Table).2-5 In practical terms, these studies raise the question of how long you should wait for an antidepressant to “work.”
Table
Variables in antidepressant response
It is not surprising that onset of antidepressant response in some patients varies. The new data—derived mainly from meta-analyses of studies using the Hamilton Depression Rating Scale (HAM-D)—do not tease out sources of variability in the studies, including:
|
Early indications. Here are some tips for gauging antidepressant response, depending on what you see in the first 2 to 4 weeks:
- Obtain a pretreatment score on the Beck Depression Inventory or other depression rating scale, and repeat the assessment at least once between days 7 and 10 of treatment. If there is little or no improvement, consider a modest dosage increase.
- Don’t assume that a patient who responds to an antidepressant during the first 2 weeks is experiencing a placebo effect. It may be a drug-mediated response. Some patients will retain and build on this early response, whereas others’ response may wane over subsequent weeks.
- No response to an antidepressant during weeks 1 through 4 does not bode well for most patients,5,6 although the data do not support giving up on an antidepressant after 1 to 2 weeks of nonresponse. Responses will “accumulate” during weeks 3 to 5 of treatment.7
- Patients who show little response during the first 2 weeks of treatment but experience some improvement during weeks 3 and 4 may be late responders. However, if the patient shows no improvement by week 3 or 4, consider switching to a different antidepressant, perhaps one from a different chemical class.8
- Different neurovegetative signs and symptoms of depression may improve at different rates, with some requiring >8 weeks of treatment. Insight, for example, may not improve until the second month of treatment.9
- Individualize treatment. Many treatment-refractory depressed patients—who failed to respond to 1 or more adequate drug trials—may require longer and more intensive treatment (>3 months) beffore showing a robust response.10
- “Onset of response” does not equal “clinical recovery,” nor is an improved Hamilton Depression Scale score a proxy for “high quality of life.” Patients may need ≥2 months for clinically significant improvement in interpersonal, social, and vocational function.11
Acknowledgement
The author expresses his appreciation to Michael Posternak, MD, Andrew Nierenberg, MD, and Alex J. Mitchell, MD, for their helpful comments on an early draft of this article.
1. Quitkin FM, McGrath PJ, Rabkin JG, et al. Different types of placebo response in patients receiving antidepressants. Am J Psychiatry 1991;148:197-203.
2. Posternak MA, Zimmerman M. Is there a delay in the antidepressant effect? A meta-analysis. J Clin Psychiatry 2005;66:148-58.
3. Taylor MJ, Freemantle N, Geddes JR, et al. Early onset of selective serotonin reuptake inhibitor antidepressant action. Arch Gen Psychiatry 2006;63:1217-23.
4. Mitchell AJ. Two week delay in onset of action of antidepressants: new evidence. Br J Psychiatry 2006;188:105-6.
5. Katz MM, Bowden CL, Berman N, et al. Resolving the onset of antidepressants’ clinical actions. J Clin Psychopharmacol 2006;26:549-53.
6. Nierenberg AA, Farabaugh AH, Alpert JE, et al. Timing of onset of antidepressant response with fluoxetine. Am J Psychiatry 2000;157:1423-8.
7. Stassen HH, Angst J, Delini-Stula A. Delayed onset of action of antidepressant drugs: fact or fiction? CNS Drugs 1998;3:177-84.
8. Trivedi MH, Morris DW, Grannemann BD, et al. Symptom clusters as predictors of late response to antidepressant treatment. J Clin Psychiatry 2005;66:1064-70.
9. Hirschfeld RM, Mallinckrodt C, Lee TC, et al. Time course of depression-symptom improvement during treatment with duloxetine. Depress Anxiety 2005;21(4):170-7.
10. Tew JD, Jr, Mulsant BH, Houck PR, et al. Impact of prior treatment exposure on response to antidepressant treatment in late life. Am J Geriatr Psychiatry 2006 Nov;14(11):957-65.
11. Dubini A, Bosc M, Polin V. Noradrenaline-selective versus serotonin-selective antidepressant therapy: differential effects on social functioning. J Psychopharmacol 1997;11(suppl 4):S17-S23.
Dr. Pies is clinical professor of psychiatry, Tufts University School of Medicine, Boston, MA.
Prevailing wisdom says it takes 3 to 4 weeks for an antidepressant to show clinical effect. Historically, patients who improve in the first 2 weeks have been labeled “placebo responders.”1 Several recent studies, however, demonstrate a real, drug-based response in many patients as early as the first week of treatment, depending on the medication (Table).2-5 In practical terms, these studies raise the question of how long you should wait for an antidepressant to “work.”
Table
Variables in antidepressant response
It is not surprising that onset of antidepressant response in some patients varies. The new data—derived mainly from meta-analyses of studies using the Hamilton Depression Rating Scale (HAM-D)—do not tease out sources of variability in the studies, including:
|
Early indications. Here are some tips for gauging antidepressant response, depending on what you see in the first 2 to 4 weeks:
- Obtain a pretreatment score on the Beck Depression Inventory or other depression rating scale, and repeat the assessment at least once between days 7 and 10 of treatment. If there is little or no improvement, consider a modest dosage increase.
- Don’t assume that a patient who responds to an antidepressant during the first 2 weeks is experiencing a placebo effect. It may be a drug-mediated response. Some patients will retain and build on this early response, whereas others’ response may wane over subsequent weeks.
- No response to an antidepressant during weeks 1 through 4 does not bode well for most patients,5,6 although the data do not support giving up on an antidepressant after 1 to 2 weeks of nonresponse. Responses will “accumulate” during weeks 3 to 5 of treatment.7
- Patients who show little response during the first 2 weeks of treatment but experience some improvement during weeks 3 and 4 may be late responders. However, if the patient shows no improvement by week 3 or 4, consider switching to a different antidepressant, perhaps one from a different chemical class.8
- Different neurovegetative signs and symptoms of depression may improve at different rates, with some requiring >8 weeks of treatment. Insight, for example, may not improve until the second month of treatment.9
- Individualize treatment. Many treatment-refractory depressed patients—who failed to respond to 1 or more adequate drug trials—may require longer and more intensive treatment (>3 months) beffore showing a robust response.10
- “Onset of response” does not equal “clinical recovery,” nor is an improved Hamilton Depression Scale score a proxy for “high quality of life.” Patients may need ≥2 months for clinically significant improvement in interpersonal, social, and vocational function.11
Acknowledgement
The author expresses his appreciation to Michael Posternak, MD, Andrew Nierenberg, MD, and Alex J. Mitchell, MD, for their helpful comments on an early draft of this article.
Prevailing wisdom says it takes 3 to 4 weeks for an antidepressant to show clinical effect. Historically, patients who improve in the first 2 weeks have been labeled “placebo responders.”1 Several recent studies, however, demonstrate a real, drug-based response in many patients as early as the first week of treatment, depending on the medication (Table).2-5 In practical terms, these studies raise the question of how long you should wait for an antidepressant to “work.”
Table
Variables in antidepressant response
It is not surprising that onset of antidepressant response in some patients varies. The new data—derived mainly from meta-analyses of studies using the Hamilton Depression Rating Scale (HAM-D)—do not tease out sources of variability in the studies, including:
|
Early indications. Here are some tips for gauging antidepressant response, depending on what you see in the first 2 to 4 weeks:
- Obtain a pretreatment score on the Beck Depression Inventory or other depression rating scale, and repeat the assessment at least once between days 7 and 10 of treatment. If there is little or no improvement, consider a modest dosage increase.
- Don’t assume that a patient who responds to an antidepressant during the first 2 weeks is experiencing a placebo effect. It may be a drug-mediated response. Some patients will retain and build on this early response, whereas others’ response may wane over subsequent weeks.
- No response to an antidepressant during weeks 1 through 4 does not bode well for most patients,5,6 although the data do not support giving up on an antidepressant after 1 to 2 weeks of nonresponse. Responses will “accumulate” during weeks 3 to 5 of treatment.7
- Patients who show little response during the first 2 weeks of treatment but experience some improvement during weeks 3 and 4 may be late responders. However, if the patient shows no improvement by week 3 or 4, consider switching to a different antidepressant, perhaps one from a different chemical class.8
- Different neurovegetative signs and symptoms of depression may improve at different rates, with some requiring >8 weeks of treatment. Insight, for example, may not improve until the second month of treatment.9
- Individualize treatment. Many treatment-refractory depressed patients—who failed to respond to 1 or more adequate drug trials—may require longer and more intensive treatment (>3 months) beffore showing a robust response.10
- “Onset of response” does not equal “clinical recovery,” nor is an improved Hamilton Depression Scale score a proxy for “high quality of life.” Patients may need ≥2 months for clinically significant improvement in interpersonal, social, and vocational function.11
Acknowledgement
The author expresses his appreciation to Michael Posternak, MD, Andrew Nierenberg, MD, and Alex J. Mitchell, MD, for their helpful comments on an early draft of this article.
1. Quitkin FM, McGrath PJ, Rabkin JG, et al. Different types of placebo response in patients receiving antidepressants. Am J Psychiatry 1991;148:197-203.
2. Posternak MA, Zimmerman M. Is there a delay in the antidepressant effect? A meta-analysis. J Clin Psychiatry 2005;66:148-58.
3. Taylor MJ, Freemantle N, Geddes JR, et al. Early onset of selective serotonin reuptake inhibitor antidepressant action. Arch Gen Psychiatry 2006;63:1217-23.
4. Mitchell AJ. Two week delay in onset of action of antidepressants: new evidence. Br J Psychiatry 2006;188:105-6.
5. Katz MM, Bowden CL, Berman N, et al. Resolving the onset of antidepressants’ clinical actions. J Clin Psychopharmacol 2006;26:549-53.
6. Nierenberg AA, Farabaugh AH, Alpert JE, et al. Timing of onset of antidepressant response with fluoxetine. Am J Psychiatry 2000;157:1423-8.
7. Stassen HH, Angst J, Delini-Stula A. Delayed onset of action of antidepressant drugs: fact or fiction? CNS Drugs 1998;3:177-84.
8. Trivedi MH, Morris DW, Grannemann BD, et al. Symptom clusters as predictors of late response to antidepressant treatment. J Clin Psychiatry 2005;66:1064-70.
9. Hirschfeld RM, Mallinckrodt C, Lee TC, et al. Time course of depression-symptom improvement during treatment with duloxetine. Depress Anxiety 2005;21(4):170-7.
10. Tew JD, Jr, Mulsant BH, Houck PR, et al. Impact of prior treatment exposure on response to antidepressant treatment in late life. Am J Geriatr Psychiatry 2006 Nov;14(11):957-65.
11. Dubini A, Bosc M, Polin V. Noradrenaline-selective versus serotonin-selective antidepressant therapy: differential effects on social functioning. J Psychopharmacol 1997;11(suppl 4):S17-S23.
Dr. Pies is clinical professor of psychiatry, Tufts University School of Medicine, Boston, MA.
1. Quitkin FM, McGrath PJ, Rabkin JG, et al. Different types of placebo response in patients receiving antidepressants. Am J Psychiatry 1991;148:197-203.
2. Posternak MA, Zimmerman M. Is there a delay in the antidepressant effect? A meta-analysis. J Clin Psychiatry 2005;66:148-58.
3. Taylor MJ, Freemantle N, Geddes JR, et al. Early onset of selective serotonin reuptake inhibitor antidepressant action. Arch Gen Psychiatry 2006;63:1217-23.
4. Mitchell AJ. Two week delay in onset of action of antidepressants: new evidence. Br J Psychiatry 2006;188:105-6.
5. Katz MM, Bowden CL, Berman N, et al. Resolving the onset of antidepressants’ clinical actions. J Clin Psychopharmacol 2006;26:549-53.
6. Nierenberg AA, Farabaugh AH, Alpert JE, et al. Timing of onset of antidepressant response with fluoxetine. Am J Psychiatry 2000;157:1423-8.
7. Stassen HH, Angst J, Delini-Stula A. Delayed onset of action of antidepressant drugs: fact or fiction? CNS Drugs 1998;3:177-84.
8. Trivedi MH, Morris DW, Grannemann BD, et al. Symptom clusters as predictors of late response to antidepressant treatment. J Clin Psychiatry 2005;66:1064-70.
9. Hirschfeld RM, Mallinckrodt C, Lee TC, et al. Time course of depression-symptom improvement during treatment with duloxetine. Depress Anxiety 2005;21(4):170-7.
10. Tew JD, Jr, Mulsant BH, Houck PR, et al. Impact of prior treatment exposure on response to antidepressant treatment in late life. Am J Geriatr Psychiatry 2006 Nov;14(11):957-65.
11. Dubini A, Bosc M, Polin V. Noradrenaline-selective versus serotonin-selective antidepressant therapy: differential effects on social functioning. J Psychopharmacol 1997;11(suppl 4):S17-S23.
Dr. Pies is clinical professor of psychiatry, Tufts University School of Medicine, Boston, MA.
Is it bipolar depression? ‘WHIPLASHED’ aids diagnosis
Despite much education and research, bipolar disorder is still under-recognized and inappropriately treated in many clinical settings.1 Bipolar and unipolar depression display similar symptoms, making correct diagnosis difficult. The differential diagnosis is especially problematic in patients suffering a first major depressive episode, when there is no clear history of mania or hypomania.
Nevertheless, bipolar depression does have telltale signs—remembered with the mnemonic WHIPLASHED—to guide diagnosis.2-8
Worse or “wired” when taking antidepressants. The patient complains of feeling “antsy” or being agitated or unable to sleep when taking traditional anti-depressants.
Look for numerous failed antidepressant trials, apparent tolerance to antidepressants that does not resolve with increased dose, and antidepressant-induced mania or mood cycle acceleration.
Hypomania, hyperthymic temperament, or mood swings in a patient’s history. Patients with hyperthymic temperament show persistent traits such as intense optimism, increased energy, reduced need for sleep, extroversion, and overconfidence.
Ask about periods of elevated mood or energy that might not fit formal DSM-IV-TR criteria for hypomania—such as episodes that last only a day or two. Mood lability in younger patients can be especially dramatic and poorly demarcated.
Irritable, hostile, or mixed features. Some patients show one or more hypomanic features, such as racing thoughts when depressed.
Psychomotor retardation appears more common in bipolar I depression than in unipolar major depression. Psychomotor agitation, however, is more likely in bipolar II than in unipolar major depression.
Loaded family history of mood swings, frank bipolar disorder, or affective illness. A family history of comorbid mood disorder and alcoholism may also point to bipolarity.
Abrupt onset and/or termination of depressive bouts or relatively brief episodes (
Seasonal or postpartum depression. “Winter-type” seasonal affective disorder—feeling depressed in the fall and winter, hypomanic in the spring—and postpartum psychosis have clinical and epidemiologic links with bipolar disorder.
Hyperphagia and hypersomnia—sometimes termed atypical features—are common in bipolar depression. Paradoxically, hypersomnia may co-exist with psychomotor agitation in bipolar II patients, resulting in so-called “sleepy speeders.”
Early age of onset. Major depression that appears before age 25—especially with psychotic features—may herald subsequent bipolarity.
Delusions, hallucinations, or other psychotic features are more common in bipolar than in unipolar depression.
Acknowledgment
The author thanks Nassir Ghaemi, MD, and Jim Phelps, MD, for suggesting modifications to the mnemonic.
1. Phelps JR, Ghaemi SN. Improving the diagnosis of bipolar disorder: predictive value of screening tests. J Affect Disord 2006;92(2-3):141-8.
2. Thase ME. Bipolar depression: issues in diagnosis and treatment. Harv Rev Psychiatry 2005;13(5):257-71.
3. Benazzi F, Akiskal H. Irritable-hostile depression: further validation as a bipolar depressive mixed state. J Affect Disord 2005;84(2-3):197-207.
4. Pies R. The “softer” end of the bipolar spectrum. J Psychiatr Pract 2002;8(4):189-95.
5. Albanese MJ, Pies R. The bipolar patient with comorbid substance use disorder: recognition and management. CNS Drugs 2004;18(9):585-96.
6. Chaudron LH, Pies RW. The relationship between postpartum psychosis and bipolar disorder: a review. J Clin Psychiatry 2003;64(11):1284-92.
7. Hantouche EG, Akiskal HS. Bipolar II vs. unipolar depression: psychopathologic differentiation by dimensional measures. J Affect Disord 2005;84(2-3):127-32.
8. Mitchell PB, Wilhelm K, Parker G, et al. The clinical features of bipolar depression: a comparison with matched major depressive disorder patients. J Clin Psychiatry 2001;62(3):212-6.
Dr. Pies is clinical professor of psychiatry, Tufts University School of Medicine, Boston, MA.
Despite much education and research, bipolar disorder is still under-recognized and inappropriately treated in many clinical settings.1 Bipolar and unipolar depression display similar symptoms, making correct diagnosis difficult. The differential diagnosis is especially problematic in patients suffering a first major depressive episode, when there is no clear history of mania or hypomania.
Nevertheless, bipolar depression does have telltale signs—remembered with the mnemonic WHIPLASHED—to guide diagnosis.2-8
Worse or “wired” when taking antidepressants. The patient complains of feeling “antsy” or being agitated or unable to sleep when taking traditional anti-depressants.
Look for numerous failed antidepressant trials, apparent tolerance to antidepressants that does not resolve with increased dose, and antidepressant-induced mania or mood cycle acceleration.
Hypomania, hyperthymic temperament, or mood swings in a patient’s history. Patients with hyperthymic temperament show persistent traits such as intense optimism, increased energy, reduced need for sleep, extroversion, and overconfidence.
Ask about periods of elevated mood or energy that might not fit formal DSM-IV-TR criteria for hypomania—such as episodes that last only a day or two. Mood lability in younger patients can be especially dramatic and poorly demarcated.
Irritable, hostile, or mixed features. Some patients show one or more hypomanic features, such as racing thoughts when depressed.
Psychomotor retardation appears more common in bipolar I depression than in unipolar major depression. Psychomotor agitation, however, is more likely in bipolar II than in unipolar major depression.
Loaded family history of mood swings, frank bipolar disorder, or affective illness. A family history of comorbid mood disorder and alcoholism may also point to bipolarity.
Abrupt onset and/or termination of depressive bouts or relatively brief episodes (
Seasonal or postpartum depression. “Winter-type” seasonal affective disorder—feeling depressed in the fall and winter, hypomanic in the spring—and postpartum psychosis have clinical and epidemiologic links with bipolar disorder.
Hyperphagia and hypersomnia—sometimes termed atypical features—are common in bipolar depression. Paradoxically, hypersomnia may co-exist with psychomotor agitation in bipolar II patients, resulting in so-called “sleepy speeders.”
Early age of onset. Major depression that appears before age 25—especially with psychotic features—may herald subsequent bipolarity.
Delusions, hallucinations, or other psychotic features are more common in bipolar than in unipolar depression.
Acknowledgment
The author thanks Nassir Ghaemi, MD, and Jim Phelps, MD, for suggesting modifications to the mnemonic.
Despite much education and research, bipolar disorder is still under-recognized and inappropriately treated in many clinical settings.1 Bipolar and unipolar depression display similar symptoms, making correct diagnosis difficult. The differential diagnosis is especially problematic in patients suffering a first major depressive episode, when there is no clear history of mania or hypomania.
Nevertheless, bipolar depression does have telltale signs—remembered with the mnemonic WHIPLASHED—to guide diagnosis.2-8
Worse or “wired” when taking antidepressants. The patient complains of feeling “antsy” or being agitated or unable to sleep when taking traditional anti-depressants.
Look for numerous failed antidepressant trials, apparent tolerance to antidepressants that does not resolve with increased dose, and antidepressant-induced mania or mood cycle acceleration.
Hypomania, hyperthymic temperament, or mood swings in a patient’s history. Patients with hyperthymic temperament show persistent traits such as intense optimism, increased energy, reduced need for sleep, extroversion, and overconfidence.
Ask about periods of elevated mood or energy that might not fit formal DSM-IV-TR criteria for hypomania—such as episodes that last only a day or two. Mood lability in younger patients can be especially dramatic and poorly demarcated.
Irritable, hostile, or mixed features. Some patients show one or more hypomanic features, such as racing thoughts when depressed.
Psychomotor retardation appears more common in bipolar I depression than in unipolar major depression. Psychomotor agitation, however, is more likely in bipolar II than in unipolar major depression.
Loaded family history of mood swings, frank bipolar disorder, or affective illness. A family history of comorbid mood disorder and alcoholism may also point to bipolarity.
Abrupt onset and/or termination of depressive bouts or relatively brief episodes (
Seasonal or postpartum depression. “Winter-type” seasonal affective disorder—feeling depressed in the fall and winter, hypomanic in the spring—and postpartum psychosis have clinical and epidemiologic links with bipolar disorder.
Hyperphagia and hypersomnia—sometimes termed atypical features—are common in bipolar depression. Paradoxically, hypersomnia may co-exist with psychomotor agitation in bipolar II patients, resulting in so-called “sleepy speeders.”
Early age of onset. Major depression that appears before age 25—especially with psychotic features—may herald subsequent bipolarity.
Delusions, hallucinations, or other psychotic features are more common in bipolar than in unipolar depression.
Acknowledgment
The author thanks Nassir Ghaemi, MD, and Jim Phelps, MD, for suggesting modifications to the mnemonic.
1. Phelps JR, Ghaemi SN. Improving the diagnosis of bipolar disorder: predictive value of screening tests. J Affect Disord 2006;92(2-3):141-8.
2. Thase ME. Bipolar depression: issues in diagnosis and treatment. Harv Rev Psychiatry 2005;13(5):257-71.
3. Benazzi F, Akiskal H. Irritable-hostile depression: further validation as a bipolar depressive mixed state. J Affect Disord 2005;84(2-3):197-207.
4. Pies R. The “softer” end of the bipolar spectrum. J Psychiatr Pract 2002;8(4):189-95.
5. Albanese MJ, Pies R. The bipolar patient with comorbid substance use disorder: recognition and management. CNS Drugs 2004;18(9):585-96.
6. Chaudron LH, Pies RW. The relationship between postpartum psychosis and bipolar disorder: a review. J Clin Psychiatry 2003;64(11):1284-92.
7. Hantouche EG, Akiskal HS. Bipolar II vs. unipolar depression: psychopathologic differentiation by dimensional measures. J Affect Disord 2005;84(2-3):127-32.
8. Mitchell PB, Wilhelm K, Parker G, et al. The clinical features of bipolar depression: a comparison with matched major depressive disorder patients. J Clin Psychiatry 2001;62(3):212-6.
Dr. Pies is clinical professor of psychiatry, Tufts University School of Medicine, Boston, MA.
1. Phelps JR, Ghaemi SN. Improving the diagnosis of bipolar disorder: predictive value of screening tests. J Affect Disord 2006;92(2-3):141-8.
2. Thase ME. Bipolar depression: issues in diagnosis and treatment. Harv Rev Psychiatry 2005;13(5):257-71.
3. Benazzi F, Akiskal H. Irritable-hostile depression: further validation as a bipolar depressive mixed state. J Affect Disord 2005;84(2-3):197-207.
4. Pies R. The “softer” end of the bipolar spectrum. J Psychiatr Pract 2002;8(4):189-95.
5. Albanese MJ, Pies R. The bipolar patient with comorbid substance use disorder: recognition and management. CNS Drugs 2004;18(9):585-96.
6. Chaudron LH, Pies RW. The relationship between postpartum psychosis and bipolar disorder: a review. J Clin Psychiatry 2003;64(11):1284-92.
7. Hantouche EG, Akiskal HS. Bipolar II vs. unipolar depression: psychopathologic differentiation by dimensional measures. J Affect Disord 2005;84(2-3):127-32.
8. Mitchell PB, Wilhelm K, Parker G, et al. The clinical features of bipolar depression: a comparison with matched major depressive disorder patients. J Clin Psychiatry 2001;62(3):212-6.
Dr. Pies is clinical professor of psychiatry, Tufts University School of Medicine, Boston, MA.