James Randolph Hillard, MD

All of us see patients whose recurrent depressions seem to have a seasonal component. Should we treat them differently than patients whose recurrent depressions are not related to seasons? Is there adequate evidence for the existence of seasonal affective disorder (SAD), or—as it is called in DSM-IV-TR—mood disorder with a seasonal pattern? Is bright light therapy supported by the literature, or is it just some sort of fad?

As December brings the shortest days of the year, we shine the spotlight on SAD and examine the latest evidence on its causes, diagnosis, and treatment.

Moods with a seasonal rhythm

Moods have been observed to change with the seasons since ancient times (Box 1).¹ As recently as 25 years ago, however, seasonal affective disorder was not recognized as a psychiatric diagnosis.

In the early 1980s, when researchers at the National Institute of Mental Health (NIMH) were studying the effect of bright light on melatonin secretion, they were contacted by Herbert E. Kern, a research engineer who suffered from recurrent depression. A methodical person, Kern had kept a journal of his mood variations and noticed a pattern that appeared to follow the seasons. His depression worsened in the fall and winter and improved in the spring and summer. Kern subsequently participated in an NIMH trial with phototherapy, his mood improved, and the results were published in 1982.²

Box 1

Two years later, the researchers published the first paper that described SAD as a psychiatric diagnosis.³ Criteria for the diagnosis included:

• presence of a major affective disorder
• affective episodes occurring during fall or winter and remitting in spring or summer for at least 2 consecutive years.

The paper also discussed treatment of winter depression with phototherapy.

DSM-IV-TR describes SAD as a course specifier for mood disorders, including major depressive episodes in bipolar I and II disorders and major depressive disorder (Box 2). In other words, as used in DSM-IV-TR and this article, SAD is not an independent disorder but a type of major affective disorder.

Characteristics of SAD

Symptoms. Patients with SAD suffer the typical symptoms of depression—decreased energy, guilt, and decreased libido—as well as atypical symptoms—carbohydrate craving, hypersomnia, and weight gain. They also appear less likely to exhibit psychotic symptoms and may be at lower risk for suicide than persons with major mood disorders but without SAD.¹

Changes in sleep patterns also have been observed. Rosenthal et al⁴ found increased sleep latency and increased total sleep time in patients with SAD. Delta or slow-wave sleep—the restorative part of the sleep cycle—decreased by nearly one-half (mean 46%). REM latency did not change, contrary to typical findings in depressed patients. Anderson et al⁵ also reported no change in REM latency in patients with SAD.

Comorbid conditions. Eating disorders—particularly bulimia nervosa—are more prevalent in patients with SAD.¹ Binge eating tends to worsen in the fall and winter.

Personality disorders are also common in these patients, with cluster C over-represented. Avoidant personality disorder is most common. In a sample of 45 patients with SAD, Reichborn-Kjennerud et al⁶ found any personality disorder in 58% and avoidant personality disorder in 31%. Patients with comorbid personality disorders were less likely to respond to bright light therapy.

Prevalence. The prevalence of SAD in North America is approximately 1 to 6 %, with four times as many women affected as men.¹ Data on the effect of latitude on prevalence of SAD are inconclusive.⁷

Making the diagnosis

For patients with depression, clinicians should ask about seasonality of symptoms. Onset of major depressive symptoms in the fall or winter for at least two consecutive years or remission of depressive symptoms in the spring for two consecutive years (without onset of depressive syndromes during the spring or summer) probably merits a diagnosis of SAD. The diagnosis is confirmed if seasonal patterns of depressive symptoms substantially outnumber nonseasonal occurrences over the patient’s lifetime. The diagnosis may not be appropriate if there are obvious seasonal psychosocial stressors, such as anniversary reactions in posttraumatic stress disorder.

Some patients have sub-syndromal depressive symptoms that occur seasonally. DSM-IV would probably classify them as “mood disorder, not otherwise specified,” and that group has not been studied extensively.

Box 2

What causes SAD?

Research is ongoing, but the cause of SAD is not yet fully understood, although hypotheses have been developed. The four main hypotheses relate to duration of sunlight, changes in the circadian cycle, and secretion of the “hormone of darkness,” melatonin.

Photoperiod hypothesis. The shortening of the photoperiod—duration of sunlight—during autumn and winter may explain winter depression. Some research suggests that patients with SAD have an exaggerated melatonin response to shorter days and longer nights. For example, Wehr et al⁸ found that SAD patients secrete melatonin approximately 30 minutes longer per day in the winter, compared with controls.

Phase-delay hypothesis. Core body temperature is considered one of the most reliable markers of circadian rhythm. The nadir core body temperature occurs earlier than normal in a person whose circadian rhythm is “phase-advanced” and later than usual in those with “phase-delayed” circadian rhythms. Patients with seasonal affective symptoms generally reach their lowest body temperature of the day earlier than do controls.

Lewy et al,⁹ who proposed the phase-delay hypothesis, observed that melatonin secretion appeared to be delayed in patients with SAD. Some studies have supported this hypothesis, demonstrating greater benefit of bright light treatment when administered early in the morning than later in the day. Other studies, however, have shown benefit from light exposure late in the day.¹⁰

Reduced-amplitude hypothesis. SAD sufferers have dampened circadian rhythms, and bright light may increase the amplitude of the rhythms. There is little evidence for this hypothesis.

Melatonin hypothesis. Melatonin does not appear to cause depression. Looking at melatonin secretion patterns in conjunction with circadian phases, however, may offer new insights.⁸ Several studies have shown that manipulating the timing of melatonin secretion affects mood.

Cryptochrome, a photoreceptor in the retina, may be responsible for transmitting the photosignal to the elements of the circadian clock that regulate melatonin secretion. The pineal gland modifies its secretion of melatonin in response to the amount of light exposure (Box 3).^8,11

Light therapy

Bright light therapy has been supported by placebo-controlled trials and is first-line treatment for patients with SAD.¹ Bright light therapy is usually dosed at 2,500 lux for 2 hr/day or 10,000 lux for 30 min/day at eye level.¹² The best evidence supports administering light therapy in the morning, generally between 6 and 10 AM. As described by Terman,¹³ “larks”—people who go to bed early and get up early—need earlier light than “owls”—people who stay up later and sleep later.

Box 3

HOW SUNLIGHT MAY SET THE CIRCADIAN CLOCK

When light strikes the eye, it is well known that vitamin A-based photo pigments, cones, and rods receive the signal and transmit it via the optic tracts to the occipital cortex. But if light plays a role in the pathophysiology of seasonal affective disorder, how does light signal the other elements of the circadian system?

Cryptochrome, a photoreceptor in the retina, may be responsible for transmitting the photosignal to the circadian clock.¹¹ Cryptochrome is a vitamin B2-based pigment found in the ganglion cells and on cells in the inner nuclear layer of the retina. It is thought to transmit light through the optic nerve to the suprachiasmatic nucleus, the circadian pacemaker in the hypothalamus. The signal is then transmitted through the paraventricular nucleus, down the sympathetic chain, through the superior cervical ganglion, up the nervi canarii, to its final destination—the pineal gland.⁸ The pineal gland then modifies its secretion of melatonin in response to the amount of light exposure.

Although mammals have an intrinsic rhythmicity, the circadian clock must be entrained by exogenous light. The retinohypothalamic tract is believed to be the vehicle that sets the circadian clock. If the optic nerve is cut, a person becomes blind and unable to entrain the circadian rhythm.

Light therapy can be used alone or in addition to pharmacotherapy in patients whose previously wellcontrolled depressive symptoms worsen in the fall or winter. Light therapy also can be used as prophylaxis—starting in early fall—in patients with a history of a seasonal pattern of depression. Either way, light treatments generally should continue until early spring.

Given the relatively few side effects, light therapy may be used as monotherapy in patients with mild, subsyndromal mood symptoms occurring on a seasonal basis. Light therapy should not be used without pharmacotherapy to treat a full-blown major depressive episode.

Light boxes can be found via the Internet at an average cost of $180 to $300 for a 10,000-lux unit. The boxes are small enough to be placed on a table while the patient reads or eats breakfast. Artificial lights for this therapy do not emit ultraviolet rays, which have been associated with skin cancers.

Light visors also have shown some promise in SAD treatment, as demonstrated by a 2-week, randomized, controlled trial by Joffe et al.¹⁴ Compared with light boxes, light visors are more portable, so the patient can move around during treatment. Generally, the patient wears the visor 30 minutes in the morning.

Light visors appear to be as effective as table models, although no studies have compared the two devices. A visor costs $250 to $300.

Dawn simulation in SAD treatment has been examined in a few small studies and one placebo-controlled trial with 95 patients.¹⁰ In dawn simulation, a white light gradually increases between 4:30 and 6 AM to a peak intensity of 250 lux. Dawn simulation can be done while the patient is sleeping, whereas other light treatments require the patient to wake up early enough each morning to sit before a light box for 30 minutes. More study is needed to assess this modality’s efficacy.

Light therapy precautions. Review the patient’s medications before starting light therapy. Drugs that can magnify the effects of short wave-length light—leading to severe sunburns or rashes—include tetracycline, sulfonamides, and some older antipsychotics such as chlorpromazine. Some authors recommend an ophthalmologic examination before starting light therapy and every 2 to 3 years afterwards if no complications are apparent.¹ Others believe that no ophthalmologic examination is necessary unless the patient is older than 70 or has a history of retinal disease.

Side effects of bright light therapy are usually few and mild and include headaches, eye irritation, and nausea. In some anecdotal cases, patients with bipolar disorder appear to have switched from depression to mania upon starting light therapy,¹ but such switches appear to be rare. Still, patients with bipolar disorder and their family members should be advised to watch out for switches when using light therapy.

Pharmacologic therapy

Drug therapy in SAD has not been well studied, and many of the placebo-controlled trials that have examined this mode of treatment have been small. Serotonergic agents have been most studied because serotonin, with its effects on sleep and appetite, is thought to be related to SAD pathogenesis. The largest study of a selective serotonin reuptake inhibitor for SAD¹⁵ compared sertraline with placebo. Patients who received sertraline at a mean dosage of 111 mg/d had significantly fewer depressive symptoms than did the placebo group.

A placebo-controlled, double-blind study by Thorell¹⁶ found that adding citalopram to light therapy improved measures of depressed mood, compared with light therapy alone. This study is limited by small sample size but provides direction for further research.

An open trial of reboxetine—a noradrenaline reuptake inhibitor not available in the United States—suggests that further research of agents affecting catecholamines may be worthwhile in SAD treatment.¹⁷

Psychotherapy

Psychotherapy has not been researched sufficiently to be considered a proven treatment for SAD. However, some have observed that SAD patients have a negative cognitive style that may benefit from cognitive therapy. Thus, behavioral therapy may alter a patient’s response to light.¹

Related resources

• National Organization for Seasonal Affective Disorder www.nosad.org
• Dr. Ivan’s (Ivan Goldberg, MD) Depression Central www.psycom.net/depression.central.seasonal.html
• Columbia/Presbyterian Hospital Program in Clinical Chronobiology www.light-and-iontherapy.org

Drug brand names

• Citalopram • Celexa
• Sertraline • Zoloft

Disclosure

Dr. Paradies reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Dr. Hillard reports that he is a consultant to Pfizer Inc. and Janssen Pharmaceutica, and serves on the speakers bureau of Pfizer Inc., Janssen Pharmaceutica, and Eli Lilly and Co.

All of us see patients whose recurrent depressions seem to have a seasonal component. Should we treat them differently than patients whose recurrent depressions are not related to seasons? Is there adequate evidence for the existence of seasonal affective disorder (SAD), or—as it is called in DSM-IV-TR—mood disorder with a seasonal pattern? Is bright light therapy supported by the literature, or is it just some sort of fad?

As December brings the shortest days of the year, we shine the spotlight on SAD and examine the latest evidence on its causes, diagnosis, and treatment.

Moods with a seasonal rhythm

Moods have been observed to change with the seasons since ancient times (Box 1).¹ As recently as 25 years ago, however, seasonal affective disorder was not recognized as a psychiatric diagnosis.

In the early 1980s, when researchers at the National Institute of Mental Health (NIMH) were studying the effect of bright light on melatonin secretion, they were contacted by Herbert E. Kern, a research engineer who suffered from recurrent depression. A methodical person, Kern had kept a journal of his mood variations and noticed a pattern that appeared to follow the seasons. His depression worsened in the fall and winter and improved in the spring and summer. Kern subsequently participated in an NIMH trial with phototherapy, his mood improved, and the results were published in 1982.²

Box 1

Two years later, the researchers published the first paper that described SAD as a psychiatric diagnosis.³ Criteria for the diagnosis included:

• presence of a major affective disorder
• affective episodes occurring during fall or winter and remitting in spring or summer for at least 2 consecutive years.

The paper also discussed treatment of winter depression with phototherapy.

DSM-IV-TR describes SAD as a course specifier for mood disorders, including major depressive episodes in bipolar I and II disorders and major depressive disorder (Box 2). In other words, as used in DSM-IV-TR and this article, SAD is not an independent disorder but a type of major affective disorder.

Characteristics of SAD

Symptoms. Patients with SAD suffer the typical symptoms of depression—decreased energy, guilt, and decreased libido—as well as atypical symptoms—carbohydrate craving, hypersomnia, and weight gain. They also appear less likely to exhibit psychotic symptoms and may be at lower risk for suicide than persons with major mood disorders but without SAD.¹

Changes in sleep patterns also have been observed. Rosenthal et al⁴ found increased sleep latency and increased total sleep time in patients with SAD. Delta or slow-wave sleep—the restorative part of the sleep cycle—decreased by nearly one-half (mean 46%). REM latency did not change, contrary to typical findings in depressed patients. Anderson et al⁵ also reported no change in REM latency in patients with SAD.

Comorbid conditions. Eating disorders—particularly bulimia nervosa—are more prevalent in patients with SAD.¹ Binge eating tends to worsen in the fall and winter.

Personality disorders are also common in these patients, with cluster C over-represented. Avoidant personality disorder is most common. In a sample of 45 patients with SAD, Reichborn-Kjennerud et al⁶ found any personality disorder in 58% and avoidant personality disorder in 31%. Patients with comorbid personality disorders were less likely to respond to bright light therapy.

Prevalence. The prevalence of SAD in North America is approximately 1 to 6 %, with four times as many women affected as men.¹ Data on the effect of latitude on prevalence of SAD are inconclusive.⁷

Making the diagnosis

For patients with depression, clinicians should ask about seasonality of symptoms. Onset of major depressive symptoms in the fall or winter for at least two consecutive years or remission of depressive symptoms in the spring for two consecutive years (without onset of depressive syndromes during the spring or summer) probably merits a diagnosis of SAD. The diagnosis is confirmed if seasonal patterns of depressive symptoms substantially outnumber nonseasonal occurrences over the patient’s lifetime. The diagnosis may not be appropriate if there are obvious seasonal psychosocial stressors, such as anniversary reactions in posttraumatic stress disorder.

Some patients have sub-syndromal depressive symptoms that occur seasonally. DSM-IV would probably classify them as “mood disorder, not otherwise specified,” and that group has not been studied extensively.

Box 2

What causes SAD?

Research is ongoing, but the cause of SAD is not yet fully understood, although hypotheses have been developed. The four main hypotheses relate to duration of sunlight, changes in the circadian cycle, and secretion of the “hormone of darkness,” melatonin.

Photoperiod hypothesis. The shortening of the photoperiod—duration of sunlight—during autumn and winter may explain winter depression. Some research suggests that patients with SAD have an exaggerated melatonin response to shorter days and longer nights. For example, Wehr et al⁸ found that SAD patients secrete melatonin approximately 30 minutes longer per day in the winter, compared with controls.

Phase-delay hypothesis. Core body temperature is considered one of the most reliable markers of circadian rhythm. The nadir core body temperature occurs earlier than normal in a person whose circadian rhythm is “phase-advanced” and later than usual in those with “phase-delayed” circadian rhythms. Patients with seasonal affective symptoms generally reach their lowest body temperature of the day earlier than do controls.

Lewy et al,⁹ who proposed the phase-delay hypothesis, observed that melatonin secretion appeared to be delayed in patients with SAD. Some studies have supported this hypothesis, demonstrating greater benefit of bright light treatment when administered early in the morning than later in the day. Other studies, however, have shown benefit from light exposure late in the day.¹⁰

Reduced-amplitude hypothesis. SAD sufferers have dampened circadian rhythms, and bright light may increase the amplitude of the rhythms. There is little evidence for this hypothesis.

Melatonin hypothesis. Melatonin does not appear to cause depression. Looking at melatonin secretion patterns in conjunction with circadian phases, however, may offer new insights.⁸ Several studies have shown that manipulating the timing of melatonin secretion affects mood.

Cryptochrome, a photoreceptor in the retina, may be responsible for transmitting the photosignal to the elements of the circadian clock that regulate melatonin secretion. The pineal gland modifies its secretion of melatonin in response to the amount of light exposure (Box 3).^8,11

Light therapy

Bright light therapy has been supported by placebo-controlled trials and is first-line treatment for patients with SAD.¹ Bright light therapy is usually dosed at 2,500 lux for 2 hr/day or 10,000 lux for 30 min/day at eye level.¹² The best evidence supports administering light therapy in the morning, generally between 6 and 10 AM. As described by Terman,¹³ “larks”—people who go to bed early and get up early—need earlier light than “owls”—people who stay up later and sleep later.

Box 3

HOW SUNLIGHT MAY SET THE CIRCADIAN CLOCK

When light strikes the eye, it is well known that vitamin A-based photo pigments, cones, and rods receive the signal and transmit it via the optic tracts to the occipital cortex. But if light plays a role in the pathophysiology of seasonal affective disorder, how does light signal the other elements of the circadian system?

Cryptochrome, a photoreceptor in the retina, may be responsible for transmitting the photosignal to the circadian clock.¹¹ Cryptochrome is a vitamin B2-based pigment found in the ganglion cells and on cells in the inner nuclear layer of the retina. It is thought to transmit light through the optic nerve to the suprachiasmatic nucleus, the circadian pacemaker in the hypothalamus. The signal is then transmitted through the paraventricular nucleus, down the sympathetic chain, through the superior cervical ganglion, up the nervi canarii, to its final destination—the pineal gland.⁸ The pineal gland then modifies its secretion of melatonin in response to the amount of light exposure.

Although mammals have an intrinsic rhythmicity, the circadian clock must be entrained by exogenous light. The retinohypothalamic tract is believed to be the vehicle that sets the circadian clock. If the optic nerve is cut, a person becomes blind and unable to entrain the circadian rhythm.

Light therapy can be used alone or in addition to pharmacotherapy in patients whose previously wellcontrolled depressive symptoms worsen in the fall or winter. Light therapy also can be used as prophylaxis—starting in early fall—in patients with a history of a seasonal pattern of depression. Either way, light treatments generally should continue until early spring.

Given the relatively few side effects, light therapy may be used as monotherapy in patients with mild, subsyndromal mood symptoms occurring on a seasonal basis. Light therapy should not be used without pharmacotherapy to treat a full-blown major depressive episode.

Light boxes can be found via the Internet at an average cost of $180 to $300 for a 10,000-lux unit. The boxes are small enough to be placed on a table while the patient reads or eats breakfast. Artificial lights for this therapy do not emit ultraviolet rays, which have been associated with skin cancers.

Light visors also have shown some promise in SAD treatment, as demonstrated by a 2-week, randomized, controlled trial by Joffe et al.¹⁴ Compared with light boxes, light visors are more portable, so the patient can move around during treatment. Generally, the patient wears the visor 30 minutes in the morning.

Light visors appear to be as effective as table models, although no studies have compared the two devices. A visor costs $250 to $300.

Dawn simulation in SAD treatment has been examined in a few small studies and one placebo-controlled trial with 95 patients.¹⁰ In dawn simulation, a white light gradually increases between 4:30 and 6 AM to a peak intensity of 250 lux. Dawn simulation can be done while the patient is sleeping, whereas other light treatments require the patient to wake up early enough each morning to sit before a light box for 30 minutes. More study is needed to assess this modality’s efficacy.

Light therapy precautions. Review the patient’s medications before starting light therapy. Drugs that can magnify the effects of short wave-length light—leading to severe sunburns or rashes—include tetracycline, sulfonamides, and some older antipsychotics such as chlorpromazine. Some authors recommend an ophthalmologic examination before starting light therapy and every 2 to 3 years afterwards if no complications are apparent.¹ Others believe that no ophthalmologic examination is necessary unless the patient is older than 70 or has a history of retinal disease.

Side effects of bright light therapy are usually few and mild and include headaches, eye irritation, and nausea. In some anecdotal cases, patients with bipolar disorder appear to have switched from depression to mania upon starting light therapy,¹ but such switches appear to be rare. Still, patients with bipolar disorder and their family members should be advised to watch out for switches when using light therapy.

Pharmacologic therapy

Drug therapy in SAD has not been well studied, and many of the placebo-controlled trials that have examined this mode of treatment have been small. Serotonergic agents have been most studied because serotonin, with its effects on sleep and appetite, is thought to be related to SAD pathogenesis. The largest study of a selective serotonin reuptake inhibitor for SAD¹⁵ compared sertraline with placebo. Patients who received sertraline at a mean dosage of 111 mg/d had significantly fewer depressive symptoms than did the placebo group.

A placebo-controlled, double-blind study by Thorell¹⁶ found that adding citalopram to light therapy improved measures of depressed mood, compared with light therapy alone. This study is limited by small sample size but provides direction for further research.

An open trial of reboxetine—a noradrenaline reuptake inhibitor not available in the United States—suggests that further research of agents affecting catecholamines may be worthwhile in SAD treatment.¹⁷

Psychotherapy

Psychotherapy has not been researched sufficiently to be considered a proven treatment for SAD. However, some have observed that SAD patients have a negative cognitive style that may benefit from cognitive therapy. Thus, behavioral therapy may alter a patient’s response to light.¹

Related resources

• National Organization for Seasonal Affective Disorder www.nosad.org
• Dr. Ivan’s (Ivan Goldberg, MD) Depression Central www.psycom.net/depression.central.seasonal.html
• Columbia/Presbyterian Hospital Program in Clinical Chronobiology www.light-and-iontherapy.org

Drug brand names

• Citalopram • Celexa
• Sertraline • Zoloft

Disclosure

Dr. Paradies reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Dr. Hillard reports that he is a consultant to Pfizer Inc. and Janssen Pharmaceutica, and serves on the speakers bureau of Pfizer Inc., Janssen Pharmaceutica, and Eli Lilly and Co.

All of us see patients whose recurrent depressions seem to have a seasonal component. Should we treat them differently than patients whose recurrent depressions are not related to seasons? Is there adequate evidence for the existence of seasonal affective disorder (SAD), or—as it is called in DSM-IV-TR—mood disorder with a seasonal pattern? Is bright light therapy supported by the literature, or is it just some sort of fad?

As December brings the shortest days of the year, we shine the spotlight on SAD and examine the latest evidence on its causes, diagnosis, and treatment.

Moods with a seasonal rhythm

Moods have been observed to change with the seasons since ancient times (Box 1).¹ As recently as 25 years ago, however, seasonal affective disorder was not recognized as a psychiatric diagnosis.

In the early 1980s, when researchers at the National Institute of Mental Health (NIMH) were studying the effect of bright light on melatonin secretion, they were contacted by Herbert E. Kern, a research engineer who suffered from recurrent depression. A methodical person, Kern had kept a journal of his mood variations and noticed a pattern that appeared to follow the seasons. His depression worsened in the fall and winter and improved in the spring and summer. Kern subsequently participated in an NIMH trial with phototherapy, his mood improved, and the results were published in 1982.²

Box 1

Two years later, the researchers published the first paper that described SAD as a psychiatric diagnosis.³ Criteria for the diagnosis included:

• presence of a major affective disorder
• affective episodes occurring during fall or winter and remitting in spring or summer for at least 2 consecutive years.

The paper also discussed treatment of winter depression with phototherapy.

DSM-IV-TR describes SAD as a course specifier for mood disorders, including major depressive episodes in bipolar I and II disorders and major depressive disorder (Box 2). In other words, as used in DSM-IV-TR and this article, SAD is not an independent disorder but a type of major affective disorder.

Characteristics of SAD

Symptoms. Patients with SAD suffer the typical symptoms of depression—decreased energy, guilt, and decreased libido—as well as atypical symptoms—carbohydrate craving, hypersomnia, and weight gain. They also appear less likely to exhibit psychotic symptoms and may be at lower risk for suicide than persons with major mood disorders but without SAD.¹

Changes in sleep patterns also have been observed. Rosenthal et al⁴ found increased sleep latency and increased total sleep time in patients with SAD. Delta or slow-wave sleep—the restorative part of the sleep cycle—decreased by nearly one-half (mean 46%). REM latency did not change, contrary to typical findings in depressed patients. Anderson et al⁵ also reported no change in REM latency in patients with SAD.

Comorbid conditions. Eating disorders—particularly bulimia nervosa—are more prevalent in patients with SAD.¹ Binge eating tends to worsen in the fall and winter.

Personality disorders are also common in these patients, with cluster C over-represented. Avoidant personality disorder is most common. In a sample of 45 patients with SAD, Reichborn-Kjennerud et al⁶ found any personality disorder in 58% and avoidant personality disorder in 31%. Patients with comorbid personality disorders were less likely to respond to bright light therapy.

Prevalence. The prevalence of SAD in North America is approximately 1 to 6 %, with four times as many women affected as men.¹ Data on the effect of latitude on prevalence of SAD are inconclusive.⁷

Making the diagnosis

For patients with depression, clinicians should ask about seasonality of symptoms. Onset of major depressive symptoms in the fall or winter for at least two consecutive years or remission of depressive symptoms in the spring for two consecutive years (without onset of depressive syndromes during the spring or summer) probably merits a diagnosis of SAD. The diagnosis is confirmed if seasonal patterns of depressive symptoms substantially outnumber nonseasonal occurrences over the patient’s lifetime. The diagnosis may not be appropriate if there are obvious seasonal psychosocial stressors, such as anniversary reactions in posttraumatic stress disorder.

Some patients have sub-syndromal depressive symptoms that occur seasonally. DSM-IV would probably classify them as “mood disorder, not otherwise specified,” and that group has not been studied extensively.

Box 2

What causes SAD?

Research is ongoing, but the cause of SAD is not yet fully understood, although hypotheses have been developed. The four main hypotheses relate to duration of sunlight, changes in the circadian cycle, and secretion of the “hormone of darkness,” melatonin.

Photoperiod hypothesis. The shortening of the photoperiod—duration of sunlight—during autumn and winter may explain winter depression. Some research suggests that patients with SAD have an exaggerated melatonin response to shorter days and longer nights. For example, Wehr et al⁸ found that SAD patients secrete melatonin approximately 30 minutes longer per day in the winter, compared with controls.

Phase-delay hypothesis. Core body temperature is considered one of the most reliable markers of circadian rhythm. The nadir core body temperature occurs earlier than normal in a person whose circadian rhythm is “phase-advanced” and later than usual in those with “phase-delayed” circadian rhythms. Patients with seasonal affective symptoms generally reach their lowest body temperature of the day earlier than do controls.

Lewy et al,⁹ who proposed the phase-delay hypothesis, observed that melatonin secretion appeared to be delayed in patients with SAD. Some studies have supported this hypothesis, demonstrating greater benefit of bright light treatment when administered early in the morning than later in the day. Other studies, however, have shown benefit from light exposure late in the day.¹⁰

Reduced-amplitude hypothesis. SAD sufferers have dampened circadian rhythms, and bright light may increase the amplitude of the rhythms. There is little evidence for this hypothesis.

Melatonin hypothesis. Melatonin does not appear to cause depression. Looking at melatonin secretion patterns in conjunction with circadian phases, however, may offer new insights.⁸ Several studies have shown that manipulating the timing of melatonin secretion affects mood.

Cryptochrome, a photoreceptor in the retina, may be responsible for transmitting the photosignal to the elements of the circadian clock that regulate melatonin secretion. The pineal gland modifies its secretion of melatonin in response to the amount of light exposure (Box 3).^8,11

Light therapy

Bright light therapy has been supported by placebo-controlled trials and is first-line treatment for patients with SAD.¹ Bright light therapy is usually dosed at 2,500 lux for 2 hr/day or 10,000 lux for 30 min/day at eye level.¹² The best evidence supports administering light therapy in the morning, generally between 6 and 10 AM. As described by Terman,¹³ “larks”—people who go to bed early and get up early—need earlier light than “owls”—people who stay up later and sleep later.

Box 3

HOW SUNLIGHT MAY SET THE CIRCADIAN CLOCK

When light strikes the eye, it is well known that vitamin A-based photo pigments, cones, and rods receive the signal and transmit it via the optic tracts to the occipital cortex. But if light plays a role in the pathophysiology of seasonal affective disorder, how does light signal the other elements of the circadian system?

Cryptochrome, a photoreceptor in the retina, may be responsible for transmitting the photosignal to the circadian clock.¹¹ Cryptochrome is a vitamin B2-based pigment found in the ganglion cells and on cells in the inner nuclear layer of the retina. It is thought to transmit light through the optic nerve to the suprachiasmatic nucleus, the circadian pacemaker in the hypothalamus. The signal is then transmitted through the paraventricular nucleus, down the sympathetic chain, through the superior cervical ganglion, up the nervi canarii, to its final destination—the pineal gland.⁸ The pineal gland then modifies its secretion of melatonin in response to the amount of light exposure.

Although mammals have an intrinsic rhythmicity, the circadian clock must be entrained by exogenous light. The retinohypothalamic tract is believed to be the vehicle that sets the circadian clock. If the optic nerve is cut, a person becomes blind and unable to entrain the circadian rhythm.

Light therapy can be used alone or in addition to pharmacotherapy in patients whose previously wellcontrolled depressive symptoms worsen in the fall or winter. Light therapy also can be used as prophylaxis—starting in early fall—in patients with a history of a seasonal pattern of depression. Either way, light treatments generally should continue until early spring.

Given the relatively few side effects, light therapy may be used as monotherapy in patients with mild, subsyndromal mood symptoms occurring on a seasonal basis. Light therapy should not be used without pharmacotherapy to treat a full-blown major depressive episode.

Light boxes can be found via the Internet at an average cost of $180 to $300 for a 10,000-lux unit. The boxes are small enough to be placed on a table while the patient reads or eats breakfast. Artificial lights for this therapy do not emit ultraviolet rays, which have been associated with skin cancers.

Light visors also have shown some promise in SAD treatment, as demonstrated by a 2-week, randomized, controlled trial by Joffe et al.¹⁴ Compared with light boxes, light visors are more portable, so the patient can move around during treatment. Generally, the patient wears the visor 30 minutes in the morning.

Light visors appear to be as effective as table models, although no studies have compared the two devices. A visor costs $250 to $300.

Dawn simulation in SAD treatment has been examined in a few small studies and one placebo-controlled trial with 95 patients.¹⁰ In dawn simulation, a white light gradually increases between 4:30 and 6 AM to a peak intensity of 250 lux. Dawn simulation can be done while the patient is sleeping, whereas other light treatments require the patient to wake up early enough each morning to sit before a light box for 30 minutes. More study is needed to assess this modality’s efficacy.

Light therapy precautions. Review the patient’s medications before starting light therapy. Drugs that can magnify the effects of short wave-length light—leading to severe sunburns or rashes—include tetracycline, sulfonamides, and some older antipsychotics such as chlorpromazine. Some authors recommend an ophthalmologic examination before starting light therapy and every 2 to 3 years afterwards if no complications are apparent.¹ Others believe that no ophthalmologic examination is necessary unless the patient is older than 70 or has a history of retinal disease.

Side effects of bright light therapy are usually few and mild and include headaches, eye irritation, and nausea. In some anecdotal cases, patients with bipolar disorder appear to have switched from depression to mania upon starting light therapy,¹ but such switches appear to be rare. Still, patients with bipolar disorder and their family members should be advised to watch out for switches when using light therapy.

Pharmacologic therapy

Drug therapy in SAD has not been well studied, and many of the placebo-controlled trials that have examined this mode of treatment have been small. Serotonergic agents have been most studied because serotonin, with its effects on sleep and appetite, is thought to be related to SAD pathogenesis. The largest study of a selective serotonin reuptake inhibitor for SAD¹⁵ compared sertraline with placebo. Patients who received sertraline at a mean dosage of 111 mg/d had significantly fewer depressive symptoms than did the placebo group.

A placebo-controlled, double-blind study by Thorell¹⁶ found that adding citalopram to light therapy improved measures of depressed mood, compared with light therapy alone. This study is limited by small sample size but provides direction for further research.

An open trial of reboxetine—a noradrenaline reuptake inhibitor not available in the United States—suggests that further research of agents affecting catecholamines may be worthwhile in SAD treatment.¹⁷

Psychotherapy

Psychotherapy has not been researched sufficiently to be considered a proven treatment for SAD. However, some have observed that SAD patients have a negative cognitive style that may benefit from cognitive therapy. Thus, behavioral therapy may alter a patient’s response to light.¹

Related resources

• National Organization for Seasonal Affective Disorder www.nosad.org
• Dr. Ivan’s (Ivan Goldberg, MD) Depression Central www.psycom.net/depression.central.seasonal.html
• Columbia/Presbyterian Hospital Program in Clinical Chronobiology www.light-and-iontherapy.org

Drug brand names

• Citalopram • Celexa
• Sertraline • Zoloft

Disclosure

Dr. Paradies reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Dr. Hillard reports that he is a consultant to Pfizer Inc. and Janssen Pharmaceutica, and serves on the speakers bureau of Pfizer Inc., Janssen Pharmaceutica, and Eli Lilly and Co.

All of us see patients whose recurrent depressions seem to have a seasonal component. Should we treat them differently than patients whose recurrent depressions are not related to seasons? Is there adequate evidence for the existence of seasonal affective disorder (SAD), or—as it is called in DSM-IV-TR—mood disorder with a seasonal pattern? Is bright light therapy supported by the literature, or is it just some sort of fad?

As December brings the shortest days of the year, we shine the spotlight on SAD and examine the latest evidence on its causes, diagnosis, and treatment.

Moods with a seasonal rhythm

Moods have been observed to change with the seasons since ancient times (Box 1).¹ As recently as 25 years ago, however, seasonal affective disorder was not recognized as a psychiatric diagnosis.

In the early 1980s, when researchers at the National Institute of Mental Health (NIMH) were studying the effect of bright light on melatonin secretion, they were contacted by Herbert E. Kern, a research engineer who suffered from recurrent depression. A methodical person, Kern had kept a journal of his mood variations and noticed a pattern that appeared to follow the seasons. His depression worsened in the fall and winter and improved in the spring and summer. Kern subsequently participated in an NIMH trial with phototherapy, his mood improved, and the results were published in 1982.²

Box 1

Two years later, the researchers published the first paper that described SAD as a psychiatric diagnosis.³ Criteria for the diagnosis included:

• presence of a major affective disorder
• affective episodes occurring during fall or winter and remitting in spring or summer for at least 2 consecutive years.

The paper also discussed treatment of winter depression with phototherapy.

DSM-IV-TR describes SAD as a course specifier for mood disorders, including major depressive episodes in bipolar I and II disorders and major depressive disorder (Box 2). In other words, as used in DSM-IV-TR and this article, SAD is not an independent disorder but a type of major affective disorder.

Characteristics of SAD

Symptoms. Patients with SAD suffer the typical symptoms of depression—decreased energy, guilt, and decreased libido—as well as atypical symptoms—carbohydrate craving, hypersomnia, and weight gain. They also appear less likely to exhibit psychotic symptoms and may be at lower risk for suicide than persons with major mood disorders but without SAD.¹

Changes in sleep patterns also have been observed. Rosenthal et al⁴ found increased sleep latency and increased total sleep time in patients with SAD. Delta or slow-wave sleep—the restorative part of the sleep cycle—decreased by nearly one-half (mean 46%). REM latency did not change, contrary to typical findings in depressed patients. Anderson et al⁵ also reported no change in REM latency in patients with SAD.

Comorbid conditions. Eating disorders—particularly bulimia nervosa—are more prevalent in patients with SAD.¹ Binge eating tends to worsen in the fall and winter.

Personality disorders are also common in these patients, with cluster C over-represented. Avoidant personality disorder is most common. In a sample of 45 patients with SAD, Reichborn-Kjennerud et al⁶ found any personality disorder in 58% and avoidant personality disorder in 31%. Patients with comorbid personality disorders were less likely to respond to bright light therapy.

Prevalence. The prevalence of SAD in North America is approximately 1 to 6 %, with four times as many women affected as men.¹ Data on the effect of latitude on prevalence of SAD are inconclusive.⁷

Making the diagnosis

For patients with depression, clinicians should ask about seasonality of symptoms. Onset of major depressive symptoms in the fall or winter for at least two consecutive years or remission of depressive symptoms in the spring for two consecutive years (without onset of depressive syndromes during the spring or summer) probably merits a diagnosis of SAD. The diagnosis is confirmed if seasonal patterns of depressive symptoms substantially outnumber nonseasonal occurrences over the patient’s lifetime. The diagnosis may not be appropriate if there are obvious seasonal psychosocial stressors, such as anniversary reactions in posttraumatic stress disorder.

Some patients have sub-syndromal depressive symptoms that occur seasonally. DSM-IV would probably classify them as “mood disorder, not otherwise specified,” and that group has not been studied extensively.

Box 2

What causes SAD?

Research is ongoing, but the cause of SAD is not yet fully understood, although hypotheses have been developed. The four main hypotheses relate to duration of sunlight, changes in the circadian cycle, and secretion of the “hormone of darkness,” melatonin.

Photoperiod hypothesis. The shortening of the photoperiod—duration of sunlight—during autumn and winter may explain winter depression. Some research suggests that patients with SAD have an exaggerated melatonin response to shorter days and longer nights. For example, Wehr et al⁸ found that SAD patients secrete melatonin approximately 30 minutes longer per day in the winter, compared with controls.

Phase-delay hypothesis. Core body temperature is considered one of the most reliable markers of circadian rhythm. The nadir core body temperature occurs earlier than normal in a person whose circadian rhythm is “phase-advanced” and later than usual in those with “phase-delayed” circadian rhythms. Patients with seasonal affective symptoms generally reach their lowest body temperature of the day earlier than do controls.

Lewy et al,⁹ who proposed the phase-delay hypothesis, observed that melatonin secretion appeared to be delayed in patients with SAD. Some studies have supported this hypothesis, demonstrating greater benefit of bright light treatment when administered early in the morning than later in the day. Other studies, however, have shown benefit from light exposure late in the day.¹⁰

Reduced-amplitude hypothesis. SAD sufferers have dampened circadian rhythms, and bright light may increase the amplitude of the rhythms. There is little evidence for this hypothesis.

Melatonin hypothesis. Melatonin does not appear to cause depression. Looking at melatonin secretion patterns in conjunction with circadian phases, however, may offer new insights.⁸ Several studies have shown that manipulating the timing of melatonin secretion affects mood.

Cryptochrome, a photoreceptor in the retina, may be responsible for transmitting the photosignal to the elements of the circadian clock that regulate melatonin secretion. The pineal gland modifies its secretion of melatonin in response to the amount of light exposure (Box 3).^8,11

Light therapy

Bright light therapy has been supported by placebo-controlled trials and is first-line treatment for patients with SAD.¹ Bright light therapy is usually dosed at 2,500 lux for 2 hr/day or 10,000 lux for 30 min/day at eye level.¹² The best evidence supports administering light therapy in the morning, generally between 6 and 10 AM. As described by Terman,¹³ “larks”—people who go to bed early and get up early—need earlier light than “owls”—people who stay up later and sleep later.

Box 3

HOW SUNLIGHT MAY SET THE CIRCADIAN CLOCK

When light strikes the eye, it is well known that vitamin A-based photo pigments, cones, and rods receive the signal and transmit it via the optic tracts to the occipital cortex. But if light plays a role in the pathophysiology of seasonal affective disorder, how does light signal the other elements of the circadian system?

Cryptochrome, a photoreceptor in the retina, may be responsible for transmitting the photosignal to the circadian clock.¹¹ Cryptochrome is a vitamin B2-based pigment found in the ganglion cells and on cells in the inner nuclear layer of the retina. It is thought to transmit light through the optic nerve to the suprachiasmatic nucleus, the circadian pacemaker in the hypothalamus. The signal is then transmitted through the paraventricular nucleus, down the sympathetic chain, through the superior cervical ganglion, up the nervi canarii, to its final destination—the pineal gland.⁸ The pineal gland then modifies its secretion of melatonin in response to the amount of light exposure.

Although mammals have an intrinsic rhythmicity, the circadian clock must be entrained by exogenous light. The retinohypothalamic tract is believed to be the vehicle that sets the circadian clock. If the optic nerve is cut, a person becomes blind and unable to entrain the circadian rhythm.

Light therapy can be used alone or in addition to pharmacotherapy in patients whose previously wellcontrolled depressive symptoms worsen in the fall or winter. Light therapy also can be used as prophylaxis—starting in early fall—in patients with a history of a seasonal pattern of depression. Either way, light treatments generally should continue until early spring.

Given the relatively few side effects, light therapy may be used as monotherapy in patients with mild, subsyndromal mood symptoms occurring on a seasonal basis. Light therapy should not be used without pharmacotherapy to treat a full-blown major depressive episode.

Light boxes can be found via the Internet at an average cost of $180 to $300 for a 10,000-lux unit. The boxes are small enough to be placed on a table while the patient reads or eats breakfast. Artificial lights for this therapy do not emit ultraviolet rays, which have been associated with skin cancers.

Light visors also have shown some promise in SAD treatment, as demonstrated by a 2-week, randomized, controlled trial by Joffe et al.¹⁴ Compared with light boxes, light visors are more portable, so the patient can move around during treatment. Generally, the patient wears the visor 30 minutes in the morning.

Light visors appear to be as effective as table models, although no studies have compared the two devices. A visor costs $250 to $300.

Dawn simulation in SAD treatment has been examined in a few small studies and one placebo-controlled trial with 95 patients.¹⁰ In dawn simulation, a white light gradually increases between 4:30 and 6 AM to a peak intensity of 250 lux. Dawn simulation can be done while the patient is sleeping, whereas other light treatments require the patient to wake up early enough each morning to sit before a light box for 30 minutes. More study is needed to assess this modality’s efficacy.

Light therapy precautions. Review the patient’s medications before starting light therapy. Drugs that can magnify the effects of short wave-length light—leading to severe sunburns or rashes—include tetracycline, sulfonamides, and some older antipsychotics such as chlorpromazine. Some authors recommend an ophthalmologic examination before starting light therapy and every 2 to 3 years afterwards if no complications are apparent.¹ Others believe that no ophthalmologic examination is necessary unless the patient is older than 70 or has a history of retinal disease.

Side effects of bright light therapy are usually few and mild and include headaches, eye irritation, and nausea. In some anecdotal cases, patients with bipolar disorder appear to have switched from depression to mania upon starting light therapy,¹ but such switches appear to be rare. Still, patients with bipolar disorder and their family members should be advised to watch out for switches when using light therapy.

Pharmacologic therapy

Drug therapy in SAD has not been well studied, and many of the placebo-controlled trials that have examined this mode of treatment have been small. Serotonergic agents have been most studied because serotonin, with its effects on sleep and appetite, is thought to be related to SAD pathogenesis. The largest study of a selective serotonin reuptake inhibitor for SAD¹⁵ compared sertraline with placebo. Patients who received sertraline at a mean dosage of 111 mg/d had significantly fewer depressive symptoms than did the placebo group.

A placebo-controlled, double-blind study by Thorell¹⁶ found that adding citalopram to light therapy improved measures of depressed mood, compared with light therapy alone. This study is limited by small sample size but provides direction for further research.

An open trial of reboxetine—a noradrenaline reuptake inhibitor not available in the United States—suggests that further research of agents affecting catecholamines may be worthwhile in SAD treatment.¹⁷

Psychotherapy

Psychotherapy has not been researched sufficiently to be considered a proven treatment for SAD. However, some have observed that SAD patients have a negative cognitive style that may benefit from cognitive therapy. Thus, behavioral therapy may alter a patient’s response to light.¹

Related resources

• National Organization for Seasonal Affective Disorder www.nosad.org
• Dr. Ivan’s (Ivan Goldberg, MD) Depression Central www.psycom.net/depression.central.seasonal.html
• Columbia/Presbyterian Hospital Program in Clinical Chronobiology www.light-and-iontherapy.org

Drug brand names

• Citalopram • Celexa
• Sertraline • Zoloft

Disclosure

Dr. Paradies reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Dr. Hillard reports that he is a consultant to Pfizer Inc. and Janssen Pharmaceutica, and serves on the speakers bureau of Pfizer Inc., Janssen Pharmaceutica, and Eli Lilly and Co.

All of us see patients whose recurrent depressions seem to have a seasonal component. Should we treat them differently than patients whose recurrent depressions are not related to seasons? Is there adequate evidence for the existence of seasonal affective disorder (SAD), or—as it is called in DSM-IV-TR—mood disorder with a seasonal pattern? Is bright light therapy supported by the literature, or is it just some sort of fad?

As December brings the shortest days of the year, we shine the spotlight on SAD and examine the latest evidence on its causes, diagnosis, and treatment.

Moods with a seasonal rhythm

Moods have been observed to change with the seasons since ancient times (Box 1).¹ As recently as 25 years ago, however, seasonal affective disorder was not recognized as a psychiatric diagnosis.

In the early 1980s, when researchers at the National Institute of Mental Health (NIMH) were studying the effect of bright light on melatonin secretion, they were contacted by Herbert E. Kern, a research engineer who suffered from recurrent depression. A methodical person, Kern had kept a journal of his mood variations and noticed a pattern that appeared to follow the seasons. His depression worsened in the fall and winter and improved in the spring and summer. Kern subsequently participated in an NIMH trial with phototherapy, his mood improved, and the results were published in 1982.²

Box 1

Two years later, the researchers published the first paper that described SAD as a psychiatric diagnosis.³ Criteria for the diagnosis included:

• presence of a major affective disorder
• affective episodes occurring during fall or winter and remitting in spring or summer for at least 2 consecutive years.

The paper also discussed treatment of winter depression with phototherapy.

DSM-IV-TR describes SAD as a course specifier for mood disorders, including major depressive episodes in bipolar I and II disorders and major depressive disorder (Box 2). In other words, as used in DSM-IV-TR and this article, SAD is not an independent disorder but a type of major affective disorder.

Characteristics of SAD

Symptoms. Patients with SAD suffer the typical symptoms of depression—decreased energy, guilt, and decreased libido—as well as atypical symptoms—carbohydrate craving, hypersomnia, and weight gain. They also appear less likely to exhibit psychotic symptoms and may be at lower risk for suicide than persons with major mood disorders but without SAD.¹

Changes in sleep patterns also have been observed. Rosenthal et al⁴ found increased sleep latency and increased total sleep time in patients with SAD. Delta or slow-wave sleep—the restorative part of the sleep cycle—decreased by nearly one-half (mean 46%). REM latency did not change, contrary to typical findings in depressed patients. Anderson et al⁵ also reported no change in REM latency in patients with SAD.

Comorbid conditions. Eating disorders—particularly bulimia nervosa—are more prevalent in patients with SAD.¹ Binge eating tends to worsen in the fall and winter.

Personality disorders are also common in these patients, with cluster C over-represented. Avoidant personality disorder is most common. In a sample of 45 patients with SAD, Reichborn-Kjennerud et al⁶ found any personality disorder in 58% and avoidant personality disorder in 31%. Patients with comorbid personality disorders were less likely to respond to bright light therapy.

Prevalence. The prevalence of SAD in North America is approximately 1 to 6 %, with four times as many women affected as men.¹ Data on the effect of latitude on prevalence of SAD are inconclusive.⁷

Making the diagnosis

For patients with depression, clinicians should ask about seasonality of symptoms. Onset of major depressive symptoms in the fall or winter for at least two consecutive years or remission of depressive symptoms in the spring for two consecutive years (without onset of depressive syndromes during the spring or summer) probably merits a diagnosis of SAD. The diagnosis is confirmed if seasonal patterns of depressive symptoms substantially outnumber nonseasonal occurrences over the patient’s lifetime. The diagnosis may not be appropriate if there are obvious seasonal psychosocial stressors, such as anniversary reactions in posttraumatic stress disorder.

Some patients have sub-syndromal depressive symptoms that occur seasonally. DSM-IV would probably classify them as “mood disorder, not otherwise specified,” and that group has not been studied extensively.

Box 2

What causes SAD?

Research is ongoing, but the cause of SAD is not yet fully understood, although hypotheses have been developed. The four main hypotheses relate to duration of sunlight, changes in the circadian cycle, and secretion of the “hormone of darkness,” melatonin.

Photoperiod hypothesis. The shortening of the photoperiod—duration of sunlight—during autumn and winter may explain winter depression. Some research suggests that patients with SAD have an exaggerated melatonin response to shorter days and longer nights. For example, Wehr et al⁸ found that SAD patients secrete melatonin approximately 30 minutes longer per day in the winter, compared with controls.

Phase-delay hypothesis. Core body temperature is considered one of the most reliable markers of circadian rhythm. The nadir core body temperature occurs earlier than normal in a person whose circadian rhythm is “phase-advanced” and later than usual in those with “phase-delayed” circadian rhythms. Patients with seasonal affective symptoms generally reach their lowest body temperature of the day earlier than do controls.

Lewy et al,⁹ who proposed the phase-delay hypothesis, observed that melatonin secretion appeared to be delayed in patients with SAD. Some studies have supported this hypothesis, demonstrating greater benefit of bright light treatment when administered early in the morning than later in the day. Other studies, however, have shown benefit from light exposure late in the day.¹⁰

Reduced-amplitude hypothesis. SAD sufferers have dampened circadian rhythms, and bright light may increase the amplitude of the rhythms. There is little evidence for this hypothesis.

Melatonin hypothesis. Melatonin does not appear to cause depression. Looking at melatonin secretion patterns in conjunction with circadian phases, however, may offer new insights.⁸ Several studies have shown that manipulating the timing of melatonin secretion affects mood.

Cryptochrome, a photoreceptor in the retina, may be responsible for transmitting the photosignal to the elements of the circadian clock that regulate melatonin secretion. The pineal gland modifies its secretion of melatonin in response to the amount of light exposure (Box 3).^8,11

Light therapy

Bright light therapy has been supported by placebo-controlled trials and is first-line treatment for patients with SAD.¹ Bright light therapy is usually dosed at 2,500 lux for 2 hr/day or 10,000 lux for 30 min/day at eye level.¹² The best evidence supports administering light therapy in the morning, generally between 6 and 10 AM. As described by Terman,¹³ “larks”—people who go to bed early and get up early—need earlier light than “owls”—people who stay up later and sleep later.

Box 3

HOW SUNLIGHT MAY SET THE CIRCADIAN CLOCK

When light strikes the eye, it is well known that vitamin A-based photo pigments, cones, and rods receive the signal and transmit it via the optic tracts to the occipital cortex. But if light plays a role in the pathophysiology of seasonal affective disorder, how does light signal the other elements of the circadian system?

Cryptochrome, a photoreceptor in the retina, may be responsible for transmitting the photosignal to the circadian clock.¹¹ Cryptochrome is a vitamin B2-based pigment found in the ganglion cells and on cells in the inner nuclear layer of the retina. It is thought to transmit light through the optic nerve to the suprachiasmatic nucleus, the circadian pacemaker in the hypothalamus. The signal is then transmitted through the paraventricular nucleus, down the sympathetic chain, through the superior cervical ganglion, up the nervi canarii, to its final destination—the pineal gland.⁸ The pineal gland then modifies its secretion of melatonin in response to the amount of light exposure.

Although mammals have an intrinsic rhythmicity, the circadian clock must be entrained by exogenous light. The retinohypothalamic tract is believed to be the vehicle that sets the circadian clock. If the optic nerve is cut, a person becomes blind and unable to entrain the circadian rhythm.

Light therapy can be used alone or in addition to pharmacotherapy in patients whose previously wellcontrolled depressive symptoms worsen in the fall or winter. Light therapy also can be used as prophylaxis—starting in early fall—in patients with a history of a seasonal pattern of depression. Either way, light treatments generally should continue until early spring.

Given the relatively few side effects, light therapy may be used as monotherapy in patients with mild, subsyndromal mood symptoms occurring on a seasonal basis. Light therapy should not be used without pharmacotherapy to treat a full-blown major depressive episode.

Light boxes can be found via the Internet at an average cost of $180 to $300 for a 10,000-lux unit. The boxes are small enough to be placed on a table while the patient reads or eats breakfast. Artificial lights for this therapy do not emit ultraviolet rays, which have been associated with skin cancers.

Light visors also have shown some promise in SAD treatment, as demonstrated by a 2-week, randomized, controlled trial by Joffe et al.¹⁴ Compared with light boxes, light visors are more portable, so the patient can move around during treatment. Generally, the patient wears the visor 30 minutes in the morning.

Light visors appear to be as effective as table models, although no studies have compared the two devices. A visor costs $250 to $300.

Dawn simulation in SAD treatment has been examined in a few small studies and one placebo-controlled trial with 95 patients.¹⁰ In dawn simulation, a white light gradually increases between 4:30 and 6 AM to a peak intensity of 250 lux. Dawn simulation can be done while the patient is sleeping, whereas other light treatments require the patient to wake up early enough each morning to sit before a light box for 30 minutes. More study is needed to assess this modality’s efficacy.

Light therapy precautions. Review the patient’s medications before starting light therapy. Drugs that can magnify the effects of short wave-length light—leading to severe sunburns or rashes—include tetracycline, sulfonamides, and some older antipsychotics such as chlorpromazine. Some authors recommend an ophthalmologic examination before starting light therapy and every 2 to 3 years afterwards if no complications are apparent.¹ Others believe that no ophthalmologic examination is necessary unless the patient is older than 70 or has a history of retinal disease.

Side effects of bright light therapy are usually few and mild and include headaches, eye irritation, and nausea. In some anecdotal cases, patients with bipolar disorder appear to have switched from depression to mania upon starting light therapy,¹ but such switches appear to be rare. Still, patients with bipolar disorder and their family members should be advised to watch out for switches when using light therapy.

Pharmacologic therapy

Drug therapy in SAD has not been well studied, and many of the placebo-controlled trials that have examined this mode of treatment have been small. Serotonergic agents have been most studied because serotonin, with its effects on sleep and appetite, is thought to be related to SAD pathogenesis. The largest study of a selective serotonin reuptake inhibitor for SAD¹⁵ compared sertraline with placebo. Patients who received sertraline at a mean dosage of 111 mg/d had significantly fewer depressive symptoms than did the placebo group.

A placebo-controlled, double-blind study by Thorell¹⁶ found that adding citalopram to light therapy improved measures of depressed mood, compared with light therapy alone. This study is limited by small sample size but provides direction for further research.

An open trial of reboxetine—a noradrenaline reuptake inhibitor not available in the United States—suggests that further research of agents affecting catecholamines may be worthwhile in SAD treatment.¹⁷

Psychotherapy

Psychotherapy has not been researched sufficiently to be considered a proven treatment for SAD. However, some have observed that SAD patients have a negative cognitive style that may benefit from cognitive therapy. Thus, behavioral therapy may alter a patient’s response to light.¹

Related resources

• National Organization for Seasonal Affective Disorder www.nosad.org
• Dr. Ivan’s (Ivan Goldberg, MD) Depression Central www.psycom.net/depression.central.seasonal.html
• Columbia/Presbyterian Hospital Program in Clinical Chronobiology www.light-and-iontherapy.org

Drug brand names

• Citalopram • Celexa
• Sertraline • Zoloft

Disclosure

Dr. Paradies reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Dr. Hillard reports that he is a consultant to Pfizer Inc. and Janssen Pharmaceutica, and serves on the speakers bureau of Pfizer Inc., Janssen Pharmaceutica, and Eli Lilly and Co.

All of us see patients whose recurrent depressions seem to have a seasonal component. Should we treat them differently than patients whose recurrent depressions are not related to seasons? Is there adequate evidence for the existence of seasonal affective disorder (SAD), or—as it is called in DSM-IV-TR—mood disorder with a seasonal pattern? Is bright light therapy supported by the literature, or is it just some sort of fad?

As December brings the shortest days of the year, we shine the spotlight on SAD and examine the latest evidence on its causes, diagnosis, and treatment.

Moods with a seasonal rhythm

Moods have been observed to change with the seasons since ancient times (Box 1).¹ As recently as 25 years ago, however, seasonal affective disorder was not recognized as a psychiatric diagnosis.

In the early 1980s, when researchers at the National Institute of Mental Health (NIMH) were studying the effect of bright light on melatonin secretion, they were contacted by Herbert E. Kern, a research engineer who suffered from recurrent depression. A methodical person, Kern had kept a journal of his mood variations and noticed a pattern that appeared to follow the seasons. His depression worsened in the fall and winter and improved in the spring and summer. Kern subsequently participated in an NIMH trial with phototherapy, his mood improved, and the results were published in 1982.²

Box 1

Two years later, the researchers published the first paper that described SAD as a psychiatric diagnosis.³ Criteria for the diagnosis included:

• presence of a major affective disorder
• affective episodes occurring during fall or winter and remitting in spring or summer for at least 2 consecutive years.

The paper also discussed treatment of winter depression with phototherapy.

DSM-IV-TR describes SAD as a course specifier for mood disorders, including major depressive episodes in bipolar I and II disorders and major depressive disorder (Box 2). In other words, as used in DSM-IV-TR and this article, SAD is not an independent disorder but a type of major affective disorder.

Characteristics of SAD

Symptoms. Patients with SAD suffer the typical symptoms of depression—decreased energy, guilt, and decreased libido—as well as atypical symptoms—carbohydrate craving, hypersomnia, and weight gain. They also appear less likely to exhibit psychotic symptoms and may be at lower risk for suicide than persons with major mood disorders but without SAD.¹

Changes in sleep patterns also have been observed. Rosenthal et al⁴ found increased sleep latency and increased total sleep time in patients with SAD. Delta or slow-wave sleep—the restorative part of the sleep cycle—decreased by nearly one-half (mean 46%). REM latency did not change, contrary to typical findings in depressed patients. Anderson et al⁵ also reported no change in REM latency in patients with SAD.

Comorbid conditions. Eating disorders—particularly bulimia nervosa—are more prevalent in patients with SAD.¹ Binge eating tends to worsen in the fall and winter.

Personality disorders are also common in these patients, with cluster C over-represented. Avoidant personality disorder is most common. In a sample of 45 patients with SAD, Reichborn-Kjennerud et al⁶ found any personality disorder in 58% and avoidant personality disorder in 31%. Patients with comorbid personality disorders were less likely to respond to bright light therapy.

Prevalence. The prevalence of SAD in North America is approximately 1 to 6 %, with four times as many women affected as men.¹ Data on the effect of latitude on prevalence of SAD are inconclusive.⁷

Making the diagnosis

For patients with depression, clinicians should ask about seasonality of symptoms. Onset of major depressive symptoms in the fall or winter for at least two consecutive years or remission of depressive symptoms in the spring for two consecutive years (without onset of depressive syndromes during the spring or summer) probably merits a diagnosis of SAD. The diagnosis is confirmed if seasonal patterns of depressive symptoms substantially outnumber nonseasonal occurrences over the patient’s lifetime. The diagnosis may not be appropriate if there are obvious seasonal psychosocial stressors, such as anniversary reactions in posttraumatic stress disorder.

Some patients have sub-syndromal depressive symptoms that occur seasonally. DSM-IV would probably classify them as “mood disorder, not otherwise specified,” and that group has not been studied extensively.

Box 2

What causes SAD?

Research is ongoing, but the cause of SAD is not yet fully understood, although hypotheses have been developed. The four main hypotheses relate to duration of sunlight, changes in the circadian cycle, and secretion of the “hormone of darkness,” melatonin.

Photoperiod hypothesis. The shortening of the photoperiod—duration of sunlight—during autumn and winter may explain winter depression. Some research suggests that patients with SAD have an exaggerated melatonin response to shorter days and longer nights. For example, Wehr et al⁸ found that SAD patients secrete melatonin approximately 30 minutes longer per day in the winter, compared with controls.

Phase-delay hypothesis. Core body temperature is considered one of the most reliable markers of circadian rhythm. The nadir core body temperature occurs earlier than normal in a person whose circadian rhythm is “phase-advanced” and later than usual in those with “phase-delayed” circadian rhythms. Patients with seasonal affective symptoms generally reach their lowest body temperature of the day earlier than do controls.

Lewy et al,⁹ who proposed the phase-delay hypothesis, observed that melatonin secretion appeared to be delayed in patients with SAD. Some studies have supported this hypothesis, demonstrating greater benefit of bright light treatment when administered early in the morning than later in the day. Other studies, however, have shown benefit from light exposure late in the day.¹⁰

Reduced-amplitude hypothesis. SAD sufferers have dampened circadian rhythms, and bright light may increase the amplitude of the rhythms. There is little evidence for this hypothesis.

Melatonin hypothesis. Melatonin does not appear to cause depression. Looking at melatonin secretion patterns in conjunction with circadian phases, however, may offer new insights.⁸ Several studies have shown that manipulating the timing of melatonin secretion affects mood.

Cryptochrome, a photoreceptor in the retina, may be responsible for transmitting the photosignal to the elements of the circadian clock that regulate melatonin secretion. The pineal gland modifies its secretion of melatonin in response to the amount of light exposure (Box 3).^8,11

Light therapy

Bright light therapy has been supported by placebo-controlled trials and is first-line treatment for patients with SAD.¹ Bright light therapy is usually dosed at 2,500 lux for 2 hr/day or 10,000 lux for 30 min/day at eye level.¹² The best evidence supports administering light therapy in the morning, generally between 6 and 10 AM. As described by Terman,¹³ “larks”—people who go to bed early and get up early—need earlier light than “owls”—people who stay up later and sleep later.

Box 3

HOW SUNLIGHT MAY SET THE CIRCADIAN CLOCK

When light strikes the eye, it is well known that vitamin A-based photo pigments, cones, and rods receive the signal and transmit it via the optic tracts to the occipital cortex. But if light plays a role in the pathophysiology of seasonal affective disorder, how does light signal the other elements of the circadian system?

Cryptochrome, a photoreceptor in the retina, may be responsible for transmitting the photosignal to the circadian clock.¹¹ Cryptochrome is a vitamin B2-based pigment found in the ganglion cells and on cells in the inner nuclear layer of the retina. It is thought to transmit light through the optic nerve to the suprachiasmatic nucleus, the circadian pacemaker in the hypothalamus. The signal is then transmitted through the paraventricular nucleus, down the sympathetic chain, through the superior cervical ganglion, up the nervi canarii, to its final destination—the pineal gland.⁸ The pineal gland then modifies its secretion of melatonin in response to the amount of light exposure.

Although mammals have an intrinsic rhythmicity, the circadian clock must be entrained by exogenous light. The retinohypothalamic tract is believed to be the vehicle that sets the circadian clock. If the optic nerve is cut, a person becomes blind and unable to entrain the circadian rhythm.

Light therapy can be used alone or in addition to pharmacotherapy in patients whose previously wellcontrolled depressive symptoms worsen in the fall or winter. Light therapy also can be used as prophylaxis—starting in early fall—in patients with a history of a seasonal pattern of depression. Either way, light treatments generally should continue until early spring.

Given the relatively few side effects, light therapy may be used as monotherapy in patients with mild, subsyndromal mood symptoms occurring on a seasonal basis. Light therapy should not be used without pharmacotherapy to treat a full-blown major depressive episode.

Light boxes can be found via the Internet at an average cost of $180 to $300 for a 10,000-lux unit. The boxes are small enough to be placed on a table while the patient reads or eats breakfast. Artificial lights for this therapy do not emit ultraviolet rays, which have been associated with skin cancers.

Light visors also have shown some promise in SAD treatment, as demonstrated by a 2-week, randomized, controlled trial by Joffe et al.¹⁴ Compared with light boxes, light visors are more portable, so the patient can move around during treatment. Generally, the patient wears the visor 30 minutes in the morning.

Light visors appear to be as effective as table models, although no studies have compared the two devices. A visor costs $250 to $300.

Dawn simulation in SAD treatment has been examined in a few small studies and one placebo-controlled trial with 95 patients.¹⁰ In dawn simulation, a white light gradually increases between 4:30 and 6 AM to a peak intensity of 250 lux. Dawn simulation can be done while the patient is sleeping, whereas other light treatments require the patient to wake up early enough each morning to sit before a light box for 30 minutes. More study is needed to assess this modality’s efficacy.

Light therapy precautions. Review the patient’s medications before starting light therapy. Drugs that can magnify the effects of short wave-length light—leading to severe sunburns or rashes—include tetracycline, sulfonamides, and some older antipsychotics such as chlorpromazine. Some authors recommend an ophthalmologic examination before starting light therapy and every 2 to 3 years afterwards if no complications are apparent.¹ Others believe that no ophthalmologic examination is necessary unless the patient is older than 70 or has a history of retinal disease.

Side effects of bright light therapy are usually few and mild and include headaches, eye irritation, and nausea. In some anecdotal cases, patients with bipolar disorder appear to have switched from depression to mania upon starting light therapy,¹ but such switches appear to be rare. Still, patients with bipolar disorder and their family members should be advised to watch out for switches when using light therapy.

Pharmacologic therapy

Drug therapy in SAD has not been well studied, and many of the placebo-controlled trials that have examined this mode of treatment have been small. Serotonergic agents have been most studied because serotonin, with its effects on sleep and appetite, is thought to be related to SAD pathogenesis. The largest study of a selective serotonin reuptake inhibitor for SAD¹⁵ compared sertraline with placebo. Patients who received sertraline at a mean dosage of 111 mg/d had significantly fewer depressive symptoms than did the placebo group.

A placebo-controlled, double-blind study by Thorell¹⁶ found that adding citalopram to light therapy improved measures of depressed mood, compared with light therapy alone. This study is limited by small sample size but provides direction for further research.

An open trial of reboxetine—a noradrenaline reuptake inhibitor not available in the United States—suggests that further research of agents affecting catecholamines may be worthwhile in SAD treatment.¹⁷

Psychotherapy

Psychotherapy has not been researched sufficiently to be considered a proven treatment for SAD. However, some have observed that SAD patients have a negative cognitive style that may benefit from cognitive therapy. Thus, behavioral therapy may alter a patient’s response to light.¹

Related resources

• National Organization for Seasonal Affective Disorder www.nosad.org
• Dr. Ivan’s (Ivan Goldberg, MD) Depression Central www.psycom.net/depression.central.seasonal.html
• Columbia/Presbyterian Hospital Program in Clinical Chronobiology www.light-and-iontherapy.org

Drug brand names

• Citalopram • Celexa
• Sertraline • Zoloft

Disclosure

Dr. Paradies reports no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Dr. Hillard reports that he is a consultant to Pfizer Inc. and Janssen Pharmaceutica, and serves on the speakers bureau of Pfizer Inc., Janssen Pharmaceutica, and Eli Lilly and Co.

December is a month of celebrations—Christmas, Hanukkah, Kwanzaa, and probably many others. While we’re in a festive mood, I would like to celebrate three events that have benefited our profession and our patients.

The resurgence of psychiatry

A few years ago, psychiatry was in a depression. Applications for psychiatric residencies were declining, longtime practitioners were retiring, and we all worried that there might not be jobs for us in the future. A large contingent of doomsayers predicted impending disaster because:

• New psychotropic agents (notably selective serotonin reuptake inhibitors) were so easy to use that all our patients’ psychopharmacology could be managed in primary care settings.
• The public had become convinced that various licensed and unlicensed therapists could do psychotherapy as well as we could.

These gloomy predictions have not materialized. Instead, new antidepressants and antipsychotics, new treatments for attention-deficit/hyperactivity disorder, new delivery systems, and new uses of existing agents have made prescribing not simpler but more complicated, while allowing us to help more people than ever before.

Psychopharmacologic advances have also led to increased use of combination therapy—both pharmacotherapy and psychotherapy—which research consistently shows is the most effective approach to most mental illnesses. This has led to greater demand for psychiatrists, with our training in both psychopharmacology and psychotherapy. And more people are seeking treatment for mental illnesses—rather than suffering in silence—as more effective treatments have become available and the stigma of “going to a psychiatrist” is fading.

Today we see increases in residency applications, salaries, and career opportunities in psychiatry. And those are all reasons to celebrate.

The repositioning of managed care

Managed care in the 1980s and ’90s—with its rationing through inconvenience, its view of mental health care as a commodity, discriminatory coverage, and the overriding of professional judgment—was demoralizing, Now, signs suggest that the balance of power is shifting back to providers. For example:

• Shares of stock in Magellan Behavioral Health, the national managed care company, were recently trading at less than 2 cents a share.
• The per diem paid by managed care is increasing 40% on Jan. 1 at University Hospital in Cincinnati, where I practice. When hospitals had empty beds, managed care could dictate rates. Now that beds are filled, hospitals have more leverage with managed care companies.

The launch of Current Psychiatry

With this our issue, the editors and staff of Current Psychiatry are celebrating our first full year in business. Judging by the hundreds of e-mails I have received and countless conversations I have had with readers since our launch in January, Current Psychiatry is helping psychiatrists keep pace with our rapidly changing field.

I want this journal to be relevant to psychiatry as it is really practiced. I invite you to continue telling me how Current Psychiatry can help you learn what you need to know. Now, pass the champagne!

December is a month of celebrations—Christmas, Hanukkah, Kwanzaa, and probably many others. While we’re in a festive mood, I would like to celebrate three events that have benefited our profession and our patients.

The resurgence of psychiatry

A few years ago, psychiatry was in a depression. Applications for psychiatric residencies were declining, longtime practitioners were retiring, and we all worried that there might not be jobs for us in the future. A large contingent of doomsayers predicted impending disaster because:

• New psychotropic agents (notably selective serotonin reuptake inhibitors) were so easy to use that all our patients’ psychopharmacology could be managed in primary care settings.
• The public had become convinced that various licensed and unlicensed therapists could do psychotherapy as well as we could.

These gloomy predictions have not materialized. Instead, new antidepressants and antipsychotics, new treatments for attention-deficit/hyperactivity disorder, new delivery systems, and new uses of existing agents have made prescribing not simpler but more complicated, while allowing us to help more people than ever before.

Psychopharmacologic advances have also led to increased use of combination therapy—both pharmacotherapy and psychotherapy—which research consistently shows is the most effective approach to most mental illnesses. This has led to greater demand for psychiatrists, with our training in both psychopharmacology and psychotherapy. And more people are seeking treatment for mental illnesses—rather than suffering in silence—as more effective treatments have become available and the stigma of “going to a psychiatrist” is fading.

Today we see increases in residency applications, salaries, and career opportunities in psychiatry. And those are all reasons to celebrate.

The repositioning of managed care

Managed care in the 1980s and ’90s—with its rationing through inconvenience, its view of mental health care as a commodity, discriminatory coverage, and the overriding of professional judgment—was demoralizing, Now, signs suggest that the balance of power is shifting back to providers. For example:

• Shares of stock in Magellan Behavioral Health, the national managed care company, were recently trading at less than 2 cents a share.
• The per diem paid by managed care is increasing 40% on Jan. 1 at University Hospital in Cincinnati, where I practice. When hospitals had empty beds, managed care could dictate rates. Now that beds are filled, hospitals have more leverage with managed care companies.

The launch of Current Psychiatry

With this our issue, the editors and staff of Current Psychiatry are celebrating our first full year in business. Judging by the hundreds of e-mails I have received and countless conversations I have had with readers since our launch in January, Current Psychiatry is helping psychiatrists keep pace with our rapidly changing field.

I want this journal to be relevant to psychiatry as it is really practiced. I invite you to continue telling me how Current Psychiatry can help you learn what you need to know. Now, pass the champagne!

December is a month of celebrations—Christmas, Hanukkah, Kwanzaa, and probably many others. While we’re in a festive mood, I would like to celebrate three events that have benefited our profession and our patients.

The resurgence of psychiatry

A few years ago, psychiatry was in a depression. Applications for psychiatric residencies were declining, longtime practitioners were retiring, and we all worried that there might not be jobs for us in the future. A large contingent of doomsayers predicted impending disaster because:

• New psychotropic agents (notably selective serotonin reuptake inhibitors) were so easy to use that all our patients’ psychopharmacology could be managed in primary care settings.
• The public had become convinced that various licensed and unlicensed therapists could do psychotherapy as well as we could.

These gloomy predictions have not materialized. Instead, new antidepressants and antipsychotics, new treatments for attention-deficit/hyperactivity disorder, new delivery systems, and new uses of existing agents have made prescribing not simpler but more complicated, while allowing us to help more people than ever before.

Psychopharmacologic advances have also led to increased use of combination therapy—both pharmacotherapy and psychotherapy—which research consistently shows is the most effective approach to most mental illnesses. This has led to greater demand for psychiatrists, with our training in both psychopharmacology and psychotherapy. And more people are seeking treatment for mental illnesses—rather than suffering in silence—as more effective treatments have become available and the stigma of “going to a psychiatrist” is fading.

Today we see increases in residency applications, salaries, and career opportunities in psychiatry. And those are all reasons to celebrate.

The repositioning of managed care

Managed care in the 1980s and ’90s—with its rationing through inconvenience, its view of mental health care as a commodity, discriminatory coverage, and the overriding of professional judgment—was demoralizing, Now, signs suggest that the balance of power is shifting back to providers. For example:

• Shares of stock in Magellan Behavioral Health, the national managed care company, were recently trading at less than 2 cents a share.
• The per diem paid by managed care is increasing 40% on Jan. 1 at University Hospital in Cincinnati, where I practice. When hospitals had empty beds, managed care could dictate rates. Now that beds are filled, hospitals have more leverage with managed care companies.

The launch of Current Psychiatry

With this our issue, the editors and staff of Current Psychiatry are celebrating our first full year in business. Judging by the hundreds of e-mails I have received and countless conversations I have had with readers since our launch in January, Current Psychiatry is helping psychiatrists keep pace with our rapidly changing field.

I want this journal to be relevant to psychiatry as it is really practiced. I invite you to continue telling me how Current Psychiatry can help you learn what you need to know. Now, pass the champagne!

December is a month of celebrations—Christmas, Hanukkah, Kwanzaa, and probably many others. While we’re in a festive mood, I would like to celebrate three events that have benefited our profession and our patients.

The resurgence of psychiatry

A few years ago, psychiatry was in a depression. Applications for psychiatric residencies were declining, longtime practitioners were retiring, and we all worried that there might not be jobs for us in the future. A large contingent of doomsayers predicted impending disaster because:

• New psychotropic agents (notably selective serotonin reuptake inhibitors) were so easy to use that all our patients’ psychopharmacology could be managed in primary care settings.
• The public had become convinced that various licensed and unlicensed therapists could do psychotherapy as well as we could.

These gloomy predictions have not materialized. Instead, new antidepressants and antipsychotics, new treatments for attention-deficit/hyperactivity disorder, new delivery systems, and new uses of existing agents have made prescribing not simpler but more complicated, while allowing us to help more people than ever before.

Psychopharmacologic advances have also led to increased use of combination therapy—both pharmacotherapy and psychotherapy—which research consistently shows is the most effective approach to most mental illnesses. This has led to greater demand for psychiatrists, with our training in both psychopharmacology and psychotherapy. And more people are seeking treatment for mental illnesses—rather than suffering in silence—as more effective treatments have become available and the stigma of “going to a psychiatrist” is fading.

Today we see increases in residency applications, salaries, and career opportunities in psychiatry. And those are all reasons to celebrate.

The repositioning of managed care

Managed care in the 1980s and ’90s—with its rationing through inconvenience, its view of mental health care as a commodity, discriminatory coverage, and the overriding of professional judgment—was demoralizing, Now, signs suggest that the balance of power is shifting back to providers. For example:

• Shares of stock in Magellan Behavioral Health, the national managed care company, were recently trading at less than 2 cents a share.
• The per diem paid by managed care is increasing 40% on Jan. 1 at University Hospital in Cincinnati, where I practice. When hospitals had empty beds, managed care could dictate rates. Now that beds are filled, hospitals have more leverage with managed care companies.

The launch of Current Psychiatry

With this our issue, the editors and staff of Current Psychiatry are celebrating our first full year in business. Judging by the hundreds of e-mails I have received and countless conversations I have had with readers since our launch in January, Current Psychiatry is helping psychiatrists keep pace with our rapidly changing field.

I want this journal to be relevant to psychiatry as it is really practiced. I invite you to continue telling me how Current Psychiatry can help you learn what you need to know. Now, pass the champagne!

December is a month of celebrations—Christmas, Hanukkah, Kwanzaa, and probably many others. While we’re in a festive mood, I would like to celebrate three events that have benefited our profession and our patients.

The resurgence of psychiatry

A few years ago, psychiatry was in a depression. Applications for psychiatric residencies were declining, longtime practitioners were retiring, and we all worried that there might not be jobs for us in the future. A large contingent of doomsayers predicted impending disaster because:

• New psychotropic agents (notably selective serotonin reuptake inhibitors) were so easy to use that all our patients’ psychopharmacology could be managed in primary care settings.
• The public had become convinced that various licensed and unlicensed therapists could do psychotherapy as well as we could.

These gloomy predictions have not materialized. Instead, new antidepressants and antipsychotics, new treatments for attention-deficit/hyperactivity disorder, new delivery systems, and new uses of existing agents have made prescribing not simpler but more complicated, while allowing us to help more people than ever before.

Psychopharmacologic advances have also led to increased use of combination therapy—both pharmacotherapy and psychotherapy—which research consistently shows is the most effective approach to most mental illnesses. This has led to greater demand for psychiatrists, with our training in both psychopharmacology and psychotherapy. And more people are seeking treatment for mental illnesses—rather than suffering in silence—as more effective treatments have become available and the stigma of “going to a psychiatrist” is fading.

Today we see increases in residency applications, salaries, and career opportunities in psychiatry. And those are all reasons to celebrate.

The repositioning of managed care

Managed care in the 1980s and ’90s—with its rationing through inconvenience, its view of mental health care as a commodity, discriminatory coverage, and the overriding of professional judgment—was demoralizing, Now, signs suggest that the balance of power is shifting back to providers. For example:

• Shares of stock in Magellan Behavioral Health, the national managed care company, were recently trading at less than 2 cents a share.
• The per diem paid by managed care is increasing 40% on Jan. 1 at University Hospital in Cincinnati, where I practice. When hospitals had empty beds, managed care could dictate rates. Now that beds are filled, hospitals have more leverage with managed care companies.

The launch of Current Psychiatry

With this our issue, the editors and staff of Current Psychiatry are celebrating our first full year in business. Judging by the hundreds of e-mails I have received and countless conversations I have had with readers since our launch in January, Current Psychiatry is helping psychiatrists keep pace with our rapidly changing field.

I want this journal to be relevant to psychiatry as it is really practiced. I invite you to continue telling me how Current Psychiatry can help you learn what you need to know. Now, pass the champagne!

December is a month of celebrations—Christmas, Hanukkah, Kwanzaa, and probably many others. While we’re in a festive mood, I would like to celebrate three events that have benefited our profession and our patients.

The resurgence of psychiatry

A few years ago, psychiatry was in a depression. Applications for psychiatric residencies were declining, longtime practitioners were retiring, and we all worried that there might not be jobs for us in the future. A large contingent of doomsayers predicted impending disaster because:

• New psychotropic agents (notably selective serotonin reuptake inhibitors) were so easy to use that all our patients’ psychopharmacology could be managed in primary care settings.
• The public had become convinced that various licensed and unlicensed therapists could do psychotherapy as well as we could.

These gloomy predictions have not materialized. Instead, new antidepressants and antipsychotics, new treatments for attention-deficit/hyperactivity disorder, new delivery systems, and new uses of existing agents have made prescribing not simpler but more complicated, while allowing us to help more people than ever before.

Psychopharmacologic advances have also led to increased use of combination therapy—both pharmacotherapy and psychotherapy—which research consistently shows is the most effective approach to most mental illnesses. This has led to greater demand for psychiatrists, with our training in both psychopharmacology and psychotherapy. And more people are seeking treatment for mental illnesses—rather than suffering in silence—as more effective treatments have become available and the stigma of “going to a psychiatrist” is fading.

Today we see increases in residency applications, salaries, and career opportunities in psychiatry. And those are all reasons to celebrate.

The repositioning of managed care

Managed care in the 1980s and ’90s—with its rationing through inconvenience, its view of mental health care as a commodity, discriminatory coverage, and the overriding of professional judgment—was demoralizing, Now, signs suggest that the balance of power is shifting back to providers. For example:

• Shares of stock in Magellan Behavioral Health, the national managed care company, were recently trading at less than 2 cents a share.
• The per diem paid by managed care is increasing 40% on Jan. 1 at University Hospital in Cincinnati, where I practice. When hospitals had empty beds, managed care could dictate rates. Now that beds are filled, hospitals have more leverage with managed care companies.

The launch of Current Psychiatry

With this our issue, the editors and staff of Current Psychiatry are celebrating our first full year in business. Judging by the hundreds of e-mails I have received and countless conversations I have had with readers since our launch in January, Current Psychiatry is helping psychiatrists keep pace with our rapidly changing field.

I want this journal to be relevant to psychiatry as it is really practiced. I invite you to continue telling me how Current Psychiatry can help you learn what you need to know. Now, pass the champagne!

Plaintiffs’ lawyers often try to get expert witnesses to acknowledge that “the Diagnostic and Statistical Manual of Mental Disorders is the psychiatrist’s bible, isn’t it, Doctor?” The correct answer is never to acknowledge that anything other than your professional experience and its integration with the literature is authoritative. Medicolegal considerations aside, however, DSM is more like psychiatry’s dictionary than its bible because it is revised every few years.

Fifty years ago—before the American Psychiatric Association and U.S. Public Health Service published DSM I in 1952—psychiatric diagnosis resembled 18th century English language orthography. Prior to Samuel Johnson’s dictionary in 1755, there was no standard spelling; you could spell words any way you felt like. Likewise, before DSM I, there were no standard psychiatric diagnoses.

DSM I was peculiar in many ways. For example, it used the word “reaction” in many diagnoses (e.g., “schizophrenic reaction”), reflecting the underlying assumption of William Menninger, MD, that psychiatric disorders were reactions to environmental stresses.

DSM II (1965) improved on DSM I by being better coordinated with the International Classification of Diseases and by eliminating the “reaction” part of most diagnoses. Unfortunately, it shared with DSM I a very low level of reliability. Each diagnosis included a description of a typical case, and clinicians tried to match patients to whatever diagnosis seemed most similar. Not surprisingly, two well-trained clinicians often could not agree on the diagnosis in any given case. For some diagnoses, psychiatrists showed no better agreement than would be expected by chance.

DSM III (1978) represented a fundamental change, with the now-familiar “check-list diagnoses” (e.g., the patient needs to exhibit five of the following eight symptoms). This approach greatly improved diagnostic reliability. On average, DSM III’s validity (the diagnosis corresponds to a meaningful underlying condition) was probably better, too. DSM III R (1987) and DSM IV (1994) have each tried to improve the diagnoses’ validity, as undoubtedly will DSM V (scheduled for release around 2010).

Several articles in this issue of Current Psychiatry deal with diagnoses we regularly make but that were not included in early DSM editions:

• Borderline personality disorder first appeared as a diagnostic category in DSM III. Kenneth Silk, MD, explains why the debate continues about this diagnosis—and whether it exists at all.
• Attention-deficit/hyperactivity disorder was not recognized as a diagnosis until DSM III, which seemed to include substance abuse as an exclusion criterion. In this issue, Edmund Higgins, MD, discusses antidepressant therapy for adults with both ADHD and substance abuse.
• Social phobia, discussed by Benjamin Yu, MD, et al, also was not legitimized until DSM III.

Other articles in this issue address areas of evolving knowledge. Dr. Pryor Baird’s paper on inducers of the hepatic enzyme cytochrome P-450 system explains this important prescribing problem in a way that I can understand and remember. Dr. Judy Sigmund’s article on pastoral counseling has finally let me understand what that phrase means.

As usual, Current Psychiatry has helped me keep up with our rapidly changing field. I look forward to reading this journal so much each month that if I did not receive it, I would probably develop a “psychoneurotic reaction.”

Plaintiffs’ lawyers often try to get expert witnesses to acknowledge that “the Diagnostic and Statistical Manual of Mental Disorders is the psychiatrist’s bible, isn’t it, Doctor?” The correct answer is never to acknowledge that anything other than your professional experience and its integration with the literature is authoritative. Medicolegal considerations aside, however, DSM is more like psychiatry’s dictionary than its bible because it is revised every few years.

Fifty years ago—before the American Psychiatric Association and U.S. Public Health Service published DSM I in 1952—psychiatric diagnosis resembled 18th century English language orthography. Prior to Samuel Johnson’s dictionary in 1755, there was no standard spelling; you could spell words any way you felt like. Likewise, before DSM I, there were no standard psychiatric diagnoses.

DSM I was peculiar in many ways. For example, it used the word “reaction” in many diagnoses (e.g., “schizophrenic reaction”), reflecting the underlying assumption of William Menninger, MD, that psychiatric disorders were reactions to environmental stresses.

DSM II (1965) improved on DSM I by being better coordinated with the International Classification of Diseases and by eliminating the “reaction” part of most diagnoses. Unfortunately, it shared with DSM I a very low level of reliability. Each diagnosis included a description of a typical case, and clinicians tried to match patients to whatever diagnosis seemed most similar. Not surprisingly, two well-trained clinicians often could not agree on the diagnosis in any given case. For some diagnoses, psychiatrists showed no better agreement than would be expected by chance.

DSM III (1978) represented a fundamental change, with the now-familiar “check-list diagnoses” (e.g., the patient needs to exhibit five of the following eight symptoms). This approach greatly improved diagnostic reliability. On average, DSM III’s validity (the diagnosis corresponds to a meaningful underlying condition) was probably better, too. DSM III R (1987) and DSM IV (1994) have each tried to improve the diagnoses’ validity, as undoubtedly will DSM V (scheduled for release around 2010).

Several articles in this issue of Current Psychiatry deal with diagnoses we regularly make but that were not included in early DSM editions:

• Borderline personality disorder first appeared as a diagnostic category in DSM III. Kenneth Silk, MD, explains why the debate continues about this diagnosis—and whether it exists at all.
• Attention-deficit/hyperactivity disorder was not recognized as a diagnosis until DSM III, which seemed to include substance abuse as an exclusion criterion. In this issue, Edmund Higgins, MD, discusses antidepressant therapy for adults with both ADHD and substance abuse.
• Social phobia, discussed by Benjamin Yu, MD, et al, also was not legitimized until DSM III.

Other articles in this issue address areas of evolving knowledge. Dr. Pryor Baird’s paper on inducers of the hepatic enzyme cytochrome P-450 system explains this important prescribing problem in a way that I can understand and remember. Dr. Judy Sigmund’s article on pastoral counseling has finally let me understand what that phrase means.

As usual, Current Psychiatry has helped me keep up with our rapidly changing field. I look forward to reading this journal so much each month that if I did not receive it, I would probably develop a “psychoneurotic reaction.”

Plaintiffs’ lawyers often try to get expert witnesses to acknowledge that “the Diagnostic and Statistical Manual of Mental Disorders is the psychiatrist’s bible, isn’t it, Doctor?” The correct answer is never to acknowledge that anything other than your professional experience and its integration with the literature is authoritative. Medicolegal considerations aside, however, DSM is more like psychiatry’s dictionary than its bible because it is revised every few years.

Fifty years ago—before the American Psychiatric Association and U.S. Public Health Service published DSM I in 1952—psychiatric diagnosis resembled 18th century English language orthography. Prior to Samuel Johnson’s dictionary in 1755, there was no standard spelling; you could spell words any way you felt like. Likewise, before DSM I, there were no standard psychiatric diagnoses.

DSM I was peculiar in many ways. For example, it used the word “reaction” in many diagnoses (e.g., “schizophrenic reaction”), reflecting the underlying assumption of William Menninger, MD, that psychiatric disorders were reactions to environmental stresses.

DSM II (1965) improved on DSM I by being better coordinated with the International Classification of Diseases and by eliminating the “reaction” part of most diagnoses. Unfortunately, it shared with DSM I a very low level of reliability. Each diagnosis included a description of a typical case, and clinicians tried to match patients to whatever diagnosis seemed most similar. Not surprisingly, two well-trained clinicians often could not agree on the diagnosis in any given case. For some diagnoses, psychiatrists showed no better agreement than would be expected by chance.

DSM III (1978) represented a fundamental change, with the now-familiar “check-list diagnoses” (e.g., the patient needs to exhibit five of the following eight symptoms). This approach greatly improved diagnostic reliability. On average, DSM III’s validity (the diagnosis corresponds to a meaningful underlying condition) was probably better, too. DSM III R (1987) and DSM IV (1994) have each tried to improve the diagnoses’ validity, as undoubtedly will DSM V (scheduled for release around 2010).

Several articles in this issue of Current Psychiatry deal with diagnoses we regularly make but that were not included in early DSM editions:

• Borderline personality disorder first appeared as a diagnostic category in DSM III. Kenneth Silk, MD, explains why the debate continues about this diagnosis—and whether it exists at all.
• Attention-deficit/hyperactivity disorder was not recognized as a diagnosis until DSM III, which seemed to include substance abuse as an exclusion criterion. In this issue, Edmund Higgins, MD, discusses antidepressant therapy for adults with both ADHD and substance abuse.
• Social phobia, discussed by Benjamin Yu, MD, et al, also was not legitimized until DSM III.

Other articles in this issue address areas of evolving knowledge. Dr. Pryor Baird’s paper on inducers of the hepatic enzyme cytochrome P-450 system explains this important prescribing problem in a way that I can understand and remember. Dr. Judy Sigmund’s article on pastoral counseling has finally let me understand what that phrase means.

As usual, Current Psychiatry has helped me keep up with our rapidly changing field. I look forward to reading this journal so much each month that if I did not receive it, I would probably develop a “psychoneurotic reaction.”

Plaintiffs’ lawyers often try to get expert witnesses to acknowledge that “the Diagnostic and Statistical Manual of Mental Disorders is the psychiatrist’s bible, isn’t it, Doctor?” The correct answer is never to acknowledge that anything other than your professional experience and its integration with the literature is authoritative. Medicolegal considerations aside, however, DSM is more like psychiatry’s dictionary than its bible because it is revised every few years.

Fifty years ago—before the American Psychiatric Association and U.S. Public Health Service published DSM I in 1952—psychiatric diagnosis resembled 18th century English language orthography. Prior to Samuel Johnson’s dictionary in 1755, there was no standard spelling; you could spell words any way you felt like. Likewise, before DSM I, there were no standard psychiatric diagnoses.

DSM I was peculiar in many ways. For example, it used the word “reaction” in many diagnoses (e.g., “schizophrenic reaction”), reflecting the underlying assumption of William Menninger, MD, that psychiatric disorders were reactions to environmental stresses.

DSM II (1965) improved on DSM I by being better coordinated with the International Classification of Diseases and by eliminating the “reaction” part of most diagnoses. Unfortunately, it shared with DSM I a very low level of reliability. Each diagnosis included a description of a typical case, and clinicians tried to match patients to whatever diagnosis seemed most similar. Not surprisingly, two well-trained clinicians often could not agree on the diagnosis in any given case. For some diagnoses, psychiatrists showed no better agreement than would be expected by chance.

DSM III (1978) represented a fundamental change, with the now-familiar “check-list diagnoses” (e.g., the patient needs to exhibit five of the following eight symptoms). This approach greatly improved diagnostic reliability. On average, DSM III’s validity (the diagnosis corresponds to a meaningful underlying condition) was probably better, too. DSM III R (1987) and DSM IV (1994) have each tried to improve the diagnoses’ validity, as undoubtedly will DSM V (scheduled for release around 2010).

Several articles in this issue of Current Psychiatry deal with diagnoses we regularly make but that were not included in early DSM editions:

• Borderline personality disorder first appeared as a diagnostic category in DSM III. Kenneth Silk, MD, explains why the debate continues about this diagnosis—and whether it exists at all.
• Attention-deficit/hyperactivity disorder was not recognized as a diagnosis until DSM III, which seemed to include substance abuse as an exclusion criterion. In this issue, Edmund Higgins, MD, discusses antidepressant therapy for adults with both ADHD and substance abuse.
• Social phobia, discussed by Benjamin Yu, MD, et al, also was not legitimized until DSM III.

Other articles in this issue address areas of evolving knowledge. Dr. Pryor Baird’s paper on inducers of the hepatic enzyme cytochrome P-450 system explains this important prescribing problem in a way that I can understand and remember. Dr. Judy Sigmund’s article on pastoral counseling has finally let me understand what that phrase means.

As usual, Current Psychiatry has helped me keep up with our rapidly changing field. I look forward to reading this journal so much each month that if I did not receive it, I would probably develop a “psychoneurotic reaction.”

Plaintiffs’ lawyers often try to get expert witnesses to acknowledge that “the Diagnostic and Statistical Manual of Mental Disorders is the psychiatrist’s bible, isn’t it, Doctor?” The correct answer is never to acknowledge that anything other than your professional experience and its integration with the literature is authoritative. Medicolegal considerations aside, however, DSM is more like psychiatry’s dictionary than its bible because it is revised every few years.

Fifty years ago—before the American Psychiatric Association and U.S. Public Health Service published DSM I in 1952—psychiatric diagnosis resembled 18th century English language orthography. Prior to Samuel Johnson’s dictionary in 1755, there was no standard spelling; you could spell words any way you felt like. Likewise, before DSM I, there were no standard psychiatric diagnoses.

DSM I was peculiar in many ways. For example, it used the word “reaction” in many diagnoses (e.g., “schizophrenic reaction”), reflecting the underlying assumption of William Menninger, MD, that psychiatric disorders were reactions to environmental stresses.

DSM II (1965) improved on DSM I by being better coordinated with the International Classification of Diseases and by eliminating the “reaction” part of most diagnoses. Unfortunately, it shared with DSM I a very low level of reliability. Each diagnosis included a description of a typical case, and clinicians tried to match patients to whatever diagnosis seemed most similar. Not surprisingly, two well-trained clinicians often could not agree on the diagnosis in any given case. For some diagnoses, psychiatrists showed no better agreement than would be expected by chance.

DSM III (1978) represented a fundamental change, with the now-familiar “check-list diagnoses” (e.g., the patient needs to exhibit five of the following eight symptoms). This approach greatly improved diagnostic reliability. On average, DSM III’s validity (the diagnosis corresponds to a meaningful underlying condition) was probably better, too. DSM III R (1987) and DSM IV (1994) have each tried to improve the diagnoses’ validity, as undoubtedly will DSM V (scheduled for release around 2010).

Several articles in this issue of Current Psychiatry deal with diagnoses we regularly make but that were not included in early DSM editions:

• Borderline personality disorder first appeared as a diagnostic category in DSM III. Kenneth Silk, MD, explains why the debate continues about this diagnosis—and whether it exists at all.
• Attention-deficit/hyperactivity disorder was not recognized as a diagnosis until DSM III, which seemed to include substance abuse as an exclusion criterion. In this issue, Edmund Higgins, MD, discusses antidepressant therapy for adults with both ADHD and substance abuse.
• Social phobia, discussed by Benjamin Yu, MD, et al, also was not legitimized until DSM III.

Other articles in this issue address areas of evolving knowledge. Dr. Pryor Baird’s paper on inducers of the hepatic enzyme cytochrome P-450 system explains this important prescribing problem in a way that I can understand and remember. Dr. Judy Sigmund’s article on pastoral counseling has finally let me understand what that phrase means.

As usual, Current Psychiatry has helped me keep up with our rapidly changing field. I look forward to reading this journal so much each month that if I did not receive it, I would probably develop a “psychoneurotic reaction.”

Plaintiffs’ lawyers often try to get expert witnesses to acknowledge that “the Diagnostic and Statistical Manual of Mental Disorders is the psychiatrist’s bible, isn’t it, Doctor?” The correct answer is never to acknowledge that anything other than your professional experience and its integration with the literature is authoritative. Medicolegal considerations aside, however, DSM is more like psychiatry’s dictionary than its bible because it is revised every few years.

Fifty years ago—before the American Psychiatric Association and U.S. Public Health Service published DSM I in 1952—psychiatric diagnosis resembled 18th century English language orthography. Prior to Samuel Johnson’s dictionary in 1755, there was no standard spelling; you could spell words any way you felt like. Likewise, before DSM I, there were no standard psychiatric diagnoses.

DSM I was peculiar in many ways. For example, it used the word “reaction” in many diagnoses (e.g., “schizophrenic reaction”), reflecting the underlying assumption of William Menninger, MD, that psychiatric disorders were reactions to environmental stresses.

DSM II (1965) improved on DSM I by being better coordinated with the International Classification of Diseases and by eliminating the “reaction” part of most diagnoses. Unfortunately, it shared with DSM I a very low level of reliability. Each diagnosis included a description of a typical case, and clinicians tried to match patients to whatever diagnosis seemed most similar. Not surprisingly, two well-trained clinicians often could not agree on the diagnosis in any given case. For some diagnoses, psychiatrists showed no better agreement than would be expected by chance.

DSM III (1978) represented a fundamental change, with the now-familiar “check-list diagnoses” (e.g., the patient needs to exhibit five of the following eight symptoms). This approach greatly improved diagnostic reliability. On average, DSM III’s validity (the diagnosis corresponds to a meaningful underlying condition) was probably better, too. DSM III R (1987) and DSM IV (1994) have each tried to improve the diagnoses’ validity, as undoubtedly will DSM V (scheduled for release around 2010).

Several articles in this issue of Current Psychiatry deal with diagnoses we regularly make but that were not included in early DSM editions:

• Borderline personality disorder first appeared as a diagnostic category in DSM III. Kenneth Silk, MD, explains why the debate continues about this diagnosis—and whether it exists at all.
• Attention-deficit/hyperactivity disorder was not recognized as a diagnosis until DSM III, which seemed to include substance abuse as an exclusion criterion. In this issue, Edmund Higgins, MD, discusses antidepressant therapy for adults with both ADHD and substance abuse.
• Social phobia, discussed by Benjamin Yu, MD, et al, also was not legitimized until DSM III.

Other articles in this issue address areas of evolving knowledge. Dr. Pryor Baird’s paper on inducers of the hepatic enzyme cytochrome P-450 system explains this important prescribing problem in a way that I can understand and remember. Dr. Judy Sigmund’s article on pastoral counseling has finally let me understand what that phrase means.

As usual, Current Psychiatry has helped me keep up with our rapidly changing field. I look forward to reading this journal so much each month that if I did not receive it, I would probably develop a “psychoneurotic reaction.”

Not long ago, psychiatrists were taught that adults had certain psychiatric diseases and diagnoses, and children had others. Some overlap was recognized, but it was thought to be minor. Mania, for example, was thought to be an adult disorder, and attention-deficit/hyper-activity disorder (ADHD) was for kids. When an adult presented with ADHD symptoms, we approached the diagnosis with caution. We wondered, “Is the patient just trying to get amphetamines?” When children were diagnosed with mania, we were skeptical. Could they just be overly spirited?

The misconceived separation of adult and child diagnoses developed in part because the people writing the diagnostic criteria were not the ones treating the most severely ill children. When I was in residency during the 1970s, we were discouraged from using the DSM to diagnose children. Instead, we used a set of pediatric diagnoses developed by the Group for Advancement of Psychiatry that did not translate readily into those used for adults.

In this issue, Michael Schwartz, MD, makes it clear that—yes—ADHD is a problem for many adults, but its treatment requires a different approach from that used in children. Likewise, Peter Buckley, MD, and colleagues confirm that psychotic disorders do occur in younger patients and explain how treating children and adolescents differs from treating adults. Looking to the future, Joseph DeVeaugh-Geiss, MD, previews new indications and compounds being developed specifically for psychiatric disorders in younger patients. His compilation of 21 medications in the pipeline tells me that child and adolescent psychopharmacology is poised for rapid growth.

As more effective medications and more reliable and valid diagnoses are developed for children, medication treatment should gain greater acceptance in child psychiatry. Many parents and some psychiatrists still resist the use of psychotropics in children, but that resistance is at odds with the latest findings.

Originally, our publisher did not plan to send Current Psychiatry to child and adolescent psychiatrists, as they are not surveyed by the service that rates medical journal readership (our “Nielsen ratings”). I suppose this means that the pharmaceutical industry, which buys journal advertising partly based on readership scores, does not believe that child psychiatrists prescribe many medications. Anyway, we are sending Current Psychiatry to pediatric psychiatrists, and I expect the rating system eventually will count them as “readers.” We certainly do.

I also recommend the discussion by Robert Forman, PhD, on how to guide patients to the 12-step programs that best meet their individual needs. Mutual hostility once characterized psychiatry’s relationship with 12-step programs. Today, most 12-step program leaders accept that medications have a place in managing mental and physical problems, and psychiatrists think of 12-step programs as another valuable treatment option.

Psychiatry keeps evolving, which allows us to help more people. That’s why I’m proud to be a psychiatrist. Current Psychiatry allows us to share all the changes in our profession, and that’s why I’m proud of this journal.

And, as always, we want to hear what you think. Write to Current Psychiatry at hillarjr@email.uc.edu.

Not long ago, psychiatrists were taught that adults had certain psychiatric diseases and diagnoses, and children had others. Some overlap was recognized, but it was thought to be minor. Mania, for example, was thought to be an adult disorder, and attention-deficit/hyper-activity disorder (ADHD) was for kids. When an adult presented with ADHD symptoms, we approached the diagnosis with caution. We wondered, “Is the patient just trying to get amphetamines?” When children were diagnosed with mania, we were skeptical. Could they just be overly spirited?

The misconceived separation of adult and child diagnoses developed in part because the people writing the diagnostic criteria were not the ones treating the most severely ill children. When I was in residency during the 1970s, we were discouraged from using the DSM to diagnose children. Instead, we used a set of pediatric diagnoses developed by the Group for Advancement of Psychiatry that did not translate readily into those used for adults.

In this issue, Michael Schwartz, MD, makes it clear that—yes—ADHD is a problem for many adults, but its treatment requires a different approach from that used in children. Likewise, Peter Buckley, MD, and colleagues confirm that psychotic disorders do occur in younger patients and explain how treating children and adolescents differs from treating adults. Looking to the future, Joseph DeVeaugh-Geiss, MD, previews new indications and compounds being developed specifically for psychiatric disorders in younger patients. His compilation of 21 medications in the pipeline tells me that child and adolescent psychopharmacology is poised for rapid growth.

As more effective medications and more reliable and valid diagnoses are developed for children, medication treatment should gain greater acceptance in child psychiatry. Many parents and some psychiatrists still resist the use of psychotropics in children, but that resistance is at odds with the latest findings.

Originally, our publisher did not plan to send Current Psychiatry to child and adolescent psychiatrists, as they are not surveyed by the service that rates medical journal readership (our “Nielsen ratings”). I suppose this means that the pharmaceutical industry, which buys journal advertising partly based on readership scores, does not believe that child psychiatrists prescribe many medications. Anyway, we are sending Current Psychiatry to pediatric psychiatrists, and I expect the rating system eventually will count them as “readers.” We certainly do.

I also recommend the discussion by Robert Forman, PhD, on how to guide patients to the 12-step programs that best meet their individual needs. Mutual hostility once characterized psychiatry’s relationship with 12-step programs. Today, most 12-step program leaders accept that medications have a place in managing mental and physical problems, and psychiatrists think of 12-step programs as another valuable treatment option.

Psychiatry keeps evolving, which allows us to help more people. That’s why I’m proud to be a psychiatrist. Current Psychiatry allows us to share all the changes in our profession, and that’s why I’m proud of this journal.

And, as always, we want to hear what you think. Write to Current Psychiatry at hillarjr@email.uc.edu.

Not long ago, psychiatrists were taught that adults had certain psychiatric diseases and diagnoses, and children had others. Some overlap was recognized, but it was thought to be minor. Mania, for example, was thought to be an adult disorder, and attention-deficit/hyper-activity disorder (ADHD) was for kids. When an adult presented with ADHD symptoms, we approached the diagnosis with caution. We wondered, “Is the patient just trying to get amphetamines?” When children were diagnosed with mania, we were skeptical. Could they just be overly spirited?

The misconceived separation of adult and child diagnoses developed in part because the people writing the diagnostic criteria were not the ones treating the most severely ill children. When I was in residency during the 1970s, we were discouraged from using the DSM to diagnose children. Instead, we used a set of pediatric diagnoses developed by the Group for Advancement of Psychiatry that did not translate readily into those used for adults.

In this issue, Michael Schwartz, MD, makes it clear that—yes—ADHD is a problem for many adults, but its treatment requires a different approach from that used in children. Likewise, Peter Buckley, MD, and colleagues confirm that psychotic disorders do occur in younger patients and explain how treating children and adolescents differs from treating adults. Looking to the future, Joseph DeVeaugh-Geiss, MD, previews new indications and compounds being developed specifically for psychiatric disorders in younger patients. His compilation of 21 medications in the pipeline tells me that child and adolescent psychopharmacology is poised for rapid growth.

As more effective medications and more reliable and valid diagnoses are developed for children, medication treatment should gain greater acceptance in child psychiatry. Many parents and some psychiatrists still resist the use of psychotropics in children, but that resistance is at odds with the latest findings.

Originally, our publisher did not plan to send Current Psychiatry to child and adolescent psychiatrists, as they are not surveyed by the service that rates medical journal readership (our “Nielsen ratings”). I suppose this means that the pharmaceutical industry, which buys journal advertising partly based on readership scores, does not believe that child psychiatrists prescribe many medications. Anyway, we are sending Current Psychiatry to pediatric psychiatrists, and I expect the rating system eventually will count them as “readers.” We certainly do.

I also recommend the discussion by Robert Forman, PhD, on how to guide patients to the 12-step programs that best meet their individual needs. Mutual hostility once characterized psychiatry’s relationship with 12-step programs. Today, most 12-step program leaders accept that medications have a place in managing mental and physical problems, and psychiatrists think of 12-step programs as another valuable treatment option.

Psychiatry keeps evolving, which allows us to help more people. That’s why I’m proud to be a psychiatrist. Current Psychiatry allows us to share all the changes in our profession, and that’s why I’m proud of this journal.

And, as always, we want to hear what you think. Write to Current Psychiatry at hillarjr@email.uc.edu.

Not long ago, psychiatrists were taught that adults had certain psychiatric diseases and diagnoses, and children had others. Some overlap was recognized, but it was thought to be minor. Mania, for example, was thought to be an adult disorder, and attention-deficit/hyper-activity disorder (ADHD) was for kids. When an adult presented with ADHD symptoms, we approached the diagnosis with caution. We wondered, “Is the patient just trying to get amphetamines?” When children were diagnosed with mania, we were skeptical. Could they just be overly spirited?

The misconceived separation of adult and child diagnoses developed in part because the people writing the diagnostic criteria were not the ones treating the most severely ill children. When I was in residency during the 1970s, we were discouraged from using the DSM to diagnose children. Instead, we used a set of pediatric diagnoses developed by the Group for Advancement of Psychiatry that did not translate readily into those used for adults.

In this issue, Michael Schwartz, MD, makes it clear that—yes—ADHD is a problem for many adults, but its treatment requires a different approach from that used in children. Likewise, Peter Buckley, MD, and colleagues confirm that psychotic disorders do occur in younger patients and explain how treating children and adolescents differs from treating adults. Looking to the future, Joseph DeVeaugh-Geiss, MD, previews new indications and compounds being developed specifically for psychiatric disorders in younger patients. His compilation of 21 medications in the pipeline tells me that child and adolescent psychopharmacology is poised for rapid growth.

As more effective medications and more reliable and valid diagnoses are developed for children, medication treatment should gain greater acceptance in child psychiatry. Many parents and some psychiatrists still resist the use of psychotropics in children, but that resistance is at odds with the latest findings.

Originally, our publisher did not plan to send Current Psychiatry to child and adolescent psychiatrists, as they are not surveyed by the service that rates medical journal readership (our “Nielsen ratings”). I suppose this means that the pharmaceutical industry, which buys journal advertising partly based on readership scores, does not believe that child psychiatrists prescribe many medications. Anyway, we are sending Current Psychiatry to pediatric psychiatrists, and I expect the rating system eventually will count them as “readers.” We certainly do.

I also recommend the discussion by Robert Forman, PhD, on how to guide patients to the 12-step programs that best meet their individual needs. Mutual hostility once characterized psychiatry’s relationship with 12-step programs. Today, most 12-step program leaders accept that medications have a place in managing mental and physical problems, and psychiatrists think of 12-step programs as another valuable treatment option.

Psychiatry keeps evolving, which allows us to help more people. That’s why I’m proud to be a psychiatrist. Current Psychiatry allows us to share all the changes in our profession, and that’s why I’m proud of this journal.

And, as always, we want to hear what you think. Write to Current Psychiatry at hillarjr@email.uc.edu.

Not long ago, psychiatrists were taught that adults had certain psychiatric diseases and diagnoses, and children had others. Some overlap was recognized, but it was thought to be minor. Mania, for example, was thought to be an adult disorder, and attention-deficit/hyper-activity disorder (ADHD) was for kids. When an adult presented with ADHD symptoms, we approached the diagnosis with caution. We wondered, “Is the patient just trying to get amphetamines?” When children were diagnosed with mania, we were skeptical. Could they just be overly spirited?

The misconceived separation of adult and child diagnoses developed in part because the people writing the diagnostic criteria were not the ones treating the most severely ill children. When I was in residency during the 1970s, we were discouraged from using the DSM to diagnose children. Instead, we used a set of pediatric diagnoses developed by the Group for Advancement of Psychiatry that did not translate readily into those used for adults.

In this issue, Michael Schwartz, MD, makes it clear that—yes—ADHD is a problem for many adults, but its treatment requires a different approach from that used in children. Likewise, Peter Buckley, MD, and colleagues confirm that psychotic disorders do occur in younger patients and explain how treating children and adolescents differs from treating adults. Looking to the future, Joseph DeVeaugh-Geiss, MD, previews new indications and compounds being developed specifically for psychiatric disorders in younger patients. His compilation of 21 medications in the pipeline tells me that child and adolescent psychopharmacology is poised for rapid growth.

As more effective medications and more reliable and valid diagnoses are developed for children, medication treatment should gain greater acceptance in child psychiatry. Many parents and some psychiatrists still resist the use of psychotropics in children, but that resistance is at odds with the latest findings.

Originally, our publisher did not plan to send Current Psychiatry to child and adolescent psychiatrists, as they are not surveyed by the service that rates medical journal readership (our “Nielsen ratings”). I suppose this means that the pharmaceutical industry, which buys journal advertising partly based on readership scores, does not believe that child psychiatrists prescribe many medications. Anyway, we are sending Current Psychiatry to pediatric psychiatrists, and I expect the rating system eventually will count them as “readers.” We certainly do.

I also recommend the discussion by Robert Forman, PhD, on how to guide patients to the 12-step programs that best meet their individual needs. Mutual hostility once characterized psychiatry’s relationship with 12-step programs. Today, most 12-step program leaders accept that medications have a place in managing mental and physical problems, and psychiatrists think of 12-step programs as another valuable treatment option.

Psychiatry keeps evolving, which allows us to help more people. That’s why I’m proud to be a psychiatrist. Current Psychiatry allows us to share all the changes in our profession, and that’s why I’m proud of this journal.

And, as always, we want to hear what you think. Write to Current Psychiatry at hillarjr@email.uc.edu.

Not long ago, psychiatrists were taught that adults had certain psychiatric diseases and diagnoses, and children had others. Some overlap was recognized, but it was thought to be minor. Mania, for example, was thought to be an adult disorder, and attention-deficit/hyper-activity disorder (ADHD) was for kids. When an adult presented with ADHD symptoms, we approached the diagnosis with caution. We wondered, “Is the patient just trying to get amphetamines?” When children were diagnosed with mania, we were skeptical. Could they just be overly spirited?

The misconceived separation of adult and child diagnoses developed in part because the people writing the diagnostic criteria were not the ones treating the most severely ill children. When I was in residency during the 1970s, we were discouraged from using the DSM to diagnose children. Instead, we used a set of pediatric diagnoses developed by the Group for Advancement of Psychiatry that did not translate readily into those used for adults.

In this issue, Michael Schwartz, MD, makes it clear that—yes—ADHD is a problem for many adults, but its treatment requires a different approach from that used in children. Likewise, Peter Buckley, MD, and colleagues confirm that psychotic disorders do occur in younger patients and explain how treating children and adolescents differs from treating adults. Looking to the future, Joseph DeVeaugh-Geiss, MD, previews new indications and compounds being developed specifically for psychiatric disorders in younger patients. His compilation of 21 medications in the pipeline tells me that child and adolescent psychopharmacology is poised for rapid growth.

As more effective medications and more reliable and valid diagnoses are developed for children, medication treatment should gain greater acceptance in child psychiatry. Many parents and some psychiatrists still resist the use of psychotropics in children, but that resistance is at odds with the latest findings.

Originally, our publisher did not plan to send Current Psychiatry to child and adolescent psychiatrists, as they are not surveyed by the service that rates medical journal readership (our “Nielsen ratings”). I suppose this means that the pharmaceutical industry, which buys journal advertising partly based on readership scores, does not believe that child psychiatrists prescribe many medications. Anyway, we are sending Current Psychiatry to pediatric psychiatrists, and I expect the rating system eventually will count them as “readers.” We certainly do.

I also recommend the discussion by Robert Forman, PhD, on how to guide patients to the 12-step programs that best meet their individual needs. Mutual hostility once characterized psychiatry’s relationship with 12-step programs. Today, most 12-step program leaders accept that medications have a place in managing mental and physical problems, and psychiatrists think of 12-step programs as another valuable treatment option.

Psychiatry keeps evolving, which allows us to help more people. That’s why I’m proud to be a psychiatrist. Current Psychiatry allows us to share all the changes in our profession, and that’s why I’m proud of this journal.

And, as always, we want to hear what you think. Write to Current Psychiatry at hillarjr@email.uc.edu.

When I trained in the 1970s, some older physicians still called themselves “neuropsychiatrists.” To a psychiatry resident like me, they seemed out-of-date and “uncool.” Many did electroconvulsive therapy, and some still read EEGs. An enormous chasm seemed to exist between psychiatry’s therapeutically optimistic approach to life and what I perceived as neurologists’ dreary identification of precise but untreatable lesions.

Of course psychiatry is an outgrowth of neurology, and the specialties are connected by their study of the same organ system. That explains all those American Board of Psychiatry and Neurology certificates on our walls. Over time, however, psychiatry and neurology have developed different approaches to patient care. Psychiatrists see patients for longer sessions, we generally do not treat conditions with clear physical or lab findings, and we are always thinking in terms of multidimensional diagnoses.

Comments of archneurologist Hughlings Jackson at the turn of the 20th century illustrate the estrangement of psychiatry and neurology: “Their (psychiatrists’) hospitals are not our hospitals. Their ways are not our ways.”

Sigmund Freud trained as a neurologist. He predicted that psychiatry and neurology would reunite if neuroscience caught up with psychiatric observation. This issue of Current Psychiatry shows evidence of that reconnection, as we examine the psychiatric aspects of several neurologic disorders—epilepsy and seizures, schizophrenia, Parkinson’s disease, and irritable bowel syndrome.

Neurologist Michael D. Privitera, MD, goes a long way toward making EEGs “cool” again in his article on what psychiatrists should know about EEGs and epilepsy. As director of the University of Cincinnati’s Comprehensive Epilepsy Treatment Program, he tells us what EEGs really mean and offers helpful suggestions on sorting out psychiatric from neurologic symptoms.

The negative symptoms of schizophrenia—described by Rajiv Tandon, MD, and Michael Jibson, MD, PhD—are probably a neurologic syndrome first described by Emil Kraepelin, another neuropsychiatric ancestor.

Depression, anxiety, and psychosis often complicate advanced Parkinson’s disease (PD), a chronic neurodegenerative disorder. Stephen L. Byrd, MD—a psychiatrist—and Mary D. Hughes, MD—a neurologist—describe a team approach to managing PD’s psychiatric symptoms.

Irritable bowel syndrome is a visceral hypersensitivity disorder, but psychotherapy is showing promise in the relief of its associated GI and mood disturbances. The article by Kevin W. Olden, MD, illustrates that neurologic psychiatry can offer effective treatment for some biological diseases.

Being a psychiatrist is difficult enough, but now we need to be neurologists, too. I’ve heard it said that doctors practice medicine today the way airline ticket agents would practice if they had to keep all the flight schedules in their heads. With all the information I have to manage, I frequently wish that I could get a “brain upgrade.”

A ray of hope is Current Psychiatry’s new Web site—www.currentpsychiatry.com. It provides free full-text access to our issues, links to mental health resources, listings of professional opportunities, and news and information not offered in the print edition. This month we introduce “Psyber Psychiatry,” a column by John Luo, MD, on the use of computers in psychiatry. Dr. Luo, psychiatric informatics specialist at the University of California, Davis, addresses the use of virtual reality in psychiatric therapy. Please follow Dr. Luo’s future columns on the Web site.

Hope you enjoy this issue. Contact us anytime at current.psychiatry@dowdenhealth.com to tell us what you think of Current Psychiatry—in print or online.

When I trained in the 1970s, some older physicians still called themselves “neuropsychiatrists.” To a psychiatry resident like me, they seemed out-of-date and “uncool.” Many did electroconvulsive therapy, and some still read EEGs. An enormous chasm seemed to exist between psychiatry’s therapeutically optimistic approach to life and what I perceived as neurologists’ dreary identification of precise but untreatable lesions.

Of course psychiatry is an outgrowth of neurology, and the specialties are connected by their study of the same organ system. That explains all those American Board of Psychiatry and Neurology certificates on our walls. Over time, however, psychiatry and neurology have developed different approaches to patient care. Psychiatrists see patients for longer sessions, we generally do not treat conditions with clear physical or lab findings, and we are always thinking in terms of multidimensional diagnoses.

Comments of archneurologist Hughlings Jackson at the turn of the 20th century illustrate the estrangement of psychiatry and neurology: “Their (psychiatrists’) hospitals are not our hospitals. Their ways are not our ways.”

Sigmund Freud trained as a neurologist. He predicted that psychiatry and neurology would reunite if neuroscience caught up with psychiatric observation. This issue of Current Psychiatry shows evidence of that reconnection, as we examine the psychiatric aspects of several neurologic disorders—epilepsy and seizures, schizophrenia, Parkinson’s disease, and irritable bowel syndrome.

Neurologist Michael D. Privitera, MD, goes a long way toward making EEGs “cool” again in his article on what psychiatrists should know about EEGs and epilepsy. As director of the University of Cincinnati’s Comprehensive Epilepsy Treatment Program, he tells us what EEGs really mean and offers helpful suggestions on sorting out psychiatric from neurologic symptoms.

The negative symptoms of schizophrenia—described by Rajiv Tandon, MD, and Michael Jibson, MD, PhD—are probably a neurologic syndrome first described by Emil Kraepelin, another neuropsychiatric ancestor.

Depression, anxiety, and psychosis often complicate advanced Parkinson’s disease (PD), a chronic neurodegenerative disorder. Stephen L. Byrd, MD—a psychiatrist—and Mary D. Hughes, MD—a neurologist—describe a team approach to managing PD’s psychiatric symptoms.

Irritable bowel syndrome is a visceral hypersensitivity disorder, but psychotherapy is showing promise in the relief of its associated GI and mood disturbances. The article by Kevin W. Olden, MD, illustrates that neurologic psychiatry can offer effective treatment for some biological diseases.

Being a psychiatrist is difficult enough, but now we need to be neurologists, too. I’ve heard it said that doctors practice medicine today the way airline ticket agents would practice if they had to keep all the flight schedules in their heads. With all the information I have to manage, I frequently wish that I could get a “brain upgrade.”

A ray of hope is Current Psychiatry’s new Web site—www.currentpsychiatry.com. It provides free full-text access to our issues, links to mental health resources, listings of professional opportunities, and news and information not offered in the print edition. This month we introduce “Psyber Psychiatry,” a column by John Luo, MD, on the use of computers in psychiatry. Dr. Luo, psychiatric informatics specialist at the University of California, Davis, addresses the use of virtual reality in psychiatric therapy. Please follow Dr. Luo’s future columns on the Web site.

Hope you enjoy this issue. Contact us anytime at current.psychiatry@dowdenhealth.com to tell us what you think of Current Psychiatry—in print or online.

When I trained in the 1970s, some older physicians still called themselves “neuropsychiatrists.” To a psychiatry resident like me, they seemed out-of-date and “uncool.” Many did electroconvulsive therapy, and some still read EEGs. An enormous chasm seemed to exist between psychiatry’s therapeutically optimistic approach to life and what I perceived as neurologists’ dreary identification of precise but untreatable lesions.

Of course psychiatry is an outgrowth of neurology, and the specialties are connected by their study of the same organ system. That explains all those American Board of Psychiatry and Neurology certificates on our walls. Over time, however, psychiatry and neurology have developed different approaches to patient care. Psychiatrists see patients for longer sessions, we generally do not treat conditions with clear physical or lab findings, and we are always thinking in terms of multidimensional diagnoses.

Comments of archneurologist Hughlings Jackson at the turn of the 20th century illustrate the estrangement of psychiatry and neurology: “Their (psychiatrists’) hospitals are not our hospitals. Their ways are not our ways.”

Sigmund Freud trained as a neurologist. He predicted that psychiatry and neurology would reunite if neuroscience caught up with psychiatric observation. This issue of Current Psychiatry shows evidence of that reconnection, as we examine the psychiatric aspects of several neurologic disorders—epilepsy and seizures, schizophrenia, Parkinson’s disease, and irritable bowel syndrome.

Neurologist Michael D. Privitera, MD, goes a long way toward making EEGs “cool” again in his article on what psychiatrists should know about EEGs and epilepsy. As director of the University of Cincinnati’s Comprehensive Epilepsy Treatment Program, he tells us what EEGs really mean and offers helpful suggestions on sorting out psychiatric from neurologic symptoms.

The negative symptoms of schizophrenia—described by Rajiv Tandon, MD, and Michael Jibson, MD, PhD—are probably a neurologic syndrome first described by Emil Kraepelin, another neuropsychiatric ancestor.

Depression, anxiety, and psychosis often complicate advanced Parkinson’s disease (PD), a chronic neurodegenerative disorder. Stephen L. Byrd, MD—a psychiatrist—and Mary D. Hughes, MD—a neurologist—describe a team approach to managing PD’s psychiatric symptoms.

Irritable bowel syndrome is a visceral hypersensitivity disorder, but psychotherapy is showing promise in the relief of its associated GI and mood disturbances. The article by Kevin W. Olden, MD, illustrates that neurologic psychiatry can offer effective treatment for some biological diseases.

Being a psychiatrist is difficult enough, but now we need to be neurologists, too. I’ve heard it said that doctors practice medicine today the way airline ticket agents would practice if they had to keep all the flight schedules in their heads. With all the information I have to manage, I frequently wish that I could get a “brain upgrade.”

A ray of hope is Current Psychiatry’s new Web site—www.currentpsychiatry.com. It provides free full-text access to our issues, links to mental health resources, listings of professional opportunities, and news and information not offered in the print edition. This month we introduce “Psyber Psychiatry,” a column by John Luo, MD, on the use of computers in psychiatry. Dr. Luo, psychiatric informatics specialist at the University of California, Davis, addresses the use of virtual reality in psychiatric therapy. Please follow Dr. Luo’s future columns on the Web site.

Hope you enjoy this issue. Contact us anytime at current.psychiatry@dowdenhealth.com to tell us what you think of Current Psychiatry—in print or online.

When I trained in the 1970s, some older physicians still called themselves “neuropsychiatrists.” To a psychiatry resident like me, they seemed out-of-date and “uncool.” Many did electroconvulsive therapy, and some still read EEGs. An enormous chasm seemed to exist between psychiatry’s therapeutically optimistic approach to life and what I perceived as neurologists’ dreary identification of precise but untreatable lesions.

Of course psychiatry is an outgrowth of neurology, and the specialties are connected by their study of the same organ system. That explains all those American Board of Psychiatry and Neurology certificates on our walls. Over time, however, psychiatry and neurology have developed different approaches to patient care. Psychiatrists see patients for longer sessions, we generally do not treat conditions with clear physical or lab findings, and we are always thinking in terms of multidimensional diagnoses.

Comments of archneurologist Hughlings Jackson at the turn of the 20th century illustrate the estrangement of psychiatry and neurology: “Their (psychiatrists’) hospitals are not our hospitals. Their ways are not our ways.”

Sigmund Freud trained as a neurologist. He predicted that psychiatry and neurology would reunite if neuroscience caught up with psychiatric observation. This issue of Current Psychiatry shows evidence of that reconnection, as we examine the psychiatric aspects of several neurologic disorders—epilepsy and seizures, schizophrenia, Parkinson’s disease, and irritable bowel syndrome.

Neurologist Michael D. Privitera, MD, goes a long way toward making EEGs “cool” again in his article on what psychiatrists should know about EEGs and epilepsy. As director of the University of Cincinnati’s Comprehensive Epilepsy Treatment Program, he tells us what EEGs really mean and offers helpful suggestions on sorting out psychiatric from neurologic symptoms.

The negative symptoms of schizophrenia—described by Rajiv Tandon, MD, and Michael Jibson, MD, PhD—are probably a neurologic syndrome first described by Emil Kraepelin, another neuropsychiatric ancestor.

Depression, anxiety, and psychosis often complicate advanced Parkinson’s disease (PD), a chronic neurodegenerative disorder. Stephen L. Byrd, MD—a psychiatrist—and Mary D. Hughes, MD—a neurologist—describe a team approach to managing PD’s psychiatric symptoms.

Irritable bowel syndrome is a visceral hypersensitivity disorder, but psychotherapy is showing promise in the relief of its associated GI and mood disturbances. The article by Kevin W. Olden, MD, illustrates that neurologic psychiatry can offer effective treatment for some biological diseases.

Being a psychiatrist is difficult enough, but now we need to be neurologists, too. I’ve heard it said that doctors practice medicine today the way airline ticket agents would practice if they had to keep all the flight schedules in their heads. With all the information I have to manage, I frequently wish that I could get a “brain upgrade.”

A ray of hope is Current Psychiatry’s new Web site—www.currentpsychiatry.com. It provides free full-text access to our issues, links to mental health resources, listings of professional opportunities, and news and information not offered in the print edition. This month we introduce “Psyber Psychiatry,” a column by John Luo, MD, on the use of computers in psychiatry. Dr. Luo, psychiatric informatics specialist at the University of California, Davis, addresses the use of virtual reality in psychiatric therapy. Please follow Dr. Luo’s future columns on the Web site.

Hope you enjoy this issue. Contact us anytime at current.psychiatry@dowdenhealth.com to tell us what you think of Current Psychiatry—in print or online.

When I trained in the 1970s, some older physicians still called themselves “neuropsychiatrists.” To a psychiatry resident like me, they seemed out-of-date and “uncool.” Many did electroconvulsive therapy, and some still read EEGs. An enormous chasm seemed to exist between psychiatry’s therapeutically optimistic approach to life and what I perceived as neurologists’ dreary identification of precise but untreatable lesions.

Of course psychiatry is an outgrowth of neurology, and the specialties are connected by their study of the same organ system. That explains all those American Board of Psychiatry and Neurology certificates on our walls. Over time, however, psychiatry and neurology have developed different approaches to patient care. Psychiatrists see patients for longer sessions, we generally do not treat conditions with clear physical or lab findings, and we are always thinking in terms of multidimensional diagnoses.

Comments of archneurologist Hughlings Jackson at the turn of the 20th century illustrate the estrangement of psychiatry and neurology: “Their (psychiatrists’) hospitals are not our hospitals. Their ways are not our ways.”

Sigmund Freud trained as a neurologist. He predicted that psychiatry and neurology would reunite if neuroscience caught up with psychiatric observation. This issue of Current Psychiatry shows evidence of that reconnection, as we examine the psychiatric aspects of several neurologic disorders—epilepsy and seizures, schizophrenia, Parkinson’s disease, and irritable bowel syndrome.

Neurologist Michael D. Privitera, MD, goes a long way toward making EEGs “cool” again in his article on what psychiatrists should know about EEGs and epilepsy. As director of the University of Cincinnati’s Comprehensive Epilepsy Treatment Program, he tells us what EEGs really mean and offers helpful suggestions on sorting out psychiatric from neurologic symptoms.

The negative symptoms of schizophrenia—described by Rajiv Tandon, MD, and Michael Jibson, MD, PhD—are probably a neurologic syndrome first described by Emil Kraepelin, another neuropsychiatric ancestor.

Depression, anxiety, and psychosis often complicate advanced Parkinson’s disease (PD), a chronic neurodegenerative disorder. Stephen L. Byrd, MD—a psychiatrist—and Mary D. Hughes, MD—a neurologist—describe a team approach to managing PD’s psychiatric symptoms.

Irritable bowel syndrome is a visceral hypersensitivity disorder, but psychotherapy is showing promise in the relief of its associated GI and mood disturbances. The article by Kevin W. Olden, MD, illustrates that neurologic psychiatry can offer effective treatment for some biological diseases.

Being a psychiatrist is difficult enough, but now we need to be neurologists, too. I’ve heard it said that doctors practice medicine today the way airline ticket agents would practice if they had to keep all the flight schedules in their heads. With all the information I have to manage, I frequently wish that I could get a “brain upgrade.”

A ray of hope is Current Psychiatry’s new Web site—www.currentpsychiatry.com. It provides free full-text access to our issues, links to mental health resources, listings of professional opportunities, and news and information not offered in the print edition. This month we introduce “Psyber Psychiatry,” a column by John Luo, MD, on the use of computers in psychiatry. Dr. Luo, psychiatric informatics specialist at the University of California, Davis, addresses the use of virtual reality in psychiatric therapy. Please follow Dr. Luo’s future columns on the Web site.

Hope you enjoy this issue. Contact us anytime at current.psychiatry@dowdenhealth.com to tell us what you think of Current Psychiatry—in print or online.

When I trained in the 1970s, some older physicians still called themselves “neuropsychiatrists.” To a psychiatry resident like me, they seemed out-of-date and “uncool.” Many did electroconvulsive therapy, and some still read EEGs. An enormous chasm seemed to exist between psychiatry’s therapeutically optimistic approach to life and what I perceived as neurologists’ dreary identification of precise but untreatable lesions.

Of course psychiatry is an outgrowth of neurology, and the specialties are connected by their study of the same organ system. That explains all those American Board of Psychiatry and Neurology certificates on our walls. Over time, however, psychiatry and neurology have developed different approaches to patient care. Psychiatrists see patients for longer sessions, we generally do not treat conditions with clear physical or lab findings, and we are always thinking in terms of multidimensional diagnoses.

Comments of archneurologist Hughlings Jackson at the turn of the 20th century illustrate the estrangement of psychiatry and neurology: “Their (psychiatrists’) hospitals are not our hospitals. Their ways are not our ways.”

Sigmund Freud trained as a neurologist. He predicted that psychiatry and neurology would reunite if neuroscience caught up with psychiatric observation. This issue of Current Psychiatry shows evidence of that reconnection, as we examine the psychiatric aspects of several neurologic disorders—epilepsy and seizures, schizophrenia, Parkinson’s disease, and irritable bowel syndrome.

Neurologist Michael D. Privitera, MD, goes a long way toward making EEGs “cool” again in his article on what psychiatrists should know about EEGs and epilepsy. As director of the University of Cincinnati’s Comprehensive Epilepsy Treatment Program, he tells us what EEGs really mean and offers helpful suggestions on sorting out psychiatric from neurologic symptoms.

The negative symptoms of schizophrenia—described by Rajiv Tandon, MD, and Michael Jibson, MD, PhD—are probably a neurologic syndrome first described by Emil Kraepelin, another neuropsychiatric ancestor.

Depression, anxiety, and psychosis often complicate advanced Parkinson’s disease (PD), a chronic neurodegenerative disorder. Stephen L. Byrd, MD—a psychiatrist—and Mary D. Hughes, MD—a neurologist—describe a team approach to managing PD’s psychiatric symptoms.

Irritable bowel syndrome is a visceral hypersensitivity disorder, but psychotherapy is showing promise in the relief of its associated GI and mood disturbances. The article by Kevin W. Olden, MD, illustrates that neurologic psychiatry can offer effective treatment for some biological diseases.

Being a psychiatrist is difficult enough, but now we need to be neurologists, too. I’ve heard it said that doctors practice medicine today the way airline ticket agents would practice if they had to keep all the flight schedules in their heads. With all the information I have to manage, I frequently wish that I could get a “brain upgrade.”

A ray of hope is Current Psychiatry’s new Web site—www.currentpsychiatry.com. It provides free full-text access to our issues, links to mental health resources, listings of professional opportunities, and news and information not offered in the print edition. This month we introduce “Psyber Psychiatry,” a column by John Luo, MD, on the use of computers in psychiatry. Dr. Luo, psychiatric informatics specialist at the University of California, Davis, addresses the use of virtual reality in psychiatric therapy. Please follow Dr. Luo’s future columns on the Web site.

Hope you enjoy this issue. Contact us anytime at current.psychiatry@dowdenhealth.com to tell us what you think of Current Psychiatry—in print or online.