Pearls

Paliperidone palmitate (9-hydroxyrisperidone) is an injectable, once-monthly atypical antipsychotic medication, FDA-approved in July 2009 for acute and/or maintenance treatment of schizophrenia. This aqueous-based, extremely slowly dissolving depot medication is well tolerated and causes few drug-drug interactions.¹ Clinically, paliperidone palmitate and its parent drug, intramuscular (IM) risperidone, have similarities and differences.

Clinical information

Paliperidone palmitate is available in 39-mg, 78-mg, 117-mg, 156-mg, and 234-mg formulations. Once administered, it hydrolyzes and diffuses slowly and provides paliperidone doses equivalent to 25 mg, 50 mg, 75 mg, 100 mg, and 150 mg, respectively. The 234-mg dose of paliperidone palmitate is equivalent to 12 mg oral paliperidone, 117 mg to 6 mg, and 39 to 78 mg to 3 mg, respectively (visit this article at CurrentPsychiatry.com to learn more about paliperidone palmitate).

Pharmacokinetics. This palmitate ester of paliperidone is an aqueous suspension utilizing nanocrystal molecules. The increased surface area leads to rapid medication release and a short time to steady state. Active paliperidone plasma levels were detected at day 1, meaning co-administration with the oral formulation is not necessary. Paliperidone palmitate’s slow dissolution rate results in a half-life of 25 to 49 days. The fast onset of action and long half-life simplifies administration.

Co-administration with carbamazepine decreases paliperidone levels, whereas divalproex causes an increase. Up to 60% of paliperidone is excreted unchanged through the kidneys, which means patients with impaired renal function require a lower dosage. Because the liver has only a minimal role in paliperidone palmitate’s metabolism, dose adjustment is needed only for patients with severe hepatic dysfunction.¹

Administration. Before starting this medication, test for allergy with a dose of oral paliperidone. Then administer 2 consecutive loading doses of paliperidone palmitate by deltoid IM injection; first 234 mg, and then a 156-mg dose after 7 to 10 days. Monthly injections of 117 mg are recommended, although higher or lower dosages can be used depending on the clinical situation. The first 2 injections should be in the deltoid muscle because plasma concentrations are 28% higher with deltoid vs gluteal administration. Subsequent injections can alternate between gluteal and deltoid sites.

If a dose is missed within 6 weeks of the last injection, administer the most recently used dosage. For discontinuation of 6 weeks to 6 months, administer 2 injections of the previously stabilized dose separated by 1 week, followed by the regular monthly dosage. After >6 months, begin the initial loading dose regimen.¹

Paliperidone palmitate is available in prefilled syringes that do not require refrigeration or reconstitution. Use a 22-gauge needle for deltoid injections and for patients weighing >200 lbs. Use a 23-gauge needle for gluteal injections in non-obese individuals. Do not inject into a blood vessel, and alternate injection sites between sides of the body each month.¹

Table

Paliperidone palmitate: Fast facts

Efficacy

In a 9-week, phase II, double-blind study, mean Positive and Negative Syndrome Scale (PANSS) scores improved in patients receiving paliperidone, 78 mg or 156 mg (mean change -5.2 and -7.8, respectively) compared with placebo (6.2). Two percent of the paliperidone group discontinued the agent, compared with 10% of placebo. Although extrapyramidal symptoms were comparable in all groups (1%), 5% of patients receiving 78 mg and 8% of patients receiving 156 mg reported parkinsonian adverse events, compared with 1% with placebo.²

In other double-blind, placebo-controlled trials, paliperidone dosages from 25 mg to 150 mg were associated with a decrease in positive and negative symptoms in 1,540 subjects.¹ During a 1-year study, 18% of patients taking paliperidone palmitate relapsed, compared with 48% for placebo.¹

In a 53-week study, both paliperidone palmitate and IM risperidone were effective in decreasing positive and negative symptoms; however, risperidone-treated patients showed greater therapeutic response.³ Mean PANSS score changes in patients receiving paliperidone were -11.6, compared with -14.4 with risperidone. Psychotic relapse occurred in 14% of IM risperidone patients and 18% of paliperidone palmitate patients.³

In an unpublished 13-week, randomized, double-blind study conducted by the drug’s manufacturer, paliperidone palmitate, 78 mg to 234 mg once monthly, and long-acting risperidone, 25 mg to 50 mg every other week with supplemental oral risperidone for 2 to 3 weeks, were reported as equivalent.¹ Both groups showed similar decrease in PANSS scores (-18.6 vs -17.9); however, reported adverse events were slightly higher in patients receiving paliperidone (57.9% vs 52.8%).¹

Adverse events

Common side effects include insomnia (15%), anxiety (10%), and headaches (9%). Dizziness, agitation, gastrointestinal upset, hypotension, and urinary tract infection have been reported. Rarely, tachycardia, clinically nonsignificant QTc prolongation, and tardive dyskinesia occur. Increased prolactin levels have been observed, particularly in females. This drug should not be prescribed to pregnant or lactating women or elderly patients with dementia-related psychosis. In the 13-week trial, patients gained up to 3.3 lbs. Other adverse effects include allergic reactions, blood dyscrasias, elevated liver enzymes, lower seizure thresholds, body temperature dysregulation, neuroleptic malignant syndrome, dysphagia, and motor impairments.¹

Clinically significant adverse effects were reported in 25% of paliperidone-treated subjects compared with 20% in the risperidone IM group. The discontinuation rate was 5% for paliperidone palmitate, compared with 3% for IM risperidone. Hyperkinesia with paliperidone (6%) was less prominent than with risperidone (10%).³

Drug brand names

• Carbamazepine • Tegretol
• Divalproex • Depakote
• Paliperidone • Invega
• Paliperidone palmitate • Invega Sustenna
• Risperidone IM • Risperdal Consta

Disclosure

Dr. Lindenmayer has received grant support from AstraZeneca, Otsuka, Pfizer Inc., Dainippon Sumitomo, Azur, Janssen, Eli Lilly and Company, and National Institute of Mental Health. He is a consultant to Eli Lilly and Company and Janssen. Drs. Sedky, Nazir, and Lippmann report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Acknowledgments

The authors thank Dr. Roop Parlapalli, an observer physician at University of Louisville School of Medicine, for his editorial revision.

Paliperidone palmitate (9-hydroxyrisperidone) is an injectable, once-monthly atypical antipsychotic medication, FDA-approved in July 2009 for acute and/or maintenance treatment of schizophrenia. This aqueous-based, extremely slowly dissolving depot medication is well tolerated and causes few drug-drug interactions.¹ Clinically, paliperidone palmitate and its parent drug, intramuscular (IM) risperidone, have similarities and differences.

Clinical information

Paliperidone palmitate is available in 39-mg, 78-mg, 117-mg, 156-mg, and 234-mg formulations. Once administered, it hydrolyzes and diffuses slowly and provides paliperidone doses equivalent to 25 mg, 50 mg, 75 mg, 100 mg, and 150 mg, respectively. The 234-mg dose of paliperidone palmitate is equivalent to 12 mg oral paliperidone, 117 mg to 6 mg, and 39 to 78 mg to 3 mg, respectively (visit this article at CurrentPsychiatry.com to learn more about paliperidone palmitate).

Pharmacokinetics. This palmitate ester of paliperidone is an aqueous suspension utilizing nanocrystal molecules. The increased surface area leads to rapid medication release and a short time to steady state. Active paliperidone plasma levels were detected at day 1, meaning co-administration with the oral formulation is not necessary. Paliperidone palmitate’s slow dissolution rate results in a half-life of 25 to 49 days. The fast onset of action and long half-life simplifies administration.

Co-administration with carbamazepine decreases paliperidone levels, whereas divalproex causes an increase. Up to 60% of paliperidone is excreted unchanged through the kidneys, which means patients with impaired renal function require a lower dosage. Because the liver has only a minimal role in paliperidone palmitate’s metabolism, dose adjustment is needed only for patients with severe hepatic dysfunction.¹

Administration. Before starting this medication, test for allergy with a dose of oral paliperidone. Then administer 2 consecutive loading doses of paliperidone palmitate by deltoid IM injection; first 234 mg, and then a 156-mg dose after 7 to 10 days. Monthly injections of 117 mg are recommended, although higher or lower dosages can be used depending on the clinical situation. The first 2 injections should be in the deltoid muscle because plasma concentrations are 28% higher with deltoid vs gluteal administration. Subsequent injections can alternate between gluteal and deltoid sites.

If a dose is missed within 6 weeks of the last injection, administer the most recently used dosage. For discontinuation of 6 weeks to 6 months, administer 2 injections of the previously stabilized dose separated by 1 week, followed by the regular monthly dosage. After >6 months, begin the initial loading dose regimen.¹

Paliperidone palmitate is available in prefilled syringes that do not require refrigeration or reconstitution. Use a 22-gauge needle for deltoid injections and for patients weighing >200 lbs. Use a 23-gauge needle for gluteal injections in non-obese individuals. Do not inject into a blood vessel, and alternate injection sites between sides of the body each month.¹

Table

Paliperidone palmitate: Fast facts

Efficacy

In a 9-week, phase II, double-blind study, mean Positive and Negative Syndrome Scale (PANSS) scores improved in patients receiving paliperidone, 78 mg or 156 mg (mean change -5.2 and -7.8, respectively) compared with placebo (6.2). Two percent of the paliperidone group discontinued the agent, compared with 10% of placebo. Although extrapyramidal symptoms were comparable in all groups (1%), 5% of patients receiving 78 mg and 8% of patients receiving 156 mg reported parkinsonian adverse events, compared with 1% with placebo.²

In other double-blind, placebo-controlled trials, paliperidone dosages from 25 mg to 150 mg were associated with a decrease in positive and negative symptoms in 1,540 subjects.¹ During a 1-year study, 18% of patients taking paliperidone palmitate relapsed, compared with 48% for placebo.¹

In a 53-week study, both paliperidone palmitate and IM risperidone were effective in decreasing positive and negative symptoms; however, risperidone-treated patients showed greater therapeutic response.³ Mean PANSS score changes in patients receiving paliperidone were -11.6, compared with -14.4 with risperidone. Psychotic relapse occurred in 14% of IM risperidone patients and 18% of paliperidone palmitate patients.³

In an unpublished 13-week, randomized, double-blind study conducted by the drug’s manufacturer, paliperidone palmitate, 78 mg to 234 mg once monthly, and long-acting risperidone, 25 mg to 50 mg every other week with supplemental oral risperidone for 2 to 3 weeks, were reported as equivalent.¹ Both groups showed similar decrease in PANSS scores (-18.6 vs -17.9); however, reported adverse events were slightly higher in patients receiving paliperidone (57.9% vs 52.8%).¹

Adverse events

Common side effects include insomnia (15%), anxiety (10%), and headaches (9%). Dizziness, agitation, gastrointestinal upset, hypotension, and urinary tract infection have been reported. Rarely, tachycardia, clinically nonsignificant QTc prolongation, and tardive dyskinesia occur. Increased prolactin levels have been observed, particularly in females. This drug should not be prescribed to pregnant or lactating women or elderly patients with dementia-related psychosis. In the 13-week trial, patients gained up to 3.3 lbs. Other adverse effects include allergic reactions, blood dyscrasias, elevated liver enzymes, lower seizure thresholds, body temperature dysregulation, neuroleptic malignant syndrome, dysphagia, and motor impairments.¹

Clinically significant adverse effects were reported in 25% of paliperidone-treated subjects compared with 20% in the risperidone IM group. The discontinuation rate was 5% for paliperidone palmitate, compared with 3% for IM risperidone. Hyperkinesia with paliperidone (6%) was less prominent than with risperidone (10%).³

Drug brand names

• Carbamazepine • Tegretol
• Divalproex • Depakote
• Paliperidone • Invega
• Paliperidone palmitate • Invega Sustenna
• Risperidone IM • Risperdal Consta

Disclosure

Dr. Lindenmayer has received grant support from AstraZeneca, Otsuka, Pfizer Inc., Dainippon Sumitomo, Azur, Janssen, Eli Lilly and Company, and National Institute of Mental Health. He is a consultant to Eli Lilly and Company and Janssen. Drs. Sedky, Nazir, and Lippmann report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Acknowledgments

The authors thank Dr. Roop Parlapalli, an observer physician at University of Louisville School of Medicine, for his editorial revision.

Paliperidone palmitate (9-hydroxyrisperidone) is an injectable, once-monthly atypical antipsychotic medication, FDA-approved in July 2009 for acute and/or maintenance treatment of schizophrenia. This aqueous-based, extremely slowly dissolving depot medication is well tolerated and causes few drug-drug interactions.¹ Clinically, paliperidone palmitate and its parent drug, intramuscular (IM) risperidone, have similarities and differences.

Clinical information

Paliperidone palmitate is available in 39-mg, 78-mg, 117-mg, 156-mg, and 234-mg formulations. Once administered, it hydrolyzes and diffuses slowly and provides paliperidone doses equivalent to 25 mg, 50 mg, 75 mg, 100 mg, and 150 mg, respectively. The 234-mg dose of paliperidone palmitate is equivalent to 12 mg oral paliperidone, 117 mg to 6 mg, and 39 to 78 mg to 3 mg, respectively (visit this article at CurrentPsychiatry.com to learn more about paliperidone palmitate).

Pharmacokinetics. This palmitate ester of paliperidone is an aqueous suspension utilizing nanocrystal molecules. The increased surface area leads to rapid medication release and a short time to steady state. Active paliperidone plasma levels were detected at day 1, meaning co-administration with the oral formulation is not necessary. Paliperidone palmitate’s slow dissolution rate results in a half-life of 25 to 49 days. The fast onset of action and long half-life simplifies administration.

Co-administration with carbamazepine decreases paliperidone levels, whereas divalproex causes an increase. Up to 60% of paliperidone is excreted unchanged through the kidneys, which means patients with impaired renal function require a lower dosage. Because the liver has only a minimal role in paliperidone palmitate’s metabolism, dose adjustment is needed only for patients with severe hepatic dysfunction.¹

Administration. Before starting this medication, test for allergy with a dose of oral paliperidone. Then administer 2 consecutive loading doses of paliperidone palmitate by deltoid IM injection; first 234 mg, and then a 156-mg dose after 7 to 10 days. Monthly injections of 117 mg are recommended, although higher or lower dosages can be used depending on the clinical situation. The first 2 injections should be in the deltoid muscle because plasma concentrations are 28% higher with deltoid vs gluteal administration. Subsequent injections can alternate between gluteal and deltoid sites.

If a dose is missed within 6 weeks of the last injection, administer the most recently used dosage. For discontinuation of 6 weeks to 6 months, administer 2 injections of the previously stabilized dose separated by 1 week, followed by the regular monthly dosage. After >6 months, begin the initial loading dose regimen.¹

Paliperidone palmitate is available in prefilled syringes that do not require refrigeration or reconstitution. Use a 22-gauge needle for deltoid injections and for patients weighing >200 lbs. Use a 23-gauge needle for gluteal injections in non-obese individuals. Do not inject into a blood vessel, and alternate injection sites between sides of the body each month.¹

Table

Paliperidone palmitate: Fast facts

Efficacy

In a 9-week, phase II, double-blind study, mean Positive and Negative Syndrome Scale (PANSS) scores improved in patients receiving paliperidone, 78 mg or 156 mg (mean change -5.2 and -7.8, respectively) compared with placebo (6.2). Two percent of the paliperidone group discontinued the agent, compared with 10% of placebo. Although extrapyramidal symptoms were comparable in all groups (1%), 5% of patients receiving 78 mg and 8% of patients receiving 156 mg reported parkinsonian adverse events, compared with 1% with placebo.²

In other double-blind, placebo-controlled trials, paliperidone dosages from 25 mg to 150 mg were associated with a decrease in positive and negative symptoms in 1,540 subjects.¹ During a 1-year study, 18% of patients taking paliperidone palmitate relapsed, compared with 48% for placebo.¹

In a 53-week study, both paliperidone palmitate and IM risperidone were effective in decreasing positive and negative symptoms; however, risperidone-treated patients showed greater therapeutic response.³ Mean PANSS score changes in patients receiving paliperidone were -11.6, compared with -14.4 with risperidone. Psychotic relapse occurred in 14% of IM risperidone patients and 18% of paliperidone palmitate patients.³

In an unpublished 13-week, randomized, double-blind study conducted by the drug’s manufacturer, paliperidone palmitate, 78 mg to 234 mg once monthly, and long-acting risperidone, 25 mg to 50 mg every other week with supplemental oral risperidone for 2 to 3 weeks, were reported as equivalent.¹ Both groups showed similar decrease in PANSS scores (-18.6 vs -17.9); however, reported adverse events were slightly higher in patients receiving paliperidone (57.9% vs 52.8%).¹

Adverse events

Common side effects include insomnia (15%), anxiety (10%), and headaches (9%). Dizziness, agitation, gastrointestinal upset, hypotension, and urinary tract infection have been reported. Rarely, tachycardia, clinically nonsignificant QTc prolongation, and tardive dyskinesia occur. Increased prolactin levels have been observed, particularly in females. This drug should not be prescribed to pregnant or lactating women or elderly patients with dementia-related psychosis. In the 13-week trial, patients gained up to 3.3 lbs. Other adverse effects include allergic reactions, blood dyscrasias, elevated liver enzymes, lower seizure thresholds, body temperature dysregulation, neuroleptic malignant syndrome, dysphagia, and motor impairments.¹

Clinically significant adverse effects were reported in 25% of paliperidone-treated subjects compared with 20% in the risperidone IM group. The discontinuation rate was 5% for paliperidone palmitate, compared with 3% for IM risperidone. Hyperkinesia with paliperidone (6%) was less prominent than with risperidone (10%).³

Drug brand names

• Carbamazepine • Tegretol
• Divalproex • Depakote
• Paliperidone • Invega
• Paliperidone palmitate • Invega Sustenna
• Risperidone IM • Risperdal Consta

Disclosure

Dr. Lindenmayer has received grant support from AstraZeneca, Otsuka, Pfizer Inc., Dainippon Sumitomo, Azur, Janssen, Eli Lilly and Company, and National Institute of Mental Health. He is a consultant to Eli Lilly and Company and Janssen. Drs. Sedky, Nazir, and Lippmann report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Acknowledgments

The authors thank Dr. Roop Parlapalli, an observer physician at University of Louisville School of Medicine, for his editorial revision.

Symptoms of serotonin syndrome and neuroleptic malignant syndrome (NMS) are similar—mental status changes, autonomic dysfunction, and neuromuscular abnormalities—making the syndromes difficult to differentiate. However, therapeutic interventions and the mortality rates associated with these syndromes are widely divergent.

Because many medication regimens for treatment-resistant mood disorders modulate both serotonin and dopamine systems, psychiatrists must be prepared at any time to recognize either syndrome and quickly initiate appropriate treatment. For this, we rely on disease course, lab findings and vital signs, and the physical exam.

Clinical course

Serotonin syndrome symptoms can develop within minutes to hours after the administration of an agent that increases central serotonergic tone, such as a selective serotonin reuptake inhibitor. After rapid onset, serotonin syndrome symptoms may improve or even resolve within <24 hours. NMS, on the other hand, can develop days to weeks after the administration of a dopamine antagonist—such as an antipsychotic—and may take 3 to 14 days to resolve.

Labs and vital signs

The triad of fever, leukocytosis, and increased creatine kinase (CK) are associated with NMS. Hyperthermia is present in at least 90% of cases,¹ although, some definitions of NMS list fever as a sine qua non. Leukocytosis and elevated hepatic transaminases are reported in at least 75% of NMS cases and increased CK in >90% of cases.^1,2 These signs may be present in serotonin syndrome but are less common.

Although the pathophysiology of NMS is unclear and literature is limited, some case series report iron deficiency in >95% of cases.³ If this finding were replicated on a larger scale, iron deficiency might be a sensitive, rapid, and inexpensive test to help diagnose atypical NMS presentations. Larger studies are needed before clinicians can rely on this laboratory finding to diagnose NMS.

Physical exam findings

Neuromuscular manifestations also can help distinguish serotonin syndrome from NMS. Physicians often and rightly associate muscle rigidity with NMS. This finding also is present in approximately one-half of serotonin syndrome cases, however. Hyperreflexia and myoclonus, if present, may suggest serotonin syndrome.

Symptoms of serotonin syndrome and neuroleptic malignant syndrome (NMS) are similar—mental status changes, autonomic dysfunction, and neuromuscular abnormalities—making the syndromes difficult to differentiate. However, therapeutic interventions and the mortality rates associated with these syndromes are widely divergent.

Because many medication regimens for treatment-resistant mood disorders modulate both serotonin and dopamine systems, psychiatrists must be prepared at any time to recognize either syndrome and quickly initiate appropriate treatment. For this, we rely on disease course, lab findings and vital signs, and the physical exam.

Clinical course

Serotonin syndrome symptoms can develop within minutes to hours after the administration of an agent that increases central serotonergic tone, such as a selective serotonin reuptake inhibitor. After rapid onset, serotonin syndrome symptoms may improve or even resolve within <24 hours. NMS, on the other hand, can develop days to weeks after the administration of a dopamine antagonist—such as an antipsychotic—and may take 3 to 14 days to resolve.

Labs and vital signs

The triad of fever, leukocytosis, and increased creatine kinase (CK) are associated with NMS. Hyperthermia is present in at least 90% of cases,¹ although, some definitions of NMS list fever as a sine qua non. Leukocytosis and elevated hepatic transaminases are reported in at least 75% of NMS cases and increased CK in >90% of cases.^1,2 These signs may be present in serotonin syndrome but are less common.

Although the pathophysiology of NMS is unclear and literature is limited, some case series report iron deficiency in >95% of cases.³ If this finding were replicated on a larger scale, iron deficiency might be a sensitive, rapid, and inexpensive test to help diagnose atypical NMS presentations. Larger studies are needed before clinicians can rely on this laboratory finding to diagnose NMS.

Physical exam findings

Neuromuscular manifestations also can help distinguish serotonin syndrome from NMS. Physicians often and rightly associate muscle rigidity with NMS. This finding also is present in approximately one-half of serotonin syndrome cases, however. Hyperreflexia and myoclonus, if present, may suggest serotonin syndrome.

Symptoms of serotonin syndrome and neuroleptic malignant syndrome (NMS) are similar—mental status changes, autonomic dysfunction, and neuromuscular abnormalities—making the syndromes difficult to differentiate. However, therapeutic interventions and the mortality rates associated with these syndromes are widely divergent.

Because many medication regimens for treatment-resistant mood disorders modulate both serotonin and dopamine systems, psychiatrists must be prepared at any time to recognize either syndrome and quickly initiate appropriate treatment. For this, we rely on disease course, lab findings and vital signs, and the physical exam.

Clinical course

Serotonin syndrome symptoms can develop within minutes to hours after the administration of an agent that increases central serotonergic tone, such as a selective serotonin reuptake inhibitor. After rapid onset, serotonin syndrome symptoms may improve or even resolve within <24 hours. NMS, on the other hand, can develop days to weeks after the administration of a dopamine antagonist—such as an antipsychotic—and may take 3 to 14 days to resolve.

Labs and vital signs

The triad of fever, leukocytosis, and increased creatine kinase (CK) are associated with NMS. Hyperthermia is present in at least 90% of cases,¹ although, some definitions of NMS list fever as a sine qua non. Leukocytosis and elevated hepatic transaminases are reported in at least 75% of NMS cases and increased CK in >90% of cases.^1,2 These signs may be present in serotonin syndrome but are less common.

Although the pathophysiology of NMS is unclear and literature is limited, some case series report iron deficiency in >95% of cases.³ If this finding were replicated on a larger scale, iron deficiency might be a sensitive, rapid, and inexpensive test to help diagnose atypical NMS presentations. Larger studies are needed before clinicians can rely on this laboratory finding to diagnose NMS.

Physical exam findings

Neuromuscular manifestations also can help distinguish serotonin syndrome from NMS. Physicians often and rightly associate muscle rigidity with NMS. This finding also is present in approximately one-half of serotonin syndrome cases, however. Hyperreflexia and myoclonus, if present, may suggest serotonin syndrome.

After the birth of a child, family changes can put fathers at risk for postpartum depression. Long recognized as a problem affecting some new mothers, postpartum depression also can grip men. Ten percent of new fathers and 14% of new mothers are affected by depression.¹ Still, most men and their partners fail to recognize postpartum depression—characterized by mood changes after a baby is born—when it arises.

Different causes, similar symptoms

Symptoms of postpartum depression are similar in both sexes, but the causes may be different. Hormonal changes contribute to women’s suffering, whereas sudden and unexpected lifestyle changes are thought to trigger fathers’ depression.

After the birth of a child, a father might not get the same attention from his partner and sexual activity may be reduced. His sleep is affected, and he may feel pressure to work longer hours to provide for the family economically.² Some fathers may believe the child is a binding force in an unsatisfactory marriage.³

Depressed new dads—like depressed men in general—are more likely than depressed women to engage in destructive behaviors, including alcohol or drug abuse, angry outbursts, or taking unnecessary risks such as reckless driving or extramarital sex. Other signs to look for include depressed mood, loss of interest or pleasure, weight gain or loss, oversleeping or insomnia, restlessness, fatigue, feelings of worthlessness or guilt, impaired concentration, and thoughts of suicide or death.

Treatment

Postpartum depression can began within days or weeks of a child’s delivery and can last one year or more. In both sexes, it can be successfully treated with psycho therapy, medication, or both. The family’s involvement is critical to identifying depression in a new father. Often, the woman will be the first to notice her partner’s depression. A history of depression or mental illness and having a spouse with postpartum depression increases a father’s risk of depression.

After the birth of a child, family changes can put fathers at risk for postpartum depression. Long recognized as a problem affecting some new mothers, postpartum depression also can grip men. Ten percent of new fathers and 14% of new mothers are affected by depression.¹ Still, most men and their partners fail to recognize postpartum depression—characterized by mood changes after a baby is born—when it arises.

Different causes, similar symptoms

Symptoms of postpartum depression are similar in both sexes, but the causes may be different. Hormonal changes contribute to women’s suffering, whereas sudden and unexpected lifestyle changes are thought to trigger fathers’ depression.

After the birth of a child, a father might not get the same attention from his partner and sexual activity may be reduced. His sleep is affected, and he may feel pressure to work longer hours to provide for the family economically.² Some fathers may believe the child is a binding force in an unsatisfactory marriage.³

Depressed new dads—like depressed men in general—are more likely than depressed women to engage in destructive behaviors, including alcohol or drug abuse, angry outbursts, or taking unnecessary risks such as reckless driving or extramarital sex. Other signs to look for include depressed mood, loss of interest or pleasure, weight gain or loss, oversleeping or insomnia, restlessness, fatigue, feelings of worthlessness or guilt, impaired concentration, and thoughts of suicide or death.

Treatment

Postpartum depression can began within days or weeks of a child’s delivery and can last one year or more. In both sexes, it can be successfully treated with psycho therapy, medication, or both. The family’s involvement is critical to identifying depression in a new father. Often, the woman will be the first to notice her partner’s depression. A history of depression or mental illness and having a spouse with postpartum depression increases a father’s risk of depression.

After the birth of a child, family changes can put fathers at risk for postpartum depression. Long recognized as a problem affecting some new mothers, postpartum depression also can grip men. Ten percent of new fathers and 14% of new mothers are affected by depression.¹ Still, most men and their partners fail to recognize postpartum depression—characterized by mood changes after a baby is born—when it arises.

Different causes, similar symptoms

Symptoms of postpartum depression are similar in both sexes, but the causes may be different. Hormonal changes contribute to women’s suffering, whereas sudden and unexpected lifestyle changes are thought to trigger fathers’ depression.

After the birth of a child, a father might not get the same attention from his partner and sexual activity may be reduced. His sleep is affected, and he may feel pressure to work longer hours to provide for the family economically.² Some fathers may believe the child is a binding force in an unsatisfactory marriage.³

Depressed new dads—like depressed men in general—are more likely than depressed women to engage in destructive behaviors, including alcohol or drug abuse, angry outbursts, or taking unnecessary risks such as reckless driving or extramarital sex. Other signs to look for include depressed mood, loss of interest or pleasure, weight gain or loss, oversleeping or insomnia, restlessness, fatigue, feelings of worthlessness or guilt, impaired concentration, and thoughts of suicide or death.

Treatment

Postpartum depression can began within days or weeks of a child’s delivery and can last one year or more. In both sexes, it can be successfully treated with psycho therapy, medication, or both. The family’s involvement is critical to identifying depression in a new father. Often, the woman will be the first to notice her partner’s depression. A history of depression or mental illness and having a spouse with postpartum depression increases a father’s risk of depression.

Up to 15% of the U.S. inmate population has a bona fide serious mental illness,¹ but psychiatrists working in jails or prisons also encounter manipulative inmates feigning psychiatric illness. Likewise, clinicians in the civilian sector who conduct worker’s compensation or disability evaluations need to be alert for malingering. My advice is to begin these evaluations with a thorough interview and mental status examination. Ask open-ended questions that allow patients to elaborate on their alleged complaints and their often atypical symptoms, and carefully observe the individual’s behavior and affect.

In my 20 years working in a state prison system, I have identified common clinical scenarios—represented by “3Ds”—that should raise a clinician’s suspicion about the presence of a legitimate, significant Axis I disorder.

Demanding medications. Patients with severe mental illness rarely engage in this behavior and often have to be encouraged or coaxed to adhere to medications. However, manipulative patients I have evaluated demand only certain medications. They do not request agents such as fluoxetine or risperidone but insist that only sedating psychotropics with abuse potential, such as alprazolam or quetiapine, can effectively treat their symptoms.

Divulging symptoms too eagerly or dramatically.² Typically, patients suffering from schizophrenia, bipolar disorder, or major depressive disorder are embarrassed by their symptoms and may attempt to minimize or conceal them until they have established a rapport with the clinician. To the contrary, I have seen numerous inmates feigning mental illness who immediately and openly declare, “I hear voices” or “I’m paranoid.”

Dependent or conditional threats of self-harm, violence, or litigation. Statements such as, “If you don’t do this for me, I will hurt myself or somebody else” or “I will sue you if you don’t do this” are more consistent with Axis II than Axis I pathology. Patients in the throes of severe depression or psychotic thinking usually do not possess the motivation or inclination to make conditional threats.

Although there is no substitute for a comprehensive diagnostic assessment that includes history, treatments, and mental status exam, my “3Ds” may put you on alert. These scenarios are not diagnostic, but encountering any of them is a signal to delve further into the authenticity of the individual’s presentation.

Up to 15% of the U.S. inmate population has a bona fide serious mental illness,¹ but psychiatrists working in jails or prisons also encounter manipulative inmates feigning psychiatric illness. Likewise, clinicians in the civilian sector who conduct worker’s compensation or disability evaluations need to be alert for malingering. My advice is to begin these evaluations with a thorough interview and mental status examination. Ask open-ended questions that allow patients to elaborate on their alleged complaints and their often atypical symptoms, and carefully observe the individual’s behavior and affect.

In my 20 years working in a state prison system, I have identified common clinical scenarios—represented by “3Ds”—that should raise a clinician’s suspicion about the presence of a legitimate, significant Axis I disorder.

Demanding medications. Patients with severe mental illness rarely engage in this behavior and often have to be encouraged or coaxed to adhere to medications. However, manipulative patients I have evaluated demand only certain medications. They do not request agents such as fluoxetine or risperidone but insist that only sedating psychotropics with abuse potential, such as alprazolam or quetiapine, can effectively treat their symptoms.

Divulging symptoms too eagerly or dramatically.² Typically, patients suffering from schizophrenia, bipolar disorder, or major depressive disorder are embarrassed by their symptoms and may attempt to minimize or conceal them until they have established a rapport with the clinician. To the contrary, I have seen numerous inmates feigning mental illness who immediately and openly declare, “I hear voices” or “I’m paranoid.”

Dependent or conditional threats of self-harm, violence, or litigation. Statements such as, “If you don’t do this for me, I will hurt myself or somebody else” or “I will sue you if you don’t do this” are more consistent with Axis II than Axis I pathology. Patients in the throes of severe depression or psychotic thinking usually do not possess the motivation or inclination to make conditional threats.

Although there is no substitute for a comprehensive diagnostic assessment that includes history, treatments, and mental status exam, my “3Ds” may put you on alert. These scenarios are not diagnostic, but encountering any of them is a signal to delve further into the authenticity of the individual’s presentation.

Up to 15% of the U.S. inmate population has a bona fide serious mental illness,¹ but psychiatrists working in jails or prisons also encounter manipulative inmates feigning psychiatric illness. Likewise, clinicians in the civilian sector who conduct worker’s compensation or disability evaluations need to be alert for malingering. My advice is to begin these evaluations with a thorough interview and mental status examination. Ask open-ended questions that allow patients to elaborate on their alleged complaints and their often atypical symptoms, and carefully observe the individual’s behavior and affect.

In my 20 years working in a state prison system, I have identified common clinical scenarios—represented by “3Ds”—that should raise a clinician’s suspicion about the presence of a legitimate, significant Axis I disorder.

Demanding medications. Patients with severe mental illness rarely engage in this behavior and often have to be encouraged or coaxed to adhere to medications. However, manipulative patients I have evaluated demand only certain medications. They do not request agents such as fluoxetine or risperidone but insist that only sedating psychotropics with abuse potential, such as alprazolam or quetiapine, can effectively treat their symptoms.

Divulging symptoms too eagerly or dramatically.² Typically, patients suffering from schizophrenia, bipolar disorder, or major depressive disorder are embarrassed by their symptoms and may attempt to minimize or conceal them until they have established a rapport with the clinician. To the contrary, I have seen numerous inmates feigning mental illness who immediately and openly declare, “I hear voices” or “I’m paranoid.”

Dependent or conditional threats of self-harm, violence, or litigation. Statements such as, “If you don’t do this for me, I will hurt myself or somebody else” or “I will sue you if you don’t do this” are more consistent with Axis II than Axis I pathology. Patients in the throes of severe depression or psychotic thinking usually do not possess the motivation or inclination to make conditional threats.

Although there is no substitute for a comprehensive diagnostic assessment that includes history, treatments, and mental status exam, my “3Ds” may put you on alert. These scenarios are not diagnostic, but encountering any of them is a signal to delve further into the authenticity of the individual’s presentation.

Some psychiatric patients report intolerable side effects with almost every psychotropic one reasonably could prescribe. Their psychiatric disorders remain undertreated as treatment-emergent side effects lead again and again to medication nonadherence. These patients often are frustrated by their lack of progress and in turn exasperate practitioners, creating strong transference and countertransference reactions.

To keep the therapeutic relationship on track, consider that your patient’s physiologic response to medication may be the result of genetic or psychodynamic factors you can overcome.

Start low and go slow

One option is to initiate medication far below the recommended starting dose. For example, try starting a patient on 1, 2, or 5 mg/d of fluoxetine instead of the typical 20 mg/d. These small doses can be achieved with a pill cutter or by using a liquid formulation with a measuring spoon that allows for 1-mg increments.

Some patients may report significant amelioration of symptoms even if they do not reach what is considered a therapeutic dose. These clinical observations have been confirmed by pharmacogenetic research that demonstrates metabolic variation across the population.¹ Improving patients’ well-being rather than arriving at a predetermined therapeutic dose should guide treatment.

Patients who experience multiple side effects may need extra time to acclimate to a new medication. Try initiating medication changes or increases at longer intervals, such as over months rather than weeks.

Examine psychodynamic factors

Seek to understand dynamic factors that contribute to your patient’s pattern of intolerable side effects. For example, patients’ disappointing early experiences with parents may result in angry feelings toward authority figures and a desire to frustrate them. In traumatized patients, internalized object relations consisting of pain-inflicting authority figures may be acted out through medication matters.

By understanding patients’ dynamics, we can better understand our own countertransference reactions and devise interventions that are more likely to help patients tolerate medication.

Accept patients’ sensitivity

I often tell patients, “You happen to be sensitive to side effects of medication. We might have to try a number of different medications before we find one that works and is tolerable. Furthermore, we need to start at a very low dose and take things very slowly.” This statement:

• recognizes and accepts patients’ sensitivity to psychotropics
  
• allows for externalization of some responsibility for troublesome side effects to the medication
  
• conveys a sense of therapeutic uncertainty
  
• allows patients to undertake treatment at a comfortable pace.
  

Some psychiatric patients report intolerable side effects with almost every psychotropic one reasonably could prescribe. Their psychiatric disorders remain undertreated as treatment-emergent side effects lead again and again to medication nonadherence. These patients often are frustrated by their lack of progress and in turn exasperate practitioners, creating strong transference and countertransference reactions.

To keep the therapeutic relationship on track, consider that your patient’s physiologic response to medication may be the result of genetic or psychodynamic factors you can overcome.

Start low and go slow

One option is to initiate medication far below the recommended starting dose. For example, try starting a patient on 1, 2, or 5 mg/d of fluoxetine instead of the typical 20 mg/d. These small doses can be achieved with a pill cutter or by using a liquid formulation with a measuring spoon that allows for 1-mg increments.

Some patients may report significant amelioration of symptoms even if they do not reach what is considered a therapeutic dose. These clinical observations have been confirmed by pharmacogenetic research that demonstrates metabolic variation across the population.¹ Improving patients’ well-being rather than arriving at a predetermined therapeutic dose should guide treatment.

Patients who experience multiple side effects may need extra time to acclimate to a new medication. Try initiating medication changes or increases at longer intervals, such as over months rather than weeks.

Examine psychodynamic factors

Seek to understand dynamic factors that contribute to your patient’s pattern of intolerable side effects. For example, patients’ disappointing early experiences with parents may result in angry feelings toward authority figures and a desire to frustrate them. In traumatized patients, internalized object relations consisting of pain-inflicting authority figures may be acted out through medication matters.

By understanding patients’ dynamics, we can better understand our own countertransference reactions and devise interventions that are more likely to help patients tolerate medication.

Accept patients’ sensitivity

I often tell patients, “You happen to be sensitive to side effects of medication. We might have to try a number of different medications before we find one that works and is tolerable. Furthermore, we need to start at a very low dose and take things very slowly.” This statement:

• recognizes and accepts patients’ sensitivity to psychotropics
  
• allows for externalization of some responsibility for troublesome side effects to the medication
  
• conveys a sense of therapeutic uncertainty
  
• allows patients to undertake treatment at a comfortable pace.
  

Some psychiatric patients report intolerable side effects with almost every psychotropic one reasonably could prescribe. Their psychiatric disorders remain undertreated as treatment-emergent side effects lead again and again to medication nonadherence. These patients often are frustrated by their lack of progress and in turn exasperate practitioners, creating strong transference and countertransference reactions.

To keep the therapeutic relationship on track, consider that your patient’s physiologic response to medication may be the result of genetic or psychodynamic factors you can overcome.

Start low and go slow

One option is to initiate medication far below the recommended starting dose. For example, try starting a patient on 1, 2, or 5 mg/d of fluoxetine instead of the typical 20 mg/d. These small doses can be achieved with a pill cutter or by using a liquid formulation with a measuring spoon that allows for 1-mg increments.

Some patients may report significant amelioration of symptoms even if they do not reach what is considered a therapeutic dose. These clinical observations have been confirmed by pharmacogenetic research that demonstrates metabolic variation across the population.¹ Improving patients’ well-being rather than arriving at a predetermined therapeutic dose should guide treatment.

Patients who experience multiple side effects may need extra time to acclimate to a new medication. Try initiating medication changes or increases at longer intervals, such as over months rather than weeks.

Examine psychodynamic factors

Seek to understand dynamic factors that contribute to your patient’s pattern of intolerable side effects. For example, patients’ disappointing early experiences with parents may result in angry feelings toward authority figures and a desire to frustrate them. In traumatized patients, internalized object relations consisting of pain-inflicting authority figures may be acted out through medication matters.

By understanding patients’ dynamics, we can better understand our own countertransference reactions and devise interventions that are more likely to help patients tolerate medication.

Accept patients’ sensitivity

I often tell patients, “You happen to be sensitive to side effects of medication. We might have to try a number of different medications before we find one that works and is tolerable. Furthermore, we need to start at a very low dose and take things very slowly.” This statement:

• recognizes and accepts patients’ sensitivity to psychotropics
  
• allows for externalization of some responsibility for troublesome side effects to the medication
  
• conveys a sense of therapeutic uncertainty
  
• allows patients to undertake treatment at a comfortable pace.
  

Orlistat is an FDA-approved anorexic agent for adults and adolescents that interferes with gastrointestinal lipase and prevents the absorption of 30% of dietary fat. Some clinical trials have failed to show significant weight reduction with orlistat,^1,2 but in our adolescent residential psychiatric treatment center:

• 15 patients (13 girls and 2 boys) lost an average 17.9 lbs over 4 months
  
• one patient lost 100 lbs over 8 months.
  

In a naturalistic observation, we offered orlistat plus dietary counseling to all teenage patients with a body mass index (BMI) >25 kg/m². Gastrointestinal (GI) side effects, such as odoriferous loose stools and fat-stained and occasionally soiled underwear, are common.

Factors contributing to weight loss

Motivation. Most of our patients gained weight while being treated with psychiatric medications, particularly mood stabilizers and atypical antipsychotics. These were continued during orlistat use.

Larger waist sizes and exaggerated facial and body features diminished our overweight patients’ self-respect and made them targets of bullying and rejection. Weight loss helped reverse these negative factors. Peers often supported these changes by including the teens in their circle of friends. Self-esteem, maturity, and motivation for personal growth were reflected in the teens’ social and psychotherapeutic encounters.

Overweight. Weight loss was statistically significant in teens with BMI >25 kg/m². Average pre-orlistat weight was 193 lbs and BMI 33 kg/m². Average BMI loss was 4.3 kg/m² (median loss 3.7 kg/m², standard deviation ±4.08). Although we did not treat patients with initial BMI

Diet, dosing, and activity. Our patients began a low-fat, 1,800-calorie diet in 3 meals and 2 snacks per day. They also received a daily supplement with vitamins A, D, E, and K to prevent deficiencies from the loss of fat-soluble vitamins.

Orlistat, 120 mg tid, was dispensed before meals, which enhanced awareness of healthy food choices because high-fat foods caused GI side effects.

As patients lost weight, they became more interested in exercise, and tolerance for physical activity improved.

Monitoring and support. Nursing staff weighed the teenagers weekly. Patients also had twice-monthly psychiatric assessments of orlistat’s impact on their medical, psychiatric, and psychopharmacologic status. The teens’ primary concerns included the amount of weight loss and GI side effects.

Summary. Under these conditions, orlistat may be an effective weight loss medication that can enhance self-esteem in motivated, overweight teenagers with psychiatric comorbidities.

Orlistat is an FDA-approved anorexic agent for adults and adolescents that interferes with gastrointestinal lipase and prevents the absorption of 30% of dietary fat. Some clinical trials have failed to show significant weight reduction with orlistat,^1,2 but in our adolescent residential psychiatric treatment center:

• 15 patients (13 girls and 2 boys) lost an average 17.9 lbs over 4 months
  
• one patient lost 100 lbs over 8 months.
  

In a naturalistic observation, we offered orlistat plus dietary counseling to all teenage patients with a body mass index (BMI) >25 kg/m². Gastrointestinal (GI) side effects, such as odoriferous loose stools and fat-stained and occasionally soiled underwear, are common.

Factors contributing to weight loss

Motivation. Most of our patients gained weight while being treated with psychiatric medications, particularly mood stabilizers and atypical antipsychotics. These were continued during orlistat use.

Larger waist sizes and exaggerated facial and body features diminished our overweight patients’ self-respect and made them targets of bullying and rejection. Weight loss helped reverse these negative factors. Peers often supported these changes by including the teens in their circle of friends. Self-esteem, maturity, and motivation for personal growth were reflected in the teens’ social and psychotherapeutic encounters.

Overweight. Weight loss was statistically significant in teens with BMI >25 kg/m². Average pre-orlistat weight was 193 lbs and BMI 33 kg/m². Average BMI loss was 4.3 kg/m² (median loss 3.7 kg/m², standard deviation ±4.08). Although we did not treat patients with initial BMI

Diet, dosing, and activity. Our patients began a low-fat, 1,800-calorie diet in 3 meals and 2 snacks per day. They also received a daily supplement with vitamins A, D, E, and K to prevent deficiencies from the loss of fat-soluble vitamins.

Orlistat, 120 mg tid, was dispensed before meals, which enhanced awareness of healthy food choices because high-fat foods caused GI side effects.

As patients lost weight, they became more interested in exercise, and tolerance for physical activity improved.

Monitoring and support. Nursing staff weighed the teenagers weekly. Patients also had twice-monthly psychiatric assessments of orlistat’s impact on their medical, psychiatric, and psychopharmacologic status. The teens’ primary concerns included the amount of weight loss and GI side effects.

Summary. Under these conditions, orlistat may be an effective weight loss medication that can enhance self-esteem in motivated, overweight teenagers with psychiatric comorbidities.

Orlistat is an FDA-approved anorexic agent for adults and adolescents that interferes with gastrointestinal lipase and prevents the absorption of 30% of dietary fat. Some clinical trials have failed to show significant weight reduction with orlistat,^1,2 but in our adolescent residential psychiatric treatment center:

• 15 patients (13 girls and 2 boys) lost an average 17.9 lbs over 4 months
  
• one patient lost 100 lbs over 8 months.
  

In a naturalistic observation, we offered orlistat plus dietary counseling to all teenage patients with a body mass index (BMI) >25 kg/m². Gastrointestinal (GI) side effects, such as odoriferous loose stools and fat-stained and occasionally soiled underwear, are common.

Factors contributing to weight loss

Motivation. Most of our patients gained weight while being treated with psychiatric medications, particularly mood stabilizers and atypical antipsychotics. These were continued during orlistat use.

Larger waist sizes and exaggerated facial and body features diminished our overweight patients’ self-respect and made them targets of bullying and rejection. Weight loss helped reverse these negative factors. Peers often supported these changes by including the teens in their circle of friends. Self-esteem, maturity, and motivation for personal growth were reflected in the teens’ social and psychotherapeutic encounters.

Overweight. Weight loss was statistically significant in teens with BMI >25 kg/m². Average pre-orlistat weight was 193 lbs and BMI 33 kg/m². Average BMI loss was 4.3 kg/m² (median loss 3.7 kg/m², standard deviation ±4.08). Although we did not treat patients with initial BMI

Diet, dosing, and activity. Our patients began a low-fat, 1,800-calorie diet in 3 meals and 2 snacks per day. They also received a daily supplement with vitamins A, D, E, and K to prevent deficiencies from the loss of fat-soluble vitamins.

Orlistat, 120 mg tid, was dispensed before meals, which enhanced awareness of healthy food choices because high-fat foods caused GI side effects.

As patients lost weight, they became more interested in exercise, and tolerance for physical activity improved.

Monitoring and support. Nursing staff weighed the teenagers weekly. Patients also had twice-monthly psychiatric assessments of orlistat’s impact on their medical, psychiatric, and psychopharmacologic status. The teens’ primary concerns included the amount of weight loss and GI side effects.

Summary. Under these conditions, orlistat may be an effective weight loss medication that can enhance self-esteem in motivated, overweight teenagers with psychiatric comorbidities.

Since 2005, I’ve had the opportunity to peer review Pearls articles submitted for publication in Current Psychiatry. In that time, I have read many worthwhile papers written by authors who may not be entirely clear about what constitutes a Pearl. The mnemonic PEARL could help authors:

• decide if their article or idea is appropriate for Pearls
• construct the article to conform to the Pearls format.

Precise. A Pearls article should make an accurate and concise statement. It should not be an elaborate or generalized idea based on either limited or copious information.

Easy to remember. Lengthy, highly detailed articles may be helpful and informative but are not consistent with the purpose of Pearls.

Alert. A Pearl should alert a physician to identify a problem, diagnosis, or adverse effect that they might otherwise miss or take unnecessary time to identify. Classic examples are the “handshake diagnosis” of hyperthyroidism,¹ or the “3 little words that can diagnose mild cognitive impairment.”²

References. A professional article of any length should include references. References add immediate credibility to the information presented. For a Pearl, even one reference is acceptable. A writer can easily search PubMed and the Internet to find references to confirm or support their ideas.

Less is more. Architect Mies van der Rohe’s minimalist concept applies to Pearls. A Pearl—like its namesake—is small, polished, and valuable. Simplicity is its essence.

I hope this mnemonic is useful for clinicians interested in sharing their ideas or experiences to help others in the field. I look forward to reviewing many more Pearls in the future.

Since 2005, I’ve had the opportunity to peer review Pearls articles submitted for publication in Current Psychiatry. In that time, I have read many worthwhile papers written by authors who may not be entirely clear about what constitutes a Pearl. The mnemonic PEARL could help authors:

• decide if their article or idea is appropriate for Pearls
• construct the article to conform to the Pearls format.

Precise. A Pearls article should make an accurate and concise statement. It should not be an elaborate or generalized idea based on either limited or copious information.

Easy to remember. Lengthy, highly detailed articles may be helpful and informative but are not consistent with the purpose of Pearls.

Alert. A Pearl should alert a physician to identify a problem, diagnosis, or adverse effect that they might otherwise miss or take unnecessary time to identify. Classic examples are the “handshake diagnosis” of hyperthyroidism,¹ or the “3 little words that can diagnose mild cognitive impairment.”²

References. A professional article of any length should include references. References add immediate credibility to the information presented. For a Pearl, even one reference is acceptable. A writer can easily search PubMed and the Internet to find references to confirm or support their ideas.

Less is more. Architect Mies van der Rohe’s minimalist concept applies to Pearls. A Pearl—like its namesake—is small, polished, and valuable. Simplicity is its essence.

I hope this mnemonic is useful for clinicians interested in sharing their ideas or experiences to help others in the field. I look forward to reviewing many more Pearls in the future.

Since 2005, I’ve had the opportunity to peer review Pearls articles submitted for publication in Current Psychiatry. In that time, I have read many worthwhile papers written by authors who may not be entirely clear about what constitutes a Pearl. The mnemonic PEARL could help authors:

• decide if their article or idea is appropriate for Pearls
• construct the article to conform to the Pearls format.

Precise. A Pearls article should make an accurate and concise statement. It should not be an elaborate or generalized idea based on either limited or copious information.

Easy to remember. Lengthy, highly detailed articles may be helpful and informative but are not consistent with the purpose of Pearls.

Alert. A Pearl should alert a physician to identify a problem, diagnosis, or adverse effect that they might otherwise miss or take unnecessary time to identify. Classic examples are the “handshake diagnosis” of hyperthyroidism,¹ or the “3 little words that can diagnose mild cognitive impairment.”²

References. A professional article of any length should include references. References add immediate credibility to the information presented. For a Pearl, even one reference is acceptable. A writer can easily search PubMed and the Internet to find references to confirm or support their ideas.

Less is more. Architect Mies van der Rohe’s minimalist concept applies to Pearls. A Pearl—like its namesake—is small, polished, and valuable. Simplicity is its essence.

I hope this mnemonic is useful for clinicians interested in sharing their ideas or experiences to help others in the field. I look forward to reviewing many more Pearls in the future.

The Mini-Mental State Examination (MMSE) is widely used in psychiatry and throughout the medical community to evaluate a patient’s cognitive status. The MMSE score is the common language for communicating a patient’s cognitive level among psychiatrists, primary care physicians, social workers, nursing staff, psychologists, long-term care and assisted living facility staff, and insurance companies.

Although the MMSE is highly useful and should continue to be used as a cognitive screening instrument, in some clinical situations time is too limited to allow a full assessment, which could take up to 30 minutes. In my clinical experience, I’ve discovered I can estimate the MMSE score range for a patient I suspect has dementia by asking 2 simple questions.

What is your date of birth (DOB)? When a patient cannot accurately state his or her complete DOB, usually the MMSE is ≤10, indicating severe dementia. Often this observation has been confirmed when another clinician later would do a complete MMSE and return a score close to one I predicted. DOB is a highly personal piece of information that an individual should be able to provide quickly and directly. If a patient is unable to give this information, consider the rest of the patient’s history to be inaccurate and check with collateral sources such as family or close friends.

Can you name 10 vegetables? If a patient is unable to list 10 vegetables—for example, if he or she cannot name 10 vegetables within a minute, repeats them, or mixes them up with fruits or other foods—the MMSE range usually is between 10 to 20, indicating moderate dementia. Instead of vegetables, you can ask your patient to name animals, fruits, or familiar items in other categories.

Clinical value. These 2 bedside questions do not take the place of performing a full MMSE or another established cognitive screen, such as the Montreal Cognitive Assessment¹ or the Mini-Cog.² My quick assessment—which has not been validated by research—is merely a tip that in certain situations may help you get a rough estimate of a patient’s cognitive status.

The Mini-Mental State Examination (MMSE) is widely used in psychiatry and throughout the medical community to evaluate a patient’s cognitive status. The MMSE score is the common language for communicating a patient’s cognitive level among psychiatrists, primary care physicians, social workers, nursing staff, psychologists, long-term care and assisted living facility staff, and insurance companies.

Although the MMSE is highly useful and should continue to be used as a cognitive screening instrument, in some clinical situations time is too limited to allow a full assessment, which could take up to 30 minutes. In my clinical experience, I’ve discovered I can estimate the MMSE score range for a patient I suspect has dementia by asking 2 simple questions.

What is your date of birth (DOB)? When a patient cannot accurately state his or her complete DOB, usually the MMSE is ≤10, indicating severe dementia. Often this observation has been confirmed when another clinician later would do a complete MMSE and return a score close to one I predicted. DOB is a highly personal piece of information that an individual should be able to provide quickly and directly. If a patient is unable to give this information, consider the rest of the patient’s history to be inaccurate and check with collateral sources such as family or close friends.

Can you name 10 vegetables? If a patient is unable to list 10 vegetables—for example, if he or she cannot name 10 vegetables within a minute, repeats them, or mixes them up with fruits or other foods—the MMSE range usually is between 10 to 20, indicating moderate dementia. Instead of vegetables, you can ask your patient to name animals, fruits, or familiar items in other categories.

Clinical value. These 2 bedside questions do not take the place of performing a full MMSE or another established cognitive screen, such as the Montreal Cognitive Assessment¹ or the Mini-Cog.² My quick assessment—which has not been validated by research—is merely a tip that in certain situations may help you get a rough estimate of a patient’s cognitive status.

The Mini-Mental State Examination (MMSE) is widely used in psychiatry and throughout the medical community to evaluate a patient’s cognitive status. The MMSE score is the common language for communicating a patient’s cognitive level among psychiatrists, primary care physicians, social workers, nursing staff, psychologists, long-term care and assisted living facility staff, and insurance companies.

Although the MMSE is highly useful and should continue to be used as a cognitive screening instrument, in some clinical situations time is too limited to allow a full assessment, which could take up to 30 minutes. In my clinical experience, I’ve discovered I can estimate the MMSE score range for a patient I suspect has dementia by asking 2 simple questions.

What is your date of birth (DOB)? When a patient cannot accurately state his or her complete DOB, usually the MMSE is ≤10, indicating severe dementia. Often this observation has been confirmed when another clinician later would do a complete MMSE and return a score close to one I predicted. DOB is a highly personal piece of information that an individual should be able to provide quickly and directly. If a patient is unable to give this information, consider the rest of the patient’s history to be inaccurate and check with collateral sources such as family or close friends.

Can you name 10 vegetables? If a patient is unable to list 10 vegetables—for example, if he or she cannot name 10 vegetables within a minute, repeats them, or mixes them up with fruits or other foods—the MMSE range usually is between 10 to 20, indicating moderate dementia. Instead of vegetables, you can ask your patient to name animals, fruits, or familiar items in other categories.

Clinical value. These 2 bedside questions do not take the place of performing a full MMSE or another established cognitive screen, such as the Montreal Cognitive Assessment¹ or the Mini-Cog.² My quick assessment—which has not been validated by research—is merely a tip that in certain situations may help you get a rough estimate of a patient’s cognitive status.

Psychogenic polydipsia (PPD) is a chronic, relapsing, and potentially life-threatening disorder characterized by compulsive consumption of large quantities of water resulting in “delutional hyponatremia.” PPD occurs in 6% to 20% of psychiatric patients, most often with schizophrenia.¹

In most patients with PPD, an electrolyte disturbance remains asymptomatic. However, superimposed and sudden ingestion of 3 to 4 liters of water can rapidly further dilute plasma and overwhelm the body’s compensatory reserves, leading to brain edema, seizures, coma, and even death.

The following prevention and treatment strategies might reduce morbidity and mortality in hospitalized patients diagnosed with PPD and lessen the cost of treating this serious illness.

Develop rapport. Understand that your patient has little control over his or her compulsive water intake. Remain nonjudgmental to help gain your patient’s trust.

Inquire about underlying psychiatric symptoms that might contribute to PPD. Does your patient have an overwhelming anxiety, delusional belief, or both? Effectively targeting specific symptoms will improve your chances of success.

Encourage communication among treatment team members. PPD patients are notoriously creative in sneaking water from unexpected places such as toilets and shower rooms. Staff vigilance is required to detect and prevent such clandestine behaviors.

Consult with an internist when necessary, especially if your patient has a comorbid cardiac condition that requires a low-sodium diet and/or diuretics.

Review psychotropic medications. In case reports of schizophrenia patients with PPD, switching from a typical to an atypical antipsychotic has shown efficacy in treating PPD.²

Restricting fluids to 2 to 3 liters a day combined with “a token economy”—a method of positive reinforcement to increase desired behavior—has been used to successfully treat the disorder.²

Monitor adherence by weighing patients twice a day and checking serum sodium levels frequently. Normal water retention is cyclic and peaks in the early afternoon; therefore, early-morning screening for hyponatremia may not accurately reflect the severity of water abuse. A diurnal weight gain of ≥0.6% is unusual and might point to PPD.²

Consider administering an angiotensin-converting enzyme (ACE) inhibitor. In clinical trials 60% of patients taking ACE inhibitors show decreased water consumption.²

Order 24-hour, 1-to-1 observation if you suspect continuous water abuse.

Think about placing a patient with severe PPD in a locked unit in a long-term psychiatric institution, away from all water sources.

Psychogenic polydipsia (PPD) is a chronic, relapsing, and potentially life-threatening disorder characterized by compulsive consumption of large quantities of water resulting in “delutional hyponatremia.” PPD occurs in 6% to 20% of psychiatric patients, most often with schizophrenia.¹

In most patients with PPD, an electrolyte disturbance remains asymptomatic. However, superimposed and sudden ingestion of 3 to 4 liters of water can rapidly further dilute plasma and overwhelm the body’s compensatory reserves, leading to brain edema, seizures, coma, and even death.

The following prevention and treatment strategies might reduce morbidity and mortality in hospitalized patients diagnosed with PPD and lessen the cost of treating this serious illness.

Develop rapport. Understand that your patient has little control over his or her compulsive water intake. Remain nonjudgmental to help gain your patient’s trust.

Inquire about underlying psychiatric symptoms that might contribute to PPD. Does your patient have an overwhelming anxiety, delusional belief, or both? Effectively targeting specific symptoms will improve your chances of success.

Encourage communication among treatment team members. PPD patients are notoriously creative in sneaking water from unexpected places such as toilets and shower rooms. Staff vigilance is required to detect and prevent such clandestine behaviors.

Consult with an internist when necessary, especially if your patient has a comorbid cardiac condition that requires a low-sodium diet and/or diuretics.

Review psychotropic medications. In case reports of schizophrenia patients with PPD, switching from a typical to an atypical antipsychotic has shown efficacy in treating PPD.²

Restricting fluids to 2 to 3 liters a day combined with “a token economy”—a method of positive reinforcement to increase desired behavior—has been used to successfully treat the disorder.²

Monitor adherence by weighing patients twice a day and checking serum sodium levels frequently. Normal water retention is cyclic and peaks in the early afternoon; therefore, early-morning screening for hyponatremia may not accurately reflect the severity of water abuse. A diurnal weight gain of ≥0.6% is unusual and might point to PPD.²

Consider administering an angiotensin-converting enzyme (ACE) inhibitor. In clinical trials 60% of patients taking ACE inhibitors show decreased water consumption.²

Order 24-hour, 1-to-1 observation if you suspect continuous water abuse.

Think about placing a patient with severe PPD in a locked unit in a long-term psychiatric institution, away from all water sources.

Psychogenic polydipsia (PPD) is a chronic, relapsing, and potentially life-threatening disorder characterized by compulsive consumption of large quantities of water resulting in “delutional hyponatremia.” PPD occurs in 6% to 20% of psychiatric patients, most often with schizophrenia.¹

In most patients with PPD, an electrolyte disturbance remains asymptomatic. However, superimposed and sudden ingestion of 3 to 4 liters of water can rapidly further dilute plasma and overwhelm the body’s compensatory reserves, leading to brain edema, seizures, coma, and even death.

The following prevention and treatment strategies might reduce morbidity and mortality in hospitalized patients diagnosed with PPD and lessen the cost of treating this serious illness.

Develop rapport. Understand that your patient has little control over his or her compulsive water intake. Remain nonjudgmental to help gain your patient’s trust.

Inquire about underlying psychiatric symptoms that might contribute to PPD. Does your patient have an overwhelming anxiety, delusional belief, or both? Effectively targeting specific symptoms will improve your chances of success.

Encourage communication among treatment team members. PPD patients are notoriously creative in sneaking water from unexpected places such as toilets and shower rooms. Staff vigilance is required to detect and prevent such clandestine behaviors.

Consult with an internist when necessary, especially if your patient has a comorbid cardiac condition that requires a low-sodium diet and/or diuretics.

Review psychotropic medications. In case reports of schizophrenia patients with PPD, switching from a typical to an atypical antipsychotic has shown efficacy in treating PPD.²

Restricting fluids to 2 to 3 liters a day combined with “a token economy”—a method of positive reinforcement to increase desired behavior—has been used to successfully treat the disorder.²

Monitor adherence by weighing patients twice a day and checking serum sodium levels frequently. Normal water retention is cyclic and peaks in the early afternoon; therefore, early-morning screening for hyponatremia may not accurately reflect the severity of water abuse. A diurnal weight gain of ≥0.6% is unusual and might point to PPD.²

Consider administering an angiotensin-converting enzyme (ACE) inhibitor. In clinical trials 60% of patients taking ACE inhibitors show decreased water consumption.²

Order 24-hour, 1-to-1 observation if you suspect continuous water abuse.

Think about placing a patient with severe PPD in a locked unit in a long-term psychiatric institution, away from all water sources.