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Case report: ECT for delirious mania
Delirious mania is a diagnostic term used in variety of settings, including the emergency department and inpatient psychiatry, but it does not have formal criteria established in the DSM-5. Delirious mania was first described in the 1800s and was referred to as “Bell’s Mania.”
As the late Max Fink, MD, wrote in the journal Bipolar Disorders (2002 Feb 23. doi: 10.1034/j.1399-561.1999.10112.x), delirious mania is considered to be a syndrome of the acute onset of the excitement, grandiosity, emotional lability, delusions, and insomnia characteristic of mania, and the disorientation and altered consciousness characteristic of delirium.
Such patients can be considered as having a component of bipolar I disorder, comprising mania with psychotic features. Delirious mania is associated with higher rates of morbidity and mortality, and demonstrates limited response to conventional treatment guidelines. Therefore, early detection and decisive treatment are imperative. The concurrence of delirium and mania is not unusual, yet currently there are no universal accepted treatment guidelines for delirious mania (BMC Psychiatry. 2012 Jun 21. doi: 10.1186/1471-244X-12-65). The purpose of this case report is to inspire and support community psychiatric clinicians in managing such complex cases and to improve behavioral health care outcomes. To protect our patient’s identity, we changed several key identifiers.
The treatment plan emerges
This case is of a middle-aged man with an established diagnosis of bipolar disorder. He was referred to the ED because of worsening manic symptoms marked by mood lability, pressured speech, grandiose delusions, tangential thought processes, poor insight, and impaired sleep.
Laboratory studies in the ED revealed hyponatremia and serum sodium of 126meq/l (ref. range: 135-146). The patient’s toxicology screen was positive for benzodiazepines. He was stabilized on the medical floor and then transitioned to inpatient psychiatry.
Before his admission to psychiatry, the patient’s medications were alprazolam 1 mg at bed time, bupropion 100 mg twice daily, loxapine 25 mg morning and 50 mg at bed time, olanzapine 20 mg at bedtime and 5 mg twice daily, risperidone 2 mg twice daily and oxcarbazepine 900 mg twice daily.
The bupropion was discontinued because of manic behavior, and the patient’s dose of oxcarbazepine was lowered from 900 mg twice daily to 450 mg twice daily because of hyponatremia. Our team continued to administer risperidone, olanzapine, loxapine, and alprazolam to the patient. However, he was agitated and disorganized on the psychiatry floor. In addition, we noticed that the patient exhibited confusion, disorientation, an inability to connect with reality, and periods of profound agitation.
The patient was frequently restrained physically, and medications were administered to him for safety and containment. The use of benzodiazepines and anticholinergics was minimized. However, we noticed that the patient acted paranoid, disinhibited, and combative, and he became difficult to restrain. He seemed to have a high pain tolerance, responded to internal stimuli, and began hallucinating and displaying aggressive behavior toward staff persons.
It became apparent that the patient’s circadian rhythm had been altered. He slept for only a couple of hours during the day. During the course of treatment, in one incidence, the patient became agitated and charged at a nurse. Subsequently, the patient hit his head on a wall and fell – suffering a head strike and lacerations.
The team conducted investigations, including labs and neuroimaging, to make sure that the patient was OK. His CT head scan proved unremarkable. Liver function tests revealed mild transaminitis. His TSH, folate, B12, and B1 levels were normal.
We then placed the patient in a single room with continuous behavior monitoring. His recovery seemed to take a long time with trials of different antipsychotic medications, including olanzapine, loxapine, risperidone, and paliperidone. Because of his poor response to medications, the team considered using electroconvulsive therapy (ECT).
However, the patient was unable to give informed consent for ECT because of his impaired mental status. At this point, our team submitted a substitute treatment plan that included ECT to the court for approval, and the court approved our plan.
After receiving approximately four bilateral ECT procedures three times a week, the patient’s condition started to improve gradually. He received total of 11 procedures.
Our patient became alert to time, place, and person, and his circadian rhythm normalized. Soon, his delirium cleared, and he demonstrated marked improvement in both insight into his illness and behavioral control. His grandiose delusions were still present, but he was easily redirectable. In addition, our patient demonstrated improved reality testing. He was able to be discharged home following medication adjustments and with community supports within a few short weeks of receiving ECT.
As Bo-Shyan Lee, MD, and associates reported (BMC Psychiatry. 2012 Jun 21;12:65. doi: 10.1186/1471-244X-12-65), delirious mania is closely related to catatonia. Although there are different definitions for delirium and catatonia, even the most lethal form of catatonia meets the criteria for delirium. ECT is a well established first-line treatment for catatonia. This tool has been shown to be highly effective in the treatment of delirious mania. Delirious mania can be life-threatening and should be managed aggressively. The most common causes of death are heart failure from arrhythmias, cardiac arrest, and respiratory failure. ECT is a safe treatment, and, as Dr. Fink argued, the mortality rate is even less than that associated with normal pregnancies (World J Biol Psychiatry. 2001 Jan;2[1]:1-8). In light of the safety and effectiveness of ECT, we think the tool should be considered not only in university hospital settings but as an early intervention in community settings. This case warrants further research in exploring hyperactive delirium and delirious mania.
Dr. Lamba is BR-2 unit medical director at BayRidge Hospital in Lynn, Mass. Ms. Kennedy is an attending clinician at BayRidge. Dr. Vu is medical director at BayRidge. He also serves as associate chief of psychiatry at Beverly (Mass.) Hospital and at Addison Gilbert Hospital in Gloucester, Mass. Dr. Lamba, Ms. Kennedy, and Dr. Vu have no disclosures.
Delirious mania is a diagnostic term used in variety of settings, including the emergency department and inpatient psychiatry, but it does not have formal criteria established in the DSM-5. Delirious mania was first described in the 1800s and was referred to as “Bell’s Mania.”
As the late Max Fink, MD, wrote in the journal Bipolar Disorders (2002 Feb 23. doi: 10.1034/j.1399-561.1999.10112.x), delirious mania is considered to be a syndrome of the acute onset of the excitement, grandiosity, emotional lability, delusions, and insomnia characteristic of mania, and the disorientation and altered consciousness characteristic of delirium.
Such patients can be considered as having a component of bipolar I disorder, comprising mania with psychotic features. Delirious mania is associated with higher rates of morbidity and mortality, and demonstrates limited response to conventional treatment guidelines. Therefore, early detection and decisive treatment are imperative. The concurrence of delirium and mania is not unusual, yet currently there are no universal accepted treatment guidelines for delirious mania (BMC Psychiatry. 2012 Jun 21. doi: 10.1186/1471-244X-12-65). The purpose of this case report is to inspire and support community psychiatric clinicians in managing such complex cases and to improve behavioral health care outcomes. To protect our patient’s identity, we changed several key identifiers.
The treatment plan emerges
This case is of a middle-aged man with an established diagnosis of bipolar disorder. He was referred to the ED because of worsening manic symptoms marked by mood lability, pressured speech, grandiose delusions, tangential thought processes, poor insight, and impaired sleep.
Laboratory studies in the ED revealed hyponatremia and serum sodium of 126meq/l (ref. range: 135-146). The patient’s toxicology screen was positive for benzodiazepines. He was stabilized on the medical floor and then transitioned to inpatient psychiatry.
Before his admission to psychiatry, the patient’s medications were alprazolam 1 mg at bed time, bupropion 100 mg twice daily, loxapine 25 mg morning and 50 mg at bed time, olanzapine 20 mg at bedtime and 5 mg twice daily, risperidone 2 mg twice daily and oxcarbazepine 900 mg twice daily.
The bupropion was discontinued because of manic behavior, and the patient’s dose of oxcarbazepine was lowered from 900 mg twice daily to 450 mg twice daily because of hyponatremia. Our team continued to administer risperidone, olanzapine, loxapine, and alprazolam to the patient. However, he was agitated and disorganized on the psychiatry floor. In addition, we noticed that the patient exhibited confusion, disorientation, an inability to connect with reality, and periods of profound agitation.
The patient was frequently restrained physically, and medications were administered to him for safety and containment. The use of benzodiazepines and anticholinergics was minimized. However, we noticed that the patient acted paranoid, disinhibited, and combative, and he became difficult to restrain. He seemed to have a high pain tolerance, responded to internal stimuli, and began hallucinating and displaying aggressive behavior toward staff persons.
It became apparent that the patient’s circadian rhythm had been altered. He slept for only a couple of hours during the day. During the course of treatment, in one incidence, the patient became agitated and charged at a nurse. Subsequently, the patient hit his head on a wall and fell – suffering a head strike and lacerations.
The team conducted investigations, including labs and neuroimaging, to make sure that the patient was OK. His CT head scan proved unremarkable. Liver function tests revealed mild transaminitis. His TSH, folate, B12, and B1 levels were normal.
We then placed the patient in a single room with continuous behavior monitoring. His recovery seemed to take a long time with trials of different antipsychotic medications, including olanzapine, loxapine, risperidone, and paliperidone. Because of his poor response to medications, the team considered using electroconvulsive therapy (ECT).
However, the patient was unable to give informed consent for ECT because of his impaired mental status. At this point, our team submitted a substitute treatment plan that included ECT to the court for approval, and the court approved our plan.
After receiving approximately four bilateral ECT procedures three times a week, the patient’s condition started to improve gradually. He received total of 11 procedures.
Our patient became alert to time, place, and person, and his circadian rhythm normalized. Soon, his delirium cleared, and he demonstrated marked improvement in both insight into his illness and behavioral control. His grandiose delusions were still present, but he was easily redirectable. In addition, our patient demonstrated improved reality testing. He was able to be discharged home following medication adjustments and with community supports within a few short weeks of receiving ECT.
As Bo-Shyan Lee, MD, and associates reported (BMC Psychiatry. 2012 Jun 21;12:65. doi: 10.1186/1471-244X-12-65), delirious mania is closely related to catatonia. Although there are different definitions for delirium and catatonia, even the most lethal form of catatonia meets the criteria for delirium. ECT is a well established first-line treatment for catatonia. This tool has been shown to be highly effective in the treatment of delirious mania. Delirious mania can be life-threatening and should be managed aggressively. The most common causes of death are heart failure from arrhythmias, cardiac arrest, and respiratory failure. ECT is a safe treatment, and, as Dr. Fink argued, the mortality rate is even less than that associated with normal pregnancies (World J Biol Psychiatry. 2001 Jan;2[1]:1-8). In light of the safety and effectiveness of ECT, we think the tool should be considered not only in university hospital settings but as an early intervention in community settings. This case warrants further research in exploring hyperactive delirium and delirious mania.
Dr. Lamba is BR-2 unit medical director at BayRidge Hospital in Lynn, Mass. Ms. Kennedy is an attending clinician at BayRidge. Dr. Vu is medical director at BayRidge. He also serves as associate chief of psychiatry at Beverly (Mass.) Hospital and at Addison Gilbert Hospital in Gloucester, Mass. Dr. Lamba, Ms. Kennedy, and Dr. Vu have no disclosures.
Delirious mania is a diagnostic term used in variety of settings, including the emergency department and inpatient psychiatry, but it does not have formal criteria established in the DSM-5. Delirious mania was first described in the 1800s and was referred to as “Bell’s Mania.”
As the late Max Fink, MD, wrote in the journal Bipolar Disorders (2002 Feb 23. doi: 10.1034/j.1399-561.1999.10112.x), delirious mania is considered to be a syndrome of the acute onset of the excitement, grandiosity, emotional lability, delusions, and insomnia characteristic of mania, and the disorientation and altered consciousness characteristic of delirium.
Such patients can be considered as having a component of bipolar I disorder, comprising mania with psychotic features. Delirious mania is associated with higher rates of morbidity and mortality, and demonstrates limited response to conventional treatment guidelines. Therefore, early detection and decisive treatment are imperative. The concurrence of delirium and mania is not unusual, yet currently there are no universal accepted treatment guidelines for delirious mania (BMC Psychiatry. 2012 Jun 21. doi: 10.1186/1471-244X-12-65). The purpose of this case report is to inspire and support community psychiatric clinicians in managing such complex cases and to improve behavioral health care outcomes. To protect our patient’s identity, we changed several key identifiers.
The treatment plan emerges
This case is of a middle-aged man with an established diagnosis of bipolar disorder. He was referred to the ED because of worsening manic symptoms marked by mood lability, pressured speech, grandiose delusions, tangential thought processes, poor insight, and impaired sleep.
Laboratory studies in the ED revealed hyponatremia and serum sodium of 126meq/l (ref. range: 135-146). The patient’s toxicology screen was positive for benzodiazepines. He was stabilized on the medical floor and then transitioned to inpatient psychiatry.
Before his admission to psychiatry, the patient’s medications were alprazolam 1 mg at bed time, bupropion 100 mg twice daily, loxapine 25 mg morning and 50 mg at bed time, olanzapine 20 mg at bedtime and 5 mg twice daily, risperidone 2 mg twice daily and oxcarbazepine 900 mg twice daily.
The bupropion was discontinued because of manic behavior, and the patient’s dose of oxcarbazepine was lowered from 900 mg twice daily to 450 mg twice daily because of hyponatremia. Our team continued to administer risperidone, olanzapine, loxapine, and alprazolam to the patient. However, he was agitated and disorganized on the psychiatry floor. In addition, we noticed that the patient exhibited confusion, disorientation, an inability to connect with reality, and periods of profound agitation.
The patient was frequently restrained physically, and medications were administered to him for safety and containment. The use of benzodiazepines and anticholinergics was minimized. However, we noticed that the patient acted paranoid, disinhibited, and combative, and he became difficult to restrain. He seemed to have a high pain tolerance, responded to internal stimuli, and began hallucinating and displaying aggressive behavior toward staff persons.
It became apparent that the patient’s circadian rhythm had been altered. He slept for only a couple of hours during the day. During the course of treatment, in one incidence, the patient became agitated and charged at a nurse. Subsequently, the patient hit his head on a wall and fell – suffering a head strike and lacerations.
The team conducted investigations, including labs and neuroimaging, to make sure that the patient was OK. His CT head scan proved unremarkable. Liver function tests revealed mild transaminitis. His TSH, folate, B12, and B1 levels were normal.
We then placed the patient in a single room with continuous behavior monitoring. His recovery seemed to take a long time with trials of different antipsychotic medications, including olanzapine, loxapine, risperidone, and paliperidone. Because of his poor response to medications, the team considered using electroconvulsive therapy (ECT).
However, the patient was unable to give informed consent for ECT because of his impaired mental status. At this point, our team submitted a substitute treatment plan that included ECT to the court for approval, and the court approved our plan.
After receiving approximately four bilateral ECT procedures three times a week, the patient’s condition started to improve gradually. He received total of 11 procedures.
Our patient became alert to time, place, and person, and his circadian rhythm normalized. Soon, his delirium cleared, and he demonstrated marked improvement in both insight into his illness and behavioral control. His grandiose delusions were still present, but he was easily redirectable. In addition, our patient demonstrated improved reality testing. He was able to be discharged home following medication adjustments and with community supports within a few short weeks of receiving ECT.
As Bo-Shyan Lee, MD, and associates reported (BMC Psychiatry. 2012 Jun 21;12:65. doi: 10.1186/1471-244X-12-65), delirious mania is closely related to catatonia. Although there are different definitions for delirium and catatonia, even the most lethal form of catatonia meets the criteria for delirium. ECT is a well established first-line treatment for catatonia. This tool has been shown to be highly effective in the treatment of delirious mania. Delirious mania can be life-threatening and should be managed aggressively. The most common causes of death are heart failure from arrhythmias, cardiac arrest, and respiratory failure. ECT is a safe treatment, and, as Dr. Fink argued, the mortality rate is even less than that associated with normal pregnancies (World J Biol Psychiatry. 2001 Jan;2[1]:1-8). In light of the safety and effectiveness of ECT, we think the tool should be considered not only in university hospital settings but as an early intervention in community settings. This case warrants further research in exploring hyperactive delirium and delirious mania.
Dr. Lamba is BR-2 unit medical director at BayRidge Hospital in Lynn, Mass. Ms. Kennedy is an attending clinician at BayRidge. Dr. Vu is medical director at BayRidge. He also serves as associate chief of psychiatry at Beverly (Mass.) Hospital and at Addison Gilbert Hospital in Gloucester, Mass. Dr. Lamba, Ms. Kennedy, and Dr. Vu have no disclosures.
Reducing clozapine-induced hypersalivation
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Hypersalivation is a well-documented side effect of clozapine that may affect nearly 30% of patients who take this medication.1 Because clozapine has anticholinergic properties that are expected to reduce secretions, hypersalivation is considered a paradoxical effect. This paradox can be explained by examining clozapine’s actions at the molecular level.
Clozapine has antagonistic activity at many types of receptors, including D1 to D5 dopaminergic, α1 and α2 adrenergic, serotonergic, histaminergic, and M1, M2, M3, and M5 cholinergic.2 By contrast, clozapine’s activity at M4 cholinergic receptors is agonistic. The combination of clozapine’s antagonist activity at α2 adrenergic receptors and agonist activity at muscarinic M4 receptors results in hypersalivation.3 Clozapine also increases pooling of saliva in the mouth by diminishing esophageal motility, which gives the appearance of hypersalivation as a result of reduced saliva clearance through normal swallowing.4
Practical lifestyle changes
Excessive saliva secretion and pooling can be reduced by practical behavioral and/or pharmacologic interventions. Patients who chew gum during the day will increase their swallowing unconsciously5; recommend sugarless gum to help avoid tooth decay and gum disease. If hypersalivation is particularly bothersome at night, patients may find it useful to cover their pillows with an absorbent towel.
Pharmacologic treatments
Pharmacologic interventions rely on counteracting clozapine’s secretion-inducing effects by opposing M4 agonism, α2 antagonism, or both. Antimuscarinic medications such as benztropine, trihexyphenidyl, amitriptyline, or pirenzepine often are used to reduce hypersalivation,6 although 1 systematic review concluded further evidence is needed to support the effectiveness of this approach.7 The α2 antagonism can be opposed by using the α2 agonist clonidine, which can be administered as a weekly transdermal patch of 0.1 to 0.2 mg.8 In 1 retrospective study, the cholinergic and adrenergic mechanisms of hypersalivation were addressed by combining benztropine (2 mg/d in a divided dose) with the α1 antagonist terazosin (2 mg/d). This combination reduced hypersalivation significantly in all patients after 12 weeks, exceeding the efficacy of either benztropine or terazosin administered alone.9
Hypersalivation is an inconvenient, potentially embarrassing aspect of clozapine treatment that can cause avoidable distress. One or more of these suggestions may help control an adverse effect that could diminish patient satisfaction and undermine treatment compliance.
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Safferman A, Lieberman JA, Kane JM, et al. Update on the clinical efficacy and side effects of clozapine. Schizophr Bull. 1991;17(2):247-261.
2. Zorn SH, Jones SB, Ward KM, et al. Clozapine is a potent and selective muscarinic M4 receptor agonist. Eur J Pharmacol. 1994;269(3):R1-R2.
3. Berlan M, Montastruc JL, Lafontan M. Pharmacological prospects for alpha 2-adrenoceptor antagonist therapy. Trends Pharmacol Sci. 1992;13(7):277-282.
4. Sadock BJ, Sadock VA. Kaplan and Sadock’s comprehensive textbook of psychiatry. 7th ed. Philadelphia PA: Lippincott Williams & Wilkins; 2000.
5. Bourgeois JA, Drexler KG, Hall MJ. Hypersalivation and clozapine. Hosp Community Psychiatry. 1991;42(11):1174.-
6. Cree A, Mir S, Fahy T. A review of the treatment options for clozapine-induced hypersalivation. The Psychiatrist. 2001;25:114-116.
7. Syed R, Au K, Cahill C, et al. Pharmacological interventions for clozapine-induced hypersalivation. Cochrane Database Syst Rev. 2008;(3):CD005579.-
8. Grabowski J. Clonidine treatment of clozapine-induced hypersalivation. J Clin Psychopharmacol. 1992;12(1):69-70.
9. Reinstein MJ, Sirotovskaya LA, Chasanov MA, et al. Comparative efficacy and tolerability of benztropine and terazosin in the treatment of hypersalivation secondary to clozapine. Clin Drug Investig. 1999;17(2):97-102.
Discuss this article at www.facebook.com/CurrentPsychiatry
Hypersalivation is a well-documented side effect of clozapine that may affect nearly 30% of patients who take this medication.1 Because clozapine has anticholinergic properties that are expected to reduce secretions, hypersalivation is considered a paradoxical effect. This paradox can be explained by examining clozapine’s actions at the molecular level.
Clozapine has antagonistic activity at many types of receptors, including D1 to D5 dopaminergic, α1 and α2 adrenergic, serotonergic, histaminergic, and M1, M2, M3, and M5 cholinergic.2 By contrast, clozapine’s activity at M4 cholinergic receptors is agonistic. The combination of clozapine’s antagonist activity at α2 adrenergic receptors and agonist activity at muscarinic M4 receptors results in hypersalivation.3 Clozapine also increases pooling of saliva in the mouth by diminishing esophageal motility, which gives the appearance of hypersalivation as a result of reduced saliva clearance through normal swallowing.4
Practical lifestyle changes
Excessive saliva secretion and pooling can be reduced by practical behavioral and/or pharmacologic interventions. Patients who chew gum during the day will increase their swallowing unconsciously5; recommend sugarless gum to help avoid tooth decay and gum disease. If hypersalivation is particularly bothersome at night, patients may find it useful to cover their pillows with an absorbent towel.
Pharmacologic treatments
Pharmacologic interventions rely on counteracting clozapine’s secretion-inducing effects by opposing M4 agonism, α2 antagonism, or both. Antimuscarinic medications such as benztropine, trihexyphenidyl, amitriptyline, or pirenzepine often are used to reduce hypersalivation,6 although 1 systematic review concluded further evidence is needed to support the effectiveness of this approach.7 The α2 antagonism can be opposed by using the α2 agonist clonidine, which can be administered as a weekly transdermal patch of 0.1 to 0.2 mg.8 In 1 retrospective study, the cholinergic and adrenergic mechanisms of hypersalivation were addressed by combining benztropine (2 mg/d in a divided dose) with the α1 antagonist terazosin (2 mg/d). This combination reduced hypersalivation significantly in all patients after 12 weeks, exceeding the efficacy of either benztropine or terazosin administered alone.9
Hypersalivation is an inconvenient, potentially embarrassing aspect of clozapine treatment that can cause avoidable distress. One or more of these suggestions may help control an adverse effect that could diminish patient satisfaction and undermine treatment compliance.
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Discuss this article at www.facebook.com/CurrentPsychiatry
Hypersalivation is a well-documented side effect of clozapine that may affect nearly 30% of patients who take this medication.1 Because clozapine has anticholinergic properties that are expected to reduce secretions, hypersalivation is considered a paradoxical effect. This paradox can be explained by examining clozapine’s actions at the molecular level.
Clozapine has antagonistic activity at many types of receptors, including D1 to D5 dopaminergic, α1 and α2 adrenergic, serotonergic, histaminergic, and M1, M2, M3, and M5 cholinergic.2 By contrast, clozapine’s activity at M4 cholinergic receptors is agonistic. The combination of clozapine’s antagonist activity at α2 adrenergic receptors and agonist activity at muscarinic M4 receptors results in hypersalivation.3 Clozapine also increases pooling of saliva in the mouth by diminishing esophageal motility, which gives the appearance of hypersalivation as a result of reduced saliva clearance through normal swallowing.4
Practical lifestyle changes
Excessive saliva secretion and pooling can be reduced by practical behavioral and/or pharmacologic interventions. Patients who chew gum during the day will increase their swallowing unconsciously5; recommend sugarless gum to help avoid tooth decay and gum disease. If hypersalivation is particularly bothersome at night, patients may find it useful to cover their pillows with an absorbent towel.
Pharmacologic treatments
Pharmacologic interventions rely on counteracting clozapine’s secretion-inducing effects by opposing M4 agonism, α2 antagonism, or both. Antimuscarinic medications such as benztropine, trihexyphenidyl, amitriptyline, or pirenzepine often are used to reduce hypersalivation,6 although 1 systematic review concluded further evidence is needed to support the effectiveness of this approach.7 The α2 antagonism can be opposed by using the α2 agonist clonidine, which can be administered as a weekly transdermal patch of 0.1 to 0.2 mg.8 In 1 retrospective study, the cholinergic and adrenergic mechanisms of hypersalivation were addressed by combining benztropine (2 mg/d in a divided dose) with the α1 antagonist terazosin (2 mg/d). This combination reduced hypersalivation significantly in all patients after 12 weeks, exceeding the efficacy of either benztropine or terazosin administered alone.9
Hypersalivation is an inconvenient, potentially embarrassing aspect of clozapine treatment that can cause avoidable distress. One or more of these suggestions may help control an adverse effect that could diminish patient satisfaction and undermine treatment compliance.
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Safferman A, Lieberman JA, Kane JM, et al. Update on the clinical efficacy and side effects of clozapine. Schizophr Bull. 1991;17(2):247-261.
2. Zorn SH, Jones SB, Ward KM, et al. Clozapine is a potent and selective muscarinic M4 receptor agonist. Eur J Pharmacol. 1994;269(3):R1-R2.
3. Berlan M, Montastruc JL, Lafontan M. Pharmacological prospects for alpha 2-adrenoceptor antagonist therapy. Trends Pharmacol Sci. 1992;13(7):277-282.
4. Sadock BJ, Sadock VA. Kaplan and Sadock’s comprehensive textbook of psychiatry. 7th ed. Philadelphia PA: Lippincott Williams & Wilkins; 2000.
5. Bourgeois JA, Drexler KG, Hall MJ. Hypersalivation and clozapine. Hosp Community Psychiatry. 1991;42(11):1174.-
6. Cree A, Mir S, Fahy T. A review of the treatment options for clozapine-induced hypersalivation. The Psychiatrist. 2001;25:114-116.
7. Syed R, Au K, Cahill C, et al. Pharmacological interventions for clozapine-induced hypersalivation. Cochrane Database Syst Rev. 2008;(3):CD005579.-
8. Grabowski J. Clonidine treatment of clozapine-induced hypersalivation. J Clin Psychopharmacol. 1992;12(1):69-70.
9. Reinstein MJ, Sirotovskaya LA, Chasanov MA, et al. Comparative efficacy and tolerability of benztropine and terazosin in the treatment of hypersalivation secondary to clozapine. Clin Drug Investig. 1999;17(2):97-102.
1. Safferman A, Lieberman JA, Kane JM, et al. Update on the clinical efficacy and side effects of clozapine. Schizophr Bull. 1991;17(2):247-261.
2. Zorn SH, Jones SB, Ward KM, et al. Clozapine is a potent and selective muscarinic M4 receptor agonist. Eur J Pharmacol. 1994;269(3):R1-R2.
3. Berlan M, Montastruc JL, Lafontan M. Pharmacological prospects for alpha 2-adrenoceptor antagonist therapy. Trends Pharmacol Sci. 1992;13(7):277-282.
4. Sadock BJ, Sadock VA. Kaplan and Sadock’s comprehensive textbook of psychiatry. 7th ed. Philadelphia PA: Lippincott Williams & Wilkins; 2000.
5. Bourgeois JA, Drexler KG, Hall MJ. Hypersalivation and clozapine. Hosp Community Psychiatry. 1991;42(11):1174.-
6. Cree A, Mir S, Fahy T. A review of the treatment options for clozapine-induced hypersalivation. The Psychiatrist. 2001;25:114-116.
7. Syed R, Au K, Cahill C, et al. Pharmacological interventions for clozapine-induced hypersalivation. Cochrane Database Syst Rev. 2008;(3):CD005579.-
8. Grabowski J. Clonidine treatment of clozapine-induced hypersalivation. J Clin Psychopharmacol. 1992;12(1):69-70.
9. Reinstein MJ, Sirotovskaya LA, Chasanov MA, et al. Comparative efficacy and tolerability of benztropine and terazosin in the treatment of hypersalivation secondary to clozapine. Clin Drug Investig. 1999;17(2):97-102.