- Email: [email protected]
Atypical Neuroleptic Malignant Syndrome Associated with Iloperidone Administration
Letters to the Editor administration of valpromide 900 mg/d divided in 3 doses. Psychotropic intervention resulted in significant mood stabilization and significant improvement of self-injury and aggression. The valpromide was continued at the same dose, which was well tolerated, no laboratory abnormalities were noted, and no recurrence of psychiatric symptoms were observed. Mr. A’s written informed consent was obtained. Adverse effects during TCL therapy are generally of the type common to all immunosuppressive regimens, including nephrotoxicity, gastrointestinal symptoms (diarrhea, nausea, vomiting), pruritus, alopecia, disturbances in glucose metabolism and diabetes mellitus, neurotoxicity (hand tremors, headache), neuropsychological and behavioral symptoms, severe insomnia, aggressiveness, and anxious behavior.1 Neuropsychiatric side effects are among the most debilitating side effects because of their impact on mental status and cognition, and particularly problematic after LTX. Neurotoxicity following LTX can be evoked by various perioperative factors or can develop because of drug-specific toxicity of immunosuppression. However, the tolerability of TCL appears to be doserelated, less problematic as the dose is reduced and the symptoms of TCL associated neurotoxicity may be reversed in most patients by substantially reducing the dosage or discontinuing the drug.2 All side effects are fully reversible after discontinuation of TCL. Little is known about the acute overdosing of TCL. Although the prescribing information for mycophenolic acid reports depression as an adverse event, only few descriptions of the onset or manifestation of this idiosyncratic reaction or other effect on mood have been published. Cumulative data indicate that psychiatric complications of corticosteroid
treatment are not rare and range from clinically significant anxiety and insomnia to severe mood and psychotic disorders, delirium, and dementia. While tapering or discontinuation of the corticosteroid treatment may remedy these adverse side effects, psychotropic medications are often required because of the medical necessity of the corticosteroid or the severity of the psychiatric symptom. Few studies describe the deleterious psychiatric effects associated with corticosteroids. Naturally, in a case such as that here described, characterized by multiple medical treatments, it is impossible to determine exactly which therapy may have triggered the onset of the psychiatric disorder,3,4 but the only different variable during the observation period was the accidental acute TCL overdose. The mechanism of action responsible for the immunosuppressive drugs-linked mood disorders is as yet unknown. Maria Carolina Hardoy, M.D., Ph.D. Fausto Zamboni, M.D. Laura Mameli, M.D. Azienda Ospedaliera Brotzu Cagliari, Italy Joseph R. Calabrese, M.D. Bipolar Disorders Research Center University Hospitals Case Medical Center Case Western Reserve University Cleveland, OH
Conflict of Interest Statement: J.R.C. has received research grant support from Abbott, AstraZeneca, BristolMyers Squibb, Cephalon, Eli Lilly, GlaxoSmithKline, Janssen, Repligen, Sunovion/DSPA, Takeda, and Wyeth; consulted to or served on advisory boards of AstraZeneca, Bristol-Myers Squibb, Cephalon, Sunovion/DSPA, Forest, GlaxoSmithKline, Janssen, Johnson and Johnson, Lundbeck, Neurosearch, OrthoMcNeil, Otsuka, Pfizer, Repligen, Schering-Plough, Servier, Solvay, Supernus, Synosia, and Wyeth; and has provided
Psychosomatics 53:6, November-December 2012
CME lectures supported by Abbott, AstraZeneca, Bristol-Myers Squibb, GlaxoSmithKline, Janssen, Johnson and Johnson, Lundbeck, Merck, Sanofi Aventis, Schering-Plough, Pfizer, Solvay, and Wyeth. No speaker bureaus for the past 10 years. No stock, no equity, and no patents. The remaining authors (M.C.H., F.Z., and L.M.) report no financial relationships with competing or commercial interests.
References
1. Scott LJ, McKeage K, Keam SJ, Plosker GL: Tacrolimus: a further update of its use in the management of organ transplantation. Drugs 2003; 63:1247–1297 2. Bechstein WO: Neurotoxicity of calcineurin inhibitors: impact and clinical management. Transpl Int 2000; 13:313–326 3. Fireman M, DiMartini AF, Armstrong SC, Cozza KL: Immunosuppressants. Psychosomatics 2004; 45:354 –360 4. Armstrong SC, Cozza KL, Pimentel EA: Immunosuppressants. Psychosomatics 2002; 43:424 – 427
Atypical Neuroleptic Malignant Syndrome Associated with Iloperidone Administration TO THE EDITOR: Neuroleptic malignant syndrome (NMS) is a complication seen in 0.02%– 0.25% of patients prescribed antipsychotics.1 The DSM-IV-TR proposes criteria for the diagnosis of NMS, however, many reports describe atypical presentations that appear to have similar clinical relevance, particularly with second-generation antipsychotics.1 The atypical presentations commonly lack the core features of hyperthermia and muscle rigidity, thus making a definitive diagnosis more challenging and potentially hindering treatment, increasing morbidity and mortality.1 Here, we present a case of atypical NMS associated with iloperidone, which has www.psychosomaticsjournal.org
603
Letters to the Editor recently been introduced as a secondgeneration antipsychotic approved for treating schizophrenia.2 We have not found reports in the literature to date of neuroleptic malignant syndrome with iloperidone. Case Report Ms. B is a 37-year-old African-American woman with a history of paranoid schizophrenia admitted to the medical intensive care unit (MICU) for suspected NMS. Ms. B was in her usual state of health until 4 hours prior to presentation, when she exhibited decreased verbal responsiveness and muscle stiffness. In the emergency department (ED), mutism, diaphoresis, and diffuse lead pipe rigidity were present. Heart rate was 112, temperature was 99.8°F (37.7°C), blood pressure was 132/78, and respiratory rate was 16. The remainder of the physical exam was within normal limits. Chest X-ray and EKG showed no abnormalities. Laboratory results were negative for metabolic disturbances, drugs, creatinine kinase elevation, or infection. History revealed a medication adjustment due to amenorrhea. Risperidone 2 mg PO BID, taken for 1–2 years, was abruptly discontinued, and iloperidone 1 mg PO at bedtime was started instead, 6 days prior to presentation. Due to the presence of severe lead pipe rigidity, in association with the above symptoms and a history of antipsychotic use, NMS was suspected, and treatment of NMS was promptly and aggressively initiated by the ED physician with IV dantrolene. She was admitted to the MICU 4 hours later. After 12 hours of supportive care, rigidity improved, creatinine kinase did not rise (value 103), tachycardia ranged from 100 to 130, and she remained afebrile. On mental status 604
www.psychosomaticsjournal.org
exam, she exhibited intense eye contact, blunted affect, selective mutism, and no overt psychotic symptoms. After tachycardia improved to a heart rate of 90 –100, she was transferred to the inpatient psychiatric unit on lorazepam 1 mg PO TID. In the psychiatric unit, lorazepam 1 mg PO TID was continued because of mutism. Due to concern about the possibility of rebound psychosis following discontinuation of risperidone, she was challenged with 1 mg of risperidone on day 7 of hospitalization by the inpatient psychiatrist. Within a few hours, symptoms suggestive of NMS recurred, including a worsening of tachycardia, which improved to a degree after administration of IM lorazepam. However, she remained moderately tachycardic, and the medical team recommended a d-dimer (value 7569) and chest CT scan. This revealed pulmonary emboli in the right interlobar artery and segmental branches. IV anticoagulation was then instituted on the medical floor. Once medically stabilized, she was transferred to psychiatry. Slowly, her catatonia resolved. Lorazepam was tapered to 1 mg PO BID, escitalopram 10 mg PO daily was added with good effect for mood symptoms, and she was discharged 3 weeks later on no antipsychotics. Discussion The DSM-IV-TR defines NMS as a syndrome consisting of hyperthermia (temperature ⬎100.4°F [38 °C]), muscle rigidity, and two of the following: diaphoresis, dysphagia, incontinence, altered consciousness, mutism, hypertension, labile blood pressure, CK elevation, tremor, or tachycardia.2 According to the International Consensus Study of Neuroleptic Malignant Syndrome Diagnostic Criteria proposed by Gurrera et al., hyperthermia ranked
second in importance among diagnostic features of typical NMS.3 According to the DSM, Ms. B met criteria for NMS with the exception of hyperthermia, which did not reach criterion levels on presentation. The lack of hyperthermia in Ms. B may be related to her early presentation and the rapid initiation of appropriate treatment. Cases of NMS have been described with initial symptoms of mental status changes and muscle rigidity that only later progressed to autonomic instability and hyperthermia.4 The clinical pattern seen in Ms. B is consistent with such a clinical course, which also implies that early detection of NMS symptoms may result in fewer typical cases of NMS. An alternative explanation is that Ms. B experienced what may be a related but possibly a distinct syndrome of atypical NMS, described in several reports as NMS-like syndromes lacking certain core features of the DSMIV-TR criteria, especially hyperthermia.2 Atypical NMS has often been associated with atypical antipsychotics.2 A review by Zarouff et al. reported cases of NMS with aripiprazole, clozapine, and olanzapine lacking hyperthermia, rigidity, and CK elevation.1 It has been postulated that unlike typical NMS, which involves central dopaminergic blockade, atypical NMS also involves the epinephrine, serotonin, and norepinephrine systems.5 Some authors have suggested alternative, more flexible criteria for diagnosing and categorizing NMS.6 While not meeting the full DSMIV-TR criteria for NMS, Ms. B’s presentation was consistent with the alternate criteria described by Levenson. Levenson proposed that the presence of all three major manifestations (fever, rigidity, elevated CK), or two major and four minor manifestations (tachycardia, abnormal blood pressure,
Psychosomatics 53:6, November-December 2012
Letters to the Editor tachypnea, altered consciousness, diaphoresis, and leukocytosis) be considered high-probability evidence of NMS in appropriate clinical contexts.7 The differential diagnosis for NMS includes lethal catatonia, meningitis, status epilepticus, stroke, hyperthyroidism, pheochromocytoma, acute porphyria, serotonin syndrome, malignant hyperthermia, and anticholinergic syndrome.2 Considering the clinical history and laboratory results, lethal catatonia might be considered as an alternative diagnosis. Lethal catatonia is characterized by fever, mutism, stereotypic movements, posturing, and autonomic instability.8 Unlike NMS, which typically begins with rigidity, lethal catatonia has been associated with a prodromal phase characterized by mood lability, insomnia, anorexia, excitement, and agitation prior to the onset of rigidity.9,10 Further, in lethal catatonia, catatonic episodes typically begin prior to neuroleptic administration.9 NMS therefore appears to be the more likely diagnosis in Ms. B. The re-emergence of NMS symptoms following challenge with risperidone 1 week later is also consistent with the initial presentation being NMS, since NMS events are a risk factor for future episodes.2 A review of re-challenge with atypical antipsychotics after earlier NMS showed that 19 out of 45 patients experienced recurrence of NMS symptoms.11 NMS is also considered a contributing factor to the development of pulmonary emboli, as a consequence of protracted immobility, rigidity, and subsequent
rhabdomyolysis, which increase the chances of thromboemboli.4
2.
Conclusion Despite NMS being a relatively rare occurrence, it may develop in patients taking atypical antipsychotics, including iloperidone, which has not been reported previously.4 Since prompt identification and treatment may prevent progression of symptoms and mortality, a high index of suspicion is advisable when patients prescribed anti-psychotics present with NMS-like symptoms, even if full criteria are not met. Further studies to elucidate the relationship between atypical NMS symptomatology and the standard presentation with respect to diagnostic heterogeneity and clinical course are needed. Nicole Guanci, M.D. Psychiatry Resident New Jersey Medical School University of Medicine and Dentistry of New Jersey Rashi Aggarwal, M.D. Assistant Professor Department of Psychiatry New Jersey Medical School University of Medicine and Dentistry of New Jersey Steven Schleifer, M.D. Assistant Professor Department of Psychiatry New Jersey Medical School University of Medicine and Dentistry of New Jersey References
1. Zarrouf FA, Bhanot V: Neuroleptic malignant syndrome: don’t let your
Psychosomatics 53:6, November-December 2012
3.
4.
5.
6.
7.
8.
9.
10.
11.
guard down yet. Curr Psychiatry 2007; 6:89 –95 Citrome L: Iloperidone for schizophrenia: a review of the efficacy and safety profile for this newly commercialized second-generation antipsychotic. Int J Clin Practice 2009; 63:1237–1238 Gurrera RJ, Caroff SN, Cohen A, Carroll BT, DeRoos F, Francis A, et al: An International Consensus Study of Neuroleptic Malignant Syndrome Diagnostic Criteria Using the Delphi Method. J Clin Psychiatry 2011; 72:1222–1228 Picard LS, Lindsay S, Strawn JR, Kaneria RM, Patel NC, Keck PE: Atypical neuroleptic malignant syndrome: diagnostic controversies and considerations. Pharmacotherapy 2008; 28:530 –535 Balzan MV: The neuroleptic malignant syndrome: a logical approach to the patient with temperature and rigidity. Postgrad Med J 1998; 74:72–76 Pope HG, Keck PE, McElroy SL: Frequency and presentation of neuroleptic malignant syndrome in a large Psychiatric hospital. Am J Psychiatry 1986; 143: 1227–1233 Levenson JL: Neuroleptic malignant syndrome. Am J Psychiatry 1985; 142:1137– 1145 Weder ND, Muralee S, Penland H, Tampi RR: Catatonia: a review. Ann Clin Psychiatry 2008; 20:97–107 Sheil AT, Collins KA, Schandl CA, Harley, RA: Fatal neurotoxic response to neuroleptic medications: a case report and review of the literature. Am J Forensic Med Pathol 2007; 28:116 –120 Mann SC, Caroff SN, Bleier HR, Welz WK, Kling MA, Hayashida M: Lethal catatonia. Am J Psychiatry 1986; 143: 1374 –1380 Mendhekar DN, Jiloha RC, Mehndiratta MM, War L: Challenge with atypical antipsychotic drugs in risperidone induced neuroleptic malignant syndrome: a case report. Indian J Psychiatry 2002; 44:387– 390
www.psychosomaticsjournal.org
605
treatment are not rare and range from clinically significant anxiety and insomnia to severe mood and psychotic disorders, delirium, and dementia. While tapering or discontinuation of the corticosteroid treatment may remedy these adverse side effects, psychotropic medications are often required because of the medical necessity of the corticosteroid or the severity of the psychiatric symptom. Few studies describe the deleterious psychiatric effects associated with corticosteroids. Naturally, in a case such as that here described, characterized by multiple medical treatments, it is impossible to determine exactly which therapy may have triggered the onset of the psychiatric disorder,3,4 but the only different variable during the observation period was the accidental acute TCL overdose. The mechanism of action responsible for the immunosuppressive drugs-linked mood disorders is as yet unknown. Maria Carolina Hardoy, M.D., Ph.D. Fausto Zamboni, M.D. Laura Mameli, M.D. Azienda Ospedaliera Brotzu Cagliari, Italy Joseph R. Calabrese, M.D. Bipolar Disorders Research Center University Hospitals Case Medical Center Case Western Reserve University Cleveland, OH
Conflict of Interest Statement: J.R.C. has received research grant support from Abbott, AstraZeneca, BristolMyers Squibb, Cephalon, Eli Lilly, GlaxoSmithKline, Janssen, Repligen, Sunovion/DSPA, Takeda, and Wyeth; consulted to or served on advisory boards of AstraZeneca, Bristol-Myers Squibb, Cephalon, Sunovion/DSPA, Forest, GlaxoSmithKline, Janssen, Johnson and Johnson, Lundbeck, Neurosearch, OrthoMcNeil, Otsuka, Pfizer, Repligen, Schering-Plough, Servier, Solvay, Supernus, Synosia, and Wyeth; and has provided
Psychosomatics 53:6, November-December 2012
CME lectures supported by Abbott, AstraZeneca, Bristol-Myers Squibb, GlaxoSmithKline, Janssen, Johnson and Johnson, Lundbeck, Merck, Sanofi Aventis, Schering-Plough, Pfizer, Solvay, and Wyeth. No speaker bureaus for the past 10 years. No stock, no equity, and no patents. The remaining authors (M.C.H., F.Z., and L.M.) report no financial relationships with competing or commercial interests.
References
1. Scott LJ, McKeage K, Keam SJ, Plosker GL: Tacrolimus: a further update of its use in the management of organ transplantation. Drugs 2003; 63:1247–1297 2. Bechstein WO: Neurotoxicity of calcineurin inhibitors: impact and clinical management. Transpl Int 2000; 13:313–326 3. Fireman M, DiMartini AF, Armstrong SC, Cozza KL: Immunosuppressants. Psychosomatics 2004; 45:354 –360 4. Armstrong SC, Cozza KL, Pimentel EA: Immunosuppressants. Psychosomatics 2002; 43:424 – 427
Atypical Neuroleptic Malignant Syndrome Associated with Iloperidone Administration TO THE EDITOR: Neuroleptic malignant syndrome (NMS) is a complication seen in 0.02%– 0.25% of patients prescribed antipsychotics.1 The DSM-IV-TR proposes criteria for the diagnosis of NMS, however, many reports describe atypical presentations that appear to have similar clinical relevance, particularly with second-generation antipsychotics.1 The atypical presentations commonly lack the core features of hyperthermia and muscle rigidity, thus making a definitive diagnosis more challenging and potentially hindering treatment, increasing morbidity and mortality.1 Here, we present a case of atypical NMS associated with iloperidone, which has www.psychosomaticsjournal.org
603
Letters to the Editor recently been introduced as a secondgeneration antipsychotic approved for treating schizophrenia.2 We have not found reports in the literature to date of neuroleptic malignant syndrome with iloperidone. Case Report Ms. B is a 37-year-old African-American woman with a history of paranoid schizophrenia admitted to the medical intensive care unit (MICU) for suspected NMS. Ms. B was in her usual state of health until 4 hours prior to presentation, when she exhibited decreased verbal responsiveness and muscle stiffness. In the emergency department (ED), mutism, diaphoresis, and diffuse lead pipe rigidity were present. Heart rate was 112, temperature was 99.8°F (37.7°C), blood pressure was 132/78, and respiratory rate was 16. The remainder of the physical exam was within normal limits. Chest X-ray and EKG showed no abnormalities. Laboratory results were negative for metabolic disturbances, drugs, creatinine kinase elevation, or infection. History revealed a medication adjustment due to amenorrhea. Risperidone 2 mg PO BID, taken for 1–2 years, was abruptly discontinued, and iloperidone 1 mg PO at bedtime was started instead, 6 days prior to presentation. Due to the presence of severe lead pipe rigidity, in association with the above symptoms and a history of antipsychotic use, NMS was suspected, and treatment of NMS was promptly and aggressively initiated by the ED physician with IV dantrolene. She was admitted to the MICU 4 hours later. After 12 hours of supportive care, rigidity improved, creatinine kinase did not rise (value 103), tachycardia ranged from 100 to 130, and she remained afebrile. On mental status 604
www.psychosomaticsjournal.org
exam, she exhibited intense eye contact, blunted affect, selective mutism, and no overt psychotic symptoms. After tachycardia improved to a heart rate of 90 –100, she was transferred to the inpatient psychiatric unit on lorazepam 1 mg PO TID. In the psychiatric unit, lorazepam 1 mg PO TID was continued because of mutism. Due to concern about the possibility of rebound psychosis following discontinuation of risperidone, she was challenged with 1 mg of risperidone on day 7 of hospitalization by the inpatient psychiatrist. Within a few hours, symptoms suggestive of NMS recurred, including a worsening of tachycardia, which improved to a degree after administration of IM lorazepam. However, she remained moderately tachycardic, and the medical team recommended a d-dimer (value 7569) and chest CT scan. This revealed pulmonary emboli in the right interlobar artery and segmental branches. IV anticoagulation was then instituted on the medical floor. Once medically stabilized, she was transferred to psychiatry. Slowly, her catatonia resolved. Lorazepam was tapered to 1 mg PO BID, escitalopram 10 mg PO daily was added with good effect for mood symptoms, and she was discharged 3 weeks later on no antipsychotics. Discussion The DSM-IV-TR defines NMS as a syndrome consisting of hyperthermia (temperature ⬎100.4°F [38 °C]), muscle rigidity, and two of the following: diaphoresis, dysphagia, incontinence, altered consciousness, mutism, hypertension, labile blood pressure, CK elevation, tremor, or tachycardia.2 According to the International Consensus Study of Neuroleptic Malignant Syndrome Diagnostic Criteria proposed by Gurrera et al., hyperthermia ranked
second in importance among diagnostic features of typical NMS.3 According to the DSM, Ms. B met criteria for NMS with the exception of hyperthermia, which did not reach criterion levels on presentation. The lack of hyperthermia in Ms. B may be related to her early presentation and the rapid initiation of appropriate treatment. Cases of NMS have been described with initial symptoms of mental status changes and muscle rigidity that only later progressed to autonomic instability and hyperthermia.4 The clinical pattern seen in Ms. B is consistent with such a clinical course, which also implies that early detection of NMS symptoms may result in fewer typical cases of NMS. An alternative explanation is that Ms. B experienced what may be a related but possibly a distinct syndrome of atypical NMS, described in several reports as NMS-like syndromes lacking certain core features of the DSMIV-TR criteria, especially hyperthermia.2 Atypical NMS has often been associated with atypical antipsychotics.2 A review by Zarouff et al. reported cases of NMS with aripiprazole, clozapine, and olanzapine lacking hyperthermia, rigidity, and CK elevation.1 It has been postulated that unlike typical NMS, which involves central dopaminergic blockade, atypical NMS also involves the epinephrine, serotonin, and norepinephrine systems.5 Some authors have suggested alternative, more flexible criteria for diagnosing and categorizing NMS.6 While not meeting the full DSMIV-TR criteria for NMS, Ms. B’s presentation was consistent with the alternate criteria described by Levenson. Levenson proposed that the presence of all three major manifestations (fever, rigidity, elevated CK), or two major and four minor manifestations (tachycardia, abnormal blood pressure,
Psychosomatics 53:6, November-December 2012
Letters to the Editor tachypnea, altered consciousness, diaphoresis, and leukocytosis) be considered high-probability evidence of NMS in appropriate clinical contexts.7 The differential diagnosis for NMS includes lethal catatonia, meningitis, status epilepticus, stroke, hyperthyroidism, pheochromocytoma, acute porphyria, serotonin syndrome, malignant hyperthermia, and anticholinergic syndrome.2 Considering the clinical history and laboratory results, lethal catatonia might be considered as an alternative diagnosis. Lethal catatonia is characterized by fever, mutism, stereotypic movements, posturing, and autonomic instability.8 Unlike NMS, which typically begins with rigidity, lethal catatonia has been associated with a prodromal phase characterized by mood lability, insomnia, anorexia, excitement, and agitation prior to the onset of rigidity.9,10 Further, in lethal catatonia, catatonic episodes typically begin prior to neuroleptic administration.9 NMS therefore appears to be the more likely diagnosis in Ms. B. The re-emergence of NMS symptoms following challenge with risperidone 1 week later is also consistent with the initial presentation being NMS, since NMS events are a risk factor for future episodes.2 A review of re-challenge with atypical antipsychotics after earlier NMS showed that 19 out of 45 patients experienced recurrence of NMS symptoms.11 NMS is also considered a contributing factor to the development of pulmonary emboli, as a consequence of protracted immobility, rigidity, and subsequent
rhabdomyolysis, which increase the chances of thromboemboli.4
2.
Conclusion Despite NMS being a relatively rare occurrence, it may develop in patients taking atypical antipsychotics, including iloperidone, which has not been reported previously.4 Since prompt identification and treatment may prevent progression of symptoms and mortality, a high index of suspicion is advisable when patients prescribed anti-psychotics present with NMS-like symptoms, even if full criteria are not met. Further studies to elucidate the relationship between atypical NMS symptomatology and the standard presentation with respect to diagnostic heterogeneity and clinical course are needed. Nicole Guanci, M.D. Psychiatry Resident New Jersey Medical School University of Medicine and Dentistry of New Jersey Rashi Aggarwal, M.D. Assistant Professor Department of Psychiatry New Jersey Medical School University of Medicine and Dentistry of New Jersey Steven Schleifer, M.D. Assistant Professor Department of Psychiatry New Jersey Medical School University of Medicine and Dentistry of New Jersey References
1. Zarrouf FA, Bhanot V: Neuroleptic malignant syndrome: don’t let your
Psychosomatics 53:6, November-December 2012
3.
4.
5.
6.
7.
8.
9.
10.
11.
guard down yet. Curr Psychiatry 2007; 6:89 –95 Citrome L: Iloperidone for schizophrenia: a review of the efficacy and safety profile for this newly commercialized second-generation antipsychotic. Int J Clin Practice 2009; 63:1237–1238 Gurrera RJ, Caroff SN, Cohen A, Carroll BT, DeRoos F, Francis A, et al: An International Consensus Study of Neuroleptic Malignant Syndrome Diagnostic Criteria Using the Delphi Method. J Clin Psychiatry 2011; 72:1222–1228 Picard LS, Lindsay S, Strawn JR, Kaneria RM, Patel NC, Keck PE: Atypical neuroleptic malignant syndrome: diagnostic controversies and considerations. Pharmacotherapy 2008; 28:530 –535 Balzan MV: The neuroleptic malignant syndrome: a logical approach to the patient with temperature and rigidity. Postgrad Med J 1998; 74:72–76 Pope HG, Keck PE, McElroy SL: Frequency and presentation of neuroleptic malignant syndrome in a large Psychiatric hospital. Am J Psychiatry 1986; 143: 1227–1233 Levenson JL: Neuroleptic malignant syndrome. Am J Psychiatry 1985; 142:1137– 1145 Weder ND, Muralee S, Penland H, Tampi RR: Catatonia: a review. Ann Clin Psychiatry 2008; 20:97–107 Sheil AT, Collins KA, Schandl CA, Harley, RA: Fatal neurotoxic response to neuroleptic medications: a case report and review of the literature. Am J Forensic Med Pathol 2007; 28:116 –120 Mann SC, Caroff SN, Bleier HR, Welz WK, Kling MA, Hayashida M: Lethal catatonia. Am J Psychiatry 1986; 143: 1374 –1380 Mendhekar DN, Jiloha RC, Mehndiratta MM, War L: Challenge with atypical antipsychotic drugs in risperidone induced neuroleptic malignant syndrome: a case report. Indian J Psychiatry 2002; 44:387– 390
www.psychosomaticsjournal.org
605