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Case report: treatment of catatonia in an adolescent male
JOURNAL OF ADOLESCENT HEALTH 2000;27:69–71
CASE REPORT
Case Report: Treatment of Catatonia in an Adolescent Male MELISSA P. DelBELLO, M.D., KEITH D. FOSTER, M.D., AND STEPHEN M. STRAKOWSKI, M.D.
KEY WORDS: Adolescent Atypical antipsychotics Catatonia Psychosis Schizophrenia
Catatonia is a life-threatening stuporous state that can be associated with various neurologic, medical, and psychiatric disorders (1). Although there have been several case reports of catatonia in children and adolescents, little is known about effective treatments for this syndrome. In 1997, Dhossche and Bouman (2,3) reviewed the literature and found 30 cases of childhood or adolescent catatonia. We found two additional cases of catatonia in adolescents, one treated successfully with electroconvulsive therapy (ECT) and lorazepam (4) and the other with zolpidem (5). Although olanzapine, an atypical antipsychotic, has been used to treat children and adolescents (6,7), to our knowledge there have been no reported cases using it in the treatment of catatonia. We report a case of a 16-year-old boy successfully treated for catatonia using lorazepam, valproic acid, and olanzapine; review the literature on the treatment of catatonia in adolescents; and discuss therapeutic issues.
From the Department of Child and Adolescent Psychiatry, Children’s Hospital Medical Center/University of Cincinnati (M.P.D., K.D.F.); and the Department of Psychiatry, Psychology and Neuroscience at University of Cincinnati College of Medicine (S.M.S.), Cincinnati, Ohio Address correspondence to: Dr. DelBello, Department of Psychiatry, University of Cincinnati College of Medicine, 231 Bethesda Ave., P.O. Box 670559, Cincinnati, OH 45267-0559. Manuscript accepted January 20, 2000.
Case Report A.G., a 16-year-old African-American boy, was admitted to the pediatric service with the diagnosis of “change in mental status.” The patient was completely mute; therefore, a history was obtained from his mother. During the previous month A.G. had become increasingly noncommunicative. He did not speak during the previous week except to make “burping” sounds. Before becoming mute, he reported his name being called from outside. His hygiene had deteriorated. Although he had exhibited no symptoms or signs of euphoria, irritability, or depression, during the previous week he had not slept. A.G. had no significant psychiatric or major medical history. According to his mother, A.G. was always a “loner”; however, during the previous year he had been particularly difficult to engage. A.G. was enrolled in ninth-grade special education classes for a learning disability. His grades had deteriorated over the past year, as his mother was unable to persuade him to attend school. His father had a history of alcohol dependence; however, there were no other psychiatric illnesses in his family as reported by his parents when they were questioned specifically about mood, psychotic, anxiety, disruptive behavior, and substance use disorders, as well as learning disabilities and mental retardation. His parents never married, but he maintained good relationships with both. While on the pediatric service, A.G. had a negative computed tomography (CT) scan and an electroencephalogram (EEG) to investigate the possibility of focal lesions. The EEG revealed diffuse mild slowing without any evidence of seizure activity. His vital
© Society for Adolescent Medicine, 2000 Published by Elsevier Science Inc., 655 Avenue of the Americas, New York, NY 10010
1054-139X/00/$–see front matter PII S1054-139X(00)00109-9
70
DelBELLO ET AL.
signs and physical examination initially were normal; therefore, he was transferred to the psychiatry unit, at which time he was mute and exhibited negativism and waxy flexibility. He was unable to follow simple commands or eat and was incontinent of urine and feces. He exhibited stereotypic behaviors including shoulder shrugging and burping noises and slept most of the day. Lyme, Venereal Disease Research Laboratory (VDRL), Epstein-Barr virus (EBV), and human immunodeficiency virus (HIV) titers and a lumbar puncture were obtained to evaluate for infectious etiologies of catatonia. A magnetic resonance image (MRI) was obtained to further rule out focal lesions and evaluate for whitematter diseases. Liver function tests and ceruloplasmin were obtained to rule out Wilson disease. A creatine phosphokinase (CPK), complete blood count (CBC), renal panel, and heavy mental screen were obtained to investigate other metabolic causes of catatonia. A urine toxicology screen was obtained to evaluate for substance-induced psychotic disorders. All of the above tests were negative. The differential diagnosis included psychotic disorder “not otherwise specified,” schizophrenia, major depression, and bipolar disorder. On Day 2 of admission, lorazepam was initiated at a dose of 1 mg q.i.d., with no improvement. A.G.’s lorazepam dose was increased to 2 mg t.i.d. with no further improvement for 1 week. On Day 4, valproic acid was initiated and titrated to 1000 mg/day (blood level of 85 g/mL) because bipolar disorder was still being considered. On Day 7 of hospitalization, olanzapine was added and titrated up to 10 mg b.i.d, based on dosing used in adults. During the next 2 weeks, A.G. began playing video games, and although he was still disorganized he attempted to wash and dress himself. He also began interacting with staff by answering questions with one word and playing cards. His stereotypic behaviors decreased in frequency. On Day 21, lorazepam was tapered and discontinued because A.G. was experiencing excessive sedation after the addition of the olanzapine. Valproic acid was discontinued on Day 28 after further review of A.G.’s history revealed no personal or family history of bipolar disorder. Six weeks after admission, A.G. interacted with peers, participated in some of the groups on the unit, and communicated in full sentences. He was discharged 8 weeks after admission, after receiving olanzapine monotherapy for 1 month. At the time of discharge he continued to experience occasional auditory hallucinations of a man’s mumbling voice. A.G. was given a diagnosis of schizophrenia-catatonic type
JOURNAL OF ADOLESCENT HEALTH Vol. 27, No. 1
based on criteria from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSMIV) (8); presence of hallucinations lasting at least 3 months, grossly disorganized and catatonic behavior lasting at least 1 month, negative symptoms (affective flattening and avolition) during the previous year; and impairment in social and academic functioning. At three months after discharge, A.G. remained on 20 mg/day of olanzapine and was steadily improving. He exhibited a wider range of affect and attended to all of his activities of daily living without difficulty. He interacted with peers at his transitional therapeutic school and was eager to reintegrate into his previous public school. He admitted to occasional auditory hallucinations of a motor sound but exhibited no stereotypic behavior and was sleeping and eating without difficulty. Although weight gain may occur as a side effect of olanzapine therapy (7), A.G. had not experienced this or any other adverse effect from his treatment. There has been no recurrence of his catatonia after 1 year.
Discussion This case illustrates many of the typical features of DSM-IV (8) criteria for catatonia, including catalepsy (limbs are stiff and remain in the position in which they are placed), negativism, stupor, and stereotyped movements. Catatonia may be the initial presentation of major mood disorders (bipolar disorder and major depression), schizophrenic disorders (schizophrenia, schizophreniform disorder, schizoaffective disorder, and psychotic disorder not otherwise specified), or neurologic and medical disorders. Little is known about the epidemiology of catatonia. However, in contrast to adults with catatonia, who have higher reported rates of underlying mood rather than schizophrenic disorders, children and adolescents have higher rates of psychotic disorder not otherwise specified and schizophrenia (3,9). Initially, the disorder underlying a catatonic episode may be difficult to diagnose accurately, thereby making treatment of this life-threatening disorder challenging. During the course of A.G.’s hospitalization, because nonpsychiatric conditions were excluded and additional information was gathered, it became evident that A.G. had auditory hallucinations before becoming catatonic and had no major symptoms of a mood disorder. Therefore, the diagnosis of schizophrenia was given at discharge from the hospital. In a recent review of all cases of malignant catatonia (febrile catatonia) since 1960, the mortality rate
July 2000
was reported to be 60% (1). Despite its mortality, there are relatively few case series and no doubleblind trials evaluating treatments for catatonia in adults or children and adolescents. In the few reports of catatonia in children and adolescents, electroconvulsive therapy (ECT) and benzodiazepines have shown the most promise for treatment. However, ECT may not be widely available at children’s hospitals and benzodiazepines were efficacious in only half of the 12 catatonic child and adolescent case reports in which it was used (2). Recently, there have been reports of the atypical antipsychotics, risperidone (3,10 –13) and clozapine (14,15) successfully treating catatonia in adults and children. A.G. exhibited minimal clinical improvement when treated with lorazepam monotherapy. However, A.G.’s catatonic symptoms were successfully treated with a combination of lorazepam, valproic acid, and olanzapine. Although we are unable to definitively conclude whether valproic acid, olanzapine, or a combination of the two in conjunction with lorazepam led to improvement in A.G.’s symptoms, to our knowledge there have been no previous reports using olanzapine in treating catatonia. Typical antipsychotics such as haloperidol traditionally have been used cautiously in treating patients with catatonia, especially malignant catatonia, because there is often confusion in differentiating it from neuroleptic malignant syndrome (1,16). Neuroleptic malignant disorder is a neuroleptic-induced disorder with a high mortality rate (up to 20%) involving a mental status change, severe akinesia, muscular rigidity, and autonomic instability. Moreover, the addition of an antipsychotic may exacerbate and/or complicate the clinical situation (17). D2 receptor inhibition has been implicated in the pathophysiology of catatonia (16). Atypical antipsychotics such as olanzapine have decreased D2 receptor binding affinity compared with typical antipsychotics, and therefore may be less likely to precipitate neuroleptic malignant syndrome and/or worsen catatonia (18). The potential role of valproic acid in A.G.’s recovery needs to be considered. There have been several reports that suggest mood stabilizers may be helpful in treating catatonia, however, usually when there is an underlying mood disorder (19). At presentation to the hospital A.G. had not slept for a week, and it was unclear whether before the onset of catatonia he had had other symptoms of a mood disorder. Therefore, when lorazepam did not result in symptom improvement, valproic acid was initiated. After further review with collateral sources revealed that A.G. had
TREATMENT OF CATATONIA
71
no symptoms of a mood disorder, valproic acid was discontinued. However, valproic acid may have contributed to A.G.’s improvement in symptoms. We report the successful use of olanzapine in conjunction with lorazepam and valproic acid in the treatment of catatonia. Olanzapine, an atypical antipsychotic, may be a promising treatment for catatonia. Additional studies are necessary to evaluate the efficacy of atypical antipsychotics, mood stabilizers, ECT, and benzodiazepines in the treatment of catatonia.
References 1. Mann SC, Caroff SN, Bleir HR, et al. Lethal catatonia. Am J Psychiatry 1986;143:1374 – 81. 2. Dhossche DM, Bouman NH. Catatonia in children and adolescents [letter]. J Am Acad Child Adolesc Psychiatry 1997;36: 870 –1. 3. Dhossche D, Bouman N. Catatonia in an adolescent with Prader-Willi syndrome. Ann Clin Psychiatry 1997;9:247–53. 4. Petrides G, Divadeenam KM, Bush G, et al. Synergism of lorazepam and electroconvulsive therapy in the treatment of catatonia. Biol Psychiatry 1997;42:375– 81. 5. Zaw ZF, Bates GDL. Replication of zolpidem test for catatonia in an adolescent. Lancet 1997;349:114. 6. Kumra S, Jacobsen LK, Lenane M, et al. Childhood-onset schizophrenia: An open-label study of olanzapine in adolescents. J Am Acad Child Adolesc Psychiatry 1988;37:377– 85. 7. Krishnamoorthy J, King BH. Open-label olanzapine in five preadolescent children. J Child Adolesc Psychopharm 1988;8: 107–13. 8. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th ed (DSM-IV). Washington, DC: American Psychiatric Association, 1994. 9. Rogers D. Catatonia: A contemporary approach. J Neuropsych Clin Neurosci 1991;3:334 – 40. 10. Cook EH, Olson K, Pliskin N. Response of organic catatonia to risperidone. Arch Gen Psychiatry 1996;53:82–3. 11. Dhossche D, Petrides G. Negative symptoms or catatonia? [letter]. J Am Acad Child Adolesc Psychiatry 1997;36:302. 12. Zuddas A, Pintor M, Chianchetti C. Risperidone for negative symptoms. J Am Acad Child Adolesc Psychiatry 1996;35:838 –9. 13. Zuddas A, Pintor M, Chianchetti C. In reply. J Am Acad Child Adolesc Psychiatry 1997;36:302–3. 14. Battegay R, Cotar B, Fleischauer J, et al. Results and side effects of treatment with clozapine. Comp Psychiatry 1977;18: 423– 8. 15. Rommel O, Tegenthoff M, Widdig W, et al. Organic catatonia following frontal lobe injury: response to clozapine. J Neuropsych Clin Neurosci 1998;10:237– 8. 16. Philbrick KL, Rummans TA. Malignant catatonia. J Neuropsych Clin Neurosci 1994;6:1–13. 17. Gelenberg AJ, Mandel MR. Catatonic reactions to high-potency neuroleptic drugs. Arch Gen Psychiatry 1997; 34:947–50. 18. Weller M, Kornhuber J. Does clozapine cause neuroleptic malignant syndrome? J Clin Psychiatry 1993;54:70 –1. 19. Hawkins JM, Archer KJ, Strakowski SM, et al. Somatic treatment of catatonia. Int J Psychiatry Med 1995;25:345– 69.
CASE REPORT
Case Report: Treatment of Catatonia in an Adolescent Male MELISSA P. DelBELLO, M.D., KEITH D. FOSTER, M.D., AND STEPHEN M. STRAKOWSKI, M.D.
KEY WORDS: Adolescent Atypical antipsychotics Catatonia Psychosis Schizophrenia
Catatonia is a life-threatening stuporous state that can be associated with various neurologic, medical, and psychiatric disorders (1). Although there have been several case reports of catatonia in children and adolescents, little is known about effective treatments for this syndrome. In 1997, Dhossche and Bouman (2,3) reviewed the literature and found 30 cases of childhood or adolescent catatonia. We found two additional cases of catatonia in adolescents, one treated successfully with electroconvulsive therapy (ECT) and lorazepam (4) and the other with zolpidem (5). Although olanzapine, an atypical antipsychotic, has been used to treat children and adolescents (6,7), to our knowledge there have been no reported cases using it in the treatment of catatonia. We report a case of a 16-year-old boy successfully treated for catatonia using lorazepam, valproic acid, and olanzapine; review the literature on the treatment of catatonia in adolescents; and discuss therapeutic issues.
From the Department of Child and Adolescent Psychiatry, Children’s Hospital Medical Center/University of Cincinnati (M.P.D., K.D.F.); and the Department of Psychiatry, Psychology and Neuroscience at University of Cincinnati College of Medicine (S.M.S.), Cincinnati, Ohio Address correspondence to: Dr. DelBello, Department of Psychiatry, University of Cincinnati College of Medicine, 231 Bethesda Ave., P.O. Box 670559, Cincinnati, OH 45267-0559. Manuscript accepted January 20, 2000.
Case Report A.G., a 16-year-old African-American boy, was admitted to the pediatric service with the diagnosis of “change in mental status.” The patient was completely mute; therefore, a history was obtained from his mother. During the previous month A.G. had become increasingly noncommunicative. He did not speak during the previous week except to make “burping” sounds. Before becoming mute, he reported his name being called from outside. His hygiene had deteriorated. Although he had exhibited no symptoms or signs of euphoria, irritability, or depression, during the previous week he had not slept. A.G. had no significant psychiatric or major medical history. According to his mother, A.G. was always a “loner”; however, during the previous year he had been particularly difficult to engage. A.G. was enrolled in ninth-grade special education classes for a learning disability. His grades had deteriorated over the past year, as his mother was unable to persuade him to attend school. His father had a history of alcohol dependence; however, there were no other psychiatric illnesses in his family as reported by his parents when they were questioned specifically about mood, psychotic, anxiety, disruptive behavior, and substance use disorders, as well as learning disabilities and mental retardation. His parents never married, but he maintained good relationships with both. While on the pediatric service, A.G. had a negative computed tomography (CT) scan and an electroencephalogram (EEG) to investigate the possibility of focal lesions. The EEG revealed diffuse mild slowing without any evidence of seizure activity. His vital
© Society for Adolescent Medicine, 2000 Published by Elsevier Science Inc., 655 Avenue of the Americas, New York, NY 10010
1054-139X/00/$–see front matter PII S1054-139X(00)00109-9
70
DelBELLO ET AL.
signs and physical examination initially were normal; therefore, he was transferred to the psychiatry unit, at which time he was mute and exhibited negativism and waxy flexibility. He was unable to follow simple commands or eat and was incontinent of urine and feces. He exhibited stereotypic behaviors including shoulder shrugging and burping noises and slept most of the day. Lyme, Venereal Disease Research Laboratory (VDRL), Epstein-Barr virus (EBV), and human immunodeficiency virus (HIV) titers and a lumbar puncture were obtained to evaluate for infectious etiologies of catatonia. A magnetic resonance image (MRI) was obtained to further rule out focal lesions and evaluate for whitematter diseases. Liver function tests and ceruloplasmin were obtained to rule out Wilson disease. A creatine phosphokinase (CPK), complete blood count (CBC), renal panel, and heavy mental screen were obtained to investigate other metabolic causes of catatonia. A urine toxicology screen was obtained to evaluate for substance-induced psychotic disorders. All of the above tests were negative. The differential diagnosis included psychotic disorder “not otherwise specified,” schizophrenia, major depression, and bipolar disorder. On Day 2 of admission, lorazepam was initiated at a dose of 1 mg q.i.d., with no improvement. A.G.’s lorazepam dose was increased to 2 mg t.i.d. with no further improvement for 1 week. On Day 4, valproic acid was initiated and titrated to 1000 mg/day (blood level of 85 g/mL) because bipolar disorder was still being considered. On Day 7 of hospitalization, olanzapine was added and titrated up to 10 mg b.i.d, based on dosing used in adults. During the next 2 weeks, A.G. began playing video games, and although he was still disorganized he attempted to wash and dress himself. He also began interacting with staff by answering questions with one word and playing cards. His stereotypic behaviors decreased in frequency. On Day 21, lorazepam was tapered and discontinued because A.G. was experiencing excessive sedation after the addition of the olanzapine. Valproic acid was discontinued on Day 28 after further review of A.G.’s history revealed no personal or family history of bipolar disorder. Six weeks after admission, A.G. interacted with peers, participated in some of the groups on the unit, and communicated in full sentences. He was discharged 8 weeks after admission, after receiving olanzapine monotherapy for 1 month. At the time of discharge he continued to experience occasional auditory hallucinations of a man’s mumbling voice. A.G. was given a diagnosis of schizophrenia-catatonic type
JOURNAL OF ADOLESCENT HEALTH Vol. 27, No. 1
based on criteria from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSMIV) (8); presence of hallucinations lasting at least 3 months, grossly disorganized and catatonic behavior lasting at least 1 month, negative symptoms (affective flattening and avolition) during the previous year; and impairment in social and academic functioning. At three months after discharge, A.G. remained on 20 mg/day of olanzapine and was steadily improving. He exhibited a wider range of affect and attended to all of his activities of daily living without difficulty. He interacted with peers at his transitional therapeutic school and was eager to reintegrate into his previous public school. He admitted to occasional auditory hallucinations of a motor sound but exhibited no stereotypic behavior and was sleeping and eating without difficulty. Although weight gain may occur as a side effect of olanzapine therapy (7), A.G. had not experienced this or any other adverse effect from his treatment. There has been no recurrence of his catatonia after 1 year.
Discussion This case illustrates many of the typical features of DSM-IV (8) criteria for catatonia, including catalepsy (limbs are stiff and remain in the position in which they are placed), negativism, stupor, and stereotyped movements. Catatonia may be the initial presentation of major mood disorders (bipolar disorder and major depression), schizophrenic disorders (schizophrenia, schizophreniform disorder, schizoaffective disorder, and psychotic disorder not otherwise specified), or neurologic and medical disorders. Little is known about the epidemiology of catatonia. However, in contrast to adults with catatonia, who have higher reported rates of underlying mood rather than schizophrenic disorders, children and adolescents have higher rates of psychotic disorder not otherwise specified and schizophrenia (3,9). Initially, the disorder underlying a catatonic episode may be difficult to diagnose accurately, thereby making treatment of this life-threatening disorder challenging. During the course of A.G.’s hospitalization, because nonpsychiatric conditions were excluded and additional information was gathered, it became evident that A.G. had auditory hallucinations before becoming catatonic and had no major symptoms of a mood disorder. Therefore, the diagnosis of schizophrenia was given at discharge from the hospital. In a recent review of all cases of malignant catatonia (febrile catatonia) since 1960, the mortality rate
July 2000
was reported to be 60% (1). Despite its mortality, there are relatively few case series and no doubleblind trials evaluating treatments for catatonia in adults or children and adolescents. In the few reports of catatonia in children and adolescents, electroconvulsive therapy (ECT) and benzodiazepines have shown the most promise for treatment. However, ECT may not be widely available at children’s hospitals and benzodiazepines were efficacious in only half of the 12 catatonic child and adolescent case reports in which it was used (2). Recently, there have been reports of the atypical antipsychotics, risperidone (3,10 –13) and clozapine (14,15) successfully treating catatonia in adults and children. A.G. exhibited minimal clinical improvement when treated with lorazepam monotherapy. However, A.G.’s catatonic symptoms were successfully treated with a combination of lorazepam, valproic acid, and olanzapine. Although we are unable to definitively conclude whether valproic acid, olanzapine, or a combination of the two in conjunction with lorazepam led to improvement in A.G.’s symptoms, to our knowledge there have been no previous reports using olanzapine in treating catatonia. Typical antipsychotics such as haloperidol traditionally have been used cautiously in treating patients with catatonia, especially malignant catatonia, because there is often confusion in differentiating it from neuroleptic malignant syndrome (1,16). Neuroleptic malignant disorder is a neuroleptic-induced disorder with a high mortality rate (up to 20%) involving a mental status change, severe akinesia, muscular rigidity, and autonomic instability. Moreover, the addition of an antipsychotic may exacerbate and/or complicate the clinical situation (17). D2 receptor inhibition has been implicated in the pathophysiology of catatonia (16). Atypical antipsychotics such as olanzapine have decreased D2 receptor binding affinity compared with typical antipsychotics, and therefore may be less likely to precipitate neuroleptic malignant syndrome and/or worsen catatonia (18). The potential role of valproic acid in A.G.’s recovery needs to be considered. There have been several reports that suggest mood stabilizers may be helpful in treating catatonia, however, usually when there is an underlying mood disorder (19). At presentation to the hospital A.G. had not slept for a week, and it was unclear whether before the onset of catatonia he had had other symptoms of a mood disorder. Therefore, when lorazepam did not result in symptom improvement, valproic acid was initiated. After further review with collateral sources revealed that A.G. had
TREATMENT OF CATATONIA
71
no symptoms of a mood disorder, valproic acid was discontinued. However, valproic acid may have contributed to A.G.’s improvement in symptoms. We report the successful use of olanzapine in conjunction with lorazepam and valproic acid in the treatment of catatonia. Olanzapine, an atypical antipsychotic, may be a promising treatment for catatonia. Additional studies are necessary to evaluate the efficacy of atypical antipsychotics, mood stabilizers, ECT, and benzodiazepines in the treatment of catatonia.
References 1. Mann SC, Caroff SN, Bleir HR, et al. Lethal catatonia. Am J Psychiatry 1986;143:1374 – 81. 2. Dhossche DM, Bouman NH. Catatonia in children and adolescents [letter]. J Am Acad Child Adolesc Psychiatry 1997;36: 870 –1. 3. Dhossche D, Bouman N. Catatonia in an adolescent with Prader-Willi syndrome. Ann Clin Psychiatry 1997;9:247–53. 4. Petrides G, Divadeenam KM, Bush G, et al. Synergism of lorazepam and electroconvulsive therapy in the treatment of catatonia. Biol Psychiatry 1997;42:375– 81. 5. Zaw ZF, Bates GDL. Replication of zolpidem test for catatonia in an adolescent. Lancet 1997;349:114. 6. Kumra S, Jacobsen LK, Lenane M, et al. Childhood-onset schizophrenia: An open-label study of olanzapine in adolescents. J Am Acad Child Adolesc Psychiatry 1988;37:377– 85. 7. Krishnamoorthy J, King BH. Open-label olanzapine in five preadolescent children. J Child Adolesc Psychopharm 1988;8: 107–13. 8. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th ed (DSM-IV). Washington, DC: American Psychiatric Association, 1994. 9. Rogers D. Catatonia: A contemporary approach. J Neuropsych Clin Neurosci 1991;3:334 – 40. 10. Cook EH, Olson K, Pliskin N. Response of organic catatonia to risperidone. Arch Gen Psychiatry 1996;53:82–3. 11. Dhossche D, Petrides G. Negative symptoms or catatonia? [letter]. J Am Acad Child Adolesc Psychiatry 1997;36:302. 12. Zuddas A, Pintor M, Chianchetti C. Risperidone for negative symptoms. J Am Acad Child Adolesc Psychiatry 1996;35:838 –9. 13. Zuddas A, Pintor M, Chianchetti C. In reply. J Am Acad Child Adolesc Psychiatry 1997;36:302–3. 14. Battegay R, Cotar B, Fleischauer J, et al. Results and side effects of treatment with clozapine. Comp Psychiatry 1977;18: 423– 8. 15. Rommel O, Tegenthoff M, Widdig W, et al. Organic catatonia following frontal lobe injury: response to clozapine. J Neuropsych Clin Neurosci 1998;10:237– 8. 16. Philbrick KL, Rummans TA. Malignant catatonia. J Neuropsych Clin Neurosci 1994;6:1–13. 17. Gelenberg AJ, Mandel MR. Catatonic reactions to high-potency neuroleptic drugs. Arch Gen Psychiatry 1997; 34:947–50. 18. Weller M, Kornhuber J. Does clozapine cause neuroleptic malignant syndrome? J Clin Psychiatry 1993;54:70 –1. 19. Hawkins JM, Archer KJ, Strakowski SM, et al. Somatic treatment of catatonia. Int J Psychiatry Med 1995;25:345– 69.