- Email: [email protected]
Catatonia Associated with Coadministration of Tramadol and Meperidine
CASE REPORT
Catatonia Associated with Coadministration of Tramadol and Meperidine Si-Sheng Huang, Shaw-Hwa Jou,* Nan-Ying Chiu Tramadol and meperidine are frequently prescribed medications in the management of oncologic patients. The pharmacologic interaction of these two drugs may induce mental disturbance. This was demonstrated by our case of a 39-year-old woman with gastric mucosa associated lymphoid tissue lymphoma (MALToma), stage III after chemotherapy. She was admitted to our medical ward with the complaint of abdominal pain. Pantoprazole 40 mg and tramadol 150 mg daily were prescribed with intravenous route after hospitalization. Two days later, the patient developed transient visual hallucinations and disorientation afterr additional injection of meperidine (25 mg). Six hours later, catatonic features appeared. The duty doctorr stopped all the medications. Two days later, the catatonic features disappeared. From the clinical course, we suggest that the catatonia was caused by drug interactions between tramadol and meperidine. The pharmacodynamic mechanism might be related to the dopamine and serotonin systems. [J Formos Med Assoc 2007;106(4):323–326] Key Words: catatonia, meperidine, tramadol
Tramadol and meperidine are both synthetic phenylpiperidine-derivative opiate agonists. They are strong analgesics used in the relief of moderate to severe pain. Tramadol has adverse effects such as dry mouth, constipation, urinary retention, visual disturbance, and confusion. Meperidine has been observed to have clinical manifestations of central nervous system (CNS) stimulation such as seizures, agitation, irritability, disorientation, nervousness, tremors, twitches, and myoclonus.1 These effects may be related to serum levels of meperidine and its active metabolite normeperidine.2 Opioids can increase muscle tone and may cause muscle rigidity. Opioid-induced rigidity is probably related to a catatonic state, which can be induced by opioids.3 Catatonic features can be observed in a subtype of schizophrenia, major depressive disorder,
and bipolar disorder. Catatonia may also be caused by a variety of medical or surgical conditions, such as neoplasms, encephalitis, head trauma, diabetes, and other metabolic disorders. Its clinical manifestations include motor immobility, excessive motor activity, extreme negativism or mutism, peculiarities of voluntary movement, echolalia, and echopraxia. In addition, medications, such as antipsychotics, could induce catatonia.4 Delirium is characterized by a disturbance off consciousness and a change in cognition or development of a perceptual disturbance. The disturbance develops over a short period of time and tends to fluctuate during the course of the day. Associated clinical features of delirium include sleep-wake cycle disturbance, disturbed psychomotor behavior, and emotional disturbance. Depending on the etiology, delirium can be associated
©2007 Elsevier & Formosan Medical Association . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Department of Psychiatry, Changhua Christian Hospital, Changhua, Taiwan. Received: April 18, 2006 Revised: May 26, 2006 Accepted: September 5, 2006
*Correspondence to: Dr Shaw-Hwa Jou, Department of Psychiatry, Changhua Christian Hospital, 135 Nanhsiao Street, Changhua 500, Taiwan. E-mail: [email protected]
J Formos Med Assoc | 2007 • Vol 106 • No 4
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with many nonspecific neurologic abnormalities such as tremor, myoclonus, asterixis, and reflex or muscle tone changes.5 A diminution in cholinergic function—an excess of dopamine, norepinephrine, and glutamate—and disturbances in serotonergic and γ-aminobutyric acid activities have been implicated in its pathogenesis.6 We report a patient who developed delirium and catatonic features following coadministration of tramadol and meperidine. We also review related articles and discuss the possible pathophysiologies.
Case Report In May 2005, a 39-year-old woman was diagnosed with gastric mucosa associated lymphoid tissue lymphoma (MALToma), stage III. She suffered from abdominal pain and dysphagia, at first, in March 2005. She underwent chemotherapy with cyclophosphamide 1000 mg, epirubicin hydrochloride 100 mg, vincristine sulfate 2 mg, and prednisolone 100 mg shortly after the diagnosis. She received pantoprazole, amoxicillin, clarithromycin, lamivudine, and prednisolone after chemotherapy. However, 1 week later, she visited our emergency department because of abdominal pain. Meperidine 50 mg was injected for pain. One hour later, irritable mood, restlessness, and derealized sensation were noted. Five minutes after injection, the symptoms were remitted spontaneously. Then, she was admitted to our medical ward for further evaluation. Pantoprazole 40 mg and tramadol 150 mg daily were prescribed with intravenous route. Two days later, meperidine 25 mg was injected additionally for her pain around 9 am. Two hours later, she stated that her hands and feet did not belong to her. The patient had confused consciousness, irritable mood, and inappropriate grasping behaviors around 1 pm. She reported seeing a man on the wall and many spiders around her bed. At 3 pm, she claimed that she was dead and did not know why her husband could see her. She could walk to the toilet for urination with fair f gait at 324
that time. Then, she developed mutism, immobile standing beside her bed, refusal to sit down, and reluctance to undergo physical examinations. She stood still throughout that night. The duty doctorr stopped all the medications. The results of neurologic examinations revealed isocoric pupil, positive bilateral light reflex, no obvious facial palsy, symmetric limbs muscle power, and normal deep tendon reflex. Next day, stupor consciousness, inattention, mutism, fixed posture, and negativism were still observed. Tracing back her history, there was no head trauma, epilepsy, and no overt psychiatric features. During the period of catatonia, the laboratory data showed normal findings in complete blood count, electrolytes, renal function, and liver function. Brain image and electroencephalographic examinations were not performed due to the absence of obvious focal signs. On the morning of the 3rd day, she woke up and spoke to others spontaneously. All catatonicc features had disappeared. The patient did nott receive any psychotropic during those 2 days. She was discharged 2 days later, and followed up att our hematology department afterwards.
Discussion At the emergency department, the patient developed irritable mood and derealization lasting forr 5 minutes after injection of meperidine 50 mg. However, following admission, the full symptoms of delirium and catatonia in this patient occurred with a lower dose meperidine (25 mg) subsequentt to the treatment of tramadol and pantoprazole. It suggests that the symptoms are related to a drugg interaction. Pantoprazole, a proton-pump inhibitor, is mainly metabolized by cytochrome P-450 2C19 (CYP2C19).7 Tramadol is a syntheticc 4-phenylpiperidine. O-demethylation and Ndemethylation are two main metabolic pathways of tramadol.8 As to meperidine, its main metabolicc pathway is N-demethylation.9 There is no case report about pantoprazole-induced or tramadolinduced delirium and catatonia on MEDLINE, butt there is one case report of meperidine-induced J Formos Med Assoc | 2007 • Vol 106 • No 4
Catatonia associated with tramadol and meperidine
delirium.10 The complete CYP P450 enzyme information of pantoprazole, tramadol, and meperidine is not available, and so the pharmacokinetic interaction of these drugs cannot be concluded. Some overlaps of metabolic pathways are noted between tramadol and meperidine. Tramadol and meperidine are both synthetic opioid compounds in the group of phenylpiperidine series. According to available data and pharmacologic action of these three agents, we speculate that the etiologies of delirium and catatonia in this patient were probably related to tramadol and meperidine, and less likely to be related to pantoprazole. Pharmacodynamic explanations of catatonia involve the dopamine system in the basal ganglia,4 serotonin system,11 and γ-aminobutyric acid (GABA) system.12 Northoff et al13 reported that dopaminergic metabolites in the plasma of acute catatonic patients were increased. These results suggest hyperactivity in the dopaminergic system in catatonia. However, hypoactivity in this system was also assumed.4 In addition to the dopamine system, Lauterbach12 reported that serotonergic drugs could induce catatonic syndrome because of increased 5-HT1A receptor stimulation and GABAb receptor stimulation. Tramadol and meperidine are not only anticholinergic agents but also potent inhibitors of serotonin reuptake into presynaptic neurons.14,15 Based on the findings of our case, we speculate two possible mechanisms of catatonia. First, dopamine and acetylcholine have a reciprocal relationship in the nigrostriatal pathway. A balance between the dopaminergic and cholinergic system is necessary for controlling voluntary movement.16 Anticholinergic effects of these two medications may result in an imbalance between these two systems. Second, serotonergic activity may be related to catatonia.17,18 This model could also explain the catatonic features in this patient. Fogarty and Murray1 reported a patient who developed agitation and visual hallucinations after using meperidine 930 mg daily for 4 days. Psychiatric symptoms, including anxiety, fearfulness, and hypervigilance, resolved over the next 12 hours after meperidine was discontinued. J Formos Med Assoc | 2007 • Vol 106 • No 4
Eisendrath et al10 reported six cases of meperidineinduced delirium. Their daily doses of meperidine ranged from 225 to 1400 mg. In our case, the patient’s delirium was noted 4 hours after a single dose (25 mg) of meperidine. Before injection off meperidine, our patient had regularly received tramadol 150 mg daily. From the pharmacodynamic aspect, the etiology of delirium was highlyy related to the anticholinergic effect of tramadol and meperidine.17,18 The CNS receptor level’s interaction of opioids and their metabolites mayy contribute to the pathogenesis of delirium. Moreover, the patient’s anticancer drugs, cyclophosphamide and prednisolone, can also cause delirium because of their strong anticholinergic effects. Unfortunately, there is no clear support for a diagnosis of delirium such as cognitive examination or thorough assessment of a broad range off delirium symptoms as in the use of a specificc symptom rating scale over time. These could be ictal symptoms (complex partial, even confusional status) perhaps associated with some CNS lesions including meningeal lymphoma, yet neither an electroencephalogram nor magnetic resonance imaging was done in this at-risk patient. Further, there is the possibility that this episode was onlyy coincidentally related in time to the injection off meperidine. A design with another injection off meperidine following recovery could strengthen the association to this drug with increased causality. In addition, the diagnosis of delirium can be verified with an electroencephalographic examination or physostigmine injection test.
References 1. Fogarty T, Murray GB. Psychiatric presentation of meperidine toxicity. J Clin Psychopharmacol 1987;7:116–7. 2. Stambaugh JE, Wainer IW, Sanstead JK, et al. The clinical pharmacology of meperidine—comparison of routes off administration. J Clin Pharmacol 1976;16:245–56. 3. Bailey PL, Egan TD, Stanley TH. Intravenous opioid anesthetics. In: Miller RD, ed. Anesthesia, 5th edition. Philadelphia: Churchill Livingstone, 2000:276–92. 4. Northoff G. Catatonia and neuroleptic malignant syndrome: psychopathology and pathophysiology. J Neural Transm 2002;109:1453–67.
325
S.S. Huang, et al
5. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th edition, Text Revision (DSM-IV-TR). Washington, DC: American Psychiatric Association, 2000:136–8. 6. Trepacz PT. Is there a final common pathway in delirium? Cholinergic and dopaminergic mechanisms. Semin Clin Neuropsychiatry 2000;5:132–48. 7. Andersson T. Pharmacokinetics, metabolism and interactions of acid pump inhibitors: focus on omeprazole, lansoprazole and pantoprazole. Clin Pharmacokinet 1996;31:9–28. 8. Grond S, Sablotzki A. Clinical pharmacology of tramadol. Clin Pharmacokinet 2004;43:879–923. 9. Edwards DJ, Svensson CK, Visco JP, et al. Clinical pharmacokinetics of pethidine: 1982. Clin Pharmacokinet 1982; 7:421–33. 10. Eisendrath SJ, Goldman B, Douglas J, et al. Meperidineinduced delirium. Am J Psychiatry 1987;144:1062–5. 11. Kasture SB, Mandhane SN, Chopde CT. Baclofen-induced catatonia: modification by serotonergic agents. Neuropharmacology 1996;35:595–8.
326
12. Lauterbach EC. Catatonia-like events after valproic acid with risperidone and sertraline. Neuropsychiatr Neuropsychol Behav Neurol 1998;11:157–63. 13. Northoff G, Demisch L, Wenke J, et al. Plasma homovanillic acid concentrations in catatonia. Biol Psychiatry 1996; 39:436–43. 14. Mittino D, Mula M, Monaco F. Serotonin syndrome associated with tramadol-sertraline coadministration. Clin Neuropharmacol 2004;27:150–1. 15. Rogers KJ, Thornton JA. The interaction between monoamine oxidase inhibitors and narcotic analgesics in mice. Br J Pharm 1969;36:470–80. 16. Groves PM, Wilson CJ, Young SJ, et al. Self-inhibition by dopaminergic neurons. Science 1975;190[4214]:522–8. 17. Shiga Y, Minami K, Shiraishi M, et al. The inhibitory effects of tramadol on muscarinic receptor-induced responses in Xenopus oocytes expressing cloned M(3) receptors. Anesth Analg 2002;95:1269–73. 18. Latta KS, Ginsberg B, Barkin RL. Meperidine: a critical review. Am J Ther 2002;9:53–68.
J Formos Med Assoc | 2007 • Vol 106 • No 4
Catatonia Associated with Coadministration of Tramadol and Meperidine Si-Sheng Huang, Shaw-Hwa Jou,* Nan-Ying Chiu Tramadol and meperidine are frequently prescribed medications in the management of oncologic patients. The pharmacologic interaction of these two drugs may induce mental disturbance. This was demonstrated by our case of a 39-year-old woman with gastric mucosa associated lymphoid tissue lymphoma (MALToma), stage III after chemotherapy. She was admitted to our medical ward with the complaint of abdominal pain. Pantoprazole 40 mg and tramadol 150 mg daily were prescribed with intravenous route after hospitalization. Two days later, the patient developed transient visual hallucinations and disorientation afterr additional injection of meperidine (25 mg). Six hours later, catatonic features appeared. The duty doctorr stopped all the medications. Two days later, the catatonic features disappeared. From the clinical course, we suggest that the catatonia was caused by drug interactions between tramadol and meperidine. The pharmacodynamic mechanism might be related to the dopamine and serotonin systems. [J Formos Med Assoc 2007;106(4):323–326] Key Words: catatonia, meperidine, tramadol
Tramadol and meperidine are both synthetic phenylpiperidine-derivative opiate agonists. They are strong analgesics used in the relief of moderate to severe pain. Tramadol has adverse effects such as dry mouth, constipation, urinary retention, visual disturbance, and confusion. Meperidine has been observed to have clinical manifestations of central nervous system (CNS) stimulation such as seizures, agitation, irritability, disorientation, nervousness, tremors, twitches, and myoclonus.1 These effects may be related to serum levels of meperidine and its active metabolite normeperidine.2 Opioids can increase muscle tone and may cause muscle rigidity. Opioid-induced rigidity is probably related to a catatonic state, which can be induced by opioids.3 Catatonic features can be observed in a subtype of schizophrenia, major depressive disorder,
and bipolar disorder. Catatonia may also be caused by a variety of medical or surgical conditions, such as neoplasms, encephalitis, head trauma, diabetes, and other metabolic disorders. Its clinical manifestations include motor immobility, excessive motor activity, extreme negativism or mutism, peculiarities of voluntary movement, echolalia, and echopraxia. In addition, medications, such as antipsychotics, could induce catatonia.4 Delirium is characterized by a disturbance off consciousness and a change in cognition or development of a perceptual disturbance. The disturbance develops over a short period of time and tends to fluctuate during the course of the day. Associated clinical features of delirium include sleep-wake cycle disturbance, disturbed psychomotor behavior, and emotional disturbance. Depending on the etiology, delirium can be associated
©2007 Elsevier & Formosan Medical Association . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Department of Psychiatry, Changhua Christian Hospital, Changhua, Taiwan. Received: April 18, 2006 Revised: May 26, 2006 Accepted: September 5, 2006
*Correspondence to: Dr Shaw-Hwa Jou, Department of Psychiatry, Changhua Christian Hospital, 135 Nanhsiao Street, Changhua 500, Taiwan. E-mail: [email protected]
J Formos Med Assoc | 2007 • Vol 106 • No 4
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S.S. Huang, et al
with many nonspecific neurologic abnormalities such as tremor, myoclonus, asterixis, and reflex or muscle tone changes.5 A diminution in cholinergic function—an excess of dopamine, norepinephrine, and glutamate—and disturbances in serotonergic and γ-aminobutyric acid activities have been implicated in its pathogenesis.6 We report a patient who developed delirium and catatonic features following coadministration of tramadol and meperidine. We also review related articles and discuss the possible pathophysiologies.
Case Report In May 2005, a 39-year-old woman was diagnosed with gastric mucosa associated lymphoid tissue lymphoma (MALToma), stage III. She suffered from abdominal pain and dysphagia, at first, in March 2005. She underwent chemotherapy with cyclophosphamide 1000 mg, epirubicin hydrochloride 100 mg, vincristine sulfate 2 mg, and prednisolone 100 mg shortly after the diagnosis. She received pantoprazole, amoxicillin, clarithromycin, lamivudine, and prednisolone after chemotherapy. However, 1 week later, she visited our emergency department because of abdominal pain. Meperidine 50 mg was injected for pain. One hour later, irritable mood, restlessness, and derealized sensation were noted. Five minutes after injection, the symptoms were remitted spontaneously. Then, she was admitted to our medical ward for further evaluation. Pantoprazole 40 mg and tramadol 150 mg daily were prescribed with intravenous route. Two days later, meperidine 25 mg was injected additionally for her pain around 9 am. Two hours later, she stated that her hands and feet did not belong to her. The patient had confused consciousness, irritable mood, and inappropriate grasping behaviors around 1 pm. She reported seeing a man on the wall and many spiders around her bed. At 3 pm, she claimed that she was dead and did not know why her husband could see her. She could walk to the toilet for urination with fair f gait at 324
that time. Then, she developed mutism, immobile standing beside her bed, refusal to sit down, and reluctance to undergo physical examinations. She stood still throughout that night. The duty doctorr stopped all the medications. The results of neurologic examinations revealed isocoric pupil, positive bilateral light reflex, no obvious facial palsy, symmetric limbs muscle power, and normal deep tendon reflex. Next day, stupor consciousness, inattention, mutism, fixed posture, and negativism were still observed. Tracing back her history, there was no head trauma, epilepsy, and no overt psychiatric features. During the period of catatonia, the laboratory data showed normal findings in complete blood count, electrolytes, renal function, and liver function. Brain image and electroencephalographic examinations were not performed due to the absence of obvious focal signs. On the morning of the 3rd day, she woke up and spoke to others spontaneously. All catatonicc features had disappeared. The patient did nott receive any psychotropic during those 2 days. She was discharged 2 days later, and followed up att our hematology department afterwards.
Discussion At the emergency department, the patient developed irritable mood and derealization lasting forr 5 minutes after injection of meperidine 50 mg. However, following admission, the full symptoms of delirium and catatonia in this patient occurred with a lower dose meperidine (25 mg) subsequentt to the treatment of tramadol and pantoprazole. It suggests that the symptoms are related to a drugg interaction. Pantoprazole, a proton-pump inhibitor, is mainly metabolized by cytochrome P-450 2C19 (CYP2C19).7 Tramadol is a syntheticc 4-phenylpiperidine. O-demethylation and Ndemethylation are two main metabolic pathways of tramadol.8 As to meperidine, its main metabolicc pathway is N-demethylation.9 There is no case report about pantoprazole-induced or tramadolinduced delirium and catatonia on MEDLINE, butt there is one case report of meperidine-induced J Formos Med Assoc | 2007 • Vol 106 • No 4
Catatonia associated with tramadol and meperidine
delirium.10 The complete CYP P450 enzyme information of pantoprazole, tramadol, and meperidine is not available, and so the pharmacokinetic interaction of these drugs cannot be concluded. Some overlaps of metabolic pathways are noted between tramadol and meperidine. Tramadol and meperidine are both synthetic opioid compounds in the group of phenylpiperidine series. According to available data and pharmacologic action of these three agents, we speculate that the etiologies of delirium and catatonia in this patient were probably related to tramadol and meperidine, and less likely to be related to pantoprazole. Pharmacodynamic explanations of catatonia involve the dopamine system in the basal ganglia,4 serotonin system,11 and γ-aminobutyric acid (GABA) system.12 Northoff et al13 reported that dopaminergic metabolites in the plasma of acute catatonic patients were increased. These results suggest hyperactivity in the dopaminergic system in catatonia. However, hypoactivity in this system was also assumed.4 In addition to the dopamine system, Lauterbach12 reported that serotonergic drugs could induce catatonic syndrome because of increased 5-HT1A receptor stimulation and GABAb receptor stimulation. Tramadol and meperidine are not only anticholinergic agents but also potent inhibitors of serotonin reuptake into presynaptic neurons.14,15 Based on the findings of our case, we speculate two possible mechanisms of catatonia. First, dopamine and acetylcholine have a reciprocal relationship in the nigrostriatal pathway. A balance between the dopaminergic and cholinergic system is necessary for controlling voluntary movement.16 Anticholinergic effects of these two medications may result in an imbalance between these two systems. Second, serotonergic activity may be related to catatonia.17,18 This model could also explain the catatonic features in this patient. Fogarty and Murray1 reported a patient who developed agitation and visual hallucinations after using meperidine 930 mg daily for 4 days. Psychiatric symptoms, including anxiety, fearfulness, and hypervigilance, resolved over the next 12 hours after meperidine was discontinued. J Formos Med Assoc | 2007 • Vol 106 • No 4
Eisendrath et al10 reported six cases of meperidineinduced delirium. Their daily doses of meperidine ranged from 225 to 1400 mg. In our case, the patient’s delirium was noted 4 hours after a single dose (25 mg) of meperidine. Before injection off meperidine, our patient had regularly received tramadol 150 mg daily. From the pharmacodynamic aspect, the etiology of delirium was highlyy related to the anticholinergic effect of tramadol and meperidine.17,18 The CNS receptor level’s interaction of opioids and their metabolites mayy contribute to the pathogenesis of delirium. Moreover, the patient’s anticancer drugs, cyclophosphamide and prednisolone, can also cause delirium because of their strong anticholinergic effects. Unfortunately, there is no clear support for a diagnosis of delirium such as cognitive examination or thorough assessment of a broad range off delirium symptoms as in the use of a specificc symptom rating scale over time. These could be ictal symptoms (complex partial, even confusional status) perhaps associated with some CNS lesions including meningeal lymphoma, yet neither an electroencephalogram nor magnetic resonance imaging was done in this at-risk patient. Further, there is the possibility that this episode was onlyy coincidentally related in time to the injection off meperidine. A design with another injection off meperidine following recovery could strengthen the association to this drug with increased causality. In addition, the diagnosis of delirium can be verified with an electroencephalographic examination or physostigmine injection test.
References 1. Fogarty T, Murray GB. Psychiatric presentation of meperidine toxicity. J Clin Psychopharmacol 1987;7:116–7. 2. Stambaugh JE, Wainer IW, Sanstead JK, et al. The clinical pharmacology of meperidine—comparison of routes off administration. J Clin Pharmacol 1976;16:245–56. 3. Bailey PL, Egan TD, Stanley TH. Intravenous opioid anesthetics. In: Miller RD, ed. Anesthesia, 5th edition. Philadelphia: Churchill Livingstone, 2000:276–92. 4. Northoff G. Catatonia and neuroleptic malignant syndrome: psychopathology and pathophysiology. J Neural Transm 2002;109:1453–67.
325
S.S. Huang, et al
5. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th edition, Text Revision (DSM-IV-TR). Washington, DC: American Psychiatric Association, 2000:136–8. 6. Trepacz PT. Is there a final common pathway in delirium? Cholinergic and dopaminergic mechanisms. Semin Clin Neuropsychiatry 2000;5:132–48. 7. Andersson T. Pharmacokinetics, metabolism and interactions of acid pump inhibitors: focus on omeprazole, lansoprazole and pantoprazole. Clin Pharmacokinet 1996;31:9–28. 8. Grond S, Sablotzki A. Clinical pharmacology of tramadol. Clin Pharmacokinet 2004;43:879–923. 9. Edwards DJ, Svensson CK, Visco JP, et al. Clinical pharmacokinetics of pethidine: 1982. Clin Pharmacokinet 1982; 7:421–33. 10. Eisendrath SJ, Goldman B, Douglas J, et al. Meperidineinduced delirium. Am J Psychiatry 1987;144:1062–5. 11. Kasture SB, Mandhane SN, Chopde CT. Baclofen-induced catatonia: modification by serotonergic agents. Neuropharmacology 1996;35:595–8.
326
12. Lauterbach EC. Catatonia-like events after valproic acid with risperidone and sertraline. Neuropsychiatr Neuropsychol Behav Neurol 1998;11:157–63. 13. Northoff G, Demisch L, Wenke J, et al. Plasma homovanillic acid concentrations in catatonia. Biol Psychiatry 1996; 39:436–43. 14. Mittino D, Mula M, Monaco F. Serotonin syndrome associated with tramadol-sertraline coadministration. Clin Neuropharmacol 2004;27:150–1. 15. Rogers KJ, Thornton JA. The interaction between monoamine oxidase inhibitors and narcotic analgesics in mice. Br J Pharm 1969;36:470–80. 16. Groves PM, Wilson CJ, Young SJ, et al. Self-inhibition by dopaminergic neurons. Science 1975;190[4214]:522–8. 17. Shiga Y, Minami K, Shiraishi M, et al. The inhibitory effects of tramadol on muscarinic receptor-induced responses in Xenopus oocytes expressing cloned M(3) receptors. Anesth Analg 2002;95:1269–73. 18. Latta KS, Ginsberg B, Barkin RL. Meperidine: a critical review. Am J Ther 2002;9:53–68.
J Formos Med Assoc | 2007 • Vol 106 • No 4