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The advent of neuroleptics in the mid 1950s revolutionized the treatment of both acute and chronic psychosis (1). The antipsychotic property of these medications was identified as being primarily attributable to their dopaminergic activity. Unfortunately, because this activity targets the nigrostriatal pathways of the brain, it causes extrapyramidal symptoms (EPS) (1). The prevalence of these motor abnormalities with first-generation antipsychotics has been nothing short of spectacular. The range of patients affected by these side effects has varied from 2% to 90% (2,3). The most serious EPS, tardive dyskinesia (TD), has occurred in approximately 25% of patients medicated with these agents (4). The relatively recent introduction of second-generation antipsychotics has demonstrated improvements in efficacy and various other outcome dimensions (5–11). Owing to their decreased propensity to target dopamine receptors, second- generation antipsychotics have demonstrated a decreased risk of producing EPS (12,13,15). These medications however, have not been totally free of EPS, nor have they totally abolished these side effects in patients who have acquired them either from previous treatment with first-generation antipsychotics or directly from the pathology of schizophrenia spectrum disorders (14–18). EPS have been associated with a vast array of important clinical and medicolegal consequences. These have included behavioural disturbances, functional impairment, stigma, the need for adjunct medications, nonadherance, the potential for misdiagnosis, suicidality, and poorer quality of life (19–21). These consequences have highlighted the importance of prompt recognition and treatment. Unfortunately, psychiatrists have not demonstrated adequate skills in assessing EPS (22,23). This is not surprising, given that a study of psychiatric residents revealed the under- recognition of motor abnormalities in patients receiving antipsychotic medications (24). The American Psychiatric Association’s Tardive Dyskinesia: A Task Force Report (25,26) and the Canadian Psychiatric Association’s Canadian Clinical Practice Guidelines for the Treatment of Schizophrenia (27) recommend regular assessments for motor abnormalities. Further, these publications indicate that results must be recorded and recommend standard rating scales. Despite these important guidelines, very few studies have examined the assessment and documentation of EPS. Of the limited studies available, all have identified significant deficiencies in this domain (22,28,29). Our study examined the level of assessment and documentation of EPS by attending physicians and nursing staff treating hospitalized patients with psychosis. MethodWe retrospectively examined the charts of 204 consecutive admissions (between January 1 and December 31, 1996) to a provincial psychiatric hospital and to the psychiatric ward of a general hospital, looking for documentation indicating the assessment of EPS. All patients had regular treatment with antipsychotic medication, regardless of psychiatric diagnosis. We identified demographics, length of hospitalization, diagnosis, and antipsychotic and adjunct medication. We reviewed medical records, including admission assessments, consultation reports, progress notes, nursing notes, and discharge summaries for documentation indicating that motor abnormalities were assessed and monitored. EPS were classified into dystonia, parkinsonism, akathisia, and tardive dyskinesia (TD). Charts were rated by 2 independent raters. Each type of EPS was rated based on the quality of assessment according to dimensions of severity, location, and laterality. We constructed a rating scale of 0 to 5 in which a score of 0 represented “no description” and a score of 5 represented the use of a standardized movement disorder scale (Table 1).
In addition to rating assessment quality, we also determined the frequencies of the various assessment qualities for each area of documentation and for each type of EPS. The data were analyzed for correlations between the quality and quantity of documentation for each type of motor abnormality and for demographic and clinical factors. Statistical significance was tested using the Spearman Rank Correlation Test and a conservative P = 0.01 was taken as significant because of the number of correlations. ResultsMost patients were diagnosed with a primary psychotic disorder (57.4%), followed by mood disorder (30.4%) (Table 2). There was a slight preponderance of male patients (55.4%). The age range of all patients was 17 to 92 years, with a mean age of 38.4 years. Length of hospitalization varied from 1 to 706 days, with a mean duration of 43.3 days.
The rating for each type of EPS was very similar, with most having no description. However, the rating for parkinsonism and akathisia was slightly better than that for TD and dystonia. Specifically, the percentage of medical records with “no description” for each type of EPS was as follows: dystonia (89%), parkinsonism (71%), akathisia (67%), and TD (94%). Surprisingly, the only standardized movement disorder scale found in all the charts was an Abnormal Involuntary Movement Scale (AIMS) used to assess TD (Table 3).
We found significant correlations between the presence of assessments across all the records in the chart and several clinical variables. TD was assessed more in older patients (r = 0.199, P = 0.004). Length of hospitalization was positively correlated with parkinsonism (r = 0.320, P = 0.001) and akathisia assessments (r = 0.368, P = 0.001). Use of conventional antipsychotics was associated with more assessments of parkinsonism (r = 0.224, P = 0.001). The data on adjunctive medication use contained multiple correlations. Use of adjunct sedatives was associated with increased assessments of akathisia (r = 0.194, P = 0.005). Use of antiparkinsonian medication was associated with increased assessments of dystonia (r = 0.224, P = 0.001) and parkinsonism (r = 0.262, P = 0.001). Similarly, use of beta blockers was associated with increased assessments of parkinsonism (r = 0.198, P = 0.005) and akathisia (r = 0.180, P = 0.01). No significant correlations were found between use of second-generation antipsychotics and sex . Assessments were found more frequently in nursing notes for all types of EPS except TD (Table 4). The extent of interrater agreement regarding EPS documentation was found to be 91.1%.
ConclusionsThis study highlights the exceedingly high rate of failure to document the assessment and course of EPS caused by neuroleptics. This finding suggests that clinicians have not recognized the importance of documenting these significant adverse events. Fortunately, this shortcoming is correctable with increased awareness and systematic attention to these difficulties. Despite its high prevalence and potentially disfiguring and persistent effects, TD was documented in only 5.5% of patient records. Of this minimal number, advanced age appeared to be the only factor associated with documentation. Presumably, the elderly were correctly identified as being among patients at higher risk or showing more clinical signs of TD. Possibly, sensitivity to other risk factors (see Table 4) of this phenomenon, such as length of exposure to antipsychotics, female sex, the affective component of the illness, noninsulin-dependent diabetes mellitus, cigarette smoking, and previous EPS, may have increased the attention given to this serious motor abnormality. In our study, the longer the patient’s hospitalization, the greater the likelihood that parkinsonism would be recorded. However, this motor difficulty was not documented in 71% of patient records, although it is the most common form of EPS (30). This presents a discouraging dilemma, because akinesia is not only the most common form of parkinsonism, but also the most rapid in onset (31,32). Thus, one may assume that this movement abnormality continues to be missed early in the course of antipsychotic treatment. Other factors correlating with documentation of parkinsonism were the use of conventional antipsychotics and the use of adjunct medications such as anticholinergics and beta blockers. It is encouraging that clinicians documented assessments of EPS more frequently when patients were treated with conventional antipsychotics. There is abundant and clear literature describing the higher liability of motor abnormalities with first-generation antipsychotics, compared with their second-generation counterparts. The increased documentation for patients on adjunct drugs may reflect a higher level of severity or relentlessness in parkinsonian adverse effects in these patients. Akathisia has been noted to be one of the most subjectively difficult EPS. Psychological complications have included “acting out,” suicidality, exacerbated psychosis, depression, hopelessness, and feelings of mistrust toward clinicians (33–39). In this study, 67% of cases had no documented assessment or monitoring for this serious motor abnormality. Documentation of akathisia was significantly correlated with increased length of hospitalization, adjunct sedatives, and beta blockers. The latter 2 have been common interventions for akathisia. Length of hospitalization may, unfortunately, reflect clinicians’ latent practice of assessing for this type of EPS or, possibly, their mistaking akathisia for psychotic agitation. With respect to dystonia, documentation was lacking in 89% of cases. The misperception that dystonia is a rare form of EPS, drastic in its presentation and occurring only in the emergency room or only shortly after admission, may be responsible for clinicians’ neglect to assess document this adverse event. This study demonstrates that patients treated with second- generation antipsychotic medications had less documentation of EPS in their hospital records. Granted, these medications have clearly shown a decreased risk of producing EPS and possibly have EPS-treating qualities, but they have not been totally free of causing motor abnormalities. In addition, numerous studies have demonstrated spontaneous motor abnormalities in drug-naïve schizophrenia patients (39–43). Thus, established treatment guidelines indicating the need to assess and document EPS prior to and during antipsychotic treatment should continue to be respected. Poor documentation of EPS may reflect clinicians’ nonrecognition of motor abnormalities. A study by Weiden demonstrated that physicians have alarmingly poor diagnostic skills in regard to neuroleptic-induced movement disorders (22). Understandably, limited assessment skills would discourage documentation of the presence or absence of these adverse effects. Quite possibly, and optimistically, one must consider that clinicians have indeed assessed and monitored patients for EPS. Documenting their history gathering and physical examination for motor abnormalities may have been neglected or considered trivial. However, where positive findings exist and interventions are warranted, documentation is imperative in clinical records. In the absence of positive findings, documentation is important to ascertain that motor abnormalities have been investigated. Without documentation, it may be unclear whether there has been clinical error or negligence. In the US, there have been numerous TD-related lawsuits (28,44). It may be only a matter of time before Canadian physicians are challenged by similar legal consequences. The limited assessment of EPS quite possibly suggests a neglect in the regular monitoring of anticholinergic medication. Indiscriminate use may be increasing exposure to medications such as benztropine that quite possibly cause significant and potentially serious adverse effects (45). This study has several limitations. The findings are specific to a mid-sized city and thus may not reflect nationwide patterns. The subjects were exclusively inpatients and may not reflect similar documentation practices in an outpatient setting. By contrast, however, the acute condition of inpatients may warrant more vigilant and more thorough documentation. This study exclusively focused on the assessment and monitoring habits of psychiatrists. The results may not reflect the practices of other physician groups using antipsychotics, such as general practitioners, neurologists, and other MD groups. Other methodological questions relate to the timing of the study. Patient charts were examined from the beginning of 1996 to the beginning of 1997. This was generally a time in which clinicians were just beginning to acquire clinical familiarity with second-generation antipsychotics. Paradoxically, even though first-generation antipsychotics have shown increased risk of motor abnormalities, the second-generation antipsychotics may have directed more attention to EPS. Thus, it is quite possible that documentation may now be improved. This study underscores several important issues in regard to neuroleptic-induced EPS. First, clinicians must be sensitive to the significant clinical consequences of these side effects in their patients. Clinicians must become more responsible in documenting their assessments of motor abnormalities to assure vigilant monitoring and to intervene with appropriate treatments. Second, a comprehensive and systematic assessment may be ensured by using standardized measures regularly. Because poor monitoring may reflect poor training in physically examining for EPS, it highlights the urgent need to provide such training to all clinicians caring for patients receiving antipsychotic medication. Brief but specific training has been shown to be successful (46). Specific skills training may need to be initiated at the undergraduate and postgraduate level of medical education. Finally, with the recent availability of EPS-sparing antipsychotics, neuroleptic-induced side effects may potentially become a medicolegal challenge in Canada. Optimistically, all these concerns are remediable. Whether clinicians will appropriately and urgently rise to this challenge remains a matter of speculation and hope. AcknowledgementThe authors express their appreciation to Ms Mary Tonelotto for her impeccable transcription of this manuscript. References1. Casey DE. Neuroleptic-induced acute extrapyramidal syndromes and tardive dyskinesia. Psychiatr Clin North Am 1993;16:589–609. 2. Casey DE, Keepers GA. Neuroleptic side effects: acute extrapyramidal syndromes and tardive dyskinesia. In: Casey DE, Christensen AV, editors. Psychopharmacology: current trends. Berlin: Springer-Verlag; 1988. p 74–93. 3. Sovner R, DiMascio A. Extrapyramidal syndromes and other neurological side effects of psychotropic drugs. In: Lipton MA, Dimascio A, Killam KF, editors. Psychopharmacology: a generation of progress. New York: Raven Press; 1978. p 1021–32. 4. Kane JM, Woerner M, Lieberman J. Tardive dyskinesia: prevalence, incidence and risk factors. J Clin Psychopharmacol 1988;8(Suppl 4):52–6. 5. American Psychiatric Association. Practice guidelines for the treatment of patients with schizophrenia. Am J Psychiatry 1997;154(Apr Suppl):1–63. 6. Kane J, Honigfeld G, Singer J, and others. Clozapine for the treatment-resistant schizophrenic: a double-blind comparison with chlorpromazine. Arch Gen Psychiatry 1988;45:789–96. 7. Chouinard G, Jones B, Remington C, and others. A Canadian multi-centre placebo-controlled study of fixed doses of risperidone and haloperidol in the treatment of chronic schizophrenic patients. J Clin Psychopharmacol 1993;13:25–40. 8. Tollefson D, Bensley CM J, Tran PV, and others. Olanzapine versus haloperidol in the treatment of schizophrenia and schizo-affective and schizophreniform disorders: results of an international collaborative trial. Am J Psychiatry 1997;154:457–65. 9. Borison RL, Arvanitis LA, Miller BG. ICI 204,636. An atypical antipsychotic: efficacy and safety in a multi-centre, placebo controlled trial in patients with schizophrenia. US Seroquel Study Group. J Clin Psychopharmacol 1996;16:158–69. 10. Meltzar HY. Outcome in schizophrenia: beyond symptom reduction. J Clin Psychiatry 1999;60(Suppl 3):3–7. 11. Awad AG, Voruganti LN: Quality of life and new antipsychotics in schizophrenia: are patients better off? Int J Soc Psychiatry 1999;45:268–75. 12. Kapur S, Zipowsky R, Jones C, and others. Relationship between dopamine D2 occupancy, clinical responses, and side effects: a double-blind PET study of first-episode schizophrenia. Am J Psychiatry 2000;157:514–20. 13. Leucht S, Pitschel-Walz G, Abraham D, Kissling W. Efficacy and extrapyramidal side-effects of the new antipsychotics olanzapine, quetiapine, risperidone, and sertindole compared to conventional antipsychotics and placebo: a meta-analysis of randomized controlled trials. Schizophr Res 1999;35:51–68. 14. Tran PV, Hamilton SH, Kuntz AJ, and others. Double-blind comparison of olanzapine versus risperidone in the treatment of schizophrenia and other psychotic disorders. J Clin Psychopharmacol 1997;17:407–18. 15. Cortese L, and others. Extrapyramidal symptoms in drug-naive patients with schizophrenia. Abstract presented at the International Congress on Schizophrenia Research; April 2001; Whistler (BC). 16. Kopala LC. Spontaneous and drug-induced movement disorders in schizophrenia. Acta Psychiatr Scand 1996;94:12–7. 17. Caligiuri MP, Lohr JB, Jeste DV. Parkinsonism in neuroleptic-naive schizophrenic patients. Am J Psychiatry 1993;150:1343–8. 18. Chatterjee A, Chakos M, Koreen A, and others. Prevalence and clinical correlates of extrapyramidal signs and spontaneous dyskinesia in never-medicated schizophrenic patients. Am J Psychiatry 1995;152:1724–9. 19. Drake RE, Erlich J. Suicide attempts associated with akathisia. Am J Psychiatry 1985;142:499–501. 20. Weiden P, Shaw E, Mann JJ. Causes of neuroleptic non compliance. Psychiatr Ann 1986;16:571–85. 21. Voruganti L, Cortese L, Oyewumi L, Cernovsky Z, Zirul S, Awad A. Comparative evaluation of conventional and novel antipsychotic drugs with reference to their subjective tolerability, side-effect profile and impact on quality of life. Schizophr Res 2000;43:135–45. 22. Weiden PJ, Mann J, Haas G, Mattson M, Francis A. Clinical nonrecognition of neuroleptic-induced movement disorders: a cautionary study. Am J Psychiatry 1987;139:372–3. 23. Hansen TE, Brown WL, Weigel RM, Casey DE. Underrecognition of tardive dyskinesia and drug-induced parkinsonism by psychiatric residents. Gen Hosp Psychiatry 1992;14:340–4. 24. Rigby JC, Oswald AG. An evaluation of the performing and recording of physical examinations by psychiatric trainees. Br J Psychiatry 1986;150:533–5. 25. Task Force on Late Neurological Effects of Antipsychotic Drugs. Tardive dyskinesia: summary of a task force report. Am J Psychiatry 1980;137:1163–72. 26. Tardive dyskinesia: a task force report. Washington (DC): American Psychiatric Association; 1992. 27. Canadian Psychiatric Association. Canadian clinical practice guidelines for the treatment of schizophrenia. Can J Psychiatry 1998;43(Suppl 2 Revised). 28. Benjamin S, Munetz MR. CMHC Practices related to tardive dyskinesia screening and informed consent for neuroleptic drugs. Hosp Community Psychiatry 1994;45:343–6. 29. Schachter D, Keinman I. Psychiatrists’ documentation of informed consent. Can J Psychiatry 1998;43:1012–7. 30. Muscettola G, Barbato G, Pampallona S, Casiello M, Bollini P. Extrapyramidal syndromes in neuroleptic-treated patients : prevalence, risk factors, and association to tardive dyskinesia. J Clin Psychopharmacol 1999;19:203–8. 31. Wichmann T, Delung MR. Hypokinetic movement disorders. In: Watts RL, Koller WC, editors. Movement disorders : neurologic principles and practice. New York: McGraw-Hill; 1997. p 90–1. 32. Tsai CH, Lu CS. Early onset parkinsonism in Chinese. J Formos Med Assoc 1991;90:964–9. 33. Cem Atbasoglu E, Schultz SK, Andreasen NC. The relationship of akathisia with suicidality and depersonalization among patients with schizophrenia. J Neuropsychiatry Clin Neurosci 2001;13:336–41. 34. Siris SG. Suicide and schizophrenia. J Psychopharmacol 2001;15:127–35. 35. Van Putten T, Marder SR. Behavioral toxicity of antipsychotic drugs. J Clin Psychiatry 1987;480160-6689:13–9. 36. Siris SG. Three cases of akathisia and “acting out.” J Clin Psychiatry 1985;46:395–7. 37. Drake RE, Ehrlich J. Suicide attempts associated with akathisia. Am J Psychiatry 1985;142:499–501. 38. Shear MK, Frances A, Weiden P. Suicide associated with akathisia and depot fluphenazine treatment. J Clin Psychopharmacol 1983;3:235–6. 39. Van Putten T. Vulnerability to extrapyramidal side effects. Clin Neuropharmacol 1983;60362-5664:527–34. 40. Fenton WS. Prevalence of spontaneous dyskinesia in schizophrenia. J Clin Psychiatry 2000;6161:10–4. 41. Puri BK, Barnes TR, Chapman MJ, Hutton SB, Joyce EM. Spontaneous dyskinesia in first episode schizophrenia. J Neurol Neurosurg Psychiatry 1999;66(1):76–8. 42. Gervin M, and others. Spontaneous abnormal involuntary movements in first-episode schizophrenia and schizophreniform disorder: baseline rate in a group of patients from an Irish catchment area. Am J Psychiatry 1998;155:1202–6. 43. Chatterjee A, and others. Prevalence and clinical correlates of extrapyramidal signs and spontaneous dyskinesia in never-medicated schizophrenic patients. Am J Psychiatry 1995;152:1724–9. 44. Mossman D, Lehrer D. Conventional and atypical antipsychotics and the evolving standard of care. Psychiatr Serv 2000;51:1528–35. 45. Katzung BG. Adverse effects of muscarinic receptor-blocking drugs. In: Katzung BG, editor. Basic and clinical pharmacology.7th ed. Stamford (CT): Appleton and Lange; 1998. p 113–4. 46. Dixon L, Weiden PJ, Frances AJ, Rupkin B. Management of neuroleptic-induced movement disorders: effects of physician training. Am J Psychiatry 1989;146:1:104–6. Author(s)Manuscript received April 2003, revised, and accepted August 2003. Previously presented as an abstract at the 10th Biennial Winter Workshop in Schizophrenia; February 5 11, 2000; Davos, Switzerland. 1. Director of Clinical Services, Specialized Mental Health Program, Windsor Regional Hospital; Associate Professor, University of Western Ontario, London, Ontario. . 2. Consultant Neurologist, Department of Neurology, University of Western Ontario, London Health Sciences Centre, London, Ontario. 3. Consultant Psychiatrist, Department of Psychiatry, Alexandra Marine and General Hospital, Goderich, Ontario. 4. Resident Psychiatrist, Department of Psychiatry, University of British Columbia, Vancouver, British Columbia. 5. Research Assistant, Department of Psychiatry, University of Western Ontario, London Health Sciences Centre, London, Ontario. Address for correspondence: Dr L Cortese, Windsor Regional Hospital, 1453 Prince Road, Windsor ON N9C 3Z4 e-mail: leonardo.cortese@wrh.on.ca
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