Underrecognition of tardive dyskinesia and drug-induced parkinsonism by psychiatric residents

Underrecognition of Tardive Dyskinesia and Drug-Induced Parkinsonism by Psychiatric Residents Thomas E. Hansen, M.D., William L. Brown, M.D., Ronald M. Weigel, Ph.D.,“, and Daniel E. Casey, M.D.

Abstract: Recognition

of tardive dyskinesia (TD) and other neuroleptic, drug-induced, extrapyramidal side effects presents a major challenge in modern clinical psychopharmacology. Failure to recognize these disorders can lead to poor patient care and may contribute to societal pressure for external control of psychiatric practice. This study reports the occurrence of tardive dyskinesia and drug-induced parkinsonism (DIP) in 101 inpatients, and documents underrecognition of both disorders by resident physicians. Researchers noted TD in 28% of cases azzd residents only described TD (or symptoms of TD) in 12%. TIze researcher determined DIP prevalence rate of 26% corztrasted with an 11% rate found by residents. Patients with psychotic disorders were more likely than other patients to have researcher-identified TD, whereas DIP (researcher cases) occurred more often in patients z&h affective diagnoses. Residents tended to miss milder cases of TD, and to miss DIP in younger patients and in pafiezzts with affective disorders. Improved teaching and clinical exams are recommended to improve recognition.

Introduction Recognition neuroleptic,

of tardive dyskinesia (TD) and other drug-induced, extrapyramidal side ef-

From the Portland Veterans Affairs Medical Center, Oregon Health Sciences University, Portland Oregon. Address reprint requests to: Thomas E. Hansen, M.D., Portland VA Medical Center, 116A-I’, P.O. Box 1034, Portland, OR 97207. Current address: College of Veterinary Medicine, University of Illinois at Urbana-Champaign, Presented to the New Research Section at the Annual Meeting of the American Psychiatric Association, Washington, D.C., May 1986.

340 ISSN 0163~8343/92/$5.00

fects (EPS) remains problematic despite the major impact these disorders have on psychiatric patients. This is especially evident in the wide range of prevalence figures reported for TD-from as low as 5% to more than 70% [l-4]. This variation in TD prevalence can be attributed partially to differences in patient characteristics (i.e., risk factors), and case definition (e.g., less rigorous criteria lead to higher rates) [4,5]. Claims that physicians fail to identify and treat akathisia, drug-induced parkinsonism (DIP), and dystonia suggest that these EPS are also underrecognized [6-91. The importance for adequate patient care of recognizing and documenting acute EPS and TD cannot be overemphasized. If acute EPS go untreated, poor medication compliance results and future treatment may be compromised [lo]. The occurrence of very mild DIP may indicate that neuroleptic dose is adequate and should not be further increased [ 111. Also, ineffective management of EPS, especially TD, may lead to increased demands for external regulation of psychiatric practice [12]. Despite increasing prevalence and public concerns about TD and EPS, many clinicians still report that they do not observe TD occurring at rates comparable to those seen in research settings. This study prospectively determines TD and DIP recognition rates for clinicians and researchers, examines factors affecting syndrome occurrence and clinician recognition, and makes suggestions to improve clinical evaluation.

Gcrwal Hvsyifal Psychiaty 14, 340-344, 1992

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Underrecognition

Method

of TD and DIP

specific descriptions (e.g., “tremor,“ “mouth and so forth) or provisional diagmovements,” noses of TD and DIP as positive cases.

PUtiOZtS

Included were psychiatric inpatients (N = 101) admitted consecutively over a 6-month period to the Portland Department of Veterans Affairs Medical Center who had taken neuroleptic medication for a minimum of 3 months at some point prior to admission (determined by direct patient inquiry and chart review). The first author (TEH) was a staff psychiatrist on these patients’ ward. All patients gave informed consent.

Ra tiqs We rated patients with the Abnormal Involuntary Movement Scale (AIMS) [13] and the Set. Hans Extrapyramidal Disorders Scale [14] within 72 hours of admission. The Set. Hans scale includes separate evaluations for dyskinesia (e.g., TD) and parkinsonism on a O-6 scale. The raters (TEH and WLB) achieved acceptable interrater reliability (Spearman’s rho = 0.89 for total AIMS and rho = 0.83 for total Set. Hans parkinsonism). A researcher TD diagnosis required symptoms of moderate severity (i.e., AIMS = 3) in one body area or of mild severity (i.e., AIMS = 2) in two body areas (these are the severity thresholds for Research Diagnosis of TD) [15]. A researcher DIP diagnosis required that the global Set. Hans parkinsonism score be mild or greater. Researchers rated patients blind to the resident physicians’ chart notes and diagnoses.

Chart Review At study conclusion we reviewed charts for age, DSM-III diagnosis, and resident physician recognition of movement disorders. Twelve first- and second-year psychiatric residents admitted patients during the study period. We reviewed each patient’s admission evaluation (assessments coinciding with researcher ratings) and scored either

Data Analysis We calculated TD and DIP prevalence for researcher and resident diagnoses. Risk factors analyzed for each disorder included the presence of the other disorder, age, and DSM-III diagnoses classified along two dimensions: 1) ysydrotic (schizophrenia, mania, delusional depression) versus nonpsychotic, and 2) Qfectizle (16 bipolar, and 12 with major or delusional depression) vs nonnffectivc. Multiple logistic regression analyses determined which characteristics were associated with resident physicians failing to identify researcher ‘I’D and DIP cases. The variables entered included age, psychotic and/or affective diagnosis, severity of TD, severity of DIP, and location of TD (oral vs extremity). All y-values reported in the study are two-tailed. As TD measures were highly correlated (total AIMS and Set. Hans Dyskinesia scores, Spearman’s rho = 0.98, !J < 0.001; total AIMS and global AIMS scores, rho = 0.93, p < O.OOl), we used total AIMS to indicate TD severity. Total Set. Hans Parkinsonism score was used to measure DIP severity.

Results TD Prevalence and Risk Factors Table 1 lists characteristics of patients with researcher and resident-identified TD. Residents recognized TD significantly less often than did researchers (12% vs 28%) ~7 < 0.01, McNemar test). Researchers concurred with all cases noted by the residents. Older age was significantly associated with TD prevalence for both researchers and residents (Mann-Whitney U-test; p = 0.01 for researchers, p < 0.05 for residents). Patients with psychotic diagnoses were more likely than nonpsychotic pa-

Table 1. TD patient characteristics

Group All patients Researcher diagnosed Resident diagnosed

Mean age

Researcher AIMS score

N

(SD)

(SD)

Psychotic diagnosis

Affective diagnosis

101 28 (28%) 12 (12%)

40 (12.1) 46 (14.9) 48 (13.5)

3.2 (2.9) 7.2 (1.9) 6.7 (2.9)

67 25 (37%) 8 (12%)

28 6 (21%) 2 (7%)

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Table 2. DIP patient characteristics Mean age

Researcher DIP score

Group

N

(SD)

(SD)

Psychotic diagnosis

Affective diagnosis

All patients Researcher diagnosed Resident diagnosed

101 26 (26%) 11 (11%)

40 (12.1) 47 (14.9) 50 (16.4)

2.7 (3.6) 3.6 (3.0) 4.5 (3.5)

67 17 (25%) 9 (13%)

28 12 (43%) 3 (11%)

tients to have researcher-identified TD (Chi-square = 7.8, df = 1, p < 0.005). Affective diagnoses did not affect researcher-identified TD prevalence (Chisquare, NS). Neither diagnostic group influenced resident-identified TD prevalence (Chi-square, NS). The correlation between researcher scores for TD and DIP was not significant (rho = 0.13, p > O.lO), indicating that DIP did not obscure TD and vice versa.

DIP Prevalence and Risk Factors Table 2 lists characteristics of patients with researcher and resident-identified DIP. Residents recognized DIP significantly less often than did researchers (11% vs 26%, p < 0.001, McNemar test). Researchers concurred with all cases identified as having DIP by the residents. Older age was significantly associated with higher DIP prevalence determined by researchers and residents (MannWhitney U-test, p < 0.05 for both groups). Patients with affective diagnoses were more likely than the others to have researcher-identified DIP (Chisquare = 4.76, df = 1, p < 0.05). Psychotic diagnosis did not influence either researcher or resident-identified DIP, and affective disorders did not affect resident-identified DIP.

Logistic Regression and TD Underrecognition Logistic regression analysis of resident-correct TD diagnosis (N = 12) vs resident-missed diagnosis (N = 16) revealed a trend for residents to miss less severe TD (p = 0.07). Age, presence of DIP, and psychiatric diagnosis did not contribute to the classification difference. To further examine the effect of TD score on resident recognition, we repeated the logistic regression analysis with separate oralfacial and extremity scores (calculated from the individual items on the AIMS exam) entered instead of total score. Lower oral-facial scores were significantly associated with resident-missed diagnoses (p = 0.03) but extremity scores were not associated with accuracy of resident diagnosis. 342

Logistic Regression and DIP Underrecognition. Logistic regression analysis of resident-correct DIP diagnosis (N = 11) vs resident-missed diagnosis (N = 15) revealed that severity of DIP did not influence accuracy of resident physician recognition. Resident missed diagnosis was associated with younger age (p < 0.01) and affective diagnosis (p < 0.05) when the affective/nonaffective variable was used in the regression equation and with younger age (p < O.Ol), and nonpsychotic diagnosis (p < 0.05) when the psychotic/nonpsychotic variable was used. The high negative correlation (r = -0.64, p < 0.001) between affective and psychotic diagnosis prevented analysis of the relative impact of each simultaneously.

Discussion This study primarily demonstrates underrecognition of TD and DIP by resident physicians. The possibility that researchers overdiagnosed TD and DIP seems unlikely as researcher criteria were more rigorous than those applied to the resident cases. This study also found prevalence rates for TD (28%) and DIP (26%) in the range commonly reported for chronically medicated patients [l-3,16]. The correlation between increased age and prevalence for both TD and DIP further agrees with previous reports [16,17]. In this study, underrecognition undoubtedly included both failure to observe and failure to document the syndromes. Factors influencing documentation were not specifically studied. We speculate, based on conversations with physicians at all levels of training, that concern about the significance of TD and a lack of awareness about the clinical importance of DIP could contribute to underdocumentation. Severity of TD significantly affected resident underrecognition but only when oral-facial and extremity scores were analyzed separately. This finding, which must be viewed as tentative given the small sample size used in the regression anal-

Underrecognition

ysis, suggests that residents recognize TD when it occurs with relatively greater severity in an obvious and expected location (e.g., the face), but fail to notice TD regardless of severity when it occurs elsewhere. (Similarly, as severity did not affect DIP recognition, residents appear to neglect DIP even in more severe cases). At least for TD, greater sensitivity in examination may improve recognition rates by enabling residents to see the milder cases. The presence of an affective diagnosis significantly influenced DIP recognition, with researchers more likely to diagnose DIP in such patients than in others, and residents less likely to do so. The symptoms of depression can be hard to distinguish from DIP, and misattribution of symptoms could have occurred with both the researchers and the residents. However, only 12 of the 28 affective disorder patients had depression, so this is a partial explanation at best. Given that younger age also predicted failure to recognize DIP, perhaps residents had more trouble recognizing DIP when they did not expect it. The failure to note an association between TD and affective disorder in this report differs with literature which suggests the latter is a TD risk factor [17]. Two other reports [6,18] have identified resident physician underrecognition of TD and DIP. In an evaluation of physical examinations, two of three TD cases and three of five DIP cases were missed by psychiatric resident physicians [18]. The frequency of TD (6%) and DIP (5%) was low, suggesting that the number of patients at risk was small (the number of patients on neuroleptics was not given). In the other study [6], 48 patients were on neuroleptics for at least 1 week, and researchers examined entire hospital charts. Symptoms consistent with TD were described in only four of ten (40%) researcher-diagnosed TD cases (the actual diagnosis was made by a resident in just one TD case), and DIP was diagnosed 17 of 29 times (59%) [6]. Though methodologic differences prevent direct comparison to our data, the authors found severity influenced recognition of oral TD, but not DIP (extremity TD was interestingly more likely to be recognized if it was less severe). Comparison between researchers and residents in the current and above reports reflects the prominent role resident physicians have in academic settings. Whether findings with residents can be applied to psychiatrists in general is unclear. Residents in most programs do many more physical exams than general psychiatrists and the intensity

of ‘I’D and DIP

of this activity is likely to offset the greater experience of the psychiatrist in practice. On balance, we suspect underrecognition of TD and DIP also occurs with general psychiatrists. The importance of accurate recognition of TD and DIP extends beyond work done by psychiatrists with inpatients. Psychiatric patients will have their standard neuroleptic medications continued when treated by physicians for other conditions, for instance, while hospitalized on a medical or surgical ward. Nonpsychiatrists may prescribe standard neuroleptic medications because of convenience, economics, or unavailability of psychiatrists (e.g., as medical backup to nonpsychiatrist mental health professionals, in nursing homes, and in rural areas). Also, medications with neuroleptic properties may be used for nonpsychiatric purposes (e.g., metoclopramide for gastrointestinal tract conditions, neuroleptics for pain management). Practitioners in all of these situations need to be aware of TD and DIP so they can obtain informed consent from their patients. They also need to be able to recognize these disorders, so that they can safely manage their patients. Improved teaching and use of more specific clinical exams might improve recognition rates. One study claimed that resident physicians who took a course in EPS demonstrated better management of EPS than did residents 2 years previously who had not taken the course [19]. Improved EPS recognition after teaching remains to be proved, as groups receiving or not receiving the course in the same year must be studied to control for changes in sensitivity over time not related to the course. In conclusion, we report underrecognition of TD and DIP by psychiatric resident physicians in an inpatient setting. Possible contributing problems include insensitive or incomplete exam techniques and reluctance to report findings. We suggest the following approaches may lead to improved recognition of EPS: 1. A specific examination for TD and DIP should be completed in all patients with past, current, or anticipated neuroleptic treatment, regardless of diagnosis. 2. Attention should be focused on the oral cavity for TD (e.g., more than the standard screening pharyngeal exam). 3. Hand movements must be observed at rest and with activation maneuvers (i.e., finger tapping and walking) to facilitate detection of TD in the

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extremities. Observed movements should be characterized as tremor (more likely DIP) or choreoathetoid (more likely TD). Symptoms of DIP must be specifically assessed (global impressions will miss symptoms). Symptoms include rigidity, bradykinesia (slowness of movement), tremor, facial expression, gait, and posture. Symptoms should not be automatically dismissed because of resemblance to psychiatric symptoms. Both presence and absence of signs and symptoms should be recorded.

This work was supported in part by the Veterans Administration Research SerzGce (Drs. Hurtsen, Weigel, Casey) and National Institute of Mental Health grant number MH36657 (Dr. Casey). The authors thank Melinda Lowe and Sondm K. Long for help in manuscript preparation.

References 1. Casey DE: Tardive dyskinesia. In Meltzer HY (ed), Psychopharmacology: The Third Generation of Progress. New York, Raven Press, 1987, pp 1411-1419 2. Kane JM, Smith JM: Tardive dyskinesia: prevalence and risk factors 1959 to 1979. Arch Gen Psychiatry 39:473-481, 1982 3. Jeste DV, Wyatt RJ: Changing epidemiology of tardive dyskinesia: an overview. Am J Psychiatry 138: 297-309, 1981 4. Hansen TE, Casey DE, Vollmer WM: Is there an epidemic of tardive dyskinesia? In Casey DE, Gardos G (eds), Tardive Dyskinesia: From Dogma to Reason. New York, American Psychiatric Press, 1986, pp 214 5. Asnis GM, Leopold MA, Duvoisin RC, Schwartz AH: A survey of tardive dyskinesia in psychiatric outpatients. Am J Psychiatry 134:1367-1370, 1977

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6. Weiden PJ, Mann JJ, Haas G: Clinical nonrecognition of drug-induced movement disorders: a cautionary study. Am J Psychiatry 1441148-1153, 1987 7. Van Putten T: Why do schizophrenic patients refuse to take their drugs? Arch Gen Psychiatry 31:67-72, 1974 8. Rifkin A, Quitkin F, Klein DF: Akinesia: a poorly recognized drug-induced extrapyramidal behavior disorder. Arch Gen Psychiatry 32:672-674, 1975 9. Keepers GA, Casey DE: Clinical management of acute neuroleptic-induced extrapyramidal syndromes. Curr Psychiatr Ther 23:139-157, 1986 10. Keepers GA, Hansen TE, Casey DE: Prospective prediction of vulnerability to neuroleptic-induced extrapyramidal syndromes (abstract) Proc Sot Biol Psychiatry 66:222, 1986 11. McEvoy JP: The neuroleptic threshold as a marker of minimum effective neuroleptic dose. Compr Psychiatry 27:327-335, 1986 12. Baldessarini RJ, Cohen BM: Regulation of psychiatric practice. Am J Psychiatry 143:750-751, 1986 13. Guy W: ECDEU assessment manual for psychopharmacology (revised). Washington, DC, US Department of Health, Education, and Welfare, USGPO 534-537, 1976 14. Gerlach J: Tardive dyskinesia. Dan Med Bull 26:209244, 1979 15. Schooler NR, Kane JM: Research diagnoses for tardive dyskinesia. Arch Gen Psychiatry 391486-487, 1982 extrapyr16. Ayd FJ Jr: Early-onset neuroleptic-induced amidal reactions: a second survey, 1961-1981. In Coyle JT, Enna SJ (eds), Neuroleptics: Neurochemical, Behavioral and Clinical Perspectives. New York, Raven Press, 1983, pp 75-92 17. Casey DE: Tardive dyskinesia and affective disorders. In Gardos G, Casey DE (eds), Tardive Dyskinesia and Affective Disorders. Washington, DC, American Psychiatric Press, 1984, pp l-20 18. Rigby JC, Oswald AG: An evaluation of the performing and recording of physical examinations by psychiatric trainees. Br J Psychiatry 150:533-535, 1986 19. Dixon L, Weiden PJ, Frances AJ, Rapkin B: Management of neuroleptic-induced movement disorders: effects of physician training. Am J Psychiatry 146:104-106, 1989