General Hospital Psychiatry 14, 340-344, 1992

 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 under recognition of both disorders by resident physicians. Researchers noted TD in 28% of cases and residents only described TD (or symptoms of TD) in 12%. The researcher determined DIP prevalence rate of 26% contrasted 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 with affective diagnoses. Residents tended to miss milder cases of TD, and to miss DIP in younger patients and in patients with affective disorders. Improved teaching and clinical exams are recommended to improve recognition. 


Recognition of tardive dyskinesia (TD) and other neuroleptic, drug-induced, extrapyramidal side effects (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% [1-4]. 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 [6-9].

 The importance for adequate patient care of recognizing and documenting acute EPS and TD can not be overemphasized. If acute EPS go untreated, poor medication compliance results and future treatment may be compromised [10] The occurrence of very mild DIP may indicate that neuroleptic dose is adequate and should not be further increased [11]. 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. 


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. 


We rated patients with the Abnormal Involuntary Movement Scale (AIMS) [13] and the Sct. Hans Extrapyramidal Disorders Scale [14] within 72 hours of admission. The Sct. Hans scale includes separate evaluations for dyskinesia (e.g., TD) and parkinsonism on a 0-6 scale. The raters (TEH and WLB) achieved acceptable interrater reliability (Spearman's rho = 0.89 for total AIMS and rho = 0.83 for total Sct. 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 Sat. 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 specific descriptions (e.g., “tremor,” “mouth movements” and so forth) or provisional diagnoses of TD and DIP as positive cases. 

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) psychotic (schizophrenia, mania, delusional depression) versus nonpsychotic, and 2) affective (16 bipolar, and 12 with major or delusional depression) vs. nonaffecive. Multiple logistic regression analyses determined which characteristics were associated with resident physicians failing to identify researcher TD 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 p-values reported in the study are two-tailed. As TD measures were highly correlated (total AIMS and Sct. Hans Dyskinesia scores, Spearman's rho = 0.98, p < 0.001; total AIMS and global AIMS scores, rho = 0.93. p < 0.001), we used total AIMS to indicate TO severity. Total Sct. Hans Parkinsonism score was used to measure DIP severity. 


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%, p < 0.01, McNemar test). Researchers concurred with all cases noted by the residents. Older age was significantly associated with ID 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 patients to have researcher-identified TD) (Chi-square  7.8, df = 1, p <0.005). Effective diagnoses did not affect researcher-identified TD prevalence (Chi-square, 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> 0.10), 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). Researcher 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 (Mann Whitney U-test, p<0.05 for both groups). Patients with affective diagnoses were more likely than the others to have researcher-identified DIP (Chi-Square = 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-connect 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 oral-facial 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. 

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 < 0.01), 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. 


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 [1-3,16]. 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 analysis, 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 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 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 inpatients 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 pharyngeal exam).

3.   Hand movements must be observed at rest with activation maneuvers (i.e., finger tapping and walking) to facilitate detection of TD in the extremities. Observed movements should be characterized as tremor (more likely DIP) or choreoathetoid (more likely TD).

4.   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.

5.   Both presence and absence of signs and symptoms should be recorded.

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



1.        Casey DE: Tardive dyskinesia. In Meltzer MY (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 RI: 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 2-14

5.        Asnis GM, Leopold MA, Duvoisin RC, Schwartz AM: A survey of tardive dyskinesia in psychiatric outpatients. Am J Psychiatry 134:1367-1370.1977

6.        Weiden E, Mann JJ. Haas G: Clinical nonrecognition of drug-induced movement disorders: a cautionary study. Am J Psychiatry 144:1148-1153, 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 P, 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 Soc 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 psycho-pharmacology (revised). Washington, DC, US Department of Health, Education. and Welfare, USGPO 534-537, 1976

14.     Gerlach J: Tardive dyskinesia. Dan Med Bull 26:209-244.1979

15.     Schooler NR, Kane JM: Research diagnoses for tardive dyskinesia. Arch Gen Psychiatry 39:486-487, 1982

16.     Ayd FJ Jr: Early-onset neuroleptic-induced extrapyramidal reactions; a second survey, 1961-1981. In Coyle JT, Enni 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 1-20

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 disorder: effects of physician training. Am J Psychiatry 146:104-106, 1989


From the Portland Veterans Affairs Medial Center, Oregon Health Sciences University. Portland Oregon.
Address reprint requests to: Thomas E. Hansen, M.D., Portland VA Medical Center, 116A-P, 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.


© 1992 Elsevier Science Publishing Co., Inc. 

The New England Journal of Medicine -- December 3, 1998 -- Vol. 339, No. 23
Munchausen's Microbes?

To the Editor:

  Infection induced by a patient is a difficult problem. (1) The diagnosis is often delayed because objective signs are absent. The microbiology laboratory may provide clues to the diagnosis. (2)

A 30-year-old patient, a nurse's aide, was transferred from another hospital with a history of recurrent episodes of septic arthritis of the right ankle. Over a period of 3 years, she had been hospitalized for 168 days and had undergone 15 surgical interventions. A total of 72 wound samples (including biopsy  specimens and tissue fragments obtained during debridement of the ankle) and 110 blood specimens were sent for culture. Apart from "conventional" bacteria such as staphylococci, streptococci, and coliforms, cultures of both wound and blood samples grew unusual nonfermenting, gram-negative rods.

(Table 1). These organisms included Alcaligenes denitrificans subspecies xylosoxidans, A. faecalis, flavobacterium species, Comamonas testosteroni, Sphingomonas paucimobilis, and Stenotrophomonas  maltophilia as identified by a commercial biochemical test panel (API 20 NE, BioMerieux, Marcy-l'Etoile, France).

Blood specimens for culture were obtained during febrile episodes by the hospital phlebotomy team or the medical staff. The bacteremic episodes were recurrent, and 10 of 13 positive blood cultures contained multiple organisms. All the polymicrobial blood cultures were obtained when the patient had an intravenous catheter in place, but none of the catheters that were removed grew bacteria. Unusual nonfermenting bacteria account for only 0.2 percent of all blood-culture isolates in our hospital.

In the context of the patient's manipulation of thermometers and the recurrent malfunctioning of her intravenous catheters, the microbiologic findings suggested self-induced infection. It was strongly suspected that she rinsed her wounds with water from a toilet, which was considered to be the probable source of contamination. When confronted with this suspicion, the patient denied it. Over a three-year follow-up period, however, no further infections occurred.

Nonfermenting bacteria live in soil, water, and sea water. They are ubiquitous in the hospital, where their growth is supported by a humid atmosphere. (3) Isolation of these microorganisms from the blood generally points to an exogenous source of infection, such as a hemodialysis system. (4) These organisms are opportunistic and affect severely immunocompromised patients such as those with neutropenia. (5)

In this case, the isolation of unusual nonfermenting bacteria, in the absence of other likely explanations, suggested deliberate contamination. Self-induced infection should be suspected if a patient without an underlying malignant or immunosuppressive condition has recurrent polymicrobial infections with unusual gram-negative rods.

Nico E.L. Meessen, M.D., Ph.D.
Geert H.I.M. Walenkamp, M.D., Ph.D.z
Jan A. Jacobs, M.D., Ph.D.
University Hospital Maastricht
6202 AZ Maastricht, the Netherlands


 1. Reich P, Gottfried LA. Factitious disorders in a teaching hospital. Ann Intern Med 1983;99:240-7.

 2. Wallach J. Laboratory diagnosis of factitious disorders. Arch Intern Med 1994;154:1690-6.

 3. du Moulin G. Minimizing the potential for nosocomial pneumonia: architectural, engineering, and environmental considerations for the intensive care unit. Eur J Clin Microbiol Infect Dis 1989;8:69-74.

4. Reverdy ME, Freney J, Fleurette J, et al. Nosocomial colonization and infection by Achromobacter  xylosoxidans. J Clin Microbiol 1984;19:140-3.

5. Jacobs JA, Stobberingh EE, Schouten HC. Fatal infection due to Alcaligenes xylosoxidans subsp. xylosoxidans in a neutropenic host. Clin Microbiol Newslett 1992;14:182-4.


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