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CASE REPORTS

Adolescents on Neuroleptic Medication: Is This Population at Risk for Tardive Dyskinesia?

Stephanie A McDermid, HonBSc¹, Jane Hood, PhD², Sandra Bockus, RN³, Enzo D'Alessandro, MD, FRCPC⁴

Objective: To assess the incidence of tardive dyskinesia (TD) in a sample of adolescents treated with neuroleptic medication and to identify the presence of any risk factors for TD within the affected group.

Method: A retrospective chart review was conducted for 40 cases. The Abnormal Involuntary Movement Scale (AIMS) was used to measure side effects from medication at 6-month intervals over 2 years. Drug exposure was converted to chlorpromazine (CPZ) equivalents and the presence of risk factors for TD, such as a diagnosis of affective disorder, medication noncompliance, early age of illness onset, and concomitant antiparkinsonian medication, was also noted.

Results: Of the 40 cases reviewed, 2 patients (5%) met diagnostic criteria for TD, and another 5 patients (12.5%) showed symptoms of TD.

Conclusions: TD is a serious risk at any age. Medication noncompliance, early age of illness onset, and concomitant use of antiparkinsonian medication may increase susceptibility to TD and should be carefully monitored.

(Can J Psychiatry 1998;43:629­631)

Key Words: tardive dyskinesia, neuroleptic medication, Abnormal Involuntary Movement Scale (AIMS)

Tardive dyskinesia (TD), a disorder of abnormal involuntary movements, is a rare but serious side effect of prolonged exposure to typical neuroleptic medication. Risk factors associated with TD include a diagnosis of affective disorder (1), an early age of onset of psychosis (1), medication noncompliance (2), and concomitant antiparkinsonian medication (3). The incidence of TD in adult samples is reported to be 5% after 1 year of neuroleptic treatment and increasing by 5% for each year of exposure (4). Relatively few studies have investigated the development of TD in children and adolescents. A prospective, longitudinal study of neuroleptic-related dyskinesias in children with autism estimated a 50% incidence of TD and withdrawal dyskinesias (WD) after 873 days (5). Additionally, Dorevitch and others reported a prevalence rate of 17.6% in their adolescent inpatient psychiatric ward (6). Given the increasing tendency to treat children and adolescents with neuroleptic medication as well as the paucity of research available for this group, it seems important to determine the incidence of TD in this younger population.

Method

The Psychosis Clinic at the Hospital for Sick Children in Toronto treats adolescents referred by pediatricians and psychiatrists within the metropolitan area, as well as patients referred from the hospital's inpatient units. Patient charts were reviewed to identify all patients who were treated with neuroleptic medication. Patients were included if their medication history was documented for a period of at least 2 years and the Abnormal Involuntary Movement Scale (AIMS) (7) was administered every 6 months during that 2-year period. A retrospective chart review assessed the patient's age of onset of illness, medication noncompliance (identified when physicians documented that a patient was "not complying with their medication" or had "taken themselves off of the medication"), and the concomitant use of antiparkinsonian medication. Neuroleptic medications were converted to chlorpromazine (CPZ) equivalents, and the patient's average daily dose was calculated for the 2-year period. A research diagnosis of TD was determined using the criteria outlined by Schooler and Kane (8), which are as follows: 1) at least 3 months of cumulative neuroleptic exposure; 2) at least moderate abnormal involuntary movements in 1 or more body areas or mild movements in 2 or more body areas; and 3) the absence of other conditions that produce involuntary hyperkinetic dyskinesias. Symptoms of TD were considered to be present if "mild" involuntary movements were noted in 1 body area over the 2-year period.

Results

Among the 40 patients who met the inclusion criteria, indications for neuroleptic treatment included bipolar disorder (35%, n = 14), schizophrenia (20%, n = 8), schizophreniform disorder (17.5%, n = 7), depression with psychotic symptoms (15%, n = 6), and schizoaffective disorder (12.5%, n = 5). All patients were receiving typical neuroleptics. The mean age for the 22 females and 18 males in the sample was 14.8 years (sd = 1.49). Two patients (5%), 1 male and 1 female, met the diagnostic criteria for TD, and 5 patients (12.5%), 3 males and 2 females, showed symptoms of TD. These 7 patients comprised the "TD group" (17.5%) and were compared with the remaining 33 patients comprising the "non-TD group." There was a significant difference in mean daily drug exposure between the 2 groups (t[36 ] = 2.37, P = 0.02). The average daily dose in the TD group was 268.6 mg CPZ (SD = 96.0), while in the non-TD group it was 150.4 mg CPZ (SD = 123.4). Figure 1 shows the presence of risk factors in the affected and nonaffected groups. Patients in the TD group were significantly more likely to have a history of medication noncompliance (P < 0.01), an early age of onset of psychotic symptoms (P < 0.01), and/or concomitant use of antiparkinsonian drugs (P < 0.05).

Discussion

The incidence of TD in this sample of adolescents after 2 years of neuroleptic exposure was 17.5%. Of particular interest is the similarity to the rate of complications determined by Dorevitch and others (6). Future studies will require more systematic methodologies to accurately ascertain the incidence of TD in this population.

There was a number of significant differences between the affected and nonaffected groups. Patients in the TD group had, on average, greater daily neuroleptic exposure than those in the non-TD group, suggesting that higher doses may contribute to the development of the disorder (1). Further, several risk factors for TD were more prevalent in the TD group, particularly an earlier age of illness onset, medication noncompliance, and concomitant antiparkinsonian medication. Clearly, these factors must be considered when prescribing neuroleptics to a younger population.

This study was subject to the limitations inherent in conducting retrospective chart reviews. For example, several patients had been treated at other institutions prior to their assessment at the hospital, thereby precluding the administration of a baseline AIMS. Moreover, a measure of lifetime neuroleptic exposure was not available for these patients, restricting the present study to a 2-year medication history. A better design would include a measure of cumulative neuroleptic exposure, calculated as a function of the patient's weight. Further, studies should consider the possible relationships between the severity of illness and neuroleptic dose as well as the possible correlation of an earlier age of onset with severity of illness. These methodological issues are currently being addressed in a prospective, longitudinal study.

Conclusions

Despite the limitations inherent in retrospective chart reviews, the present findings clearly suggest that the risk for TD is serious at any age. The initiation of neuroleptic treatment must be carefully considered, and extensive follow-up once medication is prescribed is essential.

References

1. Casey DE. Neuroleptic drug-induced extrapyramidal syndromes and tardive dyskinesia. Schizophr Res 1991;4:109­20.

2. Jeste DV, Caligiuri MP. Tardive dyskinesia. Schizophr Bull 1993;19:303­15.

3. Muscettola G, Pampallona S, Barbato G, Casiello M, Bollini P. Persistent tardive dyskinesia: demographic and pharmacological risk factors. Acta Psychiatr Scand 1993;87:29­36.

4. Latimer PR. Tardive dyskinesia: a review. Can J Psychiatry 1995;40(2 Suppl):49S­54S.

5. Campbell M, Armenteros JL, Malone RP, Adams PB, Eisenberg ZW, Overall JE. Neuroleptic-related dyskinesias in autistic children: a prospective, longitudinal study. J Am Acad Child Adolesc Psychiatry 1997;36:835­43.

6. Dorevitch A, Meretyk I, Umansky Y, Galili-Weisstub E. Antipsychotic drugs and tardive dyskinesia: preliminary results in an adolescent psychiatric ward. J Clin Pharm Ther 1995;20:63­5.

7. Guy W. ECDEU assessment manual for psychopharmacology. Revised. Washington (DC): US Department of Health, Education and Welfare; 1976.

8. Schooler NR, Kane JM. Research diagnoses for tardive dyskinesia. Arch Gen Psychiatry 1982;39:486­7.

Résumé

Objectif : Évaluer l'incidence de la dyskinésie tardive (DT) chez un échantillon d'adolescents traités par neuroleptiques et reconnaître la présence de tout facteur de risque de la DT dans le groupe atteint.

Méthode : Une étude de courbes rétrospective a été menée pour 40 cas. L'échelle des mouvements involontaires anormaux (EMIA) a servi à mesurer les effets secondaires des médicaments par intervalles de 6 mois, sur 2 ans. L'exposition aux médicaments a été convertie en équivalents de chlorpromazine (CPZ) et la présence de facteurs de risque de la DT, comme un diagnostic de trouble affectif, la non-observance de la médication, l'âge précoce d'apparition de la maladie et la médication antiparkinsonienne concomitante ont également été observés.

Résultats : Des 40 cas à l'étude, 2 patients (5 %) répondaient aux critères diagnostiques de la DT, et 5 autres (12,5 %) présentaient des symptômes de la DT.

Conclusions : La DT est un risque sérieux à tout âge. La non-observance de la médication, l'âge précoce d'apparition de la maladie et la médication antiparkinsonienne concomitante peuvent accroître la susceptibilité à la DT et doivent être soigneusement surveillés.

A version of this article was presented at the World Psychiatric Association regional meeting, Rome, Italy, June 13, 1997.

¹Research Assistant (at time of research), Department of Psychiatry, The Hospital for Sick Children, Toronto, Ontario.

²Postdoctoral Fellow (at time of research), Department of Psychiatry, The Hospital for Sick Children, Toronto, Ontario.

³Nurse Clinician, Psychosis Clinic, The Hospital for Sick Children, Toronto, Ontario.

⁴Director, Psychosis Clinic, The Hospital for Sick Children, Toronto, Ontario.

Address for correspondence: SA McDermid, Department of Psychology, University of Toronto, 100 St George Street, Toronto, ON M5S 3G3

email: stephani@psych.utoronto.ca

Can J Psychiatry, Vol 43, August 1998