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Clinical Course and Cellular Pathology of Tardive Dyskinesia

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Clinical Course and Cellular Pathology of Tardive Dyskinesia 126 CLINICAL COURSE AND CELLULAR PATHOLOGY OF TARDIVE DYSKINESIA CAROL A. TAMMINGA MARGARET G. WOERNER Tardive dyskinesia (TD) is an iatrogenic human hyperkinetic GABAergic) in gray matter regions in the segregated, paral- movement disorder associated with chronic antipsychotic lel frontal-subcortical modulatory motor circuits (35). drug treatment. The cause of the syndrome, namely, chronic dopamine-receptor blockade, is specifically known and is straightforward to model. Thus, disease pathophysiol- ogy has been approached with surrogate preparations. Tra- CLINICAL FEATURES AND COURSE OF ditionally, factors mediating TD have been sought in striatal TARDIVE DYSKINESIA dopaminergic transmission. However, several incompatibil- ities have developed between the characteristics of the dopa- The presentation of TD is typical of a dyskinesia, with oro- minergic model and the presentation of the disorder (10). facial, axial, and extremity hyperkinetic movements. The ␥-aminobutyric acid (GABA)–ergic transmission within the movements worsen with stress and concomitant physical basal ganglia has also been targeted as the putative patho- activity and diminish or disappear during sleep. TD onset is physiologic agent in TD. Here, although biochemical char- defining, in that all dyskinesias with their first onset within 6 acteristics between the model and the disease have appeared months of ongoing antipsychotic treatment are diagnosed compatible, therapeutic implications have not been fully as TD (50). Consequently, it is expected that the diagnosis met, possibly because of inadequate pharmacologic tools will be confounded by other categories of dyskinesia, includ- (10). ing dyskinesias of schizophrenia and of the elderly. TD is Research has suggested that both these transmitter altera- distinguished from parkinsonism, the other major category tions, dopaminergic and GABAergic, may reflect an action of antipsychotic-induced movements, by being hyperki- of antipsychotic drugs on neuronal activity within the basal netic, with delayed onset and delayed resolution after medi- ganglia thalamocortical motor circuit. Clinically, antipsy- cation discontinuation, and by its contrasting pharma- chotic drug action overall tends to normalize mental status cology. in psychosis and produces symptom remission in diverse Movements in TD are typically suppressed by antipsy- psychotic illnesses, including schizophrenia, bipolar disease, chotic drugs, and they are suppressed or even show remis- and dementia (8); parkinsonism characteristically occurs sion with potent GABA agonists; dopamine agonists exacer- with traditional antipsychotics as a major side effect (42). bate the movements, as can anticholinergic drugs (11). On a cellular basis, gradual alterations produced by these Although TD has a characteristic pharmacology, none of drugs over time, within selected subcortical brain regions the drugs that suppress movements in probe studies are and at selected synapses of this circuit, likely result in TD. potent enough to be used as a treatment (36). Treatment The mechanism of all these clinical actions is thought to approaches for TD are discussed later. begin with dopamine-receptor blockade, but thereafter it is Although TD risk is inevitable with the traditional anti- critically mediated by altered neuronal activity (including psychotics, the risk appears to have dropped significantly with the second-generation antipsychotic drugs, including clozapine, olanzapine, and risperidone, with which reduced risk has been demonstrated (38,63,66), and with quetia- Carol A. Tamminga: Maryland Psychiatric Research Center, University pine, with which reduced risk is probable. Therefore, even of Maryland School of Medicine, Baltimore, Maryland. Margaret G. Woerner: Department of Psychiatry Research, Hillside Hos- though TD may be diminishing as a significant clinical risk pital, Long Island Jewish Health System, Glen Oaks, New York. with modern antipsychotic treatment, its study has enabled 1832 Neuropsychopharmacology: The Fifth Generation of Progress TABLE 126.1. CUMULATIVE INCIDENCE OF TARDIVE DYSKINESIA Tardive Dyskinesia Persistent Tardive Neuroleptic Cumulative Incidence, Dyskinesia, (85% CI) Tardive Dyskinesia Exposure (y) (95% CI) Cumulative Incidence Hazard Ratea 1 .05 (.04–.07) .03 (.02–.04) — 5 .27 (.23–.31) .20 (.17–.23) 6.1% 10 .43 (.38–.47) .34 (.30–.39) 4.7% 15 .52 (.46–.57) .42 (.36–.47) 3.3% 20 .56 (.50–.63) .49 (.41–.57) 2.1% aHazard Rate is the rate of tardive dyskinesia occurrence per year among those remaining at risk. The number represents the average yearly hazard rate over the 5-year block of time. identification of cellular and circuit determinants of dyski- additional antipsychotic exposure. Regardless of the dura- nesias in mammalian brain. tion of the initial TD episode, if it remitted, there was a high The clinical course of TD varies by psychiatric diagnosis, likelihood (61%) of developing a second episode within 1 age, sex, and concomitant medical or neurologic illness. year. Data from a prospective study of 971 young adult psychiat- Preliminary data suggest that prognosis for TD remission ric patients followed for up to 20years indicated a increasing is better for patients who are treated for shorter times within cumulative incidence rate of TD over the 20-year interval the follow-up period after TD diagnosis and for those (Table 126.1). The cumulative incidence of persistent TD treated with lower doses of antipsychotic during follow-up was lower but increased proportionally (40). These data are (41). These facts about TD encourage future study in ani- consistent with a declining rate of TD over time, illustrated mals and humans on TD mechanisms and treatment and by the declining hazard rate (Table 126.1). A similar pattern facilitate the research by providing a firm baseline and a develops in the hazard rates over 20years for persistent TD. clear description of course. A decline in hazard rate over time was also reported by Morganstern and Glazer (46), although their data show a sharper decline after the first 5 years. FUNCTIONAL HUMAN NEUROANATOMY OF Rates of TD are significantly affected by the age and ANTIPSYCHOTIC DRUG ACTION other characteristics of the several samples studied. An in- creased vulnerability to TD associated with increasing age The human central nervous system (CNS) has been the is the most consistently reported finding in TD research. focus of studies to determine the mechanism of antipsy- A prospective study of 261 geriatric patients with a mean chotic drug action with both acute and chronic antipsy- age of 77 years revealed cumulative rates of 25%, 34%, and chotic drug administration. These antipsychotic data are 53% after, 1, 2, and 3 years of antipsychotic drug treatment relevant to TD mechanisms insofar as the localization of (74). Similar findings were reported by Jeste et al. (37) and the neural pathways subserving antipsychotic drug action by Yassa et al. (75). In the younger adult sample (40), the can suggest the regions that likely contain the neurochemi- hazard rate for TD was lowest for patients in their twenties cal disorder underlying TD. The firm association between and thirties at study entry, increased for those in their for- striatal dopamine-receptor blockade and antipsychotic drug ties, and sharply increased for those aged 50to 60years. action was established early and has been consistently con- Other variables associated with a significantly increased firmed in subsequent study (4,7,53). It has been suggested TD risk in the prospective study (Table 126.1) included the that antipsychotic drugs deliver their full antipsychotic ac- presence of extrapyramidal symptoms during antipsychotic tion by blocking the D2 dopamine receptors in limbic cor- treatment, diagnosis of unipolar depression, the number of tex (25,54). Alternatively, as argued here, antidopaminergic peaks in dosage of antipsychotic drug (more than 1,000 mg drugs could deliver their antipsychotic action by altering in chlorpromazine equivalents), and intermittent antipsy- activity in neuronal populations within the long-loop feed- chotic treatment. Treatment with lithium is associated with back neurons in the basal ganglia thalamocortical pathways, a lower risk of TD development. at least in part, thereby modulating neocortical activity indi- In this prospective study of 971 psychiatric patients rectly. The mechanisms responsible for TD may well occur (Table 126.1), the initial episode of TD was persistent for at sites within these modulatory pathways. at least 3 months for half of the cases. Of these persistent Early investigators observed an elevation of neuronal ac- cases, 68% remitted within the next 2 years. For the half tivity in the human caudate and putamen with antipsy- whose initial episode was transient, there was a high risk chotic drug treatment using functional in vivo imaging (33, (32%) of developing a persistent episode within 1 year of 69). To refine the localization of the signal, our laboratory Chapter 126: Tardive Dyskinesia 1833 FIGURE 126.1. The regions of color indicate quantitativelythe areas of regional cerebral blood flow (rCBF) activation (ON-30 day OFF) or inhibition (30 dayOFF-ON) with subchronic haloperidol treat- ment (0.3 mg/kg/day). In the top and 00 mm 04מ two figures, at from the anterior commisure/poste- rior commissure line (ACPC) plane, the basal ganglia show significant rCBF activation with haloperidol. In and 04מ the bottom two figures, at mm from the ACPC plane, both 04ם the anterior cingulate
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