Research reportMotor and cognitive aspects of motor retardation in depression
Introduction
Current diagnostic criteria for major depression include the presence of psychomotor retardation which, according to DSM-IV, “…must be severe enough to be observed by others” (American Psychiatric Association, 1994; p. 321). Most features of motor retardation are easily observed. These consist of reduced speed, slow speaking rate, delayed motor initiation, body immobility, loss of facial expression, and postural abnormalities (Parker et al., 1993). Parker et al. (1993) suggested a ‘trunk and branch’ analogy as a means of modeling motor disturbances in depression. In this model, a truncal psychic component arborises into retarded and agitated branches. While the model accounts for three potentially overlapping factors, it ignores the possibility that the ‘root’, which gives rise to the truncal component, may contain elements shared by other neuropsychiatric disorders, such as Parkinson’s disease (PD). Restricting the criteria for motor disturbances in depression to those that are observable, as suggested by DSM-IV, minimizes the likelihood that the neurobiology of depression can be fully understood.
It is noteworthy that the motor signs which characterize motor retardation are indistinguishable from characteristics of idiopathic PD. This has led some investigators to hypothesize the presence of a common neurobiological mechanism for motor retardation in depression and parkinsonism (Sachdev and Aniss, 1994), while others have found marked differences in the motor behavior of PD and depressed patients (Fleminger, 1992). The evidence for a mechanistic overlap between depression and parkinsonism is strong. Depression has been reported as a feature in PD (Rogers et al., 1987; Tom and Cummings, 1988; Tandberg et al., 1997) and psychosis (Prosser et al., 1987), and it is possible that some aspects of motor retardation may actually signal the presence of specific neuromotor pathology or a medication side effect (Casey, 1994). Overall, the overt signs associated with slowness, such as reduced movement velocities, increased reaction times, and increased movement times are similar in depression and parkinsonism.
In a previous study, (Caligiuri et al., 1998a), we described a novel approach for separating motor slowing into two components: a basic neuromotor component derived from movement velocity and a higher level cognitive or attentional component derived from a measure of reaction time. The purpose of this dichotomy is to distinguish patients whose slowness is driven by neuromotor factors, such as medication side effects, from those whose slowness is related to cognitive factors. Using wrist movement velocity, we measured the subject’s ability to program (or scale) movement velocity in anticipation of changing target distances. The idea that neuromotor slowing would manifest as impaired velocity scaling stems from extensive research on the mechanism of parkinsonian bradykinesia (Draper and Johns, 1964; Berardelli et al., 1986; Warabi et al., 1986; Benecke, 1989; Hufschmidt and Lucking, 1995). Our findings confirmed the presence of a motor programming disorder in all of the Parkinsonian patients studied and in nearly one-third of the psychosis patients. In a follow-up study of motor performance of the depressed and nondepressed psychosis patients (Caligiuri et al., 1998b), the nondepressed patients exhibited normal psychomotor performance, but scored in the abnormal range on measures of motor programming. Conversely, depressed patients exhibited abnormal psychomotor performance, but scored within normal limits on measures of motor programming, even after controlling for medication and age. These findings suggest that motor slowing may have a cognitive basis in the presence of depression and a neuromotor basis in the absence of depression.
In the present study, we used the velocity scaling measure together with a battery of traditional psychomotor measures to test the hypothesis that a significant proportion of depressed patients exhibit motor programming disturbances. Disturbances in the programming of movement velocity have been thought of as contributing to the bradykinesia seen in patients with Parkinson’s disease (Hallett and Khoshbin, 1980; Hallet, 1985). Impaired motor programming in depression would suggest that for these patients, their motor retardation may stem from disturbed dopamine neurotransmission within the basal ganglia. Alternatively, motor slowing in the absence of a velocity programming deficit would suggest a more cognitive origin of the slowness in depression.
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Patients
Thirty-six depressed outpatients (12 women and 24 men) and 22 nondepressed healthy controls (nine women and 13 men) were studied. The patients had a mean (S.D.) age of 45.1 (10.7) years and the controls had a mean age of 46.7 (16.6) years. Thirty-one of the patients met DSM-IV criteria for major depressive disorder; whereas five patients met DSM-IV criteria for bipolar II disorder. Patients were recruited from the VA San Diego Healthcare System Clinical Research Center within the Department of
Instrumental measures of motor slowing
Table 1 shows the descriptive statistics for patients and controls for the instrumental motor measures. Results of independent t-tests indicated significant differences between depressed patients and nondepressed healthy controls on all of the instrumental motor measures. Depressed patients exhibited significantly longer reaction times, lower velocities, and lower scores on the velocity scaling measure.
Additional analyses were performed on the individual data to estimate the prevalence of
Discussion
The results of the present study are consistent with the notion that motor retardation is an essential feature of major depressive disorder. As a group, the patients in the present study exhibited longer reaction times and lower peak velocities compared with healthy control subjects. Over 40% of the depressed exhibited mild impairment on traditional measures of psychomotor function. Similar results have been previously reported for reaction times (see Sobin and Sackeim, 1997, for review).
In
Conclusions
Patients may meet DSM-IV criteria for major depressive disorder without exhibiting overt signs of motor retardation. DSM-IV explicitly defined psychomotor retardation as an observable phenomena. The results from the present study suggest that over 30% of the unipolar depressed patients and 80% of the bipolar depressed patients exhibited a fundamental disturbance in motor programming and that this disturbance may remain hidden from the clinical presentation of motor retardation. The existence of
Acknowledgements
This research was supported in part from USPHS grants (P30-MH496771, T32-MH19934), the UCSD Mental Health Clinical Research Center (MH30914), and the Department of Veteran Affairs VISN-22 MIRECC. The authors wish to thank the following individuals for their assistance on this research: Dr Chris Gillin, Dr John McQuaid, Kathy Resovsky, Lorraine Goyette, and Grace Shiao.
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