Motor and cognitive aspects of motor retardation in depression

Abstract

Background: Motor retardation is a common feature of major depressive disorder having potential prognostic and etiopathological significance. According to DSM-IV, depressed patients who meet criteria for psychomotor retardation, must exhibit motor slowing of sufficient severity to be observed by others. However, overt presentations of motor slowing cannot distinguish slowness due to cognitive factors from slowness due to neuromotor disturbances. Methods: We examined cognitive and neuromotor aspects of motor slowing in 36 depressed patients to test the hypothesis that a significant proportion of patients exhibit motor programming disturbances in addition to psychomotor impairment. A novel instrumental technique was used to assess motor programming in terms of the subject’s ability to program movement velocity as a function of movement distance. A traditional psychomotor battery was combined with an instrumental measure of reaction time to assess the cognitive aspects of motor retardation. Results: The depressed patients exhibited significant impairment on the velocity scaling measure and longer reaction times compared with nondepressed controls. Approximately 40% of the patients demonstrated abnormal psychomotor function as measured by the traditional battery; whereas over 60% exhibited some form of motor slowing as measured by the instruments. Approximately 40% of the patients exhibited parkinsonian-like motor programming deficits. A five-factor model consisting of motor measures predicted diagnosis among bipolar and unipolar depressed patients with 100% accuracy. Limitations: The ability of motor measures to discriminate bipolar from unipolar patients must be viewed with caution considering the relatively small sample size of bipolar patients. Conclusions: These findings suggest that a subgroup of depressed patients exhibit motor retardation that is behaviorally similar to parkinsonian bradykinesia and may stem from a similar disruption within the basal ganglia.

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.