M P Caligiuri1, J Ellwanger. 1. Department of Psychiatry (0603), Movement Disorders Laboratory, University of California at San Diego, La Jolla, CA 92093, USA. mcaligiuri@ucsd.edu
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.
BACKGROUND:Motor retardation is a common feature of major depressive disorder having potential prognostic and etiopathological significance. According to DSM-IV, depressedpatients 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 depressedpatients 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 depressedpatients 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 depressedpatients 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 bipolarpatients. CONCLUSIONS: These findings suggest that a subgroup of depressedpatients exhibit motor retardation that is behaviorally similar to parkinsonian bradykinesia and may stem from a similar disruption within the basal ganglia.
Authors: Andrew M Farrar; Mariana Pereira; Francisco Velasco; Jörg Hockemeyer; Christa E Müller; John D Salamone Journal: Psychopharmacology (Berl) Date: 2006-10-27 Impact factor: 4.530