title: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Psychiatry (0603), Movement Disorders Laboratory, University of California at San Diego, La Jolla, CA 92093, USA. mcaligiuri@ucsd.edu
authors.forename: M P
authors.initials: MP
authors.lastname: Caligiuri
authors.forename: J
authors.initials: J
authors.lastname: Ellwanger
mesh_terms: D000928:Antidepressive Agents / Q000627:therapeutic use; D014150:Antipsychotic Agents / Q000627:therapeutic use; D001479:Basal Ganglia / Q000503:physiopathology; D001714:Bipolar Disorder / Q000523:psychology / Q000628:therapy; D003072:Cognition Disorders / Q000175:diagnosis / Q000209:etiology*; D015928:Cognitive Behavioral Therapy / Q000379:methods; D003865:Major Depressive Disorder / Q000503:physiopathology* / Q000628:therapy; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011569:Psychiatric Status Rating Scales; D011596:Psychomotor Disorders / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D011930:Reaction Time; D012720:Severity of Illness Index
chemical_list: D000928:Antidepressive Agents; D014150:Antipsychotic Agents