Motor activity, posture and facial expression have revealed mood in human beings, since earliest civilizations. The psychiatrist Karl Kleist (1879-1960) pointed that, psychomotor activity also implies subjective experiences. He assigned these experiences to the frontal lobe and the psychomotor performance to basal nuclei.1

Sigmund Freud (1856-1939) attempted to associate the neurochemical issues with instinctual drives, in order to show the way to the individual human unconscious/conscious mind. Instinctual patterns demand from the nervous system much more than external stimuli. They force it to complex activities, without these emotional and perceptual feelings, all what is related to the mental representation aspects, fails. Excitement flows, the affective tone does not take place and the limited psychic inscription cannot stop quantitative transmission of drive.2

Breakthrough of neuroscience allowed proving that prefrontal cortex (anterior and inferior frontal lobe, area 8) is involved for the planning, initiation and sequence of voluntary movements. This requires on the drive and the initiative to execute that, which is thought or planned. Motivation is mediated through the cortex frontal-orbital pathway (limbic areas extension), which can blockade prefrontal or liberate frontal areas, and generate disorders in frontal-basal pathways (promoting passive or aggressive behaviors). Movement depends on the continuous inflow of information from afferent sensory connections to prefrontal areas. If this information becomes unnecessary, it extinguishes by inhibition of frontal-orbital impulses.3
Psychomotor retardation, or generalized slowing down of body movements (motility, attitude and impairments of speech), is perceived by the patient. Inhibition, lost of interest and lack of pleasure (anhedonia) takes to diagnosis of major depressive illness (DSM-IV).

Up today, there is no biological correlate with psychomotor retardation in depressive patients because it depends on the disturbance of several neurotransmitters types, especially the noradrenergic and dopaminergic system. Plasma arginine-vasopressin concentrations were low in depressive patients with daytime psychomotor retardation, and showed elevated in those who experienced increased motor activity during sleep.4 As well, growth hormone pulses were lower in female patients with major depressive illness, associated with higher scores on the retardation item of the Hamilton depression rating scale.5

Studies with fluoxetine treatments shows that it is more efficient in inhibited depressive illness in patients with low scores for psychomotor retardation, then, it is possible, the serotonin system play a secondary role.6
Psychomotor retardation may be the most consisttently predictive of good response to tricyclic antidepressants and indicate the start of good social functioning.7

The new antidepressant agents look at a rapid disinhibition of patient’s motor retardation behaviors. It was necessary to develop scales that reveal this phenomenon. The psychomotor retardation improves slowly with antidepressive treatment. Although, the professional’s clinical impression accounts, on the physical manifestation and gestures of the depressive patient, it is not useful as medical evidence in short / mid term clinical trials.

Parametric assessment to evidence the patient’s subjective impressions emerging at the interview, is a way to document on objective impressions, in order to confirm the improvement or worsening of pharmacological treatment.
The Wildöcher scale and the Depressive Retardation Rating Scale have shown their versatility to document and correlate the psychomotor retardation with the absence of pleasure of these patients. Due the common alteration of the neurotransmission mechanisms, it would be important to correlate these types of scales with negative symptoms of schizoaffective and/or schizophrenic patients 8,9,10


REFERENCES

1. Kleist K.: Los trastornos psicomotores, catatónicos y miostáticos del tallo cerebral (séptima comunicación, 1933), en Kleist, K. Introducción a las localizaciones cerebrales en neuropsiquiatría, Editorial Polemos, Buenos Aires, 1997
2. Freud S.: Pulsiones y destinos de pulsión, Editorial Amorrortu (tomo XIV), Buenos Aires, 1993
3. Nidermeyer E.: Frontal lobe functions and dysfunctions. Clin Electroencephalogr 1998; 29 (2): 79-90.
4. Van Loden L.; Kerkhof G.A.; Van den Berg F. et al : Plasma arginine vasopressin and motor activity in major depression. Biol. Psychiatry 1998; 42(3): 196-204
5. Fiasche R..; Fideleff F.; Moizeszowicz J. et al.: Growth hormone neurosecretory dysfunction in major depressive illness. Psychoneuroendocrinology 1995; 20 (7): 727-733
6. Dantchev N.; Wildöcher D.J.: The measurement of retardation in depression. J Clinical Psychiatry 1998; 59 (suppl 14): 19-25.
7. Lamelin S.; Baruch P.: Clinical psychomotor retardation and attention in depression, J Psychiatric Res. 1998; 32(2) 812-88
8. Sobin C.; Sackheim, H. A.: Psychomotor symptoms of depression. American J Psychiatry 1997;154: 4-17.
9. Lemke M.R.; Puhl P.; Koethe N.; Winkler T.: Psychomotor retardation and anhedonia in depression, Acta Psych Scandinavica 1999; 84 (4): 252-256
10. Moizeszowicz J.: Psicofarmacología Psicodinámica IV. Estrategias terapéuticas y psiconeurobiológicas", Editorial Paidós, Buenos Aires, 1998.