The Biology of Psychomotor Retardation

Image by Gerd Altmann from Pixabay

While psychomotor retardation (slowing of movement and thoughts) has long been recognized as a symptom of depression, I think it’s probably not on the average person’s radar when they think about depression. The biology of psychomotor retardation is also poorly understood.

What psychomotor retardation is

Psychomotor retardation (PMR) is most often associated with the melancholic subtype of depression. It encompasses a range of disturbances, including:

  • slowed movements
  • lack of facial expressiveness (“flat affect”)
  • decreased eye contact
  • speech changes: decreased volume, slow and monotonous speech with increased pauses, delayed verbal responses
  • slumped posture
  • reduced mobility in trunk and proximal limbs (upper legs and arms)
  • increased self-touching

This has always been a pretty significant element in my own depression, and is currently what’s most disabling. So why am I so slow?

Science doesn’t really know.

Possible biological mechanisms

Dopamine appears to be the major neurotransmitter involved, although norepinephrine and GABA may play a role as well. Serotonin may also play a role in the cognitive aspect. The dopamine factor is likely why taking a stimulant (dextroamphetamine) is helpful for my PMR.

Structural changes in the basal ganglia are thought to play a role. It’s an area of the brain that has a number of functions, including being involved in movement. Changes in dopamine receptors in the basal ganglia are thought to be the cause of tardive dyskinesia from antipsychotics. Parkinson’s disease affects this same region, and it’s been suggested that there could be some form of shared underlying pathology.

Other structural changes have also been suggested, including a correlation between white matter hyperintensities (a type of brain lesion) and PMR.

Decreased blood flow to several areas of the brain, including the prefrontal cortex, has been observed in people with psychomotor retardation. Decreased blood flow to the supplemental motor area has also been observed. Difficulty generating signals to the motor cortex region has also been suggested as a potential contributing factor.

There’s some indication that the hypothalamic-pituitary-adrenal (HPA) axis is involved. The HPA axis is how the brain and the adrenal glands communicate to regulate the release of the stress hormone cortisol.

One major type of brain circuit runs from the cortex (the outer, most advanced part of the brain) to the striatum (which is in the basal ganglia region and is involved in motor activity, and then swings by the thalamus before returning back to the cortex. Structural and functional imaging studies in people with PMR have shown abnormalities in these circuits. The thalamus is part of the limbic system, and abnormal signals originating in that part of the brain may tie together the aspects of cognition, emotion, and movement.

So what now?

Clearly, science hasn’t figured out much yet. And in terms of research priorities, I suspect it’s relatively low on the list.

My hope is that at some point, a researcher somewhere will get an AHA moment and figure out what’s really going on with the biology of psychomotor retardation. More than simple scientific curiosity, that matters because the current bunch of treatments available aren’t all that effective. Perhaps if it was better understood, a more targeted treatment could be identified to add on top of the usual depression treatment options.

Until then, I’ll be that person moving only slightly faster than a snail.


Originally published at on July 27, 2020.




Author of 4 books — latest is A Brief History of Stigma | Mental health blogger | Former MH nurse | Living with depression |

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Ashley L. Peterson

Ashley L. Peterson

Author of 4 books — latest is A Brief History of Stigma | Mental health blogger | Former MH nurse | Living with depression |

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