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Learning About Why Depression Makes Me So Slow

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While psychomotor retardation (a slowing of movement and thoughts) has long been recognized as a symptom of depression, it’s not on most people’s radar when they think of depression. It’s a symptom I’ve experienced throughout much of the course of my depressive illness, and it’s a significant factor in the level of disability from my illness. However, it’s also quite difficult to effectively convey to people what it’s like unless they’re actually able to see me when I’m slow.

What is psychomotor retardation

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

  • slowed movements that are objectively observable by others
  • 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

It feels like trying to walk through molasses. It’s different from feeling fatigued; my body simply won’t move any faster. The changes in movement are objectively visible to anyone who happens to be looking my way. Most people wouldn’t know why I’m so slow, but they would immediately recognize that I’m somehow impaired.

There’s a slowing of thought, too, although I find it hard to quantify because there’s no objective reference point. The slowness of thought and movement can combine to have significant impacts on my speech. It becomes very halting, as I can only get out a couple of words before I need to pause to let brain and mouth catch up.

So why am I so slow? It turns out that science doesn’t really know.

Possible biological mechanisms

Dopamine appears to be the major neurotransmitter involved, although various others may play a role as well. The dopamine factor is likely why taking a stimulant (dextroamphetamine) is helpful for my PMR. I most certainly don’t look like someone who’s taking a stimulant, but without it, I’m even slower.

Structural changes in parts of the brain appear to play a role. The basal ganglia is an area involved in movement, and it’s involved in Parkinson’s disease and likely in tardive dyskinesia that can occur as a side effect from antipsychotics.

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Decreased blood flow to several areas of the brain, including areas involved in movement, have been observed in people with psychomotor retardation. Another possibility is disruptions in the hypothalamic-pituitary-adrenal (HPA) axis, which regulates the release of the stress hormone cortisol. Yet another possible factor is changes in the brain circuits running from the cortex, in the outermost part of the brain, to the striatum, which is in the basal ganglia region, and back to the cortex.

That’s a lot of possibilities with a big lack of certainty.

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, it 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.

Is this a symptom you’ve dealt with as part of your own illness?

Originally published: August 31, 2020
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