In this series, I dig a little deeper into the meaning of psychological terms. This week’s term is psychomotor retardation (PMR).
Psychomotor retardation, one of the less common but more outwardly observable symptoms of depression, involves a slowing of movement and thoughts. It’s been described as far back as Ancient Greek times.
PMR is one of the DSM-5’s symptom criteria for a major depressive episode, and it’s one of the cluster of symptoms in the melancholic features specifier. One study found that a higher number of previous depressive episodes was associated with more severe psychomotor symptoms, and the researchers suggested that PMR may be like a scar of past depressive episodes.
What does psychomotor retardation look like?
PMR can affect multiple aspects of movement, including:
- slowed movements that are noticeable by others
- walking is slow, with abnormal gait
- lack of facial expressiveness of emotion (“flat affect”)
- decreased eye contact, fixed gaze
- speech changes: decreased volume, slow and monotonous speech with increased pauses, delayed verbal responses and spontaneous speech
- slumped posture
- reduced movement in the trunk and proximal limbs, i.e. upper legs and arms
Non-clinicians may notice PMR in others, but not understand what they’re seeing. My experience has been that general practitioners don’t tend to be familiar with what PMR (or at least severe PMR) looks like, and I have to tell them what they’re seeing.
In this video, I’m not moving far enough to get much of a sense of how ridiculously slow my walking is, but my speech impairment is quite obvious, as is the flat affect. When I’m well, I smile frequently and have done a fair bit of public speaking.
Effects on speech
Speaking involves both cognitive planning tasks and complex motor tasks. PMR can get in the way of both. PMR affects speech in a number of ways, and there are similarities to speech changes in Parkinson’s disease.
Tone, Inflection, articulation, and volume are decreased, so speech is quiet, monotone, and less fluent. There are also more and longer pauses. Responses are delayed and of decreased length. Changes in glottalization, an effect sometimes described as creaky voice, may be a result of changes in laryngeal muscle tension in the throat.
Speech impairment and depression severity
Not everyone with severe depression experiences psychomotor retardation, but changes in speech can be indicative of depression severity. In one study, objectively measured changes in speech, specifically speech rate, pause time, and response time, were partially correlated to severity scores on the HAM-D, a commonly used test for measuring depression severity.
Another study found that several acoustic features were associated with greater depression severity, including features indicative of decreased precision in motor control, as well as decreased variability in certain speech parameters.
While the two main rating scales used to assess PMR rely on a clinician’s subjective evaluation of a patient’s speech, there is technology that can objectively evaluate this. However, the challenge lies in figuring out what’s best to measure and being able to separate out the various other factors that can affect speech.
I’ve done a Youtube video here focusing on speech impairment due to psychomotor retardation.
It isn’t known exactly how PMR happens biologically, but a number of possibilities have been identified. Dopamine appears to be the major neurotransmitter involved, particularly in relation to the basal ganglia region of the brain, although norepinephrine and GABA may play a role as well. Serotonin may also play a role in the cognitive aspect.
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. This is known as the cortico-striatal-thalamo-cortical (CSTC) loop.
Structural and functional imaging studies in people with PMR have shown abnormalities in these CSTC 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.
Structural changes in the basal ganglia are thought to play a role. The basal ganglia region of the brain has a number of functions, including involvement in motor activity. 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 with depression.
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, which influences inflammation in the brain and body.
A study by Goldsmith and colleagues observed a relationship between psychomotor speed in depressed patients and levels of the inflammatory markers interleukin 6 (IL-6) and monocyte chemotactic protein (MCP-1). Research has also identified various other inflammatory molecules that may play a role.
What does psychomotor retardation feel like?
Psychomotor retardation feels a lot like moving through molasses, both mentally and physically. It’s not a matter of lack of energy; if anything, I find that moving so slowly produces fatigue rather than the other way around, since moving feels like I need to push through physical resistance.
In terms of speech, I notice an impact on the cognitive elements of putting together words and word-finding, but what feels subjectively most difficult is what I would describe as finding and implementing the motor scripts for words. It’s easier for me to say a multi-syllable word than having to say multiple short words of the same overall syllable length, as it feels like I need to retrieve each word one at a time.
Making eye contact requires more mental energy than I have available. If I’m concentrating on getting words out, I find myself looking up at the ceiling, which you can see me doing in the video. The video also shows that I blink rapidly as I’m fishing for words. I actually hadn’t realized that prior to watching the video, but as far as I can tell, it seems to be as I’m looking for the motor scripts for words rather than looking for the words themselves.
My pattern over time
Slowed psychomotor activity has appeared off and on throughout the course of my illness. It was particularly bad during my second hospitalization, which lasted two months. As time has passed, though, there’s been a pattern of abrupt onset (or worsening) of PMR in response to major environmental stressors, which seems like it may relate to the HPA-axis/cortisol stress response. It generally starts when I wake up the day following the stressor, and tends to last a few weeks. In the past, the PMR would resolve between stress-induced spikes, but that’s no longer the case.
I’ve always been aware of PMR when it’s happening, although that awareness doesn’t help me do anything about it. It feels like my body just can’t go any faster. When it’s mild, it’s mostly walking that’s affected, but when it’s bad, it has a significant impact on my speech.
Psychomotor retardation can be difficult to treat, and it doesn’t always respond as well to antidepressant therapy as other symptoms do. Research has shown mixed results as to whether some antidepressants are likely to work better than others.
Electroconvulsive therapy (ECT) can be helpful. You can read about my experiences getting ECT here.
The addition of a stimulant medication is also an option. I’ve found that dextroamphetamine (Dexedrine) has helped. I don’t notice any changes immediately after taking a dose, but I notice a difference after being on it (or off it) for several days.
Infliximab, also known as Remicade, is a monoclonal antibody that targets an element of the body’s inflammatory system called TNF-alpha. There is some research to indicate that it can reduce depressive symptoms, including PMR.
Is psychomotor retardation a symptom you’ve experienced with your illness? Have you noticed any patterns with it?
You can find the rest of the what is… series in the Psychology Corner.
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