When the Brain’s “Go Signal” Runs Low: Could Dopamine Explain Why Mind and Body Slow Down Together?

Psychomotor retardation is the medical term for a noticeable slowing of movement, speech and, sometimes, thinking. It is often linked with severe depression and catatonia, but it can also appear in neurological conditions that seem very different, including Parkinson’s disease.

This paper asks whether these illnesses might share part of the same underlying brain problem. In particular, the authors focus on dopamine in the striatum, a group of brain areas involved in starting actions and deciding how much effort to put into them.

Their idea is that reduced dopamine signalling here might act like a weakened “go signal”: the person can still have the ability to move, but getting movement started and giving it enough speed and energy becomes harder.

This matters because medicine usually separates conditions such as Parkinson’s disease, depression and catatonia into different diagnostic boxes. The authors instead take a transdiagnostic approach. This means looking across diagnoses and asking whether the same biological process might help explain a symptom that they share.

Their main question is therefore: could less dopamine ‘signalling’ in the striatum, particularly its upper or “dorsal” part, help explain psychomotor slowing across several neurological and psychiatric disorders?

Importantly, this was not a new experiment involving a fresh group of participants. It was a narrative review, bringing together evidence from clinical observations, population studies, brain imaging, laboratory studies and treatment research. The authors compare a few different conditions (mainly Parkinson’s disease, drug-induced parkinsonism, neuroleptic malignant syndrome, catatonia, depression).

The paper is best understood as an expert argument built from different strands of research rather than a systematic attempt to find and combine every relevant study using numbers (statistics). Because of this, there is no single sample size or main statistical test for the paper itself. Instead, the authors report statistics from studies that they review.

People with Parkinson’s disease, depression and catatonia can all show a similar slowing of movement, speech and sometimes thinking. In Parkinson’s disease, this slowing is strongly linked to reduced dopamine activity in a brain area called the striatum, which helps us start and control movement. People may walk more slowly, take smaller steps, speak more quietly and have difficulty getting movements started.

Interestingly, some people with depression can look quite similar. Around one-quarter to one-half of people with depression may show visible psychomotor slowing, including slower movement, speech and walking. Catatonia can involve even more severe slowing, such as hardly moving or speaking at all. Parkinson’s disease and catatonia can also share features such as stiffness, reduced facial expression and periods where movement seems to “freeze”. However, catatonia usually develops much more quickly than Parkinson’s disease.

The authors also suggest that physical slowing may be connected with slower thinking and reduced motivation. For example, slowed movement in Parkinson’s disease is linked with slowed thinking, while slowing in both Parkinson’s disease and depression is associated with loss of pleasure or motivation. This does not mean these conditions are the same, but their shared features raise the possibility that changes in dopamine may be one part of the explanation.

There is also a useful clue from treatments. In broad terms, drugs that block dopamine can cause or worsen slowed movement, while treatments that increase dopamine can improve it in some conditions. Levodopa (which allows the body to make more dopamine) is a core treatment for Parkinson’s disease, while dopamine-blocking antipsychotics (which are sometimes given to people living with schizophrenia) can cause something called parkinsonism (which looks similar to Parkinson’s disease) and sometimes worsen catatonia.

There is some evidence that dopamine-enhancing treatments may also help slowness in depression and catatonia, but here the evidence is much less secure. The authors themselves describe the evidence in these psychiatric conditions as preliminary, with small samples and too few good clinical trials.

One of the most interesting ideas in the paper is that dopamine may not simply control whether a muscle can move (hinting at a structural problem). Instead, it may help the brain decide whether an action is “worth the energy”. Imagine the brain having an invisible dial that determines how much energy to put into an action. With healthy dopamine signalling, getting up, walking across a room or answering a question may feel worth the effort. When that system is disrupted, the energetic “price” of acting may feel higher. In Parkinson’s disease, people can sometimes physically move faster but naturally choose slower movements because faster movement effectively costs them more effort. Similar processes may contribute to the loss of drive, slow movement and slowed thinking seen in depression making it more of a functional problem.

There are real strengths to the paper. Rather than relying on one type of evidence, it asks whether clinical symptoms, population studies, brain scans, biology and treatment effects all point in roughly the same direction. When several very different methods tell a similar story, that is more persuasive. The transdiagnostic approach is also valuable because it may help researchers move beyond diagnostic labels and study groups of people who actually share the symptom of interest.

However, those strengths need to be weighed against weaknesses. Psychomotor retardation has not been measured consistently across studies. Some researchers use rating scales, others measure reaction times, and others use wearable activity monitors. It can also be difficult to tell whether someone is moving slowly because their motor system is slowed, because their thinking is slower, because attention or memory is impaired, or because their motivation has changed. The authors explicitly recognise these problems.

There is another important limitation: dopamine is probably only part of the story. Other chemical messengers in the brain (like GABA, serotonin, glutamate and acetylcholine) also interact with these brain systems. Catatonia, for example, responds strongly to benzodiazepines, which mainly affect GABA. The authors therefore warn against treating dopamine as a single master switch controlling all psychomotor behaviour.

A better picture may be a sound mixing desk rather than one volume control: dopamine may be an important slider, but several other sliders influence the final output.

The evidence is convincing that dopamine loss contributes strongly to slowed movement in Parkinson’s disease. There is also good evidence that changes in dopamine may play a part in slowing movement and thinking in depression, and possibly in catatonia too.

But the evidence does not yet prove that low dopamine in this part of the brain is the same cause of slowing across all these conditions. The authors say we still do not know exactly where in the brain the problem happens or how it works, especially in mental health conditions.

Because this was a narrative review rather than a systematic review, while many pieces of the puzzle seem to fit, some important pieces could still be missing.

One important idea is that diagnoses such as depression may include people with very different underlying brain changes. Some people with depression have clear psychomotor slowing, while others do not. The authors therefore suggest that future studies should group people according to their movement symptoms, rather than treating everyone with the same diagnosis as if they are biologically alike.

The authors also call for larger and better studies of treatments that increase dopamine, especially in people with depression who have clear psychomotor slowing. They also suggest using newer and shorter types of brain scanning, which may be easier for very unwell people to tolerate.

The authors declared competing interests, although nothing in the paper establishes that these affected the conclusions. These relationships are worth being aware of because the review discusses drug treatments, but they are openly declared and should not on their own be taken as evidence of bias.

Overall, this paper offers a strong hypothesis rather than a final answer. It suggests that the slowing seen in Parkinson’s disease, depression and catatonia may sometimes be different outward signs of disruption in a shared dopamine system. Future research now needs to test that idea directly, particularly by studying carefully selected people with clear psychomotor slowing, using better brain imaging and well-designed treatment trials.

The most powerful possibility raised by this paper is that when a person’s body and thoughts seem to slow down, the problem may not simply be a lack of will or motivation: somewhere deep in the brain, the signal that turns intention into action may itself have become quieter.