This is a common phenomenon associated with fluctuations in the effectiveness of treatment. There are two biological explanations; one is that there is, for example, a narrowing in or around a joint or nerve root in the spine, and when the medication is less effective, this leads to the muscles tensing (becoming shorter) and the narrowing becoming even more constricted, resulting in pain, for example. In this case, the constriction is the root cause, but it is the varying effect of Parkinson’s on muscle tension that gives rise to the varied symptoms. It may also be the muscle tension itself that causes the pain – this is common in the early symptoms of Parkinson’s disease, often before diagnosis, and may be mistaken for chronic tennis elbow, shoulder pain, etc. The pain may also vary in these cases, but is then not related to medication but to normal activity.
Another, probably less common cause of pain or aches – though it may manifest as various sensory symptoms – is that the dopamine deficiency can give rise to symptoms in the thalamus, which plays a key role in the interaction between muscle control and sensory functions (the thalamus integrates information about, for example, the position of an arm and coordinates movement by, for example, reading the arm’s position relative to the body so that the muscles can be controlled. The thalamus may therefore, due to a dopamine deficiency, misinterpret sensory signals so that they are perceived as pain during an ‘off’ phase.
It need not be actual damage to a joint or muscle that gives rise to varying symptoms, but stiff muscles during ‘off’ periods place greater strain on (tender) muscle attachments, and make narrow passages for nerve fibres even narrower, which gives rise to pain.
Håkan Widner