Pain is one of the most common and distressing non-motor symptoms associated with Parkinson’s disease (PD). While the cardinal features of PD involve motor dysfunction, pain affects between 30% and 85% of patients and can even predate the onset of movement problems by years. This pain is significantly more prevalent and severe in the Parkinson’s population compared to the general population. The experience of pain in PD is complex and multifactorial, stemming from a combination of mechanical problems, central nervous system changes, and secondary effects of the disease.
Motor Symptom Pain
Pain often arises directly from the physical manifestations of the disease, leading to what is classified as musculoskeletal or nociceptive pain. The muscular stiffness, or rigidity, that characterizes PD causes chronic tension in the muscles and joints. This constant, involuntary resistance to movement can lead to a persistent, deep aching or tightness, particularly in the neck, back, and limbs.
Bradykinesia, or the slowness of movement, further compounds this issue by limiting the natural range of motion and protective limb movements. Reduced spontaneous activity, such as the diminished arm swing while walking, can contribute to shoulder and joint strain, sometimes presenting as a “frozen shoulder.” The combination of rigidity and reduced movement restricts the stretching and relaxing of muscles, resulting in chronic fatigue and localized discomfort.
A particularly painful manifestation is dystonia, which involves sustained or repetitive muscle contractions that cause twisting and abnormal postures. Dystonic pain frequently affects the feet, legs, and neck, sometimes causing toes to curl painfully or the foot to invert. This type of pain often occurs during “off” periods when dopaminergic medication levels are low, highlighting its direct link to the underlying neurochemical deficiency. Even tremor can lead to localized pain and muscle fatigue from the persistent muscular activity required to manage the movement.
Nerve and Sensory Dysfunction
Beyond the mechanical causes of pain, discomfort originates within the nervous system. The loss of dopamine-producing neurons alters the central processing of pain signals. This deficiency leads to dysfunction in the brain’s pain inhibition pathways, making the person hypersensitive to painful stimuli.
This change in central processing is the basis for Central Parkinsonian Pain, discomfort felt without clear physical injury. Patients may experience diffuse, burning, or aching sensations that are poorly localized. The brain’s altered perception of pain, or nociplastic pain, intensifies normal sensations into painful ones.
Another category is radicular or neuropathic pain, which involves damage or compression to peripheral nerves. This manifests as sharp, shooting, burning, or tingling pain along the path of a nerve, such as sciatica. This pain can be exacerbated by the disease’s motor features and postural changes. Akathisia, a distinct sensory phenomenon, is a source of intense discomfort, characterized by an inner restlessness and a painful inability to be still.
Secondary and Non-Motor Contributors
Pain in PD is often aggravated by secondary factors. A common contributor is the progressive change in posture, particularly the development of a stooped, forward-flexed posture known as camptocormia. This abnormal alignment places chronic, uneven strain on the muscles and ligaments of the back, neck, and hips, leading to persistent axial pain.
Gastrointestinal dysfunction, such as severe constipation and gastroparesis (slowed stomach emptying), is highly prevalent and can cause abdominal cramping, bloating, and visceral discomfort.
The psychological state of the patient also has a profound impact on the experience of pain. Depression and anxiety, which are common in PD, can lower the pain threshold and intensify discomfort. This reciprocal relationship means persistent pain can worsen mood, while mood disorders amplify pain signals. Chronic fatigue, another non-motor symptom, reduces the body’s overall tolerance for discomfort.
Categorizing Pain for Diagnosis
Understanding the causes of pain in Parkinson’s disease is fundamental because effective treatment depends on accurate diagnosis of the pain type. A clinician must determine whether the pain is mechanical (nociceptive), nerve-related (neuropathic), or a result of central processing issues (nociplastic) to select the correct therapeutic approach. Pain due to muscle stiffness may require adjustments to dopaminergic medication or physical therapy, while neuropathic pain requires specific nerve-blocking agents.
Clinicians often use a framework to categorize PD-related pain into five subtypes: musculoskeletal, dystonic, radicular/neuropathic, central, and akathisia. Patients play a crucial role by accurately describing the location, quality, and timing of their pain, particularly noting whether it fluctuates with their medication cycle or occurs during “on” versus “off” periods. This detailed reporting allows the medical team to pinpoint the underlying mechanism and tailor a specific, mechanism-based treatment plan.