Parkinson's Disease and Chronic Pain

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Chronic pain is very common in Parkinson's disease, affecting more than two thirds of all patients, and it tends to worsen as the disease progresses. The spine is the most frequent area of pain. Patient's usually don't realise that pain is part of the disease process. There is a lack of data around how to effectively manage pain in those affected.

Classification

Pain in Parkinson's disease may be multifactorial.The classification system by Ford is the most commonly used. It classifies pain into musculoskeletal, radicular/neuropathic, dystonia-related, akathic discomfort/pain, and central pain. Musculoskeletal type pain is considered to be the most frequent type of pain. In the presence of radiographic osteoarthritis, pain is twice as common, suggesting central processes.

It is difficult in clinical practice to differentiate between different purported pain mechanisms. Furthermore, because Parkinson's disease occurs later in life, it is also common to have non Parkinson's disease associated pain (i.e. Hickums dictum).

Ford's pain classification

Pain type	Pain features
Musculoskeletal pain	Aching, cramping, arthralgic, myalgic sensations in joints, and muscles; Associated findings may include muscle tenderness, arthritic changes, skeletal deformity, limited joint mobility, postural abnormalities, and antalgic gait; May be exacerbated by parkinsonian rigidity, stiffness, and immobility, and relieved by mobility; May fluctuate with medication dosing, and improve with levodopa
Radicular/neuropathic pain	Pain in a root or nerve territory, associated with motor or sensory signs of nerve or root entrapment
Dystonic pain	Associated with sustained twisting movements and postures; muscular contractions often very forceful and painful; Dystonia may involve any limb or extremity, as well as facial and pharyngeal musculature; May fluctuate closely with medication dosing: early morning dystonia, off dystonia, beginning-of-dose and end-of-dose dystonia, peak dose dystonia
Central or primary pain	Burning, tingling, formication, ‘‘neuropathic’’sensations, often relentless and bizarre in quality, not confined to root or nerve territory; Pain may have an autonomic character, with visceral sensations or dyspnea, and vary in parallel with the medication cycle as a non-motor fluctuation; Not explained by rigidity, dystonia, musculoskeletal or internal lesion
Akathisia	Subjective sense of restlessness, often accompanied by an urge to move; May fluctuate with medication effect, and improve with levodopa

Pathophysiology

Central pain:

Central pain in Parkinson's Disease (PD) arises from disturbances in pain processing and perception within the ascending and descending pathways. These disturbances are due to the involvement of numerous pain processing structures that are directly implicated in the spread of PD pathoanatomy within the nervous system across different neuropathological stages. The basal ganglia play a significant role in central pain processing, with dopaminergic deficits leading to reduced multimodal pain thresholds. Spinal excitability alterations and local neurodegenerative changes, such as painful hyperactivity in primary afferent nociceptors and diminished dopaminergic descending inhibition, are pathophysiologically relevant in PD.

Moreover, the impact of dopaminergic replacement therapy on pain thresholds remains controversial, particularly for levodopa. Abnormal central nociceptive pain processing is influenced by other neurodegeneratively affected regions in PD, including cortical areas, limbic structures, thalamus, brainstem nuclei, periaqueductal grey matter, and the spinal cord. Additionally, molecular alterations in the cytoskeleton and mitochondria in PD may contribute to nociceptor hyperactivity, resulting in neuropathic pain and increased pain sensitivity due to reduced nociception thresholds.

Nociceptive pain

Pain in PD patients is more commonly observed as musculoskeletal or nociceptive pain rather than central pain, with roughly half of the PD population experiencing pain due to secondary diseases such as spinal or peripheral joint osteoarthritis. Although this pain may be exacerbated by akinesia and rigidity, there is no clear correlation between the severity of motor symptoms and reported pain levels. This suggests that pain and motor impairment may not share identical pathogenetic mechanisms.

It is important to consider that musculoskeletal pain, particularly on one side of the body (e.g., shoulder-arm syndrome) and adhesive capsulitis, is a common early manifestation of akinesia and rigidity in PD. This type of pain may be frequently misdiagnosed or overlooked, further complicating the understanding of pain presentation and progression in PD patients.

Other than

Risk Factors

Risk factors for pain include female gender, dyskinesia, postural abnormalities, motor complications, depression, diabetes mellitus, osteoporosis, rheumatic diseases, and arthritis.

Management

Unfortunately there is limited data guiding the treatment of pain in PD. Furthermore no specific treatments exist. Medications include dopaminergic drugs, non-opoid drugs, opioids, anticonvulsants, and antidepressants. Unfortunately, pain is often resistant to treatment.

Resources

Pain in Parkinson's Disease - Ford 2010.pdf - 138 KB (f)

Pain in Parkinson's Disease - Buhmann 2020.pdf - 327 KB (f)

Pisa syndrome in Parkinson's disease - Barone 2016.pdf - 1.69 MB (f)