Dr. Ruth Geldati is the director of the Movement Disorders Unit at the Rabin Medical Center. In this article she writes about pain and sensory disturbances in Parkinson's disease.

Parkinson's disease is usually diagnosed by motor signs such as tremors at rest, slowness, stiffness and difficulty walking. At the stage when these signs appear, there is already a degeneration of 70-50% of the dopaminergic cells. Because the motor symptoms in Parkinson's disease are so prominent, they often overshadow other signs of the disease such as depression, fatigue, impaired sense of smell, autonomic nervous system disorders, and sensory disturbances.

The sensory disturbances include pain, impairment of the sense of smell, visual hallucinations, auditory and tactile hallucinations, and a feeling of numbness or currents. Today it is already known that the non-motor signs can precede the appearance of the motor signs by several years. However, being non-specific, great clinical sensitivity is required to diagnose Parkinson's disease based on them alone.

This review will focus on pain, which is the most severe non-motor disorder among the sensory disorders in Parkinson's disease and its impact on the quality of life of patients with the disease.

Physiology and anatomy of pain

The involvement of the basal ganglia in the processing of the sensation of pain in Parkinson's disease is becoming clear recently at the same time as their involvement in their motor function. The surrounding nuclei have branched connections with the thalamus nucleus (responsible for processing that sensation) and with the cerebral cortex. In addition, cells in the basal ganglia have the ability to process sensory signals.

Studies in laboratory animals have shown that cells in the black substance (substantia nigra) respond to mechanical stimulation, electrical stimulation and heat and pain stimulation. Injection of 6-hydroxydopamine, a toxic substance into the basal ganglia, causes an increase in the stimulus threshold for pain in rats. Imaging tests such as brain mapping (SPECT) also support that the surrounding nuclei are involved in pain responses. Bilateral pain stimulation causes an increase in cerebral metabolic activity in the area of ​​the thalamus and basal ganglia. In several clinical syndromes of chronic pain, a decrease in the uptake of labeled dopamine was observed, similar to the picture obtained in Parkinson's patients.