Pain and other nonmotor symptoms in PD are increasingly recognized as a major cause of reduced health-related quality of life. Pain in PD may be categorized into a number of different subtypes, including musculoskeletal, dystonic, radicular neuropathic, and central pain. The onset of pain can vary in relation to motor symptoms, and may precede the appearance of motor symptoms by several years, or occur after the diagnosis of PD has been made. Pain in PD is frequently under-recognized and is often inadequately treated. Levodopa-related dystonia may respond to manipulation of dopaminergic medication. Dopaminergic therapy may also improve musculoskeletal pain related to rigidity and akinesia, as well as akathisia in PD. Botulinum toxin injections can be effective for treatment of painful focal dystonia. Pain and dysesthesia have been reported to improve with DBS, in some cases. Increased understanding of basal ganglia pathways has provided further insights into the pathogenesis of pain in PD, but the exact mechanism of pain processing and modulation remains unclear.

With predictive testing allowing the identification of gene-positive individuals prior to disease onset, the prodromal stage of Huntington's disease provides an ideal period for the use of disease-modifying therapy. A quantifiable and reliable biomarker for monitoring disease progression is crucial for clinical studies of neuroprotection, and this remains an area of active research. Understanding of the underlying pathophysiological mechanisms continues to grow, based mainly on cellular and animal models of Huntington's disease.

No abstract

Individuals with huntingtin gene CAG repeats in the intermediate (27-35) range should be considered at risk for the development of HD, particularly if they have a family history of HD, whether they exhibit clinical features of the disease.