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Research Article

Introduction

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Pages 1-2 | Published online: 31 Oct 2011

Parkinson's disease (PD) is a neurodegenerative disorder that affects an estimated 5,000,000 persons throughout the world, and it is estimated that the prevalence will double by the year 2030 [Citation1]. The loss of dopamine in the substantia nigra is the primary neurochemical change associated with PD; however, it is increasingly recognized that there are multiple neurochemicals and multiple brain areas affected by this disease [Citation2, 3]. The cardinal features of PD include bradykinesia, resting tremor, rigidity, and in the later stages postural instability. However, it is estimated that by the time these symptoms appear, there has already been a loss of 60%–80% of dopamine neurons [Citation4].

A current research goal in PD is to identify nonmotor symptoms that predate the development of motor symptoms such that those at risk for PD can be identified earlier. A number of premotor symptoms have been identified, including olfactory dysfunction; visual changes; autonomic changes including constipation, orthostatic hypotension, and cardiac abnormalities; sleep disorders; and neurobehavioral and cognitive changes [Citation5]. Earlier identification of persons at risk for PD would warrant earlier treatment options that could slow or stop disease progression. There are currently no definitively neuroprotective treatments available for PD. However, multiple compounds have been studied or are currently under study including the monoamine oxidase type B (MAO-B) inhibitors, rasagiline [Citation6] and selegiline [Citation7], co-enzyme Q10 [Citation8], pramipexole [Citation9], levodopa [Citation10], and creatine [Citation11] among others.

Although PD is one of the most common movement disorders, the diagnosis and treatment can be a challenge. In fact, in one study, it was shown that primary care physicians misdiagnosed PD in nearly 50% of cases, general neurologists in 25%, and movement disorder specialists in 8% [Citation1]. There are multiple disorders that have features similar to PD and can therefore be mistaken for PD including the atypical forms of parkinsonism such as multiple system atrophy, progressive supranuclear palsy, dementia with Lewy bodies and corticobasal degeneration, drug-induced parkinsonism, vascular parkinsonism, psychogenic disorders, Alzheimer's disease, essential tremor, and normal pressure hydrocephalus. The use of the United Kingdom Parkinson's Disease Society Brain Bank Clinical Diagnostic Criteria for the diagnosis of PD can significantly improve diagnostic accuracy [Citation12].

The decision to initiate treatment in PD should be based on the symptoms and situation of each individual. Symptom severity, disability, social activities, and employment obligations can all influence when treatment should be initiated. In early disease, there are multiple treatment options including the MAO-B inhibitors rasagiline and selegiline, the dopamine agonists pramipexole and ropinirole, carbidopa/levodopa, amantadine, and rarely anticholinergics [Citation13]. In addition to treatment of motor symptoms, it is important to recognize and treat the nonmotor symptoms of PD. Common nonmotor symptoms include cognitive impairment, psychosis, apathy, depression, anxiety, sleep disorders, orthostatic hypotension, constipation, urological disorders, sexual dysfunction, excessive sweating, pain, and sensory disturbances among others [Citation14]. As the disease progresses, in addition to increased symptom severity, motor complications, such as on/off motor fluctuations and dyskinesia, occur in the majority of patients [Citation13]. Treatments for advanced PD include the MAO-B inhibitors rasagiline, selegiline, and orally disintegrating selegiline; the dopamine agonists ropinirole, pramipexole, and apomorphine; and the catechol-O-methyltransferase inhibitors entacapone and tolcapone for motor fluctuations and amantadine for dyskinesia. In both early and more advanced disease, it is important to understand the safety concerns related to the medications used. Deep brain stimulation is a surgical treatment option, typically performed when medical treatment options can no longer maintain a consistent control of symptoms [Citation13]. Finally, there are a number of new treatment options under investigation as potential neuroprotective agents and also to improve the symptomatic treatment of PD.

This supplement contains seven peer-reviewed manuscripts covering the latest information regarding the recognition, diagnosis, and treatment of PD. Specific topics include premotor and other nonmotor symptoms of PD, compounds investigated as potentially neuroprotective and the various study designs used for evaluation of these compounds, the diagnosis and initiation of treatment, treatment of advanced PD, safety concerns related to PD medications, and, finally, future treatment options for PD.

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