What Is Parkinsons Disease

Here’s a description of Parkinsons Disease from CME Medscape together with the treatments available.

Parkinson’s Disease: Early Intervention: Introduction

Introduction

Parkinson’s disease (PD) is the second most common neurodegenerative disease in the United States, and it affects more than a million people.[1] The cause of PD remains unknown but is attributed to a complex interaction between genetic and environmental factors.[2] Clinically, PD is characterized by a triad of rigidity, bradykinesia, and rest tremor, and is often associated with postural instability. Although motor disability is the hallmark of PD, a broad spectrum of nonmotor manifestations can significantly contribute to disease-related disability (Table 1).

Table 1. Nonmotor Manifestations of Parkinson’s Disease

Neuropsychiatric symptoms
Depression, apathy, anhedonia, anxiety
Dementia
Impulse control disorders
Hallucinations, delusions (usually medication induced)
Sleep dysfunction
Disorders of sleep initiation and maintenance
Insomnia, poor sleep efficiency
Primary sleep disorders
Restless legs syndrome, periodic limb movement disorder
Sleep apnea (obstructive and central)
Parasomnias
RBD
Non-REM sleep-related movement disorders
Vivid dreaming
Excessive daytime somnolence
Autonomic dysfunction
Bladder dysfunction
Orthostatic hypotension
Hyperhydrosis
Sexual dysfunction
Gastrointestinal symptoms
Constipation
Hypersalivation
Dysphagia
Sensory symptoms
Pain
Olfactory dysfunction
Visual symptoms (diplopia, vision blurring)
Other symptoms
Fatigue
Weight loss
Weight gain (can be medication induced)

RBD = REM sleep behavior disorder; REM = rapid eye movement

The motor manifestations of the disease are linked to degeneration of dopaminergic neurons in the substantia nigra pars compacta of the midbrain. However, the neuropathologic changes of PD are widespread, affecting multiple nondopaminergic pathways including degeneration of noradrenergic, serotoninergic, and cholinergic neurons. According to the hypothesis of Braak and coworkers,[3] degeneration of these neurons may precede the earliest neuropathologic changes seen in the substantia nigra pars compacta and may explain the wide spectrum of nonmotor symptoms that can be present even early in the course of PD.

Traditionally, treatment of PD has been focused on improving motor disability. A change in the score on the Unified Parkinson’s Disease Rating Scale (UPDRS) is the most commonly used measure of efficacy in early-stage PD interventional studies.[4] The UPDRS consists of 4 parts: part I is a brief evaluation of mentation, behavior, and mood; part II assesses activities of daily living (ADL); part III is the objective assessment of motor disability; and part IV is the assessment of complications of therapy (ie, dyskinesia and motor fluctuations). The current version of the UPDRS is heavily weighted toward measuring the degree of motor disability. However, multiple studies of disease-related quality of life (QOL) impairment clearly indicate that nonmotor symptoms, specifically depression, are the major variables responsible for the change in QOL.[5,6] A new version of the UPDRS has been recently developed to expand the assessment of nonmotor disability.[7]

Treatment of PD is limited to symptomatic interventions aimed at reduction of disease-related disability. In the absence of curative therapy, our interventions should focus on impact on disease-related QOL and reduction of long-term treatment-related complications. There is a wide armamentarium of agents approved for management of early PD (Table 2). This article will briefly review recent studies on the efficacy and side effect profile of the 3 major classes of agents — levodopa, dopamine agonists, and monoamine oxidase B inhibitors (MAO-Bs) — as treatment options for early PD, focusing on the side effect profile of each group of agents. Anticholinergic agents and amantadine are also used for treatment of early PD; however, no recent studies have assessed their efficacy.

Table 2. Classes of Agents Approved for Monotherapy in Early Parkinson’s Disease

Class Agent Brand Name
MAO-B inhibitor Rasagiline
Selegiline
Azilect®
Levodopa replacement Carbidopa/levodopa Sinemet®
Sinemet CR®
Parcopa®*
Dopamine agonists Pramipexole
Ropinirole
Rotigotine†
Mirapex®
Mirapex ER®
Requip®
Requip XL®
Neupro®
NMDA antagonist Amantadine Symmetrel®

*Orally dissolvable preparation of carbidopa/levodopa
†Currently off the market in the United States
CR = controlled release; ER = extended release; MAO-B = monoamine oxidase B; NMDA = N-methyl-D-aspartate; XL = extended release

The second part of this review will discuss the scope of nonmotor manifestations associated with early PD. Motor disability is the target of most studies; however, clinicians should weigh the impact of the intervention on nonmotor disability against the side effect profile to guide them in selection of a treatment agent. Neuroprotection in PD was reviewed in a recent Medscape publication.[8]

 

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One Response to What Is Parkinsons Disease

  1. Pingback: As Long As I’m Doing Tests Today… — Parky Bill's PD Place

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