eMedicine Specialties > Physical Medicine and Rehabilitation > Movement Disorders

Parkinson Disease

Author: Jeff Blackmer, MD, FRCP(C), Associate Professor, Medical Director, Neurospinal Service, Division of Physical Medicine and Rehabilitation, The Rehabilitation Centre; Executive Director, Office of Ethics, Canadian Medical Association
Contributor Information and Disclosures

Updated: Mar 10, 2009

Introduction

Background

James Parkinson first described Parkinson disease (or Parkinson's disease) in 1817. The disorder is one of a number of chronic, progressive, neurodegenerative central nervous system (CNS) diseases that typically occur in adults older than 65 years.¹  The first symptom of Parkinson's disease (PD) usually is a unilateral resting tremor of the hand (pill-rolling tremor). Other common clinical features include cogwheeling rigidity, bradykinesia, and postural instability. Rigidity and bradykinesia tend to be more disabling than the tremor. The basic pathophysiology of PD is a lack of dopamine-producing cells in the basal ganglia. This disorder can be treated surgically and medically; physical therapy often is included in the treatment program as well, although its effectiveness remains somewhat controversial.

Related eMedicine topics:
Parkinson Disease [Neurology]
Parkinson-Plus Syndromes

Pathophysiology

Parkinson's disease (PD) is a disorder of the extrapyramidal system, that is, the motor structures in the basal ganglia. (See image below and Image 1.) PD may be caused by degeneration of dopamine-producing cells in the substantia nigra, resulting in decreased levels of dopamine in the striatum. The exact effects of dopamine on movement are difficult to ascertain, in part because each of the 4 known types of postsynaptic receptors for dopamine has its own anatomic distribution and pharmacologic action. Symptoms of PD usually begin to appear when dopamine levels drop by at least 50%. Associated hyperactivity of cholinergic neurons in the caudate nuclei results in an imbalance in the normal dopamine-to-acetylcholine ratio, which contributes to the symptoms.

The exact cause of these changes remains unknown.² Theories include accelerated aging, genetic susceptibility, environmental toxins (eg, cyanide, manganese, carbon disulfide, pesticides, well water, methanol, organic solvents, lead), as well as oxidative stress. The oxidative stress theory is complex and essentially involves cell death resulting from free radicals produced by oxidation of dopamine. Although the oxidative stress theory seems to receive the most support, many authors feel that the disease is probably caused by a combination of the above 4 factors.³

Evidence shows that whole-body, lifetime occupational exposure to lead is an independent risk factor for the development of PD. In addition, a study conducted in Finland indicates that increasing body mass index (BMI) is related to an increased risk of PD development, further supporting a multifactorial and complex etiology for the condition. Please refer to Causes. Some evidence also indicates that certain environmental factors (including smoking and coffee drinking) may actually have protective associations.⁴

Frequency

United States

The frequency of Parkinson's disease in the United States is similar to that found internationally.

International

The overall incidence of Parkinson's disease, based on several worldwide studies, is about 10-20 cases per 100,000 population per year. Prevalence estimates tend to vary, but the currently accepted figure is approximately 100-200 cases per 100,000 population.

Mortality/Morbidity

The clinical symptoms of Parkinson's disease (PD) worsen over time. Prior to the introduction of levodopa (L-dopa), PD caused severe disability or death in 25% of patients within 5 years of onset, in 65% in the next 5 years, and in 89% of those who survived for 15 years. The mortality rate from PD was 3 times that of the general population matched for age, sex, and racial origin. With the introduction of L-dopa, the mortality rate dropped approximately 50%, and longevity was extended by several years, although no evidence suggests that L-dopa actually alters the underlying pathologic process or stems the progressive nature of the disease.^5,6

Race

Although Parkinson's disease is widespread, some populations seem to have a lower incidence, including the black populations of South Africa and Nigeria; however, black persons living in Mississippi seem to be affected to the same degree as the white population. Lower incidence has also been reported in Asian populations but not in Asian Americans. Lower incidence also may not exist in the Taiwanese.

Sex

The male-to-female ratio for Parkinson's disease is 3:2.

Age

The prevalence of Parkinson's disease (PD) increases with age. In patients younger than 40 years, the prevalence is 5 cases per 100,000 population, increasing to 300-700 cases per 100,000 population in the seventh decade and rising to more than 700 cases per 100,000 population in persons older than 70 years.

However, a 2009 report by Driver et al suggested that the incidence of PD decreases after age 89 years.⁴ The investigators began with a prospective cohort of almost 22,000 US male physicians, aged 40-84 years. Over a 23-year follow-up period, 563 of the participants were found to have developed PD, with the cumulative incidence of PD being 9.9% in persons aged 45-100 years. Although the age-specific incidence rate began to climb steeply in participants at age 60 years, peaking between the ages of 85 and 89 years, the rate declined in participants aged 90 years or more. The lifetime risk for PD was 6.7% in participants aged 45-100 years. The investigators cautioned, however, that despite the evidence in their report, it remains to be established whether a true decrease in PD risk occurs in men after age 89 years.

Related eMedicine topic:
Parkinson Disease in Young Adults

Clinical

History

Symptoms and signs of Parkinson's disease (PD) typically begin in one extremity or side but eventually involve the other limbs and trunk. The classic triad of PD is tremor, rigidity, and akinesia. Historical features reported by patients with PD can include the following:

• Stiffness and slowed movements
• Tremor or shaking at rest
• Difficulty getting out of a chair or rolling over in bed
• Frequent falls or tripping
• Difficulty walking
• Memory loss
• Shifting forward of posture into a stoop
• Speech changes (eg, whispering, rapid speech)
• Smaller handwriting
• Slowness in performing activities of daily living (ADL)
• Sialorrhea
• Decreased sense of smell

Physical

Findings on physical examination in patients with Parkinson's disease can include the following:

• Muscle rigidity
• Cogwheeling-type rigidity (often the initial presentation)
• Bradykinesia
• General slowing of movements
• Postural instability
  • Assumption by patient of a stooped-forward posture
  • Presence, usually, of a festinating gait pattern (stumbling forward); however, retropulsion also can occur
  • Decreased arm swing during ambulatory activity
• Resting tremor
• Pill-rolling tremor, often bilateral but may be asymmetric, usually 3-5 Hz frequency
• Hands preferentially affected, but legs, chin, and head generally involved with more advanced disease
• Painful dystonia, usually occurring in the early morning
• Dementia, often a late feature, ultimately occurring in about one third of patients
• Autonomic symptoms
  • Slowed enteric motility and constipation
  • Urinary retention and incontinence
  • Orthostatic hypotension
  • Masklike facies
  • Micrographia
  • Hypokinetic dysarthria
• Rapid, monotonous, low-volume speech
• Olfactory dysfunction (hyposmia), which may be present prior to motor symptoms and often is not recognized by the patient
• Dysphagia
• Depression
  • Can affect up to 50% of patients
  • Suicide risk
• Akathisia (inability to sit still)
• Seborrheic dermatitis, usually of the face and scalp
• Poor olfactory function, which appears to be correlated with loss of dopamine receptors in the nigrostriatal region

Related eMedicine topics:
Dementia in Motor Neuron Disease
Laryngeal Manifestations of Parkinson Disease
Parkinson Disease Dementia

Causes

• Accelerated aging
  • Normal aging is associated with clinical features that may resemble PD.
  • Aging is associated with a decline of pigmented neurons in the substantia nigra and with decreased levels of striatal dopamine and dopa decarboxylase.
  • Some authorities believe that PD may result from the effects of aging superimposed on an insult to the nigrostriatal system earlier in life.
• Oxidative stress
  • This theory receives much support and attention in the literature.
  • PD patients may suffer the combined effects of multiple factors, culminating in damage from free radicals.
  • Dopamine oxidation can result in the formation of hydrogen peroxide, as well as the superoxide anion radical.
  • Hydrogen peroxide can undergo reactions with ferrous ions, resulting in formation of the highly toxic hydroxyl radical.
  • These hydroxyl radicals can cause cell membrane damage.
• Genetic susceptibility
  • Twin studies often have proven inconclusive.
  • Genetic factors seem to play a greater role in PD that has an earlier onset.
  • An increased incidence of a family history of PD is observed in affected individuals (16% vs 4% of control population).
• Environmental toxins include the following:
  • Cyanide
  • Manganese
  • Carbon disulfide
  • Pesticides
  • Well water
  • Lead
  • Methanol
  • Organic solvents
• Medications that can cause parkinsonian symptoms but not PD itself include the following:
  • Metoclopramide
  • Domperidone
  • Reserpine-containing antihypertensives
  • Neuroleptics
• Increased BMI was shown in one study to be associated with an increased risk of PD development. This effect was found to be graded (the greater the BMI, the higher the risk) and independent of other risk factors.

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