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SOURCE

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Source: Chen JJ, Dashtipour K. Parkinson disease. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017. http://accesspharmacy.mhmedical.com/content.aspx?bookid=1861&sectionid=134127873.

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DEFINITION

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  • Progressive, chronic disorder of central nervous system (CNS) characterized by impaired muscular coordination and tremor.

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ETIOLOGY

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  • Unknown; likely result of interactions between aging, genetic constitution, and environmental factors.

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PATHOPHYSIOLOGY

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  • Loss of neurons and presence of Lewy bodies in substantia nigra pars compacta.

  • Degree of nigrostriatal dopamine loss correlates directly with severity of motor symptoms.

  • Reduced activation of dopamine-1 and dopamine-2 receptors results in greater inhibition of thalamus.

  • Loss of presynaptic nigrostriatal dopamine neurons inhibits thalamic activity and reduces activation of motor cortex.

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EPIDEMIOLOGY

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  • Affects up to 1 million individuals in United States.

  • Annual incidence ranges from 10 to 120 per 100,000 persons depending on age.

  • Affects 0.5% of people in their sixties and 2.5% of those older than age 80.

  • Usual age at diagnosis is 55–65 years.

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RISK FACTORS

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  • Increasing age.

  • Male sex.

  • Heredity (close relative with disease)

  • Toxin exposure (eg, herbicides, pesticides)

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CLINICAL PRESENTATION

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SIGNS AND SYMPTOMS
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  • General features.

    • Resting tremor.

    • Muscular rigidity.

    • Bradykinesia (usually asymmetric)

    • Postural instability in advanced disease.

  • Motor symptoms.

    • Decreased manual dexterity.

    • Difficulty arising from seated position.

    • Diminished arm swing during ambulation.

    • Dysarthria.

    • Dysphagia.

    • Festinating gait.

    • Flexed posture.

    • “Freezing” at initiation of movement.

    • Hypomimia.

    • Hypophonia.

    • Micrographia.

  • Autonomic and sensory symptoms.

    • Bladder and anal sphincter disturbances.

    • Constipation.

    • Diaphoresis.

    • Fatigue.

    • Olfactory impairment.

    • Orthostatic blood pressure changes.

    • Pain.

    • Paresthesias.

    • Paroxysmal vascular flushing.

    • Seborrhea.

    • Sexual dysfunction.

    • Sialorrhea.

  • Mental status changes.

    • Anxiety.

    • Apathy.

    • Bradyphrenia.

    • Cognitive impairment.

    • Depression.

    • Hallucinosis/psychosis (typically drug-induced)

    • Sleep disorders.

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DIAGNOSIS

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MEANS OF CONFIRMATION AND DIAGNOSIS
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  • Bradykinesia and at least one of the following:

    • Restring tremor.

    • Rigidity.

    • Postural instability.

  • Exclude other types of parkinsonism or tremor disorders (see Differential Diagnosis)

  • Presence of at least three supportive positive criteria:

    • Asymmetry of motor signs/symptoms.

    • Unilateral onset.

    • Progressive disorder.

    • Resting tremor.

    • Excellent response to carbidopa/L-dopa.

    • L-dopa response for 5 years or longer.

    • Presence of L-dopa dyskinesias.

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LABORATORY TESTS
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  • None available to diagnose Parkinson disease.

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IMAGING
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  • Neuroimaging may be useful for excluding other diagnoses.

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DIFFERENTIAL DIAGNOSIS
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  • Essential tremor.

  • Pharmaco toxicity (drug-induced)

    • Antiemetics (metoclopramide, prochlorperazine)

    • Antipsychotics (chlorpromazine, fluphenazine, haloperidol, olanzapine, risperidone, thioridazine)

    • Other drugs (α-methyldopa, cinnarizine, flunarizine, tetrabenazine)

  • Environmental toxicity (manganese, organophosphates)

  • Infections (HIV, subacute sclerosing panencephalitis)

  • Metabolic disorder (hypothyroidism, parathyroid abnormalities)

  • Neoplasms, strokes, traumatic lesions involving the nigrostriatal pathways.

  • Normal-pressure hydrocephalus.

  • Parkinsonism with other neuronal system degenerations.

  • Dementia with Lewy bodies.

  • Multiple system atrophy.

  • Progressive supranuclear palsy.

  • Familial parkinsonism.

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