INTRODUCTION: Parkinson’s disease is a slowly progressive degenerative neurologic disorder affecting the brain centers that are responsible for control and regulation of movement. The degenerative or idiopathic form of Parkinson’s disease is the most common; there is also a secondary form with a known or suspected cause. The cause of the disease is mostly unknown but research suggests several causative factors (eg, genetics, atherosclerosis, viral infections, head trauma). The disease usually first appears in the fifth decade of life and is the fourth most common neurodegenerative disease.
PATHOPHYSIOLOGY: Parkinson’s disease is associated with decreased levels of dopamine resulting from destruction of pigmented neuronal cells in the substantia nigra in the basal ganglia region of the brain. Dopamine The loss of dopamine stores in this area of the brain results in more excitatory neurotransmitters than inhibitory neurotransmitters, leading to an imbalance that affects voluntary movement. Cellular degeneration causes impairment of the extrapyramidal tracts that control semiautomatic functions and coordinated movements; motor cells of the motor cortex and the pyramidal tracts are not affected.
CLINICAL MANIFESTATIONS: The cardinal signs of Parkinson’s disease are tremor, rigidity, bradykinesia (abnormally slow movements), and postural instability. Resting tremors: a slow, unilateral turning of the forearm and hand and a pill-rolling motion of the thumb against the fingers; tremor at rest and increasing with concentration and anxiety. Resistance to passive limb movement characterizes muscle rigidity; passive movement may cause the limb to move in jerky increments (lead-pipe or cog-wheel movements); stiffness of the arms, legs, face, and posture are common; involuntary stiffness of passive extremity increases when another extremity is engaged in voluntary active movement. Impaired movement: Bradykinesia includes difficulty in initiating, maintaining, and performing motor activities. Loss of postural reflexes, shuffling gait, loss of balance (difficulty pivoting); postural and gait problems place the patient at increased risk for falls.
OTHER CHARACTERISTICS: Autonomic symptoms that include excessive and uncontrolled sweating, paroxysmal flushing, orthostatic hypotension, gastric and urinary retention, constipation, and sexual dysfunction. Psychiatric changes may include depression, dementia, delirium, and hallucinations; psychiatric manifestations may include personality changes, psychosis, and acute confusion. Auditory and visual hallucinations may occur. Hypokinesia (abnormally diminished movement) is common. As dexterity declines, micrographia (small handwriting) develops. Masklike facial expression. Dysphonia (soft, slurred, low-pitched, and less audible speech).
ASSESSMENT AND DIAGNOSTIC METHODS: Patient’s history and presence of two of the four cardinal manifestations: tremor, rigidity, bradykinesia, and postural changes. Positron emission tomography (PET) and single photon emission computed tomography (SPECT) scanning have been helpful in understanding the disease and advancing treatment. Medical history, presenting symptoms, neurologic examination, and response to pharmacologic management are carefully evaluated when making the diagnosis.
MEDICAL MANAGEMENT: Goal of treatment is to control symptoms and maintain functional independence; no approach prevents disease progression.
PHARMACOLOGIC THERAPY: Levodopa is the most effective agent and the mainstay of treatment. Anticholinergic agents to control tremor and rigidity. Amantadine hydrochloride (Symmetrel), an antiviral agent, to reduce rigidity, tremor, and bradykinesia. Dopamine agonists (eg, pergolide, bromocriptine mesylate), ropinirole, and pramipexole are used to postpone the initiation of carbidopa and levodopa therapy. Monoamine oxidase inhibitors (MAOIs) to inhibit dopamine breakdown. Catechol-O-methyltransferase (COMT) inhibitors to reduce motor fluctuation. Antidepressant drugs. Antihistamine drugs to allay tremors.
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