- Also called:
- primary parkinsonism, paralysis agitans, or idiopathic parkinsonism
Parkinson disease
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What is Parkinson's disease?
Parkinson's disease is a progressive neurological condition that belongs to a group of disorders known as parkinsonism. It is characterized by tremor, muscle rigidity, slow movement, and postural instability.
The disease is caused by the degeneration of cells in the substantia nigra and locus ceruleus, which are pigmented nuclei in the brainstem, as well as their connections with the basal ganglia. This degeneration results in a deficiency of dopamine, a neurotransmitter that plays a crucial role in motor control, leading to inhibited activity within the basal ganglia.
Onset typically occurs between 60 and 70 years of age. While the cause of Parkinson's is unknown, it is believed that a combination of genetic predisposition and environmental factors are risk factors.
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What part of the brain is mainly affected by Parkinson's disease?
Parkinson's disease primarily affects the substantia nigra, a region in the brainstem responsible for producing dopamine, a neurotransmitter that helps to control movement. In Parkinson's disease, the dopamine-producing neurons in the substantia nigra degenerate, leading to a dopamine deficiency, which disrupts signaling to the basal ganglia and impairs motor control. The cause of this degeneration is unclear, but it may involve the accumulation of a protein called alpha-synuclein into Lewy bodies, mitochondrial dysfunction, and inflammation.
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What causes the brain cells to stop working properly in Parkinson's disease?
In Parkinson's disease, the degeneration of cells in the substantia nigra and locus ceruleus, both pigmented nuclei in the brainstem, and their connections to the basal ganglia causes brain cells to stop working properly. The basal ganglia, situated above the brainstem, are involved in initiating and patterning voluntary movements. This motor control system uses the neurotransmitters dopamine and acetylcholine. Parkinsonism involves a deficiency of dopamine as a result of the degeneration of neurons in the substantia nigra, which leads to the inhibition of activity within the basal ganglia.
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What chemical messenger is reduced in the brains of people with Parkinson's disease?
In Parkinson's disease, the level of dopamine, a neurotransmitter that inhibits nerve impulses in the brain, is markedly reduced. This reduction occurs primarily in the substantia nigra region of the brain as a result of the loss of dopaminergic neurons. These neurons normally synthesize and use dopamine to communicate with other neurons in parts of the brain that regulate motor function. The cause of decreased dopamine levels is unclear.
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What are Lewy bodies, and how are they related to Parkinson's disease?
Lewy bodies are abnormal deposits of alpha-synuclein protein that accumulate in the brain. They're named after German physician Friedrich Heinrich Lewy, who first described them in the context of Parkinson's disease.
In Parkinson's disease, Lewy bodies appear in the substantia nigra, a brain region that produces the neurotransmitter dopamine. The decrease of dopamine in the brain has been noted in patients with Parkinson's disease. The accumulation of alpha-synuclein from Lewy bodies may lead to neuronal degeneration; however, it is not clear whether Lewy bodies are a cause or a result of the disease. Lewy bodies are also associated with dementia with Lewy bodies, a chronic, progressive disease that causes a deterioration of intellectual capacity.
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How do the changes in the brain from Parkinson's disease lead to its symptoms, like tremors and movement problems?
In Parkinson's disease, the degeneration of neurons in the substantia nigra leads to a dopamine deficiency, disrupting signals to the basal ganglia, which control voluntary movement. This dopamine deficiency causes an imbalance, inhibiting activity within the basal ganglia. The disruption leads to the hallmark symptoms of parkinsonism: tremors, muscle rigidity, slowness of movement, and postural instability. While the exact cause of this neuronal deterioration is unknown, the accumulation of alpha-synuclein protein forming Lewy bodies, mitochondrial dysfunction, and heightened sensitivity to inflammation-causing cytokines may be involved.
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Parkinson disease, a degenerative neurological disorder that is characterized by the onset of tremor, muscle rigidity, slowness in movement (bradykinesia), and stooped posture (postural instability). The disease was first described in 1817 by British physician James Parkinson in his “Essay on the Shaking Palsy.” Parkinson disease is the primary form of parkinsonism, a group of chronic disorders in which there is progressive loss of motor function due to the degeneration of neurons in the area of the brain that controls movement. Parkinson disease is distinguished from other types of parkinsonism because it is idiopathic, meaning it occurs in the absence of an identifiable cause.
Risk factors
It is thought that, in the majority of cases, Parkinson disease arises from a combination of genetic predisposition and certain environmental factors, such as exposure to pesticides or certain solvents, including trichloroethylene. Although Parkinson disease is rarely inherited, individuals who have first-degree relatives with the disease appear to be at increased risk. In addition, mutations in a gene called PRKN, which encodes a protein known as parkin, have been associated with early-onset (before age 40) Parkinson disease and with some cases of late-onset (after age 50) Parkinson disease. Mutations in several other genes have been linked to noninherited forms of the disease.
Onset and symptoms
The onset of Parkinson disease typically occurs between the ages of 60 and 70, although in about 5 to 10 percent of cases onset occurs before age 40. The worldwide incidence of Parkinson disease is estimated to be about 160 per 100,000 persons, with about 16 to 19 new cases per 100,000 persons appearing each year. Men are slightly more affected than women, and there are no apparent racial differences. Parkinson disease often begins with a slight tremor of the thumb and forefinger, sometimes called “pill-rolling,” and slowly progresses over a period of 10 to 20 years. Advanced disease is often characterized by loss of facial expression, reduced rate of swallowing leading to drooling, severe depression, dementia, and paralysis.
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Neuropathology
A marked decrease in the level of dopamine, a neurotransmitter that plays an important role in the inhibition of nerve impulses in the brain, has been noted in patients with Parkinson disease. This decrease, which occurs primarily in a region of the brain called the substantia nigra, has been attributed to the loss of so-called dopaminergic neurons that normally synthesize and use dopamine to communicate with other neurons in parts of the brain that regulate motor function. The cause of decreased dopamine levels is unclear. A protein known as alpha synuclein appears to be involved in neuronal degeneration. Alpha synuclein is produced by dopaminergic neurons and is broken down by other proteins, such as parkin and neurosin. Defects in any of the proteins that break down alpha synuclein may lead to its accumulation, resulting in the formation of deposits called Lewy bodies in the substantia nigra. However, other mechanisms affecting the accumulation of alpha synuclein have been identified, and it is not clear whether Lewy bodies are a cause of or occur as a result of the disease. Other findings in people affected by Parkinson disease include mitochondrial dysfunction, leading to increased production of free radicals that cause significant damage to brain cells, and heightened sensitivity of the immune system and neurons to molecules called cytokines, which stimulate inflammation.
Treatment
The most effective treatment for Parkinson disease is administration of the metabolic precursor to dopamine, known as levodopa (l-dopa). Levodopa crosses the blood-brain barrier (a physiological partition blocking the entry of large molecules into the central nervous system) via special transport proteins and is converted to dopamine in the brain, primarily in the region containing the substantia nigra. Although initially beneficial in causing a significant remission of symptoms, levodopa frequently is effective for only 5 to 10 years, and serious side effects—including uncontrolled movements, hallucinations, persistent nausea and vomiting, and changes in behaviour and mood—often accompany treatment. Cotreatment with a drug called carbidopa, which inhibits an enzyme that breaks down levodopa prior to crossing the blood-brain barrier, allows higher concentrations of levodopa to reach the brain. Thus, levodopa-carbidopa combination therapy enables lower doses of levodopa to be administered, thereby reducing side effects. This combination therapy has allowed many patients to live reasonably normal lives. A drug known as entacapone, which slows the metabolism of levodopa, may be given with levodopa and carbidopa.
Other drugs used to relieve the symptoms of Parkinson disease include agents that stimulate dopamine production in the brain, such as pergolide and bromocriptine, and agents that slow the degradation of dopamine, such as selegiline. In addition, the antiviral agent amantadine can reduce certain symptoms of the disease.
In some cases, surgery may be necessary to alleviate advanced symptoms. For example, a surgical procedure known as deep brain stimulation (DBS) has been successful in decreasing involuntary movements, improving debilitating problems with gait and slowness of movement, and reducing doses of medications. In DBS an electrode is implanted in the brain and is attached via a lead wire to a neurostimulator inserted under the skin, usually near the collarbone. The neurostimulator sends electrical signals to the electrode. These signals work by disrupting the physiological impulses that cause disordered movement.
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Spinal cord stimulation, an experimental therapy, has also shown some benefit in improving movement in patients with Parkinson disease. In this therapy, electrodes are implanted into the epidural space along the spinal cord. When switched on, the device emits electrical pulses at a frequency that stimulates the spinal cord and potentially boosts communication between the spinal cord and areas of the brain that control motor activity. In a clinical study involving a small number of Parkinson disease patients, spinal cord stimulation reduced the number of freezing episodes (instances in which individuals are suddenly unable to move) and improved standing ability, step length, and walking speed.