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Parkinsons
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Background: Parkinson disease (PD) is a progressive neurodegenerative disorder associated with a loss of dopaminergic nigrostriatal neurons. It is named after James Parkinson, the English physician who described the shaking palsy in 1817.
PD is recognized as one of the most common neurological disorders, affecting approximately 1% of individuals older than 60 years. Cardinal features include resting tremor, rigidity, bradykinesia, and postural instability.
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Pathophysiology: The major neuropathologic findings in PD are a loss of pigmented dopaminergic neurons in the substantia nigra and the presence of Lewy bodies. The loss of dopaminergic neurons occurs most prominently in the ventral lateral substantia nigra. Approximately 60-80% of dopaminergic neurons are lost before the motor signs of PD emerge.
Lewy bodies are concentric, eosinophilic, cytoplasmic inclusions with peripheral halos and dense cores. The presence of Lewy bodies within pigmented neurons of the substantia nigra is characteristic, but not pathognomonic, of idiopathic PD. Lewy bodies also are found in the cortex, nucleus basalis, locus ceruleus, intermediolateral column of the spinal cord, and other areas. Lewy bodies are not specific to PD, as they are found in some cases of atypical parkinsonism, Hallervorden-Spatz disease, and other disorders. Incidental Lewy bodies are found at postmortem in patients without clinical signs of parkinsonism. The prevalence of incidental Lewy bodies increases with age. Incidental Lewy bodies have been hypothesized to represent the presymptomatic phase of PD.
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No standard criteria exist for the neuropathologic diagnosis of PD, as the specificity and sensitivity of the characteristic findings have not been established clearly. Individuals presenting with primary dementia may exhibit neuropathologic features indistinguishable from those of PD.
Alpha-synuclein recently was discovered to be a major structural component of Lewy bodies. All Lewy bodies stain for alpha-synuclein and most also stain for ubiquitin.
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The basal ganglia motor circuit modulates cortical output necessary for normal movement (see Image 1). Signals from the cerebral cortex are processed through the basal ganglia-thalamocortical motor circuit and return to the same area via a feedback pathway. Output from the motor circuit is directed through the internal segment of the globus pallidus (GPi) and the substantia nigra pars reticulata (SNr). This inhibitory output is directed to the thalamocortical pathway and suppresses movement.
Two pathways exist within the basal ganglia circuit; they are referred to as the direct and indirect pathways. In the direct pathway, outflow from the striatum directly inhibits GPi and SNr. The indirect pathway comprises inhibitory connections between the striatum and the external segment of the globus pallidus (GPe) and the GPe and the subthalamic nucleus (STN). The subthalamic nucleus exerts an excitatory influence on the GPi and SNr. The GPi/SNr sends inhibitory output to the ventral lateral (VL) nucleus of the thalamus. Striatal neurons containing D1 receptors constitute the direct pathway and project to the GPi/SNr. Striatal neurons containing D2 receptors are part of the indirect pathway and project to the GPe.
Dopamine is released from nigrostriatal (SNc) neurons to activate the direct pathway and inhibit the indirect pathway. In PD, decreased striatal dopamine causes increased inhibitory output from the GPi/SNr (see Image 2). This increased inhibition of the thalamocortical pathway suppresses movement. Via the direct pathway, decreased striatal dopamine stimulation causes decreased inhibition of the GPi/SNr. Via the indirect pathway, decreased dopamine inhibition causes increased inhibition of the GPe, resulting in disinhibition of the STN. Increased STN output increases GPi/SNr inhibitory output to the thalamus.
Frequency:
Internationally: The incidence has been estimated to be 4.5-21 cases per 100,000 population per year. Estimates of PD prevalence range from 18-328 per 100,000 population, with most studies yielding a prevalence of approximately 120 per 100,000.
Sex: PD is about 1.5 times more common in men than in women.
Age: The incidence and prevalence of PD increase with age. The average age of onset is approximately 60 years. Onset in persons younger than 40 years is relatively uncommon.
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