The Basics of Parkinson Disease
How a Loss of Specific Neurons Leads to a Loss of Movement Control
Mar 1, 2008
As many as 1 in 100 people over the age of 60 suffer from Parkinson disease. Characterized by the presence of isolated tremors while at rest, slowness of movement, and loss of coordination, these and other symptoms are related to the inability to properly control voluntary movement. The disease and its symptoms appear because of the loss of neurons in the brain region known as the substantia nigra.
How Does the Brain Control Movement
The ability to move certain muscles when necessary is taken for granted by most people. The action of motor neurons to tell skeletal muscle to contract seems to be the simplest of physiologic requests. The control of purposeful movement is vastly more complicated than that. Voluntary movement is regulated, in part, by neural activity in two interconnected regions deep in the brain, the basal ganglia and the substantia nigra. Literally translated to “black substance”, because of the darkly colored pigmentation of the nerve cells in this region, loss of neurons within the substantia nigra is a hallmark of the pathology of PD.
What causes Parkinson disease
As is the case with many other neurodegenerative disorders, the vast majority of Parkinson disease cases occur spontaneously with no known genetic inheritance from generation to generation. These so-called sporadic cases make up more than 90% of all cases of PD. However, inherited forms of PD have been identified of both the dominant and the recessive type. With both early and late age onset forms, the various gene defects responsible have pointed to selected biochemical pathways that could serve as key targets for future therapeutic intervention. One area of particular interest is the role played by oxidative damage in the substantia nigra as a causal factor in PD.
Medication Therapy for PD
Many of the nerve cells in the subtantia nigra produce and utilize the neurotransmitter known as dopamine for communication with other nerve cells. Because of the loss of these 'dopaminergic' neurons, the mainstays of PD treatment and symptom control have been drugs that increase the levels of dopamine in the remaining neurons (drugs containing the compounds L-DOPA and carbodopa such as Sinemet) or compounds that enhance signaling through the pathways typically activated by dopamine (compounds known as ‘dopamine agonists’ such as bromocriptine, ropinirole and pergolide).
Surgical Therapy for PD
Surgical interventions of varying types for limiting the symptoms of PD have emerged over the last three decades. While treatment with medications is always the first choice, these surgical treatments have proven useful for many people. The earliest surgical treatments involved intentionally damaging specific structures in the brain that are involved in modulating movement control. The idea behind this is that some of the symptoms of PD, largely the tremors, could be dampened. These included procedures known as pallidotomy (damaging a brain region known as the globus pallidus) and thalamotomy (damaging a specific area of the thalamus).
More recently, surgical interventions for PD therapy have focused on the use of deep brain stimulation. Miniature electrodes are surgically placed in specific brain regions and are used to deliver controlled, extremely small electrical currents. This can change the activity of surrounding cells and has provided measurable benefits to patients with symptoms that have proven more resistant to drug therapy. Other treatments currently being tested include the direct infusion into the brain of factors that help to keep the remaining nerve cells alive and the introduction of cell transplants directly into the affected areas of the brain.
