Parkinson’s disease is a slowly progressive neurologic disorder caused by the loss of dopamine (DA)-secreting cells in the substantia nigra and basal ganglia of the brain. DA is a neurotransmitter responsible for synaptic trans -mission in the nerve pathways coordinating smooth and focused activity of skeletal muscles. Loss of DA-secreting cells is associated with a classic pattern of symptoms, including the following:  Resting tremor in the limb, especially of the hand when in a relaxed position; tremor usually increases during stress and is often more severe on one side of the body  Rigidity or increased tone (stiffness) in all muscles  Slowness of movement (bradykinesia) and inability to initiate movement (akinesia)  Lack of spontaneous movements  Loss of postural reflexes, which leads to poor balance and abnormal walking (festinating gait)  Slurred speech, slowness of thought, and small, cramped handwriting The cause of idiopathic Parkinson’s disease, in which DA-secreting neurons in the substantia nigra are damaged and lost by degeneration or apoptosis, is not known. However, some evidence suggests a hereditary predisposition; about 20% of Parkinson’s patients have a family member with similar symptoms. Symptoms that resemble idiopathic Parkinson’s dis-ease may also result from infections (e.g., encephalitis), toxins (e.g., MPTP), drugs used in the treatment of neuro-logic disorders (e.g., neuroleptics used to treat schizophre-nia), and repetitive trauma. Symptoms with these causes are called secondary parkinsonism. On the microscopic level, degeneration of neurons in the substantia nigra is very evident. This region loses its typical pigmentation, and an increase in the number of glial cells is noticeable (gliosis). In addition, nerve cells in this region display characteristic intracellular inclusions called Lewy bodies, which represent accumulation of intermedi-ate neurofilaments in association with proteins -synuclein and ubiquitin. Treatment of Parkinson’s disease is primarily symp-tomatic and must strike a balance between relieving symp-toms and minimizing psychotic side effects. L-Dopa is a precursor of DA that can cross the blood–brain barrier and is then converted to DA. It is often the primary agent used to treat Parkinson’s disease. Other drugs that are used in-clude a group of cholinergic receptor blockers and aman-tadine, a drug that stimulates release of DA from neurons. If drug therapies are not effective, several surgical op-tions can be considered. Stereotactic surgery, in which nuclei in selective areas of the brain (globus pallidus, thalamus) are destroyed by a thermocoagulative probe in-serted into the brain, can be effective in some cases. Sev-eral new surgical procedures are being developed and are still in experimental stages. These include transplantation of DA-secreting neurons into the substantia nigra to replace lost neurons.
bodies and Golgi cisternae. Microtubules, neurofilaments, mitochondria, and vesicles, however, pass through the axon hillock into the axon. The region of the axon between the apex of the axon hillock and the beginning of the myelin sheath (see below) is called the initial segment. The initial segment is the site at which an action potential is generated in the axon. The action potential (described in more detail below) is stimulated by impulses carried to the axon hillock on the membrane of the cell body after other impulses are received on the dendrites or the cell body itself.
Some large axon terminals are capable of local protein synthesis, which may be involved in memory processes.