Parkinson's Disease

Course overview

Purpose The purpose of this course is to explain the, clinical manifestations and the pathophysiology of Parkinson's disease. Also be able to discuss the treatment options of Parkinson's disease. Objectives •Define what Parkinson's disease is. •Discuss the pathophysiology of Parkinson's disease, •Describe common symptoms of Parkinson's disease • •Describe the most recognized common medication used to treat Parkinson's disease. • Discuss deep brain stimulation Introduction Parkinson's disease is known as a progressive neurological movement disorder of the basal ganglia caused by loss of dopamine producing cells. Signs and symptoms are rigidity, resting tremor, bradykinesia (which is slow movement), postural instability, and unsteady gait with shuffling noted. Parkinson's disease increases with age, and increases in the 50s. It is very difficult to be able to diagnose Parkinson's since there is no specific diagnostic test that confirms the disease process. Therefore in order to diagnose a diagnosis of Parkinson's, clinical manifestations are the key to examine. Approximately 1 million people in the US have been diagnosed with Parkinson's disease. Parkinson's disease is 1 and half higher in men than women. Pathophysiology Dopamine (DA) which a neurotransmitter, is the most critical element with Parkinson's disease. It results in progressive degeneration of the pigmented dopamine-producing neurons in the substantia nigra of the midbrain. This disrupts the normal balance between DA and acetylcholine (ACh) in the basal ganglia area of the brain. The basal ganglia are a large group of nuclei at the base of the cerebral cortex. The basal ganglia control movement and coordination and affect voluntary movement. The basal ganglia interact with other important brain structures, such as the cerebral cortex. Dopamine is produced from levodopa (L-DOPA). This is what occurs in an active normal brain. It is produced from tyrosine, through the interaction with the enzyme, tyrosine hydroxylase. Neurotransmitters are either excitatory (such as ACh) or inhibitory (such as DA), and in a normal brain the balance of neurotransmitters controls complex body movements. Nigrostriatal fibers project from the substantia nigra to the corpus striatum, carrying messages to the higher motor centers in the cerebral cortex. The loss of dopamine stores results in more excitatory neurotransmitters than inhibitory transmitters. This imbalance affects voluntary movement. Symptoms usually become evident when 60% of pigmented neurons are lost and dopamine levels fall about 80%. The extrapyramidal tracts that control semiautomatic function and coordination of movements are impaired although motor cells are not damaged. The damage to the extrapyramidal tracts results in tremors, rigidity, bradykinesia, and postural instability, the key symptoms of Parkinson's disease. Forms of Parkinsonism Parkinson's disease is the most common form of Parkinsonism, it is defined as a syndrome characterized by similar symptoms but with various etiologies. Idiopathic This form has no known cause and has onset usually in the 50s or 60s. This is the most common and seen in most cases of Parkinson's disease. Toxin-associated Carbon monoxide, manganese (from exposure in copper mines), carbon disulfide. Medication associated Reserpine, methyldopa, lithium, haloperidol, and phenothiazine, metoclopramide have all been implicated. Symptoms may be reversible if the medications are discontinued. Illicit-drug associated Methyl-4-phenyl-1, 2, 5, 6-tetrahydropyridine (MPTP), amphetamine, methamphetamine may cause Parkinsonism. MPTP is a neurotoxin that selectively destroys dopaminergic neurons in the substantia nigra. AGE OCCURENCE Early-onset PD (Early-onset PD) Is believed to be related to genetic defects and affects about 10% of those with Parkinson's disease. Symptoms are similar to idiopathic Parkinson's disease. Juvenile-onset PD (<20) This rare form is us