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Parkinson’s Disease Historical Perspective First described by British doctor James Parkinson Identified its major symptoms and called it “the shaking palsy” Research progressed slowly until the 1960’s 60’s linked the disease to the loss of cells that produce dopamine Initial Symptoms First signs can be mistaken for another condition. Can be considered by the patient as a normal part of the aging process. Persistent mild fatigue Handwriting might become “shaky” Person might feel unbalanced or have difficulty performing sit-to-stands Agitation, irritability, & depression Lack of affect (masked face phenom) Initial symptoms can go on for years Movement Disorders Hand tremors Muscles associated with movement all Typically involves a have opposing rhythmic back-andmuscles - when one is forth motion of the activated, the other is thumb at 3 bpm. relaxed. Most evident when Brain’s signals in PD the limb is at rest or patients become under stress confused causing both Patients report rigidity sets of muscles to or resistance to remain engaged and movement contracted. Movement Disorders cont’d Spontaneous movements can become progressively slower and may actually cease. This is known as bradykinesia Impaired balance and coordination (known as postural instability) Causes PD pt.’s to lean unnaturally backward or forward Common to see someone with head down, stooped stance Movement Disorders cont’d Become vulnerable to falls Those who tend to lean backward have to step step backward first before they begin walking (known as retropulsion) Some develop a midstride halting which creates a risk for falls. Most common gait characteristics are short, quick steps. Can appear as if they are scrambling forward to keep their balance. Secondary Symptoms Depression Emotional Changes (Irritable, pessimistic, fearful, become dependent or isolated) Memory Loss (slower thought processes) Swallowing Difficulties Speech Problems Bladder/Bowel Prob’s Excessive sweating Sleep Disturbance Causes Basal Ganglia and Dopamine is Substantia Nigra cell responsible for the death or dysfunction transmission of signals associated These neurons with smooth, produce the controlled, muscular neurotransmitter activity from the (neuro-chemical) substantia nigra to the dopamine corpus striatum Causes cont’d PD “occurs” when these neurons die or fail to function properly. Without enough dopamine, neurons in the corpus striatum do not function in the usual coordinated manner. The result is an inability to direct or control the body’s movements normally. Typical PD pt. has an 80% reduction of dopamine producing cells. Theories about cell death Nerve cells are Damage is normally damaged by free controlled by other radicals - unstable chemicals called molecules generated antioxidants. by normal chemical Not understood yet reactions. what mechanistic Free radicals lack one event prevents this electron and attempt “checks and balances” to replace it by reacting with nearby procedure to take molecules in a process place. called oxidation. Theories about cell death cont’d Toxins destroy Genetic factors dopamine producing 1/5th of PD pt.s have neurons. at least 1 relative with Exposure to pesticides parkinsonian or a toxic substance in symptoms the food supply. Investigating the Not proven theory that the roots conclusively. of PD are in a facet of DNA. Incidence 500,000 Americans have the diagnosis of PD 50,000 new cases each year (in the U.S. alone) Numbers are higher because of dismissal of symptoms or misdiagnosis. Not gender-specific Avg. age of onset is 60 yrs. Old Estimated that 5-10% of pt.s experience symptoms before the age of 40. Diagnosis Neuropsychological tests CAT (computerized tomography) MRI (magnetic resonance) These are used to rule out other diagnosis Side effects of medications Multiple Strokes Progressive Supranuclear Palsy Shy-Drager Syndrome Wilsons Disease Treatment Cure does not exist Tx is usually comprised of medications and therapies that relieve symptoms. Levodopa (Sinemet) First used in the 1960’s Delays the onset of symptoms for 75% of PD pt.s Used to make dopamine, which itself cannot be injected into the body because it cannot pass the blood-brain barrier. Treatment cont’d When Levodopa is combined with Carbidopa, L-dopa holds back the conversion of levodopa into dopamine until it reaches the brain. Effective in treating bradykinesia and rigidity Less effective in reducing tremor Often ineffective in relieving problems related to balance. Levodopa Side Effects Nausea Vomiting Low Blood Pressure Restlessness Twitching, nodding, jerking (large doses) Lower dosage limits the side effects but symptoms then reoccur. Long-term use diminishes effectiveness Taking frequently but in smaller amounts is an occasionally effective solution. Lecture Home