1. 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

2. 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

3. Movement Disorders  Hand tremors  Typically involves a rhythmic back-and- forth motion of the thumb at 3 bpm.  Most evident when the limb is at rest or under stress  Patients report rigidity or resistance to movement  Muscles associated with movement all have opposing muscles - when one is activated, the other is relaxed.  Brain’s signals in PD patients become confused causing both sets of muscles to remain engaged and contracted.

4. 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

5. 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 mid- stride 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.

6. 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

7. Causes  Basal Ganglia and Substantia Nigra cell death or dysfunction  These neurons produce the neurotransmitter (neuro-chemical) dopamine  Dopamine is responsible for the transmission of signals associated with smooth, controlled, muscular activity from the substantia nigra to the corpus striatum

8. 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.

9. Theories about cell death  Nerve cells are damaged by free radicals - unstable molecules generated by normal chemical reactions.  Free radicals lack one electron and attempt to replace it by reacting with nearby molecules in a process called oxidation.  Damage is normally controlled by other chemicals called antioxidants.  Not understood yet what mechanistic event prevents this “checks and balances” procedure to take place.

10. Theories about cell death cont’d  Toxins destroy dopamine producing neurons.  Exposure to pesticides or a toxic substance in the food supply.  Not proven conclusively.  Genetic factors  1/5th of PD pt.s have at least 1 relative with parkinsonian symptoms  Investigating the theory that the roots of PD are in a facet of DNA.

11. 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.

12. 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

13. 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.

14. 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.

15. 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 Lecture Home