MSCI M131 Lecture 12(Unit 2)Outline of Past Lecture I. Neuromuscular disordersa. Myasthenia Gravisb. Multiple SclerosisOutline of Current lectureI. Multiple SclerosisII. Parkinson’s DiseaseCurrent LectureI. Multiple Sclerosisc. Signs and symptomsi. Sensory, physiological issues; depressiond. Diagnosisi. Very difficult to diagnose in early stagesii. In most cases, antibodies can be detectediii. Eventually scans will show “scarring” in braine. Clinical importancei. Incidence increasing (could be toxins and pollution or just diagnosing more)ii. Most diagnosed at 25-35iii. Symptoms often make people stay away from social interactioniv. Inability to workf. Risk factorsi. Not contagiousii. Not directly inherited, but some genetic factorsiii. Environment; infectionsg. Treatmentsi. No cureii. Immunosuppression, general; immunomodulators (specific, side effects worse)iii. Plasmapheresis (filter out antibodies)iv. Various rehab therapiesh. PrognosisThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.i. Depends on progression ratesii. Rarely fatal on its own (respiratory or cardiac complications)iii. 85% end up in a wheelchairiv. Average lifespan 5-10 years shorterv. Relapses occurII. Parkinson’s Diseasea. Pathophysiologyi. Basal ganglia – several structures that help fine-tune movement1. Substantia nigra – main role is muscle inhibitionii. Dopamine helps motor control by creating damping effectiii. Cell death in substantia nigra causes a bias towards excitation due to decreased baseline inhibitionb. Etiologyi. Most cases unknown (idiopathic)ii. However, a few factors can cause PD1. Genetic (small, usually young-onset cases)2. Concussion (brain damage)3. Toxins (pesticides and drugs)iii. Signs and symptoms1. Tremor and spasticity2. Early diagnosis difficult – no blood tests can diagnose PD – relies on severity of symptomsiv. Risk factors - genetics, toxins, concussions, use of antipsychotics (wear down dopamine center)v. Treatments1. Pharmaceuticala. L-DOPA – converted to dopamine, crosses the blood brainbarrierb. Many other drugs to deal with symptoms2. Surgicala. Pallidotomy – destroy globus pallidusi. Cuts the excitatory pathway, chance of damage somewhere elseb. Deep brain stimulationi. Reactivates inhibitory pathwayvi. Clinical importance1. When symptoms appear, about 80% of substantia nigra already dead2. Tolerance to and side effects from PD drugs is a problemvii. Prognosis1. Not good – no cure2. Not fatal on its own, but decreased lifespan; death from