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Pathology F10

Parkinson Disease

Parkinson Disease is caused by ____________________ a loss of dopamine
How many dopamine producing neurons must a person loose before Parkinson symptoms begin to show? 70-80%
Primary Parkinson is ____________. idiopathic
Etiology of Parkinson -idiopathic (primary parkinson) -Post-infectious -Toxic -more likely to be multifactorial & the trigger can be different for every person
Infections that have been reported to lead to Parkinson: -measles -CMV -rubella -herpes
Toxic triggers of Parkinson: manganese, carbon monoxide, synthetic heroine, cyanide
Parkinson-Plus Syndrome (PPS) -distinguishing factor: if you give someone with Parkinson extra dopamine (L-dopa) their symptoms do not improve -worse that Primary Parkinson because there is no treatment or comfort)
Parkinson Disease -chronic progressive disease of motor function of CNS
Incidence of Parkinson Disease -1% of those over 55 years of age -incidence increases with age -mean age of onset is between 58-62 -10% of cases have an early onset (before 40)
Three Cardinal Features of Parkinson Disease -Rigidity -Bradykinesia -Tremor
Rigidity -increased tone of agonist & antagonist (equal resistance to flexion & extension) -patient becomes progressively more rigid in the later stages
Bradykinesia -slow movement -loose trunk rotation and coordination, leading to akinesia or freezing movement
Tremor -appears first -in Parkinson Disease there's a resting tremor -postural instability and festinating gait
Festinating gait -a shuffle or gallop -arm swing may be first to go -putting music on may change motor program to get them walking again (freezing movement)
Cogwheel tremor -cogwheel has teeth (stops, lets go, stops, etc) -as PT is moving a patient, the it goes, then stops, releases and moves further then stops, etc -due to tremors modifying rigidity (shaking it loose)
Pathogenesis of Parkinson -dysfunction within the subcortical grey matter in basal ganglia -pathologic hallmark is the degeneration of substantia nigra in association with production of Lewy bodies -substantia nigra loses its ability to produce dopamine
where is dopamine produced? substantia nigra pars compacta
Pathophysiology of Parkinson -Basal gangli disorder -involves underactive direct pathway & overactive indirect pathway -decline in the ability to initiate movement -depletion of dopamine -80% loss before symptoms show -writing probs may be 1st thing noticed
How are Tremors caused? lesion of the connection between the basal ganglia and the cerebellar-red-nucleus pathway
Basal Ganglia -presets the motor system based on sensory movements -may need to see movement in periphery sometimes to be able to walk -excitatory direct pathwway activates thalamocortical pathway -inhibitory indirect pathway inhibits thalamocortical pathway
lesion of the basal ganglia causes changes in the character of movement (slowing of movement, poor coordination & loss of adaptive control)
Clinical Manifestations -hallmark= movement disorder -problem with movement activation tremor is the most common initial manifestation (pill rolling at rest) -tremor disappears during sleep -loss of ext against gravity -loss of up & out movement
systemic manifestations -poverty of movement (move less & less) -fatigue -masked faces -flexion dystonia -festinating gait -dysphagia -visual/sensorimotor probs -depression -dementia (late phases) -bradyphrenia -dysautonomia -CV abnormality -airway obstruction -free
flexed dystonia -proximal stiffness -face gets stiff
Masked Faces -loss of facial expression muscles -person may think they are smiling but aren't
dysphagia trouble swallowing
bradyphrenia slowness of thought
dysautonomia -autonomic NS involvement is gone: -excessive sweat -increased salivation/drooling -bladder dysfunction -GI motility
air trapping -associated with airway obstruction -bronchioles collapse & trap air behind collapse & kills alveolar sacs
freezing when periphery stops moving
Diagnosis of Parkinson -look for the classic triad (tremor, rigidity and bradykinesia) -Asymmetry of signs and symptoms, resting tremor -a good response to Levodopa (diagnosis of IDP) -CT or MRI to assess dopamine levels
Stages of Disease Progression Hoehn & Yahr Stages: Stage I=Min or absent signs Stage II=Min bilateral w/o balance impairment Stage III=Impaired postural responses, capable of living ind Stage IV=Severe disability, able to stand & walk w/ assistance Stage V=Wheelchair or bed depen
Clinical Course of Parkinson -Benign= if in stage I or II and its been 4 years after diagnosis -Progressive -Malignant= progresses to stage II within a year of diagnosis
Treatment of Parkinson -symptomatic= increase mobility -drug therapy -deep brain stimulation -implant electrodes in brain & stimulate to decr tremors -pallidotomy= make a lesion in brain (globis pallidis of basal ganglis) to decr rigidity
Pharmacological Management of Parkinson -Selegiline or deprenyl (Eldepryl)= neuroprotective drug that buys times before L-dopa -Levodopa -Artane, Parsidol -Amantadine= acts like dopamine & anticholinergic -Bromocriptine & Pergolide
L-dopa -Levodopa -allows more dopamine to basal ganglia -only affective for 5-7 yr then a neg response occurs -worsening of sympt when coming off meds -dyskinesia; facial grimacing; twitch of tongue & lips -On-Off phenom (sudden periods of immobility -dys
Artane, Parsidol -anticholinergics -body begins to make more acetylcholine which adds to tremors so this is ANTI
dystonia from long term use of L-dopa twisting; axial & prox extremities
Medical/Surgical management -nutrition is crucial (high cal- low protein diet) -Stereotaxic surgery (pallidotomy, thalamotomy, deep brain stim) -transplantation (fetal/stem cells into basal ganglia- not perfected yet)
high cal - low protein diet -high protein will block effectiveness of L-dopa
Created by: CWestrick
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