Parkinsons Disease

Parkinsons Disease Slowly progressing neurologic movement disorder that leads to disability. Affects men more than women s/s usually appear in the 5th decade of life , but can be as early as 30 yrs old. Can either be DEGENERATIVE(IDIOPATHIC) or SECONDAY (with a known or suspected cause) PATHOPHYISIOLOGY: Due to decreased levels of neurotransmitter → DOPAMINE Loss of dopamine in areas of the brain result in more excitatory neurotransmitters than inhibitory, leading to an imbalance that affects voluntary movement. S/S don’t start until 60% of pigmented neurons are lost and the striatal dopamine level is decreased by 80%. CLINICAL MANIFESTATIONS: Gradual onset w s/s that progress slowly over a chronic prolonged period of time. Cardinal S/S → TREMOR, RIGIDITY, BRADYKINESIA/AKINESIA & POSTURAL INSTABILITY. TREMOR: slow unilateral resting tremor is present in most pts at time of dx. Resting tremor disappears w purposeful movement and during sleep but is evident when the extremities are motionless or at rest. RIGIDITY: limbs are resistant to passive movement . passive movement can cause limbs to move in jerky increments, referred to as lead-pipe or cogwheel movements. Involuntary stiffness of the passive extremity increases when another extremity is engaged in voluntary active movement. Stiffness or the arms, legs, face, and posture is common BRADYKINESIA: overall slowing of active movement POSTURAL INSTABILITY: develops postural and gait problems; stand w the head bent fwd and walks w a propulsive gait. Posture is caused by the fwd flexion of the neck, hips, knees and elbows. Pt may walk faster and faster trying to move the feet fwd under the bodys center of gravity (shuffling gait) OTHER: effect of PD on basal ganglia produces autonomic s/s that include: uncontrolled sweating, drooling, paroxysmal flushing, orthostatic hypotension, gastric and urinary retention., constipation and sexual dysfunction. Dysphagia Neurogenic orthostatic hypotension Psych changes including: depression , anxiety, dementia, delirium, hallucinations and psychosis. ASSESSMENT AND DX FINDINGS Currently the disease is dx clinically from the pts hx and presence of 2/4 of the cardinal s/s (tremor, rigidity, bradykinesia, postural changes) Dx is often confirmed by a positive response to a levodopa trial . MEDICAL MANAGEMENT: Tx is directed towards controlling s/s and maintaining functional independence bc no medical or sx procedures are in current use to prevent disease progression. PHARMACOLOGIC TX: Antiparkinsonian meds increase striatal dopaminergic activity, reducing the excessive influence of excitatory cholinergic neurons on the extrapyramidal tract, thereby restoring a balance between dopaminergic and cholinergic activities, or acting on NT pathways other than the dopaminergic pathway. Levodopa is the most effective agent and mainstay of tx – its converted to dopamine in the basal ganglia producing symptom relief. Carbidopa is often added to levodopa to avoid metabolism of levodopa therapy before it can reach the brain Benefits of levodopa diminish over time. Within 5-10 yrs pts develop a response to the med (characterized by dyskinesia, facial grimacing, rhythmic jerking movement of the hands, head bobbing, chewing, smacking movements, involuntary movements of the trunk and extremitites.)