parkinson's Flashcards
what keeps dopamine in balance in Parkinson’s
acetocholine
Parkinson’s
Progressive disorder with degeneration of nerve cells in the basal ganglia with generalized decline in muscular function.
There is depigmentation of the substania nigra of the basal ganglia.
Is a disorder of the extrapyramidal system. This includes all descending fibers in the cortical and subcortical motor centers that reach the medulla and spinal cord by pathways other than corticospinal tracts. Important in maintenance of equilibrium & muscle tone.
effects of Parkinson’s
Selective depletion of dopamine producing neurons in the substania nigra in midbrain.
Dopamine influences purposeful movement. Without it there is a loss of the inhibitory influence of the excitatory mechanisms of acetycholine which goes unopposed.
Depletion of dopamine results in degeneration of the basal ganglia
Statistics of Parkinson’s
Affects men more than women.
Cause is unknown. Predominately idiopathic but research suggests several causative factors: genetics, atherosclerosis, excessive accumulation of oxygen free radicals, viral infections, head trauma, chronic antipsychotic medication and some environmental exposures.
100 to150 persons/ 100,000 or about 50,000 new cases per year.
Symptoms usually appear in fifth decade but some have been diagnosed by age 30.
Four classic symptoms of of Parkinson’s
Tremors
Rigidity
Akinesia
Postural Instability
Tremors in parkinson
a slow, unilateral, resting tremor present in about 70% at the time of diagnosis. Disappears with purposeful movement. Starts on one side and progresses to the other.
usually have resting tremors that will go away with purposeful movement
rigidity in parkinsons
have stiffness of neck, trunk and shoulders commonly. Cogwheel rigidity common.
Akinesia
(bradykinesia)
slowness of movement. May exhibit “freezing phenomenon”. As dexterity declines, micrographia develops.
tiny tiny writing is common in parkinsons
Postural Instability
loss of postural reflexes. Stands with head bent forward. Shuffling, propulsive gait.
autonomic symptoms of parkinsons
sweating, paroxyzsmal flushing, lacrimation, orthostatic hypotension, gastric and urinary retention, constipation, drooling, sensitivity to heat and sexual disturbances.
psychiatric changes in parkinsons
depression, dementia, sleep disturbances, and hallucinations. May have cognitive, perceptual, & memory deficits though intellect is usually not affected. May see personality changes, psychosis, dementia and acute confusion in the elderly.
what is a parkinsons patient at risk for as the disease progresses
respiratory & urinary infection, skin breakdown, and injury from falls.
stage 1 of parkinson’s
mild tremors. unilateral . patient doesn’t even realize there is something going. inconsistent. Little problem with locomotion
stage 2 of parkinson’s
symptoms are bilateral. slightly more tremors. Friends and family start to see something is wrong.
stage 3 of parkinson’s
starting to slow with body motion . moderately severe disability. More issues with gait and stability.
stage 4 parkinson’s
at this point they can’t live alone. very rigid. full blown tremors.
stage 5 parkinson’s
they can’t stand or walk. Require nursing care
what is usually the final demise of Parkinson’s patients
urinary tract or respiratory infection. They go septic
diagnostic findings in parkinsons
Laboratory and imaging studies are not helpful in diagnosing condition. PET scanning is used to evaluate levodopa ( precursor to dopamine ) uptake.
Disease is diagnosed by history and presence of 2 or more of the cardinal manisfestations.
medical management of parkinson’s
control the symptoms
Directed at controlling symptoms and maintaining functional independence because there is no medical or surgical treatment to prevent or cure the disease.
We now have better symptom control measures.
pharmacological therapy in parkinsons acts by
Increasing striatal dopaminergic activity
b. Reducing excessive influence of excitatory cholinergic neurons. c. Acting on neurotransmitter pathways other than dopaminergic pathways.
surgical management of parkinson’s
Thalamotomy and pallidotomy are effective in relieving many symptoms. Interrupts nerve pathways and alleviates tremor and rigidity.
b. During thalamotomy stereotactic electrical stimulator destroys a portion of the thalmus to decrease tremors. Complications can be ataxia and hemiparesis.
c. Pallidotomy destroys part of globus pallidum. Helps to decrease rigidity, bradykinesia & dyskinesia. Improves motor function and ADLs. Complications:
stroke, visual changes, hemiparesis
Use MRIs, CT scans and angiography to localize appropriate site. Have a stereotactic frame and make a burr hole to pass the electrode through it to target the area.
Stereotactic procedures are completed on one side of the brain at a time. If there are bilateral symptoms, 6 months interval is suggested.
neural transplantation in parkinson’s
Implantation of adrenal medulla tissue into corpus striatum to reestablish normal dopamine release.
Research to transplant human fetal brain cells or genetically engineered cells .
Recently (2000) fetal pig neuronal cells survived transplantation so may be alternate to human cell transplants.
deep brain stimulation in parkinson’s
Recently approved by the FDA, pacemaker like brain implants show promising results in relieving tremors.
Stimulation can be bilateral or unilateral. Electrode is placed in thalmus and connected to a pulse generator implanted in a subcutaneous subclavicular or abdominal pouch.
Generator sends high frequency impulses through a wire placed under the skin to a lead anchored in the skull. The electrode blocks nerve pathways in the brain that cause tremor. Complication: lead leakage.