Epidemiology

Parkinsons DiseaseBy: Ashley Caceres, Sofiya Dupliy, Rachel Hervold, Alexandra Raccuia, and Kerry QuiltyDescription of DiseaseParkinsons disease is a slowly progressing neurologic movement disorder that eventually leads to disabilityIt is the fourth most common neurodegenerative disease, and 50,000 new cases are reported each year in the United States The disease affects men more often than women. Symptoms usually first appear in the fifth decade of lifeCases have been diagnosed as early as 30 years of age. The degenerative or idiopathic form of Parkinsons disease is the most commonThere is also a secondary form with a known or suspected cause.Although the cause of most cases is unknown, research suggests several causative factors, including genetics, atherosclerosis, excessive accumulation of oxygen free radicals, viral infections, head trauma, chronic use of antipsychotic medications, and some environmental exposures.

Risk FactorsEnvironmental risk factors commonly associated with the development of Parkinsons disease include use of pesticides, living in a rural environment, consumption of well water, exposure to herbicides, and proximity to industrial plants or quarriesThe National Institutes of Health-AARP Diet and Health Study, as well as a meta-analysis of prospective studies, found that higher caffeine intake was associated with lower risk of Parkinson disease in both men and women. A similar association was found for smoking and Parkinson disease risk.

SymptomsParkinsons disease has a gradual onset, and symptoms progress slowly over a chronic, prolonged course. The cardinal signs are:TremorRigidityBradykinesia abnormally slow movementsPostural instability

SymptomsTremorAlthough symptoms are variable, a slow, unilateral resting tremor is present in the majority of patients at the time of diagnosis characteristically disappears with purposeful movement but is evident when the extremities are motionless.The tremor may manifest as a rhythmic, slow turning motion (pronationsupination) of the forearm and the hand and a motion of the thumb against the fingers as if rolling a pill between the fingers.RigidityResistance to passive limb movement characterizes muscle rigidity. Passive movement of an extremity may cause the limb to move in jerky increments, referred to as lead-pipe or cog-wheel movementsInvoluntary stiffness of the passive extremity increases when another extremity is engaged in voluntary active movement. Stiffness of the arms, legs, face, and posture are commonSYMPTOMSBradykinesiaoverall slowing of active movement may also take longer to complete activities and have difficulty initiating movement, such as rising from a sitting position or turning in bedPostural InstabilityThe patient commonly develops postural and gait problems.A loss of postural reflexes occurs, and the patient stands with the head bent forward and walks with a propulsive gait.The posture is caused by the forward flexion of the neck, hips, knees, and elbowsThe patient may walk faster and faster, trying to move the feet forward under the bodys center of gravity (shuffling gait).Difficulty in pivoting causes loss of balance (either forward or backward).Gait impairment and postural instability place the patient at increased risk for falls

Other ManifestationsThe effect of Parkinsons disease on the basal ganglia often produces autonomic symptoms that include excessive and uncontrolled sweating, paroxysmal flushing, orthostatic hypotension, gastric and urinary retention, constipation, and sexual dysfunctionPsychiatric changes include depression, dementia (progressive mental deterioration), delirium, and hallucinationsMental changes may appear in the form of cognitive, perceptual, and memory deficits, although intellect is not usually affected. A number of psychiatric manifestations (personality changes, psychosis, dementia, and acute confusion) are common in elderly patients with Parkinsons disease. Other manifestationsHypokinesia (abnormally diminished movement) is also common and may appear after the tremorThe freezing phenomenon refers to a transient inability to perform active movement and is thought to be an extreme form of bradykinesiaAdditionally, the patient tends to shuffle and exhibits a decreased arm swing. Micrographia (small handwriting) developsThe face becomes increasingly masklike and expressionless, and the frequency of blinking decreases. Dysphonia (soft, slurred, low-pitched, and less audible speech) may occur as a result of weakness and incoordination of the muscles responsible for speech. In many cases, the patient develops dysphagia, begins to drool, and is at risk for choking and aspiration.

ComplicationsComplications associated with Parkinsons disease are common and are typically related to disorders of movement.As the disease progresses, patients are at risk for respiratory and urinary tract infection, skin breakdown, and injury from falls. The adverse effects of medications used to treat the symptoms are associated with numerous complications such as dyskinesia or orthostatic hypotension EpidemiologyRecognized as the most common neurologic disorders, affecting approximately 1% of individuals older than 60 years. The incidence of Parkinson disease has been estimated to be 4.5-21 cases per 100,000 population per yearEstimates of prevalence range from 18 to 328 cases per 100,000 population, with most studies yielding a prevalence of approximately 120 cases per 100,000 populationThe wide variation in reported global incidence and prevalence estimates may be the result of a number of factors, including the way data are collected, differences in population structures and patient survival, case ascertainment, and the methodology used to define casesThe incidence and prevalence of Parkinson disease increase with age, and the average age of onset is approximately 60 years. Onset in persons younger than 40 years is relatively uncommon

EtiologyAlthough the etiology of Parkinson disease is still unclear, most cases are hypothesized to be due to a combination of genetic and environmental factors. Currently known genetic causes of Parkinsons disease account for approximately 10% of cases.

EtiologyThe oxidation hypothesis suggests that free radical damage, resulting from dopamine's oxidative metabolism, plays a role in the development or progression of Parkinson disease.Although the mechanisms by which genetic mutations cause Parkinson disease is not known, evidence to date converges on mechanisms related to abnormal protein aggregation, defective ubiquitin-mediated protein degradation, mitochondrial dysfunction, and oxidative damage. Preventing the propagation of abnormal alpha-synuclein aggregation may be the key to slowing or stopping Parkinson disease progression.

ETIOLOGYPsychological vs. biologicalSeveral studies found higher prevalence of depression and anxiety disorders up to 20 years before PD onsetChanges reported in:Subcortical nuclei and the frontal lobesStriatal-thalamic-frontal cortex neural circuitsBrainstem monoamine and indolamine systems (i.e., dopamine, serotonin, norepinephrine, and acetylcholine)PathophysiologyNo specific, standard criteria exist for the neuropathologic diagnosis of Parkinson disease, as the specificity and sensitivity of its characteristic findings have not been clearly established. However, the following are the 2 major neuropathologic findings in Parkinson disease:Loss of pigmented dopaminergic neurons of the substantia nigra pars compactaThe presence of Lewy bodies and Lewy neuritesSome individuals who were thought to be normal neurologically at the time of their deaths are found to have Lewy bodies on autopsy examination. These incidental Lewy bodies have been hypothesized to represent the presymptomatic phase of Parkinson disease. The prevalence of incidental Lewy bodies increases with age.

15Pathophysiology

PathophysiologyParkinsons disease is primarily associated with the gradual loss of cells in the substantia nigra of the brain. This area is responsible for the production of dopamine. Dopamine is a chemical messenger that transmits signals between two regions of the brain to coordinate activity. For example, it connects the substantia nigra and the corpus striatum to regulate muscle activity.If there is deficiency of dopamine in the striatum the nerve cells in this region fire out of control. This leaves the individual unable to direct or control movements. This leads to the initial symptoms of Parkinsons disease. As the disease progresses, other areas of the brain and nervous system degenerate as well causing a more profound movement disorder. The exact cause for the loss of cells is unknown. Possible causes include both genetic and environmental factors.

Pathophysiology

DiagnosisUnfortunately, there is currently no standard diagnostic test for Parkinsons DiseaseOften times the initial diagnosis of Parkinsons Disease is made by a family physician who is familiar enough with the patient to notice subtle changesUltimately, the diagnosis is based onA thorough medical and family historyA neurological examinationDiagnosisIf Parkinsons is suspected, the physician may observe for several sign and symptoms:If your expression is animated or flatIf you experience tremors in your arms (present either at rest or extended)If there is any stiffness in the arms or neckIf you rise from a chair easilyIf you walk normally or with short steps (shuffling gait) and if your arms swing symmetricallyYour doctor may also pull you backwards while standing to observe how quickly you can regain your balanceDiagnosisAlthough there is no standard test used to diagnose Parkinsons Disease, there are some options to help physicians arrive at a diagnosis. These include:Treatment with a Parkinson drugLab TestsPETscan

DiagnosisBeginning treatment with a Parkinsons drug is one option. If the symptoms respond to treatment, the diagnosis is Parkinsons.The drug of choice is Carbidopa-levodopa, which is the most effective PD medication. It restores dopamine to adequate levels, since dopamine is depleted in this disease.Performing certain lab tests to diagnose other conditions with similar symptoms.Blood tests to check for abnormal levels of thyroid hormone or liver damageCT scan or MRI to check for stroke, brain tumor or hydrocephalusPETscan to test for low levels of dopamine in the brain, a key sign of Parkinsons.In 2011, the FDA approved the DaTscan, which captures detailed images of dopamine levels, even more so then a PETscanHowever, both of these options are incredibly expensive, not covered by insurance, and not available in many hospitalsTherefore, response to drug treatment is a more affordable indicator leading to a diagnosis of PD.

TreatmentThere is currently no treatment to cure Parkinsons disease, however the available treatment options can significantly relieve symptoms and markedly improve the quality of life Care is individualized for each patient based on presenting symptoms and social, occupational, and emotional needs.

Treatment for Parkinson's disease may include any or all of the following:MedicationSurgery Rehabilitation programClinical research trials

Treatment Drug Therapy Antiparkinsonian medications act by:(1) increasing striatal dopaminergic activity(2) reducing the excessive influence of excitatory cholinergic neurons on the extrapyramidal tract, thereby restoring a balance between dopaminergic and cholinergic activities(3) acting on neurotransmitter pathways other than the dopaminergic pathway.Levodopa (Larodopa) is the most effective agent . Levodopa is converted to dopamine in the basal ganglia, producing symptom relief.Used with Cabidopa, which blocks eary conversion of Levodopa into dopamine Within 5 to 10 years, most patients develop a response to the medication characterized by dyskinesia (abnormal involuntary movements), including:Facial grimacingRhythmic jerking movements of the handsHead bobbing, chewing and smacking movementsInvoluntary movements of the trunk and extremities

Treatment Drug therapy (contd)Other medications used include: Anticholinergic Agents [Cogentin] to help control tremors and rigidity and counteract the action of acetylcholine Antiviral Agents [Symmetrel] to reduce rigidity, tremors, and postural changes Dopamine Agonists [Parlodel, Permax] for early Parkinson's disease as well as secondary drug therapy when other drugs lose effectiveness Monoamine Oxidase Inhibitors [Eldepryl, Azilect] delays or reduces dopamine breakdown Catechol O Methyltransferase Inhibitors - increase duration of action of cabidopa and levodopa, reduce motor fluctuations in patients with advanced Parkinsons disease Antidepressants [Elavil, Prozac, Wellbutrin] Antihistamines [Benadryl, Banflex] may reduce tremors Treatment Surgery Surgical Management: Surgery is only considered as a treatment for Parkinson's disease when medication cannot adequately control symptoms. The limitations of levodopa therapy and the recent advances in neurosurgical procedures decrease potential complications and allow for better treatment.In patients with disabling tremors, rigidity, or severe levodopa-induced dyskinesia, surgery may be considered. Although surgery provides symptom relief in selected patients, it has not been shown to alter the course of the disease or to produce permanent improvement.Surgical options include: Stereotactic Procedures [Thalamotomy and Pallidotomy]Neural Transplantation Deep Brain Stimulation Treatment surgery (contd)Thalamotomy: It is thought that the abnormal brain activity that causes tremor is processed through the thalamus. Thalamotomy destroys part of the thalamus to block the abnormal brain activity from reaching the muscles and causing tremor. Pallidotomy: It is thought that the part of the brain called the globus pallidus becomes overactive in Parkinson's disease. This overactivity acts like a brake and slows or diminishes bodily movement. Pallidotomy surgery permanently destroys the overactive globus pallidus to lessen the symptoms of Parkinson's disease. This treatment can eliminate rigidity and significantly reduce tremor, bradykinesia and balance problemsPallidotomy can also enhance the effect of medication in people with an advanced form of the disease

Treatment surgery (contd)Deep Brain Stimulation: Pacemakerlike brain implants are used to relieve tremors. The stimulation can be bilateral or unilateral; bilateral stimulation is thought to be of greater benefit to patients than results achieved with thalamotomy or pallidotomy. In deep brain stimulation, an electrode is placed in the thalamus and connected to a pulse generator that is implanted in a subcutaneous subclavicular or abdominal pouch. The battery-powered pulse generator sends high-frequency electrical impulses through a wire placed under the skin to a lead anchored to the skull. The electrode blocks nerve pathways in the brain that cause tremors. These devices are not without complications that can result from both the surgical procedure needed for implantation and the device itself

Treatment surgery (contd)Neural Transplantation:Ongoing research is exploring transplantation of porcine neuronal cells, human fetal cells, and stem cells Legal, ethical, and political concerns surrounding the use of fetal brain cells and stem cells have limited the implementation of these procedures.

Treatment physical therapyRegular exerciseRecommended throughout the life of disorder.Helps maintain and improve mobility and strength.Physical exercise aids in rigidity relief, muscle strength and flexibility, balance, etc.

NCLEX QuestionThe client diagnosed with Parkinsons disease (PD) is being admitted with a fever and patchy infiltrates in the lung fields on the chest x-ray. Which clinical manifestations of PD would explain these assessment data?

Masklike face and shuffling gait.Difficulty swallowing and immobility.Pill rolling of fingers and flat affect.Lack of arm swing and bradykinesia.ANSWER & RationaleAnswer: B. Difficulty Swallowing and Immobility

Choice A is not correct. Masklike face is responsible for lack of expression and is part of the motor manifestations of Parkinsons disease but is not related to the symptoms listed. Shuffling is also a motor deficit and does pose a risk for falling, but fever and patchy infiltrates on a chest x-ray do not result from a gait problem. They are manifestations of a pulmonary complication.Choice B is correct.Difficulty swallowing places the client at risk for aspiration. Immobility predisposes the client to pneumonia. Both clinical manifestations place the client at risk for pulmonary complications.Choice C is not correct.Pill rolling of fingers and flat affect do not have an impact on the development of pulmonary complications.Choice D is not correct.Arm swing and bradykinesia are motor deficits.NCLEX QuestionThe nurse is conducting a support group for clients diagnosed with Parkinsons disease and their significant others. Which information regarding psychosocial needs should be included in the discussion?

The client should discuss feelings about being placed on a ventilator.The client may have rapid mood swings and become easily upset.Pill-rolling tremors will become worse when the medication is wearing off.The client may automatically start to repeat what another person says.ANSWER & RATIONALEAnswer: B. The client may have rapid mood swings and become easily upset.

Choice A is not correct.This is information that should be discussed when filling out an advance directive form. A ventilator is used to treat a physiological problem.Choice B is correct.These are psychosocial manifestations of PD. These should be discussed in the support meeting.Choice C is not correct.The reduction in the unintentional pill-rolling movement of the hands is controlled at times by the medication; this is a physiological problem.Choice D is not correct.Echolalia is a speech deficit in which the client automatically repeats the words or sentences of another person; this is a physiological problem.NCLEX QuestionThe nurse is admitting a client with the diagnosis of Parkinsons disease. Which assessment data support this diagnosis?

Crackles in the upper lung fields and jugular vein distention.Muscle weakness in the upper extremities and ptosis.Exaggerated arm swinging and scanning speech.Masklike face and a shuffling gait.Answer & RationaleAnswer: D. Masklike face and a shuffling gait.

Choice A is not correct. Crackles and jugular vein distention indicate heart failure, not PD.Choice B is not correct. Upper extremity weakness and ptosis are clinical manifestations of myasthenia gravis.Choice C is not correct. The client has very little arm swing, and scanning speech is a clinical manifestation of multiple sclerosis.Choice D is correct. Both masklike face and shuffling gait are clinical manifestations of Parkinsons Disease.

NCLEX QuestionThe client diagnosed with PD is being discharged on carbidopa/levodopa (Sinemet), an antiparkinsonian drug. Which statement is the scientific rationale for combining these medications?

There will be fewer side effects with this combination than with carbidopa alone.Dopamine D requires the presence of both of these medications to work.Carbidopa makes more levodopa available to the brain.Carbidopa crosses the bloodbrain barrier to treat Parkinsons disease.ANSWER & RationaleAnswer: C. Carbidopa makes more levodopa available to the brain.

Choice A is not correct.Carbidopa is never given alone. Carbidopa is given together with levodopa to help the levodopa cross the bloodbrain barrier.Choice B is not correct.Levodopa is a form of dopamine given orally to clients diagnosed with PD.Choice C is correct.Carbidopa enhances the effects of levodopa by inhibiting decarboxylase in the periphery, thereby making more levodopa available to the central nervous system. Sinemet is the most effective treatment for PD.Choice D is not correct.Carbidopa does not cross the bloodbrain barrier.