Symptoms and Treatment of Parkinsons Disease

Symptoms and Treatment of Parkinsons ailmentParkinsons diseaseParkinsons disease is a progressive neurologic disorder affecting the mavin centers that are responsible for say-so and regulation of movement. It is characterized by bradykinesia (slowness of movement), tremor, and muscle peevedness or rigidity (Katzung, Mastes, Trevor, 2012).The major lesion appears to result in a firing of pigmented neurons, oddly those in the substantia nigra of the thinker. The substantia nigra is a disposition of midbrain nuclei that project fibers to the corpus striatum. One of the major neurotransmitters in this area of the brain, and in other move of the central nervous system, is dopamine, which has an important inhibiting function in the central control of movement (Brunton, Chabner, Knollman, 2011). Although dopamine ordinarily exists in high c at a timentration in certain parts of the brain, in Parkinsons disease it is low-down in the substania nigra and the corpus striatum. Dep letion of dopamine levels in the basal ganglia is associated with bradykinesia, rigidity, and tremors (Brunton, Chabner, Knollman, 2011).Regional cerebral blood merge is reduced in patients with Parkinsons disease, and on that point is a high prevalence of dementia. Biochemical and pathologic selective information suggest that demented patients with Parkinsons disease whitethorn fuddle coexis tent Alzheimers disease (Connelly Fox, 2012).In the majority of patients, the ca uptake of the disease is unknown. Arteriosclerotic Parkinsonism is seen more frequently in older get along with groups. It may follow encephalitis, poisoning, or toxicity (manganese, carbon monoxide), or hypoxia, or may be medicine induced. The disease most frequently attacks persons in their fifties and sixties and is the second most common neurologic disorder of the elderly (Brunton, Chabner, Knollman, 2011).The clinical manifestations of Parkinsons disease are impaired movement, muscle rigidity, tremor, muscle weakness, and detriment of postural reflexes. earliest signs embroil a stiffening of the extremities and a wax-like rigidity in the performance of only movements. The patient has difficulty in initiating, maintaining, and performing motor activities, and experiences some delay in carrying out formula activity (Kofman).As the disease progresses, the tremor begins, frequently in one hand and arm, then the other, and later on in the head, although the tremor may remain unilateral. The tremor is characteristic it is a slow, turning motion (pronation-supination) of the gird and the hand, and motion of the thumb against the fingers as if rolling a pill between the fingers. It increases when the patient is concentrating or feels intent (Connelly Fox, 2012).Other characteristics of the disease affect the face, stature, and gait. thither is loss of normal arm swing. Eventually, the rigid extremities become weaker. Since there is limited movement in the muscles, the face has so little expression that it is said to be masklike (with tenuity of blinking), a feature that digest be recognized at a glance (Connelly Fox, 2012).There is a loss of postural reflexes, and the patient stands with head bent forward and walks as if in danger of move forward. Difficulty in pivoting and loss of balance may lead to frequent falls (Katzung, Mastes, Trevor, 2012).Frequently, these patients show signs of depression, and it has non been established whether the depression is a reaction to the disorder or related to a biochemical abnormality. noetic manifestations may appear in the form of cognitive, perceptual, and memory deficits. A number of psychiatric manifestations (personality changes, psychosis, dementia, confusion) are particularly common among the elderly (Kofman). Complications from immobility (pneumonia, urinary tract infection) and the consequences of falls and accidents are major safaris of death (Kofman).Early diagnosis of Parkinsons disease corporatio n be difficult, as the patient can rarely smash when symptoms started. Often someone close to the patient notices a change such as stooped posture, stiff arm, a slight limp, or tremor. Handwriting changes may be an early diagnostic clue. The diagnosis of Parkinsons disease can usually be made with certainty when there is evidence of tremor, rigidity, and bradykinesia (Brunton, Chabner, Knollman, 2011). The results of the patients history and neurological examination are carefully evaluated. Without treatment Parkinsons disease progresses over ten to fifteen years to a rigid, akinetic state in which patients are incapable of caring for themselves (Brunton, Chabner, Knollman, 2011). The availability of impelling pharmacological treatment has altered the prognosis of Parkinsons disease in most cases, functional mobility can be maintained for many years. Life expectancy of adequately treated patients is increased substantially (Brunton, Chabner, Knollman, 2011). The figurehead of dysphagia is associated with shorter survival times. Motor impairment of the muscles in the throat impairs swallowing and poses a take chances for aspiration pneumonia. Other complications of Parkinsons disease include sleep disorders, sexual dysfunction, bowel and bladder complications, and sensory problems, such as the loss of smell (Kofman).There is no cure for Parkinsons disease. Treatment mainly relies on replacing dopamine with focus on controlling symptoms and improving quality of life (Katzung, Mastes, Trevor, 2012). Because Parkinsons disease symptoms are out-of-pocket to a deficiency of the brain chemical dopamine, the brain medicine treatment help increase dopamine levels in the brain. Levodopa, usually in combination with carbidopa, is the standard drug treatment (Katzung, Mastes, Trevor, 2012). For patients who do not answer to levodopa, dopamine agonists may be prescribed. Physical therapy is an important part of Parkinsons disease treatment. Rehabilitation can help amend balance, mobility, speech and functional abilities. No treatment method has been proven to change the manakin of the disease. For early disease, with little or no impairment, drug therapy may not be necessary (Kofman).There is no cure for Parkinsons disease, but medications, physical therapy, and surgical interventions can help control symptoms and improve the quality of life (Connelly Fox, 2012). The goals of treatment are to relieve disabilities and balance the problems of the disease with the berth effect of the medications. A number of issues must be considered in choosing a medication for treatment. These include the effectiveness of the medication, the side effectuate of the medication, and the loss of effectiveness over time (Brunton, Chabner, Knollman, 2011).Levodopa (L-dopa) has been utilize for years and is the gold standard for treatment. L-dopa increases brain levels of dopamine. It is probably the most effective drug for controlling symptoms and is e mploy in all phases of the disease. The standard preparations, Sinemet and Atamet, desegregate levodopa with carbidopa, a drug that slows the breakdown of levodopa. Levodopa is better at improving motor problems than dopamine agonists but increases the risk of involuntary movements. Effectiveness tends to decrease after four to five years of use (Brunton, Chabner, Knollman, 2011).Dopamine agonists drugs copy dopamine to stimulate the dopamine system in the brain. The drugs included are pramipexole (Mirapex), ropinirole (Requip), bromocriptine (Parlodel), and rotigotine (Neupro) (Katzung, Mastes, Trevor, 2012).Monoamine oxidase B inhibitors may have some mild well-beings in initial therapy they include selegiline (Eldepryl) and rasagiline (Azilect), and they slow the breakdown of dopamine that occurs naturally in the brain and dopamine produced by levodopa (Katzung, Mastes, Trevor, 2012).Entacapone (comtan) is a catechol-o-methyl transferase (COMT) inhibitor that helps to prolo ng the make of levodopa by gormandizeing an enzyme that breaks down dopamine (Brunton, Chabner, Knollman, 2011).Medications to treat other symptoms associated with Parkinsons disease include antidepressants. Tricyclics, particularly Amitriptyline (Elavil), studies indicate that the use of SSRIs may worsen symptoms. Anti-psychotics include clozapine and quetiapine help with psychotic symptoms seen with Parkinsons disease (Brunton, Chabner, Knollman, 2011). The cholinesterase inhibitor drugs donepezil (Aricept) and rivastigmine (Exelon) are used to treat Alzheimers disease and are sometimes used for Parkinsons disease. The benefits are small and may not be noticed. Daytime sleepiness and fatigue may be treated with modafinil (Provigil) a drug used to treat narcolepsy or methylphenidate (Ritalin) may be considered for fatigue. Glycopyrrolate, scopolamine, and injections of botulinum toxin may be used to relieve drooling symptoms (Brunton, Chabner, Knollman, 2011).Advanced Parkins ons disease poses challenges for the patient and caregivers. Eventually, symptoms such as stooped posture, freezing, and speech difficulties may no longer respond to drug therapy. Surgery (deep brain stimulation) may be considered. Patients become progressively dependent on others for care and require assistance with daily tasks. The goal of treatment for advanced Parkinsons disease should be on providing safety, comfort, and quality of life (Brunton, Chabner, Knollman, 2011).The toxic effects of Levodopa with carbidopa are considerable. Dyskinesia, the ability to control muscles, can take many forms, most often uncontrolled flailing of the arms and legs or chorea, rapid and exigent motions that can affect the limbs, face, tongue, mouth, and neck (Brunton, Chabner, Knollman, 2011). Hypotension is a common problem during the archetypical few weeks of therapy. Cardiac arrhythmias and gastrointestinal difficulties are common, with the potential of gastric bleeding. Levodopa can ca use disturbances in breathing function, but may benefit patients with upper airway obstructions. Hair loss and mental and psychiatric side effects including confusion, extreme emotional states, especially anxiety, vivid dreams, visual and auditory hallucinations, sleepiness, and effects on learning are other side effects of levodopa (Connelly Fox, 2012). Levodopa causes few psychiatric side effects than other drugs including anticholinergics, selegiline, amantadine, and dopamine agonists. Psychiatric side effects often occur at night, therefore, some doctors recommend reducing the evening dose (Connelly Fox, 2012).Monoamine Oxidase B (MAO-B) inhibitors block monoamine oxidase B, an enzyme that degrades dopamine. Selegiline was commonly used in early onset disease in combination with L-dopa for victuals (Brunton, Chabner, Knollman, 2011). Concerns of the significant side effects have been raised. Azilect, a newer MAO-B Inhibitor, is used alone during early stage Parkinsons dise ase and in combination with L-dopa for moderate to advanced Parkinsons disease. position effects of MAO-B inhibitors include orthostatic hypotension, hypertension if combined with drugs that increase serotonin levels, such as many antidepressants (Brunton, Chabner, Knollman, 2011). A mordacious increase in blood pressure may occur if patients eat foods rich in the amino group acid tyramine, while taking selegiline or rasagiline, and for two weeks after stopping the medications. Patients should avoid foods such as aged cheeses, processed lunch meats, pickled herring, yeast extracts, aged red wine, draft beers, sauerkraut, and soy act (Connelly Fox, 2012).Dopamine agonists stimulate dopamine receptors in the substantia nigra. Dopamine agonists are effective in delaying motor complications during the first years of treatment (Katzung, Mastes, Trevor, 2012). Newer dopamine agonists, Mirapex (pramipexole) and Requip (ropinirol) are the most commonly prescribed. Mirapex appears to w ork better and have fewer side effects than requip. Side effects include nausea, vomiting, constipation, headache, nasal congestion, nightmares, hallucinations, and psychosis. Bromocriptine is the only ergot dopamine agonist approved for treatment in the US (Connelly Fox, 2012). Apomorphine is a dopamine agonist used as a rescue drug in people having on- attain effects severe enough to require going false L-dopa for a few days. Because it causes severe nausea and vomiting, it must be taken with an anti-emetic. Rotigotine (Neupro) is a once daily transdermal patch to treat early and advanced stage Parkinsons disease (Connelly Fox, 2012).Catechol-O- methyl group Transferase Inhibitors (COMT Inhibitors) increase concentrations of existing dopamine in the brain. Entacapone (Comtan, Stalevo) is the current standard COMT inhibitor. It improves motor fluctuations related to weaning off effects. The side effects include involuntary muscle movement, confusion, hallucinations, nausea, vom iting, insomnia, headache, urinary retention, cramps, diarrhea, less common constipation, susceptibility to respiratory infection, sweating and dry mouth (Brunton, Chabner, Knollman, 2011). A major concern is reports of death from liver damage in patients taking tolcapone (Tasmar) and is recommended only for patients unable to tolerate other drugs. Entacapone does not appear to have the same effects on the liver and does not require the same monitoring (Katzung, Mastes, Trevor, 2012).Anticholinergic drugs were the first used in the treatment for Parkinsons disease. They are used only for control of tremors in early stages (Brunton, Chabner, Knollman, 2011). Side effects are dry mouth, nausea, urinary retention, blurred vision, and constipation. They can increase heart rate and constipation. They may cause mental problems including memory loss, confusion, and hallucinations (Brunton, Chabner, Knollman, 2011).Amantadine stimulates the release of dopamine and may be used with early mild symptoms. Side effects include swollen ankles, and mottled skin, visual hallucinations. Overdose can cause serious and atrocious toxicity (Brunton, Chabner, Knollman, 2011).ReferencesBrunton, L., Chabner, B., Knollman, B. (2011). Goodman Gilmans The pharmacological basis of therapeutics (12 ed.). McGraw-Hill.Connelly, B., Fox, S. (2012, December). Drug treatments for the neuropsychiatric complications of Parkinsons disease. Retrieved from Medscape.com http//www.medscape.com/viewarticles/777166Katzung, B., Mastes, S., Trevor, A. (2012). Basic clinical pharmacology (12 ed.). McGraw-Hill.Kofman, O. (n.d.). Complications of therapy in Parkinsons disease. CKP-MFC, 12, 87-91. Retrieved from http//www.ncbi.nih.gov/pmc/articles/pmc2153537