HOW IS PARKINSON’S DISEASE TREATED
Are there treatment options for Parkinson’s?
Are they cost effective?
Or cost prohibitive?
Currently, there is no cure for Parkinson’s disease. Instead, therapy is directed at treating the symptoms that are most bothersome to an individual with Parkinson’s disease. For this reason, there is no standard or “best” treatment for Parkinson’s disease that applies to every patient. Treatment approaches include medication and surgical therapy. Other treatment approaches include general lifestyle modifications (rest and exercise), physical therapy, support groups, occupational therapy and speech therapy. In this section, you will become more familiar with the different types of medications commonly prescribed for PD, other alternative therapies, and surgical treatment options. Recent studies have implicated that a treatment is better than no treatment. In other words, medications and therapies may modify the progression of Parkinson’s disease.
Treatment for Parkinson’s Disease (PD), due to its chronic nature, requires broad-based management including patient and family education, support group services, general wellness maintenance, exercise, and nutrition. At present, there is no cure for PD, but medications or surgery can provide relief from the symptoms. There are so many forms of therapy (or treatment) and medications for Parkinson’s, that I could make a small handbook from all the material available. This is but a brief look to some treatments/therapies available and not meant to slight some others.
While many medications treat Parkinson’s, none actually reverse the effects of the disease or cure it. Furthermore, the gold standard treatment varies with the disease state. People with Parkinson’s therefore often must take a variety of medications to manage the disease’s symptoms. Several medications currently in development seek to better address motor fluctuations and non-motor symptoms of PD. However, none are yet on the market with specific approval to treat Parkinson’s.
The main families of drugs useful for treating motor symptoms are Levodopa (L-DOPA), dopamine agonists and MAO-B inhibitors. The most commonly used treatment approach varies depending on the disease stage. Two phases are usually distinguished: an initial phase in which the individual with PD has already developed some disability for which he needs pharmacological treatment, and a second stage in which the patient develops motor complications related to levodopa usage. Treatment in the initial state aims to attain an optimal tradeoff between good management of symptoms and side-effects resulting from enhancement of dopaminergic function. The start of L-DOPA treatment may be delayed by using other medications such as MAO-B inhibitors and dopamine agonists, in the hope of causing the onset of dyskinesia’s to be retarded. In the second stage the aim is to reduce symptoms while controlling fluctuations of the response to medication. Sudden withdrawals from medication, and overuse by some patients, also have to be controlled. When medications are not enough to control symptoms, surgical techniques such as deep brain stimulation can relieve the associated movement disorders. L-DOPA has been the most widely used treatment for over 30 years. L-DOPA is transformed into dopamine in the dopaminergic neurons by dopa-decarboxylase. Since motor symptoms are produced by a lack of dopamine in the substantia nigra the administration of L-DOPA temporarily diminishes the motor symptomatology.
There are some indications that other drugs may be useful as treatment of motor symptoms in early and late PD, but since quality of evidence on efficacy is reduced they are not first choice treatments. In addition to motor PD is accompanied by an ample range of different symptoms. Different compounds are used to improve some of these problems. A preliminary study indicates that taking the drug Aricept may help prevent falls in people with Parkinson’s. Donepezil boosts levels of the neurotransmitter acetylcholine, and is currently an approved therapy for the cognitive symptoms of Alzheimer’s disease. In the study, participants taking donepezil experienced falls half as often as those taking a placebo, and those who previously fell the most showed the most improvement.
Treating PD with surgery was once a common practice. But after the discovery of levodopa, surgery was restricted to only a few cases. Studies in the past few decades have led to great improvements in surgical techniques, and surgery is again being used in people with advanced PD for whom drug therapy is no longer sufficient. Less than 10% of PD sufferers qualify as suitable candidates for a surgical response. There are three different mechanisms of surgical response for PD: ablative surgery, (the irreversible burning or freezing of brain tissue), stimulation surgery or deep brain stimulation (DBS), and transplantation or restorative surgery.
Neuroablative Lesion surgery (NAS) locates and destroys, by heat, the parts of the brain that are associated with producing Parkinsonian neurological symptoms. The procedures generally involve a thalamotomy and/or pallidotomy. Because it is difficult to accurately measure the amount of tissue to be destroyed, it is not uncommon for tremors to persist through multiple courses of surgery since tissue is irreversibly damaged and removed and it is safer to test smaller areas of tissue to prevent serious complications, such as a stroke or paralysis. This method has been generally replaced by deep brain surgery.
Deep brain stimulation (DBS) is presently the most used method of surgical treatment because it does not destroy brain tissue, it is reversible, and it can be tailored to each individual at their particular stage of disease. DBS employs three hardware components: a neuro-stimulator, also called an implanted pulse generator (IPG), which generates electrical impulses used to modulate neural activity, a lead wire which directs the impulses to a number of metallic electrodes towards the tip of the lead near the stimulation target, and an extension wire that connects the lead to the IPG. The IPG, which is battery-powered and encased in titanium, is traditionally implanted under the collarbone, and is connected by the subcutaneous extension to the lead, which extends from outside the skull under the scalp down into the brain to the target of stimulation. The entire three component system is sometimes referred to as a brain pacemaker, as the system operates on many of the same principles as medical cardiac pacing.
The pre-operative targeting of proper implantation sites can be accomplished via the indirect and direct methods.
Electrophysial functional mapping (EFM), a tool utilized in both methods in order to verify the target nuclei, has come under scrutiny due to its associated risks of hemorrhages, dysarthria or tetanic contractions. DBS is recommended to PD patients without important neuropsychiatric contraindications who suffer motor fluctuations and tremor badly controlled by medication, or to those who are intolerant to medication. DBS is effective in suppressing symptoms of PD, especially tremor. A recent clinical study led to recommendations on identifying which Parkinson’s patients are most likely to benefit from DBS.
Muscles and nerves that control the digestive process may be affected by PD, therefore, it is common to experience constipation and gastroparesis (food remaining in the stomach for a longer period of time than normal). A balanced diet is recommended to help improve digestion. Diet should include high-fiber foods and plenty of water. Levodopa and proteins use the same transportation system in the intestine and the blood–brain barrier, competing between them for access. When taken together the consequences of such competition is a reduced effectiveness of the drug. Therefore when levodopa is introduced excessive proteins are discouraged, while in advanced stages additional intake of low-protein products such as bread or pasta is recommended for similar reasons. To minimize interaction with proteins levodopa is recommended to be taken 30 minutes before meals. At the same time, regimens for PD restrict proteins during breakfast and lunch and are usually taken at dinner.
There is partial evidence that speech or mobility problems can improve with rehabilitation although studies are scarce and of low quality. Regular physical exercise and/or therapy can be beneficial to maintain and improve mobility, flexibility, strength, gait speed, and quality of life. Exercise may also improve constipation. Exercise interventions have been shown to benefit patients with Parkinson’s disease in regards to physical functioning, health-related quality of life, balance and fall risk. In a review of 14 studies examining the effects of exercise on persons with Parkinson’s disease, no adverse events or side-effects occurred following any of the exercise interventions. There are five proposed mechanisms by which exercise enhances neuroplasticity. 1) intensive activity maximizes synaptic plasticity; 2) complex activities promote greater structural adaptation; 3) activities that are rewarding increase dopamine levels and therefore promote learning/relearning; 4) dopaminergic neurons are highly responsive to exercise and inactivity (“use it or lose it”); 5) where exercise is introduced at an early stage of the disease, progression can be slowed. Occupational therapy (OT) aims to promote health and quality of life by helping people with the disease to participate in as many activities of their daily living as possible. There have been few studies on the effectiveness of OT and their quality is poor, although there is some indication that it may improve motor skills and quality of life for the duration of the therapy.
Palliative care is often required in the final stages of the disease, often when dopaminergic treatments have become ineffective. The aim of palliative care is to achieve the maximum quality of life for the person with the disease and those surrounding him or her. Some central issues of palliative are; caring for patients at home while adequate care can be given there; reducing or withdrawing dopaminergic drug intake to reduce drug side effects and complications; preventing pressure ulcers by management of pressure areas of inactive patients; facilitating the patient’s end of life decisions for the patient as well as involved friends and relatives.
Present treatments of Parkinson disease provide satisfactory disease control for most early stages patients. However, present gold standard treatment of Parkinson disease using Levodopa, is associated with motor complications, and does not prevent disease progression. More effective and long term treatment of Parkinson disease are urgently needed to control the progression of the disease. In vivo gene therapy is a new approach for treatment of Parkinson disease. The use of somatic-cell gene transfer to alter gene expression in brain neurochemical systems is a novel alternative conventional treatment.
Gene therapy is currently under investigation. It involves the use of a non-infectious virus to shuttle a gene into a part of the brain. The gene used leads to the production of an enzyme which helps to manage PD symptoms or protects the brain from further damage.
One of the gene therapy based approach involves gene delivery of neurturin and gilial-cell-derived nuerotrophic factor (GDNF) to the putamen in patients with advanced Parkinson’s disease. GDNF protects dopamine neurons in vitro and animal models of parkinsonism; neurturin is a structural and functional analogue of GDNF that protected dopamine neuron in animal model of the disease. Despite the open-label trials have shown benefits of continuous infusion of GDNF, the results were not confirmed in double-blind studies. This may be due to the distribution factor; the trophic factor was not distributed sufficiently throughout the target place.
Investigations on neuro-protection are at the forefront of PD research. Currently, there are no proven neuro-protective agents or treatments available for Parkinson Disease. While still theoretical, neuro-protective therapy is based on the idea that certain neurons that produces dopamine and are susceptible to premature degeneration and cell death can be protected by the introduction of neuro-protective pharmaceuticals. This protection can occur before any symptoms manifest based on genetic risk, and also during early or late-stage PD when other treatments have ceased their impact due to the progression of the disease. Accordingly, neuro-protective therapy seeks to delay the introduction of levodopa.
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