Parkinson's disease by daniel tarsy

Parkinson's DiseaseBy Daniel Tarsy

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Contents
Background
Epidemiology of Parkinson’s disease
Pathology of Parkinson’s disease
Clinical features of Parkinson’s disease
Differential diagnosis of Parkinson’s disease
Treatment of Parkinson’s disease
Education and support
Diet and lifestyle
Exercise and physical/speech therapy
Treatment with medications
Diet and lifestyle
Newly diagnosed patients often inquire about the amount of protein they should consume after reading that protein may interfere with gastrointestinal absorption of levodopa. This is actually more important in patients with advanced PD who experience motor fluctuations in response to levodopa. Certain large amino acids derived from protein may reduce levodopa absorption in the intestine and transport from the blood into the brain, thereby potentially interfering with its clinical efficacy. In such cases, levodopa should not be taken less than 30 minutes before or 60 minutes after meals. A protein redistribution diet which limits most protein intake to an evening meal is only necessary in occasional patients.
Nausea or vomiting after levodopa or dopamine agonists is alleviated by taking these medications during or following meals. In patients with early PD and a stable medication response this will not compromise therapeutic efficacy.
Large, high fat meals which slow gastric emptying may interfere with medication absorption and should be avoided.
Patients should consume sufficient fiber and fluid to prevent constipation, which is frequently associated with PD.
Weight loss is sometimes associated with PD or treatment with levodopa. Elderly patients are at greater risk for poor nutrition and weight loss. Recognition and management of this problem is important to avoid loss of bone and muscle mass. Dietary calorie and vitamin supplements may be indicated. In postmenopausal women, calcium supplements and medications to prevent osteoporosis are recommended.
Coenzyme Q10 enhances mitochondrial function. PD is associated with reduced platelet mitochondrial and serum coenzyme Q10 activity. In clinical trials in PD patients, coenzyme Q10 , 1200 mg/day has been proven safe and has been associated with slightly less progressive motor disability, compared with placebo.
Large doses of vitamin E do not slow progression of PD.
Large doses of vitamin B6 (pyridoxine) interfere with L-dopa metabolism and should be avoided in the currently very rare patient who takes L-dopa without carbidopa, a peripheral dopa decarboxylase inhibitor. This is not a practical concern when levodopa is combined with carbidopa.
Patients should be encouraged to assume a positive attitude, remain professionally and socially active, and assume a generally healthy lifestyle with emphasis on regular exercise and good general nutrition.
Exercise and physical/speech therapy
Regular exercise promotes a feeling of physical and mental well-being, important in the management of PD. Although exercise does not slow progression of PD symptoms it can prevent or alleviate orthopedic effects of akinesia, rigidity and flexed posture such as shoulder, hip, and back pain and has also been shown to improve some motor functions. Supervised training including cardiovascular fitness exercise, muscle stretching and strengthening, and balance training have been found to be useful in some short- and long-term studies. Occupational therapy to assess home safety, supervise use of walking aids, and provide instruction concerning sensory cuing plays a greater role in more advanced PD associated with gait and balance deficits. Tai Chi may be useful for balance training. Controlled trials have shown that acupuncture does not improve PD motor symptoms.
Loss of voice volume often becomes a significant problem in more advanced PD. Patients should be encouraged to be more consciously aware of their voice output and concentrate on projecting more loudly than they think is necessary. Lee Silverman voice therapy is a special technique which emphasizes increased volume production and has been demonstrated to be helpful in PD. More information regarding this may be obtained at www.lsvt.org
Treatment with medications
Treatment with medications is dictated by whether one is dealing with PD, atypical parkinsonism, or secondary parkinsonism. Antiparkinson medications are highly effective in PD but relatively ineffective in most patients with atypical parkinsonism. Secondary parkinsonism such as drug-induced parkinsonism, vascular parkinsonism, and normal pressure hydrocephalus are treated according to underlying causes. However, although there are established criteria for diagnosis of PD, they are not foolproof and a trial of antiparkinson medications is warranted in all patients with parkinsonism. However, patients with atypical parkinsonism are more liable to experience medication side effects.
The first consideration is when to initiate medication. Currently available medications are given to improve symptoms; they have no proven ability to slow progression of the underlying disease. Therefore, drug treatment should be initiated only when symptoms begin to interfere with routine activities of daily living, employment, lifestyle, or physical appearance. Patient age and level of physical and professional productivity are also important considerations. The decision on when to begin treatment and which medications to use should be considered jointly by the physician, patient, and patient’s family. Active research is ongoing to identify disease modifying or neuroprotective drugs to slow disease progression. To date no proven agents have emerged from the many medications which have been screened. The following groups of medications are for treatment of only the motor symptoms of PD, which are tremor, bradykinesia (slowness), and rigidity and are listed in the table. They are listed approximately in the order in which they are often introduced into treatment but it should be realized that different patients may require different medications and that there is no firm or absolute rule for the order of using these medications.
Treatment of non-motor PD symptoms In addition to the well known motor symptoms of PD, non-motor symptoms are currently attracting increased interest and concern.
Sleep disorders are extremely common in PD; they affect 90% of patients. Poor night-time sleep and excessive daytime drowsiness are common. Possible causes include sedative effects of some antiparkinson medications such as the dopamine agonists, poor sleep hygiene, and poor sleep at night due to obstructive sleep apnea, restless legs syndrome, REM sleep behavior disorder, depression, anxiety, nocturnal stiffness, and fragmented sleep of unknown cause. Proper treatment relies on identifying the cause in a particular patient. REM sleep behavior disorder commonly precedes the onset of motor symptoms and is relieved by clonazepam taken before sleep. Sudden onset of sleep while driving (“sleep attacks”) have also been described, particularly in patients taking dopamine agonists although this is not necessarily associated with specific antiparkinson drugs.
Fatigue is a related problem but more common in advanced PD. Treatable causes include poor sleep, depression, and bradykinesia but it may also be an independent symptom. Empiric treatment with methylphenidate, modafinil, or selegiline may be considered but the response to these is usually disappointing.
Depression and anxiety often appear for the first time in early PD and may even be presenting symptoms. Treatment of these is important and will help patients to tolerate otherwise relatively mild motor symptoms. SSRI antidepressants are effective for both depression and anxiety and are usually well tolerated in patients with PD. Patients with PD may also exhibit apathy, with lack of motivation and emotional reactivity, in the absence of true depression. When severe enough to warrant pharmacologic intervention, this complaint may be responsive to methylphenidate.
Psychosis and visual hallucinations occur in more advanced PD where they are usually side effects of antiparkinson drugs. They are managed by adjustment of medications or introduction of antipsychotic medications that do not exacerbate motor symptoms of PD, such as clozapine or quetiapine. Other antipsychotic drugs, all of which interfere with dopamine transmission, should be avoided in PD. This does not include antidepressants and anti-anxiety medications which may be safely used in PD and do not exacerbate parkinsonism. Cognitive impairment of varying severity occurs in up to one-third of patients with PD. More severe cognitive impairment or dementia must be distinguished from other causes of dementia in older patients such as Alzheimer’s disease, cerebrovascular disease, normal pressure hydrocephalus, hypothyroidism, and vitamin deficiency. When due to PD the pattern of deficits differs from Alzheimer’s disease in that frontal lobe functions such as multitasking, judgement, and personality are affected more than recent memory, language function, and spatial orientation. Treatment with cholinesterase inhibitors such as donepezil, galantamine, rivastigmine, or memantine is recommended, and are often more effective in PD than in Alzheimer’s disease. The presence of psychosis, visual hallucinations, or dementia in early PD raises the possibility of dementia with Lewy bodies.Autonomic symptoms are not usually present in early PD, by contrast with multiple system atrophy, where they often appear before or together with onset of motor symptoms and are a major cause of difficulty. Nonetheless, proper attention should be paid to management of constipation, low blood pressure with standing (orthostatic hypotension), urinary frequency, and impotence. Constipation is managed with high fiber diet, stool softeners, and laxatives. Bladder symptoms usually require consultation with a urologist to identify the specific pattern of bladder dysfunction, to guide medication treatment, and to exclude other causes.
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