Wednesday, December 22, 2010
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What is Parkinson's disease?
Parkinson disease (Parkinson's disease, PD) is a progressive neurodegenerative disorder associated with a loss of dopaminergic nigrostriatal neurons. It is named after James Parkinson, the English physician who described the shaking palsy in 1817.
Parkinson disease is recognized as one of the most common neurological disorders, affecting approximately 1% of individuals older than 60 years. Cardinal features include resting tremor, rigidity, bradykinesia, and postural instability.
Parkinson's disease is a disease that slowly progressive condition resulting from a deficiency in the brain of a chemical called dopamine. Dopamine is one of neurotransmitters in the brain that allow nerve cells to communicate with each other.
People with Parkinson’s disease experience a loss of nerve cells in the part of their brains responsible for controlling voluntary movements. This part of the brain is called the substantia nigra. The nerve cells in the substantia nigra usually produce a chemical called dopamine which helps transmit messages from the brain to the rest of the body via the central nervous system. As these cells are lost, people with Parkinson’s disease experience a loss of dopamine and the messages controlling movement stop being transmitted efficiently.
Over 180 years ago, James Parkinson described a neurodegenerative disease that bears his name.
The term "parkinsonian syndrome" or "parkinsonism" refers to idiopathic Parkinson disease , genetic forms, cases with known environmental causes, and the other atypical forms of parkinsonism, including progressive supranuclear palsy, multiple systems atrophy, and corticobasal degeneration. The latter three are often referred to as "parkinson-plus" syndromes, since each includes features not found in idiopathic Parkinson disease.
The table below shows the classification of Parkinson syndrome.
Distribution of Parkinson Syndromes (PS) | |
Syndrome | % of PS Cases |
Idiopathic PD | 85% |
Neuroleptic-induced | 7%-9% |
MSA | ~2.5% |
PSP | ~1.5% |
Vascular | ~3% |
Known toxins | Very rare |
Recurrent head trauma | Very rare |
From Hughes et al. Neurology. 2001 Nov;57(10 Suppl 3):S34-8.
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DEMOGRAPHICS
Age distribution
D Twelves et al. Systematic review of incidence studies in Parkinson's Disease. Movement Disorders 2003 18: 19-31.
The prevalence rises exponentially with age, after the age of 65. Approximately 0.3% of the general population and 3% of people over the age of 65 have idiopathic Parkinson’s disease diagnosed clinically. About 10% of patients have an onset of disease before the age of 40 - "young-onset" Parkinson's disease
Race
Asians and African blacks have the lowest reported incidence of the disease. To what extent this reflects environmental or genetic differences or differences in ascertainment is not clear, but the prevalence of Lewy bodies in the brains of Nigerians is similar to that of Western populations
Smoking
There is no significant smoking and this disease. It is associated with a lowered risk for the development of Parkinson’s diseaseThe odds ratio of ever having smoked among Parkinson's disease patients compared with the general population was 0.5 about 95%. The implications of this association are not clear.
Rural living
Living in a rural environment has often been associated with an increased risk of idiopathic Parkinson’s disease, possible relating to the influence of pesticide chemicals or consumption of well water. However, the magnitude of this risk in the population of affected individuals is only 10% .
Diet
Diet has been evaluated in many studies to determine if antioxidants present in food protect predisposed patients from the disease. Most of these studies are small or inconclusive. Therefore diet has small percentage that lead to this disease
Genes
A recent large study found high concordance among monozygotic twins when one twin has early-onset disease. Several multigenerational families have been described, with pathologically confirmed Parkinson's disease although in these there are usually atypical features such as rapid rate of progression or a high frequency of dementia. Mutations in 1 exon of the alpha-synuclein gene were recently discovered in a large Italian and 3 smaller Greek families that may have been related and in another exon of the same gene in a German family. However, the disease is rapidly progressive and has a young age onset in these families. Moreover, mutations in this gene have not been found in other families and sporadic IPD. In young-onset Parkinson's disease, the frequency of mutations in the PARKIN gene is high when a first degree family member is also affected. Mutations in this gene were originally described in autosomal recessive Japanese pedigrees with prominent sleep benefit, sensitivity to extrapyramidal side effects of L-DOPA and absence of nigral Lewy bodies in pathologically studied cases. A susceptibility locus on chromosome 2 in familial PD with features more closely resembling sporadic IPD has been described in 6 families with autosomal dominant inheritance with low penetrance .
Causes
Researchers have been unable to identify specific causes of Parkinson's disease but there are many theories regarding factors which may individually or in combination play a role in its development. These include:
· Genetics - Researchers have found gene mutations related to juvenile and early-onset PD. Recently, a new mutation was identified on the LRRK2 gene that is believed to be related to idiopathic PD.
· Family history - According to the National Institute of Neurologic Disorders and Stroke (NINDS) approximately 15-20% of patients with Parkinson's disease have a close relative who exhibited a parkinsonian symptom. Estimates are that the risk for developing PD for family members of a patient with PD is 3-4 times that of the general population. There is a theory that if the right factors come together in an individual with a predisposition based on family history, that individual will develop Parkinson's disease.
· Oxidative damage - Free radicals (unstable molecules) circulating in the brain may cause oxidation resulting in damage to neurons. Some researchers refer to free radicals as endogenous toxins (toxins produced by the body).
· Toxins - Exposure to environmental toxins such as pesticides may cause degeneration of the dopamine producing cells. It is known that exposure to the herbicide Paraquat elevates the risk for PD. Although not clearly understood, it appears that smoking lowers the risk of developing PD.
· Occupational exposure - There is a higher prevalence in certain occupations such as welders, farmers, cabinet makers, and cleaners. In addition, drinking well water and industrial exposure to heavy metals (such as iron, zinc, copper, mercury, and magnesium) also elevate the risk of PD.
· Accelerated aging of neural cells - This theory proposes that for unknown reasons, the normal age-related death of brain cells is accelerated in patients with Parkinson's disease, causing the dopamine-producing cells to "age" and die faster than normal.
Pathophysiology of of Parkinson's Disease
Deep in the brain, below the cerebral cortex, there are interconnected areas of grey matter collectively known as the basal ganglia (literally "basement structures"). These structures include the caudate nucleus, putamen, and globus pallidum internus (GPi) which are involved in controlling voluntary movement. The nerve cells in the substantia nigra (a cluster of cells located next to the basal ganglia) produce dopamine, an essential neurotransmitter that is responsible for transmitting electrical signals between nerve cells. The substantia nigra sends out fibers to the corpus striatum (grey and white bands of tissue in the caudate nucleus and putamen) where the dopamine is released. The transmission of dopamine and its release into the corpus striatum is necessary for smooth, coordinated muscle movement.
Parkinson's disease occurs when there is a disruption of dopamine production which leads to impaired neurotransmission (communication between brain cells) in the basal ganglia. The reduced level of dopamine causes the nerve cells to fire out of control and causes a loss of smooth, controlled muscle activity. The death of dopamine-producing cells in the substantia nigra, resulting in a reduced level of dopamine in the corpus striatum, is the primary pathology in Parkinson's disease. By the time symptoms develop, there is at least a 60% loss of dopamine-producing cells in the substantia nigra and an 80-90% loss of dopamine in the corpus striatum.
There are five major pathways in the brain connecting other brain areas with the basal ganglia. These are known as the
● motor
● oculo-motor
● associative
● limbic
● orbitofrontal circuits
The names indicate the main projection area of each circuit. All of them are affected in PD, and their disruption likely explains much of the symptomatology of the disease since these circuits are involved in a wide variety of functions including movement, attention or learning. Scientifically, the motor circuit has been examined the most intensively.
A particular conceptual model of the motor circuit divides the efferent neurons from the striatum into two different projection systems, known as the direct and indirect pathways.
The direct pathway connects the putamen directly with the globus pallidus pars interna (GPi)- substantia nigra pars reticulata (SNr), and facilitates movement by reducing the output of the basal ganglia. The indirect pathway consists of three links, first a projection from the putamen to the globus pallidus pars externa (GPe); second a projection from GPe to the subthalamic nucleus (STN); and third a projection from STN to SNr.
The indirect pathway, as opposed to the direct, inhibits movement by increasing activity in the basal ganglia. According to this model, dopamine reduction in PD produces functional consequences related to motor symptoms of the disease. The most important consequence is increased activity in the indirect pathway, leading to excessive inhibition of movement and thus to hypokinetic symptoms.
IN NORMAL PERSON
+ and - signs at the point of the arrows indicate respectively whether the pathway is excitatory or inhibitory in effect.
Green arrows refer to excitatory glutamatergic pathways
Red arrows refer to inhibitory GABAergic pathways
Turquoise arrows refer to dopaminergic pathways that are excitatory on the direct pathway and inhibitory on the indirect pathway.
Dis-inhibitory pathways are in effect excitatory on the feedback to the cortex, while dis-dis-inhibitory pathways are inhibitory
There are 4 important signs
1) Shaking at rest (tremor)
2)Rigidity
3)slow in initiate the movement (bradykinesia)
4)Postural instability (occur late in the disease)
1)Tremor at rest
-tremor may appear like rolling or oscillating the hand or arms
-earlier only arm affected but after a few months or years, both arms may be affected
-the tremor is start and stop (on and off)
-it is worsen when under stress
-it is relieve during rest or sleep
-tremor usually involve tongue, lips or chin
2)Rigidity
-rigidity means increase the resistance when someone else want to move your joint such as during flexion or extension of affected limb
-The resistance can be either smooth (lead-pipe) or start and stop (cog wheeling).
3)Bradykinesia
-meaning slow during movement, unplanned movement and decrease size of movement
-also expressed as micrographia (small handwriting), hypomimia (decreased facial expression), decreased blink rate, and hypophonia (soft speech).
4)Postural instability
-this is due to imbalance and loss of reflexes which it is very important to keep in upright positio
Other symptoms
-experience freezing when starting to walk (start-hesitation), during turning, or crossing a threshold such as going through a doorway.
-Flexed postures of neck, trunk, and limbs may occur.
-Altered mental status generally occurs late in PD and affects 15-30% of people with PD.
-Short-term memory and visio-spacial function may be impaired.
-The onset of PD is typically lopsided, with the most common initial finding being an asymmetric rest tremor in one arm. About 20% of people first experience clumsiness in 1 hand.
-Over time, you will notice symptoms related to progressive bradykinesia, rigidity, and problems with walking (called gait disturbances).
The initial symptoms of PD may be nonspecific and include fatigue and depression.
- Some people experience a subtle decrease in dexterity and may notice a lack of coordination with activities such as golf, dressing, or climbing stairs.
- Some people complain of aching or tightness in the calf or shoulder region.
- The first affected arm may not swing fully when walking, and the foot on the same side may scrape the floor.
- Over time, posture becomes progressively flexed and your stride becomes shorter leading to a shuffling gait.
- Decreased swallowing may lead to excess saliva and ultimately drooling.
- Symptoms of problems with your involuntary nervous system are common and may include constipation, sweating abnormalities, and sexual dysfunction.
- Sleep disturbances are also common.
Several other conditions can mimic the neurologic symptoms of Parkinson's disease and must be excluded before the diagnosis is established. It is important to differentiate between true idiopathic (unknown cause) Parkinson's disease and parkinsonian symptoms that develop secondary to some underlying condition or medication.
The three most common categories of conditions that may be mistaken for Parkinson's disease include medication-induced parkinsonism, Parkinson-plus syndrome, and essential tremor.
- Medication-induced parkinsonism - Certain medications may either cause parkinsonian symptoms or exacerbate the severity of symptoms in the individual diagnosed with Parkinson's disease. It is important to determine whether symptoms are related to medications, in which case discontinuing the medications can result in cessation of symptoms over time, or to actual Parkinson's disease. The most common medications that can induce parkinsonian symptoms include:
- antipsychotics - Examples include haloperidol, thioridazine (Mellaril), risperidone (Risperdal), lithium (Eskalith), chlorpromazine (Thorazine), and olanzapine (Zyprexa). Parkinsonian side-effects of these medications can last 1-2 years after stopping the medications.
- antiemetics - These drugs are used to treat nausea and vomiting. Examples include prochlorperazine (Compazine) and metoclopramide (Reglan).
- antihypertensives - These drugs are used to treat high blood pressure. Examples include methyldopa (Aldomet) and reserpine (Harmonyl).
- antianginals - Heart medications used to treat angina or chest pain such as dilitiazem (Cardizem).
- antineoplastics - These drugs are used to treat various types of cancers.
- Parkinson-Plus syndromes - This is a group of disorders which presents with parkinsonism in association with other distinct clinical features, such as autonomic disturbances (Shy-Drager syndrome) or ataxia (multi-system atrophy). These syndromes show poor or short-lived therapeutic response to Parkinson's disease medications and include symptoms or patterns of symptoms that do not appear in Parkinson's disease such as:
- signs of dementia early after onset of symptoms
- incidences of falling soon after onset of symptoms
- feet set wide apart while walking
- abnormal eye movements
- symmetric (bilateral) signs of parkinsonism
- severe disability within five years of onset of symptoms
- Essential tremor - tremors that are similar to those of PD but are identified based on the following characteristics:
- typically bilateral
- often accompanied by head tremor or tremulous voice
- handwriting is typically large and tremulous
- signs of bradykinesia and rigidity are absent
Other conditions which should be ruled out when a patient presents with Parkinson-like symptoms include:
- Multi-infarct disease (multiple small strokes), also called arteriosclerotic or vascular parkinsonism.
- Other degenerative brain diseases such as Alzheimer's disease (destroys memory and cognition) and Huntington's disease (causes uncontrolled movements and cognitive loss). Parkinsonian features occur in many patients with Alzheimer's disease and other dementias.
- Dementia with Lewy bodies.
- Normal Pressure Hydrocephalus which is an excessive accumulation of cerebrospinal fluid in the cerebral ventricles of the brain.
- Brain tumors.
- Exposure to toxins such as manganese dust, carbon disulfide and carbon monoxide
- Abuse of drugs containing MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), often found in heroin, which was found to cause a permanent form of Parkinson's. This finding in the 1980's actually heralded an important breakthrough in Parkinson's disease research as scientists could induce a simulated Parkinson's disease in animals for further study.
Pharmacological
1)Dopaminergic agents
- To restore dopamine levels or acticvity
Eg,Dopamine precursor, Cathecol-O-methyl transferase(COMT)inhibitor, Dopamine agonist, Amantadine, Monoamine oxidase inhibitor
2) Antimuscaranic agents
- · In Parkinson disease,reduced dopamine levels cause a relative cholinergic activity.Antimuscarinic is used to restore the balance
Dopamine precursor
Levodopa and carbidopa combined (Sinemet®) is the mainstay of Parkinson's therapy. Levodopa is rapidly converted into dopamine by the enzyme dopa decarboxylase (DDC), which is present in the central and peripheral nervous systems. Much of levodopa is metabolized before it reaches the brain.
Carbidopa blocks the metabolism of levodopa in the liver, decreasing nausea and increasing the amount of levodopa that reaches the brain. Levodopa is most effective in treating bradykinesia and rigidity, less effective in reducing tremor, and often ineffective in relieving problems with balance.
Side effects include nausea, especially early in treatment, low blood pressure (hypotension), and abnormal movements (dyskinesias). Slow dosage adjustment and taking medication with food can reduce these effects and using the lowest effective dose may prevent or delay the appearance of motor dysfunction. Levodopa can become ineffective over time.
Depression, confusion, and visual hallucinations also may occur with these medications, especially in the elderly.
Dopamine Agonists
Dopamine agonists mimic dopamine's function in the brain. They are used primarily as adjuncts to levodopa/carbidopa therapy. In some cases, these drugs are used as monotherapy, but they are generally less effective in controlling symptoms.
Side effects are similar to those produced by levodopa and include nausea, sleepiness, dizziness, and headache.
Dopamine agonists include the following:
- Bromocriptine (Parlodel®)
- Pramipexole (Mirapex®)
- Ropinirole (Requip®)
Amantadine (Symmetryl®) is an antiviral drug with dopamine agonist properties. It increases the release of dopamine and is often used to treat early-stage Parkinson's disease, either alone, with an anticholinergic drug, or with levodopa. Generally, it loses its effectiveness within 3 to 4 months.
Side effects of amantadine include mottling of the skin, edema, confusion, blurred vision, insomnia, and anxiety.
MAO-B Inhibitors
Dopamine is oxidized by monoamine oxidase B (MAO-B). Rasagiline (Azilect®) and selegiline (Carbex®) inhibit MAO-B, increasing the amount of available dopamine in the brain. MAO-B inhibitors boost the effects of levodopa.
Side effects may include nausea, dizziness, abdominal pain, confusion, hallucinations, and dry mouth.
MAO-B inhibitors are contraindicated for patients taking tricyclic antidepressants (e.g., Pamelor®) , SSRIs (e.g., Prozac®), or meperidine (Demerol®) and other opiates. Patients who are taking MAO-B inhibitors must follow their physician's recommendations regarding a number of dietary precautions.
COMT (catechol-O-methyl transferase) Inhibitors
These medications augment levodopa therapy by inhibiting the COMT enzyme, which breaks down dopamine after it is released in the brain. These drugs are only effective when used with levodopa.
COMT inhibitors include entacapone (Comtan®) and tolcapone (Tasmar®).
Side effects of these medications include vivid dreams, visual hallucinations, nausea, sleep disturbances, daytime drowsiness, headache, and dyskinesias.
Carbidopa, levodopa, and entacapone are combined in Stalevo®, which is available in flexible dosing and indicated for patients who experience a reduced effectiveness of their PD medication.
Common side effects of Stalevo® include dyskinesias and nausea, which may be controlled by altering the dosing schedule.
Other side effects include the following:
- Abdominal pain
- Constipation
- Diarrhea
- Discolored urine
- Dizziness
- Fatigue
- Hallucinations
- Hyperkinesias
Anticholinergics
Anticholinergics reduce the relative overactivity of the neurotransmitter acetylcholine to balance the diminished dopamine activity. This class of drugs is most effective in the control of tremor, and they are used as adjuncts to levodopa.
These drugs include the following:
- Benztropine mesylate (Cogentine®)
- Biperiden (Akineton®)
- Diphenhydramine (Benadryl®)
- Trihyxyphenidyl (Artane®)
Side effects associated with anticholinergic drugs include dry mouth, blurred vision, constipation, and urinary retention. In higher doses, these medications may impair memory.
Non-pharmalogical
Deep brain stimulation.
In deep brain stimulation, surgeons implant electrodes into a specific area of your brain. The electrodes are connected to a generator that sends electrical pulses to your brain and may help control your Parkinson's disease symptoms. Surgery may involve risks, and your surgeon will work with you to determine if surgery is the most appropriate treatment for you.
Physical therapy
Goals of physical therapy include maintaining or increasing activity levels, decreasing rigidity and bradykinesia, optimizing gait, and improving balance and motor coordination. Features of the PT program may include:
- Regular exercise, such as walking (1+ miles/day), swimming, golf, or dancing, depending on the patient's preferences and abilities
- Stretching and strengthening
- Exaggerated or patterned movements, such as high stepping and weight shifting
- Mobility aids, orthotics (such as braces or splints)
- Training in transfer techniques
- Training in techniques to improve posture and walking
Occupational therapy
Goals of occupational therapy include maximizing fine motor coordination, especially of the upper extremities, reducing energy expenditure, increasing safety and independence, and improved efficiency of activities of daily living. Features of the OT program may include:
- Use of orthoses and adaptive equipment
- Home and workplace modification, improving accessibility, and removing obstructions
- Adaptation and simplification of utensils, toileting articles, beds, etc
Speech and swallowing
Low voice volume (hypophonia) often occurs in PD. Several PD-specific voice training programs have been developed, which share an emphasis on consciously increasing voice volume as a key strategy. Other features may include modification of speech patterns such as use of shorter sentences, breathing exercises, and range-of-motion exercises for the muscles of speech.
Drooling (sialorrhea) can be a common feature of advanced PD. The origin of the problem is not in increased saliva production, but reduced spontaneity of swallowing. Awareness of the problem, and consciously swallowing more often, may be effective. If not, treatments may include a small dose of an anticholinergic medication under the tongue, or injection of botulinum toxin into the salivary glands to temporarily paralyze them. Both of these reduce saliva production.
Management of swallowing difficulties may include instruction to take smaller bites, to completely empty the mouth before taking the next bite, and eating softer foods.
Sexuality
Sexual dysfunction affects a large proportion of patients with PD and their spouses. Difficulties include erectile dysfunction in males, vaginal dryness, and loss of libido. Hypersexuality from levodopa and dopamine agonists also occurs. Many PD patients are reluctant to talk about these issues with their doctor, and may not connect the symptom to the disease at all. There are useful treatments, both medical and nonmedical, for many of these problems. Patients should always have a thorough urological or gynecological evaluation to rule out non-PD related problems. Sildenafil (Viagra®) has been shown to be safe and effective in men in PD to treat erectile dysfunction.
Driving
PD patients tend to do worse than controls on tests of driving safety, because of increased reaction times and movement times caused by PD. Vehicular control skills are generally well preserved, but attention to safety landmarks declines. Decline in performance seems to be related to a worsening of motor abilities. Patients tend not to be good judges of their loss of driving safety, and family members may need to intervene. A good way to determine driving capability is to have the patient undergo a driving examination at a rehabilitation facility.
Constipation
A good bowel regimen can greatly reduce constipation. Increased fluid intake, a diet rich in vegetables and fruits, use of stool softeners, and increased dietary and supplemental fiber are just some interventions that can help. Working with one's physician and/or a gastroenterologist is the approach to take.
-PD is not considered to be a fatal disease by itself, but it progresses with time. The average life expectancy of a PD patient is generally lower than for people who do not have the disease. Parkinson's disease is rarely the direct cause of death; more commonly, people die from complications associated with PD rather than from the disease itself.
- In the late stages of the disease, PD may cause complications such as choking, pneumonia, and falls that can lead to death.
-With appropriate treatment, most people with PD can live productive lives for many years after diagnosis. There are some indications that Parkinson's disease acquires resistance to drug treatment by evolving into a Parkinson-plus disorder, usually Lewy Body Dementia, although transitions to Progressive Supranuclear Palsy or Multiple System Atrophy are not unknown.
Research scientists have not yet discovered a way to prevent Parkinson's disease.
One of the theories as to the cause of Parkinson's disease is that free radicals may contribute to nerve cell death, thereby leading to Parkinson's disease. Free radicals are unstable and potentially damaging molecules generated by normal chemical reactions in the body.
Normally, free radical damage is kept under control by antioxidants, chemicals that protect cells from this damage. Many naturally occurring antioxidants or substances are thought to have antioxidant properties. Some of these include:
Vitamin E
- Works along with vitamin C to slow the progression of Parkinson's disease and postpone the need for drug therapy. These antioxidants are free radical scavengers that work to protect the brain from free radical damage. Large amounts of both vitamin C & E are recommended for the disease. These amounts can not be gotten from food sources so must be gotten through supplementation.
Vitamin C
- An antioxidant that may slow the progression of the disease and postpone the need for drug therapy.In a 1979 study of patients with early Parkinson's disease who were given 3,000 mg of Vitamin C and 3,200 IU's of Vitamin E daily, progression of the disease was slowed for up to three years.
B Vitamins
- Extremely important in brain function and enzyme activity.
Vitamin B5
- Aids in speeding messages from one nerve cell to another.
Vitamin B3
- Improves brain circulation. Caution: do not take B3 (niacin) if you have a liver disorder,gout or high blood pressure.
Vitamin B6
- Brain dopamine production depends on adequate supplies of this vitamin. Caution: Do not take this supplement if you are taking a levodopa preparation.
Coenzyme Q10(CoQ10)
- Is a powerful antioxidant and also increases oxygenation of cells and is involved in the generation of cellular energy.
Ginkgo biloba
- Over time improves circulation and delivery of oxygen to improve brain function, minimize leg cramps and tremors, and increase a feeling of well-being.
Selenium
- A powerful antioxidant.
Calcium
- Works with magnesium. Needed for nerve impulse transmission.
Magnesium
- Works with calcium. Needed for nerve impulse transmission.
Antioxidant versus free radicals Nerve cells are the main source of Parkinson's disease. Since their destruction can be blamed on free radicals, there is good reason for those looking for preventive ways to counter the free radicals which are potentially damaging molecules that enter our bodies through unnoticed sources. Antioxidants are known to keep these free radicals away from the body in order to minimize the damage caused to nerve cells. Preventive Medicine Scientists believe that a dose of antioxidants can have good reason to predict the destruction of the molecules that cause damage to nerve cells. Parkinson's syndrome comes by when the destruction of nerve cells has reached a situation when the person is virtually brain-dead. This situation is a gradual development that is unfelt when the destruction begins and strikes only when the disease has taken over one's mental faculties. Otherwise except for a few visible initial symptoms it is hard to tell. Caffeine is also a food source of antioxidants and helps in keeping free radicals away. besides that,there are other certain ways that you can take,such as :
Make sure that three-fourths of your dietary intake comes from raw food sources (seeds, nuts, grains, raw milk for example).
Since the amino acid L-phenylalanine may help alleviate the symptoms of Parkinson's disease include foods such as almonds, Brazil nuts, fish, pecans, pumpkin, sesame seeds, lima beans, chickpeas, and lentils in your diet.
Limit your the amount of protein in your diet to seven grams per day. Instead of meat and poultry eat other sources of protein such as barley, tofu, yogurt, beans, lentils, etc. If you are taking levodopa concentrate your protein consumption in the evenings as some of the amino acids in these foods may prevent the levodopa from reaching the brain.
B6 may interfere with the potency of this drug so if you are on levodopa monitor your intake of B6 foods such as bananas, fish, beef, liver, oatmeal, peanuts, potatoes, and whole grains. Do not take supplemental B6 if you must take levodopa.
If you have Parkinson's disease take seven grams of carbohydrates to one gram of protein.
This bean contains dopamine and eating more than 1/2 cup of these beans along with a daily dose of the drug levodopa can cause symptoms of a dopamine overdose. The fava bean is primarily used in Mediterranean and Middle Eastern dishes.
Physical therapy and daily moderate exercise can help maintain normal muscle tone and function. Choose exercises such as walking, jogging, stretching, swimming, etc. that get the muscles moving and the heart pumping.
Pesticides, cleaners, and other chemicals routinely used in household cleaning, and in agriculture and lawn care have been linked to Parkinson's disease. Although exposure may be very minimal, even small amounts can cause problems in children, elderly, and people already ill. When these substances are avoided there is a better chance that symptoms will improve.Research on possible preventionExtensive research is on regarding finding a way to prevent Parkinson's disease. According to medical opinion it is quite a challenge and tests involve a number of complicated procedures to filter out, find a pattern or anything that can help doctors find a uniform way to prevent it in all human beings. One of the advanced techniques called the positron emission tomography (PET) is expected to expand the scientists' findings at a faster rate and allow scientists to come to a stronger position in finding a prevention method. Positron emission tomography (PET) scanning may lead to important advances in our knowledge about Parkinson's disease. PET scans of the brain produce pictures of chemical changes as they occur in the living brain. Using PET, research scientists can study the brain's dopamine receptors (the sites on nerve cells that bind with dopamine) to determine if the loss of dopamine activity follows or precedes degeneration of the neurons that make this chemical. This information could help Parkinson's disease research scientists better understand the disease process and may potentially lead to improved treatments and eventually prevention of Parkinson's disease. |
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