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Overview |
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Definition |
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Parkinson's disease is a chronic, progressive disorder of the central nervous
system (CNS) characterized by gait difficulty, postural instability, rigidity,
and tremor due to the loss of dopaminergic neurons in the substantia nigra,
which leads to dopamine depletion. Parkinson's disease is the most common form
of parkinsonism and is classified as idiopathic or primary. Rate of occurrence
is higher in later life (age 50 and above; average age of onset, 60); 5% to 10%
of patients are under the age of 40, and 5% of all patients have a familial
history of the disease. The disease affects men and women equally. The other
major subtypes of parkinsonism are listed below.
- Postencephalitic parkinsonism
- Drug-induced parkinsonism
- Striatonigral degeneration
- Arteriosclerotic parkinsonism
- Toxin-induced parkinsonism
- Parkinsonism-dementia complex of
Guam
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Etiology |
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A combination of oxidative damage, environmental toxins, genetic
predisposition, and accelerated aging have been identified as the most likely
etiologic factors. True etiology is unknown. |
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Risk Factors |
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- Environmental factors or toxicants (such as pesticides and
viruses)
- Family history of parkinsonism (due to a mutant alpha synuclein gene)
- Endogenous neurochemicals (free radicals)
- Normal age-related wearing away of dopamine-producing
neurons
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Signs and Symptoms |
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- Tremor, most present unilaterally; increases with stress and improves
with rest
- Rigidity
- Bradykinesia; creates gait disturbance and postural
abnormalities
- Poor balance
- Walking problems
- Blepharospasm
Secondary symptoms may include the following.
- Memory loss
- Sleep disturbances
- Stooped posture
- Ocular abnormalities
- Constipation or incontinence through dysautonomia
- Dementia in 20% of patients
- Speech, breathing, and swallowing
problems
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Differential
Diagnosis |
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- Essential (benign, familial) tremor
- Shy–Drager syndrome (multiple system
atrophy)
- Progressive supranuclear palsy
- Wilson's disease
- Huntington's disease
- Hallervorden–Spatz syndrome
- Alzheimer's disease
- Creutzfeldt–Jakob disease
- Depression
- Diffuse Lewy body disease
- Olivopontocerebellar atrophy
- Post-traumatic
encephalopathy
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Diagnosis |
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Physical Examination |
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Patient exhibits consistent presence of tremors and one or more of the other
physical symptoms, including relatively immobile face with widened palpebral
fissures, infrequent blinking, and fixity of facial expression; seborrhea of the
scalp and face is common. |
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Laboratory Tests |
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There are no objective tests for Parkinson's disease. |
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Pathology/Pathophysiology |
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The presence of Lewy bodies are considered the hallmark of the disease but
can be identified only at autopsy. |
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Imaging |
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Neuroimaging techniques hold promise in providing markers for the disease.
PET can quantify activity of the dopamine system by measuring activity of the
dopamine transporter (DAT). MRI can be used to rule out a mass lesion in the
brain, multiple but clinically silent cerebral infarcts, or normal pressure
hydrocephalus. |
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Other Diagnostic
Procedures |
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- As this is a neurodegenerative disease that is treatable, a
therapeutic response to levodopa should confirm the diagnosis.
- Clinician interview and observation assesses symptoms and degree of
severity. A careful patient history, such as the Schwab and English Activities
of Daily Living Scale, can be used to confirm diagnosis and severity of
symptoms.
- Evaluate for substance abuse and other medical
conditions.
Several standardized instruments can help in assessment and determination of
appropriate treatment.
- Activities of Daily Living (ADL) Scale
- NYU Parkinson Disease Disability Scale
- Hoehn and Yahr Scale
- Columbia University Scale
- Cornell–UCLA Scale
- Webster Scale
- University of British Columbia
Scale
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Treatment Options |
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Treatment Strategy |
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Depending on the type, number, and severity of symptoms, treatment options
include the following.
- Pharmacotherapy
- Surgery (e.g., cryothalamotomy and pallidotomy)
- Exercise to improve mobility and physical, occupational, or speech
therapy as required
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Drug Therapies |
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- Levodopa (L-3,4-dihydroxyphenylalanine; 25/100 mg increased gradually
to 25/250 mg; tid for both), a dopamine precursor, is transformed into dopamine
by nerve cells; most effective for bradykinesia and rigidity; side effects
include severe nausea and vomiting, low blood pressure, involuntary movements,
restlessness.
- Carbidopa is used in combination with levodopa; available in combined
form as Sinemet (25/100 or 50/200 mg); prevents levodopa from being metabolized
until it reaches the brain; allows for smaller doses of levodopa and reduces
levodopa's side effects.
- Selegiline (deprenyl) inhibits enzyme monoamine oxidase B (MAO-B),
which metabolizes dopamine in the brain; prolongs response to levodopa by
protecting dopamine-producing neurons from toxic effect; side effects include
nausea, orthostatic hypotension, insomnia; contraindicated for patients taking
fluoxetine and meperidine.
- Anticholinergics such as benztropine (Cogentin; 0.5 to 2 mg tid) and
biperiden (Akineton; 1 to 3 mg qid) block action of acetylcholine; used when
symptoms are mild and before Sinemet; side effects include dry mouth,
constipation, urinary retention, hallucinations, memory loss, blurred vision,
and confusion.
- Amantadine (110 mg bid) potentiates the release of endogenous
dopamine; side effects include restlessness, confusion, skin rashes, edema,
disturbances of cardiac rhythm; may be combined with anticholinergics
- Dopamine antagonists such as bromocriptine (Parlodel; 2.5 to 10 mg
tid) and pergolide (Permax; 1 mg tid) activate dopamine receptors; taken alone
or with Sinemet.
- Catechol-O-methyltransferase (COMT) inhibitors such as tolcapone
(Tasmar) increase availability of levodopa in the brain; can be taken with
levodopa
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Complementary and Alternative
Therapies |
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CAM therapies do not take the place of pharmaceutical treatment. They may,
however, provide some relief of symptoms and slow the progression of the
disease. The primary focus is decreasing oxidation. Hair analysis may be useful
to determine if there is heavy metal toxicity. |
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Nutrition |
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- Essential fatty acids are anti-inflammatory. Dietary manipulation
includes reducing animal fats and increasing fish. A mix of omega-6 (evening
primrose, black currant, borage, pumpkin seed) and omega-3 (flaxseed and fish
oils) may be most optimum (2 tbsp. oil/day or 1,000 to 1,500 mg bid).
- Antioxidants vitamin C (1,000 mg tid), vitamin E (400 to 800 IU/day),
and the trace mineral selenium (200 mcg) may slow progression of Parkinson's,
and are often found in a complex together. Other antioxidants that are often
recommended are alpha-lipoic acid, grape seed extract, and pycnogenol.
- Vitamin B6 (10 to 100 mg/day) may help with symptom control, but
should be given with zinc (30 mg/day) to counteract B6's ability to interfere
with lerodopa metabolism.
- A vitamin B complex is helpful.
- Manganese: Excessive exposure increases the risk of
Parkinson's.
- Amino acids: Low protein diets may help control tremors. However,
D-tyrosine (100 mg/kg/day) increases dopamine turnover. Patients with
Parkinson's may be deficient (since the major source is meats, dairy, and eggs),
and supplementation may be beneficial.
- Glutathione: antioxidant, found in low levels in patients with
Parkinson's (200 mg bid)
- Choline increases brain function; thus, various forms are recommended
including lecithin, phosphatidylcholine, and DMAE (dimethylaminoethanol), which
stimulates the production of choline.
- Neurotransmitters made from amino acids such as glutamic acid and
GABA (gamma-aminobutyric acid) often are used in treating
Parkinson's.
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Herbs |
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Herbs are generally a safe way to strengthen and tone the body's systems. As
with any therapy, it is important to ascertain a diagnosis before pursuing
treatment. Herbs may be used as dried extracts (capsules, powders, teas),
glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless
otherwise indicated, teas should be made with 1 tsp. herb per cup of hot water.
Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for
roots. Drink 2 to 4 cups/day. Tinctures may be used singly or in combination as
noted.
- Gotu kola (Centella asiatica): traditionally used as a CNS
stimulant, with historic use in Parkinson's. One cup tea bid, or 30 to 60 drops
tincture bid
- Ginkgo (Ginkgo biloba): circulatory stimulant, increases
cerebral vascular sufficiency and antioxidant (as a supplement 120
mg/day)
- Hawthorn (Crataegus monogyna): circulatory stimulant,
antioxidant (2 to 5 g/day)
- Herbs specific to the liver such as milk thistle (Silybum
marianum), globe artichoke (Cynara scolymus), and bupleurum
(Bupleurum falcatum) provide liver support and reduce free radical
damage.
- Nervine herbs such as St. John's wort (Hypericum perforatum),
skullcap (Scutellaria lateriflora), oats (Avena sativa), and lemon
balm (Melissa officinalis) help support the structure of the nervous
system.
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Homeopathy |
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An experienced homeopath should assess individual constitutional types and
severity of disease to select the correct remedy and potency. For acute
prescribing use 3 to 5 pellets of a 12X to 30C remedy every one to four hours
until acute symptoms resolve. For chronic prescribing use 30C 5 pellets once or
twice daily.
- Argentum nitricum for ataxia, trembling, awkwardness, painless
paralysis
- Causticum for Parkinson's with restless legs at night,
contractures, especially when patient prefers wet, rainy weather
- Mercurius vivus for Parkinson's that is worse at night,
especially with panic attacks
- Plumbum metallicum for Parkinson's, especially with a history
of arteriosclerosis
- Zincum metallicum for Parkinson's with great restlessness,
especially with depression
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Physical Medicine |
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Chelation therapy with I.V. EDTA may be effective if the Parkinson's is due
to heavy metal toxicity or environmental toxins. |
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Acupuncture |
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May be helpful, particularly for the tremor associated. |
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Massage |
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May help with increasing circulation, decreasing muscle spasm, and increasing
the overall sense of well-being. |
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Patient Monitoring |
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Patients receiving pharmacological therapy must be closely monitored for drug
effectiveness, side effects, and adjustments. Concomitant medical conditions and
their pharmacological therapies may influence the treatment of Parkinson's;
these conditions include glaucoma, heart disease, high blood pressure, and
stomach/intestinal diseases. Psychotherapy can help reduce anxiety and
depression; however, medications for anxiety and depression may worsen symptoms
of Parkinson's disease in some patients. |
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Other
Considerations |
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Prevention |
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There are no known ways to prevent or avoid Parkinson's disease. Early use of
selegiline may delay progression of symptoms. Avoid drugs known to cause tardive
dyskinesia. |
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Complications/Sequelae |
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Patients over 60 may have increased side effects from certain pharmacological
interventions such as anticholinergic drugs, including hallucinations,
confusion, and psychosis. |
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Prognosis |
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Parkinson's disease is irreversible and progressive. Choosing the proper
pharmacotherapies can improve symptoms, especially in the early to mid
stages. |
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References |
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Bartram T. Encyclopedia of Herbal Medicine. Dorset, England: Grace
Publishers; 1995:328-329.
Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic
Guide to Herbal Medicines. Boston, Mass: Integrative Medicine
Communications; 1998:138.
Fauci AS, Braunwald E, Isselbacher KJ, et al., eds. Harrison's Principles
of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998.
Morrison R. Desktop Guide to Keynotes and Confirmatory Symptoms.
Albany, Calif: Hahnemann Clinic Publishing; 1993:32-33, 111-113, 244-247,
303-304, 401-403.
National Institutes of Health. Accessed at
www.ninds.nih.gov/healinfo/disorder/parkinso/pdhtr.htm on January 16, 1999.
Parkinson's Disease Foundation. Accessed at www.pdf.org on January 16,
1999.
Perry TL, Godin DV, Dansen S. Parkinson's disease: a disorder due to nigral
glutathione deficiency. Neurosci Lett. 1982;33:305-310.
Tierney LM Jr, McPhee SJ, Papadakis MA. Current Medical Diagnosis &
Treatment 1999. 38th ed. Stamford, Conn: Appleton & Lange; 1999.
Werbach M. Nutritional Influences on Illness. New Canaan, Conn: Keats
Publishing; 1988:346-349. |
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Copyright © 2000 Integrative Medicine
Communications This publication contains
information relating to general principles
of medical care that should not in any event be construed as specific
instructions for individual patients. The publisher does not accept any
responsibility for the accuracy of the information or the consequences arising
from the application, use, or misuse of any of the information contained herein,
including any injury and/or damage to any person or property as a matter of
product liability, negligence, or otherwise. No warranty, expressed or implied,
is made in regard to the contents of this material. No claims or endorsements
are made for any drugs or compounds currently marketed or in investigative use.
The reader is advised to check product information (including package inserts)
for changes and new information regarding dosage, precautions, warnings,
interactions, and contraindications before administering any drug, herb, or
supplement discussed herein. | |