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

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.

• 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

• 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

• 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

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.

There are no objective tests for Parkinson's disease.

The presence of Lewy bodies are considered the hallmark of the disease but can be identified only at autopsy.

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.

• 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

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

• 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

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.

• 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.

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.

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

Chelation therapy with I.V. EDTA may be effective if the Parkinson's is due to heavy metal toxicity or environmental toxins.

May be helpful, particularly for the tremor associated.

May help with increasing circulation, decreasing muscle spasm, and increasing the overall sense of well-being.

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.

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.

Patients over 60 may have increased side effects from certain pharmacological interventions such as anticholinergic drugs, including hallucinations, confusion, and psychosis.

Parkinson's disease is irreversible and progressive. Choosing the proper pharmacotherapies can improve symptoms, especially in the early to mid stages.

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.