Parkinson’s Disease

BASICS

DESCRIPTION

An adult-onset neurodegenerative disorder of the extrapyramidal system characterized by a combination of tremor at rest, rigidity and bradykinesia. The diagnosis requires therapeutic response to levodopa which implies normal striatal neurons. This is the only neurodegenerative disease which is treatable long-term.

System(s) affected: Nervous, Musculoskeletal
Genetics: Genetic factors do not play a major role in causing typical PD, especially when onset after age 50
Incidence/Prevalence in USA: 50,000 per year; .3% 55-64, 1% 65-74, 3.1% 75-84; 4.3% 85-94
Predominant age: Age 60 with 5% between the ages of 21 and 39
Predominant sex: Male > Female (1.4:1)

SIGNS AND SYMPTOMS

Cardinal signs
- Tremor (4–8 Hz) in repose: Diagnostic, but not required; relieved with activity, concentration, and sleep; increases with stress; 10% of patients present with only tremor, 30% present without; most begin with unilateral tremor.
- Bradykinesia: required for diagnosis; most disabling symptom; movement initiation difficult, can be overcome with will; causes the gait and postural abnormalities
- Rigidity: lead pipe type; cog-wheeling with tremor
Other associated signs and symptoms
- Speech is poorly enunciated, low volume, clipped
- Ocular abnormalities: decreased blinking, blepharospasm, impaired upward gaze
- Seborrhea
- Dysautonomia with constipation, incontinence, sexual dysfunction
- Depression in 2/3 of patients
- Dementia in 20% of patients; more common in patients whose disease onset was bilateral – mild to moderate, 90% with Folstein MMSE > 15
- Gait disturbances including no arm swing, en bloc turning, problems getting up from chair, festination, freezing
- Leaning posture
- Propulsion or retropulsion
- Micrographia
- Masked facies
- Neglect of swallowing with drooling
Hoehn and Yahr scale of disability in Parkinson's disease
- Stage 1: unilateral, minimal functional impairment
- Stage 2: bilateral without impairment of balance
- Stage 3: bilateral, postural instability, physically independent
- Stage 4: severe disability, can walk or stand without assistance but markedly incapacitated
- Stage 5: wheelchair bound or bedridden unless aided

CAUSES

Unknown
Loss of dopaminergic neurons in the substantia nigra with rate of loss 1% per year in patients with Parkinson's versus 0.5% in normal aging
Probably not genetic, rather toxic or infectious
Known toxins: MPTP, pesticides. Other non-dopaminergic neurons can be affected.

RISK FACTORS

Unknown in the idiopathic disease

DIAGNOSIS

LABORATORY

N/A

Drugs that may alter lab results: N/A
Disorders that may alter lab results: N/A

PATHOLOGICAL FINDINGS

Typical changes that allow precise pathological diagnosis. Lewy bodies.

SPECIAL TESTS

N/A

IMAGING

CT or MRI help rule out other disorders
PET scanning

DIAGNOSTIC PROCEDURES

Diagnostic criteria:

Clinically possible – any one of:
- Rest tremor
- Rigidity
- Bradykinesia
Clinically probable – any 2 of:
- Rest tremor
- Rigidity
- Bradykinesia
- Impaired postural reflexes, or
- One of first three displaying asymmetry
Clinically definite – any 3 of:
- Rest tremor
- Rigidity
- Bradykinesia
- Impaired postural reflexes, or
- Any 2 of above with one of first 3 displaying asymmetry

TREATMENT

APPROPRIATE HEALTH CARE

Outpatient

GENERAL MEASURES

Drugs have therapeutic and toxic effects
Acute worsening may indicate depression, non-compliance, or supervening illness
Course is progressive with or without drugs. Life-long therapy directed toward symptom control – treat disability
Investigate for drug-induced cause; if found, discontinue drug. Symptom resolution may take weeks to months.
Physical, occupational, and speech therapy
Physical limitations require adjustments in the home, e.g., special chairs, elevated toilet seat, eating utensils, dressing oneself

SURGICAL MEASURES

Adrenal medullary transplants, fetal midbrain with substantia nigra neurons
Thalamotomy – akinesia
Stereotactic pallidotomy – akinesia
Deep brain stimulation – dyskinesia, tremor response 88%

ACTIVITY

Maintain activity to whatever degree possible; use cane for walking

DIET

Small frequent meals if difficulty in eating
High liquid intake important; high bulk foods
Reduced protein diet is unnecessary

PATIENT EDUCATION

Local support groups
United Parkinson Foundation, 360 W. Superior St., Chicago, IL 60610, 312-664-2344
American Parkinson's Disease Foundation, 1250 Hyland Blvd., Staten Island, NY 10305, 800-223-2732

FOLLOW UP

PREVENTION/AVOIDANCE

Avoid drugs known to cause tardive dyskinesia, such as: Fluphenazine, perphenazine, prochlorperazine, thiopropazate, trifluoperazine, promazine, thioridazine, haloperidol, droperidol, benperidol, fluspirilene, pimozide, trifluperidol, chlorprothixene, clopenthixol, thiothixene

POSSIBLE COMPLICATIONS

Dementia, depression, aspiration pneumonia, falls, freezing, dyskinesias; also associated with a twofold increase risk of death

EXPECTED COURSE AND PROGNOSIS

More rapid progression: older age at disease onset; dementia
Milder disease: the predominant feature is tremor

MISCELLANEOUS

ASSOCIATED CONDITIONS

Psychosis; depression

AGE-RELATED FACTORS

Pediatric: May occur as secondary parkinsonism in this age group
Geriatric:Common among elderly
Others: N/A

PREGNANCY

N/A

OTHER NOTES

New approaches in treatment undergoing study

ABBREVIATIONS

COMT = catechol-O-methyltransferase

Clinical Investigations

ROLE OF HOMOEOPATHY

Holistic healing that treats the person, not just the disease. Experience gentle, lasting wellness with expert constitutional care.