I was told that some of the text may have been deleted from the handout about
parkinsonism that was recently distributed.  Apparently the explaination of
anticholinergic meds was deleted.
I'm retransmitting the entire handout.
The following handout contains information that may answer some frequenly
asked questions on the PARKINSN mailing list.  I distribute this handout to
talks I give to parkinson support groups.
 
Introduction
 
Parkinson's Disease (PD) was first formally described by James Parkinson in
1817.  Prior to James Parkinson during the 18th century, the features were
noted but the disease was not fully described.  In the early 1900's a
epidemic of Encephalitis lethargica in Europe  left many people with
Parkinson's-like malady as a residual illness after surviving flu-like
condition.  This outbreak greatly increased the number of patients with
parkinsonism and was important in that it taught us that all that shakes is
not PD. It was than realized that other causes of bradykinesia (slow
movements) and tremor exist.  The first breakthrough in therapy came with the
introduction of Levo-Dopa therapy in the 1960's.  Today there are numerous
new therapies to treat different aspects of PD and to slow the progression of
the disease.
Another exciting advance in the understanding of PD came about when it was
discovered that a street drug called MPTP caused PD by producing neurotoxins
in the brain.  This lead to the discovery that drugs that inhibit the
formation of neurotoxins are partially protective for PD.
 
Scope of the Problem
 
Parkinson's Disease is not rare.  There are over 300,000 sufferers of PD with
40,000 new cases diagnosed per year.  The cost is tremendous.  This
represents hundreds of millions of dollars of lost revenue, not to mention
the cost of medications,  therapies, and to care givers.
 
Risk Factors
 
PD commonly affects the age group of 40-90 year olds.  It affects men
slightly more than women, and affects the white race more that the Japanese,
Chinese and African races.  There may be a slight genetic predisposition
(keep in mind that there are many PD look-alikes which are inherited).  There
has not been a proven association with exposure to rural homes, farming, well
water, herbicides or pesticides.  Infection of a fetus with the flu may
increase the risk of developing PD later in life.  Trauma has not been shown
to increase the risk of PD, however boxers may develop pugalistic PD after
long careers in boxing.  Emotional stress is though to be a risk factor.
 
Protective Factors
 
The protective effects of cigarettes, vitamin C, E, beta-carotene, cod liver
oil or protein calories or lack of protein has not been proven.  Protein in
food is known to decrease the absorption of Sinemet by competing with binding
sites in the gut.
 
Clinical Features of PD
 
The first symptom that a patient may notice may be tremor, rigidity, akinesia
(freezing), postural disturbance or balance problems.  Tremor is the most
common complaint.  There may also be dystonia (abnormal movements), fatigue,
depression, anxiety, restlessness, poor handwriting, quieting of voice,
change in posture, muscle aches, cramping or paresthesias (tingling
feelings).  The gait is shuffling with a stooped posture, narrow base and
flexed knees with turning en bloc.  The severity of PD is divided into 5
stages, and the treatment is tailored to the stage.
 
Parkinsonism Look-Alikes
 
Pathologic studies into the underlying cause of PD have lead to the discovery
of a number of other diseases which share clinical features to PD.
 Approximately 80% of patients who present with the symptoms above will be
found to have idiopathic PD.  Approximately 8% have secondary PD (due to
toxins, drugs, trauma, metabolic disorder, infection stroke, brain tumor).
 About 10% have Parkinson plus syndromes, a group of disorders with multiple
system degeneration with neurologic involvement beyond the typical features
of PD.  These include eye movement problems in Progressive Supranuclear Palsy
(PSP), dysautonomia (problems with blood pressure, digestion, etc...) in Shy
Drager Syndrome (SDS), ataxia (poor coordination) in OlivoPontoCerebellar
Atrophy (OPCA), apraxia (poor fine motor control), myoclonus (jerking) and
alien hand in CorticoBasal Ganglionic Degeneration (CBGD), dementia in
Alzheimer's Disease with Parkinsonism (ADP) or diffuse Lewy Body Disease
(LBD), dementia with motor neuron disease with Parkinsonism Dementia
Amyotrophic Lateral Sclerosis (PD-ALS).
These diseases usually have less tremor, early problems with gait and poor
response to Sinemet.
 
Progressive Surpanuclear Palsy
 
This disorder accounts for 7% of parkinsonism and merits special mention
here.  The gait is stiff, extended, broad based with pivoting instead of
turning en bloc.  The earliest problems are with balance and have had falls.
 There is dysarthia (slurred speech) dysphagia (swalling problems) and
emotional incontinence.  There is paralysis of downward gaze.  The response
to medications is less than in PD.
The other PD look-alikes will not be discussed further due to time
constraints.
 
 
Treatment with Sinemet
 
Most of the audience is familiar with Levo-Dopa/Carbidopa therapy.  L-Dopa is
converted to Dopamine in the brain in cells in the substantia nigra.
 Carbidopa prevents some of the side effects of conversion outside the brain.
 Sinemet requires intact cells in the brain and places some stress on these
cells.  For this reason, Sinemet is sometimes withheld until the later stages
of the disease, and has a limited length of time for its use.  Other
medications may be tried with and without Sinemet to protect the cells and to
lessen the requirement for Sinemet.  Problems with On/Off effects and
dystonia have been lessened by the use of continuous release Sinemet (CR).
 
Treatment with Selegiline (Deprenyl, Edepryl)
 
Selegiline increases the length of action and the magnitude of the effects of
Sinemet. It is thought that it also slows the progression of PD by inhibiting
the production of toxins in the brain which destroy brain cells.
Treatment with Dopamine Agonists
Drugs that act directly on receptors rather than requiring the conversion to
dopamine by intact brain cells were developed to address some limitations of
Sinemet.  These drugs are believed not to put as much strain on brain cells
and allow the dosage of Sinemet to be lessened.  Examples of these drugs are
bromocriptine (Parlodel), pergolide (Permax), Lisuride (available in Europe
only) and apomorphine.
 
Treatment with Anticholinergic Medications
 
Drugs that block transmission of acetyl choline are useful in the treatment
of PD.  These medications also alleviate depression and reduce tremor.
 Examples include  (Symmetrel), benztropine (Cogentin), amitryptiline
(Elavil), bedadryl and trihexiphenidyl (Artane).
 
Other Treatments
 
All patients with PD receive extensive evaluation in my clinic.  Patients are
helped with  problems with sleep, depression and daily activities and there
is extensive help for care givers as well.  Recently medicare has approved
the reimbursement for at home nurses and therapists for PD.  PD patients
often require canes, walkers, dietary changes, modifications of their home
and work environments and assistance in their daily activities.
 
PD Surgery
 
Our staff is experienced with state of the art surgery for PD.  This consists
of neurosurgical transplantation of fetal cells into the the brain to produce
dopamine.  This treatment is indicated for a small, select group of patients.
 
Reference:
Neurologic Clinics "Parkinson's Disease" May 1992, Editors JM Cedarbaum, ST
Gancher, Publisher WB Saunders, Harcourt Brace. Page 341.
 
I hope this helps you.
 
Steven A. Norris, M.D.
Peninsula Medical Associates, Bradenton, Florida
Steve52N.aol.com (Steve Norris)