Print

Print


I'm having server problems and am not receiving all of my mail.  I
haven't seen Don's posts, but received Ken's response. Don is an ARIES,
not a Taurus. Vivian says that's why Don and I are so much alike, 'cause
I'm an ARIES too.
The following was posted a long time ago, but thought it pertinent...

Parkinson's Disease: Treating Foot Cramps

Reprinted from Medical Sciences Bulletin published by Pharmaceutical
Information Associates, Ltd.

Drugs mentioned:
     levodopa/carbidopa (Sinemet/Dupont-MSD)
     selegiline (Eldepryl/Somerset)
     pergolide (Permax/Lilly)
     bromocriptine (Parlodel/Sandoz)
     trihexyphenidyl (Artane/Lederle)
     cyclobenzaprine (Flexeril/Merck)
     baclofen (Lioresal/Geigy)
     clonazepam (Klonopin/Roche)
     botulinum toxin (Botox/Allergan).

Aching and cramping of the feet are common complaints, often occurring
after injury (strains and sprains) or excessive exercise,
or in association with arthritis or poor circulation in the legs. In
Parkinson's disease (PD), cramping of the feet is also very
common, but the cause is central rather than peripheral. Foot cramping
is just one of several focal dystonias -- abnormal,
sustained tightening of muscles -- that appear to be due to
neurochemical abnormalities in the basal ganglia, that part of the brain
involved in PD. Patients show a particular type of cramping
characterized by downward clenching of the toes or inward turning
of the foot. Cramping can occur throughout the day or night, and can be
especially annoying when it interferes with sleep. Foot
cramping is more common among those individuals whose PD affects just
one side of the body.

Dystonias are often mistaken for other causes of cramping or painful
muscles. Some individuals with orthopedic foot problems,
such as "hammer toes," are actually suffering from Parkinsonian
dystonia. Patients with dystonias may be entirely unaware of
any Parkinsonism; indeed, muscle cramping can precede the onset of
Parkinsonian symptoms by years. There are no laboratory
tests that distinguish dystonia from other causes of cramping, although
a thorough neurologic examination and specialized tests
should pinpoint the cause. Some dystonic features -- such as
blepharospasm (involuntary closing of the eyelids) or torticollis
(involuntary turning of the neck) -- are common in the general
population.

In the PD patient receiving levodopa/carbidopa (Sinemet/DuPont
Pharmaceuticals), focal dystonias may be caused by either
too much of the drug or too little. Patients may experience dystonia
when peak drug levels are attained 1 to 2 hours after
administration, or hours later when drug effects wear off. Changing the
dose or dosage schedule of Sinemet, or using the
sustained-release product (Sinemet CR) may help. The monoamine-oxidase B
inhibitor selegiline (Eldepryl/Somerset) may
also help. A bedtime dose of Sinemet CR, pergolide (Permax/Lilly), or
bromocriptine (Parlodel/Sandoz) may prevent foot
dystonia during early- morning hours. Some patients respond to
anticholinergics such as trihexyphenidyl (Artane/Lederle),
muscle relaxants such as cyclobenzaprine (Flexeril/Merck) and baclofen
(Lioresal/Geigy), and the anticonvulsant
clonazepam (Klonopin/Roche). Another treatment giving excellent relief
is botulinum toxin (Botox/Allergan). Injected into the
dystonic or cramping muscle, botulinum toxin reduces the intensity of
the spasms; the effects may last months after injec-tion.
The toxin is also used for Parkinsonian tremors, benign essential
tremor, and a number of dystonias not always associated with
PD. These include blepharospasm, torticollis, dysphonia (cramping of the
vocal cords), strabismus (wandering eye), stuttering,
and large-muscle spasms associated with conditions such as stroke, head
trauma, and multiple sclerosis.

A careful evaluation of the temporal relationship between foot cramping
and the levodopa dosage schedule should help the
physician decide how best to treat this uncomfortable manifestation of
PD. Modifying the levodopa regimen or adding other
anti-PD agents can alter signals from the brain that trigger the
contractions, or the muscle itself can be "paralyzed" with
botulinum toxin. (LeWitt PA. UPF Newsl. 1993; #3: 3-4).
--
Judith Richards, London, Ontario, Canada
<[log in to unmask]>
                         ^^^
                         \ /
                       \  |  /   Today’s Research
                       \\ | //         ...Tomorrow’s Cure
                        \ | /
                         \|/
                       ```````