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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 =D2hammer toes,=D3 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).
Hope this is helpful, =
Gail Vass cg for sister with PD
