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My husband (pd for 8 years) recently sensed weakness in his right ankle. Compounding the shuffling of his left foot and his problems with balance= , the weakness is causing havoc with his walking. He saw his neurologist w= ho diagnosed the problem with his right foot due to a pinched nerve caused b= y a slipped disk in his back. Then I came across the following article, which talks about a downward clenching of the toes due to pd, which is what hubby exhibits, but only w= hen he walks. At rest he does not have any cramping. Also sinemet provides re= lief for all his symptoms except for the weakness in his right foot. Has anyone experience anything similar? Helen Medical Sciences Bulletin Contents follows: Aching and cramping of the feet are common complaints, often occurring af= ter 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 t= he 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 abnormali= ties 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 ca= n occur throughout the day or night, and can be especially annoying when it interferes with slee= p. 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 musc= les. Some individuals with orthopedic foot problems, such as =D2hammer toes,=D3 are actually su= ffering 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 a= re no laboratory tests that distinguish dystonia from other causes of cramping, although a thoro= ugh 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, o= r 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, pergolid= e (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), a= nd the anticonvulsant clonazepam (Klonopin/Roche). Another treatment giving excellent relief is botulinum toxin (Botox/Allergan). Injected into the dystonic or cramping muscle, botulinu= m toxin reduces the intensity of the spasms; the effects may last months after injec-tion. Th= e 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 associate= d with conditions such as stroke, head trauma, and multiple sclerosis. A careful evaluation of the temporal relationship between foot cramping a= nd 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). =20