<<Disclaimer: Verify this information before applying it to your situation.>> At 01:44 PM 2/26/96 -0600, Rene Delehanty <[log in to unmask]> wrote: > which is now combined with horrible burning sensations >in her extremities (legs especially). Does anyone else ever have these >kinds of symptoms? I keyed this in from the Merck Manual (16th ed): Peripheral Neuropathy ... Nutritional deficiency and metabolic disorders may result in polyneuropathy. Deficiency of B vitamins is often the cause (eg, in alcoholism, beriberi, pernicious anemia, isoniazid-induced pyridoxine deficiency, malabsorption syndromes, and hyperemesis gravidarum). Polyneuropathy also occurs in hypothyroidism, porphyria, sarcoidosis, amyloidosis, and uremia. Diabetes mellitus causes several forms of neuropathy; sensorimotor distal polyneuropathy (most common), multiple mononeuropathy, and focal mononeuropathy (eg, of oculomotor or abducens cranial nerves). ... Polyneuropathy is relatively symmetric; sensory, motor, and vasomotor fibers often are involved simultaneously. (An acute, rapidly progressive form, the Guillain-Barre syndrome, and hereditary neuropathies are discussed separately below.) The most common form of polyneuropathy, seen with metabolic disease (eg, diabetes mellitus, renal failure, malnutrition), develops slowly, often over months or years; it frequently begins with sensory abnormalities in the lower extremities. Abnormalities are often more severe distally than proximally. Peripheral tingling, numbness, burning pain, or deficiencies in joint proprioception and vibratory sensation often are prominent. Pain is often worse at night and may be aggravated by touching the affected area or by temperature changes. In severe cases, objective signs of sensory loss, typically with stocking-and-glove distribution, can be shown. The Achilles and other deep tendon reflexes are diminished or absent. Painless ulcers on the digits or Charcot's joints may be seen when sensory loss is profound. Sensory or proprioceptive deficits may lead to gait abnormalities. Motor involvement results in distal muscle weakness and atrophy. The autonomic nervous system may be additionally or selectively involved, leading to nocturnal diarrhea, bladder and bowel incontinence, impotence, or postural hypotension. Vasomotor symptoms are variable. The skin may be paler and drier than normal or there may be excess sweating and/or dusky discoloration. Trophic changes are common in severe and prolonged cases; they consist of smooth, shiny skin, pitted or ridged nails, and osteoporosis. Uncommonly, an exclusively sensory polyneuropathy is seen, which begins with peripheral pains and paresthesias and progresses centrally to a loss of all forms of sensation. This occurs as a remote effect of carcinoma, especially bronchogenic, after megadose intoxication with pyridoxine (B6), in amyloidosis, hypothyroidism, myeloma, and uremia. ... ======================================================================= Peripheral neuropathy is listed as one of the possible symptoms of celiac disease, or gluten intolerance. CD is a malabsorption syndrome, and the patient can become deficient in fat soluble vitamins and minerals, due to damaged intestinal villi. In the Celiac Sprue Association/USA flyer on celiac disease (Box 31700, Omaha, NE 68131 402-558-0600) among the symptoms it lists peripheral neuropathy as numbness and tingling in fingers and toes. ======================================================================= A Medline abstract: TI- [Celiac disease in adults revealed by sensory-motor neuropathy] TI- <Original> Maladie coeliaque de l'adulte revelee par une neuropathie sensitivo-motrice. AU- Viader F; Chapon F; Dao T; Rivrain Y; Lechevalier B CS- Service de Neurologie, CHRU de Caen. JN- Presse Med; 24 (4) p222-4 PY- Jan 28 1995 AB- Central or peripheral nervous system complications are occasionally observed in adult patients with celiac disease. Several mechanisms have been proposed including vitamin deficiency, vascular inflammation and a direct effect of gluten intolerance. Typical nerve fiber damage due to demyelinization has been suggested. We observed a 65-year old woman with a right peroneal nerve palsy superimposed on a diffuse peripheral neuropathy who was found to have folic acid deficiency which in turn led to the diagnosis of adult celiac disease. Electrophysiological and histological studies demonstrated a predominantly demyelinating peripheral neuropathy which responded first to parenteral folic acid supplementation and second to a gluten-free diet. The mechanisms of peripheral nerve damage in adult celiac disease are briefly discussed and the possible role of folic acid deficiency is emphasized.