Where pain and sensitivity of the feet are the major complaints, the pressure of bedclothes may be avoided by placing a cradle support over the legs. Aching of the limbs may be related to their immobility, in which case they should be moved passively on frequent occasions. Aspirin or acetaminophen is usually sufficient to control hyperpathia and allodynia; occasionally codeine or methadone must be added. Obviously, opiates and addicting synthetic analgesics should be avoided if possible, but we have resorted to fentanyl patches for short periods in a few severely affected patients. Some of our patients with severe burning pain (similar to causalgia) in the feet had in the past been helped temporarily by blocking the lumbar sympathetic ganglia or by epidural injection of analgesics. The response to phenytoin, carbamazepine, and gabapentin has been inconsistent, but they are widely used. Adrenergic-blocking medication has been of little value and mexiletine, in our experience, of uncertain benefit.
The regeneration of peripheral nerves, which may take many months, will be of little avail if the muscles have been allowed to undergo contracture and the joints to become fixed. In cases of severe paralysis, molded splints should be applied to the arms, hands, legs, and feet during periods of rest. Pressure on the heels and elbows can be avoided by padding the splints and by turning the patient frequently or by asking the patient to do so. As function returns, more vigorous physiotherapeutic measures can be undertaken.
Recovery from nutritional polyneuropathy is a slow process. In the mildest cases there may be a considerable restoration of motor function in a few weeks. In severe forms of the disease, many months may pass before the patient is able to walk unaided. The sensory features and pain in particular may be slower to recover, having taken over a year in one of our recently observed patients. The slowness of recovery creates a special problem for the alcoholic patient, in whom the great danger to continued recovery is the resumption of drinking and inadequate diet.
Whether or not riboflavin deficiency leads to neurologic symptoms has been controversial. In the past, there were claims that glossitis, cheilosis, and neuropathy were caused by riboflavin deficiency, but its effects were never isolated. It is a component of general malnutrition, making it difficult to separate the cause of various disorders. Night blindness seems, however, to be caused by B2 deficiency. Antozzi and coworkers reported that a metabolic disorder similar to the Reye syndrome can be caused by riboflavin deficiency and is correctable by administration of riboflavin alone. The affected infants in their studies were hypoglycemic, hypotonic, and episodically weak and unresponsive. Generally, 15 mg per day in divided doses is used for replacement, but restoration of a normal diet is paramount.
Antozzi and colleagues also recorded instances of disease in older children and adults, manifesting as a type of lipid storage polymyopathy as a result of either a deficiency or malabsorption of riboflavin. Presumably, a disorder of flavin metabolism had caused an impairment of both beta-oxidation of fatty acids and respiratory chain I and II complexes. Serum creatine phosphate was normal in these individuals, but carnitine was reduced. The oral administration of 200 mg of riboflavin and 4 g of carnitine per day relieved the symptoms. We have seen one case with a significant recovery after supplementation was instituted.
PELLAGRA (NIACIN, NICOTINIC ACID,