Mieloneuropatía periférica y óptica en un paciente alcohólico deficiente en ácido fólico

Abstract

In Western countries, neurological disorders secondary to toxic nutritional problems usually present as isolated cases that are generally associated to identifiable causes (alcoholism, eating disorders, absorption disorders, use of medicines) that reduce the availability of basic nutrients, especially B group vitamins, but also folic acid (FA). The optic nerves and the peripheral axons are frequent target organs in this type of pathology, but leukoencephalopathy and spinal cord involvement may also appear, often in combination. We describe the case of a 38-year-old female smoker with a heavy alcohol habit, who developed a subacute clinical pattern of, predominantly axonal, sensitive peripheral polyneuropathy, with vegetative fibre involvement. She also presented involvement of the posterior spinal cord, which gave rise to an ataxic disorder in the gait, as well as a severe bilateral retrobulbar optic neuropathy. Likewise, she presented macrocytosis (MCV: 118) due to megaloblastosis. She was also found to have a FA deficit but a normal vitamin B12 metabolism. With the help of supplementary vitamins, stopping drinking and the regularisation of her diet, the patient presented progressive clinical improvement, and was able to walk without support at 3 months and almost completely recovered her sight, which was corroborated by an improvement in the studies of both visual and somatosensorial evoked potentials. In our community, alcoholism is a frequent cause of nutritional deficiencies, which lead to neurological problems. FA is one of the nutrients that become deficient in alcoholics. More and more descriptions are being reported of peripheral polyneuropathy, retrobulbular optic neuropathy, myelopathy or leukoencephalopathy associated to FA deficiency, above all in patients with a history of alcoholism.