Notwithstanding the extensive studies on the nervous syndrome of the achylic deficiency conditions, particularly in Addison-Biermer's disease, its etiopathogeny still remains obscure; that is probably one of the reasons of the inefficient results of the available therapeutic procedures, which are mainly aimed at the hematologic changes. However, there is no clinical and etiopathogenic parallelism between the nervous syndrome and the anemia, neither is the latter a necessary feature of the clinical picture. On the other hand, disturbances of gastric secretion represent a fundamental aspect of the condition. Hence, the writer's suggestion to denominate the condition achylic demyelinating neuropathy (neuro-achylia), instead of neuro-anemia. Based on the study of 53 cases of funicular myelosis associated to gastric achylia and/or megaloblastosis (including 4 cases without anemia), which are compared to those reported in the literature, the writer discusses the symptomatology of the neuro-achylias, symptoms being classified as neuritic, spinal and encephalic. The first ones are especially represented by parethesias (98.1 per cent of the presented cases), superficial hypos-thesia with peripheral distribution and muscular tenderness. In discussing the spinal syndrome, the importance of the disturbances of vibration sense (96.2 per cent of the cases) is stressed, the anatomo-physiopathology of which is considered. The frequency of the dissociation between vibration and position senses (30.2 per cent) is emphasized. In the encephalic syndrome, the mental and optic disturbances are discussed. The histopathology of each syndrome is briefly reviewed. In the discussion of the etiopathogeny, the rôle of the constitutional factor and achylia is emphasized. Reference is made to the toxi-infectious (Hurst), deficiency (avitaminosis A and B, and dyslipoidosis) and allergic theories, as well as to the toxic, ischemic and autonomic concepts. The importance of the allergic theory, as indicated by the studies of Ferraro, co-workers and others on the experimental demyelinating encephalomyelitis, is stressed. The etiopathogeny of the achylic deficiency diseases, according to present knowledge, can be shortly stated as follows: anemia and myelosis have in common gastrointestinal disturbances (especially gastric achy lia) but diverge in the subsequent pathogenic stages. The anemia has a strictly deficiency basis (lack of vitamin B12) ; allergy is the ground of myelosis (the allergens being the insufficiently disintegrated proteins of the gastrointestinal tract). The classic therapeutic procedures of Addison-Biermer's disease are reviewed and attention is drawn to the manner of evaluating the changes in the nervous conditions. The changes in the plantar reflexes and especially those of pallesthesia, are reliable criteria; improvement of parethesias, gait and muscle power does not always mean a therapeutic effect on the neural lesion, but might only indicate improvement of general conditions; changes of the deep reflexes, on the other hand, may even be an evidence of aggravation of the disease. Finally, the writer discusses the newer therapeutic procedures (folic acid and vitamin B12), which, like liver therapy, are mainly related to the blood changes, and only secondarily to the nervous syndrome. The specific treatment of the latter has not received the proper attention yet, and one can only refer, among therapeutic procedures with this purpose, intrathecal thiaminotherapy, and the use of vitamins A and B. The writer suggests that, in view of the possible allergic ground of the demyelinations, anti-histaminic drugs (prophylaxis) and adrenocorticotropic hormone (curative treatment) be tried in cases of neuro-achylia.