[Myelopathy associated with HTLV-1: clinical electrophysiologic study]. / Mielopatía asociada al HTLV-1: estudio clinicoelectrofisiológico.

Clinical and electrophysiological studies have been performed in 9 cases of HTLV-I associated myelopathy (7 female, 2 male). Spastic paraparesis and neurogenic bladder were present in 8; sensory disturbances were detected only in 4. The conduction velocities of the posterior tibial and sural nerves were reduced in 2 cases. Median nerve SSEP revealed a delay of N11, N13, N14, N20 peak latencies and an increase of N9-N20, N13-N14 and N13-N20 interpeak latencies. The electrophysiological studies are the most accurate indicators of the diffuse involvement not only of central motor and sensory pathways but also of the peripheral nervous system.

[Post-sectional antral peptic ulcer and antrofundic re-anastomosis in rats (manifestation of a probable antrofundic neuroendocrine center)]. / Ulcera péptica antral postsección y reanastomosis antrofúndica en la rata (puesta de manifiesto de un probable centro neuroendócrino antrofúndico).

The antrum-fundic section and re-anastomosis (AESR), liberates, in Wistar male rats, genuine antral peptic ulcers. They start within 20 days. They are progressive evolution, penetrating into all gastric walls. Between 7 and 8 months, they involve near organs (spleen, liver, pancreas) and produce a great inflammatory reaction of the peripancreatic ganglions. The antral peptic ulcer is induced if the gastric lesser curvature's nerves are sectioned and a concomitant pyloroplasty is done or not. The gastric hemisection, if anterior or posterior, break out the peptic ulcer only on the same side of the antrum-fundic interruption. In all this situations, except in cases of concomitant pyloroplasty, it is proved a pronounced and significantly increase of the gastric (g/kg), but not pancreatic index. In the AFSR series with nervous section on the lesser curvature and without pyloroplasty, the percentage of antral peptic ulcers in 56%. It is postulated the probably existence, at an antrum-fundic level, of a neuroendocrine center. Its nullification or disturbance by the section and re-anastomosis procedure could generate the antral ulcer and other histologic changes (increase of the "G" cells, hyperplasia of the parietal, ECL and "A like" cells) by one or various hypothetical ways: 1. Direct action, nullifying the normal blocking function of somatostative over the "G" cells and or parietal cells. 2. Disturbing or nullifying the motor pump effect of the gastric antrum, and on this way, enhancing the duodenum-gastric reflux with all know deleterious effects of the bile in the antrum particularly in an acid milieu. 3. Modifying, in the opposite direction, the sensitivity by one hand, of the "G" cells mass and by the other one, of the parietal, ECL and "A like" cells. The depression of the fundic sensitivity will induce the hyperplasia of the "G" cells, the hypersecretion of gastrin and, "a posteriori", all the secretory effects and trophic characteristic of it. 4. Disturbing the prostaglandins secretion, perhaps through a deficit of the nervous innervation, with the resulting epiphenomenon of a cytoprotection deficit mediated through the mucus and bicarbonate production. It is probably that the proposed physiopathogenic mechanism are associated and that the final result, the antral peptic ulcer is the consequence of an increase of the aggressive factors (acid, bile) and a concomitant depression of the defensive factors (cytoprotection), starting normally by the prostaglandins through the mucus and bicarbonate secretion.

Ulcera péptica antral postsección y reanastomosis antrofúndica en la rata (puesta de manifiesto de un probable centro neuroendócrino antrofúndico). / [Post-sectional antral peptic ulcer and antrofundic re-anastomosis in rats (manifestation of a probable antrofundic neuroendocrine center)]

The antrum-fundic section and re-anastomosis (AESR), liberates, in Wistar male rats, genuine antral peptic ulcers. They start within 20 days. They are progressive evolution, penetrating into all gastric walls. Between 7 and 8 months, they involve near organs (spleen, liver, pancreas) and produce a great inflammatory reaction of the peripancreatic ganglions. The antral peptic ulcer is induced if the gastric lesser curvatures nerves are sectioned and a concomitant pyloroplasty is done or not. The gastric hemisection, if anterior or posterior, break out the peptic ulcer only on the same side of the antrum-fundic interruption. In all this situations, except in cases of concomitant pyloroplasty, it is proved a pronounced and significantly increase of the gastric (g/kg), but not pancreatic index. In the AFSR series with nervous section on the lesser curvature and without pyloroplasty, the percentage of antral peptic ulcers in 56

. It is postulated the probably existence, at an antrum-fundic level, of a neuroendocrine center. Its nullification or disturbance by the section and re-anastomosis procedure could generate the antral ulcer and other histologic changes (increase of the [quot ]G[quot ] cells, hyperplasia of the parietal, ECL and [quot ]A like[quot ] cells) by one or various hypothetical ways: 1. Direct action, nullifying the normal blocking function of somatostative over the [quot ]G[quot ] cells and or parietal cells. 2. Disturbing or nullifying the motor pump effect of the gastric antrum, and on this way, enhancing the duodenum-gastric reflux with all know deleterious effects of the bile in the antrum particularly in an acid milieu. 3. Modifying, in the opposite direction, the sensitivity by one hand, of the [quot ]G[quot ] cells mass and by the other one, of the parietal, ECL and [quot ]A like[quot ] cells. The depression of the fundic sensitivity will induce the hyperplasia of the [quot ]G[quot ] cells, the hypersecretion of gastrin and, [quot ]a posteriori[quot ], all the secretory effects and trophic characteristic of it. 4. Disturbing the prostaglandins secretion, perhaps through a deficit of the nervous innervation, with the resulting epiphenomenon of a cytoprotection deficit mediated through the mucus and bicarbonate production. It is probably that the proposed physiopathogenic mechanism are associated and that the final result, the antral peptic ulcer is the consequence of an increase of the aggressive factors (acid, bile) and a concomitant depression of the defensive factors (cytoprotection), starting normally by the prostaglandins through the mucus and bicarbonate secretion.