Study of spontaneous recurrent seizures and morphological alterations after status epilepticus induced by intrahippocampal injection of pilocarpine.

Epileptic seizures are clinical manifestations of neuronal discharges characterized by hyperexcitability and/or hypersynchrony in the cortex and other subcortical regions. The pilocarpine (PILO) model of epilepsy mimics temporal lobe epilepsy (TLE) in humans. In the present study, we used a more selective approach: microinjection of PILO into the hilus of the dentate gyrus (H-PILO). Our main goal was to evaluate the behavioral and morphological alterations present in this model of TLE. Seventy-six percent of all animals receiving H-PILO injections had continuous seizures called status epilepticus (SE). A typical pattern of evolution of limbic seizures during the SE with a latency of 29.3 ± 16.3 minutes was observed using an analysis of behavioral sequences. During the subsequent 30 days, 71% of all animals exhibited spontaneous recurrent seizures (SRSs) during a daily 8-hour videotaping session. These SRSs had a very conspicuous and characteristic pattern detected by behavioral sequences or neuroethiological analysis. Only the animals that had SE showed positive Neo-Timm staining in the inner molecular layer of the dentate gyrus (sprouting) and reduced cell density in Ammon's horn pyramidal cell subfield CA1. However, no correlation between the intensity of sprouting and the mean number and total number of SRSs was found. Additionally, using Fluoro-Jade staining, we observed neurodegeneration in the hilus and pyramidal cell subfields CA3 and CA1 24 hours after SE. These data indicate that H-PILO is a reliable, selective, efficient, low-mortality model that mimics the acute and chronic behavioral and morphological aspects of TLE.

Neurochemistry study of spinal cord in non-human primate (Sapajus spp.).

The spinal cord is involved in local, ascending and descending neural pathways. Few studies analyzed the distribution of neuromediators in the laminae of non-human primates along all segments. The present study described the classic neuromediators in the spinal cord of the non-human primate Sapajus spp. through histochemical and immunohistochemical methods. Nicotinamide adenine dinucleotide hydrogen phosphate-diaphorase (NADPH-d) method showed neuronal somata in the intermediolateral column (IML), central cervical nucleus (CCN), laminae I, II, III, IV, V, VI, VII, VIII and X, besides dense presence of nerve fibers in laminae II and IX. Acetylcholinesterase (AChE) activity was evident in the neuronal somata in laminae V, VI, VII, VIII, IX, CCN, IML and in the Clarke's column (CC). Immunohistochemistry data revealed neuronal nitric oxide synthase (nNOS) immunoreactivity  in neuronal somata and in fibers of laminae I, II, III, VII, VIII, X and IML; choline acetyltransferase (ChAT) in neuronal somata and in fibers of laminae VII, VIII and IX; calcitonin gene-related peptide (CGRP) was noticed in neuronal somata of lamina IX and in nerve fibers of laminae I, II, III, IV, V, VI and VII; substance P (SP) in nerve fibers of laminae I, II, III, IV, V, VI, VII, VIII, IX, X, CCN, CC and IML; serotonin (5-HT) and vesicular glutamate transporter-1 (VGLUT1) was noticed in nerve fibers of all laminae;  somatostatin (SOM) in neuronal somata of laminae III, IV, V, VI, VII, VIII and IX and nerve fibers in laminae I, II, V, VI, VII, X and IML; calbindin (Cb) in neuronal somata of laminae I, II, VI, VII, IX and X; parvalbumin (PV) was found in neuronal somata and in nerve fibers of laminae III, IV, V, VI, VII, VIII, IX and CC; finally, gamma-amino butyric acid (GABA) was present in neuronal somata of laminae V, VI, VII, VIII, IX and X. This study revealed interesting results concerning the chemoarchitecture of the Sapajus spp. spinal cord with a distribution pattern mostly similar to other mammals. The data corroborate the result described in literature, except for some differences in CGRP, SP, Cb, PV and GABA immunoreactivities present in neuronal somata and in nerve fibers. This could suggest certain specificity for the neurochemistry distribution in this non-human primate species, besides adding relevant data to support further studies related to processes involving spinal cord components.

Inhibition of long-term potentiation in the schaffer-CA1 pathway by repetitive high-intensity sound stimulation.

High-intensity sound can induce seizures in susceptible animals. After repeated acoustic stimuli changes in behavioural seizure repertoire and epileptic EEG activity might be seen in recruited limbic and forebrain structures, a phenomenon known as audiogenic kindling. It is postulated that audiogenic kindling can produce synaptic plasticity events leading to the spread of epileptogenic activity to the limbic system. In order to test this hypothesis, we investigated if long-term potentiation (LTP) of hippocampal Schaffer-CA1 synapses and spatial navigation memory are altered by a repeated high-intensity sound stimulation (HISS) protocol, consisting of one-minute 120 dB broadband noise applied twice a day for 10 days, in normal Wistar rats and in audiogenic seizure-prone rats (Wistar Audiogenic Rats - WARs). After HISS all WARs exhibited midbrain seizures and 50% of these animals developed limbic recruitment, while only 26% of Wistar rats presented midbrain seizures and none of them had limbic recruitment. In naïve animals, LTP in hippocampal CA1 neurons was induced by 50- or 100-Hz high-frequency stimulation of Schaffer fibres in slices from both Wistar and WAR animals similarly. Surprisingly, HISS suppressed LTP in CA1 neurons in slices from Wistar rats that did not present any seizure, and inhibited LTP in slices from Wistar rats with only midbrain seizures. However HISS had no effect on LTP in CA1 neurons from slices of WARs. Interestingly HISS did not alter spatial navigation and memory in both strains. These findings show that repeated high-intensity sound stimulation prevent LTP of Schaffer-CA1 synapses from Wistar rats, without affecting spatial memory. This effect was not seen in hippocampi from audiogenic seizure-prone WARs. In WARs the link between auditory stimulation and hippocampal LTP seems to be disrupted which could be relevant for the susceptibility to seizures in this strain.

Sleep disturbances in hepatitis C patients undergoing treatment: minisleep questionnaire as a screening tool.

AIM: Sleep disturbances are frequently reported by patients with chronic hepatitis C virus (HCV) during treatment with interferon (IFN) α plus ribavirin. Poor sleep quality is related to the onset of depression and impaired quality of life in patients receiving treatment. The aims of this study were to apply the Mini Sleep Questionnaire (MSQ) as a screening tool to assess the self-reported sleep quality and the prevalence of sleep disorders. METHODS: We conducted a transversal, observational, descriptive study comprising 41 subjects with HCV, divided into two groups, treatment (N.=16) and control (N.=25). A structured questionnaire was used to collect sociodemographic and clinical data and the MSQ was applied to assess the sleep quality. A Chi-square test was applied to compare sleep quality between groups. RESULTS: Significant differences between groups in the classification of sleep quality were observed (P<0.05). The group of patients under treatment presented higher frequency of sleep disorders (63%) when compared to the control group (12%). Additionally, the apnea domain was the most impacted. CONCLUSION: This study identified a higher prevalence of sleep disorders and self-reported poor sleep quality in HCV patients under treatment. The MSQ may be useful as a screening tool for sleep disorders in HCV patients during the treatment with IFN-α plus ribavirin.

Tryptophan metabolism in alcoholic pellagra patients: measurements of urinary metabolites and histochemical studies of related muscle enzymes.

Biochemical and enzymatic aspects of tryptophan-niacin metabolism were studied in 15 adult alcoholic pellagra patients and in 14 controls. In addition to the clinical signs of niacin deficiency, most of the pellagra patients had other signs of malnutrition. Plasma tryptophan in pellagra patients was 2.07 +/- 1.27 mumol/dl, and in the controls 4.84 +/- 2.21 mumol/dl (p less than 0.001). The erythrocyte glutamic oxaloacetic transaminase index was 1.94 +/- 0.77 in the pellagra patients and 1.58 +/- 0.73 in the controls. The urinary levels of 3-hydroxyanthranilic acid were 34.49 +/- 21.47 mumol/g of creatinine in the pellagra patients and 14.51 +/- 8.02 mumol/g creatinine in the controls (p less than 0.02). The urinary levels of N'methylinicotinamide were 2.13 +/- 1.18 mg/g creatinine in the pellagra patients and 4.76 +/- 1.94 mg/g creatinine in the controls (p less than 0.01). The excretion of N'-methyl-2-pyridone-5-carboxamide (2-pyridone) was 2.94 +/- 2.37 mg/g creatinine in the pellagra patients and 10.19 +/- 7.49 mg/g creatinine in the controls (p less than 0.01). The histoenzymological activity of 3-hydroxyanthranilate oxidase in the deltoid muscle was higher in the pellagra patients than in the controls, whereas alpha-glycerophosphate dehydrogenase activity was higher in the controls. These results suggest that for alcoholic pellagra patients the tryptophan-niacin pathway is inhibited after the 3-hydroxyanthranilate oxidase step.

Pulmonary tumour embolism from squamous cell carcinoma of the oesophagus.

Pulmonary tumour embolism and subacute "cor pulmonale" have been reported in association with tumours of different origins. Even though these features were first described in a patient with carcinoma of the oesophagus, the frequency and importance of oesophageal tumours as the source of pulmonary tumour embolism have not been studied. In the present investigation, the lungs of 16 autopsied patients with squamous cell carcinoma of the oesophagus were studied prospectively. The lungs were removed as a block and 15 sections (3 from each lobe) were analysed. Pulmonary tumour embolism was detected in 7 cases. The lymphatic vessels were involved in all of them, and were associated with arteries and arterioles in 2. 2 patients presented a classical picture of subacute cor pulmonale, and dyspnoea was present in 3 other cases. The present study permitted us to conclude that carcinomas of the oesophagus frequently evolve toward carcinomatous lymphangitis and that pulmonary tumour embolism should be included in the differential diagnosis of the dyspnoea presented by the patients.

Limbic epileptogenicity, cell loss and axonal reorganization induced by audiogenic and amygdala kindling in wistar audiogenic rats (WAR strain).

Audiogenic seizures are a model of generalized tonic-clonic brainstem-generated seizures. Repeated induction of audiogenic seizures, in audiogenic kindling (AuK) protocols, generates limbic epileptogenic activity. The present work evaluated associations between permanence of AuK-induced limbic epileptogenicity and changes in cell number/gluzinergic terminal reorganization in limbic structures in Wistar audiogenic rats (WARs). Additionally, we evaluated histological changes after only amygdala kindling (AmK) and only AuK, and longevity of permanence of AuK-induced limbic epileptogenicity, up to 160 days. WARs and Wistar non-susceptible rats were submitted to AuK (80 stimuli) followed by both 50 days without acoustic stimulation and AmK (16 stimuli), only AmK and only AuK. Cell counting and gluzinergic terminal reorganization were assessed, respectively, by using Nissl and neo-Timm histochemistries, 24 h after the last AmK stimulus. Evaluation of behavioral response to a single acoustic stimulus after AuK and up to 160 days without acoustic stimulation was done in another group. AuK-induced limbic epileptogenicity developed in parallel with a decrease in brainstem-type seizure severity during AuK. AmK was facilitated after AuK. Permanence of AuK-induced limbic epileptogenicity was associated with cell loss only in the rostral lateral nucleus of amygdala. Roughly 20 generalized limbic seizures induced by AuK were neither associated with hippocampal cell loss nor mossy fiber sprouting (MFS). AmK developed with cell loss in hippocampal and amygdala nuclei but not MFS. Main changes of gluzinergic terminals after kindling protocols were observed in amygdala, perirhinal and piriform cortices. AuK and AuK-AmK induced a similar number and type of seizures, higher than in AmK. AmK and AuK-AmK were associated with broader cell loss than AuK. Data indicate that permanent AuK-induced limbic epileptogenicity is mainly associated to gluzinergic terminal reorganization in amygdala but not in the hippocampus and with no hippocampal cell loss. Few AmK-induced seizures are associated to broader and higher cell loss than a higher number of AuK-induced seizures.

Tetrasomy 9p caused by idic (9) (pter----q13----pter).

Cytogenetic investigation on a malformed male infant showed an extra chromosome similar to chromosome 9 in all metaphases studied. GTG, CBG, and G-11 staining suggested that the extra chromosome was an abnormal 9, permitting the identification of the chromosome constitution as 47,XY,+idic (9) (pter----q13----pter).

Typical and atypical lung carcinoids: clinical and morphological diagnosis.

Forty cases of carcinoid tumors of the lung were studied retrospectively from 1989-1993 in the Pathology Department of Hospital Pulido Valente in Lisbon. The mean age of patients was 44 years old, and the presenting symptoms included hemoptysis, cough, thoracic pain, fever, and dyspnea. An endobronchial mass was seen in 75% of the cases. The histopathological study was based on the following morphological criteria: disorganized architecture with increased cellularity (8 cases; 20%), nuclear pleomorphism (14 cases; 22%), the presence of coarse chromatin (19 cases; 30%), increased mitotic activity (13 cases; 21%), enlarged nucleoli (17 cases; 27%), necrosis (12 cases; 25%), vascular permeation (8 cases; 15%), distant metastasis (6 cases; 14%). Chromogranin was the most strongly reliable immunostaining for the diagnosis. In our series the initial routine diagnosis and the diagnosis after morphological criteria evaluation matched, and in 14 cases the final diagnosis was of atypical carcinoids.

A prospective study of the morphological aspects of tumor involvement of the pulmonary vessels.

A prospective morphological study of tumor involvement of the pulmonary vessels (TIPV) was undertaken on 203 consecutive autopsy cases of malignancies. The lungs were removed as a block and 15 sections (3 from each lobe) were analyzed. Site of origin, histological type and staging of the tumor, topographic distribution of the tumor emboli in the lungs, right ventricular hypertrophy and dilatation, pulmonary infarct, pulmonary vascular sclerosis and lung metastases were recorded in each case. TIPV was detected in 84 (41.4%) cases, the highest frequency reported until now. In 28 cases, TIPV was considered to be the main cause of death. The breast, liver, and pancreas were primary sites in more than 50% of the cases in which TIPV was observed. TIPV was more prevalent in epithelial neoplasms and showed a strong correlation with advanced disease. There was no significant difference among topographic regions of the lungs. The cases with TIPV were correlated with a high frequency of right ventricular hypertrophy and dilatation, vascular sclerosis and pulmonary metastases but not with pulmonary infarcts.

Myocardial ventricular mass related to coronary artery distribution in human hearts.

This prospective study of 120 autopsy collected human hearts correlates the "Right Ventricle/Left Ventricle" free walls mass ratio and the ventricular mass fraction supplied by the right coronary ("Right Coronary/Ventricular Weight"). Different coloured gel injected through both coronary artery's capillary beds allowed ventricular myocardium separation to obtain the weights. In hearts without hypertrophy, mean +/- standard deviation of the "Right Ventricle/Left Ventricle" mass ratio was 0.54 +/- 0.09 for males and 0.62 +/- 0.23 for females; "Right Coronary/Ventricular Weight" mass ratios were 0.39 +/- 0.08 and 0.39 +/- 0.04, respectively. Mean +/- standard deviation of the "Right Ventricle/Left Ventricle" and "Right Coronary/Ventricular Weight" ratios were 0.37 +/- 0.05 and 0.36 +/- 0.10, respectively in hearts with "Left Ventricle Hypertrophy"; 0.56 +/- 0.07 and 0.38 +/- 0.11 in hearts "Without Hypertrophy"; 0.54 +/- 0.08 and 0.39 +/- 0.08 in hearts with "Biventricular Hypertrophy"; 0.89 +/- 0.16 and 0.49 +/- 0.06 in hearts with "Right Ventricle Hypertrophy". Means and variances are narrower for the "Right Coronary/Ventricular Weight" than that observed for the "Right Ventricle/Left Ventricle" mass ratio. It is due to the special double coronary arrangement in which every artery irrigates both ventricles. These results suggest that the usual pattern of the human coronary arteries' anatomy acts as a buffer for the ventricular mass distribution to be irrigated by both arteries in hypertrophy.

Pulmonary tumor embolism to alveolar septal capillaries. An unusual cause of sudden cor pulmonale.

Although metastatic spread of tumor to the lungs is common, subsequent production of cor pulmonale is not. The involvement of pulmonary alveolar capillaries causing sudden cor pulmonale is very rare. We describe a patient who presented with chest pain and sudden shortness of breath. Autopsy disclosed diffuse pulmonary microembolism to septal capillaries caused by tumor cells from a squamous cell carcinoma of the cervix. To our knowledge, this is the second report of this kind of pulmonary tumor embolism.

Pulmonary tumor embolism to alveolar septal capillaries. A prospective study of 12 cases.

Pulmonary tumor embolism leading to subacute cor pulmonale has been extensively studied. However, to our knowledge, the involvement of pulmonary alveolar capillaries has not previously been studied in detail. A prospective study was conducted on 112 autopsied patients with cancer to determine the presence of microembolism in the alveolar septal capillaries. Fifteen sections of predetermined lung areas were obtained and examined. Tumor embolism to alveolar septal capillaries was detected in 12 cases (10.7%), with simultaneous involvement of other vascular territories in 11. Seven patients had dyspnea; four, right ventricular failure; four, hypertrophy of the right ventricle; and three, arterial vascular sclerosis. The present data have led us to conclude that pulmonary tumor embolism to alveolar septal capillaries occurs in association with the involvement of arterial or lymphatic vessels and should be analyzed within the context of the study of subacute cor pulmonale.

Pulmonary tumor embolism to arterial vessels and carcinomatous lymphangitis. A comparative clinicopathological study.

A prospective study of 222 consecutive autopsies of cancer cases was undertaken to investigate whether carcinomatous lymphangitis and pure arterial tumor embolism of the lungs are different clinicopathological entities. The lungs were removed as a block and 15 sections (three from each lobe) were analyzed. A protocol containing clinical (ie, dyspnea, cyanosis, right ventricular failure, engorgement of jugular veins, and peripheral edema as main cause of death) and morphological (ie, right ventricle thickness and dilatation, vascular sclerosis, pulmonary infarct) data were carefully recorded in each case. Arterial tumor embolism was detected in 19 cases (8.5%) and carcinomatous lymphangitis in 44 cases (19.8%). We found no differences in relation to signs and symptoms of arterial tumor embolism and carcinomatous lymphangitis, but respiratory distress as the main cause of death was significantly more frequent in the cases with arterial involvement by tumor emboli. Morphologically, however, right ventricular hypertrophy-dilatation, histological signs of pulmonary hypertension, and hemorrhagic infarcts were more prevalent in the cases with arterial tumor embolism. This study permits us to conclude that although arterial tumor embolism and carcinomatous lymphangitis are clinically similar diseases, they are morphologically different entities. Our results suggest that the most probable pathogenesis of pulmonary endarteritis and subsequent pulmonary hypertension is the injury to the vascular endothelium caused by the arrest of tumor emboli.

Experimental micropolycystic ovarian disease. I. Measurement of body weight, ovarian weight and histochemical activity of 17 beta-hydroxysteroid dehydrogenase.

The effects of administration of 1.25 mg testosterone propionate between the 2nd and 5th day of life on body weight, ovarian weight, food and water consumption, and the histochemical activity of 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) were studied in female Wistar rats during the evolution of experimental micropolycystic ovaries. Biometric studies showed a 9.9 day delay of vaginal opening for the treated animals and that the increased body weight of the animals during the disease was not related to food intake and thus presumably due to the induced metabolic disorder. Reduced histochemical activity of the 17 beta-HSD of testosterone-treated rats was detected at ages 30, 60 and 90 days before the onset of morphological alterations of the ovaries. The possible participation of 17 beta-HSD in the disequilibrium between androstenedione and testosterone and in the genesis of the disease is discussed.

Acute administration of human chorionic gonadotropin reverts some of the inhibitory effects of an LH-RH agonist on testicular steroidogenesis.

An LH-RH agonist, des-Gly10,[DTrp6]-LH-RH ethylamide (LH-RH A), was administered chronically to adult male cats in order to determine its effect on the steroidogenesis of the testis during the stimulatory action of human chorionic gonadotropin (hCG). Measurement of plasma testosterone levels were combined with the histochemical analysis of some steps of the testicular steroidogenic pathway. Chronic daily treatment with LH-RH A (20 micrograms/kg) for 67 days inhibited the early testicular response to hCG during the initial 0.5, 1 and 24 h, whereas the inhibitory effect was not observed 48 and 72 h after hCG administration. The maximal responses to hCG were obtained both in LH-RH A-treated animals and in their control group 48 and 72 h after hCG administration. Under these conditions, LH-RH A-treated cats showed no alteration in 3 beta-hydroxysteroid dehydrogenase (3 beta-Host-D) activity, whereas a marked inhibition was observed in the activity of alcohol dehydrogenase (ADII) which reflects the activity of 20,22-desmolase and/or 17,20-desmolase.

Histochemical and histological analysis of the Leydig cells of cats treated with a supraphysiological dose of LH-RH analog.

An LH-RH analog (des-Gly10,[D-Trp6]-LH-RH ethylamide, LH-RH A) was administered to adult male cats for 67 days (20 micrograms/kg, sc) in order to study its inhibitory effects on the structure of Leydig cells, as determined by histological and histochemical-morphometric techniques. Histological examination showed that LH-RH A promotes a decrease in the volume of the interstitial tissue. In addition, Leydig cell nuclei exhibited marked structural alterations. Morphometric analyses utilizing histochemistry of the enzyme 3-beta-hydroxysteroid dehydrogenase (3-beta-HOST-D) as a marker of Leydig cells also demonstrated a significant decrease of the relative volume occupied by the Leydig cells in the testis.

Effect of corn and sorghum diets in N1 methylnicotinamide excretion and hepatic enzymes in rats.

This study was carried out to compare the effects of corn (Zea mays) and sorghum (Sorghum vulgare) diets on urinary N1 methylnicotinamide (N'MN) excretion and on the activity of hepatic enzyme in young adult rats. Thirty rats, weighing an average of 174.3 g at the beginning of the experiments, were divided into three groups and studied for 13 weeks. The two experimental diets supplied 7% protein, and a casein diet was used as control. Niacin was excluded from the vitamin mixture used in the corn and sorghum diets. The activities of the following enzymes were studied: betaHOB-D, G6P-D, NADH2-TR, NADPH2-TR, and 3 HOA-0. Urinary excretion of N'MN was statistically different among the three groups, the corn group having the lowest level. The corn-fed animals appeared to have more obvious alterations in liver enzyme activity. The changes found in corn and sorghum-fed animals are different and cannot be explained as due to niacin deficiency. The different amino acid compositions of the two grains and their relationship with the discrepancies in the result are also discussed.

Heart aneurysm in Chagas' disease.

This prospective study on 41 autopsy collected human hearts concerns the "apical" lesion in Chagas' disease. Previous report did not show a correlation between lesion frequency and heart weight then discarding a vascular factor in its pathogenesis. The present paper involves other variables besides the heart weight to evaluate the relative coronary insufficiency. Distinct colored gel (green and red) injected through the capillary beds of both coronary arteries defined the extent of both vessels before separating the atria and removing the sub-epicardium fat. The Right Ventricle (RV) and Left Ventricle (LV) free walls furnished the RV/LV mass ratio. The myocardium mass colored green (right coronary artery--RC) and the whole Ventricular Weight (VW) determined the RC/VW mass ratio. The heart weight plus these mass ratios, graded and added, composed a score inversely proportional to the myocardium irrigation condition. It intended to be a more sensitive morphologic evaluation of the relative ischaemia to correlate to the apical lesion. This study showed a right deviation for the relative accumulated frequency of lesions plotted as a score function and a significant difference for higher scores in hearts with aneurysm. It suggests a ischaemic factor intervening in the apical lesion pathogenesis in Chagas' cardiopathy.

Assessment of ivermectin therapeutic efficacy on third-stage larvae of Lagochilascaris minor in mice experimentally infected.

In this study we evaluated the potential action of ivermectin on third-stage larvae, both at migratory and encysted phases, in mouse tissues after experimental infection with Lagochilascaris minor. Study groups I and II consisted of 120 mice that were orally administered 1,000 parasite eggs. In order to assess ivermectin action upon migratory larvae, group I (60 mice) was equally split in three subgroups, namely I-A, I-B, and I-C. On the 7th day after inoculation (DAI), each animal from the subgroup I-A was treated with 200 micrograms/Kg ivermectin while subgroup I-B was given 1,000 micrograms/Kg, both groups received a single subcutaneous dose. To assess the drug action on encysted larvae, group II was equally split in three subgroups, namely II-A, II-B, II-C. On the 45th DAI each animal was treated with ivermectin at 200 micrograms/Kg (subgroup II-A) and 1,000 micrograms/Kg (group II-B) with a single subcutaneous dose. Untreated animals of subgroups I-C and II-C were used as controls. On the 60th DAI all animals were submitted to larva search. At a dose of 1,000 micrograms/Kg the drug had 99.5% effectiveness on third-stage migratory larvae (subgroup I-B). Ivermectin efficacy was lower than 5% on third-stage encysted larvae for both doses as well as for migratory larvae treated with 200 micrograms/Kg.