Causas de ataxia aguda en un hospital de tercer nivel de complejidad / Causes of acute ataxia at a tertiary level hospital

La ataxia es una alteración de la coordinación motora voluntaria y del control postural. Es una entidad poco frecuente en la infancia, siendo la principal causa de ataxia aguda descripta en la bibliografía, de origen inmunológico (post infecciosa), seguida de las intoxicaciones. Para el diagnóstico es fundamental una anamnesis detallada, cronología de los síntomas, antecedentes infecciosos o de contacto con sustancias tóxicas y un examen neurológico completo. El objetivo de nuestro estudio fue analizar retrospectivamente la causa de ataxia aguda como signo neurológico predominante en pacientes que consultaron en el Hospital Juan P. Garrahan. Diseño: Se trata de un estudio descriptivo, observacional, retrospectivo y de corte transversal. Población: niños de 1 a 18 años, con o sin patología previa conocida, que consultaron al servicio de emergencias del hospital por ataxia entre enero de 2013 y octubre de 2018. Método: recolección y análisis de historias clínicas comprendidas en esa fecha, con alteración en la marcha como síntoma de consulta. Resultados: de un total de 237 pacientes, la causa más frecuente de ataxia aguda fue la inmunológica (incluyendo en este grupo a las postinfecciosas y a las no asociadas a infección). Conclusión: En nuestro hospital con tercer nivel de atención, la causa más frecuente de ataxia aguda fue la inmunológica. En segundo lugar, las intoxicaciones y, en tercer lugar, las enfermedades neurológicas. (AU)

Ataxia is a disorder of voluntary motor coordination and postural control, which is rare in childhood. The main cause of acute ataxia described in the literature is immune-mediated inflammation (postinfectious), followed by intoxication. A detailed anamnesis, chronology of symptoms, history of infection or contact with toxic substances, and a complete neurological examination are essential in the diagnostic work-up. The aim of our study was to retrospectively analyze the cause of acute ataxia as a predominant neurological sign in patients who consulted at Hospital Juan P. Garrahan. Study design: A descriptive, observational, retrospective, cross-sectional study was conducted. Study population: children aged 1 to 18 years, with or without known previous disease, who presented to the hospital emergency department for ataxia between January 2013 and October 2018. Method: collection and analysis of medical records from that period of patients with gait disturbance as the reason for consultation. Results: out of a total of 237 patients, the most frequent cause of acute ataxia was immune-mediated inflammation (both post-infectious and noninfectious). Conclusion: In our tertiary care hospital, the most frequent cause of acute ataxia was immune-mediated inflammation. The second most frequent cause was intoxication and the third neurological diseases (AU)

Síndrome de opsoclonia-mioclonia-ataxia em paciente com AIDS / Opsoclonus-myoclonus-ataxia syndrome in an AIDS patient

É relatado aqui o caso de uma mulher de 38 anos com AIDS que desenvolveu a síndrome de opsoclonia-mioclonia-ataxia em um período diferente dos outros casos já relatados na literatura. A síndrome de opsoclonia-mioclonia-ataxia já tinha sido relatada como manifestação inicial de AIDS, assim como no momento da soroconversão de HIV e na síndrome de reconstituição imune. Este caso é único, uma vez que a paciente tinha contagem elevada de CD4 e carga viral negativa no momento em que a síndrome de opsoclonia-mioclonia-ataxia ocorreu.

We report the case of a 38-year-old woman with AIDS who developed opsoclonus-myoclonus-ataxia syndrome during a period different from other cases reported in literature. Opsoclonus-myoclonus-ataxia syndrome had already been reported as the initial neurological presentation of AIDS, as well as at the time of HIV-seroconversion and immune reconstitution syndrome. Our case is unique since the patient had an elevated CD4 count and negative viral load in the period when the opsoclonus-myoclonus-ataxia syndrome occurred.

Effect of isopregnanolone on rapid tolerance to the anxiolytic effect of ethanol / Influência da isopregnenolona na tolerância rápida ao efeito ansiolítico do etanol

OBJETIVE: It has been shown that neurosteroids can either block or stimulate the development of chronic and rapid tolerance to the incoordination and hypothermia caused by ethanol consumption. The aim of the present study was to investigate the influence of isopregnanolone on the development of rapid tolerance to the anxiolytic effect of ethanol in mice. METHOD: Male Swiss mice were pretreated with isopregnanolone (0.05, 0.10 or 0.20 mg/kg) 30 min before administration of ethanol (1.5 g/kg). Twenty-four hours later, all animals we tested using the plus-maze apparatus. The first experiment defined the doses of ethanol that did or did not induce rapid tolerance to the anxiolytic effect of ethanol. In the second, the influence of pretreatment of mice with isopregnanolone (0.05, 0.10 or 0.20 mg/kg) on rapid tolerance to ethanol (1.5 g/kg) was studied. CONCLUSIONS: The results show that pretreatment with isopregnanolone interfered with the development of rapid tolerance to the anxiolytic effect of ethanol.

OBJETIVO: Estudos prévios têm mostrado que os neuroesteróides podem bloquear ou estimular o desenvolvimento da tolerância rápida e crônica aos efeitos de incoordenação e hipotermia produzidos pelo etanol. O objetivo do presente estudo foi investigar a influência da isopregnenolona sobre o desenvolvimento da tolerância rápida ao efeito ansiolítico do etanol em camundongos. MÉTODO: Camundongos suíços, machos, foram pré-tratados com isopregnenolona (0,05, 0,10 ou 0,20 mg/kg) 30 minutos antes da administração de etanol (1,5 g/kg). Após 24 horas, todos os animais foram testados no labirinto em cruz elevado. O primeiro experimento foi realizado com o intuito de selecionar uma dose de etanol que produzisse tolerância rápida ao efeito ansiolítico do etanol. No segundo experimento, o objetivo foi investigar o efeito da isopregnenolona (ISO; 0,05, 0,10 ou 0,20 mg/kg) sobre a tolerância rápida ao etanol (1,5 g/kg). CONCLUSÕES: Os resultados mostram que o tratamento prévio com isopregnenolona interferiu no desenvolvimento da tolerância rápida ao efeito ansiolítico etanol.

A comparative study of delayed neurotoxicity in hens following repeated administration of organophosphorus compounds.

Hens treated with Mipafox (10 mg/kg, sc), sarin (50 micrograms/kg, sc) or parathion (1 mg/kg, sc) daily for 10 days exhibited severe, moderate and no ataxia respectively on 14th day after the start of exposure. The neurotoxic esterase (NTE) activity was significantly inhibited in the brain, spinal cord and platelets of hens treated with mipafox or sarin whereas no change was noticed with parathion treatment. All three compounds significantly inhibited acetylcholinesterase (AChE) activity in the platelets. Spinal cord of hens treated with mipafox, sarin or parathion showed axonal degeneration heavy, moderate and none respectively. It is concluded that repeated administration of equitoxic doses of mipafox, sarin and parathion to hens are marked, moderate and non-delayed neurotoxic respectively.

The development of tolerance to ataxia and to diuresis induced by ethanol in rats is not simultaneous

The present study was conducted to determine whether behaviorally accelerated development of tolerance to the disruptive effects of ethanol on rotarod performance paralleled the development of tolerance to ethanol-induced diuresis and to determine the effect of pre-and post-training ethanol administration on the development of tolerance to both of these effects. Male Wistar rats were treated with ethanol (2gKg-1 day-1, ip) over a preiod of 5 weeks under one of the following schemes: ethanol injections before training (pre-training ethanolgroup) or after training (post-training ethanol group). Control animals received 0.9% NaCl, ip, after training. The effect of ethanol on diuresis was assessed once a week. Data are reported as means ñ SEM of 6 animals. Significant tolerance to the uncoordinating effect of ethanol was detected from the 17th day of treatment onwards in animals of the pre-training group (2nd day = 1.7 ñ 0.6s vs 17th day = 39.0 ñ 8.1s, Student t-test for related samples)but was not observed in animnals of the post-training ethanol group until 34 day of treatment (pre-training ethanol group = 56.1 ñ 8.5s; post-training ethanol group= 29.8 ñ 9.6s vs control group = 12.6 ñ 7.6s, Newman-Kleuls test). In contrast, the development of tolerance to the diuretic effect of ethanol was similar in both groups and appeared after 4 weeks of treatment (pre-training ethanol group: 28th day = 1.9 ñ 0.7 ml vs lst day = 4.0 ñ 0.5ml, Student t-test for related samples; post-training ethanol group: 28th day = 1.0 ñ ml vs 1st day = 3.1 ñ 0.30.6ml vs 1st day = 3.1 ñ 0.3ml, Student t-test for related samples). These data suggest that tolerance to the motor incapacitating effect of ethanol does not affect the time course of tolerance of ethanol-induced diuresis and thus, the two processes involve independent mechanisms. Moreover, the data confirm that tolerance to the disruptive effect of ethanol on rotarod performance can be influenced by the scheme f training