Inhalation of dimethyl fumarate-encapsulated solid lipid nanoparticles attenuate clinical signs of experimental autoimmune encephalomyelitis and pulmonary inflammatory dysfunction in mice.

RATIONALE: The FDA-approved Dimethyl Fumarate (DMF) as an oral drug for Multiple Sclerosis (MS) treatment based on its immunomodulatory activities. However, it also caused severe adverse effects mainly related to the gastrointestinal system. OBJECTIVE: Investigated the potential effects of solid lipid nanoparticles (SLNs) containing DMF, administered by inhalation on the clinical signs, central nervous system (CNS) inflammatory response, and lung function changes in mice with experimental autoimmune encephalomyelitis (EAE). MATERIALS AND METHODS: EAE was induced using MOG35-55 peptide in female C57BL/6J mice and the mice were treated via inhalation with DMF-encapsulated SLN (CTRL/SLN/DMF and EAE/SLN/DMF), empty SLN (CTRL/SLN and EAE/SLN), or saline solution (CTRL/saline and EAE/saline), every 72 h during 21 days. RESULTS: After 21 days post-induction, EAE mice treated with DMF-loaded SLN, when compared with EAE/saline and EAE/SLN, showed decreased clinical score and weight loss, reduction in brain and spinal cord injury and inflammation, also related to the increased influx of Foxp3+ cells into the spinal cord and lung tissues. Moreover, our data revealed that EAE mice showed signs of respiratory disease, marked by increased vascular permeability, leukocyte influx, production of TNF-α and IL-17, perivascular and peribronchial inflammation, with pulmonary mechanical dysfunction associated with loss of respiratory volumes and elasticity, which DMF-encapsulated reverted in SLN nebulization. CONCLUSION: Our study suggests that inhalation of DMF-encapsulated SLN is an effective therapeutic protocol that reduces not only the CNS inflammatory process and disability progression, characteristic of EAE disease, but also protects mice from lung inflammation and pulmonary dysfunction.

A Fully Adapted Headstage With Custom Electrode Arrays Designed for Electrophysiological Experiments.

Electrophysiological recordings lead amongst the techniques that aim to investigate the dynamics of neural activity sampled from large neural ensembles. However, the financial costs associated with the state-of-the-art technology used to manufacture probes and multi-channel recording systems make these experiments virtually inaccessible to small laboratories, especially if located in developing countries. Here, we describe a new method for implanting several tungsten electrode arrays, widely distributed over the brain. Moreover, we designed a headstage system, using the Intan® RHD2000 chipset, associated with a connector (replacing the expensive commercial Omnetics connector), that allows the usage of disposable and inexpensive cranial implants. Our results showed high-quality multichannel recording in freely moving animals (detecting local field, evoked responses and unit activities) and robust mechanical connections ensuring long-term continuous recordings. Our project represents an open source and inexpensive alternative to develop customized extracellular records from multiple brain regions.

Epilepsy as a dynamical system, a most needed paradigm shift in epileptology.

The idea of the epileptic brain being highly excitable and facilitated to synchronic activity has guided pharmacological treatment since the early twentieth century. Although tackling epilepsy's seizure-prone feature, by tonically modifying overall circuit excitability and/or connectivity, the last 50 years of drug development has not seen a substantial improvement in seizure suppression of refractory epilepsies. This review presents a new conceptual framework for epilepsy in which the temporal dynamics of the disease plays a more critical role in both its understanding and therapeutic strategies. The repetitive epileptiform pattern (characteristic during ictal activity) and other well-defined electrographic signatures (i.e., present during the interictal period) are discussed in terms of the sequential activation of the circuit motifs. Lessons learned from the physiological activation of neural circuitry are used to further corroborate the argument and explore the transition from proper function to a state of instability. Furthermore, the review explores how interfering in the temporally dependent abnormal connectivity between circuits may work as a therapeutic approach. We also review the use of probing stimulation to access network connectivity and evaluate its power to determine transitional states of the dynamical system as it moves towards regions of instability, especially when conventional electrographic monitoring is proven inefficient. Unorthodox cases, with little or no scalp electrographic correlate, in which ictogenic circuitry and/or seizure spread is temporally restricted to neurovegetative, cognitive, and motivational areas are shown as possible explanations for sudden death in epilepsy (SUDEP) and other psychiatric comorbidities. In short, this review presents a paradigm shift in the way that we address the disease and is aimed to encourage debate rather than narrow the rationale epilepsy is currently engaged in. This article is part of the Special Issue "NEWroscience 2018".

Amygdala inhibition impairs fear conditioning but increases the stimulus-driven activity in the inferior colliculus.

It has been shown that fear conditioning improves the steady-state evoked potentials driven by a long lasting amplitude modulated tone in the inferior colliculus. In this work we tested the hypothesis that the amygdala modulates this effect, since it plays a crucial role in assessing the biological relevance of environmental stimuli. We inhibited the basolateral nucleus of the amygdala of rats by injecting a GABAa receptor agonist (muscimol) before the recall test session of an auditory fear conditioning paradigm and recorded the evoked activity in the central nucleus of the inferior colliculus. According to our results, the treatment with muscimol decreased the expression of freezing behavior during the recall test session, but did not impair the entrainment of the evoked activity in the inferior colliculus induced by fear conditioning. We repeated the injection protocol with another group of rats but without pairing the tone to an aversive stimulus and observed that the inhibition of the basolateral amygdala enhances the stimulus-driven activity in the inferior colliculus regardless of the conditioning task. Our findings suggest that the basolateral amygdala exerts a tonic modulation over the encoding of sensory information at the early stages of the sensory pathway.

A Custom Microcontrolled and Wireless-Operated Chamber for Auditory Fear Conditioning.

Animal behavioral paradigms, such as classical conditioning and operant conditioning, are an important tool to study the neural basis of cognition and behavior. These paradigms involve manipulating sensory stimuli in a way that learning processes are induced under controlled experimental conditions. However, the majority of the commercially available equipment did not offer flexibility to manipulate stimuli. Therefore, the development of most versatile devices would allow the study of more complex cognitive functions. The purpose of this work is to present a low-cost, customized and wireless-operated chamber for animal behavior conditioning, based on the joint operation of two microcontroller modules: Arduino Due and ESP8266-12E. Our results showed that the auditory stimulation system allows setting the carrier frequency in the range of 1 Hz up to more than 100 kHz and the sound stimulus can be modulated in amplitude, also over a wide range of frequencies. Likewise, foot-shock could be precisely manipulated regarding its amplitude (from ∼200 µA to ∼1500 µA) and frequency (up to 20 pulses per second). Finally, adult rats exposed to a protocol of cued fear conditioning in our device showed consistent behavioral response and electrophysiological evoked responses in the midbrain auditory pathway. Furthermore, the device developed in the current study represents an open source alternative to develop customized protocols to study fear memory under conditions of varied sensory stimuli.

Seizure Susceptibility Corrupts Inferior Colliculus Acoustic Integration.

Evidence suggests that the pathophysiology associated with epileptic susceptibility may disturb the functional connectivity of neural circuits and compromise the brain functions, even when seizures are absent. Although memory impairment is a common comorbidity found in patients with epilepsy, it is still unclear whether more caudal structures may play a role in cognitive deficits, particularly in those cases where there is no evidence of hippocampal sclerosis. This work used a genetically selected rat strain for seizure susceptibility (Wistar audiogenic rat, WAR) and distinct behavioral (motor and memory-related tasks) and electrophysiological (inferior colliculus, IC) approaches to access acoustic primary integrative network properties. The IC neural assemblies' response was evaluated by auditory transient (focusing on bottom-up processing) and steady-state evoked response (ASSR, centering on feedforward and feedback forces over neural circuitry). The results show that WAR displayed no disturbance in motor performance or hippocampus-dependent memory tasks. Nonetheless, WAR animals exhibited significative impairment for auditory fear conditioning (AFC) along with no indicative of IC plastic changes between the pre-conditioning and test phases (ASSR coherence analysis). Furthermore, WAR's IC response to transient stimuli presented shorter latency and higher amplitude compared with Wistar; and the ASSR analysis showed similar results for WAR and Wistar animals under subthreshold dose of pentylenetetrazol (pro-convulsive drug) for seizure-induction. Our work demonstrated alterations at WAR IC neural network processing, which may explain the associated disturbance on AFC memory.

Deep brain stimulation probing performance is enhanced by pairing stimulus with epileptic seizure.

The unpredictability of spontaneous and recurrent seizures significantly impairs the quality of life of patients with epilepsy. Probing neural network excitability with deep brain electrical stimulation (DBS) has shown promising results predicting pathological shifts in brain states. This work presents a proof-of-principal that active electroencephalographic (EEG) probing, as a seizure predictive tool, is enhanced by pairing DBS and the electrographic seizure itself. The ictogenic model used consisted of inducing seizures by continuous intravenous infusion of pentylenetetrazol (PTZ - 2.5 mg/ml/min) while a probing DBS was delivered to the thalamus (TH) or amygdaloid complex to detect changes prior to seizure onset. Cortical electrophysiological recordings were performed before, during, and after PTZ infusion. Thalamic DBS probing, but not amygdaloid, was able to predict seizure onset without any observable proconvulsant effects. However, previously pairing amygdaloid DBS and epileptic polyspike discharges (day-1) elicited distinct preictal cortically recorded evoked response (CRER) (day-2) when compared with control groups that received the same amount of electrical pulses at different moments of the ictogenic progress at day-1. In conclusion, our results have demonstrated that the pairing strategy potentiated the detection of an altered brain state prior to the seizure onset. The EEG probing enhancement method opens many possibilities for both diagnosis and treatment of epilepsy.

Auditory fear conditioning modifies steady-state evoked potentials in the rat inferior colliculus.

The rat inferior colliculus (IC) is a major midbrain relay for ascending inputs from the auditory brain stem and has been suggested to play a key role in the processing of aversive sounds. Previous studies have demonstrated that auditory fear conditioning (AFC) potentiates transient responses to brief tones in the IC, but it remains unexplored whether AFC modifies responses to sustained periodic acoustic stimulation-a type of response called the steady-state evoked potential (SSEP). Here we used an amplitude-modulated tone-a 10-kHz tone with a sinusoidal amplitude modulation of 53.7 Hz-as the conditioning stimulus (CS) in an AFC protocol (5 CSs per day in 3 consecutive days) while recording local field potentials (LFPs) from the IC. In the preconditioning session (day 1), the CS elicited prominent 53.7-Hz SSEPs. In the training session (day 2), foot shocks occurred at the end of each CS (paired group) or randomized in the inter-CS interval (unpaired group). In the test session (day 3), SSEPs markedly differed from preconditioning in the paired group: in the first two trials the phase to which the SSEP coupled to the CS amplitude envelope shifted ~90°; in the last two trials the SSEP power and the coherence of SSEP with the CS amplitude envelope increased. LFP power decreased in frequency bands other than 53.7 Hz. In the unpaired group, SSEPs did not change in the test compared with preconditioning. Our results show that AFC causes dissociated changes in the phase and power of SSEP in the IC.NEW & NOTEWORTHY Local field potential oscillations in the inferior colliculus follow the amplitude envelope of an amplitude-modulated tone, originating a neural response called the steady-state evoked potential. We show that auditory fear conditioning of an amplitude-modulated tone modifies two parameters of the steady-state evoked potentials in the inferior colliculus: first the phase to which the evoked oscillation couples to the amplitude-modulated tone shifts; subsequently, the evoked oscillation power increases along with its coherence with the amplitude-modulated tone.

Wistar audiogenic rats display abnormal behavioral traits associated with artificial selection for seizure susceptibility.

Accumulating evidence from different animal models has contributed to the understanding of the bidirectional comorbidity associations between the epileptic condition and behavioral abnormalities. A strain of animals inbred to enhance seizure predisposition to high-intensity sound stimulation, the Wistar audiogenic rat (WAR), underwent several behavioral tests: forced swim test (FST), open-field test (OFT), sucrose preference test (SPT), elevated plus maze (EPM), social preference (SP), marble burying test (MBT), inhibitory avoidance (IAT), and two-way active avoidance (TWAA). The choice of tests aimed to investigate the correlation between underlying circuits believed to be participating in both WAR's innate susceptibility to sound-triggered seizures and the neurobiological substrates associated with test performance. Comparing WAR with its Wistar counterpart (i.e., resistant to audiogenic seizures) showed that WARs present behavioral despair traits (e.g., increased FST immobility) but no evidence of anhedonic behavior (e.g., increased sucrose consumption in SPT) or social impairment (e.g., no difference regarding juvenile exploration in SP). In addition, tests suggested that WARs are unable to properly evaluate degrees of aversiveness (e.g., performance on OFT, EPM, MBT, IAT, and TWAA). The particularities of the WAR model opens new venues to further untangle the neurobiology underlying the co-morbidity of behavioral disorders and epilepsy. This article is part of a Special Issue entitled "Genetic and Reflex Epilepsies, Audiogenic Seizures and Strains: From Experimental Models to the Clinic".

Triggering Different Brain States Using Asynchronous Serial Communication to the Rat Amygdala.

Inputting information to the brain through direct electrical microstimulation must consider how underlying neural networks encode information. One unexplored possibility is that a single electrode delivering temporally coded stimuli, mimicking an asynchronous serial communication port to the brain, can trigger the emergence of different brain states. This work used a discriminative fear-conditioning paradigm in rodents in which 2 temporally coded microstimulation patterns were targeted at the amygdaloid complex. Each stimulus was a binary-coded "word" made up of 10 ms bins, with 1's representing a single pulse stimulus: A-1001111001 and B-1110000111. During 3 consecutive retention tests (i.e., day-word: 1-B; 2-A, and 3-B), only binary-coded words previously paired with a foot-electroshock elicited proper aversive behavior. To determine the neural substrates recruited by the different stimulation patterns, c-Fos expression was evaluated 90 min after the last retention test. Animals conditioned to word-B, after stimulation with word-B, demonstrated increased hypothalamic c-Fos staining. Animals conditioned to word-A, however, showed increased prefrontal c-Fos labeling. In addition, prefrontal-cortex and hypothalamic c-Fos staining for, respectively, word-B- and word-A-conditioned animals, was not different than that of an unpaired control group. Our results suggest that, depending on the valence acquired from previous learning, temporally coded microstimulation activates distinct neural networks and associated behavior.

Neuroprotective effect of exercise in rat hippocampal slices submitted to in vitro ischemia is promoted by decrease of glutamate release and pro-apoptotic markers.

The role of physical exercise as a neuroprotective agent against ischemic injury has been extensively discussed. Nevertheless, the mechanisms underlying the effects of physical exercise on cerebral ischemia remain poorly understood. Here, we investigate the hypothesis that physical exercise increases ischemic tolerance by decreasing the induction of cellular apoptosis and glutamate release. Rats (n = 50) were submitted to a swimming exercise protocol for 8 weeks. Hippocampal slices were then submitted to oxygen and glucose deprivation. Cellular viability, pro-apoptotic markers (Caspase 8, Caspase 9, Caspase 3, and apoptosis-inducing factor), and glutamate release were analyzed. The percentage of cell death, the amount of glutamate release, and the expression of the apoptotic markers were all decreased in the exercise group when compared to the sedentary group after oxygen and glucose deprivation. Our results suggest that physical exercise protects hippocampal slices from the effects of oxygen and glucose deprivation, probably by a mechanism involving both the decrease of glutamatergic excitotoxicity and apoptosis induction.

Temporal rearrangement of pre-ictal PTZ induced spike discharges by low frequency electrical stimulation to the amygdaloid complex.

BACKGROUND: Epilepsy is a common neurological disease affecting over 40 million people worldwide. The foremost important challenge of epileptologists has been to control and predict the recurrent and spontaneous seizures of epileptic patients. The application of low frequency electrical stimulation (LFS) in deep brain structures has shown promising results in seizure control. However, the use of LFS as a probing strategy for seizure prediction, thus contributing to a closed loop solution, is still poorly explored. OBJECTIVE: To improve seizure prediction by producing gradually increasing phase-locked pre-ictal electrographical responses, due to the short-term plastic changes in epileptogenic neural networks, thus behaving as a "programmed" surrogate marker. METHODS: Urethane anesthetized rats were divided into 3 groups: the PTZ-noES group was injected with pentylenetetrazole (PTZ 4 mg/ml/min flow rate) i.v. without electrical stimulation (ES); the ES-noPTZ group received ES (0.5 Hz, 0.1 ms pulse width and 0.6 mA) to the amygdaloid complex and the PTZ + ES group received simultaneously i.v. PTZ infusion and ES. After each condition, electrographical parameters and c-Fos expression of regions of interest were evaluated. RESULTS: Although the PTZ + ES group had no evident change in the sustained electrographic seizure onset, duration and/or frequency spectrum; c-Fos labeling showed a different expression pattern when compared to the PTZ-noES and ES-noPTZ. Also, PTZ + ES formed a gradually increasing evoked potential; confirming the strong coupling of reverberant neural networks induced by ES - phase locked to stimuli. CONCLUSION: ES induces a detectable temporal rearrangement of pre-ictal activity, which has suggestive applicability to seizure prediction.

Pharmacological induction of ischemic tolerance in hippocampal slices by sarcosine preconditioning.

Brain ischemic tolerance is a protective mechanism induced by a preconditioning stimulus, which prepare the tissue against harmful insults. Preconditioning with N-methyl-d-aspartate (NMDA) agonists induces brain tolerance and protects it against glutamate excitotoxicity. Recently, the glycine transporters type 1 (GlyT-1) have been shown to potentiate glutamate neurotransmission through NMDA receptors suggesting an alternative strategy to protect against glutamate excitotoxicity. Here, we evaluated the preconditioning effect of sarcosine pre-treatment, a GlyT-1 inhibitor, in rat hippocampal slices exposed to ischemic insult. Sarcosine (300 mg/kg per day, i.p.) was administered during seven consecutive days before induction of ischemia in hippocampus by oxygen/glucose deprivation (OGD). To access the damage caused by an ischemic insult, we evaluated cells viability, glutamate release, nitric oxide (NO) production, lactate dehydrogenase (LDH) levels, production of reactive oxygen species (ROS), and antioxidant enzymes as well as the impact of oxidative stress in the tissue. We observed that sarcosine reduced cell death in hippocampus submitted to OGD, which was confirmed by reduction on LDH levels in the supernatant. Cell death, glutamate release, LDH levels and NO production were reduced in sarcosine hippocampal slices submitted to OGD when compared to OGD controls (without sarcosine). ROS production was reduced in sarcosine hippocampal slices exposed to OGD, although no changes were found in antioxidant enzymes activities. This study demonstrates that preconditioning with sarcosine induces ischemic tolerance in rat hippocampal slices submitted to OGD.

Differential effects of swimming training on neuronal calcium sensor-1 expression in rat hippocampus/cortex and in object recognition memory tasks.

Physical activity has been proposed as a behavioral intervention that improves learning and memory; nevertheless, the mechanisms underlying these health benefits are still not well understood. Neuronal Calcium Sensor-1 (NCS-1) is a member of a superfamily of proteins that respond to local Ca(2+) changes shown to have an important role in learning and memory. The aim of the present study was to investigate the effects of swimming training on NCS-1 levels in the rat brain after accessing cognitive performance. Wistar rats were randomly assigned to sedentary (SG) or exercised groups (EG). The EG was subject to forced swimming activity, 30 min/day, 5 days/week, during 8 weeks. Progressive load trials were performed in the first and last week in order to access the efficiency of the training. After the 8 week training protocol, memory performance was evaluated by the novel object preference and object location tasks. NCS-1 levels were measured in the cortex and hippocampus using immunoblotting. The EG performed statistically better for the spatial short-term memory (0.73 ± 0.01) when compared to the SG (0.63 ± 0.02; P<0.05). No statistically significant exercise-effect was observed in the novel object preference task (SG 0.65 ± 0.02 and EG 0.68 ± 0.02; p>0.05). In addition, chronic exercise promoted a significant increase in hippocampal NCS-1 levels (1.8 ± 0.1) when compared to SG (1.17 ± 0.08; P<0,05), but had no effect on cortical NCS-1 levels (SG 1.6 ± 0.1 and EG 1.5 ± 0.1; p>0.05). Results suggest that physical exercise would modulate the state of the neural network regarding its potential for plastic changes: physical exercise could be modulating NCS-1 in an activity dependent manner, for specific neural substrates, thus enhancing the cellular/neuronal capability for plastic changes in these areas; which, in turn, would differentially effect ORM task performance for object recognition and displacement.

Anatomically dependent anticonvulsant properties of temporally-coded electrical stimulation.

In the PTZ animal model of epilepsy, electrical stimulation applied to the amygdaloid complex may result in either pro-convulsive or anticonvulsant effect, depending on the temporal pattern used (i.e. periodic-PS and non-periodic-NPS electrical stimulation). Our hypothesis is that the anatomical target is a determinant factor for the differential effect of temporally-coded patterns on seizure outcome. The threshold dose of PTZ to elicit forelimb clonus and generalized tonic-clonic seizure behavior was measured. The effect of amygdaloid complex PS on forelimb clonus threshold showed a pro-convulsive effect while NPS was anticonvulsant. NPS also significantly increased generalized tonic-clonic threshold; while PS, although at lower threshold levels, did not present statistical significance. Thalamus stimulation did not affect forelimb clonus threshold and showed similar anticonvulsant profiles for both PS and NPS on generalized tonic-clonic threshold. In summary, the anatomical target is a determinant factor on whether temporally-coded ES differentially modulates seizure outcome.

Avaliação da pressão positiva expiratória final utilizando o aparelho fisioterápico Quale / Evaluation of positive end expiratory pressure using a physiotherapy device called Quake

O objetivo deste estudo foi avaliar, em voluntários saudáveis, o valor médio da pressão positiva expiratória final (PEEP) na utilização do recurso fisioterápico Quake, relativamente novo no mercado. Participaram 62 indivíduos de ambos os sexos, entre 18 e 30 anos, que foram submetidos a: prova de função pulmonar; avaliação do pico de fluxo expiratório, da sensação subjetiva de esforço (escala de Borg) e da saturação de oxigênio; e à utilização do aparelho, acoplado a um anovacuômetro, para efetuar duas seqüências respiratórias, de 10 e 20 incursões por minuto, monitoradas por retroalimentação visual. Os dados foram tratados estatisticamente. Foi observada diferença significativa entre os valores das pressões geradas apenas na seqüência de 10 incursões por minuto (p=0,03). Na comparação das pressões entre as seqüências, os valores foram significativamente menores na de 10 incursões (29,42±8,04 cmH2O; p=0,03). Não foram encontradas correlações entre as pressões e as variáveis da espirometria, idade e pico de fluxo expiratório. Foi observada uma fraca correlação significativa antes (r=0,36; p=0,003) e depois (r=0,31; p=0,014) da seqüência de 20 incursões entre as pressões nessa seqüência e os escores de fadiga na escala de Borg, tendo o mesmo ocorrido com a saturação de oxigênio. A PEEP gerada pelo Quake em indivíduos saudáveis varia de acordo com a frequência em incursões por minuto, sendo maior durante a seqüência mais rápida, que também gera maior cansaço...

The aim of this study was to assess the mean positive end expiratory pressure(PEEP) during use of the Quake, a relatively new device, in healthy volunteers. Participants were 62 subjects of both sexes aged 18 to 30 years old, who were submitted to: pulmonary function tests; expiratory peak flow evaluation; the Borg scale; assessment of oxygen saturation; and use of the device, coupled to amanometer, in two sequences, of 10 and 20 breaths per minute, with monitoring by visual feedback. Data were statistically analysed. Significant differences between pressures were found only at the 10-breath per minute sequences (p=0.03). When comparing pressures between the sequences, values were significantly lower in the 10-breath per minute sequence (29.42±8.04 cmH2O; p=0.03). No correlations were found between pressures and pulmonary function test measures, age, or expiratory peak flow. A weak, significant correlation was found between Borg scale scores and pressures before (r=0.36; p=0.003) and after (r=0.31; p=0.014) the 20-breath per minute sequence, the same occurring with oxygen saturation. In healthy volunteers, then, Quake PEEP values are higher during the quickest (20-breath per minute) sequence, which also requires more exertion...

Prevalência de queixas urinárias e o impacto destas na qualidade de vida de mulheres integrantes de grupos de atividade física / Prevalence of urinary complaints and their impact on the quality of life of women that participate in physical activity groups

Introdução: A Sociedade Internacional de Continência define incontinência urinária como qualquer perda de urina relatada pelo paciente.É uma condição que afeta a população mundial, principalmente feminina, levando a diversas implicações. O objetivo desteestudo foi verificar a prevalência de queixas urinárias e o impacto destas na qualidade de vida das mulheres, integrantes de grupos deatividade física. Métodos: Participaram do estudo 50 mulheres, com idade a partir de 40 anos, participantes de grupos de atividadefísica conduzidos pela Fisioterapia em um Centro de Saúde de Belo Horizonte, Minas Gerais. As voluntárias foram submetidas a umaanamnese uroginecológica, e aquelas que apresentaram queixas urinárias nos últimos meses responderam o questionário ?King?s HealthQuestionnaire? para avaliação da qualidade de vida. Resultados: A prevalência de mulheres com queixas urinárias foi de 42 por cento. Ossintomas mais predominantes foram: urgência (95,24 por cento), freqüência (90,48 por cento), incontinência de esforço (85,71 por cento) e noctúria (80,95 por cento).Quanto à intensidade, os sintomas de urge-incontinência (49 por cento) e urgência (46 por cento) apresentaram os maiores índices. De acordo com a análise dos domínios, o impacto da incontinência (53,96 ± 26,83) sobressalta-se quando comparado a outros resultados, seguido pelodomínio medidas de gravidade (43,78 ± 23,01). Conclusão: A população estudada apresentou elevada prevalência de queixas urinárias e o impacto da qualidade de vida encontrado não descarta a influência negativa do quadro patológico.