Odontalgia Atípica (OA) é uma condição dolorosa orofacial crônica de intensidade moderada a severa, que ocorre nas estruturas dentoalveolares e na mucosa oral. É considerada de difícil diagnóstico por estar associada com a ausência de alterações clínicas e radiográficas perceptíveis. Seus aspectos patofisiológicos sensoriais e de manutenção e perpetuação da dor ainda são mal compreendidos. Os objetivos deste estudo foram: (1) avaliar as alterações somatossensoriais em pacientes com OA através dos testes sensoriais quantitativos (QST); (2) ampliar o conhecimento disponível sobre os mecanismos de modulação da dor através do teste de controle de modulação da dor (CPM); e (3) avaliar as condições psicológicas como ansiedade e depressão, qualidade do sono e qualidade de vida através de questionários auto-aplicáveis. Um total de 50 indivíduos foram incluídos, sendo 25 sujeitos do grupo sintomático com OA (19 mulheres, 58,25 +- 12,17 anos de idade) e 25 sujeitos saudáveis do grupo controle (19 mulheres, 58,92 +- 7,39 anos)(p>0.05). Os QSTs englobaram os testes de Limiar de Detecção Mecânica (MDT), Limiar de Sensibilidade Dolorosa Mecânica (PDT), Teste Mecânico de Alodinia com cotonete (DMA1) e escova dental (DMA2), Testes de Detecção Dolorosa do tipo quente (HPD) e gelado (CPD) e o Teste de Somação Temporal (WUR). O controle de modulação da dor foi feito através do teste CPM e as avaliações psicológicas através do Inventário de Ansiedade e Depressão de Beck, o Índice de Qualidade do Sono de Pittsburg e o Questionário de Qualidade de Vida SF-36. Os QSTs foram repetidos após a aplicação de uma pomada anestésica de Benzocaína 2%. A análise estatística foi feita através dos testes t pareado, teste t e o teste não paramétrico de Mann-Whitney, considerando-se um nível de significância de 5%. Os resultados indicaram que sujeitos com OA apresentam ganho sensorial por meio de estímulos térmicos do tipo quente (HPD) e gelado (CPD) e estímulos mecânicos dinâmicos (DMA1, DMA2 e WUR), e perda sensorial à estímulos mecânicos (MDT, PDT). Ainda, o teste CPM reduziu a intensidade da dor significativamente somente para o grupo controle. A aplicação tópica de anestesia indicou uma redução significativa na intensidade da dor nos indivíduos afetados. Além disso, sujeitos com OA apresentaram sintomas de maior depressão e ansiedade, qualidade do sono ruim e baixa qualidade de vida comparados à pacientes saudáveis. Este estudo enfatizou que alterações somatossensoriais significativas são encontradas em sujeitos com OA, onde envolve uma participação de processos periféricos de sensitização e condução da dor, associado à fenômenos de alodínia e hiperalgesia, o que sugere alterações em nível de sensitização central. O sistema modulátorio de dor mostra-se deficiente e as condições psicológicas estão afetadas em sujeitos com OA. / Atypical Odontalgia (AO) is a chronic orofacial painful condition, which occurs in dentoalveolar structures and oral mucosa. AO is difficult to diagnose because it is associated with the absence of any clinical and radiographic alterations. Repetitive dental procedures are made, with the aim to relief pain. Sensory pathophysiological aspects and pain maintenance and perpetuation are still poorly understood. The aim of this study were: (1) evaluate somatosensory abnormalities in AO patients through quantitative sensory testing (QST), (2) evaluate mechanisms of pain modulation through the controlled pain modulation test (CPM), and (3) assess the psychological features such as anxiety, depression, sleep quality and quality of life through selfreported questionnaires. A total of 50 subjects were included, consisting of 25 subjects with symptomatic AO (19 women, 58.25 +- 12.17 years old) and 25 subjects in the control group (19 women, 58.92 +- 7.39 years old)(p>0.05). QST encompassed Mechanical Detection Threshold (MDT), Pain Detection Threshold (PDT), Dynamical Mechanical Allodynia with a cotton swab (DMA1) and with a toothbrush (DMA2), Cold Pain Detection (CPD), Heat Pain Detection (HPD) and Wind-up Ratio (WUR). Pain modulation was performed by CPM and psychological evaluations through Anxiety Inventory and Beck Depression Index, the Pittsburgh Sleep Quality and Quality of Life Questionnaire SF-36. QSTs were repeated after the administration of an anesthetic cream (2% Benzocaine). Statistical analysis was performed using the \"t\" test, paired t test and nonparametric Mann-Whitney test considering a significance level of 5%. Results indicated that AO subjects showed sensory gain through heat (HPD) and cold (CPD) stimuli and dynamic mechanical stimuli (DMA1, DMA2 and WUR), and sensory loss to mechanical stimuli (MDT, PDT). Moreover, CPM reduced pain intensity significantly only in the control group. A topical anesthesia showed a significant reduction in pain intensity in affected subjects. Furthermore, subjects with AO had symptoms of depression and anxiety, poor sleep quality and poor quality of life compared to healthy individuals. This study emphasized that somatosensory abnormalities are found in subjects with AO, which involves participation of peripheral sensitization associated with allodynia and hyperalgesia, suggesting central sensitization abnormalities. Pain modulation system proves deficient and psychological conditions are affected in subjects with AO.

Introdução: Os opioides são os analgésicos mais efetivos para tratamento da dor moderada a intensa. No entanto, evidências crescentes têm demonstrado que seu uso pode levar a mudanças na sensibilidade dolorosa. Nesse contexto, a hiperalgesia induzida pelo remifentanil (r-IH) envolve um desequilíbrio nos sistemas inibitórios e excitatórios. Postula-se que um dos mecanismos centrais seja a disfunção do sistema modulador descendente da dor. Então, neste estudo, testamos a hipótese de que a estimulação transcraniana de corrente contínua (ETCC), devido aos seus efeitos analgésicos, poderia prevenir a r-IH. Os desfechos primários incluíram a escala numérica de dor (END 0-10) durante o teste repetitivo ao frio (rCOLDT), e a alteração na END (0-10) durante o teste de modulação condicionada de dor (CPM-TASK). Os desfechos secundários foram os limiares de dor ao calor (HPT) e o tempo de reação durante o teste de dor à água gelada [zero graus oC, (IPT)]. Métodos: Ensaio clínico randomizado, fatorial, duplo cego, que incluiu 48 homens saudáveis, com idades entre 19 e 40 anos. Os sujeitos foram randomizados em quatro grupos (n=12): ativo (a) - ETCC / solução salina, Sham (s) - ETCC / solução salina, a-ETCC / remifentanil e s-ETCC / remifentanil. Foi aplicado o ETCC sobre o córtex motor primário, com uma sessão única de 20 min e 2 mA. Resultados: Durante o rCOLDT, houve um efeito significativo entre os grupos nos escores cumulativos da END (P = 0,01). O grupo s-ETCC / remifentanil apresentou maiores escores de dor durante rCOLDT, [media (SD) 5,49 (1,04)] e a-ETCC / remifentanil apresentaram escores relativamente menores [4,15 (1,62)]. Este achado mostra que o efeito da ETCC bloqueou a HI-R. Os grupos a-ETCC / solução salina e s-ETCC / salina apresentaram menor índice de dor durante rCOLDT, [3.11 (1.2)] e [3.15 (1.62)], respectivamente. A incidência de hiperalgesia definida como um aumento de 15% na END durante o rCOLDT foi de: 31% no grupo s-ETCC/remifentanil; 22% no grupo a-ETCC/remifentanil; 11% no grupo a-ETCC/salina; e 8.3% no grupo s-ETCC/salina. Os grupos com remifentanil apresentaram escore positivo na END (0-10) durante a tarefa CPM, ou seja, produziu um desengate do sistema modulador descendente de dor (DPMS). Além disso, s-ETCC / Remifentanil em comparação com a-ETCC/remifentanil apresentou menor HPT e maior tempo de reação durante o IPT. Conclusão: Esses achados sugerem que os efeitos da a-ETCC previne a disfunção da capacidade inibitória do sistema modulador descendente da dor induzido pelo remifentanil durante o rCOLDT. / Background: Opioids are the most effective analgesics to treat moderate to severe pain. However, growing evidence shows that opioids can elicit unexpected changes in pain sensitivity. In this sense, remifentanil-induced hyperalgesia (r-IH) involves an imbalance in the inhibitory and excitatory systems. It postulates that one of the central mechanisms is the dysfunction of the descending pain modulating system. We tested the hypothesis that transcranial Direct Current Stimulation (t-DCS), given its analgesics effects, could prevent r-IH. The primary outcomes included the Numerical Pain Score NPS (0-10) during the repetitive cold test (rCOLDT) and the change on the NPS (0-10) during the conditioned pain modulation (CPM)-task. The secondary outcomes were the heat pain threshold (HPT) and the reaction-time during the Ice-Water Pain Test (IPT). Methods: This double blinded, explanatory factorial randomized trial included 48 healthy males, ages ranging 19 to 40 years. They were randomized into four equal groups: active (a)-tDCS/saline, sham (s)-tDCS/saline, a-tDCS/remifentanil and s-tDCS/remifentanil. We applied tDCS over the primary motor-cortex, with a single session of 20 minutes and 2mA. Results: During the rCOLDT, there was a significant group effect on the cumulative NPS scores (P=0.01). The s-tDCS/remifentanil group presented larger pain scores during rCOLDT, [mean (SD) 5.49 (1.04)] and a-tDCS/remifentanil group had relative lower pain scores [4.15 (1.62)]; showing its blocking effect on r-IH. a-tDCS/saline and s-tDCS/saline groups showed lowest pain scores during rCOLDT, [3.11(1.2)] and [3.15(1.62)], respectively. The incidence of hyperalgesia defined as a 15% increase in NPS during rCOLDT was: 30.3% in the s-tDCS / remifentanil group; 22% in the a-tDCS / remifentanil group; 11% in the a- tDCS / saline group; 8.3% in the s-tDCS / saline group. Remifentanil groups showed positive scores in the NPS (0-10) during the CPM-task, that is, it produced a disengagement of the descending pain modulatory system (DPMS). Also, s- tDCS/Remifentanil compared to a-tDCS/Remifentanil showed lower HPT and larger reaction-time during the IPT. Conclusion: These findings suggest that the effects of a-tDCS prevents the dysfunction of the inhibitory capacity of the descending modulatory pain system induced by remifentanil during rCOLDT.

Afecções musculoesqueléticas crônicas são um problema de saúde pública devido à sua alta prevalência, seu alto custo econômico e por seu impacto negativo na qualidade de vida de pacientes e seus familiares. Diante disso, pesquisadores têm estudado lesões musculares em modelos animais para melhor compreensão dos mecanismos envolvidos na iniciação e manutenção de distúrbios musculoesqueléticos. Na tentativa de esclarecer os mecanismos nociceptivos envolvidos neste processo e encontrar terapias efetivas, nosso grupo de pesquisa vem utilizando modelos experimentais de dor e potenciais tratamentos farmacológicos e não farmacológicos como objeto de estudo. O presente estudo teve como finalidade avaliar se o tratamento farmacológico com gabapentina é eficaz em reverter a dor muscular de ratos com miosite crônica induzida pela injeção de Adjuvante de Freund Completo (CFA) no músculo gastrocnêmio, e ainda, analisar a influência da gabapentina em células gliais e citocinas pró e anti-inflamatórias no sistema nervoso central e periférico destes animais. Nossos resultados demonstram o efeito da gabapentina em células gliais. Esta ação induz uma diminuição na expressão de astrócitos e microglias, levando a um aumento de citocinas anti-inflamatórias e inibição de citocinas pró-inflamatórias e consequentemente uma melhora do quadro nociceptivo em nosso modelo experimental. / Chronic musculoskeletal disorders are a public health problem due to its high prevalence, high economic cost and negative impact on patients and their relatives quality of life. Due to this, researchers have been studying muscle injury in animal models to better understand the mechanisms involved in the initiation and maintenance of musculoskeletal disturbs. To elucidate the nociceptive mechanisms involved in this process and seek for effective therapies, our research group has been using experimental models of pain and potential pharmacological and non-pharmacological treatments as object of study. The aim of this study was to assess whether the treatment with gabapentin is effective in reversing the muscle pain injury in rats with chronic myositis induced by the injection of Complete Freund\'s Adjuvant (CFA) in the gastrocnemius muscle. Also to analyze the influence of gabapentin on glial cells and pro-and anti-inflammatory cytokines in the central and peripheral nervous system of these animals. Our results demonstrate the effect of gabapentin on glial cells. This action are able to decrease expression of astrocytes and microglia, leadind to an increase in anti-inflammatory cytokines and inhibition of proinflammatory cytokines and an improvement of the nociceptive picture in our experimental mode.

Pain is the oldest medical condition and has been referenced through the ages. TENS is a non-invasive treatment for pain. Despite conflicting reports of treatment outcomes, TENS has enjoyed widespread clinical utilization. Seminal work by Sluka and colleagues reported low frequency TENS produces anti-hyperalgesia through µ-opioid receptors and high frequency TENS produces anti-hyperalgesia through ä-opioid receptors in an animal model of inflammation. The experimental results suggested that pain can be reduced by both high and low frequency TENS but by differing opioid receptors. These important findings require translational experiments to be conducted in humans. Providing an adequate placebo for experimental investigation of any physical intervention presents as a challenge. An improvement in the placebo intervention is critical to ascertain the true effects of TENS on painful conditions. Clinical TENS experiments often only examine a single outcome - resting pain. Recent work suggests TENS is less effective on resting pain as compared to movement pain. Investigation to determine which outcome measures (pain at rest, movement pain, pain sensitivity, and function) are most likely to be affected by TENS in human subjects with pain are critical to inform the design of future studies. The least investigated parameter for application of TENS electrode site determination. One method of selection employs a technique of finding points on the skin with suspected lower impedance. To date, no literature exists to determine the effectiveness of this clinical practice and speculation has existed for decades regarding the existence of distinct electrical properties associated with specific points on the body. This series of experiments accomplishes the goals of improving the TENS placebo, testing established parameters from basic science experiments in a patient population, testing multiple outcome measures to direct future investigation; and examined the effect of electrode site selection in TENS analgesia. These experiments were the first to establish a placebo that can 100% blind the TENS examiner, to test this placebo in a patient population, and to show that although there are differences in impedance between optimal and sham sites, that this difference had no effect in the amount of analgesia produced by TENS.

Adverse childhood events have been identified as a risk factor for developing chronic pain conditions in adulthood. However, previous studies have inconsistently supported the link between adverse childhood events and hypersensitivity to laboratory-induced pain. Therefore, this study intended to investigate the effects of adverse childhood events on temporal summation of second pain (TSSP). A group of 38 healthy and pain-free college students participated in laboratory pain tests after being screened for childhood trauma history. Half of participants (47.5% female) were positive for childhood trauma and the other half (63.2% female) reported no adverse childhood event. The laboratory pain tests measured TSSP using 10 thermal pulses per trial over four consecutive trials. The trauma group showed a tendency of greater sensitization within TSSP trials and lack of habituation over repeated TSSP trials. In sum, adverse childhood events predisposed adults to enhanced TSSP, which is potentially linked to an increased likelihood to develop chronic pain problems.

No description available.

In clinical situations, most of the patients suffer from inflammation and acute postoperative pain after surgery. Postoperative pain has been emphasized as a very crucial issue in improving the quality of medical care in each medical center. Therefore, management of the postoperative pain is an effective approach to reduce the painful unpleasant feeling, complications, and death rate after surgery. Surgical trauma results in the induction of COX-2, leading to the release of prostaglandins, which sensitize peripheral nociceptors and increase the excitability of spinal neurons, producing pain hypersensitivity in the surrounding uninjured tissue.The purpose of this study is to test the preventive effect of COX-2 inhibitor SC-236 for post-operative pain by rat plantar incision model.Then, we explored whether SC-236 is more effective in reducing the hyperalgesia and inflammation response administered before incision than after incision. Furthermore, we used male Sprague-Dawley rats received plantar incision were used in this study, the rats received subcutaneous injection of SC-236 before or after plantar incision. Behavior teste of mechanical allodynia¡Bthermal hyperalgesia and COX-2 expression level was determined at 4 h and 1, 2, and 3 days after surgery. Mechanical allodynia was measured by mechanical withdrawal threshold that was determined by stimulating with von Frey filaments stimulation. Thermal hyperalgesia was measured by thermal withdrawal thermal tested by radioactive thermal assay. Mechanical allodynia¡Bthermal hyperalgesia and COX-2 expression level were measured at various time points by behavior teste¡Breal-time polymerase chain reaction¡Bwestern blot and immunohistochemistry. The data from pre-incisional injection of SC-236 was compared with that from post-incisional injection of SC-236.The results revealed pre-incisional injection of COX-2 inhibitor significantly inhibited thermal hyperalgesia but not mechanical allodynia then post-incisional injection of COX-2 inhibitor group. Skin of pre-incisional injection of SC-236 show significant decreased mRNA expression of COX-2 at 1 day and 2 day after incision evidenced by real-time polymerase chain reaction. Western blot and immunohistochemistry also show significant decreased protein expression of COX-2 at 4 hours and 1 day after incision. Therefore, pre-incisional administration of SC-236 could prevent the surgical wound induced thermal hyperalgesia and decrease mRNA and protein expression level of cutaneous COX-2 at 4 hours and one day after surgical incision compared to post-incisional administration of SC-236 .

Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 5 uppsatser.

Introdução: Os opioides são os analgésicos mais efetivos para tratamento da dor moderada a intensa. No entanto, evidências crescentes têm demonstrado que seu uso pode levar a mudanças na sensibilidade dolorosa. Nesse contexto, a hiperalgesia induzida pelo remifentanil (r-IH) envolve um desequilíbrio nos sistemas inibitórios e excitatórios. Postula-se que um dos mecanismos centrais seja a disfunção do sistema modulador descendente da dor. Então, neste estudo, testamos a hipótese de que a estimulação transcraniana de corrente contínua (ETCC), devido aos seus efeitos analgésicos, poderia prevenir a r-IH. Os desfechos primários incluíram a escala numérica de dor (END 0-10) durante o teste repetitivo ao frio (rCOLDT), e a alteração na END (0-10) durante o teste de modulação condicionada de dor (CPM-TASK). Os desfechos secundários foram os limiares de dor ao calor (HPT) e o tempo de reação durante o teste de dor à água gelada [zero graus oC, (IPT)]. Métodos: Ensaio clínico randomizado, fatorial, duplo cego, que incluiu 48 homens saudáveis, com idades entre 19 e 40 anos. Os sujeitos foram randomizados em quatro grupos (n=12): ativo (a) - ETCC / solução salina, Sham (s) - ETCC / solução salina, a-ETCC / remifentanil e s-ETCC / remifentanil. Foi aplicado o ETCC sobre o córtex motor primário, com uma sessão única de 20 min e 2 mA. Resultados: Durante o rCOLDT, houve um efeito significativo entre os grupos nos escores cumulativos da END (P = 0,01). O grupo s-ETCC / remifentanil apresentou maiores escores de dor durante rCOLDT, [media (SD) 5,49 (1,04)] e a-ETCC / remifentanil apresentaram escores relativamente menores [4,15 (1,62)]. Este achado mostra que o efeito da ETCC bloqueou a HI-R. Os grupos a-ETCC / solução salina e s-ETCC / salina apresentaram menor índice de dor durante rCOLDT, [3.11 (1.2)] e [3.15 (1.62)], respectivamente. A incidência de hiperalgesia definida como um aumento de 15% na END durante o rCOLDT foi de: 31% no grupo s-ETCC/remifentanil; 22% no grupo a-ETCC/remifentanil; 11% no grupo a-ETCC/salina; e 8.3% no grupo s-ETCC/salina. Os grupos com remifentanil apresentaram escore positivo na END (0-10) durante a tarefa CPM, ou seja, produziu um desengate do sistema modulador descendente de dor (DPMS). Além disso, s-ETCC / Remifentanil em comparação com a-ETCC/remifentanil apresentou menor HPT e maior tempo de reação durante o IPT. Conclusão: Esses achados sugerem que os efeitos da a-ETCC previne a disfunção da capacidade inibitória do sistema modulador descendente da dor induzido pelo remifentanil durante o rCOLDT. / Background: Opioids are the most effective analgesics to treat moderate to severe pain. However, growing evidence shows that opioids can elicit unexpected changes in pain sensitivity. In this sense, remifentanil-induced hyperalgesia (r-IH) involves an imbalance in the inhibitory and excitatory systems. It postulates that one of the central mechanisms is the dysfunction of the descending pain modulating system. We tested the hypothesis that transcranial Direct Current Stimulation (t-DCS), given its analgesics effects, could prevent r-IH. The primary outcomes included the Numerical Pain Score NPS (0-10) during the repetitive cold test (rCOLDT) and the change on the NPS (0-10) during the conditioned pain modulation (CPM)-task. The secondary outcomes were the heat pain threshold (HPT) and the reaction-time during the Ice-Water Pain Test (IPT). Methods: This double blinded, explanatory factorial randomized trial included 48 healthy males, ages ranging 19 to 40 years. They were randomized into four equal groups: active (a)-tDCS/saline, sham (s)-tDCS/saline, a-tDCS/remifentanil and s-tDCS/remifentanil. We applied tDCS over the primary motor-cortex, with a single session of 20 minutes and 2mA. Results: During the rCOLDT, there was a significant group effect on the cumulative NPS scores (P=0.01). The s-tDCS/remifentanil group presented larger pain scores during rCOLDT, [mean (SD) 5.49 (1.04)] and a-tDCS/remifentanil group had relative lower pain scores [4.15 (1.62)]; showing its blocking effect on r-IH. a-tDCS/saline and s-tDCS/saline groups showed lowest pain scores during rCOLDT, [3.11(1.2)] and [3.15(1.62)], respectively. The incidence of hyperalgesia defined as a 15% increase in NPS during rCOLDT was: 30.3% in the s-tDCS / remifentanil group; 22% in the a-tDCS / remifentanil group; 11% in the a- tDCS / saline group; 8.3% in the s-tDCS / saline group. Remifentanil groups showed positive scores in the NPS (0-10) during the CPM-task, that is, it produced a disengagement of the descending pain modulatory system (DPMS). Also, s- tDCS/Remifentanil compared to a-tDCS/Remifentanil showed lower HPT and larger reaction-time during the IPT. Conclusion: These findings suggest that the effects of a-tDCS prevents the dysfunction of the inhibitory capacity of the descending modulatory pain system induced by remifentanil during rCOLDT.

Fundação Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro / A privação de sono paradoxal (PSP) provoca diversas alterações neuroquímicas e comportamentais relacionadas a mudanças nas funções de sistemas de neurotransmissores. São descritas na literatura respostas aumentadas a estímulos álgicos em animais privados desta fase de sono. Os métodos de PSP frequentemente utilizados têm sido associados à geração de ansiedade nos animais, e a hiperalgesia observada poderia, portanto, ser conseqüência aos estímulos ansiogênicos gerados pelo método. Neste trabalho tivemos como objetivos avaliar se o método utilizado para a PSP é ansiogênico e investigar o efeito dos fármacos ansiolítico, diazepam e analgésico, ácido acetilsalicílico sobre a ansiedade e resposta a estímulos térmicos álgicos em animais PSP. Ratos machos Wistar com 90 dias de vida foram privados de sono paradoxal por 96 horas, sendo a resposta álgica avaliada pelo tempo de retirada da pata traseira em ratos expostos à placa quente (46C). A avaliação do nível de ansiedade dos animais foi feita através do teste do campo aberto, através da relação entre a permanência nos quadrantes centrais e nos quadrantes periféricos, e também pelo teste do labirinto em cruz elevado, sendo quantificado o número de vezes que o animal entrava nos braços abertos do labirinto e o tempo gasto pelo animal nos mesmos braços. Os animais PSP apresentaram aumento no índice de locomoção em relação aos animais controles (+314,8%, p<0,05), aumento no número de entradas (+257,1%) e no tempo gasto nos braços abertos do labirinto em cruz elevado (+319,2%, p<0,05), e redução na latência de retirada da pata traseira da placa quente (-64,2%, p<0,05). O fármaco diazepam, não influenciou nas respostas apresentadas pelos animais PSP no teste de campo aberto e no teste da placa quente, mas influenciou nas repostas apresentadas por estes animais no teste do labirinto em cruz elevado tanto no tempo (+308, p<0,05), quanto no número de entradas (+316,6%, p<0,05). O fármaco ácido acetilsalicílico promoveu uma diminuição do índice de locomoção nos animais PSP submetidos ao teste de campo aberto que também foram administrados com o diazepam (-99,5%, p<0,05). No teste da placa quente o ácido acetilsalicílico não apresentou nenhuma influência na percepção de dor nos animais. Os resultados obtidos neste trabalho indicam que o método de privação de sono paradoxal por período de 96 horas não induz ansiedade, e a redução farmacológica dos níveis de ansiedade não influencia na resposta álgica induzida pela privação de sono paradoxal. / Paradoxical sleep deprivation (PSD) causes several neurochemical and behavioral changes related to alterations in neurotransmitters systems. Increased responses to nociceptive stimuli have been reported in animals deprived of this phase of sleep. The commonly used methods of PSD have been linked to the generation of anxiety in animals, and hyperalgesia could, therefore, be due to anxiety stimuli generated by the method. The purpose of this study was to investigate anxiety induced by the PSD method and the effect of the anxiolytic drug diazepam and analgesic drug acetylsalicylic acid on anxiety and response to thermal nociceptive stimuli. Male Wistar rats of 90 days of life were deprived from sleep for 96 hours and submitted to the nociceptive test on the hot plate (46C). The assessment of anxiety level of animals was performed using the open field test, where they made the link between residence in central and peripheral squares, and also by test of the elevated plus maze, whose endpoint was to quantify the number of times that the animal entered in the open arms of the maze and measure the time spent by the animal in the same arms. PSD animals showed increased rate of locomotion compared to control animals (+314.8%, p <0.05), longer time spent in open arms of elevated plus maze (+319.2%, p <0.05), largest number of entries in the same arms of the maze (+257.1%) and reductions in latency to withdraw the hind paw of the hot plate (-64.2%, p <0.05). The drug diazepam, did not influence the responses made by PSD animals in the open field and hot plate test, but influenced the answers given by these animals in test of the elevated plus maze in both time (+308, p <0.05), or the number of entries (+316.6%, p <0.05). The drug acetylsalicylic acid caused a decline in the rate of locomotion in PSD animals subjected to the open field test that also was administered with diazepam (-99.5%, p <0.05). The results of this study indicated that the method of paradoxical sleep deprivation does not appear to be anxiogenic. The results obtained in this work showed that the PSD method does not induce anxiety and the pharmacological reduction in anxiety does not interfere in the increased algic response induced by paradoxical sleep deprivation.