CAMILA SQUARZONI DALE

(Fonte: Lattes)
Índice h a partir de 2011
4
Projetos de Pesquisa
Unidades Organizacionais
BMA, ICB - Docente
LIM/62 - Laboratório de Fisiopatologia Cirúrgica, Hospital das Clínicas, Faculdade de Medicina
LIM/26 - Laboratório de Pesquisa em Cirurgia Experimental, Hospital das Clínicas, Faculdade de Medicina - Líder

Resultados de Busca

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  • article
    Electrical stimulation of the posterior insular cortex induces opioid and cannabinoid-dependent antinociception and regulates glial cells in the spinal cord
    (2022) GONÇALVES, Elizamara Santos; MATIELO, Heloísa Alonso; TEIXEIRA, Manoel Jacobsen; ANDRADE, Daniel Ciampi de; HAMANI, Clement; DALE, Camila Squarzoni
    ABSTRACT BACKGROUND AND OBJECTIVES: Half of neuropathic pain patients still end up failing clinical treatments. Electrical stimulation of the posterior insular cortex (ESI) modulates sensory and nociceptive circuits. This study evaluated the effects of a range of frequencies of ESI proposed to improve neuropathic pain. METHODS: Male Sprague Dawley rats, 280-340 g, submitted to the chronic constriction of the right sciatic nerve were tested for mechanical sensitivity using the paw pressure and von Frey flaments tests, and for thermal sensitivity using the hot plate test. The rats were submitted to ESI 10, 60 or 100 Hz (one, five or seven ESI, 15 min, 210 µs, 1V), applied to the posterior insular cortex, and were evaluated in the tests before and after ESI, or in follow-up of 48, 72 and 168h. The open field evaluated general activity after ESI 5. The involvment of opioid and cannabinoid testes were evaluated through treatment with naloxone and SR1416A - antagonist and inverse agonist/antagonist of the receptors, respectively, after ESI 5, while activation of astrocytes, marked by glial fibrillary acid protein (GFAP), and of microglia, marked by IBA-1 (glial marker), in the spinal cord evaluated by immunohistochemistry. RESULTS: Data demonstrate that 10, 60, and 100 Hz ESIs modulate mechanical and thermal sensitivity. ESI 5 increased immunoreactivity of GFAP in the spinal cord, without altering IBA-1 (glial marker). Naloxone and SR141716A reversed the antinociception of 60 Hz ESI 5. 60 Hz ESI 7 induced antinociception up to 72h. CONCLUSION: 60 Hz ESI induces opioid and cannabinoid-dependent antinociception and regulates glia. HIGHLIGHTS 60 Hz-delivered ESI was the best analgesic protocol for the insular stimulation. Data showed a prolonged analgesic effect up to 72h after repetitive ESI. ESI regulates glia activation in pain modulatory system.
  • article 4 Citação(ões) na Scopus
    Non-invasive insular stimulation for peripheral neuropathic pain: Influence of target or symptom?
    (2022) CUNHA, Pedro Henrique Martins da; Liu Dongyang; FERNANDES, Ana Mercia; THIBES, Raissa Benocci; SATO, Joao; TANAKA, Harki; DALE, Camila; LAPA, Jorge Dornellys da Silva; MORAIS, Adriano Donizeth Silva de; SOARES, Felipe Henriques Carvalho; SILVA, Valquiria Aparecida da; GRAVEN-NIELSEN, Thomas; TEIXEIRA, Manoel Jacobsen; ANDRADE, Daniel Ciampi de
    Objectives: The posterior-superior insula (PSI) has been shown to be a safe and potentially effective target for neuromodulation in peripheral neuropathic pain (PNP) in humans and animal models. However, it remains unknown whether there is a measurable responder profile to PSI stimulation. Two factors were hypothesized to influence the response of repetitive transcranial magnetic stimulation (rTMS) of the PSI: differences in rTMS target (discrete subregions of the PSI) or PNP phenotype. Methods: This is a secondary analysis from a randomized, double-blind, sham-controlled, crossover trial assessing PSI-rTMS in PNP (N = 31, 5 days rTMS) (10.1016/j.neucli.2021.06.003). Active PSI-rTMS true responders (>50% pain reduction from baseline after active but not after sham series of treatment) were compared with not true responders, to determine whether they differed with respect to 1) rTMS neuro-navigational target coordinates, and/or 2) specific neuropathic pain symptom inventory (NPSI) clusters (pinpointed pain, evoked pain, and deep pain) at baseline. Results: Mean rTMS target coordinates did not differ between true (n = 45.1%) and not true responders (p = 0.436 for X, p = 0.120 for Y, and p = 0.116 for Z). The Euclidian distance between true and not true responders was 4.04 mm. When comparing differences in responders between NPSI clusters, no participant within the evoked pain cluster was a true responder (p = 0.024). Conclusion: Response to PSI-rTMS may depend on pain cluster subtype rather than on differences in targeting within the PSI.