Each completed a questionnaire that included views of the female body and described up to 5 interstitial cystitis/painful bladder syndrome pains, noting 40 descriptors for each.
Results: Two-thirds of the 226 patients reported
multiple pains. Pain could be consolidated at 4 sites, including suprapubic, urethral, genital and nongenitourinary. Most descriptors were similar and little evidence indicated that 1 pain influenced pain at another site. Another 3 patterns were evident, including 1) a suprapubic > urethral > genital > nongenitourinary ranking in site distribution and at each site proportions that were Entrectinib solitary, the worst and the most frequent pains, and pains that responded to bladder events, 2) site specific allodynia, check details and 3) for urethral and genital pains a wider spectrum of sensations, including burning, stinging and sharp. Patients with urethral (38%) or genital (27%) pain did not differ from those without such pain in 95% of 44 important characteristics.
Conclusions: Suprapubic
prominence and changes in the voiding cycle are features consistent with but do not prove that the bladder is the pain generator in interstitial cystitis/painful bladder syndrome and the pain sites described by patients are referred from it. The patients with interstitial cystitis/painful bladder syndrome who might have been diagnosed with vulvodynia or urethral syndrome did not differ from others in important patient variables.”
“We have previously demonstrated that pallidotegmental GABAergic neurons play a crucial role in prepulse inhibition (PPI) of the startle reflex in mice through the activation of GABA(B) receptors in pedunculopontine tegmental neurons. In this study, we investigated whether PPI disruption induced by methamphetamine ( METH) or MK-801 is VEGFR inhibitor associated with the dysfunction of pallidotegmental neurons. Furthermore, we examined the effects of baclofen, a GABA(B) receptor agonist,
on METH- and MK-801-induced PPI impairment. Acute treatment with METH ( 3 mg/kg, subcutaneouly (s.c.)) and MK-801 (>0.3 mg/kg, s.c.) significantly disrupted PPI, accompanied by the suppression of c-Fos expression in lateral globus pallidus induced by PPI. Furthermore, acute treatment with METH and MK-801 stimulated c-Fos expression in the caudal pontine reticular nucleus (PnC) in mice subjected to the PPT test, although PPI alone had no effect on c-Fos expression. Repeated treatment with 1 mg/kg METH for 7 days, which did not affect PPI acutely, showed similar effects on PPI and c-Fos expression to acute treatment with METH ( 3 mg/kg). Baclofen dose-dependently ameliorated PPI impairment induced by acute treatment with METH ( 3 mg/kg) and MK-801 ( 1 mg/kg), and decreased METH- and MK-801-stimulated c-Fos expression in PnC to the basal level. These results suggest that dysfunction of pallidotegmental neurons is involved in PPI disruption caused by METH and MK-801 in mice.