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Saliva and its defence systems such as antioxidants and minerals are very important in the pathogenesis of different diseases. Cigarette smoking has many destructive effects. Oxidative stresses play an important role in the side effects of smoking. This study assessed the effect of cigarette smoking on salivary levels of catalase, vitamin C, and α-amylase.
This retrospective cohort study was carried out in Hamadan, Iran, on 510 subjects; 259 subjects were smokers (the exposed group) and 251 were non-smokers (the unexposed group). Five microliters of unstimulated saliva was collected by spitting method. Catalase, vitamin C, and α-amylase salivary levels were determined by spectrophotometric assay. Data were analyzed with t-test using STATA 12.
Vitamin C level in smokers was significantly lower than that in non-smokers. The salivary catalase levels were lower and α-amylase levels were higher in smokers, but the differences were not statistically significant (P = 0.416 and P = 0.265, respectively). Smokers were younger than non-smokers.
Smoking resulted in a change in salivary antioxidant levels. Changes in antioxidant levels can influence the deleterious effects of smoking on oral mucosa; it might also indicate systemic changes and changes in the serum levels of oxidative agents. Further studies are necessary to understand the mechanisms and real effects of smoking, to determine the benefits of supplementary antioxidants for treatment and to reduce the dangerous side effects of smoking.
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Stimulus frequency otoacoustic emissions (SFOAEs) are produced by cochlear irregularities reflecting energy from the peak region of the traveling wave (TW). Activation of medial olivocochlear (MOC) efferents reduces cochlear amplification and otoacoustic emissions (OAEs). In other OAEs, MOC activation can produce enhancements. The extent of MOC enhancements of SFOAEs has not been previously studied. In anesthetized guinea pigs, we electrically stimulated MOC fibers and recorded their effects on SFOAEs. MOC stimulation mostly inhibited SFOAEs but sometimes enhanced them. Some enhancements were not near response dips and therefore cannot be explained by a reduction of wavelet cancelations. MOC stimulation always inhibited auditory-nerve compound action potentials showing that cochlear-amplifier gain was not increased. We propose that some SFOAE enhancements arise because shocks excite only a small number of MOC fibers that inhibit a few scattered outer hair cells thereby changing (perhaps increasing) cochlear irregularities and SFOAE amplitudes. Contralateral sound activation is expected to excite approximately one third of MOC efferents and may also change cochlear irregularities. Some papers suggest that large SFOAE components originate far basal of the TW peak, basal of the region that receives cochlear amplification. Using a time-frequency analysis, we separated SFOAEs into components with different latencies. At all SFOAE latencies, most SFOAE components were inhibited by MOC stimulation, but some were enhanced. The MOC inhibition of short-latency SFOAE components is consistent with these components being produced in the cochlear-amplified region near the TW peak.
Background
SUNCT like syndrome secondary to post herpes zoster infection has not been reported in literature.
CaseWe are reporting two cases of SUNCT like syndrome secondary to post herpes zoster infection of the V1 distribution of the trigeminal nerve. Treatment with pregabalin and lamotrigine achieved complete symptomatic relief in both patients.
ConclusionSUNCT like syndrome can occur after herpetic infection of the trigeminal nerve. Unlike primary SUNCT syndrome, post-herpetic SUNCT like syndrome seems to respond well to pharmacological treatment and has a good prognosis.
