Sensorimotor responses to repeated electrical stimulation of the superior laryngeal nerve were compared in 8 patients with adductor spasmodic dysphonia (ADSD) and 11 normal controls to determine if adductor response disinhibition occurred in ADSD. Pairs of electrical pulses were presented at interstimulus intervals varying from 100 to 5,000 milliseconds (ms). Three responses were measured in thyroarytenoid muscles: ipsilateral R1 responses at 17 ms and ipsilateral and contralateral R2 responses between 60 and 75 ms. Conditioned response characteristics, the percent occurrence and percentage amplitude of initial responses, were measures of response inhibition. As a group, the patients had reduced response inhibition: their conditioned ipsilateral R1 response amplitudes were increased, as was the frequency of their conditioned contralateral muscle responses (p < or = .002) compared to normal. However, the patients' initial responses were normal in latency and frequency characteristics, demonstrating that the brain stem mechanisms for these responses were intact. These results suggest a central disinhibition of laryngeal responses to sensory input in ADSD.

Electronic cigarette (e-cigarette) usage in the USA has drastically increased in the past 5 years due to age restrictions on conventional cigarettes, aggressive marketing and a perception that e-cigarettes are a healthy alternative. E-cigarettes contain nicotine, water, glycerol, propylene glycol and optional flavouring. On inhalation, the device heats the ingredients into a vapour [1]. While tobacco cigarette smoke is known to cause deleterious effects on the cardiovascular system, angiogenesis and skin capillary perfusion by causing direct injury to blood vessel walls, increased platelet aggregation, microvascular thrombosis [2-4] and inflammation [5], the consequences of e-cigarette vapour exposure on the lung are still largely unexplored [6, 7]. Recently, LERNER et al. [8] reported that vapours produced by e-cigarettes and e-cigarette fluids with flavourings induced toxicity, oxidative stress and inflammatory response in human bronchial airway epithelial cells (H292) and fetal lung fibroblasts (HFL1) as well as mouse lung. GARCIA-ARCOS et al. [9] showed that the aerosolised nicotine-containing e-cigarette fluid increased airway hyperreactivity, distal airspace enlargement, mucin production, and cytokine and protease expression in mice, implying potential dangers of nicotine inhalation during e-cigarette use. The inflammatory response to e-cigarette use involved increased neutrophil activation and mucus production [10], and decreased mucociliary clearance [11]. In human embryonic and mouse neural stem cells, human pulmonary fibroblasts [12], and skin and lung cells [13], cytotoxicity of e-cigarette vapour was correlated with the number and concentration of chemicals used to flavour the fluids. We recently showed in the skin flap survival model in vivo that nicotine-containing e-cigarette vapour is just as harmful to the microcirculation as tobacco cigarette smoke [4]. In the present study, we examined whether long-term exposure to e-cigarette vapour or nicotine produce the same damaging effect on lung structure and vasculature as tobacco smoke in a rat model in vivo. 6-week-old, male Sprague Dawley rats (Envigo Laboratories, Denver, CO, USA) were divided into four groups of eight animals per group and exposed for 5 weeks as follows. 1) Room air. 2) Subcutaneous injections of (−)-nicotine ditartrate (Sigma Aldrich, St Louis, MO, USA) 2 mg•kg −1 twice daily; the amount of nicotine for injections was based on that known from previous studies to produce stable plasma nicotine levels of approximately 25 ng•mL −1 , which is compatible with plasma levels in habitual smokers [14, 15]. 3) Blu E-cigs (Classic Tobacco Flavour (Blu, Charlotte, NC, USA), containing 12 mg•mL −1 nicotine) vapour produced in a TE-2E e-cigarette smoking machine (Teague Enterprises, Davis, CA, USA); the coil temperature of the e-cigarettes was within the normal range usually used by vapers (200-250°C). Rats in this group were exposed to 48 mg nicotine per day [4]. Our experimental design, by subjecting rats to e-cigarette vapour, is a major imp...

Both the medium-content and high-nicotine content e-cigarette exposure groups had similar amounts of flap necrosis and hypoxia when compared with the tobacco cigarette exposure group. Nicotine-containing e-cigarette vapor is similarly toxic to skin flap survival as tobacco cigarettes.

Previously, we demonstrated that patients with adductor spasmodic dysphonia (ADSD) have a disinhibition of laryngeal responses to sensory input. In this study, sensorimotor responses to stimulation of the superior laryngeal nerve were compared between 10 subjects with abductor spasmodic dysphonia (ABSD) and 15 normal volunteers. The groups had similar latency and frequency characteristics of their unconditioned adductor responses (p>.05). The conditioned R1 (early) responses of the subjects with ABSD were greater and more variable in amplitude than those of the normal volunteers (p< or =.008). Similar R2 (late) conditioning effects were found in both groups, with a nonsignificant trend toward reduced inhibition of contralateral R2 responses at lower interstimulus intervals (p = .01) in the patient group. Thus, inhibitory mechanisms that modulate the R1 laryngeal sensorimotor pathway in the brain stem may be abnormal in subjects with ABSD. Abnormal modulation of laryngeal sensorimotor responses seems present in both types of spasmodic dysphonia.

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