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Objective: The impact of laryngeal dysfunction on airflow has not been well characterized in motor neuron disease (MND). This study aimed to detect and characterize extreme airflow oscillations informally observed during volitional cough and forced vital capacity (FVC) tasks in individuals with MND who demonstrated neurolaryngeal impairments including reduced speed and extent of vocal fold abduction compared to healthy controls during volitional cough expulsion. The extreme airflow oscillations in the MND group, when viewed as a flow-volume loop, appeared similar to the "sawtooth-sign." If the airflow oscillations are periodic in a range similar to phonation, they may reflect reduced laryngeal patency. Methods: Volitional cough and FVC airflow data (3 trials each) from 12 participants with MND with bulbar/laryngeal involvement (3 F; ages 45-76) and 12 healthy controls (6 F; ages 41-68) were analyzed for periodicity. Percent and absolute durations of periodicity of the flow oscillations were calculated by an algorithm applied to the airflow signals. In addition, the frequency, magnitude, and kurtosis of the periodic airflow oscillations were described and compared between groups. Results: In both volitional cough and FVC trials, the percent of airflow periodicity during forced expiration was significantly higher (z = 3.54) in individuals with MND, adjusted for age and sex. Periodic airflow accounted for on average 28% of the total time in participants with MND and was within a frequency range similar to phonation. Magnitude of the airflow oscillations was also larger for participants with MND (z = 3.46), and kurtosis of airflow was smaller (z = −4.70) during forced expiration, indicating persistent airflow oscillations throughout exhalation. Conclusions: The significantly larger-magnitude, lower-kurtosis, and more prominent presence of sawtooth-like airflow periodicity within a frequency range similar to phonation observed in individuals with MND with neurolaryngeal impairments suggests glottic airflow resistance during forced expiration. [ABSTRACT FROM AUTHOR]

Background: Several cases of herpes zoster‐induced psoriasis have been reported in the literature. Objective: Our nationwide retrospective cohort study is designed to examine the risk association between herpes zoster and psoriasis. Methods: From the Taiwan National Health Insurance Research Database, 26,623 patients from 1999 to 2013 with a diagnosis of herpes zoster and no prior history of psoriasis were selected as the study subjects. The control group was established during the study period from those without a herpes zoster diagnosis and was propensity score matched to minimize confounding factors. Both cohorts were followed for cases of psoriasis development. Data analysis was done via Kaplan–Meier analysis and Cox Proportional‐Hazards Models. Results: Comparing the study group to control, the adjusted hazard ratio was 1.66 (95% CI, 1.31–2.13: p < 0.05) after adjusting for covariates (age, gender, urbanization, selected comorbidities and selected medications use). Statistical analysis found no interaction effect among herpes zoster and other covariates for risk modification of psoriasis development. Conclusion: This study demonstrated an increased risk of psoriasis in patients diagnosed with herpes zoster. [ABSTRACT FROM AUTHOR]

Objectives: The purpose of the experiment was to study the effect of L-NAME (N(Omega)-nitro-L-arginine methyl ester) and its cotreatment with lidocaine on the spinal block and infiltrative cutaneous analgesia. Methods: The quality of cutaneous analgesia was examined by the block of the cutaneous trunci muscle reflexes following needle stimuli in the rat. Spinal anaesthetic potency was assessed by measuring three neurobehavioral examinations of nociceptive, proprioceptive and motor function following intrathecal injection in the rat. Key findings: L-NAME (0.6, 6 and 60 nmol) when cotreatment with lidocaine (ED50) produced dose-related cutaneous analgesia. Coadministration of L-NAME (0.6 μmol) with lidocaine intensified (P < 0.01) and prolonged (P < 0.001) cutaneous analgesia, whereas subcutaneous L-NAME (0.6 μmol) and saline did not provoke cutaneous analgesic effects. Adding L-NAME (2.5 μmol) to lidocaine intrathecally prolonged spinal sensory and motor block (P < 0.01), while intrathecal L-NAME (2.5 μmol) or 5% dextrose (vehicle) produced no spinal block. Conclusions: L-NAME at 60 nmol (the minimum effective dose) increases and prolongs the effect of cutaneous analgesia of lidocaine. L-NANE at an ineffective dose potentiates lidocaine analgesic and anaesthetic effects. [ABSTRACT FROM AUTHOR]

We report a case of late‐onset Schnitzler syndrome successfully treated with Janus‐activated kinase (JAK) inhibitors and colchicine. Schnitzler syndrome should be considered for recurrent chronic urticaria when accompanied by fever, fatigue, rapid weight loss, and poor response to antihistamine treatment. Skin biopsy, bone marrow biopsy, and electrophoresis help confirm the diagnosis. Early diagnosis and treatment can lead to complete resolution of symptoms. Besides interleukin (IL)‐1 and IL‐6 inhibitors, JAK inhibitors and colchicine may be considered as other choices of treatment. [ABSTRACT FROM AUTHOR]