Hsuan‐Te Chu

BACKGROUND: While migraines have been associated with emotional disturbances, it remains unknown whether the intensity of emotional expression is directly related to migraine frequency. OBJECTIVE: The present study investigated depression/anxiety among migraineurs. METHODS: This cross-sectional study included 588 clinical outpatients in Taiwan. Migraines were stratified by attack frequency, with and without auras, and with well-controlled confounding variables. Demographic and clinical data, including sleep characteristics, were collected. Multivariable linear regressions were employed to examine whether migraine frequency (1-4 headache days per month, 5-8 headache days per month, 9-14 headache days per month, or >14 headache days per month) was associated with depression/anxiety symptoms, as indicated by the Beck's Depression Inventory (BDI) and Hospital Anxiety and Depression Subscales (HADS). RESULTS: BDI total scores were highest in patients with chronic migraines (mean ± SD: 13.2 ± 8.5), followed by those with high frequency (12.1 ± 8.5), medium frequency (10.6 ± 8.0), low frequency (9.1 ± 7.1), and lowest in nonmigraine controls (6.6 ± 5.9), with a significant trend in frequency (P trend < .001); similar results were obtained for HADS scores. BDI and HADS scores were independently related to high-frequency episodic and chronic migraine frequency and to poor sleep quality. The relationship between BDI score and migraine frequency was present in both aura-present (P trend = .001) and aura-absent subgroups (P trend = .029). CONCLUSION: Higher migraine frequency, either with or without auras, correlated with higher symptom scores of anxiety and depression.

Young people are disproportionately affected by sexually transmitted infections (STIs). The risk of STIs in young people following first-episode schizophrenia is unknown. This study using Taiwan's National Health Insurance Research Database enrolled 44 109 adolescents and young adults with first-episode schizophrenia and 176 436 age- and sex-matched controls without schizophrenia from 2001 through 2009 and followed to the end of 2011. New-onset STIs were identified. Survival analysis was performed. Cox regression analysis was used to examine the effects of comorbid substance use disorder (SUD), schizophrenia medications, and schizophrenia severity. The E value for causality of evidence was calculated. We found that young people had a higher risk of STIs following first-episode schizophrenia compared with controls without schizophrenia (hazard ratio [HR] = 2.35, 95% CI = 2.08-2.64); these STIs included human immunodeficiency virus (HIV) (3.70, 2.60-5.28) and syphilis (5.35, 3.96-7.23). They also showed a disproportionate distribution of STIs, with an increased proportion of syphilis (20.4% vs 8.2%) and HIV (9.1% vs 6.0%). When presenting with SUD, the risks of HIV (11.00, 7.02-17.25) and syphilis (9.11, 6.16-13.47) were further increased. The severe schizophrenia group had an extremely high risk of syphilis (41.26, 27.69-61.47) and HIV (7.50, 3.85-14.62). Schizophrenia medications may provide beneficial effects against contracting STIs (0.77, 0.68-0.89). We concluded that following first-episode schizophrenia, young patients are at higher risk of STIs, particularly HIV and syphilis. The risk further increased when subjects presented with SUD or severe schizophrenia. Importantly, antipsychotic treatment may lower the risk of STIs.

AIMS: Obstructive sleep apnea (OSA) and insomnia commonly coexist; hypnotics are broadly prescribed for insomnia therapy. However, the safety of hypnotics use in OSA patients is unclear. We conducted a retrospective case-control study to investigate the risk of adverse respiratory events in hypnotics-using OSA patients. METHODS: We obtained data from the Taiwan National Health Insurance Database from 1996 to 2013. The case group included 216 OSA patients with newly-diagnosed adverse respiratory events, including pneumonia and acute respiratory failure. The control group included OSA patients without adverse respiratory events, which was randomly frequency-matched to the case group at a 1:1 ratio according to age, gender, and index year. Hypnotics exposure included benzodiazepines (BZD) and nonbenzodiazepines (non-BZD). A recent user was defined as a patient who had taken hypnotics for 1 to 30 days, while a long-term user was one who had taken hypnotics for 31 to 365 days. RESULTS: Multivariable adjusted analysis showed recent BZD use is an independent risk for adverse respiratory events (OR = 2.70; 95% CI = 1.15–6.33; P < 0.001). Subgroup analysis showed both recent and long-term BZD use increased the risk of acute respiratory failure compared to never BZD use (OR = 28.6; 95% CI = 5.24–156; P < 0.001, OR = 10.1; 95% CI = 1.51–67.7; P < 0.05, respectively). Neither BZD nor non-BZD use increased the risk of pneumonia in OSA patients. CONCLUSION: BZD use might increase the risk of acute respiratory failure in OSA patients.

Brain degeneration in patients with Alzheimer’s disease (AD) results from the accumulation of pathological amyloid-β (Aβ) plaques and tau protein tangles, leading to altered plasma levels of biomarkers. However, few studies have investigated the association between plasma biomarkers and cognitive impairment in patients with AD. In this cross-sectional study, we investigated correlations between mini-mental state examination (MMSE) scores and levels of plasma biomarkers in patients with amnestic mild cognitive impairment (aMCI) and AD. Thirteen individuals with normal cognition, 40 patients with aMCI, and 37 patients with AD were enrolled. Immunomagnetic reduction was used to assess the levels of plasma biomarkers, including amyloid Aβ1-40, Aβ1-42, total tau protein (t-Tau), and phosphorylated tau protein (threonine 181, p-Tau181). Our analysis revealed a significant negative correlation between MMSE and both measures of tau, and a trend toward negative correlation between MMSE and Aβ1-42. In a longitudinal study involving three patients with aMCI and two patients with AD, we observed strong negative correlations (r &lt; −0.8) between changes in MMSE scores and plasma levels of t-Tau. Our results suggest that plasma levels of t-Tau and p-Tau181 can be used to assess the severity of cognitive impairment in patients with AD. Furthermore, the results of our preliminary longitudinal study suggest that levels of t-Tau can be used to monitor the progression of cognitive decline in patients with aMCI/AD.