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Background and aims Renal dysfunction is a potent risk factor for cardiovascular diseases, including stroke. This study aimed to evaluate the impact of admission estimated glomerular filtration rate (eGFR) levels on short-term (1-month) and long-term (1-year) mortality in patients with acute ischemic stroke. Methods From the Taiwan Stroke Registry data, we classified ischemic stroke patients, identified from April 2006 to December 2015, into 5 groups by eGFR at admission: ≥ 90, 60–89, 30–59, 15–29, and Results Among 52,732 ischemic stroke patients, 1480 died within one month. The 1-month mortality rate was over 5-fold greater in patients with eGFR Conclusions After acute ischemic stroke, patients with reduced eGFR are at elevated risks of short-term and long-term deaths in a graded relationship.

Trans-cinnamaldehyde (TCA), an essential oil in cinnamon powder, may have beneficial effects as a treatment for stroke which is the second leading cause of death worldwide. Post-ischemic inflammation induces neuronal cell damage after stroke, and activation of microglia, in particular, has been thought as the main contributor of proinflammatory and neurotoxic factors. The purpose of this study was to investigate the neuroprotective effects of TCA in an animal model of ischemia/reperfusion (I/R)-induced brain injury and the neuroprotective mechanism was verified in LPS-induced inflammation of BV-2 microglial cells. Our results showed that TCA (10-30 mg/kg, p.o.) significantly reduced the infarction area, neurological deficit score and decreased iNOS and COX-2 protein expression level in I/R-induced injury brain tissue. It inhibited 0.5 µg/ml LPS-induced NO production in BV-2 microglial cells without affecting cell viability, reduced protein expression of iNOS and COX-2, and attenuated inhibition of p53 protein. TCA also suppressed the effects of LPS-induced nuclear translocation of NF-κB p65 and p50 and increased cytosolic IκBα. It also reduced LPS-induced mRNA expression of iNOS, COX-2, and TNFα. We concluded that TCA has a potential neuroprotective effect to against the ischemic stroke, which may be via the inhibition of neuroinflammation through attenuating iNOS, COX-2 expression and NF-κB signaling pathway.

Background Inflammation-related microvasculr disease, albuminuria, and rapid deterioration of renal function can accelerate the development of end-stage renal disease (ESRD). The role of hip fracture (HFr), a disorder that involves inflammation, in the development of ESRD has not been fully investigated. This study explored whether HFr increases the risk of ESRD. Methods Taiwan National Health Insurance inpatient claims were used to identify 83,550 patients newly diagnosed with HFr from 2000 to 2006, and 83,550 age- and sex-matched patients without HFr were randomly selected for comparison. Hazards of ESRD combined with HFr, comorbidities, including hypertension, hyperlipidemia, peripheral arterial disease, osteoporosis and asthma, and general health status, with Charlson comorbidity index (CCI), were assessed using data to the end of 2011. Results ESRD risk was 1.42-fold higher (95% confidence interval [CI]:1.29–1.33) in the HFr cohort than in the control group, which was computed using the Cox proportional model. Age-specific analysis revealed that the adjusted hazard ratios (aHRs) of ESRD for HFr patients increased slightly as age increased, with an aHR of 1.56 (95% CI:1.35–1.81) for patients 65–74 years old, which gradually decreased to 0.88 (95% CI:0.66–1.18) for patients ≥ 85 years old. ESRD risk increased as HFr severity increased, with an aHR of 6.71 (95% CI:5.90–7.63) for patients with severe HFr. Conclusion This study is the first to report that HFr, in combination with underlying osteoporosis-related chronic illness, microvascular disease and chronic inflammation, is associated with an increased risk of ESRD, particularly among relatively younger people.

Summary Purpose Inflammatory processes, which raise the unsteadiness of brain neuron membrane potentials, might enhance the development of epilepsy. Inflammation is a substantial indicator of epilepsy risk. In this study, we evaluated whether chronic osteomyelitis (COM), a chronic inflammatory disease, increases epilepsy risk. Materials and methods A Taiwanese national insurance claims dataset of more than 22 million enrollees was used to select 20,996 COM patients and 83,973 randomly selected age- and gender-matched controls to investigate epilepsy development over an 11-year follow-up period, starting on January 1, 2000 and ending on December 31, 2010. The epilepsy risk was analyzed using a Cox proportional hazards regression model. Results Comorbidities known to elevate epilepsy risk, including diabetes, hypertension, head injury, stroke, and cancer, were commonly noted in the COM cohort, which had considerably higher risk of epilepsy than did the control group. Comparing only those without comorbidities, COM patients still exhibited higher epilepsy risk than the control group did (adjusted hazard ratio [aHR] = 3.87, 95% confidence interval [CI]: 3.01–4.98). The younger population exhibited an even greater risk (age ≤39 years: aHR = 6.10, 95% CI: 4.00–9.30; age ≥65 years: aHR = 1.66, 95% CI: 1.28–2.16). Conclusion This is the first study linking COM to an increased risk in epilepsy development. The results demonstrated that COM is a significant predictor of epilepsy. Further study of COM patients, particularly young patients, is recommended to facilitate epilepsy prevention.

Background and aims This cohort study assessed the association between inflammatory bowel disease (IBD) and the risk of future ischemic stroke. Methods The IBD cohort comprised adult patients (≥ 20 years old) who had received either ambulatory or inpatient care between 1998 and 2011 and IBD-free controls were randomly selected from the general population and frequency matched according to age, sex, and index year (included 18,392 patients with IBD and 73,568 control patients). Both cohorts with ischemic stroke before the index date and the ischemic stroke cases diagnosed within one year after the index date were excluded. We observed the study patients until the incidence of ischemic stroke, death, withdrawal from the insurance program, or they were lost to follow-up, or the end of 2011. Results The risk of ischemic stroke was 1.12-fold (95% CI, 1.02–1.23) higher among the IBD cohort than among the non-IBD cohort. Compared to the subjects without IBD, the adjusted HR of ischemic stroke was 1.15 (95% CI 1.04–1.28) in the Crohn's disease (CD) patients and 1.01 (95% CI 0.84–1.21) in the ulcerative colitis (UC) group. The risk of developing ischemic stroke significantly increased with the increased frequency of IBD exacerbation and hospitalization. Furthermore, the adjusted HR among the CD patients increased in conjunction with the number of medical visits, from 1.07 to 6.36 and the adjusted HR among the UC patients also increased in conjunction with the number of medical visits, from 1.11 to 2.10. Conclusions IBD exhibited an increased risk of developing ischemic stroke.

Background/Aims: We investigated the association of hypertensive encephalopathy (HE) with subsequent dementia. Methods: Using universal insurance claims data, we identified a study cohort of 5,504 participants with HE newly diagnosed between 1997 and 2010 and a comparison cohort of 22,016 healthy participants. Incidence and risks of dementia were estimated for both cohorts until the end of 2010. Results: The dementia incidence was 1.45-fold [95% confidence interval (CI) = 1.27-1.66] higher in the study cohort than in the comparison cohort, with an adjusted hazard ratio (HR) of 1.38 (95% CI = 1.19-1.59) for the study cohort. The risk was higher for males than for females and elderly patients. With an incidence of 13.4 per 1,000 person-years, the HR of dementia increased to 2.09 (95% CI = 1.18-3.71) for the HE patients with the comorbidities of head injury and diabetes compared to those without HE and comorbidities. The risk of developing dementia declined with the follow-up time. Conclusion: Hypertensive patients with HE displayed a significantly higher risk for dementia than those without HE. The risk increased further in those with the comorbidities of head injury and diabetes. Physicians should be aware of the link between HE and dementia when assessing patients with HE.

Aim The aim of this study was to investigate the possible association between benzodiazepine (BZD) use and risk of incident stroke by utilizing data from 2000 to 2003 from the National Health Insurance system of Taiwan. Methods Study subjects consisted of 38 671 patients with new BZD use and 38 663 people without BZD use who were frequency-matched for age, sex and baseline comorbidity with BZD users. All subjects had no history of stroke. Each study patient's case was followed until a new diagnosis of stroke was made or until the patient was censored by loss to follow up, death, or termination of insurance. The study lasted until the end of 2009. A Cox proportional hazards regression model was used to estimate the incidences and hazard ratios (HR) of stroke. Results The HR of hemorrhagic stroke was significantly lower in the BZD group when compared with the non-BZD group. For patients aged 20–39 years, the HR of ischemic stroke was significantly higher in the BZD group when compared with the non-BZD group. Compared to the non-BZD group, patients with a lower annual dosage (

Botulism is a rare but serious paralytic disease caused by botulinum toxin. We report an outbreak of type B botulism in Taiwan in 2006. There were five cases involved in this outbreak. They present ileus and acute cranial nerve dysfunction including dysphagia and blurred vision. One of them had severe neurologic impairment and required mechanical ventilatory support. No patient received antitoxin administration because of delayed diagnosis. The food specimen revealed positive botulism toxin B. There were no fatalities. Consumption of fermented food was significantly associated with this outbreak. We also reviewed the characteristics of cases with botulism in Taiwan since 1985.

Objective Movement-related cortical potentials (MRCP; nomenclature of MRCP components according to Shibasaki and Hallett (Shibasaki H, Hallett M. What is the Bereitschaftspotential? Clin Neurophysiol 2006;117:2341–56) were studied in patients with Machado–Joseph disease (MJD) to elucidate the pathophysiology of voluntary movement. Methods We studied nine genetically proven MJD patients and eight age-matched healthy subjects. Multi-channel electroencephalogram (EEG) recordings were obtained during self-paced fast extensions of the wrist. EEG epochs were time-locked to electromyography (EMG) onset or offset of the voluntary EMG burst and averaged. Results In the MJD patients, the early Bereitschaftspotential (early BP, −1500 to −500 ms) was not affected but the late BP was reduced over the central midline area and contralaterally to the movement side. The amplitude of the fpMP, a post-movement MRCP component, was also reduced. In addition, the offset cortical potential in the first 500 ms after EMG offset (Moff + 500) was attenuated bilaterally over a wide cortical area. Conclusions Findings suggest that cortical activations associated with the initiation and termination of a voluntary movement are impaired in MJD patients. Significance Abnormalities of pre- and post-movement MRCP components provide researchers with pathophysiological insight into voluntary motor dysfunction in MJD.

The aim of this study was to investigate the possible association between benzodiazepine (BZD) use and risk of incident stroke by utilizing data from 2000 to 2003 from the National Health Insurance system of Taiwan.Study subjects consisted of 38,671 patients with new BZD use and 38,663 people without BZD use who were frequency-matched for age, sex and baseline comorbidity with BZD users. All subjects had no history of stroke. Each study patient's case was followed until a new diagnosis of stroke was made or until the patient was censored by loss to follow up, death, or termination of insurance. The study lasted until the end of 2009. A Cox proportional hazards regression model was used to estimate the incidences and hazard ratios (HR) of stroke.The HR of hemorrhagic stroke was significantly lower in the BZD group when compared with the non-BZD group. For patients aged 20-39 years, the HR of ischemic stroke was significantly higher in the BZD group when compared with the non-BZD group. Compared to the non-BZD group, patients with a lower annual dosage (1 g) or duration (30 days) of BZD use had a lower risk of stroke in the elder group (P 0.0001) and patients with a higher annual dosage (≥ 4 g) or duration (≥ 95 days) of BZD use had a higher risk of stroke in all age groups (P 0.0001).Our findings may suggest neuroprotection under lower-dosage BZD use and neurotoxicity under higher-dosage BZD use.

Objective Inflammatory processes, which provoke alternations of neurotransmitter metabolism, neuroendocrine function, and neuroplasticity in the brain, might promote depression. In depression patients who do not exhibit risk factors, including hypertension, diabetes, coronary heart disease, stroke, Parkinson's disease and dementia, particularly in young people, inflammation is a likely risk factor for depression. We explored whether chronic osteomyelitis (COM), a chronic inflammatory disease, increases depression risk. Methods A Taiwanese national insurance claims data set of more than 22 million enrollees was used to select 15,529 COM patients without depression history and 62,116 randomly selected age- and gender-matched controls without depression and COM history to trace depression development for an 12-year follow-up period from January 1, 1999 to December 31, 2010. The depression risk was analyzed using the Cox proportional hazards regression model. Results The above-mentioned risk factors for depression were more frequent in the COM cohort, who exhibited significantly higher depression risk than the control group did. Comparing only those without comorbidities, the COM group exhibited higher depression risk than the control group did (hazard ratio [HR] = 3.04, 95% confidence interval [CI]: 2.55–3.62). The younger population carried even greater risk (age 65: HR = 1.75, 95% CI: 1.39–2.19). Conclusions This is the first study connecting COM to increased risk of developing depression. The outcomes suggest that COM is a substantial depression predictor and call for a closer focus on these patients for more rigorous depression prevention, particularly in young people.