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Background Social functioning is crucial for daily living and is an essential indicator of dementia in patients with Parkinson's disease. The pattern of social functioning in patients with Parkinson's disease without dementia (i.e. those who are cognitively intact or have mild cognitive impairment (PD-MCI)) and its determinants are unclear. Aims In exploring the heterogeneity of social functioning among patients with Parkinson's disease-associated dementia, we determined the optimal cut-off score of the Parkinson's Disease Social Functioning Scale (PDSFS) for patients with PD-MCI, and the variables influencing patients’ social functioning. Method A total of 302 participants underwent the Mini-Mental State Examination (MMSE) and PDSFS; 120 patients with Parkinson's disease completed the measurements (MMSE, Activities of Daily Living Scale and Neuropsychiatric Inventory). Group comparisons, receiver operating characteristic curves, Spearman correlation and multiple and hierarchical regression analyses were conducted. Results The PD-MCI group scored the lowest on the PDSFS (F = 10.10, P < 0.001). The PDSFS cut-off score was 53 (area under the curve 0.700, sensitivity 0.800, specificity 0.534). The MMSE (β = 0.293, P = 0.002), Activities of Daily Living Scale (β = 0.189, P = 0.028) and Neuropsychiatric Inventory (β = −0.216, P = 0.005) scores predicted the PDSFS score. Further, there was an interaction effect between the Activities of Daily Living Scale and Neuropsychiatric Inventory scores on the PDSFS score (β = 0.305, P < 0.001). Conclusions We determined a PDSFS cut-off score for detecting PD-MCI and found that patients with PD-MCI have social dysfunction. Future research should focus on the effects of neuropsychiatry symptoms and activities of daily living on social functioning, and tailor the intervention programme for patients with Parkinson's disease.

BackgroundIndividuals with chronic viral hepatitis are at increased risk of experiencing poor sleep quality and sleep disturbances. However, it remains unclear whether the sleep disorders associated with viral hepatitis are secondary to the comorbidities related to viral hepatitis or the direct effect of hepatitis viruses on sleep. This study investigated the direct impact of viral hepatitis B and C on sleep quality.MethodsIndividuals with viral hepatitis B or C and their healthy counterparts were recruited for the present study, and they were evaluated with the Parkinson's Disease Sleep Scale-2, the Epworth Sleepiness Scale, and the Pittsburgh Sleep Quality Index in the absence of common comorbidities associated with viral hepatitis.ResultsNeither hepatitis B nor hepatitis C was found to cause significant differences in insomnia symptoms or excessive daytime sleepiness. However, individuals with hepatitis C, but not hepatitis B, tended to be less likely to experience restlessness of the legs or arms at night.ConclusionsThis study suggests that hepatitis viruses B and C may not cause a significant impact on sleep quality and related disorders directly. Sleep disturbances in individuals with chronic viral hepatitis may instead be attributable to hepatic decompensation or the comorbid factors associated with viral hepatitis.

Moderate coolness is sensed by TRPM8 ion channels in peripheral sensory nerves, but the mechanism by which noxious cold is detected remains elusive. Here, we show that somatosensory and sympathetic neurons express two distinct mechanisms to detect noxious cold. In the first, inhibition by cold of a background outward current causes membrane depolarization that activates an inward current through voltage-dependent calcium (CaV ) channels. A second cold-activated mechanism is independent of membrane voltage, is inhibited by blockers of ORAI ion channels and by downregulation of STIM1, and is recapitulated in HEK293 cells by co-expression of ORAI1 and STIM1. Using total internal reflection fluorescence microscopy we found that cold causes STIM1 to aggregate with and activate ORAI1 ion channels, in a mechanism similar to that underlying store-operated calcium entry (SOCE), but directly activated by cold and not by emptying of calcium stores. This novel mechanism may explain the phenomenon of cold-induced vasodilation (CIVD), in which extreme cold increases blood flow in order to preserve the integrity of peripheral tissues.

BackgroundThe commonly used screening tests for Parkinson’s disease (PD) are the Montreal Cognitive Assessment (MoCA) and Mini-Mental State Examination (MMSE), both of which only focus on cognitive function. A composite assessment that considers both cognitive and social dysfunction in PD would be helpful in detecting mild cognitive impairment (MCI) and PD dementia (PDD).ObjectiveWe aimed to simplify the commonly used tools and combine cognitive and social functioning tests to detect early MCI and PDD.Materials and MethodsA total of 166 participants (84 PD patients and 82 healthy) were recruited who completed the MMSE, MoCA, PD social functioning scale (PDSFS), clock drawing test, activities of daily living, comprehensive neuropsychological assessment (e.g., executive, attention, language, memory, and visuospatial functions), and movement disorder society (MDS)-unified PD rating scale. According to the MDS diagnostic criteria, the patients were grouped into PD-nonMCI, PD-MCI, or PDD.ResultsTo detect PD-MCI, the optimal cut-off scores for the simplified MoCA and the combined test were 9 and 35. The discrimination values measured by the area under the receiver operating characteristic curve (AUC) of the two tests were 0.767 (p < 0.001) and 0.790 (p < 0.001). When the simplified MoCA was 7 or the combined test 30, the patients would be classified as having PDD. The AUCs of the two tests were 0.846 (p < 0.001) and 0.794 (p = 0.003).ConclusionWe suggest considering both cognitive and social functions when detecting PD-MCI and PDD.

The direct impact of chronic hepatitis B and hepatitis C on neurocognition remains elusive due to the frequent comorbidities, and the domains of the neurocognitive functions affected have rarely been investigated comprehensively. We cross-sectionally assessed the neurocognitive functions of the individuals with chronic hepatitis B, chronic hepatitis C, treated chronic hepatitis C with a sustained virologic response, and their healthy control counterparts. Laboratory examinations were used to investigate the impact of inflammation on neurocognition, exclude the medical conditions that could interfere with neurocognition assessment, and assess liver function and fibrotic severity of the liver of the participants. This study found the detrimental impact of chronic hepatitis B on language and executive functions. In contrast, individuals with chronic hepatitis C showed deficits in executive functions, psychomotor speed, memory, and attention. Successful elimination of hepatitis C resulted in improved liver function, but not neuropsychological test performance. Moreover, erythrocyte sedimentation rate level was found to mediate the deficits in the attention of individuals with chronic hepatitis C. These results demonstrate the neurocognitive deficits and the difference in the profiles of neurocognitive deficits in individuals with chronic hepatitis B and chronic hepatitis C. Our study also provided results suggesting the mediation by systemic inflammation on the attention deficit in individuals with chronic hepatitis C.

Background: Hypomimia is a clinical feature of Parkinson’s disease (PD). Based on the embodied simulation theory, the impairment of facial mimicry may worsen facial emotion recognition; however, the empirical results are inconclusive. Objective: We aimed to explore the worsening of emotion recognition by hypomimia. We further explored the relationship between the hypomimia, emotion recognition, and social functioning. Methods: A total of 114 participants were recruited. The patients with PD and normal controls (NCs) were matched for demographic characteristics. All the participants completed the Mini-Mental State Examination and the Chinese Multi-modalities Emotion Recognition Test. In addition to the above tests, the patients were assessed with the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale and Parkinson’s Disease Social Functioning Scale (PDSFS). Results: Patients with PD with hypomimia had worse recognition of disgust than NCs (p = 0.018). The severity of hypomimia was predictive of the recognition of disgust (β= –0.275, p = 0.028). Facial emotion recognition was predictive of the PDSFS score of PD patients (β= 0.433, p = 0.001). We also found that recognizing disgust could mediate the relationship between hypomimia and the PDSFS score (β= 0.264, p = 0.045). Conclusion: Patients with hypomimia had the worst disgust facial recognition. Hypomimia may affect the social function of PD patients, which is related to recognizing the expression of disgust. Emotion recognition training may improve the social function of patients with PD.

This study aimed to understand the impact of sex on the neurocognitive function of patients with Parkinson’s disease (PD). Ninety-four participants with idiopathic PD and 167 age-matched healthy individuals as normal controls (NCs) were recruited and underwent comprehensive neuropsychological assessments. Sex differences were found in NCs, but not in patients with PD. Among male participants, patients with PD showed worse performance on the Digit Symbol Substitution (DSS) (p &lt, 0.001) test and Symbol Search (SS) (p &lt, 0.001) than NCs. Among female participants, patients with PD showed worse performance on the category score of the Modified Wisconsin Card Sorting Test (p &lt, 0.001), SS (p &lt, 0.001), and pentagon copying (p &lt, 0.001) than NCs. After controlling for the effects of age and years of education, Hoehn and Yahr stage was found to predict the performance of the Color Trails Test part A (βA = 0.241, pA = 0.036), Stroop Color and Word Test (β = −0.245, p = 0.036), and DSS (β = −0.258, p = 0.035) in men with PD. These results indicate the differential effect of sex on the neurocognitive function among healthy aging and PD populations. The disappearance of sex differences, which is present in healthy aging, in patients with PD suggests a gradual loss of the neuroprotective effect of estrogen after the initiation of the neurodegenerative process. This study also found mental flexibility and visuospatial function to be the susceptible cognitive domains in women with PD, while the disease severity could predict the working memory and processing speed in men with PD.

Viral hepatitis is a devastating disease with the risk for cirrhosis and carcinogenicity. Regulatory T cells (Tregs) play important roles in the disease course of viral hepatitis via maintaining the balance between overt‐immune responses and viral replications. We hypothesized that genetic polymorphisms of Treg‐related genes, such as interleukin‐2, transforming growth factor‐β 1 (TGF‐β1), forkhead box P3 (FOXP3), and adenylyl cyclase type 9 modulate the hosts' immune regulation under circumstances of viral hepatitis. We examined the effect of five single nucleotide polymorphisms (SNPs) of Treg‐related genes on the levels of C‐reactive protein (CRP) and erythrocyte sedimentation rate (ESR), alanine aminotransferase, and non‐invasive hepatic fibrosis marker (Fibrosis‐4 index) in a total of 138 participants with viral hepatitis. The rs1800469 (a TGF‐β1 SNP) GG genotype is associated with higher serum CRP levels, and the rs3761547 (a FOXP3 SNP) C allele in the females is associated with higher ESR levels. Besides, female participants carrying the rs3761547 C allele had a significantly higher Fibrosis‐4 (FIB‐4) index than the females carrying the TT genotype, while the rs3761547 C allele had the opposite effect in males. With linear‐regression moderation analysis, we found that sex moderated the impact of the FOXP3 SNP on the levels of FIB‐4, whereas the FOXP3 SNP caused the opposite effect between males and females on the severity of hepatic fibrosis. These results provide evidence for the participation of TGF‐β1 and FOXP3 in the inflammatory responses associated with viral hepatitis, where FOXP3 function may be moderated by sex.

Neutrophils must navigate accurately towards pathogens in order to destroy invaders and thus defend our bodies against infection. Here we show that hydrogen peroxide, a potent neutrophil chemoattractant, guides chemotaxis by activating calcium-permeable TRPM2 ion channels and thus generating an intracellular leading-edge calcium “pulse”. The thermal sensitivity of TRPM2 activation means that chemotaxis towards hydrogen peroxide is strongly promoted by small temperature elevations, suggesting that an important function of fever may be to enhance neutrophil chemotaxis by facilitating calcium influx through TRPM2. Chemotaxis towards conventional chemoattractants such as LPS, CXCL2 and C5a does not depend on TRPM2 but is driven in a similar way by leading-edge calcium pulses. Other proposed initiators of neutrophil movement, such as PI3K, Rac and lyn, influence chemotaxis by modulating the amplitude of calcium pulses. We propose that intracellular leading-edge calcium pulses are universal drivers of the motile machinery involved in neutrophil chemotaxis.

This study aimed to elucidate the role of sex in neurocognitive function in patients with Parkinson’s disease (PD). Ninety-four idiopathic PD and 167 healthy elderly as normal controls (NCs) were recruited and underwent comprehensive neuropsychological assessments. The sex difference were found in NCs but not in PD. In male, PD patients had worse performance on the Digit symbol substitution (DSS) (p

BACKGROUND Social functioning is crucial for the determinants of Parkinson's disease (PD) with dementia; however, there is no social functioning scale applicable to PD. OBJECTIVE This study aimed to develop a social functioning scale specific to PD (PDSFS) and provide a cut-off score to improve diagnosis accuracy. METHODS The items were developed through literature, interview patients, and PD expertise. After the pilot study, one hundred fifty-seven patients and 74 healthy participants were enrolled and completed the Mini-Mental State Examination, Clock Drawing Test, Activities of Daily Living, Neuropsychiatric Inventory, Adaptive Behavior Assessment System-Second Edition (ABAS-II) and part III of the Movement Disorder Society-sponsored revision of the Unified Parkinson's Disease Rating Scale (MDS-UPDRS). RESULTS The final PDSFS has 23 items. The exploratory factor analysis revealed three factors, including "Family Life, Hobbies and Self-Care", "Interpersonal Relationship and Recreational Leisure", and "Social Bond". The internal consistency coefficient was 0.883, and the test-retest reliability was 0.774, respectively. The total score of the PDSFS was significantly related to the total score of ABAS-II (r = 0.609, p

Objectives There is no analytical method for simultaneous monitoring of warfarin and novel direct oral anticoagulants (NOACs) in human urine samples in a single run in the clinics. Although several studies have reported their measurements in human blood samples, but its sample collection is more invasive and time-consuming, thereby challenging to monitor frequently. Methods In this work, we developed a fast microextraction technique (ultrasound-assisted salt-induced liquid-liquid microextraction, USA-SI-LLME) coupled with high-performance liquid chromatography-tandem mass spectrometry (HPLC–MS/MS) to rapidly quantify four commonly used NOACs drugs (apixaban, dabigatran, edoxaban, and rivaroxaban) and warfarin in human urine samples. USA-SI-LLME conditions were optimized using a water-miscible organic solvent as an extraction solvent, high salt concentrations, sample pH, and extraction time (∼5.5 min). Results and conclusions The analytical method showed excellent linearities from 0.5 to 500 μg/L for apixaban, edoxaban, rivaroxaban, warfarin, and 1 ∼ 500 μg/L for dabigatran. Intra- and inter-day precision values were 0.99 for all analytes. Limits of detection ranged between 0.07 ∼ 0.18 μg/L, and relative recoveries ranged between 92.18 and 110.15%. This method was successfully applied to analyze 15 one-spot urine samples from 15 clinical patients who regularly took warfarin or NOACs, and high accuracy was found. We concluded that this method could be used as a non-invasive high-throughput and rapid monitoring of NOACs and warfarin in human urine in clinical settings and could provide timely analysis during emergency care.

Monoamine neurotransmitters play essential roles in the regulation of arousal and sleep. Impaired metabolism of monoamine neurotransmitters could result in the accumulation of neurotoxic aldehyde metabolites and, hence, neuronal degeneration. Aldehyde dehydrogenases play an important role in the metabolism of the neurotoxic aldehyde metabolites, including the aldehyde metabolites of dopamine, serotonin, and noradrenaline. Deficient aldehyde dehydrogenase 2 (ALDH2) has been suggested to result in the accumulation of these biogenic aldehydes. An ALDH2 single nucleotide polymorphism (SNP), rs671 (A), results in significantly reduced ALDH2 enzyme activity. A total of 83 Parkinson’s disease (PD) patients were recruited in this study. In addition to the genotypes of rs671, the patients were assessed with the PD sleep scale-2nd version (PDSS-2) and the Epworth sleepiness scale (ESS) for symptoms of daytime and nocturnal sleep disturbances. The patients carrying rs671 (A) had more frequent dozing while lying down to rest in the afternoon (ESS item5) (F = 7.308, p = 0.008) than the rs671 (GG) patients. The patients with rs671 (A) reported a trend toward more frequent difficulty staying asleep than the patients with rs671 (GG). (F = 3.278, p = 0.074). The results indicate that patients carrying allele rs671 (A) are more likely to experience impairment in the regulation of arousal and sleep. The results also support the hypothesis that the accumulation of neurotoxic monoamine neurotransmitter aldehyde metabolites secondary to reduced ALDH2 enzyme activity may cause more severe monoaminergic neuronal loss and, hence, more severe symptoms in the regulation of wakefulness and sleep.

Thermal and noxious stimuli are detected by specialized nerve endings, which transform the stimuli into electrical signals and transmit the signals into central nervous system to facilitate the perception of temperature and pain. Several members within the transient receptor potential (TRP) channel family serve as the sensors for temperature and noxious stimuli and are involved in the development of pathological pain, especially inflammatory pain. Various inflammatory mediators can sensitize and modulate the activation threshold of TRP channels and result in the development of inflammatory pain behaviors. A brief review of the role of TRP channels in nociception and the modulatory mechanisms of TRP channels by inflammatory mediators, focusing on TRPV1, TRPA1, and TRPM2, will be presented. Recent advances in the development of therapeutic strategies targeting against TRP channels will also be reviewed.

The abilities to detect warmth and heat are critical for the survival of all animals, both in order to be able to identify suitable thermal environments for the many different activities essential for life and to avoid damage caused by extremes of temperature. Several ion channels belonging to the TRP family are activated by non-noxious warmth or by heat and are therefore plausible candidates for thermal detectors, but identifying those that actually regulate warmth and heat detection in intact animals has proven problematic. TRPM2 has recently emerged as a likely candidate for the detector of non-noxious warmth, as it is expressed in sensory neurons, and mice show deficits in the detection of warmth when TRPM2 is genetically deleted. TRPM2 is a chanzyme, containing a thermally activated TRP ion channel domain attached to a C-terminal motif, derived from a mitochondrial ADP ribose pyrophosphatase, that confers on the channel sensitivity to ADP ribose and reactive oxygen species such as hydrogen peroxide. Several open questions remain. Male mammals prefer cooler environments than female, but the molecular basis of this sex difference is unknown. TRPM2 plays a role in regulating body temperature, but are other warmth-detecting mechanisms also involved? TRPM2 is expressed in autonomic neurons, but does it confer a sensory function in addition to the well-known motor functions of autonomic neurons? TRPM2 is thought to play important roles in the immune system, in pain and in insulin secretion, but the mechanisms are unclear. TRPM2 has to date received less attention than many other members of the TRP family but is rapidly assuming importance both in normal physiology and as a key target in disease pathology.

Objective The use of opiate substances, such as heroin and methadone, has been proven to cause executive function damage. The extent of damage may be mediated by the activity of enzyme aldehyde dehydrogenase 2 (ALDH2), which plays an important role in neurotransmitter dopamine metabolism. The single nucleotide polymorphism Glu487Lys distributes mostly in Asia and codes for ALDH2 with greatly reduced enzyme activity. The current study aims to explore the effect of ALDH2 on executive function in opiate users. Methods A total of 94 opiate users were recruited and 58 patients finished the neuropsychological assessment and blood genotyping. Results After co-variating the influence of age and the years of education, we found that participants with ALDH2 A allele performed worse on the Category Complete index of the Modified Wisconsin Card Sorting Test (F = 5.34, p = 0.02), suggesting an impaired planning ability in this group. We also found that ALDH2 A carriers went through the Trail 2 in Color Trails Test faster (F = 8.21, p = 0.01), in part suggesting better set-shifting abilities; however, impulsiveness and lack of planning associated with this study group may also explain the faster performances. Conclusions The role that ALDH2 plays in the pathology of cognitive impairment in opiate users may lead new focus in studies of the pathophysiology in opiate usage and its consequences on cognitive function.

Thermal and noxious stimuli are detected by specialized nerve endings, which transform the stimuli into electrical signals and transmit the signals into central nervous system to facilitate the perception of temperature and pain. Several members within the transient receptor potential (TRP) channel family serve as the sensors for temperature and noxious stimuli and are involved in the development of pathological pain, especially inflammatory pain. Various inflammatory mediators can sensitize and modulate the activation threshold of TRP channels and result in the development of inflammatory pain behaviors. A brief review of the role of TRP channels in nociception and the modulatory mechanisms of TRP channels by inflammatory mediators, focusing on TRPV1, TRPA1, and TRPM2, will be presented. Recent advances in the development of therapeutic strategies targeting against TRP channels will also be reviewed.

Executive dysfunction is common in Parkinson's disease (PD) patients. The catechol-O-methyltransferase (COMT) Val158Met polymorphism has been proposed to affect executive functions (EFs) in the prefrontal cortex. The present study attempted to explore the influence of the COMT polymorphism on EFs in patients with PD. Fifty-four PD patients were recruited and underwent neuropsychological assessments for three core EFs. The COMT polymorphism was genotyped using the TaqMan SNP Genotyping Assay. Participants were divided into three study groups: Val homozygotes, heterozygotes, and Met homozygotes. The three COMT genotype groups had significantly different performances in set-shifting [χ2 (2, 54) = 9.717, p = 0.008] and working memory tasks [χ2 (2, 54) = 7.806, p = 0.020]. Post-hoc analyses revealed that PD Val homozygotes performed significantly poorer in the set-shifting task than did either the PD Met homozygotes (z = -2.628, p = 0.009) or PD heterozygotes (z = -2.212, p = 0.027). Our explorative results suggest that the putative level of prefrontal dopamine influenced set-shifting through a "cane-shaped" dopamine level-response relationship. Our results have clinical implications, which may influence PD treatment with dopamine in the future because the optimal dopamine level to maximize EFs may vary based on the clinical course and COMT polymorphism status. Further study recruiting a larger number of participants is needed to confirm our preliminary findings.

Neurotransmitter degradation has been proposed to cause the accumulation of neurotoxic metabolites. The metabolism of these metabolites involves aldehyde dehydrogenase 2 (ALDH2). The Asian-specific single nucleotide polymorphism rs671 causes reduced enzyme activity. This study aims to explore whether Parkinson’s disease (PD) patients with reduced ALDH2 activity owing to the rs671 polymorphism are at risk for neuropsychological impairments. A total of 139 PD patients were recruited. Each participant was assessed for medical characteristics and their ALDH2 genotype. The Mini-Mental State Examination (MMSE), the Clinical Dementia Rating Scale and the Frontal Behavioral Inventory were used to measure neuropsychological functions. We found that the MMSE scores were significantly lower in patients with inactive ALDH2 (U = 1873.5, p = 0.02). The presence of cognitive impairments was significantly more frequent in the inactive ALDH2 group (46.0%) than in the active ALDH2 group (26.3%) (χ2 = 5.886, p = 0.01). The inactive group showed significant deterioration in hobbies and exhibited more severe “disorganization” and “hyper-sexuality” behaviours. The additive effects of the allele on the development of cognitive impairments in PD patients may be an important finding that provides further insight into the pathogenic mechanism of cognitive dysfunction in PD.

Animals must sense temperature in the external environment in order to find ambient temperatures appropriate for different activities, such as hunting or sleeping, and to avoid even brief exposure to damaging extremes of temperature. They must also sense their internal bodily temperature in order to regulate it. Some members of the TRP channel family are activated by thermal stimuli, and are consequently named the thermoTRPs; thermally sensitive ion channels are also found in the potassium and chloride channel families. When thermoTRP channels are expressed in a sensory neuron, channel opening in response to heat leads to depolarization and generation of action potentials. It is still an open question which channels are important for sensation of thermal stimuli in the external environment, and channels involved in the sensation of internal bodily temperature for the purposes of thermoregulation are even less understood. In this chapter we review the properties of thermosensitive ion channels and their roles in thermosensation and thermoregulation, with an emphasis on TRP channels.

To investigate the skin innervation and its clinical significance in late-stage chronic kidney disease (CKD).Case series.National Taiwan University Hospital, Taipei, Taiwan.Forty consecutive nondiabetic patients with late-stage CKD (14 female and 26 male; mean [SD] age, 60.7 [12.3] years), including 2 cases with stage 3 CKD, 6 with stage 4 CKD, and 32 with stage 5 CKD, ie, end-stage kidney disease.Clinical evaluation of neurological deficits, nerve conduction study, autonomic function tests, and a 3-mm-diameter skin biopsy specimen taken from the distal leg.Quantitation of epidermal innervation, parameters of nerve conduction study, R-R interval variability, and sympathetic skin response.Clinically, 21 patients (52.5%) were symptomatic with paresthesia over the limbs or autonomic symptoms. The intraepidermal nerve fiber (IENF) density was markedly reduced in patients with CKD compared with age- and sex-matched controls (mean [SD], 2.8 [2.0] vs 8.6 [2.8] fibers/mm; P.001). Skin denervation was observed in 27 patients (67.5%). Fifteen patients (37.5%) had abnormalities on nerve conduction studies, and 29 patients (72.5%) had abnormal results on autonomic function tests. By analysis with multiple regression models, the IENF density was negatively correlated with the duration of renal disease (P = .02). Additionally, the R-R interval variability at rest was linearly correlated with the IENF density (P = .02) and the absence of sympathetic skin responses at the soles was associated with reduced IENF density (P = .03).Small-fiber sensory and autonomic neuropathies constitute the major form of neuropathy in late-stage CKD. Furthermore, skin denervation was associated with the duration of renal disease.

A 53-year-old male patient developed insidious onset of length-dependent painful neuropathy on a background of encephalopathy during prolonged treatment with metronidazole for a cumulative dose of 146 g in 88 days. The reversible encephalopathy was documented with gradual resolution of hyperintense lesions in bilateral cerebellum and brainstem on brain MRI together with the improvement in symptoms of ataxia and dysarthria. The concomitant impairment of small-diameter sensory nerves posed a diagnostic challenge. The authors took advantage of serial skin biopsies to demonstrate reversible metronidazole-induced small-fibre sensory neuropathy, that is, skin denervation after metronidazole and corresponding skin reinnervation with the disappearance of sensory symptoms.

Rwei-Ling Yu,1 Chun-Hsiang Tan,2 Ruey-Meei Wu3 1Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan; 2Wolfson Centre for Age Related Diseases, King’s College London, London, UK; 3Department of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan Objectives: The aims of this study were to explore nocturnal disturbances in patients with Parkinson’s disease (PD) and to assess their impact on quality of life (QoL).Methods: A total of 211 patients with PD were recruited for this study, and each participant was evaluated using the mini-mental state examination, PD sleep scale – second version (PDSS-2), pittsburgh sleep quality index (PSQI), PD QoL questionnaire (PDQ), Epworth sleepiness scale, Hoehn and Yahr (H&Y) staging, and unified Parkinson’s disease rating scale (UPDRS). Multiple regression analyses were performed to determine the contribution of the predictive variables on QoL.Results: There were 56.4% males (mean age: 64.08years; disease duration: 6.02years; H&Y stage: 2.25; and UPDRS: 33.01) in this study. Our patients’ actual sleep time was 5.96±1.16hours and the average sleep efficiency was 82.93%±12.79%. Up to 64.4% of patients were classified as “poor” sleepers and 23.8% suffered from daytime sleepiness. The final stepwise regression model revealed that UPDRS parts I and II, the sleep disturbance and daytime dysfunction components of the PSQI, the PD symptoms at night subscale of the PDSS-2, and the levodopa equivalent dose were significant predictors of the PDQ score (R2=53, F7,165=28.746; P

An 82-year-old female with history of hypertension, atrial fibrillation and rectosigmoid cancer status postoperation without recurrence had a sudden onset of right hemiparesis and aphasia. She had regularly taken irbesartan, atenolol, propafenone and indapamide. On arrival at the emergency room, she was globally aphasic and had right hemiparesis, hemihypoaesthesia and homonymous hemianopia. Her initial National Institutes of Health Stroke Scale Score was 20. Head CT 65 min after onset of symptoms showed a left hyperdense middle cerebral artery sign. A left middle cerebral artery infarction was diagnosed. She received recombinant tissue plasminogen activator (rt-PA) (alteplase, 0.75 mg/kg) 140 min after onset of …