Conclusion School-aged children are well able to describe adverse drug events of their anticonvulsant medication. Almost two thirds of the described events concern neurologic or psychiatric symptoms that cause an emotional burden and restrictions according to the patients.What is Known• Anticonvulsants have a high potential of adverse drug events.• In an earlier survey, parents expressed fears of severe adverse drug events such as liver failure, which seldom occur, and reported a high number of neurological and psychological adverse drug events.What is New• Many children fear that their anticonvulsants could harm them, and they fear and experience neurological and psychological adverse drug events.• According to the children, adverse drug events cause an emotional burden and restrictions in school performance and favorite leisure activities.Primary immunodeficiency disorders represent a heterogeneous spectrum of diseases, predisposing to recurrent infections, allergy, and autoimmunity. While an association between primary immunodeficiency disorders and increased risk of cancer has been suggested since the 1970s, renewed attention has been given to this topic in the last decade, largely in light of the availability of large registries as well as advances in next generation sequencing. In this narrative review, we will give an insight of the primary immunodeficiencies that are commonly responsible for the greater number of cancers in the primary immunodeficiency disorders population. We will describe clinical presentations, underlying genetic lesions (if known), molecular mechanisms for carcinogenesis, as well as some management considerations. We will also comment on the future directions and challenges related to this topic.Conclusion The awareness of the association between several primary immunodeficiencies and cancer is crucial to provide the best care for these patients.What is Known • Patients with primary immunodeficiency have an increased risk of malignancy. The type of malignancy is highly dependent on the specific primary immunodeficiency disorder.What is New • Survival in patients with primary immunodeficiency disorders has been improving, and conversely also their lifetime risk of malignancy. • International collaboration and multinational registries are needed to improve our knowledge and therapeutic strategies.INTRODUCTION Cognitive impairment is a debilitating manifestation in Parkinson’s disease (PD). We sought to investigate predictors of PD-CI (PD with cognitive impairment). METHODS We systematically searched PubMed and Cochrane Library for prospective cohort studies and pooled estimates via random-effects models. Primary analyses for all types of cognitive impairments and subgroup analyses by separate outcomes were conducted. buy A2ti-2 RESULTS A total of 28,009 studies were identified, of which 57 studies with 31 factors were included in the meta-analysis. In the primary analysis, 13 factors were associated with PD-CI, comprising advanced age [relative risk (RR) = 1.07, 95% confidence interval (CI) = 1.03-1.12], age at onset (RR = 4.43, 95% CI = 1.87-10.54), postural-instability-gait disorder (RR = 3.76, 95% CI = 1.36-10.40), higher Hoehn and Yahr stage (RR = 1.83, 95% CI = 1.35-2.47), higher UPDRS III score (RR = 1.04, 95% CI = 1.01-1.08), rapid eye movement sleep behavior disorder (RR = 3.72, 95% CI = 1.20-11.54), hallucinations (RR = 3.09, 95% CI = 1.61-5.93), orthostatic hypotension (RR = 2.98, 95% CI = 1.41-6.28), anxiety (RR = 2.59, 95% CI = 1.18-5.68), APOE ε2 (RR = 6.47, 95% CI = 1.29-32.53), APOE ε4 (RR = 3.04, 95% CI = 1.88-4.91), electroencephalogram theta power > median (RR = 2.93, 95% CI = 1.61-5.33), and alpha power  less then  median (RR = 1.77, 95% CI = 1.07-2.92). In the subgroup analysis, MAPT H1/H1 genotype increased the risk of dementia in PD. Sixty-four studies were included in the systematic review, of which 12 factors were additionally correlated with PD-CI using single studies. CONCLUSIONS Advanced age, genetic variation in APOE and MAPT, gait disturbance, motor assessments, non-motor symptoms, and electroencephalogram may be promising predictors for PD-CI.Autonomic dysfunction is a common non-motor symptom in Parkinson’s disease (PD). Dopamine and serotonin are known to play a role in autonomic regulation, and, therefore, PD-related degeneration of serotonergic and dopaminergic neurons in these regions may be associated with autonomic dysfunction. We sought to clarify the association between extrastriatal serotonergic and striatal dopaminergic degeneration and the severity of autonomic symptoms, including gastrointestinal, pupillomotor, thermoregulatory, cardiovascular, and urinary dysfunction. We performed hierarchical multiple regression analyses to determine the relationships between (extra)striatal serotonergic and dopaminergic degeneration and autonomic dysfunction in 310 patients with PD. We used [123I]FP-CIT SPECT binding to presynaptic serotonin (SERT) and dopamine (DAT) transporters as a measure of the integrity of these neurotransmitter systems, and the SCOPA-AUT (Scales for Outcomes in Parkinson’s Disease-Autonomic) questionnaire to evaluate the perceived severity of autonomic dysfunction. Motor symptom severity, medication status, and sex were added to the model as covariates. Additional analyses were also performed using five subdomains of the SCOPA-AUT cardiovascular, gastrointestinal, urinary, thermoregulatory, and pupillomotor symptoms. We found that autonomic symptoms were most significantly related to lower [123I]FP-CIT binding ratios in the right caudate nucleus and were mainly driven by gastrointestinal and cardiovascular dysfunction. These results provide a first look into the modest role of dopaminergic projections towards the caudate nucleus in the pathophysiology of autonomic dysfunction in PD, but the underlying mechanism warrants further investigation.BACKGROUND Multiple system atrophy (MSA) is an adult onset, fatal neurodegenerative disease. However, no reliable biomarker is currently available to guide clinical diagnosis and help to determine the prognosis. Thus, a comprehensive meta-analysis is warranted to determine effective biomarkers for MSA and provide useful guidance for clinical diagnosis. METHODS A comprehensive literature search was made of the PubMed, Embase, Cochrane and Web of Science databases for relevant clinical trial articles for 1984-2019. Two review authors examined the full-text records, respectively, and determined which studies met the inclusion criteria. We estimated the mean difference, standard deviation and 95% confidence intervals. RESULTS A total of 28 studies and 11 biomarkers were included in our analysis. Several biomarkers were found to be useful to distinguish MSA patients from healthy controls, including the reduction of phosphorylated tau, α-synuclein (α-syn), 42-amino-acid form of Aβ and total tau (t-tau), the elevation of neurofilament light-chain protein (NFL) in cerebrospinal fluid, the elevation of uric acid and reduction of homocysteine and coenzyme Q10 in plasma.