Stroke is a leading cause of disability and mortality all over the world. Due to an aging population, the incidence of stroke is rising significantly, which has led to devastating consequences for patients. In addition to traditional risk factors such as age, hypertension, hyperlipidemia, diabetes and atrial fibrillation, sleep disorders, as independent modifiable risk factors for stroke, have been highlighted increasingly. In this review, we provide an overview of common types of current sleep disturbances in cerebrovascular diseases, including insomnia, hypersomnia, breathing-related sleep disorders, and parasomnias. Moreover, evidence-based clinical therapeutic strategies and pitfalls of specific sleep disorders after stroke are discussed. We also review the neurobiological mechanisms of these treatments as well as their effects on stroke. Since depression after stroke is so prevalent and closely related to sleep disorders, treatments of post-stroke depression are also briefly mentioned in this review article.

Sleep disorders are one of the most common non-motor symptoms in Parkinson's disease (PD). It can cause a notable decrease in quality of life and functioning in PD patients, as well as place a huge burden on both patients and caregivers. The most cited sleep disorders in PD included insomnia, restless legs syndrome (RLS), rapid eye movement (REM), sleep behavior disorders (RBD), excessive daytime sleepiness (EDS) and sleep disordered breathing (SDB), which can appear alone or several at the same time. In this review, we listed the recommended pharmacological treatments for common sleep disorders in PD, and discussed the recommended dosages, benefits and side effects of relative drugs. We also discussed non-pharmacological treatments to improve sleep quality, including sleep hygiene education, exercise, deep brain stimulation, cognitive behavior therapy and complementary therapies. We tried to find proper interventions for different types of sleep disorders in PD, while minimizing relative side effects.

Background and Aims: Wilson’s disease (WD) is a rare hereditary disorder due to ATP7B gene mutation, causing pathologic copper storage mainly in the liver and neurological systems. Hepatocyte transplantation showed therapeutic potential; however, this strategy is often hindered by a shortage of quality donor cells and by allogeneic immune rejection. In this study, we aimed to evaluate the function and efficacy of autologous reprogrammed, ATP7B gene‐restored hepatocytes using a mouse model of WD. Approach and Results: Sufficient liver progenitor cells (LPCs) were harvested by reprogramming hepatocytes from ATP7B−/− mice with small molecules, which exhibited strong proliferation and hepatic differentiation capacity in vitro. After lentivirus‐mediated mini ATP7B gene transfection and redifferentiation, functional LPC‐ATP7B‐derived hepatocytes (LPC‐ATP7B‐Heps) were developed. RNA sequencing data showed that, compared with LPC–green fluorescent protein–Heps (LPC‐GFP‐Heps) with enrichment of genes that were mainly in pathways of oxidative stress and cell apoptosis, in LPC‐ATP7B‐Heps under high copper stress, copper ion binding and cell proliferation pathways were enriched. LPC‐ATP7B‐Heps transplantation into ATP7B−/− mice alleviated deposition of excess liver copper with its associated inflammation and fibrosis, comparable with those observed using normal primary hepatocytes at 4 months after transplantation. Conclusions: We established a system of autologous reprogrammed WD hepatocytes and achieved ATP7B gene therapy in vitro. LPC‐ATP7B‐Heps transplantation demonstrated therapeutic efficacy on copper homeostasis in a mouse model of WD.

Wilson’s disease (WD) is an inherited disease caused by mutations in ATP7B and is characterized by the pathological accumulation of copper in the liver and brain. Common clinical manifestations of WD include a wide range of liver disease and neurological symptoms. In some patients, psychiatric symptoms may be the only manifestation at the time of diagnosis. The clinical features of WD are highly variable and can mimic any disease of internal medicine. Therefore, for unexplained medical diseases, the possibility of WD should not be ignored. Early diagnosis and treatment can improve the prognosis of WD patients and reduce disability and early death. Gene sequencing is becoming a valuable method to diagnose WD, and if possible, all WD patients and their siblings should be genetically sequenced. Copper chelators including D-penicillamine, trientine, and dimercaptosuccinic acid can significantly improve the liver injury and symptoms of WD patients but may have a limited effect on neurological symptoms. Zinc salts may be more appropriate for the treatment of asymptomatic patients or for the maintenance treatment of symptomatic patients. High-quality clinical trials for the drug treatment of WD are still lacking, therefore, individualized treatment options for patients are recommended. Individualized treatment can be determined based on the clinical features of the WD patients, efficacy and adverse effects of the drugs, and the experience of the physician. Liver transplantation is the only effective method to save patients with acute liver failure or with severe liver disease who fail drug treatment.

Wilson's disease (WD), also called hepatolenticular degeneration, is an autosomal recessive inheritance disorder of copper metabolism characterized by the multiple mutations in the ATP-ase 7B gene of chromosome 13q. About half of the WD patients have neurological or psychiatric symptoms. As WD is a kind of medicable or nearly curable neurodegenerative disease in the field of medicine, early consideration/examination and without delay/ life-long treatment usually lead to better prognoses. The drugs, also named as anticopper agents, are commonly used in clinics including D-penicillamine, trientine, sodium dimercaptosuccinate, dimercaptosuccinic acid, zinc and tetrathiomolybdate. This provides detailed reviews about these medicines.

Introduction. This study investigated the influence of lockdown during the 2019 coronavirus disease (COVID-19) pandemic on the quality of life of patients with Parkinson’s disease (PD). Methods. We conducted a questionnaire survey involving 113 patients with PD from Xihu District, Hangzhou, Zhejiang. During the epidemic prevention and control period (February 1 to March 31, 2020), patients enrolled were asked to fill out questionnaires, including the “COVID-19 Questionnaire for PD Patients during the Period of Epidemic Prevention and Control” and “39-item Parkinson’s Disease Questionnaire (PDQ-39).” During the phase of gradual release of epidemic prevention and control (April 1 to April 30, 2020), all patients were followed up again, and PDQ-39 questionnaires were completed. Results. The quality of life for patients during the period of epidemic prevention and control was worse than that after epidemic prevention and control ( < 0.001). The biggest problem that they faced was that they could not receive their doctor’s advice or guidance regularly. The quality of life of patients who had difficulty getting doctors’ guidance or those who changed their routine medication due to lockdown was even worse. Telemedicine was quite effective and efficient for patients to get doctors’ guidance during lockdown. Conclusions. The inconvenient treatment during the pandemic directly caused the aggravation of patients’ symptoms and the decline in their quality of life. It is suggested that social media (such as WeChat or Tencent QQ) are used for regular interactions and follow-up appointments for patients with inconvenient medical treatment.