Autoimmune encephalitis (AE) is a category of immune-mediated disorders of the central nervous system (CNS) affecting children and adults. It is characterized by the subacute onset of altered mentation, neurocognitive issues, refractory seizures/ drug-resistant epilepsy, movement disorders, and/or autonomic dysfunction. AE is mediated by autoantibodies targeting specific surface components or intracytoplasmic antigens in the CNS, leading to functional or structural alterations. Multiple triggers that induce autoimmunity have been described, which are mainly parainfectious and paraneoplastic. The imaging features of AE often overlap with each other and with other common causes of encephalitis/encephalopathy (infections and toxic-metabolic etiologies). Limbic encephalitis is the most common imaging finding shared by most of these entities. Cortical, basal ganglia, diencephalon, and brainstem involvement may also be present. Cerebellar involvement is rare and is often a part of paraneoplastic degeneration. Owing to an improved understanding of AE, their incidence and detection have increased. Hence, in an appropriate setting, a high degree of suspicion is crucial when reporting clinical MRIs to ensure prompt treatment and better patient outcomes. In this review, we discuss the pathophysiology of AE and common etiologies encountered in clinical practice.

Autoimmune encephalitis (AE) is a category of immune-mediated disorders of the central nervous system (CNS) affecting children and adults. It is characterized by the subacute onset of altered mentation, neurocognitive issues, refractory seizures/ drug-resistant epilepsy, movement disorders, and/or autonomic dysfunction. AE is mediated by autoantibodies targeting specific surface components or intracytoplasmic antigens in the CNS, leading to functional or structural alterations. Multiple triggers that induce autoimmunity have been described, which are mainly parainfectious and paraneoplastic. The imaging features of AE often overlap with each other and with other common causes of encephalitis/encephalopathy (infections and toxic-metabolic etiologies). Limbic encephalitis is the most common imaging finding shared by most of these entities. Cortical, basal ganglia, diencephalon, and brainstem involvement may also be present. Cerebellar involvement is rare and is often a part of paraneoplastic degeneration. Owing to an improved understanding of AE, their incidence and detection have increased. Hence, in an appropriate setting, a high degree of suspicion is crucial when reporting clinical MRIs to ensure prompt treatment and better patient outcomes. In this review, we discuss the pathophysiology of AE and common etiologies encountered in clinical practice.

Autoimmune encephalitis (AE) is a category of immune-mediated disorders of the central nervous system (CNS) affecting children and adults. It is characterized by the subacute onset of altered mentation, neurocognitive issues, refractory seizures/ drug-resistant epilepsy, movement disorders, and/or autonomic dysfunction. AE is mediated by autoantibodies targeting specific surface components or intracytoplasmic antigens in the CNS, leading to functional or structural alterations. Multiple triggers that induce autoimmunity have been described, which are mainly parainfectious and paraneoplastic. The imaging features of AE often overlap with each other and with other common causes of encephalitis/encephalopathy (infections and toxic-metabolic etiologies). Limbic encephalitis is the most common imaging finding shared by most of these entities. Cortical, basal ganglia, diencephalon, and brainstem involvement may also be present. Cerebellar involvement is rare and is often a part of paraneoplastic degeneration. Owing to an improved understanding of AE, their incidence and detection have increased. Hence, in an appropriate setting, a high degree of suspicion is crucial when reporting clinical MRIs to ensure prompt treatment and better patient outcomes. In this review, we discuss the pathophysiology of AE and common etiologies encountered in clinical practice.

Objective To explore the protective effect of Anchanling serum on PCI2 cell injury induced by lactacystin and the possible mechanism.Methods The sem were obmined from rats with intragastric administration of Anchanling at small,medium and high doses.Lactacystin was used to induce proteasomal dysfunction in PCI2 cells,and the cell viability was evaluated with MTT assay.The PC 12 cells in exponential growth were divided into normal control,lactacystin injury and Anchanling-treated groups with corresponding treatments,and theexpressions of alpha-synuclein and tyrosine hydroxylase(TH)were assayed using immunohistochemical staining.Results The serum of rats with medium-dose Anchanling treatment group resulted in the highest viability of the PC 12 cells among the 3 dose groups(P＜0.05).Compared with the normal control group,lactacystin exposure significantly increased the number of alpha-synuclein-positive cells but decreased the TH-positive cells (P＜0.05);treatments with the drug-containing sera significantly lowered alpha-synuclein-positive cells and increased TH-positive cells in the PC 12 cells with lactacystin exposure(P＜0.05).Conclusion Anchanling can improve the function of the ubiquitin-proteasome system,reduce the intracellular aggregation of alpha-synuclein,and upregulate TH expression in the PC 12 cells to promote the cell survival and offer neuronal protection effects.

Autoimmune encephalitis (AE) is a category of immune-mediated disorders of the central nervous system (CNS) affecting children and adults. It is characterized by the subacute onset of altered mentation, neurocognitive issues, refractory seizures/ drug-resistant epilepsy, movement disorders, and/or autonomic dysfunction. AE is mediated by autoantibodies targeting specific surface components or intracytoplasmic antigens in the CNS, leading to functional or structural alterations. Multiple triggers that induce autoimmunity have been described, which are mainly parainfectious and paraneoplastic. The imaging features of AE often overlap with each other and with other common causes of encephalitis/encephalopathy (infections and toxic-metabolic etiologies). Limbic encephalitis is the most common imaging finding shared by most of these entities. Cortical, basal ganglia, diencephalon, and brainstem involvement may also be present. Cerebellar involvement is rare and is often a part of paraneoplastic degeneration. Owing to an improved understanding of AE, their incidence and detection have increased. Hence, in an appropriate setting, a high degree of suspicion is crucial when reporting clinical MRIs to ensure prompt treatment and better patient outcomes. In this review, we discuss the pathophysiology of AE and common etiologies encountered in clinical practice.

BACKGROUND AND PURPOSE: Non-contrast brain computed tomography (NCCT) remains the most common imaging modality employed to select patients for thrombolytic therapy in acute ischemic stroke. The current study used the Alberta Stroke Program Early CT Score (ASPECTS) to identify early ischemic changes on brain NCCT imaging with the aim to investigate whether a relationship exists between time from symptoms onset to NCCT with the presence of early ischaemic change quantified by ASPECTS. METHODS: We studied 1,329 ischemic stroke patients who had NCCT within 8 hours of stroke onset. Patients were assessed to see if they had any ASPECTS lesion and if the rate of patients with a lesion increased with time using logistic regression. RESULTS: 30% patients had an ASPECTS < 10 within the first 3 hours from symptom onset. Within the first 3 hours, the odds for a CT change (ASPECTS < 10) per minute of time was 1.00 with 95% confidence interval (CI) (0.99 to 1.00) (P=0.266). After 3 hours, there was a significant increase in odds of ASPECTS < 10 with increasing time. The odds of being ASPECTS positive increased 1% (odds ratio=1.01) per 1 minute of time with 95% CI (1.00 to 1.01) (P=0.002). CONCLUSIONS: We have identified that prior to first 3 hours of stroke there was no effect of time on odds of CT ischemic change; after the first 3 hours of stroke the odds increased with increasing time to CT scan. The occurrence of early ischemic change may be a marker of time from stroke onset rather than severity.
Alberta ; Brain ; Humans ; Logistic Models ; Stroke* ; Thrombolytic Therapy ; Tomography, X-Ray Computed

OBJECTIVETo evaluate the safety and effectiveness of totally implantable hearing aid (Carina) was assessed in adult patients with bilateral moderate to severe hearing loss.

METHODSSurgical implantations of Carina were performed in three adult patients with bilateral moderate to severe hearing loss. The safety and effectiveness were evaluated in a more than 12 months follow-up by comparison of outcomes of PTA and speech audiometry pre and post-operatively. The daily usage of implants was observed and compared with traditional hearing aids.

RESULTSThe average elevation of unaided threshold elevation on surgical side was 8.3 dB postoperatively. The average functional gain in four speech frequencies of PTA was 35.4 dB HL and the average threshold decrease of speech discrimination was 22.5 dB HL. The subjective scoring of performance of the implants is significantly higher than traditional hearing aid.

CONCLUSIONSTotally implantable hearing aid (Carina) is an ideal implant to treat moderate to severe hearing loss. Long term follow-up is needed to validate the results.

Adult ; Auditory Threshold ; Cochlear Implants ; Equipment Safety ; Female ; Hearing Aids ; Hearing Loss ; rehabilitation ; Humans ; Male ; Middle Aged

Progranulin (PGRN) has recently emerged as a key player in a subset of frontotemporal dementias (FTD). Numerous mutations in the progranulin gene have been identified in patients with familial or sporadic frontotemporal lobar degeneration (FTLD). In order to understand the molecular mechanisms by which PGRN deficiency leads to FTLD, we examined activity of PGRN in mouse cortical and hippocampal neurons and in human neuroblastoma SH-SY5Y cells. Treatment of mouse neurons with PGRN protein resulted in an increase in neurite outgrowth, supporting the role of PGRN as a neurotrophic factor. PGRN treatment stimulated phosphorylation of glycogen synthase kinase-3 beta (GSK-3β) in cultured neurons. Knockdown of PGRN in SH-SY5Y cells impaired retinoic acid induced differentiation and reduced the level of phosphorylated GSK-3β. PGRN knockdown cells were also more sensitized to staurosporine-induced apoptosis. These results reveal an important role of PGRN in neurite outgrowth and involvement of GSK-3β in mediating PGRN activity. Identification of GSK-3β activation as a downstream event for PGRN signaling provides a mechanistic explanation for PGRN activity in the nervous system. Our work also suggest that loss of axonal growth stimulation during neural injury repair or deficits in axonal repair may contribute to neuronal damage or axonal loss in FTLD associated with PGRN mutations. Finally, our study suggests that modulating GSK-3β or similar signaling events may provide therapeutic benefits for FTLD cases associated with PGRN mutations.
Animals ; Apoptosis ; Cell Culture Techniques ; Cell Differentiation ; Cell Line ; Embryo, Mammalian ; Female ; Gene Knockdown Techniques ; Glycogen Synthase Kinase 3 ; genetics ; metabolism ; Glycogen Synthase Kinase 3 beta ; Humans ; Intercellular Signaling Peptides and Proteins ; genetics ; pharmacology ; physiology ; Mice ; Neurites ; physiology ; Neurons ; cytology ; physiology ; Phosphorylation ; Pregnancy ; Progranulins ; Proto-Oncogene Proteins c-akt ; metabolism ; RNA Interference