Summary:Purpose: Prolonged and continuous epileptic seizure (status epilepticus) results in cellular changes that lead to neuronal damage. We investigated whether these cellular changes entail mitochondrial dysfunction and ultrastructural damage in the hippocampus, by using a kainic acid (KA)-induced experimental status epilepticus model.Methods: In Sprague-Dawley rats maintained under chloral hydrate anesthesia, KA (0.5 nmol) was microinjected unilaterally into the CA3 subfield of the hippocampus to induce seizure-like hippocampal EEG activity. The activity of key mitochondrial respiratory chain enzymes in the dentate gyrus (DG), or CA1 or CA3 subfield of the hippocampus was measured 30 or 180 min after application of KA. Ultrastructure of mitochondria in those three hippocampal subfields during KAinduced status epilepticus also was examined with electron microscopy.Results: Microinjection of KA into the CA3 subfield of the hippocampus elicited progressive build-up of seizure-like hippocampal EEG activity. Enzyme assay revealed significant depression of the activity of nicotinamide adenine dinucleotide cytochrome c reductase (marker for Complexes I+III) in the DG, or CA1 or CA3 subfields 180 min after KA-elicited temporal lobe status epilepticus. Conversely, the activities of succinate cytochrome c reductase (marker for Complexes II+III) and cytochrome c oxidase (marker for Complex IV) remained unaltered. Discernible mitochondrial ultrastructural damage, varying from swelling to disruption of membrane integrity, also was observed in the hippocampus 180 min after hippocampal application of KA.Conclusions: Our results demonstrated that dysfunction of Complex I respiratory chain enzyme and mitochondrial ultrastructural damage in the hippocampus are associated with prolonged seizure during experimental temporal lobe status epilepticus. Key Words: Kainic acid-Status epilepticusHippocampus-Complex I of mitochondrial respiratory chainMitochondrial ultrastructure.Mitochondria are ubiquitous intracellular organelles enclosed by a double membrane-bound structure. The primary function of mitochondria is production of cellular energy in the form of adenosine triphosphate (ATP) by way of oxidative phosphorylation through the mitochondrial respiratory chain. Mitochondrial oxidative phosphorylation consists of five enzyme complexes (Complexes I-V) located in the mitochondrial inner membrane (1). Biochemical evidence suggested that the majority of cerebral ATP consumption is used to operate the electrogenic activity of neurons (2). Adequate energy supply by mitochondria is therefore essential for neuronal excitability and neuronal survival.Seizure activity results in a large number of changes and cascades of cellular events, including gene expression, receptor composition, synaptic physiology, and activation of

IMPORTANCE Tinnitus has a prevalence of 10% to 25% and is frequently associated with numerous complications, such as neuropsychiatric disease. Traditional treatments have failed to meet the needs of patients with tinnitus. Noninvasive brain stimulation (NIBS) can focally modify cortical functioning and has been proposed as a strategy for reducing tinnitus severity. However, the results have been inconclusive.OBJECTIVE To evaluate the association between different central NIBS therapies and efficacy and acceptability for treatment of tinnitus.DATA SOURCES ClinicalKey, Cochrane CENTRAL, Embase, ProQuest, PubMed, ScienceDirect, and Web of Science databases were searched from inception to August 4, 2019. No language restriction was applied. Manual searches were performed for potentially eligible articles selected from the reference lists of review articles and pairwise meta-analyses.STUDY SELECTION Randomized clinical trials (RCTs) examining the central NIBS method used in patients with unilateral or bilateral tinnitus were included in the current network meta-analysis. The central NIBS method was compared with sham, waiting list, or active controls. Studies that were not clinical trials or RCTs and did not report the outcome of interest were excluded.DATA EXTRACTION AND SYNTHESIS Two authors independently screened the studies, extracted the relevant information, and evaluated the risk of bias in the included studies. In cases of discrepancy, a third author became involved.

Benign and inflammatory THS were highly similar in terms of nosography. The responses to glucocorticoid treatment were generally good except in patients with orbital pseudotumors.

We report a family with familial amyloid polyneuropathy (FAP), showing an early-onset and a fatal outcome before age 30. Transthyretin (TTR) gene analysis showed one point mutation (T-->C change) in the second base of codon 55, and the corresponding amino acid substitution of proline (Pro) for leucine (Leu) was confirmed at the protein level. This is the first FAP family of Taiwanese origin demonstrating a causative gene abnormality, and FAP with TTR-Pro55 was considered to be more serious compared with other forms of FAP.

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One of the factors that induces eustachian tube dysfunction caused by the invasion of nasopharyngeal carcinoma is paralysis of the tensor veli palatini muscle. Electromyography (EMG), computed tomography (CT), and/or magnetic resonance imaging (MRI) were used to study the tensor muscle and the related paratubal structures and parapharyngeal space. This study, from 44 patients with nasopharyngeal carcinoma, showed that 67% of tensor muscles on the side of the symptomatic ear yielded abnormal electromyographic waveforms, which usually indicated a neurogenic disorder. In the majority of the abnormal EMG cases, CT or MRI often revealed that the pharyngobasilar fascia and the tensor muscle were compressed anterolaterally and the upper prestyloid parapharyngeal space was infiltrated. It was found that an abnormal electromyogram of the tensor muscle generally suggested a more advanced T stage and eustachian tube dysfunction. Otitis media with effusion in the stage I cases was usually not caused by paralysis of the tensor muscle. The invasion of some early cancers, especially localized on the torus tubarius, could also cause the effusion.

The relationship between cholesterol level and hemorrhagic stroke is inconclusive. We hypothesized that low cholesterol levels may have association with intracerebral hemorrhage (ICH) severity at admission and 3-month outcomes. This study used data obtained from a multi-center stroke registry program in Taiwan. We categorized acute spontaneous ICH patients, based on their baseline levels of total cholesterol (TC) measured at admission, into 3 groups with <160, 160–200 and >200 mg/dL of TC. We evaluated risk of having initial stroke severity, with National Institutes of Health Stroke Scale (NIHSS) >15 and unfavorable outcomes (modified Rankin Scale [mRS] score >2, 3-month mortality) after ICH by the TC group. A total of 2444 ICH patients (mean age 62.5±14.2 years; 64.2% men) were included in this study and 854 (34.9%) of them had baseline TC <160 mg/dL. Patients with TC <160 mg/dL presented more often severe neurological deficit (NIHSS >15), with an adjusted odds ratio [aOR] of 1.80; 95% confidence interval [CI], 1.41–2.30), and 3-month mRS >2 (aOR, 1.41; 95% CI, 1.11–1.78) using patients with TC >200 mg/dL as reference. Those with TC >160 mg/dL and body mass index (BMI) <22 kg/m2 had higher risk of 3-month mortality (aOR 3.94, 95% CI 1.76–8.80). Prior use of lipid-lowering drugs (2.8% of the ICH population) was not associated with initial severity and 3-month outcomes. A total cholesterol level lower than 160 mg/dL was common in patients with acute ICH and was associated with greater neurological severity on presentation and poor 3-month outcomes, especially with lower BMI.