Pioglitazone (PIO), a thiazolidinedone, was reported to stimulate peroxisome proliferator-activated receptor-γ (PPAR-γ) with anti-inflammatory, anti-proliferative, anti-diabetic, and antidepressive activities. However, whether this compound exerts any perturbations on Ca2+-activated K+ and M-type K+ currents in central neurons remains largely unresolved. In this study, we investigated the effects of PIO on these potassium currents in hippocampal neurons (mHippoE-14). In whole-cell current recordings, the presence of PIO (10 μM) increased the amplitude of Ca2+-activated K+ current [IK(Ca)] in mHippoE-14 cells. PIO-induced stimulation of IK(Ca) observed in these cells was reversed by subsequent addition of paxilline, yet not by TRAM-39 or apamin. In inside-out current recordings, PIO applied to the bath concentration-dependently increased the activity of large-conductance Ca2+-activated K+ (BKCa) channels with an EC50 value of 7.6 μM. Its activation of BKCa channels in mHippoE-14 cells was voltage-dependent and accompanied by both a lengthening in mean open time and a shortening in slow component of mean closed time. The activation curve of BKCa channels after addition of PIO was shifted to less depolarized potential without any change in the gating charge. PIO also suppressed the amplitude of M-type K+ currents inherently in mHippoE-14 neurons. Taken together, in addition to its agonistic action on PPAR-γ, PIO-induced perturbation of these potassium channels may be responsible for its widely pharmacological actions on hippocampal neurons.

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Patients with optic neuritis (ON) are at an increased risk of developing multiple sclerosis (MS), an illness that may result in physical dysfunction and short life expectancy. Information on the conversion rate to MS of patients with ON is essential in determining the impact of ON on the incidence of MS. Previous Taiwanese studies on the risk of MS in patients with ON were all hospital based, thereby limiting the generalizability of the findings. We aimed to estimate the risk of MS in patients with ON using a nationally representative sample. A cohort of 2,741 patients who sought outpatient care for ON in 2000 was identified from Taiwan's National Health Insurance claims. The control group consisted of 27,330 age- and sex-matched subjects randomly selected from all beneficiaries in 2000. The person-year approach with Poisson assumption was used to estimate the incidence rate of MS from 2000 to 2008. The relative risk of outpatient visit or hospitalization for MS was estimated using the Cox proportional hazard model. The incidence rates of MS in the ON and control groups were 25.6 and 0.4, respectively, per 10,000 person-years; these values represent a relative risk estimate of 30.84 (95% confidence interval: 14.48 to 65.73) after the potential confounders were considered. Female or younger patients with ON were associated with a significantly elevated risk of developing MS. This study found that Taiwanese patients with ON are at a substantially high relative risk of developing MS. In addition to patients with ON, female and younger people should also receive intensive neurological care to further reduce their risk of developing MS.

A thrombolysis program with video-assisted therapeutic risk communication decreased DTN time and increased the treatment rate of patients with AIS.

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INTRODUCTION Nonketotic hyperglycemia–related seizures are not uncommonly encountered in clinical practice. Their presentation varies, and they may cause serious consequences if they remain unnoticed. CASE We report a case of nonketotic hyperglycemia-related seizures of unique left parieto-occipital origin and semiology, presenting as focal aware (simple partial) and impaired awareness (complex partial) seizures, including contralateral limb convulsion and apraxialike behavior. DISCUSSION Nonketotic hyperglycemia–related seizures can present with a relatively unique semiology. Careful education to the patients and family regarding attention to the paroxysmal symptoms and an effort to maintain good glycemic control are mandatory in clinical practice.

Diagnosing non-convulsive seizures (NCSs) is a great challenge for most clinicians due to a wide spectrum of clinical presentations. The complexity of the disease course usually results in a delayed diagnosis or misdiagnosis so that timely and appropriate treatment is not given. Herein, we report a case with NCSs misdiagnosed as vertebrobasilar insufficiency (VBI), in which the patient suffered from episodes of prominent dizziness, vertigo, becoming transfixed, and worsening response within a day. Brain magnetic resonance image findings were unremarkable, however electroencephalography (EEG) showed rhythmic epileptiform discharges that appeared to originate from the right frontal area with ipsilateral hemispheric involvement. We prescribed intravenous valproate and the seizures ceased. Few studies have reported a patient with NCS misdiagnosed with VBI, a very different entity. It is thus important that clinicians should be aware of the trivial symptoms of NCSs, and to consider implementing early EEG studies and anti-epileptic drug therapy.

Stimulus‐induced rhythmic, periodic, or ictal discharges (SIRPIDs), an unusual pattern in electroencephalography, have been described in critically‐ill encephalopathic patients in response to alerting stimuli. The phenomenon may be seen in patients with a broad range of aetiologies, including cerebral infarct, haemorrhage, anoxia, and degenerative diseases. Here, we report a unique case of status epilepticus presenting with SIRPIDs during funduscopic examination‐induced focal to bilateral tonic‐clonic seizures.