Eagle syndrome (ES) is a rare clinical syndrome characterized by the elongation of the temporal bone's styloid process, or calcification of stylohyoid ligament, compressing surrounding structures causing pharyngalgia. One of its variants, the styloid-carotid artery syndrome, produces symptoms by compression of the external or internal carotid arteries (ICA). Here, we present a case of a 43-year-old woman with ES and bilateral ICA dissections. The patient underwent staged bilateral angioplasty and covered stent placement, followed by styloidectomy. A computerized tomography angiogram revealed patency of both stents at a two-year follow-up.
Objectives: Reportedly, hippocampal neuronal degeneration by kainic acid (KA)-induced seizures in rats <14 days old was enhanced by lipopolysaccharide (LPS). This study was to test the hypothesis that cytokines such as interleukin (IL)-1β, IL-6 and tumor necrosis factor-α are associated with aggravated neuronal damage. Materials and Methods: Sixty male Sprague-Dawley, 14-day-old rats were used. Experiments were conducted in saline, LPS + saline, saline + KA and LPS + KA groups. Intraperitoneal LPS injections (0.04 mg/kg) were administered 3 h prior to KA injection (3 mg/kg). Results: The LPS + KA group showed a tendency toward shorter latency to seizure onset (p = 0.086) and significantly longer seizure duration (p < 0.05) compared with the KA group. Induction of the proconvulsant cytokine IL-1β in rat pup brains was significantly greater in the LPS + KA group compared to the KA group (38.8 ± 5.5 vs. 9.2 ± 1.0 pg/µg; p < 0.05); however, IL-6 levels were higher in the KA group than in the LPS + KA group (108.7 ± 6.8 vs. 60.9 ± 4.7 pg/µg; p < 0.05). The difference in tumor necrosis factor-α between the LPS + KA group and the KA group was insignificant (12.1 ± 0.6 vs. 10.9 ± 2.3 pg/µg; p = 0.64). Conclusions: Our results showed an increase in the proconvulsant cytokine IL-1β and a decrease in a potentially neuroprotective cytokine, IL-6, in rat pups treated with LPS + KA. These results warrant further investigation into the possible role of IL-1β induction and IL-6 suppression in LPS-promoted neuronal damage.
Coccidioides meningoencephalitis is a central nervous system (CNS) fungal infection withCoccidioides species which can lead to various CNS complications, such as hydrocephalus,vasculitis, and stroke. Most cases reported with Coccidioides meningoencephalitis were inimmunocompromised patients, and the radiologic characteristics on this condition are not wellestablished. Here we report a case of Coccidioides meningoencephalitis in an immunocompetentpatient with one-year follow-up brain magnetic resonance image (MRI) studies after successfultreatment with antifungal drugs. The MRI demonstrated subcortical parenchymal lesions,selectively involving the white matter, and persistent meningeal enhancement.
BackgroundAnti-GAD-related cerebellar ataxia has rarely been described as an acute cause of autoimmune ataxia.Phenomenology ShownA young female who acutely developed anti-GAD-associated ataxia with magnetic resonance imaging (MRI) showing cerebellar edema and follow-up MRI 6 months later showing cerebellar atrophy.Educational ValueRecognizing that anti-GAD-associated cerebellar ataxia can present in a young adult as an acute and severe cause of ataxia, with cerebellar changes evident on MRI.
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