Bilateral carotid dissection due to Eagle syndrome in a young female.

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.

Acute Cerebellar Ataxia Associated with Modest Elevation of Anti-GAD Antibodies in a Young Patient.

Background: Anti-GAD-related cerebellar ataxia has rarely been described as an acute cause of autoimmune ataxia. Phenomenology Shown: A 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 Value: Recognizing 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.

IL-1ß induction and IL-6 suppression are associated with aggravated neuronal damage in a lipopolysaccharide-pretreated kainic acid-induced rat pup seizure model.

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)-1ß, 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-1ß 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-1ß 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-1ß induction and IL-6 suppression in LPS-promoted neuronal damage.

Exacerbation of idiopathic paroxysmal kinesigenic dyskinesia in remission state caused by secondary hypoparathyroidism with hypocalcemia after thyroidectomy: evidence for ion channelopathy.

Most reported cases of paroxysmal kinesigenic dyskinesia (PKD) are idiopathic or familial; however, hypoparathyroidism is another unusual cause of secondary PKD. The pathomechanism of PKD remains poorly understood, and the association between idiopathic and secondary PKD remains an enigma, and has yet to be clearly elucidated. We recently encountered a patient with idiopathic PKD whose symptoms were aggravated by secondary hypoparathyroidism with hypocalcemia after having undergone a thyroidectomy. The patient's paroxysms were ameliorated by the normalization of serum calcium levels. The results discussed herein may provide support for the hypothesis that PKD is associated with neuronal ion regulation.

Favorable influence of subclinical hypothyroidism on the functional outcomes in stroke patients.

Subclinical hypothyroidism (SCH) is thought to have an influence on stroke outcomes. However, few reports demonstrate a favorable relationship between the two. We evaluated this association in acute ischemic stroke. From Jan 2005 to June 2008, 756 acute ischemic stroke patients were recruited within seven days of onset. The patients with overt hypothyroidism/hyperthyroidism or other medical conditions that may affect thyroid function were excluded. Thyroid stimulating hormone (TSH) and free thyroxine (FT4) levels were measured within two days. Patients were divided into two groups: the SCH group (TSH > 5.0 microU/mL and normal FT4 levels) and the control group. Stroke outcomes were assessed using two different criteria. In the first outcome model, favorable outcomes [I] were simply defined by modified Rankin Scale (mRS) scores (14. The changes in mRS scores and the proportion of patients with favorable outcomes [I] or [II] at the 30(th) and 90(th) day were compared between the two patient groups. Of the 756 patients, 31 (4.1%) were patients with SCH. More patients from the SCH group showed improvement in NIHSS scores on the 30(th) day compared to the control group (48.4% vs. 25.3%, p=.006). In addition, the proportion of patients who exhibited favorable outcomes [I] was significantly higher in the SCH group on the 90(th) day (74.2% vs. 55.3%, p=.027) and that trend was seen as early as the 30(th) day (p=.102). Similarly, the proportion of the patients with favorable outcomes [II] was significantly greater in the SCH group both on the 30(th) (29.0% vs. 14.6%, p=.039) and 90(th) day (58.0% vs. 31.0%, p=.003). We found that acute ischemic stroke patients with SCH at admission were more likely to show favorable functional outcomes than those without SCH. We can suggest preconditioning before the stroke combined with a reduced response to stress as a possible protective mechanism.

Cardiac troponin T elevation after stroke: relationships between elevated serum troponin T, stroke location, and prognosis.

BACKGROUND AND PURPOSE: Elevation of serum cardiac troponin T (cTnT) is regarded as a specific marker of acute coronary syndrome. Serum cTnT can be increased in patients with acute ischemic stroke, but its clinical implications remain unclear. The aim of this study was to identify the relationships between elevated cTnT and stroke severity, location, and prognosis. METHODS: From January 2005 to December 2006, this study recruited 455 consecutive patients who were admitted to Kangbuk Samsung Hospital due to acute ischemic stroke within 3 days of onset, which was confirmed by diffusion magnetic resonance imaging. A total of 416 patients was finally included and divided into 2 groups: an elevated cTnT group (n=45) and a normal cTnT group (n=371). The short-term prognosis was assessed by 30-day modified Rankin Scale responder analysis was compared between the two groups. RESULTS: Serum cTnT was elevated in 10.8% of cases, with elevated cTnT associated with greater stroke severity, as assessed by the National Institutes of Health Stroke Scale score, Insular-lobe involvement was more common in patients with elevated cTnT than in the normal cTnT group. Short-term prognosis was more unfavorable in the elevated cTnT group than in the normal cTnT group. Multivariate regression analysis indicated that elevated cTnT was independently related to insular involvement, cardioembolism, and unfavorable outcome. CONCLUSIONS: Elevated cTnT in acute ischemic stroke was associated with severe neurological deficits at stroke onset and damages to the insular lobe. The outcome of acute ischemic stroke was worse for patients with elevated cTnT than for those with normal cTnT. The pathomechanism underlying acute ischemic stroke and subclinical myocardial damage warrants further study.