Intracranial Arterial Calcificationes Can Reflect Cerebral Atherosclerosis Burden

BACKGROUND AND PURPOSE: We investigated whether the intracranial arterial calcification status reflects the overall cerebral atherosclerosis burden. METHODS: Patients with acute cerebral infarction who were admitted to a single university hospital stroke center and underwent brain computed tomography angiography (CTA) between May 2011 and December 2015 were included. We reviewed their demographic, clinical, and imaging data. Cerebral artery calcification was assessed from the cavernous portion of both internal carotid arteries, and patients were categorized into three groups according to the calcification status. The cerebral atherosclerosis score was calculated as the sum of the degree of stenosis of the major intracranial and extracranial arteries on brain CTA. RESULTS: In total, 1,161 patients were included (age=67±13 years, mean±standard deviation), of which 517 were female. Intracranial arterial calcification and atherosclerosis were detected in 921 patients. The cerebral atherosclerosis score tended to increase with the calcification status (no calcification=2.0±3.0, mild=3.8±3.8, severe=6.5±4.8; p < 0.001 in analysis of variance followed by the Bonferroni test). Multivariable logistic regression analysis including age, sex, vascular risk factors, body mass index, estimated glomerular filtration rate, high-sensitivity C-reactive protein, and calcification status showed that intracranial calcification was independently associated with an advanced cerebral atherosclerosis burden in a dose-dependent manner (compared to no calcification: odds ratio=2.0 and 95% confidence interval=1.1–3.4 for mild calcification, and odds ratio=4.7 and 95% confidence interval=2.7–8.3 for severe calcification). CONCLUSIONS: This study found that the calcification status of the cavernous portion of an internal carotid artery can reflect the overall cerebral atherosclerosis burden.

Paradoxical Response after a Voriconazole Treatment in an Immunocompetent Host with a Skull Base Osteomyelitis due to Invasive Aspergillosis

BACKGROUND: We describe a case of skull base osteomyelitis due to invasive aspergillosis which had been aggravated after antifungal treatment but significantly recovered by dexamethasone. CASE REPORT: A 74-year-old male patient presented to neurology clinic complaining of sudden onset right-sided facial palsy and headache. Brain magnetic resonance imaging (MRI) and sphenoid sinus biopsy confirmed Aspergillus infection of skull base. He was treated with voriconazole for two months, but his headache was not relieved, and he additionally complained of vertigo and dysphagia. A subsequent MRI showed reduced enhancement of initial lesions, but increased thickness of surrounding dura mater. With an impression of paradoxical inflammatory response after antifungal treatment, parenteral dexamethasone was administered for one month while maintaining voriconazole. His symptoms improved thereafter. CONCLUSION: A paradoxical inflammatory response during antifungal treatment in the skull base aspergillosis aggravates the neurological symptom by thickening the dura mater, which can be recovered by dexamethasone.

Adult Mumps Meningoencephalitis with Splenial Lesion

No abstract available.

Calcineurin Inhibitor Induced Multiple Infarctions / 대한이식학회지

Tacrolimus is the most commonly used immunosuppressant after kidney transplantation. Here, we report a patient with multiple cerebral infarctions during tacrolimus treatment after kidney transplantation. A 54-year-old female was admitted due to sudden onset right leg weakness. Brain magnetic resonance imaging (MRI) showed multiple acute infarctions but normal vasculature. Evaluations of cardiac embolism were unremarkable. After 8 months, her weakness progressed and follow-up brain MRI showed additional multiple infarctions. We changed here medication from tacrolimus to mycophenolate mofetil, and her symptoms improved gradually.

Rapid Progression of Sporadic ALS in a Patient Carrying SOD1 p.Gly13Arg Mutation

Amyotrophic lateral sclerosis (ALS), the most common adult onset motor neuron disease, is pathologically characterized by progressive loss of the upper and lower motor neurons. Mutations in the Cu/Zn superoxide dismutase gene (SOD1) account for about 20% of familial ALS cases and a small percentage of sporadic ALS (SALS) cases, and have revealed a validated genotype-phenotype correlation. Herein, we report a p.Gly13Arg mutation in SOD1 exon 1 in a patient with SALS who presented with a rapidly progressive course, predominantly affecting the lower motor neurons. A 48-year-old man presented with progressive weakness and muscle atrophy of the left upper and lower limbs, followed by muscle fasciculation and cramping. The clinical features of the patient were clearly suggestive of ALS, and implied a sporadic form with rapid progression, predominantly affecting the lower motor neurons. Sequencing of the SOD1 gene by PCR revealed a missense mutation of G to C (c.37G>C) in exon 1, and amino acid substitution of glycine by arginine (p.Gly13Arg). This is the first case identifying the p.Gly13Arg mutation of SOD1 in the Korean population, and clinical assessments of this patient revealed a different phenotype compared with other cases.