ABSTRACT
INTRODUCTION: Contrast-induced encephalopathy (CIE) is a rare complication associated with the use of contrast media. New contrast agents make contrast complications increasingly rare. The diagnosis of CIE is challenging, particularly in patients with acute ischemic stroke. Neuroimaging results for patients with CIE can also be highly variable. PATIENT CONCERNS: A 63-year-old man with severe internal carotid artery stenosis who experienced several symptoms, including dizziness, nausea, vomiting, fever, and blurred vision after being administered the contrast agent iodixanol. DIAGNOSES: Multiple CT and MRI brain scans were performed. After excluding other differential diagnoses such as electrolytes imbalance, hypo/hyperglycemia and other neurological emergencies such as cerebral hemorrhage, cerebral infarction, the final diagnosis of CIE was made. INTERVENTION: Treatment consisted of adequate hydration, intravenous dexamethasone, mannitol, and anticonvulsants. OUTCOME: The patient demonstrated progressive neurological improvement, and recovered from all symptoms on the fifth day. Follow-up at 3 months shows a good prognosis for patients. CONCLUSION: Patients with CIE may have a high signal on diffusion-weighted imaging and a low signal on apparent diffusion coefficient brain MRI. This is similar to the MRI findings in acute stroke. This needs to be distinguished from acute cerebral infarction and suggests that we should closely monitor patients' neurological symptoms at the time of cerebral angiography and after the investigations.
Subject(s)
Ischemic Stroke , Stroke , Male , Humans , Middle Aged , Cerebral Angiography , Stroke/diagnosis , Magnetic Resonance Imaging/methods , Cerebral Infarction/diagnostic imaging , Cerebral Infarction/etiologyABSTRACT
RATIONALE: Spontaneous carotid cavernous fistula (CCF) is rare, and the expression of headache caused by it can be variable. PATIENT CONCERNS: A case of a man hospitalized for high-intensity hemicranial headache which was aggravated by lying down and relieved when standing or sitting. The pain was of a pulsating character, localized on the right, behind the eye, followed by nausea and vomiting. He gradually appeared with ophthalmoplegia, decreased visual acuity and epistaxis. DIAGNOSIS: Digital subtraction angiogram (DSA) showed a pseudoaneurysm arising from the internal carotid artery (ICA) that projected anteriorly and medially into the sphenoid sinus with occluded fistula. INTERVENTIONS: The pseudoaneurysm was successfully treated with covered stent. OUTCOMES: The patient was then followed up clinically at the outpatient and seen in the outpatient clinic with no further episodes of nasal bleeding or new neurologic deficit. The vision loss and ophthalmoparesis were unchanged. LESSONS: Hemicranial postural headache may be the first and characteristic sign of spontaneous CCF.
Subject(s)
Aneurysm, False , Carotid-Cavernous Sinus Fistula , Embolization, Therapeutic , Aneurysm, False/therapy , Carotid Artery, Internal , Carotid-Cavernous Sinus Fistula/diagnosis , Carotid-Cavernous Sinus Fistula/diagnostic imaging , Embolization, Therapeutic/adverse effects , Epistaxis/etiology , Headache/etiology , Headache/therapy , Humans , MaleABSTRACT
It is well known that extracellular deposition of amyloid-ß (Aß) peptide and microglia-mediated neuroinflammation are major hallmarks of Alzheimer's disease (AD). Interferon regulatory factor-8 (IRF-8), an important transcription factor of the IRF family, is highly restricted in microglia in brains. The expression pattern and function of IRF-8 in AD need to be elucidated in order to provide novel therapies for the treatment of AD. In this study, our results indicated that expression of IRF-8 is significantly elevated in the brains and microglia of AD transgenic model Tg2576 mice. Notably, in vitro cell culture and reporter luciferase assay show that Aß1-40 treatment promotes expression of IRF-8 at the transcriptional level. Silencing of IRF-8 in microglia abolished Aß1-40-induced elevation in typical activated microglia-related genes, including the microglial innate response receptor toll-like receptor 2 (TLR2), the chemotaxis gene purinergic receptor P2Y12R, and the proinflammatory cytokine IL-1ß. However, overexpression of IRF-8 exacerbated the elevated expression of these proteins. Finally, the JAK2/STAT-1 pathway was found to mediate Aß1-40-induced elevation of IRF-8. Overall, this is the first time to report that IRF-8 is involved in microglial activation and neuroinflammation in AD.
