Dural arteriovenous fistula of the craniocervical junction.

Dural arteriovenous (AV) fistulas of the craniocervical junction can be challenging to diagnose. We describe a 70-year-old man with subacute progressive myelopathy whose MR scan of cervical spine showed serpiginous dorsal vessels, suggesting a dural AV fistula. However, a detailed diagnostic angiogram was normal, prompting additional work-up and a wider differential, which was non-revealing. His symptoms progressed over months, but the evolution of the lesion characteristics on repeat spinal imaging still suggested a dural AV fistula. Repeat angiogram identified an infratentorial dural AV fistula arising from the meningohypophyseal artery. He improved following retrosigmoid craniotomy and clipping. Initial angiography does not always demonstrate a dural AV fistula; if there is clinical and radiographic evolution, repeat angiography might identify a fistula with a rare arterial feeder.

Case Report: Ocular Manifestation of Mantle Cell Lymphoma.

SIGNIFICANCE: Mantle cell lymphoma (MCL) is a rare lymphoma that can present even more rarely in the orbit. Diagnosis, differentiation, and systemic treatment with the help of an oncologist are necessary for improved prognosis. Eye care providers must be vigilant when addressing ocular findings to determine next steps. PURPOSE: We present a case of presumed orbital fat prolapse confirmed as MCL found on routine eye examination. CASE REPORT: A 72-year-old White man presented for an annual comprehensive eye examination and was found to have conjunctival elevation in the superior and inferior fornices bilaterally. The patient had stable lymphadenopathy on positron emission tomography/computed tomography imaging 1 week before presentation. Coupled with the patient's recent diagnosis of systemic MCL, there was high suspicion that the conjunctival lesions were malignant. Biopsy of the conjunctival lesion confirmed MCL. A reevaluation of the previous imaging with a neuroradiologist confirmed the presence of orbital lesions consistent with MCL. The patient responded to treatment with low-dose focal radiation therapy. CONCLUSIONS: Primary eye care providers should be aware of limitations of orbital imaging during routine positron emission tomography and computed tomography scans in those with MCL, and consultation with neuroradiology for image review may be useful if the clinical findings are suspicious.

Sarcoidosis in the Head and Neck: An Illustrative Review of Clinical Presentations and Imaging Findings.

OBJECTIVE: Sarcoidosis is referred to as a great imitator because of its propensity to radiologically mimic a variety of pathologic entities. Symptomatic neurosarcoidosis is present in approximately 5% of patients with sarcoidosis, and it is found histopathologically in approximately 25% of asymptomatic patients. CONCLUSION: An understanding of the multifaceted imaging manifestations of head and neck sarcoidosis will aid early recognition of the diagnosis, with a goal for earlier initiation of therapy and prevention of irreversible sequelae of the disease.

Painting blood vessels and atherosclerotic plaques with an adhesive drug depot.

The treatment of diseased vasculature remains challenging, in part because of the difficulty in implanting drug-eluting devices without subjecting vessels to damaging mechanical forces. Implanting materials using adhesive forces could overcome this challenge, but materials have previously not been shown to durably adhere to intact endothelium under blood flow. Marine mussels secrete strong underwater adhesives that have been mimicked in synthetic systems. Here we develop a drug-eluting bioadhesive gel that can be locally and durably glued onto the inside surface of blood vessels. In a mouse model of atherosclerosis, inflamed plaques treated with steroid-eluting adhesive gels had reduced macrophage content and developed protective fibrous caps covering the plaque core. Treatment also lowered plasma cytokine levels and biomarkers of inflammation in the plaque. The drug-eluting devices developed here provide a general strategy for implanting therapeutics in the vasculature using adhesive forces and could potentially be used to stabilize rupture-prone plaques.

Injuries of the globe: what can the radiologist offer?

Traumatic ocular injuries are a significant cause of blindness and visual deficits. In the setting of acute orbital trauma, urgent ophthalmologic evaluation and intervention are critical in preserving vision. However, in the acute trauma setting, clinical evaluation of the globe may be difficult in the presence of surrounding periorbital soft-tissue swelling and other associated injuries, and patient cooperation may be limited because of unresponsiveness, altered mentation, or sedation. Often, rapid access to imaging is part of the initial diagnostic evaluation, and radiologists may be the first to identify traumatic injuries of the globe. Because of this, radiologists should be familiar with normal orbital and globe anatomy at various imaging modalities and have a thorough understanding of the various patterns of ocular injury and their imaging appearances. Radiologists should also be familiar with the various mimics of ocular injury, including congenital and acquired conditions that may alter the shape of the globe, various types of ocular calcifications, and the different types of material used to treat retinal detachment. Such knowledge may help radiologists make accurate diagnoses, which facilitates prompt and appropriate patient care.

Intraoperative near-infrared fluorescent cholangiography (NIRFC) in mouse models of bile duct injury.

BACKGROUND: Accidental injury to the common bile duct is a rare but serious complication of laparoscopic cholecystectomy. Accurate visualization of the biliary ducts may prevent injury or allow its early detection. Conventional X-ray cholangiography is often used and can mitigate the severity of injury when correctly interpreted. However, it may be useful to have an imaging method that could provide real-time extrahepatic bile duct visualization without changing the field of view from the laparoscope. The purpose of the present study was to test a new near-infrared (NIR) fluorescent agent that is rapidly excreted via the biliary route in preclinical models to evaluate intraoperative real-time near infrared fluorescent cholangiography (NIRFC). METHODS: To investigate probe function and excretion, a lipophilic near-infrared fluorescent agent with hepatobiliary excretion was injected intravenously into one group of C57/BL6 control mice and four groups of C57/BL6 mice under the following experimentally induced conditions: (1) chronic biliary obstruction, (2) acute biliary obstruction (3) bile duct perforation, and (4) choledocholithiasis, respectively. The biliary system was imaged intravitally for 1 h with near-infrared fluorescence (NIRF) with an intraoperative small animal imaging system (excitation 649 nm, emission 675 nm). RESULTS: The extrahepatic ducts and extraluminal bile were clearly visible due to the robust fluorescence of the excreted fluorochrome. Twenty-five minutes after intravenous injection, the target-to-background ratio peaked at 6.40 +/- 0.83 but signal was clearly visible for ~60 min. The agent facilitated rapid identification of biliary obstruction and bile duct perforation. Implanted beads simulating choledocholithiasis were promptly identifiable within the common bile duct lumen. CONCLUSIONS: Near-infrared fluorescent agents with hepatobiliary excretion may be used intraoperatively to visualize extrahepatic biliary anatomy and physiology. Used in conjunction with laparoscopic imaging technologies, the use of this technique should enhance hepatobiliary surgery.

Selective factor XIIa inhibition attenuates silent brain ischemia: application of molecular imaging targeting coagulation pathway.

OBJECTIVES: The purpose of this study was use molecular imaging targeting coagulation pathway and inflammation to better understand the pathophysiology of silent brain ischemia (SBI) and monitor the effects of factor XIIa inhibition. BACKGROUND: SBI can be observed in patients who undergo invasive vascular procedures. Unlike acute stroke, the diffuse nature of SBI and its less tangible clinical symptoms make this disease difficult to diagnose and treat. METHODS: We induced SBI in mice by intra-arterial injection of fluorescently labeled microbeads or fractionated clot into the carotid artery. After SBI induction, diffusion-weighted magnetic resonance imaging was performed to confirm the presence of microinfarcts in asymptomatic mice. Molecular imaging targeting the downstream factor XIII activity (single-photon emission computed tomography/computed tomography) at 3 h and myeloperoxidase activity (magnetic resonance imaging) on day 3 after SBI induction were performed, without and with the intravenous administration of a recombinant selective factor XIIa inhibitor derived from the hematophagous insect Triatoma infestans (rHA-Infestin-4). Statistical comparisons between 2 groups were evaluated by the Student t test or Mann-Whitney U test. RESULTS: In SBI-induced mice, we found abnormal activation of the coagulation cascade (factor XIII activity) and increased inflammation (myeloperoxidase activity) close to where emboli lodge in the brain. rHA-Infestin-4 administration significantly reduced ischemic damage (53% to 85% reduction of infarct volume, p < 0.05) and pathological coagulation (35% to 39% reduction of factor XIII activity, p < 0.05) without increasing hemorrhagic frequency. Myeloperoxidase activity, when normalized to the infarct volume, did not significantly change with rHA-Infestin-4 treatment, suggesting that this treatment does not further decrease inflammation other than that resulting from the reduction in infarct volume. CONCLUSIONS: Focal intracerebral clotting and inflammatory activity are part of the pathophysiology underlying SBI. Inhibiting factor XIIa with rHA-Infestin-4 may present a safe and effective treatment to decrease the morbidity of SBI.

Local anesthetics induce human renal cell apoptosis.

Renal cell apoptosis contributes significantly to the pathogenesis of acute renal failure. Local anesthetics induce apoptosis in neuronal and lymphocytic cell lines. We examined the effects of chronic (48 h) local anesthetic treatment (lidocaine, bupivacaine and tetracaine) on human proximal tubular (HK-2) cells. Apoptosis induction was assessed by detecting poly(ADP)-ribose polymerase fragmentation, caspase activation, terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) staining, DNA laddering and by cellular morphology. Cell death was quantified by measuring neutral red dye uptake and lactate dehydrogenase released into the cell culture medium. All 3 local anesthetics caused concentration-dependent cell death, induced HK-2 cell apoptosis and potentiated TNF-alpha induced apoptosis. Local anesthetics induced HK-2 cell apoptosis by activation of caspases 3, 6, 7, 8 and 9. ZVAD-fmk, a pan-caspase inhibitor, blocked the local anesthetic induced HK-2 cell apoptosis. Local anesthetics also inhibited the activities of anti-apoptotic kinases protein kinase B (Akt) and extracellular signal regulated mitrogen-activated protein kinase. Local anesthetic's pro-apoptotic effects are independent of sodium channel inhibition as tetrodotoxin, a selective voltage-gated sodium channel blocker, failed to mimic local anesthetic-mediated induction or potentiation of HK-2 cell apoptosis. We conclude that local anesthetics induce human renal cell apoptotic signaling by caspase activation and via inhibition of pro-survival signaling pathways.