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A literature review was performed by content experts in neuro-ophthalmology and neuroradiology using a systematic English-language Medline search (1994)(1995)(1996)(1997)(1998)(1999)(2000)(2001)(2002)(2003)(2004)(2005)(2006)(2007)(2008) limited to articles with relevance to neuro-ophthalmic and orbital imaging. The information covered in this review includes: (i) the basic mechanics, indications and contraindications for cranial and orbital computed tomography and magnetic resonance (MR) imaging; (ii) the utility and indications for intravenous contrast, (iii) the use of specific MR sequences; (iv) the techniques and ophthalmic indications for computed tomography/MR angiography and venography; and (v) the techniques and indications for functional MR imaging, positron emission tomography scanning and single photon emission computed tomography. Throughout the review accurate and timely communication with the neuroradiologist regarding the clinical findings and suspected location of lesions is emphasized so as to optimize the ordering and interpretation of imaging studies for the ophthalmologist.

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The CRI device demonstrated superior capacity over systolic blood pressure in predicting the need for posttraumatic hemorrhage intervention in the acute resuscitation phase after injury.

The interactions of two potential topcoat materials for environmental barrier coatings, Yb 2 SiO 5 and Yb 2 Si 2 O 7 , with calcium-magnesium-aluminosilicate (CMAS) engine deposits were studied. X-ray diffraction, scanning electron microscopy, energy-dispersive X-ray spectroscopy, and electron diffraction were used to investigate the phase transformation associated with the exposure of Yb 2 SiO 5 and Yb 2 Si 2 O 7 to CMAS at 1300°C. It was found that Yb 2 SiO 5 strongly reacts with CMAS to completely dissolve the Yb 2 SiO 5 and form hexagonal Ca 2 Yb 8 (SiO 4) 6 O 2 deposits. In contrast, no discernable reaction between CMAS and Yb 2 Si 2 O 7 , was observed over the 96-hour exposure.

Acute kidney injury is an unfortunate complication of acyclovir therapy secondary to crystal-induced nephropathy. It is characterized by a decrease in renal function that develops within 24–48 hours of acyclovir administration indicated by a rapid rise in the serum creatinine. Failure to quickly realize this as an etiology of acute kidney injury can lead to excessive morbidity to the patient. The case described in this vignette is an example of the clinical manifestation of acyclovir crystal obstructive nephrotoxicity. We will briefly discuss the pathophysiology, diagnosis, prevention, and management of patients that present with acyclovir nephrotoxicity.