Myelopathy after traumatic lumbar vertebral intraosseous arteriovenous fistula with epidural venous drainage treated with transvenous embolization.

Spinal epidural arteriovenous fistulas are an uncommon entity. The authors present an interesting case of a 48-year-old man involved in a MVC five months prior to presenting with bilateral lower extremity weakness and hypoesthesia below the knees. MRI demonstrated a flow void in the L1 vertebral body burst fracture along with a dilated basivertebral vein draining in to engorged epidural venous plexus. Angiography confirmed an intraosseous arteriovenous fistula fed by T12 and L1arteries and epidural venous drainage. Complete obliteration by arterial embolization was precluded by origin of the artery of Adamkiewicz from the feeding L1 lumbar artery. Embolization using a transvenous approach allowed for successful obliteration of the fistula. Following the procedure, the patient had significant immediate improvement in the lower extremity symptoms. This is the first report of a posttraumatic spinal epidural arteriovenous fistula secondary to a vertebral burst fracture successfully treated by transvenous embolization.

Acute Herpes Zoster Radiculopathy of the Lower Extremity With Dermatomal Rash and Lumbar Nerve Enhancement on MRI.

Herpes zoster is a frequent cause of neuralgia and dermatomal vesicular rash secondary to reactivation of latent varicella zoster virus. However, it rarely presents with acute lumbar radiculopathy and the diagnosis can be quite challenging in such cases. Nerve signal abnormalities on magnetic resonance imaging are well recognized in herpes zoster neuropathy or plexopathy affecting the extremities, although gadolinium enhancement is characteristically absent. In this article, we describe a case of acute herpes zoster lumbosacral radiculopathy with characteristic vesicular dermatomal rash and second ever reported finding of gadolinium enhancement of the lumbar nerve on magnetic resonance imaging.

A Case of Familial Male-Limited Precocious Puberty in a Child With Klinefelter Syndrome.

Familial male-limited precocious puberty (FMPP) is an autosomal dominant, male-limited disorder that causes peripheral precocious puberty in boys. Klinefelter syndrome (47, XXY) is the most common chromosomal aberration in males with associated infertility, hypogonadism, and learning disability. We report here a case of Klinefelter syndrome in a patient with FMPP. A 6-year-old boy was referred to our pediatric endocrinology department for accelerated linear growth and premature pubic hair development. He was diagnosed with FMPP based on clinical, laboratory, and genetic sequencing. Increased levels of gonadotropins prompted further investigation, leading to a subsequent diagnosis of Klinefelter syndrome through karyotype analysis. This case illustrates that patients with FMPP and elevated gonadotropins should encourage further investigation by physicians. We recommend the use of karyotype analysis in such patients who are not receiving aromatase inhibitor therapy. We hypothesize that his mutation or pretreatment with aromatase inhibitors may have a protective effect on testosterone production and sperm viability.