Far-out foraminal stenosis with radiculopathy caused by bony spur formation secondary to anomalous articulation between the transverse process and the sacral ala is rarely reported. We report two cases of unilateral far-out foraminal entrapment of the L5 spinal nerve below a transitional vertebra, with a review of the literature. The objective of this work was to describe the management of a rare far-out foraminal stenosis below a transitional vertebra and to evaluate the surgical and conservative procedures and results. In a previous article, decompression was performed through an anterior approach. However, we report no difficulty with decompression using a posterior approach for one patient. The diagnosis was confirmed with computed tomography, magnetic resonance imaging, and selective radiculography. First, selective nerve root blocks were performed in two cases for the purpose of nonoperative treatment. After failure of conservative treatment with selective nerve root block, one patient underwent posterior decompression by resection of the bony spur using a posterior approach. One patient obtained good relief of radicular pain with only selective nerve root block. The other patient obtained good relief of radicular pain after posterior decompression was performed. Posterior decompression through the posterior approach is an easy, safe, and useful treatment for radicular pain caused by an L5 nerve far-out foraminal stenosis below a transitional vertebra when conservative treatments have failed to obtain good relief of radicular pain.

Adipose triglyceride lipase (ATGL) deficiency manifesting neutral lipid storage disease with myopathy/triglyceride deposit cardiomyovasculopathy presents distinct fat-containing vacuoles known as Jordans' anomaly in peripheral leucocytes. To develop an automatic notification system for Jordans' anomaly in ATGL-deficient patients, we analyzed circulatory leukocyte scattergrams on automated hematology analyzer XE-5000. The BASO-WX and BASO-WY values were found to be significantly higher in patients than those in non-affected subjects. The two parameters measured by automated hematology analyzer may be expected to provide an important diagnostic clue for homozygous ATGL deficiency.

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