We performed bilateral transmuscular quadratus lumborum blocks in six cadavers using iodinated contrast and methylene blue. Computed tomography imaging was performed in four cadavers and anatomical dissection was completed in five. This demonstrated spread to the lumbar paravertebral space in 63% of specimens, laterally to the transversus abdominis muscle in 50% and caudally to the anterior superior iliac spine in 63% of specimens. There was no radiographic evidence of spread to the thoracic paravertebral space. Anatomical dissection revealed dye staining of the upper branches of the lumbar plexus and the psoas major muscle in 70% of specimens. Further clinical studies are required to confirm if the quadratus lumborum block might be a suitable alternative to lumbar plexus block.

Background Cortical and subcortical gray matter (GM) atrophy may progress differently during the course of Parkinson's disease (PD). We delineated and compared the longitudinal pattern of these PD-related changes. Methods Structural MRIs and clinical measures were obtained from 76 PD with different disease durations and 70 Controls at baseline, 18- and 36-months. Both cortical and subcortical (putamen, caudate, and globus pallidus) GM volumes were obtained, compared, and associated with PD clinical measures at baseline. Their volumes and rates of change also were compared among Controls, PDs, and PD subgroups based on duration of illness [≤1 year (PDE), 1-5 years (PDM), and >5 years (PDL)]. Results Compared to Controls, PD subjects displayed smaller cortical GM and striatal (putamen, caudate, ps≤0.001), volumes at baseline. Cortical GM volumes were negatively associated with disease duration at baseline, whereas striatal volumes were not. PD subjects demonstrated accelerated volume loss in cortical GM (p=0.006), putamen (p=0.034), and caudate (p=0.008) compared to Controls. Subgroup analyses demonstrated that accelerated cortical atrophy reached statistical significance in PD subjects with duration of illness 1-5 years (PDM, ps<0.001) and the trend of accelerated atrophy seemed to persist until later stages, whereas striatal atrophy occurred in PD subjects with PDE (p=0.021 for putamen, p=0.005 for caudate) and PDM (p=0.002 for putamen, p=0.001 for caudate) that significantly slowed down in PDL (ps for PDL vs PDE or PDM: <0.01). Conclusions The pattern of GM loss in PD differs in cortical and subcortical regions, with striatal atrophy occurring earlier and extra-striatal cortical atrophy later.

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OBJECTIVE A thorough understanding of anatomy is critical for successful carpal tunnel release. Several texts depict the median nerve (MN) as taking a course parallel to the long axis of the forearm (LAF). The authors report on their attempt to formally assess the course of the MN as it travels to the carpal tunnel in the distal wrist and discuss its potential clinical significance. METHODS The width of the wrist, the distance from the radial wrist to the MN, and the distance from the distal volar wrist crease to the point where the MN emerges between the flexor carpi radialis (FCR) tendon and the flexor digitorum superficialis (FDS) tendons were recorded during cadaveric dissection of 76 wrist specimens. The presence or absence of palmaris longus was documented. Finally, the angles between the MN and FCR tendon and between the MN and the LAF were measured using ImageJ. RESULTS The relative position of the MN at the distal wrist crease, as determined by the ratio of the distance from the MN to the radial wrist divided by wrist width, revealed a mean value of 0.48, indicating that the nerve was usually located just radial to midline. The mean distance between the distal wrist crease and the MN's emergence was 34.6 mm. The mean angle between the MN and the FCR tendon was 14.1°. The angle between the MN and the LAF had a mean value of 8.8° (range 0.0°-32.2°). The nerve was parallel to the LAF in only 10.7% of the studied wrists. Palmaris longus was absent in 14 (18.4%) of the 76 wrists. CONCLUSIONS The MN takes an angular approach to the carpal tunnel in the distal wrist in the vast majority of cases. This newly described finding will be useful to both clinicians and anatomists.

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PurposeTo determine the effect of diabetes and metabolic stress on retinal nuclear factor E2‐related factor‐2 (Nrf2) protein content after light and dark adaptation, and its effect on vision in rats. Darkness was used as a stressor because the retina is more metabolically active in the dark.MethodsLong‐Evans and Sprague‐Dawley rats were made diabetic by streptozotocin (STZ) injection and compared to age‐matched controls (CNT). One group of STZ and CNT rats was sacrificed in light‐adapted conditions; the second group was sacrificed after 24 hr dark adaptation. Retinal Nrf2 protein was determined by immunoblot after 6 and 10 weeks of STZ‐diabetes. Behavioral optokinetic testing was used to measure visual function (spatial frequency threshold and contrast sensitivity) after 6 and 10 weeks of diabetes. Statistical analysis was by ANOVA and Newman‐Keuls test.ResultsThere was significantly less Nrf2 after 6 weeks of STZ‐diabetes (p<0.05), and visual function was also significantly reduced after 6 and 10 weeks of STZ‐diabetes compared to CNT (p<0.05).ConclusionDiabetes impairs visual function in rats and reduces retinal Nrf2 protein content under metabolic stress.