Quantitative susceptibility mapping in ischemic stroke patients after successful recanalization.

Quantitative susceptibility mapping (QSM) is a novel processing method for gradient-echo magnetic resonance imaging (MRI). Higher magnetic susceptibility in cortical veins have been observed on susceptibility maps in the ischemic hemisphere of stroke patients, indicating an increased oxygen extraction fraction (OEF). Our goal was to investigate susceptibility in veins of stroke patients after successful recanalization in order to analyze the value of QSM in predicting tissue prognosis and clinical outcome. We analyzed MR images of 23 patients with stroke due to unilateral middle cerebral artery (MCA)-M1/M2 occlusion acquired 24-72 h after successful thrombectomy. The susceptibilities of veins were obtained from QSM and compared between the stroke territory, the ipsilateral non-ischemic MCA territory and the contralateral MCA territory. As outcome variables, early infarct size and functional disability (modified Rankin Scale, mRS) after 3-5 months was used. The median susceptibility value of cortical veins in the ischemic core was 41% lower compared to the ipsilateral non-ischemic MCA territory and 38% lower than on the contralateral MCA territory. Strikingly, in none of the patients prominent vessels with high susceptibility signal were found after recanalization. Venous susceptibility values within the infarct did not correlate with infarct volume or functional disability after 3-5 months. Low venous susceptibility within the infarct core after successful recanalization of the occluded vessel likely indicates poor oxygen extraction arising from tissue damage. We did not identify peri-infarct tissue with increased susceptibility values as potential surrogate of former penumbral areas. We found no correlation of QSM parameters with infarct size or outcome.

Anatomical study of the teres major muscle: description of an additional distal muscle slip.

BACKGROUND: Understanding muscle and tendon anatomy is of tremendous importance to achieve optimal surgical execution and results in tendon transfers around the shoulder. The aim of this study was to introduce and describe an additional distal muscle slip of the teres major (TM). METHODS: Sixteen fresh-frozen cadaver shoulders were dissected with the deltopectoral approach. The ventral latissimus dorsi (LD) tendon was harvested, and the shoulders were analyzed for the presence/absence of a distal teres major slip (dTMs) and its dimensions and relationship with the TM and LD tendons. RESULTS: The dTMs was identified in 12 shoulders (75%). It was always distal to the TM tendon and visible during the deltopectoral approach. There was a clear separation between the TM proximally and dTMs tendon distally. At the humeral insertion, both tendons had a common epimyseal sheet around the teres major and inserted continuously at the humerus. The mean width of the dTMs tendon at the insertion was 13 ± 4 mm (range, 7-22 mm). The total lengths of the dTMs tendon and LD tendon were 40 ± 7 mm (range, 25-57 mm) and 69 ± 7 mm (range, 57-79 mm), respectively (p < 0.001). The dTMs muscle showed direct adhesions in ten shoulders (83%) with the LD muscle. CONCLUSIONS: This is the first macroscopic description of an additional distal slip of the teres major muscle. The dTMs has a separate (distal) but continuous (mediolateral) insertion at the humerus within a common epimyseal sheet around the TM. The dTMs tendon is visible during the deltopectoral approach and can therefore provide a lead structure, particularly in ventral LD transfers with the deltopectoral approach.

Biomechanical analysis of arthroscopically assisted latissimus dorsi transfer fixation for irreparable posterosuperior rotator cuff tears-Knotless versus knotted anchors.

We compared the construct stability of traditional knotted techniques with modern knotless anchor systems used in arthroscopically assisted latissimus dorsi transfers (aLDTs) for irreparable posterosuperior rotator cuff tears. Eighteen cadaveric shoulders were age- and gender-matched to the following three groups: knotted group (two knotted anchors); knotless group (two knotless anchors); and triple anchor group (two knotless anchors; one all-suture anchor at the apex of the humeral head). All tendons were cyclically loaded in line of the aLDT over 400 cycles followed by a load to failure test. Outcome measures were the ultimate load to failure, elongation, construct stiffness, and failure modes. The triple anchor group revealed the highest ultimate load to failure (431 ± 78 N) compared with the knotted (326 ± 52 N; p = .022) and knotless (353 ± 105 N; p = .129) groups. Total elongation and construct stiffness were not significantly different comparing all three groups. The failure modes were: anchor pull-out in all specimen of the knotted group; three (50%) anchor pull-out and three suture pull-out in the knotless group (p = .046); four (67%) anchor pull-out, one (17%) suture pull-out and one tendon pull-out in the triple anchor group. Biomechanical analyses of knotless fixation techniques for aLDTs show similar construct stability and elongation compared with the traditional, knotted techniques. Bone fixation seems to be improved with the knotless anchor systems. In our practice, we continue to use the knotless fixation technique for aLDT and in the situation of weak, osteoporotic bone, we add a third (all-suture) anchor to improve construct stability.

Inhibition of calpain delays early muscle atrophy after rotator cuff tendon release in sheep.

Chronic rotator cuff (RC) tears are characterized by retraction, fat accumulation, and atrophy of the affected muscle. These features pose an intractable problem for surgical repair and subsequent recovery, and their prevention may be easier than reversal. Using an established ovine model, we tested the hypothesis that inhibition of the protease calpain mitigates m. infraspinatus atrophy by preservation of the myofibers' structural anchors in the sarcolemma (the costameres). Already 2 weeks of distal tendon release led to a reduction in muscle volume (-11.6 ± 9.1 cm3 , P = 0.038) and a 8.3% slow-to-fast shift of the fiber area (P = 0.046), which were both entirely abolished by chronic local administration of the calpain inhibitor calpeptin alone, and in combination with sildenafil. Calpain inhibition blunted the retraction of the muscle-tendon unit by 0.8-1.0 cm (P = 0.020) compared with the control group, and prevented cleavage of the costameric protein talin. Calpain 1 and 2 protein levels increased in the medicated groups after 4 weeks, counteracting the efficacy of calpeptin. Hence atrophic changes emerged after 4 weeks despite ongoing treatment. These findings suggest that the early muscular adaptations in the specific case of RC tear in the ovine model are indistinguishable from the atrophy and slow-to-fast fiber transformation observed with conventional unloading and can be prevented for 2 weeks. Concluding, calpain is a potential target to extend the temporal window for reconstruction of the ruptured RC tendon before recovery turns impossible.