Ischemia reperfusion injury is reviewed in the context of the evolution of flap research over the past decade. A description of the clinical relevance of this field is presented and the possible etiologies are reviewed. The pathophysiology of this injury is then explored in some detail. Both skin and myocutaneous flaps, in a variety of animal models, are discussed. Research performed in vitro, as well as in other organ systems similarly affected by ischemia and reperfusion, is also examined. Particular attention is placed on the function of several newly described inflammatory mediators where it appears relevant to future research and treatment in the field of reconstructive microsurgery.

BackgroundIt has long been suggested that feedback signals from facial muscles influence emotional experience. The recent surge in use of botulinum toxin (BTX) to induce temporary muscle paralysis offers a unique opportunity to directly test this “facial feedback hypothesis.” Previous research shows that the lack of facial muscle feedback due to BTX-induced paralysis influences subjective reports of emotional experience, as well as brain activity associated with the imitation of emotional facial expressions. However, it remains to be seen whether facial muscle paralysis affects brain activity, especially the amygdala, which is known to be responsive to the perception of emotion in others. Further, it is unknown whether these neural changes are permanent or whether they revert to their original state after the effects of BTX have subsided. The present study sought to address these questions by using functional magnetic resonance imaging to measure neural responses to angry and happy facial expressions in the presence or absence of facial paralysis.ResultsConsistent with previous research, amygdala activity was greater in response to angry compared to happy faces before BTX treatment. As predicted, amygdala activity in response to angry faces was attenuated when the corrugator/procerus muscles were paralyzed via BTX injection but then returned to its original state after the effects of BTX subsided. This preliminary study comprises a small sample size and no placebo condition; however, the A-B-A design affords the present sample to serve as its own control.ConclusionsThe current demonstration that amygdala responses to facial expressions were influenced by facial muscle paralysis offers direct neural support for the facial feedback hypothesis. Specifically, the present findings offer preliminary causal evidence that amygdala activity is sensitive to facial feedback during the perception of the facial expressions of others. More broadly, these data confirm the utility of using BTX to address the effect of facial feedback on neural responses associated with the perception, in addition to the experience or expression of emotion.

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Botulinum toxin type A treatment of glabellar rhytides resulted in high levels of patient satisfaction, and more than one-third of patients thought they appeared younger than they did before treatment.

Summary: Social interactions are largely dependent on the interpretation of information conveyed through facial expressions. Although facial reanimation seeks restoration of the facial expression of emotion, outcome measures have not addressed this directly. This study evaluates the use of a machine learning technology to directly measure facial expression before and after facial reanimation surgery. Fifteen study subjects with facial palsy were evaluated both before and after undergoing cross-facial nerve grafting and free gracilis muscle transfer. Eight healthy volunteers were assessed for control comparison. Video footage of subjects with their face in repose and with a posed, closed-lip smile was obtained. The video data were then analyzed using the Noldus FaceReader software application to measure the relative proportions of seven cardinal facial expressions detected within each clip. The facial expression recognition application detected a far greater happy signal in postoperative (42 percent) versus preoperative (13 percent) smile videos (p < 0.0001), compared to 53 percent in videos of control faces smiling. This increase in postoperative happy signal was achieved in exchange for a reduction in the sad signal (15 percent to 9 percent; p = 0.092) and the neutral signal (57 percent to 37 percent; p = 0.0012). For video clips of patients in repose, no significant difference in happy emotion was detected between preoperative (3.1 percent) and postoperative (1.4 percent) states (p = 0.5). This study provides the first proof of concept for the use of a machine learning software application to objectively quantify facial expression before and after surgical reanimation. CLINICAL QUESTION/LEVEL OF EVIDENCE: Diagnostic, IV.

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The use of mesh when repairing the abdominal donor site during a pedicled or free TRAM flap breast reconstruction is cost effective compared with primary fascial closure alone.

Recessive mutations in Post-GPI attachment to proteins 3 (PGAP3) cause the rare neurological disorder hyperphosphatasia with mental retardation syndrome 4 type (HPMRS4). Here, we report a novel homozygous nonsense mutation in PGAP3 (c.265C>T-p.Gln89*), in a 3-year-old boy with unique novel clinical features. These include decreased intrauterine fetal movements, dysgenesis of the corpus callosum, olfactory bulb agenesis, dysmorphic features, cleft palate, left ear constriction, global developmental delay, and hypotonia. The zebrafish functional modeling of PGAP3 loss resulted in HPMRS4-like features, including structural brain abnormalities, dysmorphic cranial and facial features, hypotonia, and seizure-like behavior. Remarkably, morphants displayed defective neural tube formation during the early stages of nervous system development, affecting brain morphogenesis. The significant aberrant midbrain and hindbrain formation demonstrated by separation of the left and right tectal ventricles, defects in the cerebellar corpus, and caudal hindbrain formation disrupted oligodendrocytes expression leading to shorter motor neurons axons. Assessment of zebrafish neuromuscular responses revealed epileptic-like movements at early development, followed by seizure-like behavior, loss of touch response, and hypotonia, mimicking the clinical phenotype human patients. Altogether, we report a novel pathogenic PGAP3 variant associated with unique phenotypic hallmarks, which may be related to the gene’s novel role in brain morphogenesis and neuronal wiring.