The evolution of facial reanimation techniques.

This review article provides an updated discussion on evidence-based practices related to the evaluation and management of facial paralysis. Ultimately, the goals of facial reanimation include obtaining facial symmetry at rest, providing corneal protection, restoring smile symmetry and facial movement for functional and aesthetic purposes. The treatment of facial nerve injury is highly individualized, especially given the wide heterogeneity regarding the degree of initial neuronal insult and eventual functional outcome. Recent advancements in facial reanimation techniques have better equipped clinicians to approach challenging patient scenarios with reliable, effective strategies. We discuss how technology such as machine learning software has revolutionized pre- and post-intervention assessments and provide an overview of current controversies including timing of intervention, choice of donor nerve, and management of nonflaccid facial palsy with synkinesis. We highlight novel considerations to mainstay conservative management strategies and examine innovations in modern surgical techniques with a focus on gracilis free muscle transfer. Innervation sources, procedural staging, coaptation patterns, and multi-vector and multi-muscle paddle design are modifications that have significantly evolved over the past decade.

Functional changes in the neural retina occur in the absence of mitochondrial dysfunction in a rodent model of diabetic retinopathy.

Diabetic retinopathy is a neurovascular diabetes complication resulting in vision loss. A wealth of literature reports retinal molecular changes indicative of neural deficits, inflammation, and vascular leakage with chronic diabetes, but the mechanistic causes of disease initiation and progression are unknown. Microvascular mitochondrial DNA (mtDNA) damage leading to mitochondrial dysfunction has been proposed to drive vascular dysfunction in retinopathy. However, growing evidence suggests that neural retina dysfunction precedes and may cause vascular damage. Therefore, we tested the hypothesis that neural mtDNA damage and mitochondrial dysfunction are an early initiating factor of neural diabetic retinopathy development in a rat streptozotocin-induced, Type I diabetes model. Mitochondrial function (oxygen consumption rates) was quantified in retinal synaptic terminals from diabetic and non-diabetic rats with paired retinal structural and function assessment (optical coherence tomography and electroretinography, respectively). Mitochondrial genome damage was assessed by identifying mutations and deletions across the mtDNA genome by high depth sequencing and absolute mtDNA copy number counting through digital PCR. Mitochondrial protein expression was assessed by targeted mass spectrometry. Retinal functional deficits and neural anatomical changes were present after 3 months of diabetes and prevented/normalized by insulin treatment. No marked dysfunction of mitochondrial activity, maladaptive changes in mitochondrial protein expression, alterations in mtDNA copy number, or increase in mtDNA damage was observed in conjunction with retinal functional and anatomical changes. These results demonstrate that neural retinal dysfunction with diabetes begins prior to mtDNA damage and dysfunction, and therefore retinal neurodegeneration initiation with diabetes occurs through other, non-mitochondrial DNA damage, mechanisms.

Facial fillers: Relevant anatomy, injection techniques, and complications.

Objective: The aim of this review article is to discuss the currently available facial fillers, their differences and indications, relevant anatomy, injection techniques, and avoidance and management of complications. Data Sources: Clinical experience and scientific papers. Conclusions: Reversal of facial aging via filler injection has been around since the late 1800s with the initial use of detrimental products. Today, many safe and effective products exist and can be tailored to the individual patient's desired effect. With the evolution of both products and injection techniques, the rate of complications with facial filler use is low. Nonetheless, providers offering facial filler injections should have detailed knowledge of facial anatomy, including facial planes and soft tissue compartments. Multiple injection techniques exist. Different techniques should be used, depending on the anatomic target. Providers should also know how to avoid and manage complications.

Soft Tissue Trauma: Critical Recognition and Timing of Intervention in Emergency Presentations.

The facial trauma surgeon will see a variety of facial injuries. Recognition of emergency cases and proper intervention is and this article aims to highlight those cases and the respective proper interventions.

Prognosis of Acute Low-Tone Hearing Loss Without Vertigo: A Scoping Review.

OBJECTIVE: Despite its relatively high prevalence, our understanding of the natural clinical course of acute low-tone hearing loss (ALHL) without vertigo remains incomplete. The purpose of this study is to summarize the findings of studies that evaluated recovery from hearing loss (HL), recurrence and/or fluctuation of HL, and progression to Meniere's Disease (MD) of patients presenting with ALHL without vertigo. METHODS: A scoping review of the English literature was performed. On May 14, 2020 and July 6, 2022, MEDLINE, Embase, and Scopus were searched to identify articles related to the prognosis of ALHL. To be included, articles had to present outcomes that were clearly distinguishable for patients with ALHL without vertigo. Two reviewers evaluated articles for inclusion and extracted data. Disagreements were adjudicated by a third reviewer. RESULTS: Forty-one studies were included. There was extensive heterogeneity between studies in regard to defining ALHL, treatment methods, and time of follow-up. Most of the cohorts (39 out of 40) reported partial or complete recovery of hearing in the majority (>50%) of patients, although reports of recurrence were relatively common. Progression to MD was infrequently reported. Shorter time from onset of symptoms to treatment predicted better hearing outcomes in 6 of 8 studies. CONCLUSION: The literature suggests that although the majority of patients with ALHL experience hearing improvement, recurrence and/or fluctuation are common, and progression to MD occurs in a minority of patients. Additional trials utilizing standardized inclusion and outcome criteria are needed to determine the ideal treatment for ALHL. LEVEL OF EVIDENCE: NA Laryngoscope, 133:2457-2469, 2023.

Loss of the antioxidant enzyme CuZnSOD (Sod1) mimics an age-related increase in absolute mitochondrial DNA copy number in the skeletal muscle.

Mitochondria contain multiple copies of the circular mitochondrial genome (mtDNA) that encodes ribosomal RNAs and proteins locally translated for oxidative phosphorylation. Loss of mtDNA integrity, both altered copy number and increased mutations, is implicated in cellular dysfunction with aging. Published data on mtDNA copy number and aging is discordant which may be due to methodological limitations for quantifying mtDNA copy number. Existing quantitative PCR (qPCR) mtDNA copy number quantification methods provide only relative abundances and are problematic to normalize to different template input amounts and across tissues/sample types. As well, existing methods cannot quantify mtDNA copy number in subcellular isolates, such as isolated mitochondria and neuronal synaptic terminals, which lack nuclear genomic DNA for normalization. We have developed and validated a novel absolute mtDNA copy number quantitation method that uses chip-based digital polymerase chain reaction (dPCR) to count the number of copies of mtDNA and used this novel method to assess the literature discrepancy in which there is no clear consensus whether mtDNA numbers change with aging in skeletal muscle. Skeletal muscle in old mice was found to have increased absolute mtDNA numbers compared to young controls. Furthermore, young Sod1 -/- mice were assessed and show an age-mimicking increase in skeletal muscle mtDNA. These findings reproduce a number of previous studies that demonstrate age-related increases in mtDNA. This simple and cost effective dPCR approach should enable precise and accurate mtDNA copy number quantitation in mitochondrial studies, eliminating contradictory studies of mitochondrial DNA content with aging.