The impact of sensory neuropathy and inflammation on epithelial wound healing in diabetic corneas

Diabetic peripheral neuropathy (DPN) is the most common complication of diabetes, with several underlying pathophysiological mechanisms, some of which are still uncertain. The cornea is an avascular tissue and sensitive to hyperglycemia, resulting in several diabetic corneal complications including delayed epithelial wound healing, recurrent erosions, neuropathy, loss of sensitivity, and tear film changes. The manifestation of DPN in the cornea is referred to as diabetic neurotrophic keratopathy (DNK). Recent studies have revealed that disturbed epithelial-neural-immune cell interactions are a major cause of DNK. The epithelium is supplied by a dense network of sensory nerve endings and dendritic cell processes, and it secretes growth/neurotrophic factors and cytokines to nourish these neighboring cells. In turn, sensory nerve endings release neuropeptides to suppress inflammation and promote epithelial wound healing, while resident immune cells provide neurotrophic and growth factors to support neuronal and epithelial cells, respectively. Diabetes greatly perturbs these interdependencies, resulting in suppressed epithelial proliferation, sensory neuropathy, and a decreased density of dendritic cells. Clinically, this results in a markedly delayed wound healing and impaired sensory nerve regeneration in response to insult and injury. Current treatments for DPN and DNK largely focus on managing the severe complications of the disease. Cell-based therapies hold promise for providing more effective treatment for diabetic keratopathy and corneal ulcers.     

A randomised controlled trial of intravenous dexmedetomidine added to dexamethasone for arthroscopic rotator cuff repair and duration of interscalene block

Prolongation of peripheral nerve blockade by intravenous dexamethasone may be extended by intravenous dexmedetomidine. We randomly allocated 122 participants who had intravenous dexamethasone 0.15 mg.kg⁻¹ before interscalene brachial plexus block for day-case arthroscopic rotator cuff repair to intravenous saline (62 participants) or intravenous dexmedetomidine 1 μg.kg⁻¹ (60 participants). The primary outcome was time from block to first oral morphine intake during the first 48 postoperative hours. Fifty-nine participants reported taking oral morphine, 25/62 after placebo and 34/60 after dexmedetomidine, p = 0.10. The time to morphine intake was shorter after dexmedetomidine, hazard ratio (95%CI) 1.68 (1.00–2.82), p = 0.049. Median (IQR [range]) morphine doses were 0 (0–12.5 [0–50]) mg after control vs. 10 (0–30 [0–50]) after dexmedetomidine, a difference (95%CI) of 7 (0–10) mg, p = 0.056. There was no effect of dexmedetomidine on pain at rest or on movement. Intra-operative hypotension was recorded for 27/62 and 50/60 participants after placebo vs. dexmedetomidine, respectively, p < 0.001. Other outcomes were similar, including durations of sensory and motor block. In conclusion, dexmedetomidine shortened the time to oral morphine consumption after interscalene block combined with dexamethasone and caused intra-operative hypotension.     

Microsurgical anatomy of the facial nerve

The facial nerve connections and pathways from the cortex to the brainstem are intricate and complicated. The extra‐axial part of the facial nerve leaves the lateral part of the pontomedullary sulcus and enters the temporal bone through the internal acoustic meatus. In the temporal bone, the facial nerve branches into fibers innervating the glands and tongue. After it emerges from the temporal bone it supplies various facial muscles. It contains a motor, general sensory, special sensory, and autonomic components. The physician needs comprehensive knowledge of the anatomy and courses of the facial nerve to diagnose and treat lesions and diseases of it so that surgical complications due to facial nerve injury can be avoided. This review describes the microsurgical anatomy of the facial nerve and illustrates its anatomy in relation to the surrounding bone, connective, and neurovascular structures.