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Anatomical analysis of antebrachial cutaneous nerve distribution pattern and its clinical implications for sensory reconstruction.

ABSTRACT: This study aimed to reveal the distribution pattern of antebrachial cutaneous nerves and provide a morphological basis for sensory reconstruction during flap transplantation. Forearm specimens containing skin and subcutaneous fat were obtained from 24 upper extremities of 12 adult cadavers. Cutaneous nerves were visualized using modified Sihler's staining. Then the data was used to show the distribution pattern and innervation area of the forearm cutaneous nerve. The anterior branch of lateral antebrachial cutaneous nerve innervates 26% of the medial anterior forearm; the posterior branch innervates 38.21% of the lateral anterior forearm and 24.46% of the lateral posterior forearm. The anterior branch of medial antebrachial cutaneous nerve innervates the medial aspect of the forearm covering 27.67% of the anterior region; the posterior branch the lateral part of the forearm covering 7.67% and 34.75% of the anterior and posterior regions, respectively. The posterior antebrachial cutaneous nerve covers 41.04% of the posterior forearm. Coaptations were found between the branches of these cutaneous nerves. The relatively dense secondary nerve branches were found in the middle 1/3 of the lateral anterior forearm and the middle 1/3 of the medial posterior forearm. The relatively dense tertiary nerve branches were the middle 1/3 and lower 1/3 of the medial anterior forearm. The intradermal nerve branches were the relatively dense in the middle 1/3 of the medial anterior and lateral posterior forearm. The middle 1/3 of the medial and lateral forearm had the relatively dense total nerve branches. These results can be used sensory matching while designing forearm flaps for reconstruction surgeries to obtain improved recovery of sensory.

SUBMITTER: Li H

PROVIDER: S-EPMC6738927 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:New findingsWhat is the central question of this study? Are sensory nerve-mediated vasodilatation and the NO-dependent contribution to that response attenuated in the cutaneous microvasculature of women who have had preeclampsia? What is the main finding and its importance? Women who have had preeclampsia demonstrate attenuated microvascular endothelium-dependent dilatation compared to women with a history of uncomplicated pregnancy. However, there are no differences in sensory nerve-mediated vasodilatation between groups. This suggests that the neurogenic response is not altered following preeclampsia, and that the NO-dependent vasodilatation of the neurogenic response is not related to endothelium-dependent NO-mediated dilatation in these women.AbstractWomen who have had preeclampsia (PE) demonstrate microvascular endothelial dysfunction, mediated in part by reduced nitric oxide (NO)-dependent mechanisms. Localized heating of the skin induces a biphasic vasodilatation response: a sensory nerve-mediated initial peak, followed by a sustained endothelium-dependent plateau. We have previously shown that the endothelium-dependent plateau is attenuated in PE. However, it is unknown if the sensory nerve-mediated initial peak is similarly attenuated. Therefore, the purpose of this study was to examine the effect of PE history on sensory nerve-mediated vasodilatation and the NO-dependent contribution to that response. We hypothesized that PE would have an attenuated initial peak and a reduced NO-dependent contribution to that response compared to women with a history of normotensive pregnancy (healthy controls, HC). Nine HC (31 ± 4 years) and nine PE (28 ± 6 years) underwent a standard local heating protocol (42°C; 0.1°C s-1 ). Two intradermal microdialysis fibres were placed in the skin of the ventral forearm for the continuous local delivery of lactated Ringer solution alone (control) or 15-mM NG -nitro-l-arginine methyl ester for nitric oxide synthase (NOS) inhibition. Red blood cell flux was measured at each site by laser Doppler flowmetry (LDF). Cutaneous vascular conductance was calculated (CVC = LDF/mean arterial pressure) and normalized to maximum (%CVCmax ; 28-mM SNP + local heat 43°C). There were no differences in the initial peak between groups (HC: 79 ± 8 vs. PE: 80 ± 10%CVCmax ; P = 0.936). NOS inhibition attenuated the initial peak in both HC (57 ± 18% CVCmax ; P = 0.003) and PE (54 ± 10%CVCmax ; P = 0.002). However, there were no differences in the NO-dependent portion of the initial peak (HC: 23 ± 16 vs. PE: 24 ± 9%; P = 0.777). The local heating plateau (HC: 99 ± 4 vs. PE: 88 ± 7%CVCmax ; P = 0.001) and NO contribution to the plateau (HC: 31 ± 9 vs. PE: 17 ± 14%; P = 0.02) were attenuated in PE. There was no relation between NO-dependent dilatation in the initial peak and NO-dependent dilatation in the plateau across groups (R2 = 0.005; P = 0.943). Women who have had PE demonstrate attenuated microvascular endothelium-dependent dilatation. However, there are no differences in sensory nerve-mediated vasodilatation following PE, suggesting that the NO-dependent vasodilatation of the neurogenic response is not related to endothelium-dependent NO-mediated dilatation in these women.

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Anatomical analysis of antebrachial cutaneous nerve distribution pattern and its clinical implications for sensory reconstruction.

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