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A Study to Determine the Incidence and Examine the Implications of Phrenic Nerve Dysfunction in Cervical Spine Hyper‐Flexion/Extension Injury
Author(s) -
Turner Kaitlin Amanda,
Walton David,
Johnson Marjorie,
Willmore Katherine,
Wilson Tim
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.748.4
Subject(s) - medicine , diaphragmatic breathing , dermatome , phrenic nerve , anatomy , cervical vertebrae , surgery , anesthesia , respiratory system , pathology , alternative medicine
The phrenic nerve (PN) is a bilateral peripheral nerve originating primarily from the anterior rami of C4 with varying contributions from C3 and C5. It courses inferiorly along the anterior scalene deep to the pre‐vertebral fascia, passes posterior to the first rib entering the thorax to innervate each hemi‐diaphragm, respectively. The PN is the only motor input to the diaphragm; its activation results in diaphragmatic contraction, facilitating inspiration, and breathing. Cervical hyper‐flexion/extension injury (CHFEI) is a common consequence of motor vehicle collisions (MVC). The extension moment may result in damage to the anterior scalene. Based on the path and anatomical location of the PN in the neck and the mechanism of CHFEIs there is potential for injury to the PN to occur during MVCs. Injury or damage to the PN can cause a range of dysfunctions including shortness of breath (SOB), altered breathing patterns (ABP), the inability to breathe independently, referred pain to C3‐5 dermatomes, and altered core control. However, to our knowledge, investigation of damage to the PN is not evaluated clinically following cervical trauma. This is a potential gap in the literature that needs to be investigated as PN injury may result in un‐ or misdiagnosed ABPs, SOB, and/or chronic pain in the C3‐5 dermatome region. This study aims to suggest potential sites of adhesion of the PN and propose treatment strategies based on its' anatomical path and determine the prevalence and implications of symptoms suggestive of PN injury secondary to CHFEI. Methodology Detailed dissection of the PN along its course in the anterior neck and thorax to its innervation of the diaphragm was completed on embalmed (n=9) and fresh/frozen (n=2) cadavers to examine potential sites where damage to the PN or adhesions of surrounding tissues would be more susceptible. Results In both embalmed and fresh/frozen cadavers the PN consistently courses along the anterior scalene either bound tightly between the anterior scalene and pre‐vertebral fascia or adhered directly to the pre‐vertebral fascia. It's consistently incorporated within the fascial sheath surrounding the subclavian artery/vein, and the mobility of the PN is minimal until the surrounding pre‐vertebral fascia and/or fascial sheath surrounding the sublacian artery/vein is removed. Discussion The limited mobility of the PN suggests that a CHFEI could result in a traction injury of the PN, which could cause ABP, SOB, and/or pain in the C3‐5 dermatome region. Injury to tissues surrounding the PN, especially the pre‐vertebral fascia, could cause adhesions and further limit mobility of the PN resulting in similar symptoms as those present with PN injury. To determine if PN injury is assessed clinically in patients that have sustained CHFEI a survey will be sent to clinicians. As well, a patient intake form will be created to determine the prevalence of symptoms present post CHFEI that could be related to PN injury. Future study will include measurements of PN mobility with cervical positions that would mimic those typically present in CHFEI's.