ABSTRACT
OBJECT: Recurrent laryngeal nerve (RLN) palsy is a well-known complication of cervical spine surgery. Nearly all previous studies were performed without laryngoscopy in asymptomatic patients. This prospective study was undertaken to discern the true incidence of RLN palsy. Because not every RLN palsy is associated with hoarseness, the authors conducted a prospective study involving the use of pre- and postoperative laryngoscopy. METHODS: Prior to anterior cervical spine surgery preoperative indirect laryngoscopy was performed in 123 patients to evaluate the status of the vocal cords as a sign of function of the RLN. To assess postoperative status in 120 patients laryngoscopy was repeated, and in cases of vocal cord malfunction follow-up examination was conducted 3 months later. In the group of 120 patients who attended follow-up examination, two (1.6%) had experienced a preoperative RLN palsy without hoarseness. Postoperatively the rate of clinically symptomatic RLN palsy was 8.3%, and the incidence of RLN palsy not associated with hoarseness (that is, clinically unapparent without laryngoscopy) was 15.9% (overall incidence 24.2%). At 3-month follow-up evaluation the rate had decreased to 2.5% in cases with hoarseness and 10.8% without hoarseness. Thus, the overall rate of early persisting RLN palsy was 11.3%. CONCLUSIONS: Laryngoscopy revealed that the true incidence of initial and persisting RLN palsy after anterior cervical spine surgery was much higher than anticipated. Especially in cases without hoarseness this could be proven, but the initial incidence of hoarseness was higher than expected. Only one third of new RLN palsy cases could be detected without laryngoscopy. Resolution of hoarseness was approximately 70% in those with preoperative hoarseness. The true rate of RLN palsy underscores the necessity to reevaluate the surgery- and intubation-related techniques for anterior cervical spine surgery and to reassess the degree of presurgical patient counseling.
Subject(s)
Cervical Vertebrae/surgery , Diskectomy , Intervertebral Disc Displacement/surgery , Postoperative Complications/etiology , Recurrent Laryngeal Nerve Injuries , Spinal Fusion , Vocal Cord Paralysis/etiology , Cross-Sectional Studies , Follow-Up Studies , Hoarseness/diagnosis , Hoarseness/epidemiology , Hoarseness/etiology , Humans , Iatrogenic Disease , Incidence , Laryngoscopy , Postoperative Complications/diagnosis , Postoperative Complications/epidemiology , Prospective Studies , Remission, Spontaneous , Vocal Cord Paralysis/diagnosis , Vocal Cord Paralysis/epidemiologyABSTRACT
Tobacco-associated carcinogens are catalyzed by microsomal epoxide hydrolase (mEH). Combinations of the Y113H and H139R polymorphic EPHX1 variants have been assumed to alter the enzyme activity and thus the risk of squamous cell head and neck cancer (SCCHN). Based on in vitro data, a putative low, medium and high mEH activity has been associated with combinations of these genotypes, and the respective activity categories have been frequently used in the estimation of risks for smoking-related cancers. We investigated the SCCHN risk for EPHX1 genotypes among 280 cases and 289 controls. We could not detect main effects of the EPHX1 genotypes, but a smaller risk of the 139HR genotype in smokers (odds ratio, OR, 0.57; 95% confidence interval, CI, 0.34-0.95). We could not confirm an increase of the SCCHN risk for genotype combinations according to a putative medium and high enzyme activity (OR 1.28, 95% CI 0.84-1.96; OR 0.98, 95% CI 0.58-1.64, respectively), but a significant heterogeneity of the estimated risks for the singular genotypes within these categories among smokers ( P=0.02). Further, p53 mutations among smoking cases were less frequent in the group with a putative high enzyme activity, although insignificant due to small numbers (OR 0.54, 95% CI 0.13-2.17). This supports uncertainties in categorizing genotypes with respect to limited enzyme activity data, especially when taken from in vitro experiments.
Subject(s)
Carcinoma, Squamous Cell/enzymology , Epoxide Hydrolases/genetics , Head and Neck Neoplasms/enzymology , Carcinoma, Squamous Cell/genetics , Carcinoma, Squamous Cell/pathology , DNA Primers/chemistry , DNA, Neoplasm/analysis , Female , Genes, p53/genetics , Genotype , Head and Neck Neoplasms/genetics , Head and Neck Neoplasms/pathology , Humans , Male , Microsomes/enzymology , Middle Aged , Mutation , Odds Ratio , Polymerase Chain Reaction , Polymorphism, Genetic , Smoking/adverse effectsABSTRACT
The gap junction protein connexin30 (Cx30) is expressed in a variety of tissues that include epithelial and mesenchymal structures of the inner ear. We generated Cx30 (Gjb6) deficient mice by deletion of the Cx30 coding region. Homozygous mutants (Cx30((-/-))) were born at the expected Mendelian frequency, developed normally and were fertile. However, they exhibit a severe constitutive hearing impairment. From the age of hearing onset, these mice lack the electrical potential difference between the endolymphatic and perilymphatic compartments of the cochlea, i.e. the endocochlear potential, which plays a key role in the high sensitivity of the mammalian auditory organ. In addition, after postnatal day 18, the cochlear sensory epithelium starts to degenerate by cell apoptosis. This degeneration process is likely to account for the concomitant decrease of the endolymphatic potassium concentration and the aggravation of the hearing loss in adult Cx30((-/-)) mice. The Cx30 ((-/-)) phenotype thus reveals the critical role of Cx30 both in generating the endocochlear potential and for survival of the auditory hair cells after the onset of hearing. The Cx30 deficient mice may represent a valuable model to study the mechanism of the hearing loss in human patients carrying a homozygous deletion of the CX30 gene (del Castillo et al., 2002, New Engl. J. Med., 346, 243-249).
