Motion-specific laryngeal reinnervation using muscle-nerve-muscle neurotization.

There is no current treatment method that can reliably restore physiologic movement to a paralyzed vocal fold. The purposes of this study were to test the hypotheses that 1) muscle-nerve-muscle (M-N-M) neurotization can be induced in feline laryngeal muscles and 2) M-N-M neurotization can restore movement to a paralyzed vocal fold. Muscle-nerve-muscle neurotization can be defined as the reinnervation of a denervated muscle via axons that are induced to sprout from nerves within an innervated muscle and that then traverse a nerve graft interposed between it and the target denervated muscle. A paralyzed laryngeal muscle could be reinnervated by axons from its contralateral paired muscle, thus achieving motion-specific reinnervation. Eighteen adult cats were divided into sham, hemilaryngeal-denervated, and M-N-M-reinnervated thyroarytenoid muscle groups. Five of the 6 reinnervated animals had histologic evidence of axons in the nerve graft, 4 of the 6 had evoked electromyographic evidence of crossed reinnervation, and 1 of the 6 had a return of appropriately phased adduction. This technique has great potential and should be further investigated.

Thyroarytenoid muscle maintains normal contractile force in chronic vocal fold immobility.

BACKGROUND: Denervation of skeletal muscle typically results in irreversible denervation atrophy over time. This finding has generated controversy as to the efficacy of reinnervation procedures for chronic vocal fold immobility related to recurrent laryngeal nerve injury. OBJECTIVE: To test the hypothesis that chronic vocal fold immobility after recurrent laryngeal nerve injury does not result in diminished maximal isometric force generation in the thyroarytenoid muscle. STUDY DESIGN: Adult random-bred cats underwent either unilateral laryngeal denervation (n = 6) or sham surgery (n = 6). After 6 months, videolaryngoscopy was performed followed by in vitro measurement of maximal isometric tetanic force produced by the thyroarytenoid muscle. RESULTS: All animals in the denervation group showed right vocal fold paralysis after the initial denervation operation; none of these animals had return of appropriately phased movement with respiration. Four had intermittent disorganized twitching movements. One had these movements plus an occasional weak adduction, and one had no movement. Normal vocal fold mobility was observed in 6 of 6 animals undergoing sham surgery. The maximal isometric tetanic force measured from the thyroarytenoid muscle in the sham group was 438 mN (+/-92 mN standard deviation [SD]). The maximal isometric tetanic force measured from the thyroarytenoid muscle in the chronically immobile group was 405 mN (+/-107 mN SD). Differences were not statistically significant. CONCLUSION: Maximal isometric force in the thyroarytenoid muscle is not diminished in chronic vocal fold immobility after recurrent laryngeal nerve injury. We conclude that the possibility for restoration of contractile force to the chronically immobile thyroarytenoid muscle exists. This finding supports the pursuit of reinnervation procedures in the treatment of chronic vocal fold immobility.

Simultaneous vocal fold and tongue paresis secondary to Epstein-Barr virus infection.

Dysphonia is a common presenting symptom in cases referred for otolaryngologic evaluation. Similarly, primary care physicians frequently see adolescents or young adults with symptomatic Epstein-Barr virus infection. Some of the patients with active Epstein-Barr virus infection who have severe clinical manifestations of infectious mononucleosis will be referred for otolaryngologic evaluation. Voice abnormalities in these patients, though, are usually limited to altered resonance due to pharyngeal crowding by hyperplastic lymphoid tissue. We describe a patient with infectious mononucleosis who was referred for evaluation of dysphonia and was diagnosed with unilateral tongue and vocal fold paresis. We also discuss the patient's clinical course and review the related literature. Although uncommon, cranial nerve palsies must be considered in the patient with Epstein-Barr virus infection who presents with voice or speech disturbance. Arch Otolaryngol Head Neck Surg. 2000;126:1491-1494

Comparison of nutshell granular activated carbons to commercial adsorbents for the purge-and-trap gas chromatographic analysis of volatile organic compounds.

Granular activated carbons (GACs) made from agricultural by-products were investigated as adsorbents for short path thermal desorption gas chromatographic analysis of selected polar and nonpolar organic compounds. GACs made from macadamia nut, black walnut and hazelnut shells were compared to four commercially available adsorbents, namely, Tenax TA, Carboxen 569, Carbosieve SIII and coconut charcoal for their properties in purge-and-trap analysis. Adsorption values and breakthrough volumes were calculated for compounds from C3 and C6-C10. GACs derived from macadamia nut shells were found to adsorb and desorb between 80% (benzene) and 277% (ethylbenzene) more acetone (C3), benzene (C6), toluene (C7), ethyl- (C8), n-propyl- (C9), or sec.-butylbenzenes (C10) purged from water at the 100 ppb level than the commercial adsorbents tested.

An allelotype of papillary thyroid cancer.

Although papillary carcinoma accounts for approximately 70% of all thyroid cancers, preliminary studies of allelic loss have thus far not identified any areas of chromosomal deletion. We evaluated 30 papillary thyroid carcinomas for chromosomal loss/allelic imbalance by testing at least 2 microsatellite markers from every autosomal arm. Fifteen of the 30 tumors tested exhibited loss of heterozygosity/allelic imbalance (LOH/AI) at one or more loci. Chromosomal arms with frequent LOH/AI included 4q, 5p, 7p and 11p. An average of 1.1 chromosomal arms displayed LOH/AI in each individual tumor. Therefore, 4q, 5p, 7p and, to a lesser extent, 11p display significant LOH/AI in papillary thyroid cancer, which indicates the presence of putative tumor-suppressor gene loci at these chromosomal arms.

Allelotype of salivary gland tumors.

To elucidate the genetic alterations that occur in salivary gland tumors, we screened every autosomal arm (and the X-chromosome) of 29 primary human salivary gland neoplasms (11 pleomorphic adenomas, 10 adenoid cystic carcinomas, 5 mucopidermoid carcinomas, and 3 carcinomas ex-mixed tumors) for allelic loss using 86 microsatellite markers. A minimum of two microsatellite markers were used per chromosomal arm to achieve informativity of at least 60% (excluding X). The pleomorphic adenomas demonstrated few areas of allelic loss; the most prominent chromosomal arm involved was 12q, lost in more than 35% of informative cases. The most significant allelic losses in adenoid cystic carcinoma were 1p, 2p, 6q, 17p, and 20p (>20% of informative cases) and 19q (40% of informative cases). Mucoepidermoid carcinoma showed 50% or greater loss at 2q, 5p, 12p, and 16q. Although losses at 9p, 3p, and 17p are common in squamous cell carcinoma of the head and neck, only the carcinoma ex-mixed tumors demonstrated loss at these loci, consistent with progression to a more aggressive phenotype. Salivary gland tumors display allelic loss patterns different from many other tumor types, suggesting distinct genetic pathways in the progression of these tumors.

Mutator phenotype in a subset of chronic lymphocytic leukemia.

The replication error phenotype (RER+), characterized by widespread microsatellite instability, is an important feature of tumors from patients with hereditary nonpolyposis colorectal carcinoma (HNPCC). This widespread instability affects repeat tracts of all lengths and is usually attributed to mutations of critical mismatch repair genes. Recently, several reports described occasional microsatellite alterations in tumors not associated with HNPCC. However, a true mutator phenotype (RER+) is very rare outside of HNPCC-associated malignancies. We examined 29 cases of chronic lymphocytic leukemia (CLL), the most common leukemia in the Western world for evidence of microsatellite instability. We identified a mutator phenotype in (2/29) 7% of the cases studied. These data suggest that the mismatch repair pathway may be altered in at least a subset of patients with CLL.

Histoplasmosis of the larynx.

Histoplasmosis commonly infects the lower respiratory tract, causing either a sub-clinical or a nonspecific pulmonary illness. It may also affect the larynx from wide-spread dissemination or in a localized form that mimics carcinoma. Hoarseness, dysphagia, and pain on swallowing are symptoms common to many diseases of the laryngopharynx, including histoplasmosis. It is therefore important to consider this fungus in the differential diagnosis. Since culture techniques alone may not establish the diagnosis, special stains of tissue preparations and serologic tests for histoplasmosis are important adjuncts. We have recently seen and treated two cases of laryngeal histoplasmosis. Amphotericin B remains the preferred drug.

Paternity testing: analysis of six blood groups and HLA markers, with particular reference to comparison of races.

Blood groups (ABO, Rh, MNSs, Kell, Duffy, and Kidd) and HLA markers were tested in cases involving 563 children of disputed parentage. In 149 (26.5%) cases, the accused men were excluded as the biologic fathers of the children in question. One hundred forty of the 149 exclusions were direct exclusions. Five exclusions were based on red blood cell data alone, i.e., HLA was non-exclusionary. Of the remaining 414 cases in which the alleged father could not be excluded as the biologic father, in 361 (87.2%) instances, the plausibility of paternity ws 95% or greater, and in 385 (93.0%) instances the comparison of men value was 20 or greater. Caucasians, blacks, and men of other races were involved in 367 (65.1%), 185 (33%), and 11 (1.9%) cases, respectively. No significant difference among races was observed in the rate of exclusion of accused men. However, of the non-excluded men, in a significantly greater proportion of black men than white men, the plausibility of paternity was below 95%. The difference was probably due to lower polymorphism of the markers tested in blacks than in whites. It is suggested that tests for additional polymorphic genes be directed towards the 12-15% of the nonexclusionary cases with plausibility of paternity values below 95%.

Sarcoidosis and fluctuating hearing loss.

Neurological manifestations of sarcoidosis occur in 5% of affected patients. Of the cranial nerves, the eighth nerve is the fourth most frequently involved. The central nervous system lesion is presumed to be a granulomatous meningitis that directly infiltrates the cranial occur in concert with other neurological findings, but may be the only presenting complaint. Sarcoidosis is not generally recognized as a cause of fluctuating sensorineural hearing loss. The fluctuating quality of the hearing loss has been noted by other investigators, but no patient has been previously reported with hearing fluctuation as the initial complaint. A chest radiograph and eye examination are mandatory. The diagnosis may be suspected from hilar adenopathy and uveitis, and confirmed by node biopsy. The hearing will usually improve on steroid therapy. Sarcoidosis represents yet another disease entity the otolaryngologist must consider in the differential diagnosis of fluctuating hearing loss.