Anterior neopharyngeal diverticulum, which may occur after total laryngectomy, is a mucosalized pouch at the base of the tongue separated from the remaining pharynx by a posterior tissue band. The diverticulum has been alternatively called a pseudo–vallecula and the posterior tissue band a pseudoepiglottis because of the appearance on barium swallow. Kirchner and Scatliff described the neopharyngeal diverticulum as a cause of postlaryngectomy dysphagia in 1962. The dysphagia is characterized by a regurgitant quality similar to that found in patients with Zenker's diverticulum. On indirect examination, the pouch can be seen and often has food or mucus in it. In the setting of postlaryngectomy dysphagia, tumor recurrence must lead the differential diagnosis, 2 but indirect examination and barium swallow may reveal the presence of a significant diverticulum. In 30 of 34 postlaryngectomy patients Kirchner et al. 3 noted such a pouch varying in size from 1 to 30 cm. A diverticulum developed in all patients in this study who had postoperative fistulas and in 9 of 13 who did not have leaks. The authors postulated dehiscence of the pharyngeal closure at the tongue base as the cause of the diverticulum. Davis et al. 4 described a ‘pseudoepiglottis’ in 21 of 28 postlaryngectomy patients. They proposed that the closure technique may affect the incidence of diverticula, noting that all patients with vertical closures had pseudoepiglottis (average length, 18.4 mm), whereas 67% of patients with a ‘T closure’ had such a finding (average length, 9.6 mm). They postulated that the superior suture line folding on itself created the pseudoepiglottis. Biller commented that the cause might be related to the approximation of the constrictor muscles. 4 No patients in Kirchner's group had surgical treatment of their anterior neopharyngeal diverticulum, whereas two patients in Davis' group underwent laser excision with improvement. Other authors describe patients with a significant ‘vallecular pseudodiverticulum’ treated with external surgical repairs. 5 Sobol et al. 6 described three patients with neopharyngeal diverticula, two of whom were treated with an endoscopic division of the posterior wall of the diverticulum. We have recently used a simple transoral method, described below, to address this problem and describe two patients with dysphagia caused by an anterior neopharyngeal diverticulum and improvement after this correction.

Laryngeal mask airway anesthesia with intraoperative fiberoptic laryngoscopy to identify the RLN is effective and safe in carefully selected patients. Advantages include decreased postoperative throat discomfort, absence of coughing during emergence from anesthesia, and elimination of the possibility of vocal cord mobility impairment secondary to RLN ischemia from the endotracheal tube balloon. In addition, this technique is applicable in operations besides thyroid surgery, in which definitive identification of the RLN is indicated.

The purpose of this study is to specify the contribution of certain frequency regions to consonant place perception for normal-hearing listeners and listeners with high-frequency hearing loss, and to characterize the differences in stop-consonant place perception among these listeners. Stop-consonant recognition and error patterns were examined at various speech-presentation levels and under conditions of low- and high-pass filtering. Subjects included 18 normal-hearing listeners and a homogeneous group of 10 young, hearing-impaired individuals with high-frequency sensorineural hearing loss. Differential filtering effects on consonant place perception were consistent with the spectral composition of acoustic cues. Differences in consonant recognition and error patterns between normal-hearing and hearing-impaired listeners were observed when the stimulus bandwidth included regions of threshold elevation for the hearing-impaired listeners. Thus place-perception differences among listeners are, for the most part, associated with stimulus bandwidths corresponding to regions of hearing loss.

Recent bioterror attacks and other world events have foc used the medical community's attention on agents that might be used in biological warfa re. One ofthese potential biological weapons is Francisella tularen sis, a gramnegative coccobacillus that is one of the most inf ectious bacteria known. Ftularensis can cause seve re, even f atal, syste mic tularemia. Unde r normal circums tances, F tularensis is transmitted by infected ticks, insects, and other animals. As a weapo n ofterrorism, the bacterium would likely be disseminated as an ae rosol and contracted by inhala tion. Because many cases of tularemia are cha racterized by head and neck symptoms, otolaryngologists should befamilia r with the diagnosis and mana gement of this disease. In this article, we describe a case of zoonotic tularemia that manifested as a neck mass, and we review the pathophysiology, diagnosis, and treatm ent of tularemia. We also summarize what is known about its potential as a biol ogical weapon.

Parathyroid hormone's cardiovascular effects were assessed in a model of experimental hypertension with known abnormalities of calcium metabolism. Mean arterial pressure (MAP) changes and serum ionized calcium responses were measured in the spontaneously hypertensive rat (SHR) and its normotensive control, the Wistar-Kyoto (WKY), following injections of synthetic human PTH 1-34. Six 22-wk-old SHR and six WKY were given intra-arterial serial injections (0.1-100 micrograms/kg) of hPTH 1-34. Both the SHR (P less than 0.001) and WKY (P less than 0.001) demonstrated log dose-dependent hypotensive responses that were maximal at 1 min, with recovery occurring between 15 and 30 min. The slopes, however, of the dose-response curves differed (P less than 0.01). The SHR experienced a greater maximal delta MAP [-93.7 +/- 2.4 (SHR) vs. -71.2 +/- 1.6 mmHg (WKY), P less than 0.01]. Furthermore, the duration of the hypotensive action of hPTH 1-34 was significantly longer (P less than 0.001) in the SHR. Even when corrected for base-line MAP the SHR demonstrated a significant (P = 0.025) enhancement of this vasodilator response at doses of 5 micrograms/kg and greater at time intervals between 3 and 9 min after injection. A transient decrease [2.25 +/- 0.10 (pre) vs. 2.17 +/- 0.11 meq/liter (1 min post), P less than 0.01] in serum ionized calcium occurred at 1 min. We conclude that hPTH 1-34 is a potent vasoactive peptide in both the normotensive WKY and the SHR. The greater maximal hypotensive response to hPTH 1-34 and the prolongation of this cardiovascular effect in the SHR may be an additional manifestation of this experimental animal's acknowledged abnormalities of cellular membrane calcium and phospholipid metabolism.