Biomedical subjects

C W Vaughan

Publications and source records attributed to C W Vaughan.

At least 37 records · Page 2Linked to original sources

PubMed1998

Symptoms in early head and neck cancer: an inadequate indicator.

Screening programs show promise in increasing the rate of early detection of head and neck cancers in high-risk populations. Prout et al (Otolaryngol Head Neck Surg 1997;116:201-8) examined the usefulness of a large-scale screening program for head and neck cancer in an inner city population by primary care physicians. Symptom assessment was based on the American Cancer Society's "Seven Warning Signs for Cancer," (Cancer manual. 8th ed. Boston: American Cancer Society, Massachusetts Division; 1990. p. 40-64) 4 of which are relevant to the head and neck. However, these signs may be insufficient for detection of early head and neck cancer. We analyzed these and other typical symptoms to determine their role in early detection. Coincident medical problems, tobacco abuse, and alcohol abuse were also analyzed. Our findings indicate that no symptom or symptom complex is strongly correlated with early head and neck cancer for any subsite except the glottis. Symptom duration is an unreliable indicator of the duration of disease. However, patients under medical supervision are more likely to have their cancers detected early, supporting the value of surveillance by the primary care physician. The absence of definite early warning signs for most head and neck cancers suggests the need to develop essential screening criteria. Defining the population that is at high risk for head and neck cancer and subjecting it to an aggressive screening protocol is essential.

Adult↗

PubMed1998

Enhancement of opioid inhibition of GABAergic synaptic transmission by cyclo-oxygenase inhibitors in rat periaqueductal grey neurones.

Cyclo-oxygenase (COX) inhibitors potentiate opioid inhibition of GABAergic synaptic transmission in rat periaqueductal grey (PAG) (Vaughan et al., 1997). In the present study, the relative contribution of cyclo-oxygenase-1 (COX-1) and COX-2 inhibition to this phenomenon was examined by use of whole-cell patch clamp recordings in brain slices. The mu-receptor partial agonist morphine (10 microM) had little effect on GABAergic synaptic transmission. Morphine reduced the frequency of spontaneous miniature inhibitory postsynaptic currents (m.i.p.s.cs) by 13%. The nonselective COX inhibitor, indomethacin, produced a dose-dependent potentiation of the morpine inhibition of m.i.p.s.c. frequency (maximum inhibition 42%, IC50=6 nM). More selective COX-2 inhibitors produced a similar potentiation of the morphine inhibition of m.i.p.s.c. frequency; however, at greater concentrations (IC50=57 nM piroxicam, 1.7 microM DFU). Maintaining slices in the protein synthesis inhibitor cycloheximide (1 microM), to prevent COX-2 induction, had no effect on the potentiation action of DFU (10 microM). These results demonstrate that the potentiation of opioid inhibition of GABAergic synaptic transmission in PAG is largely a result of inhibition of COX-1 activity. These findings suggest that COX-1, rather than COX-2 inhibition, mediates the synergistic analgesic actions of opioids and non-steroidal anti-inflammatory drugs (NSAIDs) in the midbrain PAG.

Analgesics, Opioid↗

PubMed1998

Inactivation of p53 and amplification of cyclin D1 correlate with clinical outcome in head and neck cancer.

The authors have investigated whether genetic abnormalities in two genes, loss of heterozygosity (LOH) of p53 and amplification of the cyclin D1 gene, correlate with clinical outcome in 56 matched pairs of blood and tumor from patients with squamous cell carcinoma of the head and neck (SCCHN). Frequency of p53 LOH was 47.4%, of cyclin D1 amplification 33.9%, and of both abnormalities together 23.7%. p53 LOH was associated with T4 (P = 0.003) and stage IV (P = 0.015) tumors. Cyclin D1 amplification was associated with recurrences and/or metachronous tumors (P = 0.007). The total number of p53 and cyclin D1 abnormalities (scored as zero, one, and two) show a pattern that seems to be additive; the increase in the number of these abnormalities is associated with a proportional increase in the frequency of T4, stage IV, presence of recurrences and/or metachronous tumors, and possibly a proportional decrease in the disease-free interval in the sample. The association of the markers with recurrences and/or metachronous tumors persists if the tumor stage effect is mathematically removed. The combined analysis of the p53 and cyclin D1 abnormalities seems to be more informative than either of them individually and may have predictive value in SCCHN.

Carcinoma, Squamous Cell↗

PubMed1997

How opioids inhibit GABA-mediated neurotransmission.

The midbrain region periaqueductal grey (PAG) is rich in opioid receptors and endogenous opioids and is a major target of analgesic action in the central nervous system. It has been proposed that the analgesic effect of opioids on the PAG works by suppressing the inhibitory influence of the neurotransmitter GABA (gamma-aminobutyric acid) on neurons that form part of a descending antinociceptive pathway. Opioids inhibit GABA-mediated (GABAergic) synaptic transmission in the PAG and other brain regions by reducing the probability of presynaptic neurotransmitter release, but the mechanisms involved remain uncertain. Here we report that opioid inhibition of GABAergic synaptic currents in the PAG is controlled by a presynaptic voltage-dependent potassium conductance. Opioid receptors of the mu type in GABAergic presynaptic terminals are specifically coupled to this potassium conductance by a pathway involving phospholipase A2, arachidonic acid and 12-lipoxygenase. Furthermore, opioid inhibition of GABAergic synaptic transmission is potentiated by inhibitors of the enzymes cyclooxygenase and 5-lipoxygenase, presumably because more arachidonic acid is available for conversion to 12-lipoxygenase products. These mechanisms account for the analgesic action of cyclooxygenase inhibitors in the PAG and their synergism with opioids.

Animals↗

PubMed1997

Evidence from motoneurone synchronization for disynaptic pathways in the control of inspiratory motoneurones in the cat.

1. Motoneurone synchronization was measured by cross-correlation between paired inspiratory discharges in external and internal intercostal nerves or their intramuscular branches (T3 to T8) or in the phrenic nerve (C5 root or both C5 and C6 roots independently) in anaesthetized, paralysed cats. 2. All cross-correlation histograms showed central peaks, for which the durations at half-amplitude (half-widths) from internal nerve pairs in adjacent segments were all less than for external nerve pairs in adjacent segments or within a segment (means, 1.6 ms vs. 3.4 ms for adjacent segments). Values for external-internal pairs covered the ranges for both these two. Lowest values came from two phrenic pairs (1.2 and 1.4 ms). 3. The peaks from ipsisegmental external-internal pairs were usually asymmetric and the maximum of the peak was often displaced to a lag of about -1 ms (external nerve providing the reference spikes), whereas peaks from external-external pairs were always symmetrical and centred on zero. Phrenic-internal peaks gave maxima with lags about 1 ms less than for phrenic-external peaks from the same segments. 4. Two explanations were considered possible for the differences in duration and timing: an extra synapse on the pathway to the external nerve motoneurones, or a correlation kernel for a monosynaptic connection to the external nerve motoneurones that had a slower time course than that for the internal or phrenic nerve motoneurones. Computer simulations, assuming the extra synapse, gave a good fit to the observed time courses of the correlation peaks for all categories of nerve pairs using single values of parameters (e.g. EPSP rise time) consistent with those in the literature. This could not be achieved with the different correlation kernel model. The timing of high-frequency oscillation (HFO), which was sometimes present in the correlations, was also better predicted with the extra synapse model. 5. It is concluded that most of the synchronization between external nerve motoneurones is derived from disynaptic common inputs and that any motoneurone synchronization peak with a half-width greater than about 2.2 ms should be assumed to be likely to contain di- or oligosynaptically derived components.

Animals↗

PubMed1997

Actions of the ORL1 receptor ligand nociceptin on membrane properties of rat periaqueductal gray neurons in vitro.

The actions of the endogenous ORL1-receptor ligand nociceptin on the membrane properties and synaptic currents in rat periaqueductal gray (PAG) neurons were examined by the use of whole-cell patch-clamp recording in brain slices. Nociceptin produced an outward current in all neurons tested, with an EC50 of 39 +/- 7 nM. The outward current was unaffected by naloxone. Outward currents reversed polarity at -110 +/- 3 mV in 2.5 mM extracellular potassium, and the reversal potential increased when the extracellular potassium concentration was raised (slope = 66.3 mV/log[K+]o mM). Thus, the nociceptin-induced outward current was attributable to an increased K+ conductance. Nociceptin inhibited evoked fast GABAergic (IP-SCs) and glutamatergic (EPSCs) postsynaptic currents and increased paired-pulse facilitation in a subpopulation of PAG neurons. Nociceptin inhibited evoked IPSCs and EPSCs in approximately 50% of neurons throughout the PAG, except in the ventrolateral PAG, where nociceptin inhibited evoked IPSCs in most neurons. Nociceptin decreased the frequency of spontaneous miniature postsynaptic currents (mIPSCs and mEPSCs) in a subpopulation of PAG neurons but had no effect on their amplitude distributions. Thus, nociceptin had a presynaptic inhibitory effect on transmitter release. These findings suggest that nociceptin, via its pre- and postsynaptic actions, has the potential to modulate the analgesic, behavioral, and autonomic functions of the PAG.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1997

Presynaptic inhibitory action of opioids on synaptic transmission in the rat periaqueductal grey in vitro.

1. The actions of opioids on synaptic transmission in rat periaqueductal grey (PAG) neurones were examined using whole-cell patch-clamp recordings in brain slices. 2. Methionine enkephalin (ME; 10 microM) inhibited evoked GABAergic inhibitory postsynaptic currents (IPSCs) by 57%, non-NMDA excitatory postsynaptic currents (EPSCs) by 60%, and NMDA EPSCs by 43% in PAG neurones. This inhibition was associated with an increase in paired-pulse facilitation, was mimicked by the mu-agonist DAMGO (1-3 microM) and abolished by naloxone (1 microM). Neither the kappa-agonist U69593 (1-3 microM), nor the delta-agonist DPDPE (3-10 microM) had any specific actions on evoked PSCs. 3. ME decreased the frequency of spontaneous miniature, action potential-independent postsynaptic currents (mIPSCs by 65%, mEPSCs by 54%) in all PAG neurones, but had no effect on their amplitude distributions. The reduction in mIPSC frequency persisted in nominally Ca(2+)-free, high-Mg2+ (10 mM) solutions, which also contained Cd2+ (100 microM), or Ba2+ (10 mM). Opioid inhibition of mIPSC frequency is unlikely to be mediated by presynaptic Ca2+ or K+ conductances which are sensitive to extracellular Cd2+ or Ba2+. 4. In a subpopulation of PAG neurones, ME increased a Ba(2+)-sensitive K+ conductance at potentials below -97 mV. Opioids inhibited both GABAergic and glutamatergic synaptic transmission in all PAG neurones, independent of any postsynaptic opioid sensitivity. 5. These observations are consistent with, but only partially support, the opioid disinhibition model of PAG-induced analgesia. mu-Opioids also have the potential to modulate the behavioural and autonomic functions of the PAG via modulation of both inhibitory and excitatory presynaptic mechanisms, as well as postsynaptic mechanisms.

Animals↗

PubMed1997

Head and neck cancer screening among 4611 tobacco users older than forty years.

We implemented screening for squamous cell carcinomas of the oral cavity, pharynx, and larynx with symptom assessment and systematic inspection of the oral mucosa by primary care practitioners at health care sites serving inner-city residents of Boston; 4611 tobacco users older than 40 years were screened, and 313 with specific criteria were referred to otolaryngology for diagnostic evaluations. In these screened patients, the prevalence of oral mucosal lesions was almost 13% and prevalence of persistent hoarseness was more than 11%. Although the identification of these cancers was rare (nearly 3%), abnormal findings were seen in more than 70% of referred patients. These clinical and histologic diagnoses are described. We have documented the range of pathologic conditions in high-risk patients screened for upper aerodigestive tract malignancy.

Adult↗

PubMed1996

Differential responses of lateral and ventrolateral rat periaqueductal grey neurones to noradrenaline in vitro.

1. The action of noradrenaline on the membrane properties of rat periaqueductal grey (PAG) neurones was examined using intracellular recordings in brain slices maintained in vitro. Morphological properties and the anatomical location of neurones were characterized by use of intracellular staining within biocytin. 2. Noradrenaline (0.3-100 microM) depolarized 66% (81/123) and hyperpolarized 30% (37/123) of neurones. The alpha 1- and alpha 2-adrenoceptor agonists phenylephrine and UK 14304 produced depolarizations and hyperpolarizations in all PAG neurones tested, respectively. Neurones depolarized by noradrenaline were more responsive to phenylephrine, whereas neurones hyperpolarized by noradrenaline were more responsive to UK 14304. 3. The UK 14304-induced hyperpolarizations reversed polarity at -108 +/- 2 mV (n = 11). The reversal potential increased when the extracellular potassium concentration was raised (slope = 57.8 mV/log[K+]o mM) in a manner similar to that predicted for potassium conductance. 4. The phenylephrine-induced depolarizations did not reverse polarity at negative potentials (n = 25), or did so at potentials (-119 +/- 2 mV, n = 13) more negative than the UK 14304-induced hyperpolarizations. Superfusion with low calcium (0.1 mM), high magnesium (10 mM) and either cobalt (2-4 mM), or cadmium (100 microM) usually reduced the response to phenylephrine and produced reversals near that predicted for potassium conductance. 5. The majority of the ventrolateral PAG neurones were depolarized by noradrenaline (85%, 62/73). In contrast, almost equal proportions of the lateral PAG neurones were hyperpolarized (54%, 20/37) and depolarized (46%, n = 17/37) by noradrenaline. PAG neurones depolarized or hyperpolarized by noradrenaline could not be differentiated on morphological grounds. 6. These results suggest that the net effect of noradrenaline on lateral and ventrolateral PAG neurones is to bias activity in favour of a ventrolateral PAG-mediated response pattern, which includes quiescence, hyporeactivity, hypotension and bradycardia.

Adrenergic alpha-Agonists↗

PubMed1996

Opioid inhibition of rat periaqueductal grey neurones with identified projections to rostral ventromedial medulla in vitro.

1. Rat caudal periaqueductal grey (PAG) output neurones containing rhodamine microspheres, retrogradely transported from an injection site in the rostral ventromedial medulla (RVM), were visualized in brain slices and recorded from using whole-cell patch clamp techniques. 2. The specific GABAB receptor agonist baclofen (10 microM) produced an outward current or hyperpolarization in fifty out of fifty-six caudal PAG output neurones. In 44% of these baclofen-sensitive neurones, the opioid agonist methionine enkephalin (30 microM) also produced an outward current or hyperpolarization. The opioid current reversed polarity at -104 mV and could also be produced by DAMGO, an agonist selective for the mu-subtype of opioid receptor. 3. Opioid-responding output neurones were not distributed uniformly in the caudal PAG. In horizontal slices containing lateral PAG, 56% of output neurones were inhibited by opioids, as compared with only 14% of the output neurones in slices containing ventrolateral PAG. 4. These observations are consistent with opioid disinhibition of ventrolateral PAG neurones projecting to the RVM as the predominant mechanism underlying opioid-induced analgesia in the PAG. The role of opioid receptors found on a major proportion of the output neurones in the lateral PAG remains to be established, but is assumed not be related to modulation of nociceptive function.

Analgesics↗

PubMed1996

Increase by the ORL1 receptor (opioid receptor-like1) ligand, nociceptin, of inwardly rectifying K conductance in dorsal raphe nucleus neurones.

The actions of the endogenous ORL1-receptor (opioid receptor-like1) ligand, nociceptin, on the membrane properties of rat dorsal raphe nucleus neurones were examined by use of whole-cell patch clamp recording in brain slices. Nociceptin produced an outward current in all neurones tested, with an EC50 of 12 +/- 2 nM. Dynorphin A (100 nM to 1 microM) produced little outward current. Outward currents reversed polarity near the predicted K+ equilibrium potential in both 2.5 mM (measured/predicted = -105 mV/-104 mV) and 6.5 mM (measured/predicted = -80 mV/-77 mV) extracellular K+. The conductance increase was larger between -120 and -130 mV than between -70 and -80 mV, conductance. The outward current produced by nociceptin was similar to, and occluded by, high concentrations of baclofen, demonstrating actions on the same population of K channels. Naloxone (1 microM) failed to inhibit outward currents produced by nociceptin. These results are consistent with the reported high density of ORL1 receptor mRNA in dorsal raphe nucleus and with inhibitory actions of nociceptin in cells expressing ORL1.

Animals↗

PubMed1996

Nociceptin receptor coupling to a potassium conductance in rat locus coeruleus neurones in vitro.

1. In this study we have examined the effects of nociceptin, an endogenous ligand for the opioid-like receptor ORL1 on the membrane properties of rat locus coeruleus (LC) neurones in vitro, using intracellular and whole cell patch clamp recording. 2. When locus coeruleus neurones were voltage clamped to -60 mV, application to nociceptin caused an outward current in all cells examined (n = 49), with an EC50 of 90 nM. Neither the potency nor the maximal effect of nociceptin was altered in the presence of the peptidase inhibitors, bestatin (20 microM) or thiorphan (2 microM). 3. The outward currents caused by nociceptin in 2.5 mM extracellular K+ reversed polarity at -123 mV, more negative than the predicted K+ reversal potential of -105 mV. Increasing extracellular K+ to 6.5 mM resulted in a shift of the reversal potential of +25 mV, a shift consistent with a K+ conductance. The conductance activated by nociceptin showed mild inward rectification. 4. Application of a high concentration of nociceptin (3 microM) occluded the current produced by simultaneous application of high concentrations of Met-enkephalin (10 microM), (3 microM) somatostatin and UK 14304 (3 microM), indicating that nociceptin activated the same conductance as mu-opioid and somatostatin receptors and alpha 2-adrenoceptors. 5. The actions of nociceptin were weakly antagonized by the opioid antagonist, naloxone, with pKb's estimated from 2 cells of -4.23 and -4.33. The mu-opioid antagonist, CTAP (D-Phe-Cys-Tyr-D-Trp-Arg-Pen-Thr-NH2, 1 microM), the opioid antagonist, nalorphine (30 microM) or the somatostatin antagonist, CPP (cyclo(7-aminoheptanoyl-Phe-D-Trp-Lys-Thr[Bz1]) 3 microM) did not affect the nociceptin-induced current. 6. Dynorphin A (microM), another putative endogenous ligand for ORL1, caused a robust outward current in locus coeruleus neurones that was, however, completely antagonized by moderate concentrations of naloxone (300 nM-1 microM). 7. Continuous application of nociceptin (3 microM) resulted in a decrease of the outward current to a steady level of 70% of the maximum response with a t1/2 of 120s. Desensitization was largely homologous because simultaneous application of Met-enkephalin (30 microM) during the desensitized period of the nociceptin response resulted in an outward current that was 92% of control responses to Met-enkephalin in the same cells. Conversely, continuous application of Met-enkephalin (30 microM) resulted in a decrease of Met-enkephalin current to a steady level that was 54% of the initial current. During this desensitized period application of nociceptin (3 microM) resulted in a current that was 78% of the control responses to nociceptin in the same cells. 8. Thus nociceptin potently activates an inwardly rectifying K+ conductance in locus coeruleus neurones, with a pharmacological profile consistent with activation of the ORL1 receptor. Dynorphin A does not appear to be a ligand for ORL1 in rat locus coeruleus neurones.

Amino Acid Sequence↗

PubMed1995

Sympathetic nervous system effects on feline bladder wall compliance throughout continence.

The urinary bladder is a compliant organ, high compliance being essential for useful urine storage. The extent to which the sympathetic nervous system promotes the storage of urine by increasing bladder compliance is unclear. The aim of the present study was to determine the range of bladder volumes over which the sympathetic nervous system increased bladder wall compliance. In supine, anaesthetized cats, the bladder was filled at twice the rate of natural filling, the continence cycle being interrupted at five stages. These stages were when the bladder had become globular, during prodromal contractions, soon after non-micturating contractions had commenced, approximately two-thirds of the way through the continence cycle and just prior to micturition. During each of these interruptions, bladder volume was held constant while pelvic nerve afferent activity and bladder pressure were recorded. Recordings were obtained before and during the intravenous infusion of trimethaphan, the resulting partial ganglion blockade decreasing arterial pressure by a third. Bladder pressure as well as afferent nerve activity increased significantly when the sympathetic drive was transiently blocked, indicating that there had been a prevailing net sympatho-inhibitory effect promoting bladder wall relaxation. This effect was observed during prodromal contractions and continued until the onset of micturition. This net sympatho-inhibitory effect is a potential therapeutic path for the treatment of bladder storage disorders.

Animals↗

PubMed1995

Urine storage mechanisms.

The urine storage process depends upon the coordinated control of a storage chamber, the bladder body, and its outlets, the bladder base and urethra. While urine storage disorders are of considerable clinical significance, the mechanisms underlying this process are poorly understood. Many species possess an ability to alter the duration of urine storage in the face of widely varying filling rates. The storage chamber appears largely responsible for this ability to alter capacity and compliance. However, there has been some controversy over the contribution of intrinsic smooth muscle and extrinsic neural systems to the storage process, which is partly related to the various methodologies used in experimental and clinical studies. Thus, the storage phase is greatly influenced by the filling regimes, anaesthesia, non-specific factors and infusates used in these studies. Further, the techniques used to examine and measure urine storage mechanisms often obscure the subtle nature of this process. There is little doubt that, under natural filling conditions, myogenic factors allow the bladder to store increasing volumes at low pressure. More recent studies indicate that, in addition to a quiescent parasympatho-excitatory drive, the extrinsic neural systems contribute to the storage phase with a precisely controlled sympatho-inhibitory drive. However, the sympatho-inhibitory drive does not increase capacity by promoting high compliance. Instead this drive partially reduces the level of bladder wall tension transduced by the bladder wall mechanoreceptors, and thus delays the time at which the micturition tension threshold is reached.

Humans↗

PubMed1994

Gender, bladder distension and hypogastric nerve activity in the cat.

In the pentobarbitone anaesthetised cat, postganglionic activity was recorded from the whole hypogastric nerve and from hypogastric filaments destined for the bladder wall during bladder distension. A gender difference was observed in whole hypogastric nerve recordings, cardiac-related activity obscuring other components in females with intact internal reproductive organs. In contrast, nerve activity in the vesical hypogastric filaments was dominated by bladder distension-related activity in both sexes. These observations suggest that bladder distension-related activity, which has a continence promoting action on the bladder detrusor muscle, is destined for the bladder wall, while the cardiac-related activity is largely destined for the uterine and vaginal vasculature.

Animals↗

PubMed1994

"External counterpressure" and "internal distention" for optimal laryngoscopic exposure of the anterior glottal commissure.

External laryngeal counterpressure and internal laryngeal distention produce forces that are helpful for enhancing laryngoscopic exposure of the anterior glottis. These principles were formally described in the early 20th century, but are seldom used today. Hand pressure has been the typical source for external counterpressures. Since this maneuver is unstable if provided by an assistant and wasteful if provided by the surgeon, it is often neglected. Current phonomicrosurgical techniques require wider glottal exposure; therefore, a reexamination of the value of external counterpressure and internal distention is worthwhile. During the last 2 years, 125 microlaryngoscopic procedures were performed for a variety of benign, premalignant, and malignant lesions. All patients were placed in the Boyce-Jackson position and sustained with a modified Killian gallows, with resulting elevated-vector suspension. Internal distention was achieved by placing the largest-lumen glottiscope possible between the endotracheal tube and the infrapetiole region. Exposure was also improved by using silk adhesive tape to apply external counterpressure to the lower laryngeal framework. The use of both external counterpressure and internal distention as an adjunct to microlaryngoscopy was most helpful for the surgical management of lesions located near the anterior commissure. Seemingly, the two resultant forces are in opposition to each other, but in fact they are complementary, both to each other and to the orthodox laryngoscopic principle of elevated-vector suspension.

Glottis↗

PubMed1994

Endoscopic treatment of supraglottic and hypopharynx cancer.

Transoral excision of supraglottic and hypopharynx cancer as a single modality is effective when lesions are selected for small size and endoscopic accessibility. Excisional biopsy with clear margins of larger supraglottic tumors in combination with postoperative radiotherapy provides an excellent treatment alternative for selected lesions in patients who are not candidates for open surgery. In this preliminary report, 45 cases using this minimally invasive approach are reviewed outlining oncologic rationale and functional advantages. A large bore tubed laryngoscope or the adjustable bivalve supraglottiscope was used along with a carbon dioxide laser in all cases. In 22 of the 45 patients (mostly T1), local en bloc excision of the primary cancer was performed as sole treatment on selected lesions of the supraglottis and hypopharynx. There were no local recurrences, however, 1 patient developed a neck recurrence and was salvaged by neck dissection. Twenty-three of the 45 patients had more extensive primaries (mostly T2, T3) and N0 necks. Transoral excisional biopsy was followed by full-course radiation therapy to the primary site and both necks. All 23 were followed a minimum of 2 years, and the median follow-up period was 58 months. Clear margins were obtained in 16 of 23, and there were no recurrences in the larynx. Two of 16 did fail in the neck and died despite neck dissection. Seven of 23 patients had positive margins and, despite full-course radiotherapy to the primary site and both necks, 5 of 7 failed locally or regionally. Two of the 7 died of their disease despite open salvage surgery. Therefore, 4 of 23 patients who underwent transoral excision of larger lesions followed by full-course radiotherapy died of recurrent cancer.

Combined Modality Therapy↗

PubMed1993

Vocal fold exposure in phonosurgery.

A difficult laryngeal exposure is made easier by placement of the patient's head and neck into the Boyce-Jackson "sniffing position" and then flexing them further if necessary, by selection of a laryngoscope appropriate to the patient and to the triangular glottic shape, by placement of the laryngoscope along the path of least resistance, by use of a true suspension device in order to apply the force for laryngoscopy towards the larynx and away from the teeth and gums, and by allowing time for the force to work. With these techniques, an easy exposure is made almost perfect. The true vocal folds are exposed from vocal process to anterior commissure without the need for external pressure, the endotracheal tube remains out of sight between the arytenoids, and there is no risk to the teeth, gums, and cervical spine.

Female↗