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Temporary and permanent injection medialization impotence hernia order super avana 160 mg amex, medialization laryngoplasty, arytenoid repositioning surgery, and reinnervation 3756 procedures have all been used with varying degrees of success. On the other hand, treatment options in bilateral immobility are less satisfactory, occasionally requiring the sacrifice of some voice quality to establish an adequate airway. Although the superior laryngeal nerve may or may not be affected (and in fact, may be affected alone ­ a clinical situation which will not be reviewed here), the fibers of the recurrent nerve at least must be involved to cause gross vocal fold immobility. Generally speaking, mild pressure to a peripheral nerve produces segmental demyelinization and impairs axonal transport, the degree and severity of the conduction block being proportional to the severity of the injury. Remyelinization over a preserved axon usually restores nerve conduction and function. Injuries which interrupt the axon, such as nerve section or severe crush, produce wallerian degeneration along the entire length of the nerve distal to the injury beginning within 24 hours of injury. Functional recovery depends on preservation of neural conduits for axonal regeneration. The basal lamina of the original nerve fibers may be preserved in a severe crush injury (axonotmesis), and proximal axonal sprouts may reach the appropriate muscle. If the nerve is transected (neurotmesis), the proportion of nerve fibers that find their way to the original target is low and inversely proportional to the size of the gap between proximal and distal segments. Regeneration of the recurrent nerve is more problematic than that of most peripheral nerves, because it carries a mixed population of adductor and abductor fibers. Furthermore, laryngeal paralysis turns out to be a heterogeneous condition according to many clinical criteria, eg, symptoms, vocal fold position and electromyographic evidence of the degree of nerve damage. This latter aspect is a principal reason why the Seddon classification of nerve injury, reviewed above, is not entirely useful or satisfactory in vocal fold paralysis. In addition, both human and animal studies have shown that the larynx has a strong propensity for reinnervation. In many patients, however, vocal fold reinnervation is dysfunctional and does not yield physiologic motion. This neural dysfunction extends beyond traditional notions of synkinesis, in which co-contraction of adductor and abductor fibers produces no net vocal fold motion; after all, such perfectly balanced antagonism is an extremely improbable outcome of a largely random process. Dysfunctional reinnervation may also result when nerve regrowth is appropriate but inadequate, which may result in decreased force of contraction, loss of motor unit specificity, increased muscle fatigue, and possibly also in changes in neural organization peripherally and centrally. Vocal fold innervation had traditionally been conceptualized as an all-or-none phenomenon, with paralysis, or more precisely, absence of motion, the product of a lack of neural input; this view is clearly oversimplified and inaccurate. Vocal fold paralysis is probably best considered as a continuum of neurogenic dysfunction encompassing partial denervation, complete denervation and variable degrees and patterns of reinnervation. First, differing degrees and patterns of innervation probably account for variability in the position of the paralyzed vocal fold. For most of the last century, vocal fold position was thought to reveal the site or type of lesion, beliefs that have no physiologic basis and, moreover, have been invalidated by careful clinical and laboratory work. In addition, terms like "paramedian" and "cadaveric" carry no topognostic significance, and are useful as mere descriptive conventions, if at all. Second, the natural tendency for reinnervation accounts for the general trend for voice to improve over time in unilateral vocal fold paralysis. This explanation, well 3758 supported by electrophysiologic evidence,1,2 is probably closer to reality than the notion of gradual contralateral compensation. Differences result from demographic and epidemiologic features of populations from which case series are drawn, as well as differences specific to the reporting institution. For example, an unusually high proportion of patients with laryngeal paralysis due to malignancy in a Scotch series reflects the high incidence of lung cancer in that country. The relatively high incidence of idiopathic unilateral paralysis in two Japanese series,12,13 for example, is more likely the consequence of a low prevalence of mediastinal malignancy than any heretofore unrecognized virus tending to cause laryngeal paralysis. Table 92-1 Causes of Unilateral Vocal Fold Paralysis Study Year N Tumor Trauma Idiopathic Other Laccourreye and 2003 325 9% 75% 12% - 3759 colleagues41 Loughran and 11 colleagues 2002 77 52% 22% 12% 5% intubation Yumoto and colleagues42 2002 422 19% 33% 22% 8% intubation Ramadan and 43 colleagues 1998 98 32% 30% 16% 11% intubation Benninger and colleagues44 1998 280 25% 35% 20% 8% intubation Bruggink and 45 colleagues 1998 215 25% 43% 18% - Yamada and colleagues13 1983 519 17% 12% 41% 11% intubation Tucker46 1980 210 22% 42% 14% - Hirose12 1978 600 7% 37% 41% 2% intubation Parnell and Brandenburg47 1970 100 32% 32% 10% 11% medical Clerf48 1953 299 38% 20% 12% 9% medical Work49 1941 183 14% 39% 23% 15% medical Smith and 50 colleagues 1933 173 27% 16% 17% 36% medical Adapted with permission from Sulica and colleagues14 3760 Despite such variability, it is possible to draw some conclusions regarding laryngeal paralysis. In most series, laryngeal paralysis tends to affect men more often than women, probably reflecting the underlying gender distribution of thoracic malignancy. Uniformly, the left vocal fold is affected more often than the right, in approximately a 60:40 ratio or greater, due to the greater length and more profound descent into the thorax of the left-sided nerve, and its consequent greater vulnerability to disease and surgery. Left-sided paralysis is more likely to be related to malignancy, although the possibility of malignant cause in rightsided paralysis should not be discounted. In addition to thyroidectomy, still a main source of iatrogenic laryngeal paralysis, anterior approach to the cervical spine, carotid endarterectomy, and various cardiac and thoracic procedures have all become significant sources of laryngeal nerve injury Table 92-2). Table 92-3 shows composite data for incidences of laryngeal paralysis, including information regarding permanent and temporary paralysis where available, from several recent series. The potential for recurrent nerve damage from the cuffed endotracheal tube was recognized in the 1960s and early 1970s, and continues to account for patients with vocal fold immobility which are demonstrably neural in origin and not the result of cricoarytenoid joint disruption. Table 92-2Procedures Which Place Laryngeal Nerves at Risk Cervical Operations Thyroidectomy / parathyroidectomy Anterior approach to the cervical spine Carotid endarterectomy Implantation of vagal nerve stimulator Cricopharyngeal myotomy/repair of Zenker diverticulum Thoracic Operations Pneumonectomy and pulmonary lobectomy Repair of thoracic aortic aneurysm Coronary artery bypass graft 3761 Aortic valve replacement Esophageal Surgery Tracheal suzrgery Mediastinoscopy Thymectomy Ligation of persistent ductus arteriosus Cardiac and pulmonary transplant Other Operations Skull-base operations Brainstem operations or neurosurgery which requires brainstem retraction Other Medical Procedures Central venous catheterization Endotracheal intubation Table 92-3Incidences of Vocal Fold Paralysis after Operations: Composite Data of Recent Series Surgery Type Temporary Paralysis Permanent Paralysis Overall Thyroidectomy (A) 1. Adapted with permission from Sulica and colleagues14 A number of neurogenic conditions remain important, albeit unusual causes of laryngeal paralysis (many are discussed in Chapter 91, "Neurogenic Disorders of the Larynx"). Vocal fold paralysis may appear in the wake of a stroke, almost always in conjunction with other deficits. Lateral medullary infarct (Wallenberg syndrome) is a well-known complex of neural injury featuring vocal fold paralysis, dysphagia, vertigo, ataxia, Horner syndrome and hemifacial sensory deficit and/or pain. The vocal fold paralysis tends to improve with time, although measures may be needed in the short term to prevent aspiration. The vocal fold paralysis of Arnold-Chiari malformation tends to be bilateral and is important to recognize promptly because it is reversible with timely hindbrain decompression. Charcot-Marie-Tooth disease and its variants are a heterogeneous group of hereditary motor and sensory neuropathies which may involve the laryngeal nerves.

Necessarily xarelto erectile dysfunction order 160 mg super avana amex, medialization narrows the airway and, in combination with postoperative edema and hematoma, can cause airway obstruction. For this reason, many surgeons prefer to observe patients in the hospital for one night following the procedure. Perforation typically takes place in the delicate ventricular mucosa, which lies close to the thyroid lamina, or anteriorly, where there is little soft tissue cover. Arytenoid repositioning surgery is designed to internally rotate and/or suspend the arytenoid in physiologic phonatory position. Most commonly, the muscular process of the arytenoid cartilage is approached through the inferior pharyngeal constrictor muscle and around the back of the thyroid lamina. A nonabsorbable suture is passed through the muscular process of the arytenoid and secured to the thyroid lamina to exert anterolateral traction on the muscular process and thus rotate the vocal process medially and slightly caudally, this is known as arytenoid adduction. Despite these problems, for the experienced phonosurgeon, arytenoid procedures are an essential adjunct to medialization thyroplasty in achieving an optimal voice outcome. Reinnervation using nearby nerves (both the ansa cervicalis and the hypoglossal have been studied36) would seem to be an attractive and logical approach to vocal fold paralysis. Because of the complex innervation of the vocal fold muscles, reinnervation generally improves the bulk and tone of vocal fold muscles but will not restore physiologic motion. Reinnervation is ideally suited when the vocal fold is known to be completely denervated, eg, if the recurrent nerve or vagus has been sectioned. In fact, in patients with nerve section which is recognized during the operation, immediate reanastomosis, or reinnervation if tension free nerve reanastomosis is not possible, is the treatment of choice. However, when considering reinnervation later in the course of paralysis, the surgeon should be reasonably confident that he or she is not depriving the vocal 3775 fold of existing reinnervation by sectioning a partially recovered recurrent nerve to use the distal stump. In addition, the patient must be counseled that symptom improvement may take weeks or months. For this reason, reinnervation has sometimes been combined with other rehabilitation techniques. The armamentarium of procedures to remedy unilateral laryngeal paralysis is flexible and effective enough so that, given an understanding of the underlying pathophysiology, as well as the advantages, disadvantages and technical requirements of each procedure, the otorhinolaryngologist should be able to offer meaningful symptomatic relief to nearly every patient. Thyroidectomy 3776 remains the leading surgical cause37; both nerves are also at risk at esophagectomy, tracheal resection, thymectomy and other mediastinal procedures. Similarly, tracheal, esophageal and thyroid malignancies may compromise both nerves. Amyotrophic lateral sclerosis, post-polio syndrome, Charcot-Marie-Tooth neuropathy, Arnold Chiari malformation and Guillain-Barre syndrome have been documented causes of bilateral paralysis. Some bilateral laryngeal paralyses are idiopathic, attributed to the same infectious agents as unilateral paralysis. A clinician encountering bilateral vocal fold immobility should consider the possibility of joint fixation or posterior glottic scar, particularly when the condition follows intubation. In such patients the vocal folds are not denervated, but merely appear to be because of mechanical limitation. Patients with bilateral vocal fold paralysis typically complain of dyspnea, noisy breathing and exercise intolerance. The severity of these respiratory symptoms is inversely proportional to the size of the glottic aperture between the two immobile vocal folds. Respiratory noise is worse on inspiration, as negative pressure pulls the denervated vocal folds into closer approximation and causes greater airway restriction. Voice, while not entirely normal, may not be greatly altered, and swallowing is usually not affected. When bilateral vocal fold paralysis is acute, symptoms may be dramatic and even life threatening. The typical scenario is unexpected respiratory distress after extubation from thyroid surgery, and in such a patient, securing an adequate airway is the only consideration. In patients with progressive symptoms and signs, as found in certain neurologic diseases, patients may compensate as the paralysis becomes more dense and may tolerate unexpectedly small glottic airways. Occasionally, the clinician may be surprised to discover bilateral vocal fold paralysis in relatively asymptomatic patients; close questioning about noisy inspiration or limitations in physical activity will suggest that paralysis has been present for some time. Investigation includes radiologic imaging in the manner of unilateral vocal fold paralysis, with special emphasis on the mediastinum and infra-laryngeal neck, where the recurrent nerves are in close proximity, as well as the central nervous system. Bilateral paralysis typically shows a variable (rather than 3777 fixed) extra-thoracic obstruction, as the vocal folds will passively adduct during inspiration and abduct with positive expiratory air pressure. Treatment is guided by the degree of airway limitation; except in situations of acute airway distress, the patient may be the best judge of the functional disability. Tracheostomy is frequently performed emergently and may be a reasonable treatment option for the long term as well, as it guarantees airway with minimal compromise of phonation and deglutition. Often, though, patients prefer to avoid the inconveniences of tracheostomy if possible. Other treatment options include lateralization of the vocal fold or removal of arytenoid and/or vocal fold tissue to enlarge the glottic aperture. Effort is made to preserve the membranous vocal fold to the greatest extent possible in these procedures, but voice and sometimes swallowing may be adversely affected. These procedures are destructive and irreversible, so the otorhinolaryngologist should be sure that any reasonable possibility of spontaneous improvement has been exhausted before they are considered. The irreversible nature of such interventions and their inevitable adverse effect on voice has spurred investigations into laryngeal pacemakers, currently in human trials. It should come as no surprise, then, that paresis, or incomplete paralysis in which some gross vocal fold mobility is preserved, exists alongside paralysis as a clinical entity. Symptoms of paresis are predominantly those of glottic insufficiency, even when both sides of the larynx are involved. This is because it is rare for paresis to be so dense that it impairs abduction to the extent that the airway is meaningfully narrowed. On the other hand, phonatory glottic function is affected by even mild asymmetries in neural input.

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The harmonic to noise ratio of a sound reflects the amount of energy in f0 and its harmonics divided by the energy in nonharmonic frequencies vacuum pump for erectile dysfunction in dubai super avana 160 mg order with mastercard. An unstable voice has variations in the cycles of vocal-fold vibration, in either pitch or loudness or both. Jitter is a parameter that reflects pitch instability, while shimmer measures differences in the amplitudes of neighboring cycles. Although these measures have been used for many years, they have not proven to be clinically useful or relevant. The shortterm variations in normal of near normal voices are frequently imperceptible, while in hoarse voices, the sound is too aperiodic to permit accurate derivation of perturbation measures. The phrase "strikes raindrops" has been taken from a recording of a patient reading the Rainbow Passage, a standard reading task for voice analysis. The dark vertical bands are the "noise" of the "s" consonants, with energy in a continuous range of frequencies. The three striated segments are the three voiced consonants, with resonant frequencies represented by horizontal bands, and little or no noise between. These fluctuations over longer cycles are more easily perceived, as fluctuating pitch. Pitch fluctuations are characteristic of motor control problems, as seen in neurogenic disease and with the aging voice. It can also result from laryngeal pathology, such as scarring from surgery or radiation. Thus, measurements of airflow and pressure can provide precise and objective indicators of vocal function. One can measure either steady state values, as indicators of glottal competence and vocal efficiency, or the rapid cycle-to-cycle changes that provide information about the vibratory capacity of the glottis. The airflow exiting the mouth and nose can be directly and easily measured using a facemask, usually in terms of liters per second. Mean airflow during a sustained vowel can provide an estimate of glottal competence: a high flow is seen with poor glottal closure, whereas in a strained voice, such as adductor spasmodic dysphonia, airflow is low. A decrease in phonatory airflow can indicate either an increase in laryngeal resistance or a decrease in expiratory effort. Laryngeal resistance is a derived measure, calculated from airflow and subglottic pressure, and usually expressed as centimeters of water per liter per second. Accurate measurement requires calibrated instruments, a standard protocol, and clear instructions to the subject. Mean Phonatory Flow Rate Mean phonatory flow rate has been one of the traditionally easier measures to collect and is the most common aerodynamic parameter to be reported in the literature. It should be measured during sustained phonation of a vowel at comfortable pitch and loudness, and normal mean phonatory airflow is about 200 cc/s. It is higher in conditions of glottic incompetence, such as laryngeal paralysis, a mass deficit in the vocal fold, or a mass lesion that prevents glottal closure. It is lower with increased laryngeal resistance, such as adductor spasmodic dysphonia, muscle-tension dysphonia, or vocal-fold scarring. Decreased airflow can also reflect reduced expiratory effort of pulmonary insufficiency. The pneumotachograph can also detect sudden airflow changes, such as voice breaks in patients with spasmodic dysphonia. The pneumotachograph calculates airflow by measuring the pressure decrease across a known resistance which is usually a fine wire mesh screen. The pressure produced prior to the screen and after the screen (P1-P2) allows for the 3517 calculation of airflow. It is crucial to select the appropriate pneumotachograph and transducer as stated above for the flow range to be validly measured and so that airflow will be detected with the minimal possible resistance. Some may argue that the facemask in fact interferes little with the reliability of respiratory volume and does not alter frequency measures made from a glottal airflow waveform. A body box, called body plethysmography, is most reliable but requires a great deal of space. Both extrapolate expired airflow by detecting changes in chest volume and therefore do not obstruct airflow from the mouth and nose. Indirect plethysmograpy measures the summation of changes in the cross-sectional area within the thoracic and abdominal compartments and creates a weighted summation of these changes to provide a signal that is proportional to lung volume. Careful calibration is required, body movement artifact must be kept to a minimum, and interpretation may be subject to user error. Another method of measuring airflow is the use of hot wire anemometry, which offers little resistance. The hot wire anemometer has a high- frequency response but does not measure actual volume. Further, it can be distorted by turbulence and or changes in the ambient temperature. Glottal Airflow Airflow at the level of the glottis can be estimated by using a Rothenburg mask. This mask is circumferentially vented with multiple holes covered by fine wire mesh and uses a high frequency differential pressure transducer to measure airflow from the mouth and nose. The signal is processed by "inverse filtering," which is designed to subtract the resonant frequencies of the upper vocal tract. Since glottal opening allows airflow to occur, this measure is useful for patients in whom glottal 3518 closure is deemed inadequate or incomplete (hypofunctional vocal pathologies) or in patients in whom high glottal resistance is suspected, that is, an obstruction, spasm, hyperfunction, or loud voice production.