15 Voice Disorders in the Elderly
Introduction
Older adults differ from children and young adults in terms of laryngeal and pulmonary structure and function, hormonal environment and other bodily conditions, aerobic conditioning, susceptibility to injury, intellectual function (including memory) and other factors. Just as physicians must understand functions and limitations of children, so, too, must we become familiar with the special needs, limitations, and challenges of older patients who experience vocal change. Expert diagnosis, medical treatment, voice therapy/training, and occasionally surgery usually can maintain or restore vocal stability and “youth.” This is important because voice weakness and instability are interpreted often as reflecting intellectual instability. As a result, presbyphonia can impair the credibility of societies’ wisest and most experienced elders. Presbyphonic loss of volume also makes it difficult for patients to talk with their older friends, many of whom are hearing-impaired. This may lead older voice patients to withdraw socially, substantially impairing quality of life.
As the number of individuals aged 65 and older increases, it is not surprising to note an increase in the number of older patients seeking consultations for dysphonia. The reported incidence of vocal complaints in the geriatric population is somewhere between 12% and 35%.1,2 Twenty to thirty-five percent of patients use their voices for work,3,4 suggesting that vocal health is a high priority within this subgroup of older patients. In all geriatric patients, dysphonia affects quality of life directly; and it may impair the ability to communicate significantly, particularly with hearing-impaired spouses, family and friends. Indeed, dysphonia and hearing loss frequently coexist in the elderly: those with hearing loss are more likely to have dysphonia than their counterparts without hearing loss.5 Furthermore, dysphonic seniors suffer from social isolation, anxiety and depression, indicating a need to address both dysphonia and hearing loss when treating these patients.2,6
Those over the age of 65 are subject to the same vast array of vocal diagnoses as younger adults, including benign vocal fold lesions (polyps, nodules, cysts, papillomas), chronic inflammatory laryngitis (reflux-related conditions, autoimmune disorders, medication-induced conditions), acute inflammatory laryngitis (viral, fungal and bacterial), muscle tension disorders, neurologic disorders (essential tremor, Parkinson, poststroke, spasmodic dysphonia, amyotrophic lateral sclerosis), vocal fold immobility, vocal malignancies and vocal fold atrophy. Vocal fold atrophy is unusual in younger patients except in the setting of muscle wasting diseases, paresis/paralysis, or extreme weight loss. In all cases, presbylarynx must be a diagnosis of exclusion, after all other possibilities have been considered and eliminated. Despite the high prevalence of dysphonia in the elderly, there are relatively few published studies on the subject. This may be because of the complexity of the subject: the severity of dysphonia in the geriatric patient is a function of not only the primary vocal diagnosis, but also several other factors including the functional status of the patient, co-existing morbidities, pulmonary reserve, medications, and cognitive function.
In a retrospective review of 175 elderly patients seen in a tertiary care laryngology practice in Philadelphia, the most common complaints were hoarseness in 71%, inability to project the voice or decreased volume in 45%, excessive throat clearing/phlegm in 43%, vocal fatigue in 37%, cough in 23%, and breathiness in 22%.7 Less common complaints included raspiness, pitch breaks, loss of range, globus sensation, tremor and dysphagia. Many patients had more than one complaint. The most commonly identified diagnoses, which frequently co-existed with other conditions such as presbylarynx, included laryngopharyngeal reflux, muscle tension dysphonia, paresis (diagnosed clinically and with EMG in many cases), vocal fold mass, glottic insufficiency, and varicosities/ectasias. As a result of their dysphonia, more than 50% of patients in this study reported a significant impairment in their quality of life, with potentially serious psychosocial implications.7
Anatomy and Physiology
Between the periods of young adulthood and older age, the respiratory system undergoes marked anatomic and physiologic changes. Decreased force and rate of contraction of respiratory muscles, stiffening of the thorax and loss of lung tissue elasticity undermine the power source of the voice.8–11 Lung vital capacity is decreased, and forced expiratory volume and air flow rate decline.12 These changes and others result not only in decreased power source functions, but also in changes in breathing strategy. Some of these are gender dependent. For example, in men, respiratory changes may be linked with inefficient laryngeal valving that results from the glottal gaps commonly noted with aging. In women, the age-related changes may be more likely to involve valving at the level of the velopharynx, tongue and lips, and women also experience a decline in laryngeal agility.13,14
The larynx itself also undergoes extensive anatomic and physiologic change during adulthood,15 as summarized in previous literature.16 Cartilages undergo ossification and calcification,17,18 intrinsic muscles atrophy,19–21 and joints erode.22 The nature of age-related changes in the epithelium of the vocal folds has been in dispute. Several investigators report thickening; others have found no evidence of change with aging. In women, the epithelium may progressively increase in thickness with aging, particularly after age 70.23 A variety of changes in the lamina propria have been documented, including thickening/edema of the superficial layer, degeneration/atrophy of elastic fibers, and a decline in the number of myofibrils.23,24 In males, it also has been suggested that the epithelium increases in thickness up to age 70 and then decreases with further aging. In elderly men, the mucosa stiffens and increases in viscosity in comparison with women and younger men,24 resulting in decreased ease of phonation.24,25 Changes in the larynx from young adulthood to old age are generally more extensive in men than in women, with the possible exception of muscle atrophy about which there is little information on gender differences.15
Microscopic changes noted in the superficial layer of the lamina propria in mice include a relative reduction in hyaluronic acid and elastin, with an increase in collagen. In addition, there is an increase in the density and ratio of collagen and reticular fibers which are arranged in thick, disorganized bundles.26,27 Histologic examination of aged human vocal folds has shown a decrease in the total number of cells, reduction in the intracellular organelles responsible for protein synthesis, and reduced production of extra cellular matrix (ECM) from these cells. The superficial layer of the lamina propria increases in thickness and is more edematous in both men and women, with a change in viscoelastic properties.28,29 Changes within the cricoarytenoid joint include surface irregularities and disorganization of collagen fibers.30 Laryngeal cartilages stiffen with progressive calcification and/or ossification.
A great deal of work, summarized by Thomas et al, has revealed changes in the musculature of the aging larynx, which contribute significantly to presbyphonia. Several skeletal muscle changes are known to occur with aging. Although many of these also apply to the thyroarytenoid muscle (TA), there are also notable differences. Sarcopenia refers to the loss in muscle mass, strength and quality often observed with aging. Because the loss in muscle mass is gradual, there is little noticeable loss in function, until the loss extends beyond threshold levels. At this point, functional abilities decline noticeably. Sarcopenia is likely the result of metabolic, neurologic, hormonal and environmental factors.
The TA extends from the thyroid cartilage anteriorly to the vocal process and fovea oblonga of the arytenoid cartilage. It is often thought of as being made up of a medial vocalis and more laterally positioned thyromuscularis. The latter probably plays a role in the rapid shortening of the vocal fold, while the vocalis is likely involved in “fine-tuning” tension along the vocal fold edge and in providing lateral resistance during vocal fold contact. Contraction of the TA results in thickening and stiffening of the vocal fold, and a corresponding “loosening” of the lamina propria. Compared with limb skeletal muscle, the TA differs in several ways including fiber size, contractile protein profiles, mitochondrial content, and aging patterns. Similar differences also have been found in other laryngeal muscles.
The TA in humans contains type I, IIX and IIA fibers, as well as “hybrid fibers.” Furthermore, it has been suggested that the fast and slow fibers are arranged along a gradient, with the medial aspect composed of slow fibers and the lateral aspect composed of fast fibers. This unique composition, which results in a rapidly contracting, fatigue-resistant muscle well suited for the TA’s role as a muscle of respiration, airway protection, and voice production, is unusual compared with limb skeletal muscle. Elevated levels of mitochondria have been noted in the posterior crycoarytenoid, cricothyroid and thyroarytenoid muscles compared with limb skeletal muscle. This feature may increase resistance to fatigue and facilitate the continuous action required by these muscles for respiration. The TA is richly innervated by the recurrent laryngeal and superior laryngeal branches of the vagus nerve. Motor units are small, with each motor neuron innervating only a few fibers. Laryngeal sensory information is received through mechanoreceptors, chemoreceptors, taste buds, and free nerve endings.
Although loss of muscle mass with aging in the human TA was identified first in 1941, and confirmed in subsequent studies, patterns of fiber loss have not been defined clearly. In older rats, a reduction in force, speed, and endurance has been identified. Changes in the innervation of the TA with age also have been noted. Although there appears to be no net loss of myelinated or unmyelinated fibers with age, there is an increase in myelin-abnormal and myelin-thinning fibers, suggesting an active process of degeneration/regeneration. In the superior laryngeal nerve, there is a reduction in the size and number of myelinated fibers, which correlates with the documented reduction in laryngeal sensitivity with age. Metabolic changes have also been noted in the aging TA. Mitochondrial DNA mutations consisting of the 4977-base pair deletion have been identified, and these are thought to result in the increased production of injurious free radicals. Expression of this mutation appears to increase with age, producing dysfunctional mitochondria which may negatively affect contractile properties of the TA. In addition, laryngeal blood flow decreases by ~ 50% in older rats, with a possible reduction in oxygen, and accumulation of cellular waste products. The influence of hormones on vocal maturation, and in senescence, is recognized widely, and appreciated clinically. The mechanism of action of these hormones, however, remains poorly understood.
Marked anatomic changes in the supraglottic vocal tract have been reported from young adulthood to old age. Facial bones continue to grow during this period31,32 although the magnitude of that growth (3–5%) is relatively modest. Changes in facial muscles include decreased elasticity, reduced blood supply, atrophy, and collagen fiber breakdown.33,34 The temporomandibular joints (TMJ) undergo extensive changes with aging including thinning of articular discs, reduced blood supply, and regressive remodeling of the mandibular condyle and glenoid fossa.35–40 However, age-related changes in the TMJ can be difficult to distinguish histologically from a TMJ that is involved pathologically.37,39,40 The oral mucosa loses elasticity with aging and thins, with deterioration of attachments of epithelium and connective tissue to bone.22 However, there is some disagreement as to whether these changes reflect normal aging or result from drugs, disease, or pathological conditions.40–44 Dental structures also are altered with aging, although tooth loss itself is not an inevitable consequence of aging.45 Changes in the tongue epithelium include thinning and fissuring of the tongue surface.46,47 Pharyngeal and palatal muscles also have been reported to undergo age-related degenerative changes.48–50
Loss of salivary function can produce symptoms of oral dryness, dysphagia, and oral discomfort in the elderly; susceptibility of oral infection also is reported to increase.51 The elderly have been reported to experience significant declines in tongue strength, although endurance remains relatively unaffected.52 Lingual pressure reserves during swallowing decline with aging, although maximum tongue pressures during swallow events remain stable from young adulthood to old age.53
Acoustic Changes in the Aging Voice
Mueller opined that “The voice is a mirror of personality and senescence may cloud that image.”54 The aging voice is associated with a change in vocal quality that may be perceived as reduced volume, increased breathiness, a change in pitch, decreased endurance and reduced vocal range. When listening to speech samples, listeners are reasonably accurate in distinguishing between young, middle, and older age groups. Older voices often are associated with a loss of range and described with undesirable adjectives such as “hoarse,” “raspy,” “breathy,” “unsteady,” “tremulous,” and “shaky.” The elderly are a heterogeneous group; and many of these characteristics are not solely the result of aging, but rather from poor physical conditioning that results in weak respiratory and abdominal muscles and ultimately inadequate vocal support. Several studies have shown that listeners can generally differentiate between young and old speakers. Aging affects vocal pitch, loudness, and quality, although the effects are highly variable across the aging population.55
Speaking fundamental frequency changes with age, with different patterns of change noted for men and women. In men, the fundamental frequency of speaking drops through about the fifth decade and then rises, perhaps due to vocal fold muscle atrophy or hormonal changes. In women, speaking fundamental frequency remains fairly constant or lowers slightly until menopause, after which additional lowering of fundamental frequency occurs. Interestingly, these changes are less prominent in professional singers, who tend to maintain fairly stable fundamental frequency levels throughout adulthood.56,57 Speech intensity also changes with age. Men over 70 talk louder than younger men, even after taking hearing loss into account. Elderly women do not have a similar increase in speech intensity. However, both genders experience a decrease in maximum intensity levels with advancing age.58,59 In addition, women have an elevated minimum intensity level (they cannot phonate as softly as young women).59
Although there is variability in vocal intensity with age, most studies agree that in the elderly, vocal intensity of speech and the ability to modulate it are reduced.60 Notably, these changes are much less apparent in elderly singers compared with non-singers, once again supporting a role for “vocal exercise.”
Jitter and shimmer are higher in the elderly when compared with younger people and have been associated with higher Voice Handicap Index scores.7 Both of these characteristics are related to perceptual qualities of harshness and roughness, which have been identified as characteristics of “old” voices. Singers, as well as other healthy, physically fit older individuals display less jitter and shimmer and sound “younger” compared with their counterparts in poor health.
Examination of patients with an “old voice” using strobovideolaryngoscopy may reveal changes associated with vocal atrophy including variable degrees of bowing, noted as a concavity of the medial edge of the vocal fold during both adduction and abduction, prominent vocal processes, a spindle-shaped glottic chink, and a reduction in amplitude of the mucosal wave.61,62
Although some age-related alterations cannot be avoided in specific individuals, not all of them are manifestations of irreversible deterioration. In fact, as our understanding of the aging process improves, it is becoming more and more apparent that many of these changes can be forestalled or even corrected. Woo et al reached similar conclusions recognizing that “presbylarynges is not a common disorder and should be a diagnosis of exclusion made only after careful medical and speech evaluation.”63 As physicians and teachers, we need to look closer before concluding: “I can’t help your voice; you’re just getting older.”
Medical Intervention
Certain aspects of the aging process can be controlled medically through judicious intervention. The decision to intervene much be individualized, carefully weighing the risks against benefits for each intervention. For example, as female singers approach menopause, estrogen deprivation causes substantial changes in the mucous membranes that line the vocal tract, the muscles, and other structures throughout the body. These and other hormonal effects frequently are reflected in the voice, but can be forestalled for many years through the judicious use of hormone replacement therapy in selected patients. Dosage is best determined by checking estrogen levels prior to menopause. Preparations containing androgens should be avoided whenever possible because they can cause permanent masculinization of the voice. However, treating physicians must also be aware of contraindications to hormone replacement, especially if there is a history of other health problems such as breast cancer. Other endocrine problems such as hypothyroidism also are common in the elderly and may cause prolonged dysphonia unless they are recognized and treated.
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