Laryngology Seminar
The Senescence of Voice: presbylarynges
R3 陳佳弘 2002/05/29
INTRODUCTION
age-related dysphonia, or presbylarynges (“old larynx”)
bowing; lack of closure of the middle part of vocal folds.
12% incidence of vocal dysfunction in the elderly (von Leden, 1994)
Morrison and Gore-Hickman (1986)
1) thickened, chronically edematous larynx; low-pitched dysphonia; women.
2) thinned atrophic folds; high-pitched voice; men.
3) Either condition can exist in either sex.
ANATOMICAL CHANGES
“atrophy”: loss of thyroarytenoid (TA) muscle fibers;  muscle mass or mucosal
covering; “bowing”
age-related changes: hormonal, circulatory, skeletal, and neuromuscular systems.
1) stiffening of thyroid cartilage  inferior constrictor mm. fail to improve
adduction by compressing the thyroid cartilage incomplete glottic closure (IGC)
2) hyaline cartilages (thyroid, cricoid, and most of the arytenoids) do ossify with age
since at approximately 25 y/o; (c.f. elastic cartilages [vocal process and apex of
the arytenoid, corniculate, and epiglottis] do not ossify as a part of the aging
process.)
3) cricoarytenoid (CA) joint: 1) erosion of joint surfaces thinning, irregularities;
breakdown in collagen fiber organization loosening of the joint capsule;
impairing approximation of arytenoids pitch variability; 2) ossification of CA
joint may limit the range of motion ; IGC
4) neurologic: "dying back" neuropathy; concomitant degenerative and regenerative
neural processes lack of muscle bulk, “nerve” input into the vocal cords; a
redistribution of motor units into groups or clusters (e.g., polyphasic potentials on
EMG)  affect the fine neuromuscular control
5) vocal fold (VF): difference between the sexes;
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sex hormones  in women: edematous thickening of cover   vibratory
mass;  vocal pitch;
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thinning, atrophic change in men   vocal pitch;
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common in both sexes: mucous glands ; vocalis muscle mass ;
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bowing in 58% of elderly women & 67% of elderly men;
6) alterations in lung function: trachea softens and widens; peribronchial muscles
atrophy; alveoli and bronchioles dilate; emphysema; and a reduced elasticity  
forced expiratory volume, residual volume; vital capacity may  as much as
40% ( 20 y/o  80 y/o)   subglottal driving pressures;  amplitude of mucosal
wave vibration.
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7)  effectiveness of Bernoulli effect;  medial displacement glottal gap
HISTOLOGICAL CHANGES
1)  muscle mass or mucosal cover of the VFs;
2) disarrangement /separation of collagen fibers or elastic fibers;
3)  secretions of the mucosal glands of the larynx   viscosity of the superficial
layer of lamina propria (SLLP)
4) atrophy of the mucosal cover +  dryness of the tissues   mobility of the cover.
Hirano M et al (1989); Sato K et al (2002, 1995)
1) membranous VF shortens in males;
2) mucosa/cover of VF thickens in females;
3) edema in the SLLP in both sexes;
4) intermediate layer of LP (ILLP) thins and its contour  deteriorated in males;
5) elastic fibers in ILLP  less dense and atrophy in males;
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elastic fiber ( microfibrils + amorphous substance [elastin proteins]);
variation in fiber configuration and size
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 elastin in VFs, esp. ILLP (Hammond 1998);  resistance to elastase;
crosslinks; loss of elasticity
6) deep layer of LP (DLLP) thickens in males; collagen fibers in the DLLP denser
and fibrotic in males.
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collagenous fibers  bundles, twisted, high density; (occasionally) from
the deep layer to the superficial layer of the mucosa no layered structure
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reticular fibers ; 50-nm thin; biochemical identical to collagen fiber; most
abundant around the VF edge; vibrate the most
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collagen: predominant type I& III; tensile strength by cross-linking formed
by the covalent bond between lysine and hydroxylysine residues
7) loss of acidic glycosaminoglycans (functionally combined with collagen fibrils)
less water binding; altered viscoelasticitiy (Tillmann & Schünke, 1991)
8)  number and activation of fibroblasts in maculae flavae (ant. & post. ends of
membranous VF);  synthesis of fibrous components in the VF mucosa
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SYMPTOM/SIGNS
breathiness, weakness, tremulousness, hoarseness, inability to sustain phonation,
, inadequate loudness level, vocal fatigue; pitch alteration [masculine voice
(women); feminine voice (men)];
incomplete glottic closure (IGC), or bowing during phonation
activation of muscular tension dysphonia
maladaptive supraglottic hyperfunctional compensation
DIAGNOSIS
a diagnosis of exclusion; “subjective findings” of the appearance of atrophy,
bowing, or phonatory glottal gap, or a combination of these
caution the use of measures obtained by the use of videostroboscopy in drawing
conclusions for treatment protocols and outcomes measures (Bloch 2001)
videostroboscopic findings of VF bowing or atrophy and incomplete glottal
closure
1) (at resting VF abduction); bowing index (BI)= d/L × 100, L= membranous VF
length from the anterior commissure to the tip of the vocal process;
2) (at maximal glottal closure during phonation); normalized glottal gap area
(NGGA)= (glottal gap area/L2) ×100;
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BI v.s. NGGA: a weak positive correlation (r2 = 0.31);
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the inferior (medial) VF margin was identified as the border of the glottis in
cases of VF sulcus,.
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Omori et al. (1998): 50% of VF atrophy patients with dysphonia to have no
evidence of a glottal gap.
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other presbylaryngeal changes are contributing to incomplete glottal closure
which are not well visualized stroboscopically
3) normalized laryngeal outlet (NLO)= (laryngeal outlet area/L2) ×100;
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BI vs. NLO: no correlation (r2 = 0.07);

a weak positive correlation (r2 = 0.24) between NLO and NGGA;  bowing:
not consistently predict the extent of glottal gap; not sufficiently specific to
identify presbylarynges.
4) “compensatory”: significantly smaller NLO values
TREATMENT
reassurance
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earlier recognition of this disorder and prompt intervention are key factors in
reversing vocal decompensation
specific goal-oriented speech therapy, with surgery as an adjunct
1)
2)
3)
4)
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Voice therapy
exercise the VFs;  bulk;  closure
reducing all over-activity of other muscles
eliminate the maladaptive hyperfunctional supraglottic compensation
strive to produce a pitch that is commiserate with their anatomy
use "glottal attack" exercises to improve adduction and closure of the folds. This
will increase the maximal phonatory duration and reduce fatigue
aerobic conditioning exercises will improve the pulmonary status and strengthen
this "generator" of the voice
A. Lee Silverman voice treatment (LSVT) (Ramig L, 1996)
hypokinetic dysphonia in Parkinson disease
 loudness
(1) respiratory patterns: proper abdominal breathing, little clavicular movement
on inhalation to facilitate adequate subglottal pressure
(2) pitch variation: reacquainted with their natural pitch.
(3) oral muscle tension:  buccal, lingual, and/or mandibular tension
(4) abnormalities of onset of voicing due to an abrupt attack of vowel sounds
utilizing high subglottic pressure.
B. Resonance voice therapy (Cooper 1973; Verdolini 1998)
voice with “forward focus”;  intraoral air pressure; vibratory sensations in nasal
and facial bones; the strongest, clearest voice output for the least VF stress.
Lessac approach: consonant /y/ and nasal consonants /m/, /n/, /ng/
Cooper approach: humming the consonant /m/; “m-hmmm”
VF: slightly abducted or barely adducted position
favorable for p’ts with laryngeal hyperfunction, hyper-adduction
with little effort ;  risk of injury
C. Vocal function exercise (Briess 1959; Barnes 1997; Stemple 1995)
systematic exercise;  bulk, strength, coordination of laryngeal musculature.
3 steps (1) vocal warm-up, (2) pitch glides (high-to-low and low-to-high), and (3)
prolonged /o/ at selected pitches
utilizing a resonant voice without strain
VF: barely adducted position, for maximal prolongation.
D. Pushing exercise
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E. Accent method (Smith S, 1976)
whole body movements;  pulmonary output,  laryngeal muscle tension, and a
normalized vibratory pattern
utilizing rhythmic vocalizations of consonant sounds “accents”, usu.combined
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with body movements and with stressing respiratory support for each accent.
increasingly complex accents for conversation level; rhythmic movements 
used for hyperfunctional and hypofunctional voice disorders.
Vocal fold phonsurgery
1)
thyroplasty type I with or w/o arytenoids adduction: medialization;
2)
intraoperative adjustment; limited, but sustained, vocal improvements
3)
1)
2)
3)
4)
5)
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Tucker (1985): anterior commissure laryngoplasty; limited value in the
elderly; tension is not maintained for very long
Augmentation and vocal fold injection
TeflonTM: (Polytef Paste, Mentor O & O Inc., Norwell, MA); unpredictable giant
cell foreign body reaction; poor voice results
Fat: Reinke’s space; resorption is unpredictable
Gelfoam (Upjohn Co., Kalamazoo, MI)
Silicone
Bovine collagen: management of dermal deficiencies (Knapp, 1977); Zyderm
Collagen Implant I and II®, Zyplast® and Phonogel® (Collagen Corp., Palo Alto,
CA)
FDA approved injectable bovine collagen (Zyderm) in 1981 for skin
Zyplast: cross-linked with glutaraldehyde.
hypersensitivity (<5%); antigenic: telopeptides (nonhelical portion of collagen)
intradermal testing prior to use; negative intradermal test did not assure clinical
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non-reactivity; no FDA approval for intralaryngeal use.
6) Autologous collagen compounds: Autologen® (Autogenesis Tech., Acton, MA)
(Collagenesis Inc, Beverly, MA);
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0.8 to 1.0 mL of a 3.5% solution of collagen
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site of injection: superficial layer of the lamina propria (SLLP) (Ford CN, 1995)
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preserving natural cross-linking;  graft persistence
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 inconvenience in processing and donor site morbidity
7) Homologous collagen compounds: AlloDerm® (Life Cell Corp., The Woodlands,
TX) and Dermalogen® (Collagenesis, Inc., Beverly, MA)
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AlloDerm®: acellular; appears to be permanent (ie, 20-50% at >1 year);
micronized AlloDerm®: injectable form
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Dermalogen®: decellularized; persist between 3-6 months.
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dermal cells are removed with low molecular weight non-denaturing detergents;
the matrix is stabilized through the inhibition of metalloproteinases
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freeze-drying process: preserves the integrity of the biological dermal matrix
By day 7 to 10 (left),
host fibroblast cells and
blood vessels grow.
 revascularization and
normal tissue
remodeling process
Day 90(right),
AlloDerm: integrated as
the patient's own natural
soft tissue
Fibroblasts continue to
lay down autologous
collagen.
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27-G (or 30-G) needles for collagen
injection; diameter: 400 m; bevel length:1.3 mm (Medtronic Xomed,
Jacksonville, FL)
thickness of DLLP: 400 to 600 m; the heaviest concentration of collagen;
site of injection: SLLP, medial portion of the TA muscle, or lateral portion of the
TA muscle (Courey 2001)
SLLP:  stiffness of SLLP  loss of normal vibratory patterns (Hesaka 1994,
Courey 2001)
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medial portion of the TA muscle: immediately deep to the vocal ligament, 
force of contraction to adduct vocal folds; minimal effect on the vibratory
patterns
deep layer of the lamina propria (DLLP):  numbers of covalent cross linkages
and a compact arrangement.
Dermalogen®: virtually no inflammatory cell infiltration
Fibroblast ingrowth peaks ~ D30; ==> organization of collagen fibers; stable: 3
months
(A) Graft material diffused into the
SLLP immediately superficial to the
vocal ligament. (B) Graft material
was positioned within the medial
portion of the TA muscle.
CONCLUSION
1) optimal treatment outcomes depend on accurate diagnosis
2) stepwise approach
3) therapeutic decisions: based on pts’ needs and their
perception of problems
4) multidisciplinary collaboration
5) future perspectives
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