List of voice disorders

Voice disorders are medical conditions that impair the normal vibration or movement of the vocal cords in the larynx, resulting in alterations to voice pitch, volume, quality, or endurance, with a point prevalence of about 7% and lifetime prevalence of 20-30% in the general population.^[1][2] These disorders can arise from structural abnormalities, neurological issues, improper vocal use, or psychological factors, often manifesting as hoarseness, breathiness, strain, or complete voice loss.^[3] They are broadly categorized into three main types: organic disorders, which involve physical changes to the larynx such as growths or nerve damage; functional disorders, where the vocal mechanism is structurally normal but misused, leading to inefficient phonation; and psychogenic disorders, stemming from emotional or psychological distress without organic basis.^[4] Common organic voice disorders include laryngitis, characterized by inflammation and swelling of the vocal cords often due to infection or overuse; vocal nodules, polyps, and cysts, which are benign growths from chronic irritation; vocal fold paralysis or paresis, resulting from nerve damage due to surgery, stroke, or conditions like multiple sclerosis; and spasmodic dysphonia, a neurological condition causing involuntary spasms in the laryngeal muscles.^[5][3] Functional disorders encompass muscle tension dysphonia, where excessive laryngeal muscle effort produces a strained or hoarse voice, as well as ventricular phonation and vocal fatigue from habitual misuse.^[4] Psychogenic examples include conversion dysphonia, a sudden loss of voice linked to stress, and puberphonia, persistent high-pitched voice post-puberty in males.^[4] Causes range from acute factors like viral infections and acid reflux to chronic ones such as smoking, allergies, or neurological diseases, with symptoms often including throat pain, vocal fatigue, or a sensation of tightness.^[6] Early diagnosis through laryngoscopy and voice assessment is crucial, as many disorders respond well to voice therapy, medications, or surgery, preventing long-term complications like permanent vocal cord damage.^[5]

Structural Voice Disorders

Benign Lesions

Benign lesions of the vocal folds encompass non-cancerous structural abnormalities that arise from chronic trauma, irritation, or developmental factors, leading to disruptions in vocal fold vibration and phonation. These lesions manifest as localized growths or deformities on the vocal folds, often resulting from repetitive mechanical stress or environmental irritants, and they primarily cause dysphonia through impaired glottal closure or mucosal wave propagation. Unlike diffuse inflammatory processes, which involve widespread edema without discrete masses, benign lesions present as identifiable structural changes visible on endoscopic examination.^[7] Vocal fold nodules, also known as singer's or screamer's nodes, are small, callus-like swellings that develop bilaterally at the midpoint of the vocal folds due to prolonged vocal overuse or abuse, commonly affecting professional voice users such as singers, teachers, and call center operators. These firm, symmetrical growths form as a protective response to repeated microtrauma during phonation, leading to symptoms including persistent hoarseness, vocal fatigue, and reduced vocal range, particularly noticeable after extended speaking or singing.^[8][9][10] Vocal fold polyps typically appear as unilateral, pedunculated or sessile masses filled with fluid, blood, or fibrous tissue, resulting from acute vocal trauma such as shouting, coughing, or a single episode of vocal strain. These lesions disrupt the mucosal cover, causing intermittent or progressive dysphonia characterized by a breathy, rough voice quality and sudden voice breaks, with symptoms often exacerbated by continued voice use.^[8][11][12] Vocal fold cysts are encapsulated, mucous-filled sacs embedded within the layers of the vocal fold, either congenital (mucus retention cysts) or acquired (mucus extrusion cysts from ductal obstruction), which lead to asymmetric vocal fold vibration and a breathy or strained voice quality. These submucosal lesions prevent normal pliability of the vocal fold cover, resulting in symptoms such as gradual hoarseness, pitch instability, and vocal effort, often without significant pain unless secondarily inflamed.^[13][7][14] Reinke's edema involves diffuse swelling and polypoid thickening of the superficial lamina propria (Reinke's space) due to chronic irritation, most frequently from long-term cigarette smoking or exposure to gastroesophageal reflux, presenting with a characteristic bilateral, boggy appearance that lowers the fundamental frequency, particularly in women, causing a deep, gravelly voice. Symptoms include progressive hoarseness, reduced vocal projection, and in severe cases, airway compromise from vocal fold hypertrophy, with the condition often linked to cumulative exposure rather than acute events.^[15][16] Sulcus vocalis refers to a permanent groove or furrow in the epithelium along the vocal fold edge, arising from congenital thinning of the superficial lamina propria or acquired scarring from prior trauma or surgery, which results in incomplete glottal closure and a weak, breathy voice with easy vocal fatigue. This structural defect impairs the mucosal wave, leading to symptoms such as vocal instability and limited phonatory endurance, distinct from superficial lesions by its deeper, non-reversible tethering of the mucosa to underlying structures.^[17][18][19] Diagnosis of benign vocal fold lesions relies on laryngoscopy, which reveals characteristic mass lesions or deformities without evidence of invasion or malignancy, often supplemented by videostroboscopy to assess mucosal wave abnormalities and glottal function. Flexible or rigid laryngoscopy provides direct visualization of the lesion's location, size, and symmetry, while stroboscopic imaging confirms vibratory deficits specific to each type, such as bilateral rigidity in nodules or asymmetry in cysts, enabling differentiation from inflammatory or neoplastic conditions.^[20][21][8]

Inflammatory Conditions

Inflammatory conditions of the voice encompass disorders characterized by swelling or irritation of the laryngeal structures, primarily the vocal folds, due to infectious, allergic, or irritative processes, without the formation of discrete structural lesions. These conditions often result in acute or persistent alterations in voice quality, such as hoarseness or vocal fatigue, stemming from mucosal edema or hyperemia that impairs vocal fold vibration. Common triggers include viral infections, gastroesophageal reflux disease (GERD), environmental irritants like smoking, and systemic factors such as dehydration or autoimmune diseases. Unlike neoplastic or functional disorders, inflammatory voice issues are typically reversible with targeted interventions addressing the underlying inflammation. Acute laryngitis represents the most prevalent inflammatory voice disorder, primarily caused by viral infections such as those from rhinovirus or influenza, though bacterial etiologies like Streptococcus can occur less frequently. Symptoms manifest suddenly, including hoarseness, throat pain, dry cough, and temporary aphonia, with the condition usually resolving within 1 to 2 weeks as the inflammation subsides. Diagnosis relies on clinical history and laryngoscopy revealing erythematous, swollen vocal folds, and treatment emphasizes voice rest, hydration, and humidification to reduce edema, with antibiotics reserved for confirmed bacterial cases.^[22] Chronic laryngitis involves prolonged laryngeal inflammation lasting over three weeks, often linked to non-infectious irritants including GERD-induced acid reflux, tobacco smoke exposure, or chronic inhalation of allergens. This leads to mucosal thickening and edema of the vocal folds, resulting in persistent hoarseness, vocal fatigue, frequent throat clearing, and a sensation of effortful phonation. Laryngoscopic findings typically show diffuse hyperemia and irregular vocal fold surfaces without mass formation, and management focuses on eliminating triggers—such as proton pump inhibitors for reflux or smoking cessation—alongside anti-inflammatory agents like inhaled corticosteroids to restore mucosal integrity.^[23][24] Laryngitis sicca, a subtype of chronic inflammation, arises from severe laryngeal dryness and crusting due to inadequate mucosal hydration, commonly associated with dehydration, environmental aridity, or autoimmune conditions like Sjögren's syndrome. Patients experience sticky or "glued" phonation, intermittent hoarseness, and reflexive coughing from adherent mucus debris on the vocal folds, which disrupts smooth vibration. Treatment prioritizes symptomatic relief through increased fluid intake, humidified air, and mucolytic agents or saline nebulization to rehydrate the larynx and clear crusts, often requiring ongoing management in underlying systemic diseases.^[25] Contact granuloma develops as an inflammatory response at the vocal process of the arytenoid cartilage, triggered by chronic mechanical irritation from laryngopharyngeal reflux or post-intubation trauma, leading to hyperfunctional vocal fold closure. This results in a firm, nodular swelling that causes globus pharyngeus—a persistent lump sensation in the throat—along with odynophonia (painful phonation) and mild to moderate hoarseness. Initial therapy involves voice therapy to reduce hyperfunction, combined with antireflux medications; persistent cases may require botulinum toxin injection to weaken adductors and prevent recurrence.^[26][27] Vocal fold hemorrhage occurs when forceful phonation ruptures superficial blood vessels within the vocal fold lamina propria, often exacerbated by acute overuse such as yelling or intense singing, causing immediate submucosal bleeding and stiffness. Symptoms include abrupt severe hoarseness, voice breaks, and potential pain, with untreated cases risking permanent scarring and fibrosis that impairs long-term vocal quality. Absolute voice rest for 7 to 14 days is critical, supplemented by anti-inflammatory medications like corticosteroids to minimize hematoma resolution time and prevent complications.^[28][29] Across these inflammatory conditions, treatments uniquely target the inflammatory cascade, including nonsteroidal anti-inflammatory drugs for pain and swelling reduction, alongside behavioral modifications like voice rest to allow epithelial recovery, distinguishing them from structural or neurogenic interventions. Overuse may contribute to exacerbation in cases like hemorrhage but is not the primary etiology here.^[30]

Neoplastic Conditions

Neoplastic conditions of the voice encompass abnormal cellular proliferations in the larynx that can lead to voice disorders through disruption of vocal fold function, ranging from benign tumors to malignant cancers. These disorders primarily affect the glottic region, causing symptoms such as hoarseness due to interference with phonation, and may progress to airway obstruction or more severe complications if untreated. Unlike inflammatory or functional issues, neoplastic changes involve dysregulated growth driven by viral, environmental, or genetic factors, often requiring histopathological confirmation for management.^[31] Laryngeal papillomatosis, also known as recurrent respiratory papillomatosis (RRP), is a benign neoplastic disorder characterized by wart-like growths on the vocal folds caused by human papillomavirus (HPV) types 6 and 11. It manifests as recurrent exophytic lesions that impair vocal fold vibration, leading to progressive hoarseness, and can cause airway obstruction through mass effect, particularly in juvenile-onset cases, with historical incidence rates of approximately 2-4 per 100,000 children under 18, though recent data show a decline to about 0.5 per 100,000 due to HPV vaccination.^[32] In children, transmission often occurs during childbirth from infected mothers, while adult-onset may result from reactivation of latent HPV or oral-genital contact; the condition is more aggressive in juveniles, necessitating repeated surgical interventions to maintain airway patency and voice quality.^[33][34][35] Leukoplakia of the vocal folds presents as white patches or plaques resulting from epithelial hyperkeratosis and dysplasia, serving as a premalignant condition with potential progression to invasive squamous cell carcinoma. These lesions, often linked to chronic irritation such as tobacco use, cause persistent hoarseness by altering mucosal vibration and require biopsy to assess dysplasia grade, as up to 13.9% of cases may harbor or evolve into invasive malignancy, with higher risks associated with anterior commissure involvement or vascular changes visible on narrow-band imaging. Histologically, leukoplakia encompasses a spectrum from mild hyperplasia to severe dysplasia, with transformation rates varying but emphasizing the need for vigilant surveillance and excision to prevent progression.^[36][37] Laryngeal carcinoma, predominantly squamous cell carcinoma originating from the glottic epithelium, is a malignant neoplastic disorder strongly associated with smoking and alcohol consumption, accounting for the majority of laryngeal malignancies. Early symptoms include hoarseness due to vocal fold involvement, progressing to dysphagia, odynophagia, and hemoptysis in advanced stages as the tumor invades surrounding structures; glottic tumors, comprising about 60% of cases, present earliest with voice changes. Staging follows the TNM system, where stage I limits the tumor to the larynx without nodal involvement, while stages III-IV indicate regional spread or metastasis, guiding treatments like laryngectomy or radiation.^[38][31] Rare laryngeal malignancies, such as adenocarcinoma and sarcoma, constitute less than 1% of all laryngeal tumors and typically arise from glandular or mesenchymal tissues, presenting with persistent dysphonia, hemoptysis, and airway compromise similar to squamous cell carcinoma but with distinct histologies. Adenocarcinomas, often of salivary gland origin, are exceedingly uncommon (0.35-0.5% of cases) and may mimic metastatic disease, while sarcomas like fibrosarcomas or chondrosarcomas exhibit aggressive local growth, with 5-year survival rates ranging from 32-75% depending on subtype and resectability. These entities require specialized immunohistochemical analysis for diagnosis, as their rarity complicates initial identification.^[31][39][40] Diagnosis of laryngeal neoplasms relies on a combination of endoscopic visualization, biopsy, and imaging to determine tumor extent and guide therapy. Laryngoscopy allows direct assessment of lesions, followed by biopsy for histopathological confirmation, which is essential for distinguishing benign from malignant proliferations and grading dysplasia in premalignant cases. Cross-sectional imaging with contrast-enhanced CT or MRI delineates submucosal spread, cartilage invasion (with CT sensitivity of 91%), and nodal involvement, aiding TNM staging and surgical planning without relying solely on clinical examination.^[31][41]

Functional Voice Disorders

Misuse and Overuse Disorders

Misuse and overuse disorders encompass a category of functional voice disorders resulting from habitual improper vocal techniques or excessive vocal demands, without underlying structural abnormalities or neurological impairments. These conditions often arise in individuals with vocally intensive professions, such as teachers or performers, where repetitive strain on the vocal folds leads to temporary inflammation or altered phonation patterns. Unlike structural issues, these disorders are typically reversible through behavioral modifications and voice therapy, emphasizing the role of learned habits in their onset and resolution.^[42] Vocal abuse syndrome, a common form of phonotrauma, manifests as hoarseness or vocal fatigue following prolonged yelling, screaming, or shouting, which causes acute edema in the vocal folds due to mechanical trauma. This syndrome is prevalent in scenarios involving sudden vocal intensity, such as coaching or public speaking. The resulting secondary edema impairs vocal fold vibration, producing a breathy or strained quality, but symptoms generally resolve with rest and cessation of abusive behaviors, preventing progression to chronic issues.^[42] Puberphonia, also known as mutational falsetto, is characterized by the persistence of a high-pitched, prepubertal voice in post-pubescent males due to incomplete adjustment of the vocal folds during laryngeal maturation. This functional disorder stems from psychological factors, such as anxiety or reinforcement of the higher pitch through social habits, rather than anatomical defects, leading to a falsetto register that does not descend to typical adult male frequencies. Affected individuals often exhibit a thin, unstable voice quality with pitch breaks, and the condition can persist into adulthood if untreated, impacting self-perception and communication efficacy.^[43][44] Ventricular phonation occurs when individuals substitute the false vocal folds (ventricular folds) for the true vocal folds during sound production, often as a compensatory mechanism to avoid strain on irritated or fatigued true folds. This results in a rough, low-pitched, diplophonic voice quality due to the irregular vibration of the thicker ventricular bands, which are not designed for primary phonation. Commonly observed in cases of habitual avoidance after acute overuse, it produces a harsh timbre and reduced vocal efficiency, with endoscopic evaluation confirming the false fold dominance.^[45][46] Specific behavioral patterns, such as frequent throat clearing and hard glottal attacks, contribute directly to misuse by generating excessive impact stress on the vocal folds, leading to localized trauma and hoarse voice production. Throat clearing, often triggered by perceived mucus or irritation, mimics a forceful cough that traumatizes the folds, while hard glottal attacks involve abrupt adduction before airflow, increasing collision force and promoting vocal fatigue. These habits are common in environments with allergens or dehydration, exacerbating symptoms like globus sensation and intermittent dysphonia.^[44] Prevention of misuse and overuse disorders centers on vocal hygiene practices, including adequate hydration, avoiding irritants like caffeine or smoke, and incorporating regular vocal rest periods to mitigate cumulative strain. Strategies such as using amplification devices in noisy settings and practicing gentle onset of phonation reduce the risk of phonotrauma, with education programs showing effectiveness in lowering incidence among high-risk groups like educators. Chronic persistence of these habits may lead to secondary benign lesions, such as nodules, though these are addressed elsewhere.^[47][48]

Tension-Related Disorders

Tension-related voice disorders arise from excessive or imbalanced contraction of the laryngeal and perilaryngeal muscles, often leading to inefficient phonation and vocal strain without underlying structural pathology in primary cases. These disorders, commonly encompassing muscle tension dysphonia (MTD), manifest as hyperfunctional voice production where individuals exhibit heightened muscular effort during speaking or singing, resulting in symptoms such as vocal fatigue, hoarseness, and a pressed or strained voice quality.^[49] Primary MTD specifically refers to hyperfunction occurring without an organic cause, characterized by atypical laryngeal movements and excessive tension in the extrinsic laryngeal muscles, which can develop from habitual patterns or psychosocial stressors like anxiety.^[50] In contrast, secondary MTD involves compensatory hyperfunction in response to an underlying condition, such as vocal fold paresis, where the individual exerts extra effort to achieve phonation, leading to effortful voice production and similar strained qualities.^[44] Hyperfunctional voice disorders within this category often present with elevated pitch, increased laryngeal elevation, and overall tightness in the neck and throat, particularly when anxiety amplifies the muscular response, creating a cycle of heightened tension during vocal tasks.^[51] These patterns reflect disorganized laryngeal musculature, where supraglottic constriction or undue pressure on the vocal folds disrupts normal vibration, contributing to discomfort and reduced vocal endurance. Overuse of the voice can exacerbate these tension patterns, though it is not the primary mechanism.^[49] Diagnosis of tension-related disorders relies on clinical examination findings, including palpation of the strap muscles (such as the sternohyoid and omohyoid) to detect tenderness, tightness, or asymmetry indicative of hyperfunction.^[44] Electromyography (EMG), particularly surface EMG, provides objective measurement of muscle activity patterns, revealing elevated electrical signals in perilaryngeal muscles during phonation that distinguish MTD from normal function, with moderate evidence supporting its diagnostic utility.^[52] Videostroboscopy may further confirm the absence of organic lesions in primary cases, showing hyperadduction or supraglottic squeeze without mucosal disruption.^[49] Therapy for these disorders emphasizes reducing muscular hyperfunction through targeted interventions, with voice therapy serving as the cornerstone to retrain efficient phonatory patterns. Circumlaryngeal massage, a manual technique involving gentle manipulation around the larynx to release tension in the extrinsic muscles, has demonstrated efficacy in alleviating symptoms by improving vocal fold mobility and reducing effortful phonation, often yielding rapid improvements in voice quality.^[44] Additional approaches, such as resonant voice therapy or vocal function exercises, address the hyperfunctional behaviors by promoting balanced airflow and muscle coordination, leading to sustained symptom relief in the majority of patients.^[49]

Neurogenic Voice Disorders

Paralysis and Paresis

Paralysis and paresis of the vocal folds are neurogenic voice disorders resulting from impaired innervation to the laryngeal muscles, primarily via damage to the recurrent laryngeal nerve (RLN) or superior laryngeal nerve (SLN), leading to partial or complete immobility of one or both vocal folds.^[53] These conditions disrupt normal glottic closure during phonation, causing dysphonia and potential airway or swallowing issues.^[54] Unilateral cases are more common than bilateral, with iatrogenic injury accounting for a significant portion of etiologies.^[53] Unilateral vocal fold paralysis typically arises from RLN damage during surgical procedures, such as thyroidectomy (incidence 0.5-9.5%), or from compression by tumors like lung cancer (up to 35.5% of cases).^[53] Symptoms include a breathy, hoarse voice due to incomplete glottic closure, increased aspiration risk during swallowing, and reduced vocal projection.^[55] In some instances, patients may develop compensatory muscle tension to approximate the folds, though this can exacerbate fatigue.^[54] Bilateral vocal fold paralysis often stems from iatrogenic causes like thyroid or esophageal surgery (44% of cases) or idiopathic origins (12%), resulting in both vocal folds assuming a paramedian position that compromises the airway.^[56] This leads to severe inspiratory stridor, dyspnea, and a weak, breathy voice, with lateral positioning increasing aspiration vulnerability.^[56] Airway management, such as tracheostomy, is frequently required in acute presentations.^[55] Vocal fold paresis involves partial weakness from incomplete denervation, commonly due to viral neuropathy or idiopathic neuritis, presenting with intermittent dysphonia, vocal fatigue, and diminished vocal range rather than total immobility.^[57] Unlike full paralysis, symptoms may be subtler, including diplophonia and effortful phonation.^[58] Common etiologies across these disorders include surgical trauma to the RLN during thyroidectomy, leading to transient or permanent paresis, and idiopathic inflammatory neuritis affecting nerve conduction.^[59] Viral infections, such as herpes simplex, can cause selective SLN involvement, impairing high-pitch control.^[57] Diagnosis relies on flexible laryngoscopy to observe vocal fold immobility or reduced excursion, confirming neurogenic origin by excluding mechanical fixation.^[55] Laryngeal electromyography (LEMG) further assesses muscle activity and reinnervation potential, with abnormal findings indicating denervation severity and prognosis for recovery (rates varying from 25% to 87% across studies, many within one year).^[53]

Dystonic and Tremor Disorders

Dystonic and tremor disorders of the voice encompass a group of neurogenic conditions characterized by abnormal involuntary movements or spasms in the laryngeal muscles, stemming from central nervous system dysfunction, particularly involving the basal ganglia. These disorders disrupt normal phonation by causing hyperkinetic activity, such as spasms or rhythmic oscillations, leading to inconsistent voice quality during speech production. Unlike hypokinetic disorders, they feature excessive muscle activity rather than weakness or immobility.^[60][61] Spasmodic dysphonia, also known as laryngeal dystonia, is the prototypical voice dystonia, manifesting as task-specific spasms that interfere with vocal fold vibration primarily during connected speech. The adductor type, the most prevalent form accounting for approximately 85-90% of cases, involves involuntary contractions of the laryngeal adductor muscles, causing the vocal folds to slam together and stiffen, resulting in a strained, strangled, or choked voice quality with sudden breaks and increased vocal effort. These spasms are typically absent during reflexive activities like laughing, crying, or whispering, highlighting the task-specific nature of the disorder. The underlying cause is linked to aberrant signaling in the basal ganglia, which coordinates muscle control, though genetic factors may contribute in some familial cases.^[60][61][62] The abductor type of spasmodic dysphonia, less common and comprising about 10-15% of cases, features spasms in the posterior cricoarytenoid muscles that force the vocal folds apart, preventing proper closure and airflow modulation, which produces a breathy, weak, or whispery voice with abrupt air escapes, particularly on vowel sounds. This leads to reduced vocal intensity and intelligibility during speech, while non-speech tasks remain relatively unaffected. Like the adductor variant, it arises from basal ganglia dysfunction, potentially exacerbated by prior neurological insults.^[60][61][63] Mixed spasmodic dysphonia, a rare subtype, combines elements of both adductor and abductor spasms, leading to inconsistent voice breaks that alternate between strained closures and breathy openings, complicating phonatory control and often requiring tailored diagnostic assessment. Respiratory dystonia, another focal form, primarily affects inspiratory and expiratory muscles of the larynx and respiratory system, causing spasms that disrupt breathing patterns and secondarily impair voice sustainment by limiting airflow for phonation, though it is less directly tied to speech tasks. These variants underscore the spectrum of laryngeal dystonias, all rooted in disrupted neural circuits for motor control.^[60][61][64] Essential voice tremor represents a distinct tremor disorder affecting the voice, characterized by rhythmic, oscillatory movements of the laryngeal muscles at frequencies of 4-12 Hz, resulting in quavering or wavering pitch and loudness variations that intensify with prolonged speaking or stress. This leads to a shaky, unsteady voice quality, often requiring greater effort for clear articulation, and may coexist with limb tremors in systemic essential tremor. The condition originates from dysfunction in the cerebellum or basal ganglia, which regulate motor timing and coordination, with a genetic predisposition noted in up to one-third of cases.^[65][66][67] Botulinum toxin injections serve as the primary treatment for dystonic voice disorders like spasmodic dysphonia, targeting overactive laryngeal muscles to induce temporary chemodenervation and reduce spasm severity, typically improving voice quality for 3-4 months before reinjection is needed. In adductor spasmodic dysphonia, injections into the thyroarytenoid muscles are most effective, yielding significant symptom relief in the majority of patients, though abductor and mixed types may require posterior cricoarytenoid targeting with variable outcomes. For essential voice tremor, botulinum toxin can similarly attenuate oscillations by weakening affected muscles, often combined with voice therapy to enhance control, though it is not curative and side effects like transient breathiness or dysphagia must be managed.^[60][68][69]

Psychogenic Voice Disorders

Conversion and Functional Aphonia

Conversion aphonia, also known as psychogenic aphonia, is characterized by a sudden onset of complete voice loss following psychological trauma or emotional conflict, typically manifesting as a whispery or breathy phonation while preserving a normal cough and laugh, which indicates intact laryngeal function.^[70] This disorder arises unconsciously as a conversion reaction, where psychological distress is somatized into vocal impairment without any underlying organic pathology.^[71] Patients often report the symptom as involuntary, and it may be accompanied by anxiety or depression, though the voice alteration serves no secondary gain.^[42] Functional dysphonia is distinct from psychogenic voice disorders and is generally classified under functional categories, presenting with inconsistent alterations in voice quality, such as variable hoarseness, breathiness, or strain, often triggered by stress or emotional factors but primarily due to inefficient vocal use rather than structural issues.^[44] These changes can fluctuate in severity, sometimes improving during distraction or emotional relief, and may include atypical phonation patterns like falsetto voice tied to unresolved internal conflicts.^[70] Unlike chronic tension patterns, functional dysphonia often emerges abruptly and lacks consistent hyperfunction, though its psychogenic elements can overlap in some cases.^[42] Diagnosis of conversion aphonia relies on a thorough history revealing psychosocial stressors, combined with normal findings on laryngeal visualization techniques such as flexible fiberoptic laryngoscopy or videostroboscopy, which show no anatomical or neurological abnormalities.^[44] A key diagnostic feature is the rapid, positive response to indirect suggestion during examination, such as eliciting normal voice production through play or counseling prompts, confirming the functional nature.^[70] Differential considerations include ruling out organic mimics via imaging or electromyography if needed, but the absence of persistent deficits supports the psychogenic etiology.^[42] Treatment primarily involves psychological interventions tailored to the conversion mechanism, such as cognitive-behavioral therapy or counseling to address underlying trauma and emotional conflicts, often yielding high recovery rates when combined with supportive measures.^[71] Speech-language therapy plays a crucial role, employing techniques like resonant voice therapy, inhalation phonation, or stretch-and-flow exercises to restore normal phonation patterns and build vocal confidence, with many patients achieving near-normal voice within a few sessions.^[44] In cases with comorbid anxiety, adjunctive pharmacotherapy like selective serotonin reuptake inhibitors may enhance outcomes, though the focus remains on resolving the psychogenic trigger.^[70]

Puberphonia

Puberphonia, also known as mutational falsetto or juvenile voice, is a psychogenic voice disorder characterized by the persistence of a high-pitched, pre-pubescent voice quality in individuals after puberty, typically males, due to psychological resistance to voice maturation.^[71] It arises from unresolved emotional conflicts or anxiety related to adulthood, leading to habitual use of falsetto register without organic laryngeal abnormalities. Patients may exhibit normal vocal range potential but avoid lower pitches, resulting in a voice that sounds immature or strained during attempts to speak at typical adult frequencies. Diagnosis involves perceptual evaluation of persistent high pitch post-puberty, confirmed by normal laryngeal findings on endoscopy and acoustic analysis showing elevated fundamental frequency. A history of psychological factors, such as low self-esteem or trauma, supports the psychogenic etiology, distinguishing it from organic causes like laryngeal web or neurological issues.^[44] Treatment focuses on voice therapy to facilitate pitch lowering through counseling-embedded techniques, such as biofeedback or facilitative maneuvers to access modal register, often combined with psychotherapy to address underlying psychological barriers. Success rates are high with early intervention, typically resolving within several sessions, though persistent cases may require ongoing support.^[71]

Factitious Disorders

Factitious voice disorders, distinct from unconscious psychogenic mechanisms, involve the deliberate fabrication, simulation, or induction of voice impairments to assume the sick role or obtain external incentives, as classified under factitious disorder imposed on self in psychiatric nomenclature. These conditions are intentional and conscious, unlike psychogenic disorders, and fall outside traditional psychogenic categories but are addressed here due to their psychological underpinnings in deception. In otolaryngology, such disorders are rare but can lead to extensive medical evaluations and unnecessary interventions if undetected.^[72] A key example is vocal Munchausen syndrome, characterized by fabricated dysphonia where patients present with inconsistent voice symptoms, such as intermittent hoarseness or aphonia, that resolve when unobserved. Symptoms often appear dramatic and evolve across multiple healthcare providers, with normal laryngeal findings on videostroboscopy during unguarded moments. Patients may exhibit knowledge of medical terminology and history of frequent hospitalizations, driven by a pathological need to maintain the invalid role.^[73] Vocal malingering represents another form, where voice loss is feigned intentionally for tangible benefits, such as legal claims, workplace accommodations, or insurance payouts. Presentations typically include sudden, atraumatic complete or near-complete voice loss, with an excessively high-pitched whisper or voiceless mouthing during speech attempts, contrasted by a loud, unaffected cough. Inconsistencies arise during testing, such as paradoxical voice softening or normalization when patients are asked to shout, revealing preserved vocal capability. Laryngoscopic examination usually shows normal anatomy, aiding differentiation from organic pathology.^[74] Self-induced lesions in factitious voice disorders occur through deliberate trauma to the vocal tract, such as applying chemical irritants (e.g., household cleaners or acids) to the throat to produce inflammation, edema, or ulceration mimicking laryngitis or granulomas. These actions create verifiable physical damage, like erythema or erosions on laryngoscopy, but the pattern—recurrent without plausible exposure history—raises suspicion. Such behaviors escalate risks of permanent harm, including scarring or stenosis, and are motivated by the desire for sympathy or medical attention.^[72] Detection of factitious voice disorders relies on multidisciplinary assessment, including inconsistencies in symptom presentation, normal objective tests (e.g., electromyography or acoustic analysis showing preserved phonatory function), and psychological evaluation for underlying personality traits or trauma history. Video surveillance, when ethically justified and legally permitted, can capture symptom resolution in private, confirming fabrication without direct confrontation. Speech-language pathologists play a crucial role by observing behavioral discrepancies, such as effortless whispering inconsistent with claimed aphonia.^[75] Treatment emphasizes ethical considerations to avoid reinforcing deceptive behaviors, focusing on non-confrontational psychotherapy like cognitive-behavioral therapy to address underlying emotional needs, rather than punitive measures. Multidisciplinary teams, including psychiatrists and otolaryngologists, coordinate care to limit invasive procedures, with hospitalization reserved for safety if self-harm persists. Prognosis improves with voluntary engagement, though dropout rates are high due to denial; ethical dilemmas include balancing patient autonomy with prevention of iatrogenic harm.^[76][77]

Other Voice Disorders

Age-Related Disorders

Age-related voice disorders, particularly presbyphonia, arise from degenerative changes in the larynx due to natural aging processes, affecting vocal fold structure and function in older adults.^[78] These changes typically manifest after age 60. Presbyphonia is common among elderly individuals with voice complaints, with a prevalence of up to 52% in clinical laryngology settings as of 2023, while voice disorders overall affect 4.8–29.1% of the general elderly population, leading to alterations in voice quality that can compromise communication and quality of life.^[79][80] Presbyphonia is characterized by thinning and bowing of the vocal folds resulting from atrophy of the superficial lamina propria and thyroarytenoid muscle, which reduces the folds' ability to approximate fully during phonation. Key age-related vocal fold changes include loss of elasticity in the extracellular matrix, diminished amplitude of the mucosal wave, and overall glottal incompetence, which contribute to a weakened, breathy, and tremulous voice quality as well as a reduced pitch range. These alterations often result in symptoms such as vocal fatigue, strained effort for phonation, and a limited dynamic range, with prevalence estimates indicating that 85% of asymptomatic and 87% of symptomatic elderly individuals (aged 75–101) exhibit such laryngeal findings.^[81] Incomplete glottal closure secondary to these changes heightens the risk of aspiration in seniors, potentially exacerbating swallowing difficulties and increasing susceptibility to respiratory complications.^[79] Geriatric assessments for these disorders emphasize multidimensional evaluation, including acoustic analysis to measure perturbation parameters like jitter (cycle-to-cycle frequency variability) and shimmer (cycle-to-cycle amplitude variability), which are elevated in presbyphonia and indicate irregular vocal fold vibration. Videostroboscopy is commonly used to visualize bowing, atrophy, and reduced mucosal wave propagation, aiding in differentiating age-related changes from pathologic conditions.^[81] Interventions for age-related voice disorders are tailored to the aging physiology, focusing on improving glottal closure and vocal efficiency. Vocal fold augmentation via injection laryngoplasty, using materials such as calcium hydroxyapatite or autologous fat, enhances vocal fold bulk and closure, leading to improved voice outcomes in elderly patients with atrophy. Voice therapy, including approaches like vocal function exercises and resonant voice therapy, targets organ functions and habits to strengthen the voice; systematic reviews show these yield significant improvements, such as increased maximum phonation time by 2.90–7.52 seconds and reduced jitter by 0.62%.^[82] For severe cases, surgical options like type I thyroplasty provide medialization to address glottal insufficiency.

Systemic and Iatrogenic Disorders

Systemic and iatrogenic voice disorders arise from underlying whole-body conditions or medical interventions that indirectly affect laryngeal function, often leading to dysphonia through mechanisms such as edema, inflammation, or neuromuscular disruption.^[83] These disorders differ from primary laryngeal pathologies by their extrinsic origins, requiring coordinated management of the systemic cause alongside targeted voice rehabilitation. Common manifestations include hoarseness, reduced vocal projection, and altered pitch or quality, which can significantly impair communication and quality of life.^[84] Hypothyroidism-related dysphonia typically results from myxedema, a condition involving mucopolysaccharide deposition that causes laryngeal edema and thickening of the vocal folds. This infiltration leads to a muffled, husky, or deep voice, as well as potential airway compromise in severe cases.^[85] Studies have documented this association since the 1960s, with animal models showing increased vocal fold thickness under induced hypothyroidism, confirming the structural changes responsible for the voice alterations.^[86] Uncontrolled hypothyroidism can also present with atypical symptoms like persistent dysphonia alongside other systemic effects, such as pericardial effusion.^[87] Rheumatoid arthritis can induce laryngitis through involvement of the cricoarytenoid joint, where synovial inflammation causes joint erosion, fixation, or luxation, resulting in vocal cord immobility. Patients often experience hoarseness, pain on phonation, stridor, and dyspnea due to these changes, with cricoarytenoid involvement reported in 17-70% of rheumatoid arthritis cases based on imaging and autopsy studies.^[88] Symptoms may be nonspecific, including dysphagia and odynophagia, and can mimic other laryngeal conditions, necessitating radiographic evaluation like CT to identify joint abnormalities.^[89] Iatrogenic voice disorders frequently occur following endotracheal intubation, particularly in prolonged ventilation scenarios, where mechanical trauma leads to scarring, ulceration, or granuloma formation on the vocal folds. These lesions, often located on the membranous vocal fold or arytenoid processes, cause persistent hoarseness, vocal fatigue, and reduced vocal efficiency, with granulomas being a rare but notable complication of airway instrumentation.^[90] In severe instances, such injuries can progress to laryngotracheal stenosis, further compromising airflow and voice production.^[91] Medication-induced voice changes stem from pharmacological effects on mucosal hydration, inflammation, or hormonal balance. Anticholinergics and antihistamines produce a drying effect on the vocal mucosa, leading to xerophonia or hoarse voice by reducing lubrication essential for phonation.^[92] Inhaled corticosteroids, commonly used for respiratory conditions, are associated with dysphonia in up to 35% of users due to local myopathy or candidiasis affecting the larynx.^[93] Hormonal therapies, such as anabolic steroids or estrogen modulators, can alter voice pitch and quality through changes in vocal fold mass or fluid content, with permanent lowering of pitch possible in transgender hormone treatments.^[94] Neurological secondary disorders, such as those in Parkinson's disease, manifest as hypophonia—a soft, low-volume voice—and monotone speech due to basal ganglia deficits impairing respiratory and phonatory control. Up to 90% of Parkinson's patients experience these voice impairments, characterized by reduced loudness, breathy quality, and imprecise articulation, which worsen with disease progression.^[95] While primary neurogenic aspects like vocal fold paralysis are addressed elsewhere, these systemic effects highlight the need for holistic evaluation.^[96] Management of these disorders emphasizes treating the underlying systemic condition—such as thyroid hormone replacement for hypothyroidism or disease-modifying antirheumatic drugs for rheumatoid arthritis—combined with voice therapy to restore function. Voice therapy, guided by speech-language pathologists, incorporates techniques like resonant voice training and vocal function exercises to improve projection, reduce strain, and enhance vocal efficiency, often yielding significant improvements in voice quality when initiated early.^[44] For iatrogenic or medication-related issues, discontinuing the offending agent or using spacers with inhaled steroids can mitigate symptoms, supplemented by hydration and behavioral modifications.^[97] Multidisciplinary approaches, including laryngology consultation, ensure comprehensive care tailored to the extrinsic etiology.^[98]