Spasmodic Dysphonia: Types, Symptoms, and Role of Botulinum Toxin in Treatment
Spasmodic dysphonia is a chronic neurological voice disorder that causes involuntary spasms in the laryngeal muscles during speech. These spasms lead to strained, breathy, or interrupted voice quality depending on the type of muscle group involved. The unpredictable voice quality, particularly under stress or while speaking on the phone, results in social withdrawal and psychological distress. Many patients avoid conversations altogether, contributing to isolation.
Epidemiology and Aetiology
Spasmodic dysphonia affects roughly 1 in 100,000 individuals. It predominantly affects females with an onset at around the age of 40 years. Most cases are idiopathic, though viral infections or emotional trauma may trigger the symptoms. The condition is primarily neurological due to abnormal central motor processing in the basal ganglia, which is directly related to muscle control and movements. Dysfunction in the basal ganglia can lead to movement disorders like tremors, involuntary movements, and difficulty initiating or controlling movements. This condition is a form of focal dystonia, rather than a psychogenic disorder. 8% of the patients have a positive family history of dystonia.
Clinical Features
The hallmark feature is involuntary spasms that occur only during speech. These spasms are absent during other laryngeal activities such as breathing, laughing, or singing. Alcohol intake often temporarily reduces symptoms, which helps differentiate SD from other disorders.
Diagnosis
Flexible fiberoptic laryngoscopy remains the gold standard for diagnosing SD. On laryngoscopic examination, the larynx usually appears normal at rest. However, spasmodic contractions are visible during phonation. Electromyography (EMG) may confirm abnormal muscle activity, but it is not routinely done.
Treatment. Repeated injections of Botulinum toxin is the mainstay treatment. Botulinum toxin is a neurotoxin produced by the gram-positive anaerobic bacterium Clostridium botulinum. It blocks acetylcholine release at neuromuscular junctions, relaxing hyperactive laryngeal muscles. It temporarily weakens hyperactive laryngeal muscles, reducing spasms and improving voice quality. Most clinicians use botulinum toxin type A (e.g., Botox, Dysport, Xeomin).
Types of Spasmodic dysphonia.
The condition is categorised into three types:
- Adductor SD, the most common form, produces a strangled, effortful voice.
- Abductor SD, a rarer variant, is marked by breathy voice breaks.
- Mixed SD shows features of both types. Tremor and respiratory variants also exist, adding to diagnostic complexity.
1. Adductor Spasmodic Dysphonia (ADSD)
Adductor SD is the most common subtype, representing around 90% of cases. There are spasms in the adductor muscles, mainly the thyroarytenoid muscles, that cause the vocal cords to go into adduction involuntarily. As a result, patients typically describe their voice as strained, tight, or strangled, with abrupt phonation breaks, especially during vowel-rich phrases like “we eat early” or “eighty-year eels”
Diagnosis:
- Normal laryngeal anatomy on flexible fiberoptic laryngoscopy.
- Vowel-loaded sentences worsen adductor SD, while voiceless consonant sentences improve clarity.
- Neurological workup (CT or MRI) to rule out Parkinsonism, myoclonus, pseudobulbar palsy, multiple sclerosis, cerebellar disorders, tardive dyskinesia and amyotrophic lateral sclerosis.
Treatment:
- Botulinum toxin injection into the thyroarytenoid muscle is the gold standard, which reduces spasms and improves airflow. Percutaneous electromyography (EMG) guided route through the cricothyroid space is preferred. Repeat dosing is needed every 3–4 months. Overdosage can lead to a transient breathy voice, mild dysphagia.
- Voice therapy improves the effect of botulinum toxin.
- Surgical options:
-
- Isshiki Type II Thyroplasty: A titanium bridge widens the anterior commissure, reducing adductor spasms.
- Selective Laryngeal Adductor Denervation-Reinnervation (SLAD-R): Denervates and reinnervates the affected adductor muscles.
- CO2 Laser Thyroarytenoid Myoneurectomy: Partially removes the hyperactive muscle to decrease spasm severity.
- Sectioning of the recurrent laryngeal nerve to paralyse the cord/cords, but it interferes with glottic closure, leading to a breathy and weak voice and swallowing discomfort. This treatment is still used when injection treatment fails and the spasms are severe.
- Differential diagnosis: Muscle tension (ventricular) dysphonia, psychogenic dysphonia, and upper motor neuron lesions.
2. Abductor Spasmodic Dysphonia (ABSD)
Abductor SD is far less frequent and involves spasms of the posterior cricoarytenoid muscle (the only abductor) and thus keeping the glottis open. As a result, patients typically describe their voice as a breathy voice break, especially after voiceless consonants like /p/, /s/, or /k/. Patients often struggle with phrases such as “who has hidden Harry’s hat,” where sudden glottic opening disrupts fluent phonation. The condition progressively worsens, especially under stress or while speaking on the phone.
Diagnosis:
- EMG-guided laryngoscopy during phonation
- Careful differentiation from psychogenic dysphonia and Parkinsonian hypophonia
Treatment:
- Botulinum toxin injection into the posterior cricoarytenoid muscle, delivered either percutaneously with EMG guidance or via an endoscopic approach. The benefit is comparatively less effective (50%) and has a shorter duration as compared to ADSD.
- Voice therapy improves the effect of botulinum toxin.
- Type I thyroplasty to medialize the vocal cords.
- Vocal Fold Injection Laryngoplasty
Differential diagnosis: Whispering psychogenic dysphonia and Parkinsonian syndromes.
3. Mixed Spasmodic Dysphonia
Mixed SD combines both adductor and abductor types. Patients may experience both strained and breathy voice breaks, sometimes in the same sentence. Patients often struggle with both vowel-rich phrases and voiceless consonants.
Diagnosis:
- It requires endoscopy, EMG, and phonetic stress testing.
Key Features:
- Variable symptoms that may change with botulinum toxin treatment
- Diagnosis requires EMG, nasendoscopy, and phonetic loading tasks
- Voice tremor may coexist, complicating the presentation
Treatment:
- Botulinum toxin remains the primary intervention, requiring tailored dosing targeting both adductor and abductor muscles
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Reference Textbooks.
- Scott-Brown, Textbook of Otorhinolaryngology-Head and Neck Surgery.
- Cummings, Otolaryngology-Head and Neck Surgery.
- Stell and Maran’s, Textbook of Head and Neck Surgery and Oncology.
- Ballenger’s, Otorhinolaryngology Head And Neck Surgery
- Susan Standring, Gray’s Anatomy.
- Frank H. Netter, Atlas of Human Anatomy.
- B.D. Chaurasiya, Human Anatomy.
- P L Dhingra, Textbook of Diseases of Ear, Nose and Throat.
- Hazarika P, Textbook of Ear Nose Throat And Head Neck Surgery Clinical Practical.
- Mohan Bansal, Textbook of Diseases of Ear, Nose and Throat Head and Neck Surgery.
- Hans Behrbohm, Textbook of Ear, Nose, and Throat Diseases With Head and Neck Surgery.
- Logan Turner, Textbook of Diseases of The Nose, Throat and Ear Head And Neck Surgery.
- Arnold, U. Ganzer, Textbook of Otorhinolaryngology, Head and Neck Surgery.
- Ganong’s Review of Medical Physiology.
- Guyton & Hall Textbook of Medical Physiology.
Author:

Dr. Rahul Bagla
MBBS (MAMC, Delhi) MS ENT (UCMS, Delhi)
Fellow Rhinoplasty & Facial Plastic Surgery.
Renowned Teaching Faculty
Mail: msrahulbagla@gmail.com
India
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- Please read. Juvenile Angiofibroma. https://www.entlecture.com/juvenile-angiofibroma/
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