Management of Spasmodic Dysphonia

Dr. Khurshid Alam

ENT Consultant, Doctors Hospital and Medical Centre,
Lahore

Introduction
Spasmodic Dysphonia is a chronic neurological disorder of
central motor processing characterized by task-specific action induces muscle
spasm. It has several subtypes including adductor, abductor and mixed.
Currently diagnosis is based almost exclusively on auditoryperceptual features. Muscle tension dysphonia ( MTD) which is a functional voice
disorder can mimic ADSD.
It is very important that before proceeding to any procedure
MTD should be excluded. Many studies have been done to differentiate these two
conditions. Fibreoptic laryngoscopy, phonatory airflow measurement, acoustary
analysis including spectrography variable sign based on phonatory task.
Phonatory break (absence of voicing for at least 50
millisecond) is pathognomic of ADSD. Whereas phonatory breaks are not present
in MTD.

Methods and Treatment

Patient is seen in the voice clinic in the presence of expert speech pathologist.
Fibreoptic laryngoscopy is done. Adductor spasmodic dysphonia causes
inappropriate closure of the glottis, and consequently strangled breaks in
connected speech. In Abductor dysphonia in contrast, causes inappropriate
glottal opening that produces hypophonia and breathy breaks.
Treatment options include selective resection of the recurrent laryngeal nerve,
type 2 thyroplasty but fail to show good results. Presently Botox treatment is the
treatment of choice. There is no antidystonia pharmacological agent. Oral
medications used are benzodiazepines, anticholinergics and dopamine depleters.
No drug has been reported to be useful in place of Botox.
Voice therapy may be useful after the Botox treatment. It is the principal therapy
of MTD.
Psychotherapy may help to manage the social stresses of this disorder and
thereby minimize the deterioration of voice and stress. But still there is no
convincing evidence.
Acupuncture has been tried but with not much success. Finally genetic work is
being done to understand the molecular mechanism and that may one day make
treatment.

Botulinum Toxin
SD is not a solely a matter of abnormal neural signal to laryngeal muscle but also
involve abnormal feedback from the larynx to the central nervous system.
Botox is currently the only successful treatment options for SD. For Adductor SD
it is inject in thyroarytenoid and lateral cricoarytenoid complex. And for
Abductor SD it is injected in posterior cricoarytenoid muscle. Botox is given with
EMG guided transcutaneous injection. Using EMG has a learning curve, need to
buy the EMG machine and familiarity with the EMG interpretation.
I am going to describe an alternative method of percutaneous injection technique
using direct visual guidance with the laryngoscope.
Patient is prepared and after giving local anesthesia at the cricothyroid level and
also spraying the nose and throat with 4% Xylocaine and spraying the nose with
oxymetazoline. 1.25 unit of Botox is injected in the posterior one third of the
vocal fold under direct vision.

Conclusion
Currently the standard of care for spasmodic dysphonia remains symptomatic
management of with Botox chemo denervation. Surgery is best reserved for
patients who do not benefit or cannot tolerate Botox.
SD is most likely a disorder of basal ganglia rather than the larynx, and
intervention at the end organ is unlikely to offer a true care.
SD is a very frustrating condition for the patient as many go into depression and
also loose their jobs. It is very rewarding when good results with Botox are
acquired.