Laryngeal Vibration for Spasmodic Dysphonia

Spasmodic dysphonia (SD) is a rare voice disorder that develops spontaneously during midlife.
Patients with SD typically have a strained or choked speech and report that is takes an
exhausting effort to speak. The involuntary spasms of the laryngeal musculature that give
rise to these symptoms almost always occur during speech. Progression is gradual in the first
year and then becomes chronic for life. The cause of spasmodic dysphonia is unknown, but SD
is considered to be a form of task-specific focal dystonia (FD). More women than men are
affected. Current therapeutic options are limited. SD does not respond to behavioral speech
therapy. It is treated primarily with Botulinum toxin injections (Botox), which provides
temporary symptom relief to some, but is not well tolerated by all SD patients. At present,
there is no cure for SD.

There is convergent evidence that FD is associated with kinaesthetic deficits that are also
manifest in non-dystonic musculature indicating that while the motor symptoms of dystonia are
focal, the associated somatosensory deficit is general. Recent work from our group (NIH
1R21DC011841) confirmed upper limb proprioceptive deficits in SD demonstrating that an
underlying somatosensory deficit is also a feature of SD. In our assessment this finding
opens an avenue for a missing behavioral treatment for SD. Specifically, the investigators
suggest that vibro-tactile stimulation (VTS) could be the suitable tool, given that it is
known to alter afferent signals from the vibrated mechanoreceptors in muscles and skin. The
approach seeks to show that VTS represents a non-invasive form of neuromodulation that
induces measurable improvements in the speech of SD patients. Given that SD, like other FDs,
is associated with abnormally increased cortical excitation and heightened levels of neuronal
synchronization, the investigators put forward that VTS can reduce sensorimotor cortical
excitation in SD by desynchronizing motor cortical neuron activity as has been shown in
cervical dystonia. Technically, newly available light-weight, wearable low-voltage vibrators
offer, for the first time, the possibility to apply laryngeal VTS outside a controlled
laboratory environment, which would be imperative for the technology to be clinically useful.
In general, one needs to demonstrate that a) VTS induces measurable improvements in voice
quality, b) that it induces measurable changes in somatosensory and motor cortical activation
that would provide insight into the underlying neural mechanism of its potential
effectiveness. Thus, the proposal has the following specific aims:

1. Demonstrate that a one-time, prolonged application of VTS produces acute improvements in
SD voice quality that are retained up to 60 minutes past cessation of VTS. A pre- and
post-training comparison showing significant voice improvements in the SD group as
measured by self-report (Effort Scale), clinical assessment (Consensus
Auditory-Perceptual Evaluation of Voice - CAPE-V), as the reduction in the number of
voice breaks and determining cepstral peak prominence will realize this goal. The
investigators' preliminary data show that VTS induces improvements in voice quality in
SD patients as measured by these markers.

2. Demonstrate that repeated prolonged VTS produces long lasting improvements in SD voice
quality that are retained for up to 3 months. SD patients will participate in an 8-week
in-home VTS training program. After randomization to either a treatment or sham group
(ineffective low frequency VTS), patients will start in low or high intensity training
group (1 vs. 3 sessions/wk) and cross-over after 4 weeks. Showing that significant
long-term voice improvements in the VTS treatment group as assessed by objective
measures of voice/speech production (see aim 1) will persist over a period of 11 weeks
will realize this goal.

3. Demonstrate that the application of VTS induces acute desynchronization of cortical
activity in SD, which would provide neurophysiological evidence on the assumed
effectiveness of VTS. Verifying that VTS is associated with short-latency characteristic
changes in somatosensory and motor cortical processing as measured by
electroencephalography (EEG) and documenting that these changes indicate decreased alpha
and beta-band activity in sensorimotor cortical areas will achieve this goal. The
investigators' preliminary data show that VTS suppresses low frequency neural activity
at the somatosensory and motor cortices in healthy and SD participants. Obtaining
longitudinal EEG data during VTS training (aim 2), will allow the investigators to
monitor long-term changes in cortical activation due to laryngeal VTS and to associate
them with changes in voice quality.

Impact. This is the first systematic study on the effect of VTS on SD voice symptoms. The
proposal aligns with PA-14-236 (Advancing Research in Voice Disorders) with its emphasis on
understanding voice disorders and improving diagnosis and treatment. If successful, the work
of the proposal would lay the scientific foundation for a clinical trial to examine the
usefulness of the approach in a larger patient sample. It would document the sensorimotor
cortical activation patterns associated with SD and the longitudinal changes in cortical
responses to VTS. It would promote development of wearable, user-programmable medical devices
that could apply VTS while monitoring its effect on voice production in real-time.
Ultimately, VTS would enlarge the available therapeutic arsenal by either augmenting existing
Botox therapy or becoming an alternative intervention option for patients who do not tolerate
Botox injections.

Inclusion Criteria:

- diagnosis of adductor SD for a minimum of 6 months with documented symptom relief
after botox injection

Exclusion Criteria:

- abductor SD

- patients with other voice disorders such as muscle tension dysphonia that share some
of the symptomology with SD