Neurological Concomitants in Spasmodic Dysphonia
By Lyn Dee Harrelson

neurological concomitants

Although there is controversy as the etiology of SD, Aronson (1980) reported that 80% of patients with SD show evidence of some additional neuropathology. Colton and Casper (1996) stated that other neurological signs are present in many patients with spasmodic dysphonia, including:

voice tremor
jaw and facial jerks
hand or limb tremor
hyperflexia
sucking reflex
torticollis
asymmetries in the face or palate

The spastic characteristics of SD can be related to the function of the basal ganglia and extrapyramidal tract of the brain. The function of the basal ganglia is to receive input from nearly all parts of the cerebral cortex, but especially from the motor area (Zemlin 1998). Zemlin also reported, "The basal ganglia are important components in regulation of complex motor functions such as posture, locomotion, balance, and such activities as arm swinging during walking. Lesions of the basal ganglia result in involuntary movement, increased muscle tone (rigidity), and resting tremor (which disappears during volitional movement). Some extrapyrmidal fibers of cortical origin descend to the basal ganglia, and from this level projections are sent again to inhibitory and excitatory centers of the brain. The principal function of the extrapyramidal system is to act as a coordinating mechanism for the control of the final motor pathways."

ESSENTIAL TREMOR
There is a high incidence of tremor in patients diagnosed with SD (Colton & Casper, 1996). This evidence suggests that SD is actually the symptom of an essential tremor. Other research suggests that the spastic behavior characteristics of SD are actually a compensatory strategy to try and gain control over the laryngeal tremor.

FOCAL LARYNGEAL DYSTONIA
SD is also classified as a focal laryngeal dystonia. A dystonia is a disorder of the basal ganglia. The basal ganglion is responsible for controlling muscle contractions. Without the control from the basal ganglia muscles are characterized as uncontrolled spasmodic muscle contractions (Colton & Casper 1996). Dystonias can manifest in three different ways, focal, segmental, or general.


Focal dystonia - Restricted to a few muscles.
belpharospasm (involuntary eye closures)
torticollis (head twisting)
writers cramp
spasmodic dysphonia

Segmental dystonia - involving a group of muscles

General dystonia - involving larger areas of the body
The onset of a dystonia can vary. It can be an organically based disorder and can develop early (before 26) or later on in life. Dystonia can also be triggered by trauma.

Although case history can help to identify pathologies of each patients voice disorder. Even from what is known about the pathologies of SD, it is important in developing a clear understanding of the patient's history to help generate an appropriate diagnosis.

Spasmodic dysphonia has distinctive perceptual characteristics, consistent acoustical characteristics, and visual physical characteristics that aid in determining an appropriate diagnosis. There is still much controversy as to the etiology that may never be answered. A better understanding of the etiology may aid in developing effective intervention strategies and allow professionals to make better judgments as to who will benefit from voice therapy. Currently, voice therapy is not the most favored method of treatment. Botox (Boyulinum toxin) injections provide temporary relief of th

e effects of AdSD. Another alternative to therapy is resection of the recurrent laryngeal nerve . This technique is has in most cases been replaced by Botox injections, but it is still performed on some patients with SD. These medical and surgical intervention techniques provide only temporary relief of the symptoms of AdSD. (Although surgical intervention is permanent, there have been cases of nerve reinnervation and thus a return of symptoms.)


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