the vocal folds are unable to retain subglottal air pressure (required for phonation) and breaks in phonation can be heard throughout the speech of people with spasmodic dysphonia. Regarding types of spasmodic dysphonia, the main characteristic of spasmodic dysphonia, breaks in phonation, is found along with other varying symptoms. The voice quality of adductor spasmodic dysphonia can be described as “strained-strangled” from tension in the glottal region. Voice quality for abductor spasmodic dysphonia can be described as breathy from variable widening of the glottal region. Vocal tremor may also be seen in spasmodic dysphonia. A mix and variance of these symptoms are found in mixed spasmodic dysphonia. Symptoms of spasmodic dysphonia typically appear in middle aged people, but have also been seen in people in their twenties, with symptoms emerging as young as teenage years. Cause Although the exact cause of spasmodic dysphonia is still unknown, epidemiological, genetic, and neurological pathogenic factors have been proposed in recent research. Risk factors include: Being female Being middle aged Having a family history of neurological diseases (e.g., tremor, dystonia, meningitis, and other neurological diseases) Stressful events Upper respiratory tract infections Sinus and throat illnesses Heavy voice use Cervical dystonia Childhood measles or mumps Pregnancy and parturition It has not been established whether these factors directly affect the development of spasmodic dysphonia (SD), however these factors could be used to identify possible and/or at-risk patients. Researchers have also explored the possibility of a genetic component to SD. Three genes have been identified that may be related to the development of focal or segmental dystonia: TUBB4A, THAP1 and TOR1A genes. However, a recent study that examined the mutation of these three genes in 86 SD patients found that only 2.3% of the patients had novel/rare variants in THAP1 but none in TUBB4A and TOR1A. Evidence of a genetic contribution for dystonia involving the larynx is still weak and more research is needed in order to establish a causal relationship between SD and specific genes. SD is a neurological disorder rather than a disorder of the larynx, and as in other forms of dystonia, interventions at the end organ (i.e., larynx) have not offered a definitive cure, only symptomatic relief. The pathophysiology underlying dystonia is becoming better understood as a result of discoveries about genetically based forms of the disorder, and this approach is the most promising avenue to a long-term solution. SD is classified as