No single, exclusive cause of developmental<unk>  is known. A variety of hypotheses and theories suggests multiple factors contributing to<unk> . Among these is the strong evidence that<unk>  has a genetic basis. Children who have first-degree relatives who stutter are three times as likely to develop a stutter. However, twin and adoption studies suggest that genetic factors interact with environmental factors for<unk>  to occur, and many stutterers have no family history of the disorder. There is evidence that<unk>  is more common in children who also have concurrent speech, language, learning or motor difficulties. Robert West, a pioneer of genetic studies in<unk> , has suggested that the presence of<unk>  is connected to the fact that articulated speech is the last major acquisition in human evolution. Another view is that a stutter or stammer is a complex tic. This view is held for the following reasons. It always arises from repetition of sounds or words. Young children like repetition and the more tense they are feeling, the more they like this outlet for their tension – an understandable and quite normal reaction. They are capable of repeating all types of behaviour. The more tension that is felt, the less one likes change. The more change, the greater can be the repetition. So, when a three-year-old finds he has a new baby brother or sister he may start repeating sounds. The repetitions can become conditioned and automatic and ensuing struggles against the repetitions result in prolongations and blocks in his speech. More boys stammer than girls, in the ratio of 3–4 boys : 1 girl. This is because the male hypothalamic-pituitary-adrenal (HPA) axis is more active. As males produce more cortisol than females under the same provocation, they can be tense or anxious and become repetitive. In a 2010 article, three genes were found by Dennis Drayna and team to correlate with<unk> : GNPTAB, GNPTG, and NAGPA. Researchers estimated that alterations in these three genes were present in 9% of those who have a family history of<unk> . For some people who stutter, congenital factors may play a role. These may include physical trauma at or around birth, learning disabilities, as well as cerebral palsy. In others, there could be added impact due to stressful situations such as the birth of a sibling, moving, or a sudden growth in linguistic ability. There is clear empirical evidence for structural and functional differences in the brains of stutterers. Research is complicated somewhat by the possibility that such differences could be the consequences of<unk>  rather than a cause, but recent research on older children confirms structural differences thereby giving strength to the argument that at least some of the differences are not a consequence of<unk> . Auditory processing deficits have also been proposed as a cause of<unk> .<unk>  is less prevalent in deaf and hard-of-hearing individuals, and<unk>  may be reduced when auditory feedback is altered, such as by masking, delayed auditory feedback (DAF), or frequency altered feedback. There is some evidence that the functional organization of the auditory cortex may be different in people who stutter. There is evidence of differences in linguistic processing between people who stutter and people who do not. Brain scans of adult stutterers have found greater activation of the right hemisphere, which is associated with emotions, than of the left hemisphere, which is associated with speech. In addition, reduced activation in the left auditory cortex has been observed. The capacities and demands model has been proposed to account for the heterogeneity of the disorder. In this approach, speech performance varies depending on the capacity that the individual has for producing fluent speech, and the demands placed upon the person by the speaking situation. Capacity for fluent speech may be affected by a predisposition to the disorder, auditory processing or motor speech deficits, and cognitive or affective issues. Demands may be increased by internal factors such as lack of confidence or self esteem or inadequate language skills or external factors such as peer pressure, time pressure, stressful speaking situations, insistence on perfect speech, and the like. In<unk> , the severity of the disorder is seen as likely to increase when demands placed on the person's speech and language system exceed their capacity to deal with these pressures. However, the precise nature of the capacity or incapacity has not been delineated.
Stuttering
Hoarse voice
Drooling
Spasmodic dysphonia
Stilted speech
Facial toning
Kussmaul breathing
Sleepwalking