Speech stutter feel which words cannot be pronounced

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Speech stutter feel which words cannot be pronounced

Speech is an ability that allows us to talk about our favourite food or describe a difficult concept. It is a tool that helps us to communicate with others and make agreements. For most of the people, speaking is an effortless activity, and, once learned, becomes an automatic process without conscious orientation to the structures and systems involved (Falck, 1964). But, what happens when speech becomes one of the hardest tools to use? In this essay, I will try to briefly describe stuttering and its potential causes, especially from the neuroscientific point of view.     When conscious actions and conflicting thought patterns interfere with conditioned response sequences and prevent their routine completion, we usually talk about stuttering or stammering: a speech disorder that affects fluent speech. We all sometimes experience non-fluent speech to one degree or another, especially when we are mentally and physically tired or under stressful conditions (ibid). Stuttering is indicated in speech prolongations, repeating of voices, syllables, and words, and in pauses before or during the speech. These symptoms do not occur only for one day or twice a month, on the contrary, they are present every day, but vary according to the mood and severity of the person who stutters. Pinching and blocks during talking are also very common (Ward, 2006). While speaking, people who stutter feel which words cannot be pronounced in advance. In a desire to express a word and stop stuttering, they are exposed to pressure and start stuttering even more. This agony is accompanied by head jerks, eye blinks, breath holding, vocal starters etc. (Falck, 1964). They also help themselves to pronounce a word by twisting their hands, leaning on something with one part of their body, by taking an object into their hands and squeezing it, and much more. Ironically, all these actions and attempts to inhibit stuttering are actually the stuttering (Falck, 1964; Ward, 2006). We can see that stuttering is a behaviour. It is something a person does, not something the person has. This behaviour has been learned in accordance with established laws of learning. When a person habitually does things which interfere with the sequence of events that usually result in normal speech, stuttering occurs (Falck, 1964).    Stuttering in numbers  Stuttering affects approximately 70 million people worldwide, which presents about 1% of total population in the world. Men are more often affected than women, in the ratio 4 men:1 woman (Falck, 1964; Ward, 2006; Sims 2014). One of the possible causes for such a ratio could be in the more activated hypothalamic-pituitary-adrenal axis in men, which provides them with a bigger amount of cortisol so men can be more anxious or tenser and become repetitive (Sims, 2014).    Developmental and acquired stuttering  Stuttering can be roughly divided into developmental and acquired stuttering (Ward, 2006). Developmental stuttering starts at the age between 3 – 8 and it is not transient in nature but accompanies the child first into the teenage years and then adulthood. Acquired stuttering, on the other hand, often emerges as a result of some neurological trauma, for example, stroke, tumours, head injury; and psychogenic trauma as a consequence of some distressing event as bereavement or divorce (ibid). According to Van Riper (1982) there exist another form of stuttering, called occult stuttering. It has no apparent neurological or psychological onset but emerges out of developmental stuttering which was not diagnosed in early life and is manifested later on.    What causes stuttering?  Even though there exist a lot of theories on stuttering (e.g. genetic, motoric, linguistic, neurological, psychological, auditory processing, environmental phenomenon etc.), the main cause for stuttering is not yet known (Ward, 2006). Bloodstein (1995) filtered theories of stuttering into three categories: those, related to the stuttering moment itself; those attempting to explain the aetiology of stuttering; and the ones attempting to find new frames of reference from which to examine the disorder. Among potential causes, scientists commonly involve genetic factors despite numerous stutterers without a family history of stuttering (Sermas and Cox, 1982; Guitar, 2005; Ward, 2006). Many scientists declare stuttering is inherited but many deny genetic factors. Heredity, if it truly causes stuttering, may be of two sorts, biological and social; one is a physical inheritance, and the other is a transmission by percept, example, influence, training and so on (West, Nelson and Berry, 1939). Other potential underlying mechanisms for stuttering are psychological and environmental elements. For example, the child who is exposed to a home environment containing many disrupting influences is quite likely to exhibit more speech nonfluency than is the child who is exposed to more properly balanced portions of stress and support. If a child encountered negative experience and did not know how to cope with it, his unresolved trauma could result in stuttering (Falck, 1964; Sermas and Cox, 1982).     Stuttering in the brain  What about the neurological factors? Are there any differences in the brain of persons who stutter compared to fluent speakers? Similar questions have lead scientists to start investigating whether stuttering can be explained by some abnormal neural mechanism. With the expanding progress in neuroscience, scientists indeed discovered few interesting differences in the brain of people who stutter.   Processing language information (speech perception, speech production and speech formation), normally, takes place in the right hemisphere. It was found that people who stutter have fundamentally altered hemispheric lateralization for language. This means that the normal dominance of the left hemisphere for language is not seen in the group of people who stutter, they even fail to activate left neocortical areas which are normally engaged in language processing or activate these regions bilaterally. The activation of the left hemispheric regions appears to be related to the production of stuttered speech, and the activation of right hemispheric areas could represent compensatory processes associated with attenuation of stuttering symptoms. Right hemisphere mediated compensatory processes may be associated with the attenuation of stuttered speech because the anterior and posterior perisylvian areas on the right hemisphere were activated when subjects started to speak fluently (Braun et al., 1997). Among anomalous anatomic configuration of perisylvian cortical speech-language areas, people who stutter were shown to have an unusual activation in gyral and frontal operculum and in the auditory and motor areas, as well (Foundas, Bollich, Corey, Hurley, and Heilman, 2001). Fibre tracts in premotor and motor cortex connect the sensorimotor representation of the oropharynx with the frontal operculum, involved in articulation, and the ventral premotor cortex related to the planning of motor aspects of speech. Since people who stutter showed disturbed normal temporal pattern of activation in the premotor and motor cortices, the sensorimotor integration necessary for fluent speech might be impaired because of disturbed signal transmission through the left rolandic operculum (Sommer, Koch, Paulus, Weiller, and Büchel, 2002). Rolandic operculum and sensorimotor cortex bilaterally were shown to be underactivated during speech production in the group of people who stutter relative to fluent speakers (Watkins, Smith, Davis, and Howell, 2007). Underactivation in the same group was visible also in the Heschl’s gyrus on the left. Overactivity, on the other hand, was exhibited in the anterior insula, cerebellum and midbrain bilaterally in the group of people who stutter (ibid).    According to the studies, people who stutter exhibit abnormal lateralization, atypical structures, and different activation patterns when compared with fluent speakers. It has been shown that stuttering is not a speech-limited disorder. Chang, Kenney, Loucks, and Ludlow (2009) conducted a study where participants were submitted to both speech and non-speech related tasks. People who stutter exhibited a similar difference in neural activity in both. They also showed functional activation abnormalities in regions relevant to auditory-motor integration across perception, planning, and production tasks, again in both speech and non-speech related tasks. Furthermore, compared to the fluent speakers, people who stutter had increased activation in the right STG, bilateral HG, insula, bilateral precentral SMA, and the putamen during production. On the contrary, they had decreased activation in frontal and temporoparietal regions during perception and planning. Decreased activity during production was also in the left auditory region, which could reflect decreased efferent input to this from the motor articulatory region, possibly as a result of white matter difference. Anomalies of white matter were also found by Watkins, Smith, Davis, and Howel (2008). Their data revealed reduced integrity of the white matter underlying the underactive areas in the ventral premotor cortex in people who stutter. This region is connected with posterior superior temporal and inferior parietal cortex, and those white matter tracts provide a substrate for the integration of articulatory planning and sensory feedback. When connected with primary motor cortex, it also performs execution of articulatory movements.    What is happening in the brain of people who stutter during resting state compared to fluent speakers?   Right insula and basal ganglia, especially putamen and globus pallidus were more activated in people who stutter during resting state (Ingham, Grafton, Bothe, and Ingham, 2012). In the same study brain activity during reading and monologue was tested as well. During oral reading, people who stutter showed increased activation in the right SMA, and increased activation in the frontal lobe (SMA, BA 4) during monologues, compared to fluent speakers. On the contrary, fluent speakers had stronger activation in the bilateral posterior insula and in left globus pallidus. Mentioned findings could explain why basal ganglia and right insula show abnormal activation while people who stutter just imagine stuttering. Other more activated regions in people who stutter, but not in fluent speakers, were: left BA 44, right BA 43, left STG 22, left cuneus 18, CBM lobules, left VI, right VI, IX lobule, right vermis III.     SMA and putamen are also included in the basal ganglia-thalamo-cortical network (BGTC loop) which comprises different areas that support timing of self-initiated movements, complex sequential motor control, inhibition of unwanted movements and sensorimotor learning. SMA and putamen may also interact with the cortical auditory-motor system relevant to speech processing. Children who stutter showed less connectivity within the BGTC loop, which is congruent with a known phenomenon in stuttering speakers: stuttering only occurs during the self-paced propositional speech, whereas when instructed to speak in synchrony with external pacing signals like a metronome beat, they can become dramatically more fluent (Chang and Zhu, 2013). Sommer et al. (2002) correspondingly discovered the effect external signals have on persons who stutter. They stated that fluency inducing techniques, such as chorus reading or shadowing, have a powerful effect on stuttering; both might induce fluency by providing an external clock, which might be able to functionally compensate the disconnection between frontal speech planning areas and motor areas by synchronizing their activity via a common input.     We should not forget to mention an auditory processing deficit as a potential underlying mechanism for stuttering. A specific auditory perceptual deficit restricted to the left lateralized auditory processing of speech sound was seen in people who stutter. This might underlie their speech production deficit (Corbera et al., 2005). Furthermore, it was demonstrated that people who stutter have neural encoding deficits for timing features at the early stages of the auditory pathway (Tahaei, Ashayeri, Pourbakht, and Kamali, 2014). The findings from this study also provided a possible correlation between stuttering severity and the auditory perceptual deficit in developmental stuttering which demonstrate the relevance of speech perception network to speech production. The importance of neural timing differences in auditory cortex for processing speech and non-speech stimuli were demonstrated when people who stutter did not differ from fluent speaker in the amount of speech-induced suppression of the auditory M50 or M100 amplitude, which are suppressed for word stimuli (Beal et al., 2010). Differences were shown in the timing of cortical auditory processing in people who stutter compared to fluent speakers. It might be that people who stutter have difficulties to access neural representation of speech sounds (ibid).    Impact of stuttering on people who stutter  Stuttering is hard to cope with and affects people who stutter deeply. Findings by Craig, Blumgart, and Tran (2009) indicated that stuttering does negatively impact QOL in the vitality, social functioning, emotional functioning and mental health status domains. Their results suggest that people who stutter with increased levels of severity may have a higher risk for poor emotional functioning. A lot depends on the personal characteristics of a person who stutters. Bleek et al. (2012) investigated the association between the five-factor model of personality measured by NEO Five-Factor Inventory and the Overall Assessment of the Speaker’s Experience of Stuttering (OASES), which measured the adverse impact of stuttering on a person’s life. People with higher Neuroticism and lower Extraversion scores were shown to experience a greater impact of stuttering on their daily life. It is known that people who stutter start to avoid social situations, they get anxious if they have to speak out loudly and are frightened most of the time in advance when thinking about the next occasion which would require them to speak. Peters and Hulstijn (1984) investigated the connection between stuttering and anxiety. Results showed that during first reading task, people who stutter adapted slower than the fluent speakers, and they had a more linear decrement of physiological activity compared to fluent speakers who showed a typical habituation curve. Psychologically explained, this difference could be due to the fact that during reading, the person who stutters is confronted with the disability which evokes anxiety. Physiologically speaking, in stuttering, there is a disintegration of the respiration process, which can induce a higher level of physiological activity.     There is an impact of someones’ stuttering on the fluent speakers, as well. Arousal and emotional discomfort when observing stuttering were seen in both, fluent speakers and persons who stutter (Zhang, Klinowski, Saltuklaroglu and Hudock, 2009). In both groups, skin conductance response was significantly increased and the heart rate was significantly decreased in response to stuttered versus fluent speech. People who stutter often reported how stuttering decreases when they are not thinking about or attending to speech. Kamhi and McOsker (1982) suggested that people who stutter give more attention to speech than do fluent speakers. They conducted a study in order to better understand the relationship between the attention and stuttering. People who stutter performed abysmally as compared to fluent speakers on the attention-demanding task which accompanied speech. This study serves as evidence that people who stutter are more alert to speech.     Future solutions and predictions on stuttering  Can anything be done to completely cure stuttering or should we accept the fact we can only reduce symptoms? Despite modern technology, machines and knowledge, the cure for stuttering still does not exist. Therapies are more or less primary treatment. Perkins (1985) thought that the therapy for stuttering is a dead end, where some patients demonstrate improvement fluency and others improve the ability of people who stutter to cope with their speech and with their lives. He also proposed that in the future, biochemical intervention or genetic engineering could be used to control the stuttering in regard to the potential cause of genetic factors. As already mentioned above, several studies (Sommer et al., 2002; Chang and Zhu, 2013; Tahaei et al., 2014) confirmed that fluency can be improved by so-called fluency-induced techniques. Ward (2006) listed among these techniques choral and unison speech, shadowed speech, delayed auditory feedback, masking, frequency altered feedback. Results of Corbera et al. (2005) suggested the idea of stuttering rehabilitation by means of auditory perceptual programs in addition to production programs. They proposed new training methods, such as having stutterers accurately learn to discriminate speech sound elements, to lead to improvements in speech production.     One of the clinical approaches to reducing stuttering is transcranial magnetic stimulation (TMS). George, Wasserman, and Post (1996) were exploring the use of TMS and trying to attempt if it is possible to directly modify the abnormal neural activations that stuttering speakers produce during the speech. Even though TMS use is not fully understood yet, it provides some clues as to how one might reduce stuttering. As Busan et al. (2013) proposed TMS could be used to evaluate possible changes in corticospinal excitability induced by rehabilitation and pharmacological treatment. There is also a potential in hypnotherapy for stuttering but, unfortunately, we would need more data to see whether and how hypnosis can influence neuroplasticity and rearrange cells and muscles in order to produce fluent speech (Falck, 1964). It would be more than welcome for people who stutter to start conducting research toward this direction. Another big potential for a successful treatment of stuttering, by my personal opinion, is seen in the therapy with psychedelics. They have a power to significantly change the patterns of thoughts and connections between different areas of the brain. It has been shown that psychedelics have therapeutic effects on several mental disorders, such are depression, post-traumatic stress syndrome, and anxiety (Santos et al., 2016; Johnson and Griffiths, 2017). We can also mention the therapeutic use of cannabis. It has been confirmed that cannabis has a potential to be used in the therapies, regarding its ability to calm down the human’s mind and relax the body (Baker, Peyce, Giovannoni and Thompson, 2003). Cannabinoids might be useful in the treatment of movement disorders, as Parkinson’ and Huntington’s disease are (Kluger, Triolo, Jones and Jankovic, 2015), and since we know stuttering is a disorder of motor and temporal activity patterns in the brain, it might have a positive impact in treating stuttering as well. As we can see, there is a lot of work and future research needed in order to confirm or refute possible solutions to stuttering. Hopefully, near in the future, people who stutter would be provided with a new hope to forever stop stuttering and start speaking fluently instead.  



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