الفهرس 
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Abstract
The establishment and maintenance of fluent speech comes about as a result of the successful integration of a number of complex task-specific biological systems, achieved during childhood. The breakdown of speech fluency as evidenced in stuttering can at present best be viewed as a complex multifactorial problem, resulting in a breakdown within and between these systems. Thus it is probable that the heterogeneity which is characteristic of stuttering comes about through the interplay of genetic, linguistic, neural, motor speech, environmental and psychological factors, all of which will carry different weightings for different individuals. It is also likely that the complex interplay of these varying factors not only gives rise to the appearance of stuttering in the first place, but also affects whether the disorder will develop, how it will develop, and the likelihood that it will spontaneous resolve. There is at present no proper “integrated theory” on stuttering, but the demands and capacities model does offer a simple but useable way of both capturing and making sense of the variability seen in stuttering. The speech breakdown that characterizes stuttering can be viewed as an elaborate balance between a system’s capacity to produce fluency, and demands which compromise that ability.
A commonly asked question is: “Is there something different in the brain that makes people stutter?” There is evidence from a good many sources that links stuttering to neurological anomalies. Subcortical processing of linguistic information may be different, and stuttering has been linked to the function of subcortical structures. While we cannot say that stuttering is caused by anomalous CNS functioning, there is mounting evidence to suggest that for a large number of people who stutter, at least, there are subtle differences in the processing of linguistic information that differentiate them from those who do not stutter. For some, also, there are minor but significant neuroanatomical differences.
The onset of stuttering amongst the adult population is comparatively rare and can be identified in one of two forms: neurogenic stuttering (NS) which arises due to damage to the nervous system, or psychogenic stuttering (PS) which can arise following a traumatic experience. Some clinicians also argue for a third subcategory occult stuttering .While the subtypes of acquired stuttering are now accepted as recognized forms of fluency disorders, opinion differs as to the extent these versions of stuttering are behaviorally related to the developmental condition, and how best these acquired disorders should be managed clinically. Compared with developmental (DS), acquired versions have been little studied and the data that exists is somewhat patchy. Some have claimed that acquired dysfluency must be viewed. Pathophysiologically and dealt with therapeutically as distinctly different from the developmental condition.
Stuttered speech presents as an output which is motorically disrupted or “a limitation in speech motor skill”. A common finding is that across a range of motor speech tasks which are considered to provide indices of motor control, those who stutter have been found to perform either more slowly or with greater variability (or both) than those who do not stutter. These discrepancies in motor speech performance can be seen at respiratory, laryngeal and articulatory levels. Neurological evidence, suggests that areas associated with motor planning such as Broca’s area, premotor cortex, supplementary motor area and basal nuclei are likely to be functionally implicated, as are those directly associated with motor execution. Some variability at least may represent greater flexibility in coordinated motor activity, but other may be indicative of systems which are compromised in their ability to implement accurate goal directed motor speech output.
There is a range of evidence that points to the notion that stuttering is associated with disrupted auditory processing, although the exact nature of this disruption remains obscure. Shadowed speech can produce high levels of fluency, but this may have little to do with any timing misperception induced by a faulty processing system. Delayed auditory feedback (DAF) can have dramatic fluency enhancing effects for some people who stutter, yet others remain (DAF) negative, for reasons which are currently unknown. There are reports from some people who stutter that the effects of altered feedback can wear off over time. The dichotic listening procedure provides one testable method of determining hemispheric dominance for linguistic decoding, and findings from such studies, though far from definitive, lend tentative support to the idea that auditory processing too might be a product of the right hemisphere, at least in some people who stutter. One of the biggest issues faced is that auditory processing is just one part of the communication chain and does not occur in a vacuum. Both production and perception theories must allow for the fact that one is affected by the other. Studies related to motor speech control and central auditory processing raise questions as to the nature of neuroanatomical and neurophysiological breakdown in stuttering.
Neuroimaging techniques allow this study and these techniques are categorized as ”functional” (electroencephalo-graphy (EEG), magnetoencephalography (MEG), cerebral blood flow (CBF), single photon emission computed tomography (SPECT), positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) and ”structural” (the magnetic resonance imaging (MRI),. Func¬tional neuroimaging techniques permit examination of brain activity as a function of time, which provides information on how physical and mental processes are organized and performed by the brain. Structural neuroimaging techniques permit examination of the detailed structure of the living brain. These techniques are one of the most powerful tools in psychiatric research, and have provided a wealth of new information concerning brain function and develop¬mental stuttering.
The results of noninvasive neuroimaging techniques, such as functional magnetic resonance imaging (fMRI) provide growing evidence that complex human skills are not located in highly specialized brain areas but are organized in networks connecting several different areas of both hemispheres instead. The main areas include the primary motor cortex, SMA, premotor cortex, Rolandic operculum (Brodmann area [BA] 4/43), left inferior frontal gyrus (BA47), cerebellar hemispheres (principally lobule VI), and bilateral auditory association areas. Primary and secondary visual areas (BA17/18/19) were also seen.
One way for functional imaging to advance would be to discover relationships between abnormalities of functional organization and developmental abnormalities of brain structure. Clear demonstration of structural brain abnormalities particularly if confined to the left hemisphere would suggest that the right lateralized brain activation observed with functional imaging in stuttering might best be interpreted as developmental plasticity. Abnormalities of gyral anatomy in the left and right frontal operculum have been reported. Recent research has showed decreased gray matter (GM) volume concentration in stuttering speakers was found mainly in the left side of the cerebral cortex (including the superior and medial frontal gyri, superior temporal gyrus) and the right side of the cerebellum. Interest in the idea that there may be a structural anomaly in the brains of people who stutter and by using diffusion-tensor imaging in people with developmental stuttering. The investigators reported significant reductions in diffusion in white matter (WM) in the left rolandic operculum.
Numerous neuroimaging studies have suggested that developmental stutterers display unusual neural processing during speech or non speech related tasks. EEG showed that there is:
1- Prolongation of peripheral and central conduction time.
2- Fifty-four percent of stutterers had pathological EEG findings twenty-nine percent had interhemispheric asymmetry of the dominant rhythm compared to 12% for nonstutterers.
3- Thirty-two percent had paroxysmal activity. These findings could suggest organic brain dysfunction.
MEG studies have also found that adult stutterers display unusual auditory activations during speech and an unusual sequence of neural processing of the speech signal.
SPECT results found that people with developmental stutter¬ing had more blood flow to the right hemisphere and less blood flow throughout the brain. There is evidence that developmen¬tal stuttering is related to reduced and asymmetric perfusion of the brain.
A number of researchers have used positron emission tomography (PET) scanning and functional magnetic resonance imaging (fMRI) to study more directly the involvement of cortical and subcortical brain regions in stuttering. Eight PET and fMRI studies have addressed brain func¬tion in developmental stuttering a relatively small number compared with the fifty-eight EEG studies that have been per¬formed. They found that first there is an increase in activation in lateral vocal-motor areas (especially in the right hemisphere) and decrease in activation in auditory areas (bilaterally). Second, this is accompanied by a laterality shift that brings the balance of activity toward the right hemisphere. Finally, there is prominent overactivity in three medial motor structures: SMA, cingulate motor area, and cerebellar vermis (both lobules VI and III).
The role of the basal ganglia in stuttering was first uncovered through evidence from cases of acquired stuttering due to basal ganglia damage PET studies have provided evidence of hypoactivation of the left putamen and caudate. Stuttering reflects damage to different pathways as connectivity between the basal ganglia-thalamus and pre Supplementary motor area (SMA), connectivity between the basal ganglia-thalamus and the temporal cortex and connectivity from the basal ganglia to the thalamus.
Imaging research will have minimal clinical value if it simply used to identify abnormal stuttering-related regions and then map the changes in those regions during or after therapy.