Stuttering etiology research

Personal research on the main plausible theories on the stuttering etiology

Orlin Baev

New Bulgarian University

MS Cognitive Science

Abstract:

The main plausible theories regarding stuttering etiology are considered. The main stress is put on the neurological research, unambiguously defining stuttering as pure neurological disorder. Shortly are viewed several other valuable theories, as well as psychoanalytical hypotheses. Ample empirical evidence exists to support the notion that stuttering can involve abnormalities of virtually any or all neural systems involved in speech, with a possible predominance of hypoactivity in the language processing areas and hyperactivity in the premotor and motor areas. In right-handed PWnS the left hemisphere is usually seen as the dominant hemisphere with regard to the cognitive aspects of speech. Indications are that this may not be the case in PWS and that suboptimal functioning of speech-related areas of the left hemisphere, whatever the cause, could lead to a compensatory hyperactivity in the right hemisphere. Preliminary indications are that abnormalities in the order of cerebral processing, as well as discoordination between the subsystems of speech initiation (respiration, phonation and articulation) may also be instrumental in the dysfluency of speech. Abnormalities of either cortical or subcortical systems may underlie the disturbances in coordination between these various systems. Although the implications are not quite clear it can, with a fair amount of certainty, be assumed that the hemispheric lateralisation of PWS differs from that of the rest of the population and that stuttering may perhaps be more prevalent in individuals with right hemispheric dominance.

Stuttering is a disturbance in the fluency of speech marked by involuntary, audible or silent repetitions or prolongations of sounds or syllables (Buchel & Sommer, 2004:E46). Speech impediments can have a significant impact on the psychological and, by implication, the physical health of the individual. In the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders, communication disorders like stuttering are classified under Disorders Usually First Diagnosed in Infancy, Childhood, or Adolescence (American Psychiatric Association: Diagnostic and Statistical Manual for Mental Disorders, 1994:38). Stuttering can be affected by internal (or personal) as well as external (or environmental) factors. Therefore it can be classified under the World Health Organisation's International Classification of Functioning, Disability and Health (Yaruss & Quesal, 2004:48). Stuttering is probably the most prevalent speech disorder and affects about 1% of prepubertal children (Andrews, Craig, Feyer, Hoddinott, Howie & Neilson, 1983:228). Theories about the etiology of stuttering span a continuum from the purely psychological to the physiological. Amongst the more important theories are:

a) the approach that stuttering is the result of learnt avoidance behavior, as proposed by Sheehan (Sheehan, 1953, cited in Gregory, 1986:4; Van Riper, 1992:266, 297), b) the psychoanalytic approach that views stuttering as a neurotic tendency (Hahn, 1963), c) the Cerebral Dominance Theory (Orton, 1927:671, 672; Travis, 1978:277), d) the Excess Dopamine Theory Of Stuttering (Wu, Maguire, Riley, Lee, Keator, Tang, Fallon & Najafi, 1997:767-770; Maguire, Riley, Franklin & Gottschalk, 2000:482; Louis, Winfield, Fahn & Ford, 2001), e) the Model of Central Nervous System Premotor Processing (Goldberg, 1985:567; Watson, Pool, Devous, Freeman & Finitzo, 1992:559), and f) the Maturation Hypothesis of Stuttering (Ozge, Toros & Comelekoglu, 2004:282).

Neurological Research on Stuttering

As early as the 1920s researchers began to suspect that stuttering has an organic basis but this has only been partially supported (Van Riper, 1992:353). According to Andrews et al. (1983:238) most theories about the breakdown of speech fluency stem from the proposition that people who stutter (PWS) have a reduced physiological capacity to coordinate speech. This implies a neurological basis for stuttering. The latest findings point to the hyperactivation or deactivation of one or more areas of the central nervous system during speech, as well as impaired structural communication between the areas involved in speech production, which could possibly underlie the miss-timing and discoordination to cues from other speech areas (Ingham, 2001:501; Ingham, Ingham, Finn & Fox, 2003:297; Peters, Hulstijn & Van Lieshout, 2000:104). It is always easier to understand the abnormal against the background of the normal and, for the convenience of the reader, a recent model of the neural basis of normal speech production can help for understanding stuttering.

The Cerebral Dominance Theory proposes stuttering as the consequence of a failure to establish dominance of the left hemisphere over the right. This concept was initially proposed by Orton (1927:671, 672), but continues to be debated to this day (Travis, 1978:275; Gelfer, 1996:155; Brosch, Haege, Kalehne & Johanssen, 1999:71). An interesting observation implicating a difference in cerebral dominance between PWS and people who do not stutter (PWnS) has been reported with regard to ear preference, handedness and stuttering. While it is generally assumed that right-handed PWnS, display a right-ear preference 75% of the time, indicating left hemisphere dominance, Curry and Gregory (1969), showed that only 45% of right-handed PWS exhibited a right-ear preference in dichotic listening exercises (Curry & Gregory, 1969, cited in Ingham, 2001:494). This implication that PWS display less left hemispheric speech dominance than PWnS, has also been reported by others (Fox, Ingham, Ingham, Hirsch, Downs, Martin, Jerabek, Glass & Lancaster, 1996:158; Braun, Varga, Stager, Schulz, Selbie, Maisog, Carson & Ludlow, 1997:762). Another confounding factor is the fact that females on average show relatively less hemispheric dominance than males, thus one would expect stuttering to be more prevalent in female, yet chronic stuttering is not more common in females (Ingham, 2001:494).

It appears that PWS show either bilateral dominance, as reported by Jones (Jones, 1966, cited in Van Riper, 1992:338), or right hemispheric dominance with regard to language (Braun et al. 1997:766). The results of Braun and co-workers were based on a comprehensive study of the patterns of cerebral activity that manifests during speech and language production, which showed that cerebral function is fundamentally different in PWS (Braun et al. 1997:761).

It is well-known that some individuals will cease to stutter at some stage, while the problem will persist in others. Brosch et al. (1999:240), who studied cerebral dominance in terms of chronicity of stuttering, proposed handedness to be related to the probability that a child's stuttering will become chronic. It would appear that lefthanded children show a significantly greater tendency towards chronic dysfluency. Although results from several laboratories support the concept of a link between stuttering and the pattern of cerebral dominance, with a higher incidence of stuttering in left-handers, workers such as Webster and Poulos (1987:708) could for instance not find evidence to suggest a higher incidence of left-hand preference in PWS than in PWnS. Thus further research is required for more definite conclusions on the role of cerebral dominance in stuttering.

Despite all these controversies, it does seem that the results of recent studies generally support the concept of abnormal interhemispheric relations and most point towards hyperactivity of the right, relative to the left hemisphere (Braun et al. 1997:762, 778; Buchel & Sommer, 2004:e49; Neumann, Preibish, Euler, Von Gudenberg, Lanfermann, Gall & Giraud, 2005:23). Neumann and co-workers reported abnormality in the white matter in the speech areas of the left hemisphere with hyperactivity of the right hemisphere (Neumann et al. 2005:23). Most of the recent conclusions are based on results of positron emission tomography, neuroimaging and functional magnetic resonance imaging. The concept of hyperactivity in the right hemisphere is further supported by the results of [H.sub.2.sup.15]OPET imaging studies during different speech tasks in stutterers and controls (Ingham et al. 2003:308). More evidence of differences between PWS and PWnS, with regard to hemispheric activity, is described under the discussion of neurological correlates of stuttering.

Neurological Correlates of Stuttering

Although conclusive evidence for specific cortical correlates of stuttering has, as yet, not been found, a pattern would appear to be surfacing (Sandak & Fiez, 2000:446). A fairly general consensus exists that stuttering is a disorder that involves most of the multiple neural systems used for speech (Fox et al. 1996:158). Evidence is emerging that implicates cortical areas, such as the mouth presentation in the primary motor cortex (M1, Brodmann's area 4, BA 4), Broca's area (left inferior frontal region), the supplementary motor area (SMA, also known as Penfield's area), Brodmann's area 6 (BA 6, which is the SMA and superior lateral premotor region), the inferior lateral premotor cortex (BA 6/44), Wernicke's area, the auditory processing system, which includes the primary auditory cortex (BA 41/42), the auditory association cortex (BA 21/22), the anterior insula, the anterior cingulate cortex (ACC), as well as the somatic sensory area (Brodal, 1981:835; Fox et al. 1996:159). In addition, subcortical areas such as the basal nuclei, the thalamus and cerebellum may all play a role in the mechanisms that bring about stuttering (Watson et al. 1992:560; Fox et al. 1996:159; Braun et al. 1997:776).

Cortical areas

Hypo/ Hyper activity

When reading, impulses are sent from the occipital region to the angular gyrus where reading is changed to "hearing" and from here to Wernicke's area, where thoughts are formed. From Wernicke's area, these thoughts are sent to Broca's area via the arcuate fasciculus. The left inferior frontal regions, which include Broca's area, are involved in processing the information into a vocalisation pattern (Ganong, 2001:266), while the motor and premotor regions are involved in activating the motor response. In general, PWS exhibit hypo-activity in cortical areas associated with language processing, but hyperactivity in areas associated with motor function (Sandak & Fiez, 2000:446).

Failure in the articulatory code preparation. Discoordination of speech initiation

Magneto electro-encephalogram (MEG) investigations also showed that, when PWnS read aloud, activation of the cortical areas involved occurs in the order of occipital areas to left inferior frontal areas (Broca's area) to premotor (for articulatory programming) and motor cortices (for motor preparation). PWS, on the other hand, exhibit a slightly altered pattern, that is, occipital region to premotor and motor regions to left inferior frontal areas (Broca's area) (Sandak & Fiez, 2000:447; Salmelin, Schnitzler, Schmitz & Freund, 2000:1184). On the grounds of this observation it was postulated that PWS initiate vocalisation patterns before the articulatory code is prepared (Sandak & Fiez, 2000:447).

Another theory is that stuttering can be characterised as a disorder in the timing and coordination of subsystems involved in speech production (that is respiration, phonation and articulation). The research of Peters et al. (2000:103) has shown that, while PWS and PWnS, may perhaps not differ in the way they assemble speech-motor plans, the way in which they initiate those plans, however differs. Electromyogram (EMG) recordings of laryngeal and articulatory muscle activity during stuttering correlate highly with neurological findings (Peters et al. 2000:104). This begs the questions that if a discoordination of speech initiation exists in PWS, why do PWS not stutter all the time? PWS move along a continuum extending from normal speech movements to excessive deviances (Peters et al. 2000:105). The degree of fluency would largely depend on the nature of the task. When PWS are asked to perform relatively difficult (dysfluency-evoking) tasks, for example, spontaneous speech, there is a processing overload in the left inferior frontal areas. The result is dysfluent speech. During the performance of relatively easy tasks, the degree of activation required in Broca's area decreases, while fluent speech is produced (Sandak & Fiez, 2000:448). It should, however, be obvious to anyone involved with this kind of speech impediment that other factors such as emotional and cognitive elements would also come into play. It seems feasible to suggest that the effects of emotions on the respiratory pattern--known to occur in most people, whether they suffer from speech dysfluency or not could contribute to the exacerbation of dysfluency in PWS.

It is generally accepted that Broca's and Wernicke's areas which, in right-handed individuals, are predominantly found in the left hemisphere, are involved with stuttering, but many other areas are also implicated, including the SMA, anterior insula and cerebellum (Goldberg, 1985:567; Ingham, 2001:498). The central portion of Wernicke's area (BA 22) is said to be inactive in PWS (Braun et al. 1997:766). In 1985, Goldberg proposed a model of central nervous system premotor processing (Goldberg, 1985:567; Watson et al. 1992:559). This model has since been used to explain stuttering in terms of a disruption in this processing system, implicating a dysfunction in the SMA as the cause of stuttering (Watson et al. 1992:559; Chung, Im, Lee & Lee, 2004:1106). In a positron emission tomography (PET) study of chorus and solo reading in PWS and fluent controls, researchers found that PWS show a prominent right hemisphere hyperactivation of BA 6, which includes the SMA and the superior lateral premotor region (Fox et al. 1996:161). It was noticed that if stuttering was reduced after treatment, this activity shifted to the left hemisphere (Ingham, 2001:494,496). The same authors also described hypoactivity of the primary auditory areas (BA 41/42) and a largely deactivated auditory association area (BA 21/22), especially in the right hemisphere (Ingham, 2001:496). This supports previously published results by Sandak and Fiez (2000:446), mentioned earlier in this section. These abnormal activations and deactivations associated with PWS were found to occur even when the PWS are merely imagining that they were stuttering, while reading silently (Ingham, 2001:498).

However, these results could not be supported by cerebral blood flow (CBF) patterns for PWS and PWnS when not speaking (Braun et al. 1997:761; Ingham, 2001:498). Differences in CBF patterns apparently only occur when PWS actually speak (Ingham, 2001:498).

Slightly different patterns of cortical abnormalities are reported between female PWS and male PWS. There seems to be similar levels of activation in the SMA of female PWS and female PWnS (Ingham, 2001:499). Male PWS, on the other hand, display different levels of activation to both groups. Inconsistencies in the activity of the anterior insula, an area known to be important in the planning of phonation, occur in PWS. Although increased activity of the anterior insula has been reported during stuttering in both genders, the activity appears to be higher in the left hemisphere of females (Ingham, 2001:499).

Hyperactivity of the anterior cingulate cortex (ACC) in PWS

There are some inconsistencies in reports on the activity of the anterior cingulate cortex (ACC). This area aids in speech motor activities and is of interest to many theories of stuttering. Researchers, who suggest that the right inferior ACC is hyperactivated during speech of PWS, but not in the speech of PWnS, include Braun et al. (1997:768) and Ingham et al. (2003:312). This view is supported by evidence from neuroimaging that shows increased regional CBF to the inferior and superior anterior cingulate cortex when PWS speak (Braun et al. 1997:769). The work of Fox et al. (1996:161) does however, not support this idea of activation of the ACC in PWS. These conflicting results may be due to task related experimental differences between the different laboratories, as it is known that ACC activation diminishes as task familiarity increases (Petersen, Van Mier, Fiez & Raichle, 1998:853; Ingham, 2001:501).

Unutilization of the somatic sensory information for orofacial movements production

As mentioned previously, the somatic sensory area is implicated as one of the cortical areas involved in speech disorders such as stuttering. It appears that most PWS do not use their somatic sensory information in full for orofacial movements. These findings of De Nil and Abbs (1991:2145) could explain some breakdowns in speech.

Insula connectivity break down

A right hyperactivity, similar to that mentioned under cerebral dominance, has also been reported with regard to the insula. It is known that the left insula cortex forms an anatomical bridge between Broca and Wernicke's areas that most speech functions involve the dorsal left anterior insula, and that damage to the left insula contributes to dyspraxia (Ingham et al. 2003:312). It was therefore suggested that excessive activity in the right insula cortex of PWS during speech might be due to a takeover of the left insula's speech functions by the right insula (Ingham et al. 2003:312).

Delayed cerebral maturation

Recently a different interpretation of the hemispheric left-hypoactivity-right-hyperactivity view was proposed by Ozge et al. 2004:269. They also investigated the possible role of delayed cerebral maturation, hemispheric asymmetry and regional brain differences by means of conventional EEG and quantitative EEG in children who stutter. In contrast to the view of most that hyperactivity of the right hemisphere reflects compensation for the primary hypoactivity of the left, they suggested a primary right hemispheric defect, possibly right frontal region, which may be related to SMA. Their results also give some support to the maturation hypothesis that suggests stuttering to be at least partially due to a delay in cerebral maturation (Ozge et al. 2004:270, 282). This concept that stuttering may be the result of delayed maturation dates to the 1940s when Karlin (1947) and others before him believed that the delayed myelinisation process of the cortical areas subserving speech and language in male children compared to female children, may be the cause of the higher incidence of stuttering in males (Karlin, 1947, cited in Van Riper, 1992:42). Previously in this discussion a possible association between handedness and the potential to outgrow childhood stuttering was mentioned (Ozge et al. 2004:282). Another view about recovery from childhood stuttering relates to the above described concept of stuttering as a consequence of delayed cerebral maturation where recovery is suggested to reflect the eventual maturation of the mechanisms of speech motor control (Forster & Webster, 2001:125).

Subcortical Areas

Subcortical areas implicated in stuttering are the basal nuclei, parts of the thalamus, as well as the cerebellum (Fox et al. 1996:161).

Cerebellum hyperactivity in PWS

The cerebellum, especially the vermis and the paramedian regions, is involved in the control of laryngeal and respiratory mechanisms during speech (Holmes, 1939). Lesions of the cerebellum could therefore disrupt the coordination of the muscles involved in speech. Several research groups reported enhanced cerebellar activity in PWS. De Nil, Kroll and Houle (2001:79) investigated the activity of the cerebellum of a control group of PWnS and a group of PWS. Cerebellar activity was measured before and after participation in an intensive programme to ameliorate stuttering. PWS were found to exhibit higher cerebellar activation than PWnS, both pre--and postprogramme, and therefore this overactivity of the cerebellar motor system has been included in the neural system of stuttering (Fox et al. 1996:161). PET images of blood flow studies showed that the right cerebellum hemisphere is prominent (Fox, Ingham, Ingham, Zamrripa, Xiong & Lancaster, 2000:1985).

Basal ganglia and speech articulation, procedural memory and auditory feedback. High/ low dopamine in the basal nuclei

The role of the basal nuclei in language processing has become of great interest since the late 1990s. These subcortical motor nuclei are generally known to be involved in the routine voluntary actions of speech production such as articulation (Lebrun, 1998:121) and if damaged, seem to impact negatively on such functions. This may affect mechanisms related to the execution and termination of auditory feedback, which is used in the control of voice frequency (Kiran & Larson, 2001:795). The involuntary muscle contractions, which often accompany dysfluency in PWS, are brought on directly by subcortical nuclei (Lebrun, 1998:121). It is assumed that the left putamen plays a role in articulation, specifically in the second language, which is normally learnt after a child's fifth year (Klein, Zatorre, Milner & Evans, 1994:2295). The subputaminal nucleus, which is normally best developed on the left at the anterointermediate level, may be connected to the cortical speech area and it is hypothesised that progressive aphasia may be related to disorders of the subputaminal nucleus (Simiae, Mrzljak, Fucic, Winblad, Lovric & Kostovic, 1999:73). It has also been reported that the basal nuclei may modulate the unaffected primary speech and language areas, which results in stuttering (Ludlow & Loucks, 2003:273). In addition, dopamine, a major basal nuclei neurotransmitter, has been under research as a possible cause for stuttering. Many researchers support the Excess Dopamine Theory of Stuttering (Wu et al. 1997; Maguire et al. 2000:482; Louis et al. 2001). However, this theory is partially refuted by evidence that L-dopa, which causes an increase in the amount of dopamine in the brain, improves speech fluency in Parkinson patients (Koller, 1983:175; Leder, 1996:475). Thus, the hypothesis might be amended to state that speech dysfluencies may be related to either increases or decreases in dopamine levels in the brain (Goberman & Blomgren, 2003:55), in other words, aberrant levels of dopamine release. A perhaps more feasible possibility, well reviewed by Alm (2004:325, 355), is that the basal nuclei's contribution to stuttering may be multifactorial. The core dysfunction in this proposed multifactorial contribution is seen as an impaired ability of the basal ganglia to produce timing cues with contributing defects found at receptor level, for example, high density D2-receptors and a low D1/ D2 ratio in the putamen, as well as abnormalities in the basal ganglia-thalamocortical circuit (Alm, 2004:325, 355).

Contradicting Thalamic involvement into Stuttering Production

Contradicting results have been reported with regard to the thalamus. Some researchers reported the production of stuttering-like behaviours upon stimulating the ventrolateral thalamic region (Penfield & Welch, 1951; Ojemann & Ward, 1971:679). A more anterior part, as well as the pulvinar (posterior) part of the dominant hemispheric thalamus has also been associated with language disturbances (Penfield & Roberts, 1959). In contrast, Bhatnagar and Andy (1989:1182) reported that stuttering could be reduced by thalamic stimulation.

Abnormalities in the order of cerebral processing

Magnetoencephalography (MEG) is the method of choice to investigate fine-grained temporal sequence of brain activity. Consequently, MEG was used to investigate stutterers and fluent controls reading single words (Salmelin et al. 2000). Importantly, stutterers were reported to have read most single words fluently. Nevertheless, the data showed a clear-cut difference between stutterers and controls. Whereas fluent controls activated left frontal brain areas involved in language planning before central areas involved in speech execution, this pattern was absent, even reversed, in stutterers. This was the first study to directly show a neuronal correlate of a hypothesized speech timing disorder in stutterers (Van Riper 1982).

Thus, functional neuroimaging studies have revealed two important facts: (i) in stutterers, the right hemisphere seems to be hyperactive, and (ii) a timing problem seems to exist between the left frontal and the left central cortex. The latter observation also fits various observations that have shown that stutterers have slight abnormalities in complex coordination tasks, suggesting that the underlying problem is located around motor and associated premotor brain areas.

Abnormalities in the gyrification pattern

Are there structural abnormalities that parallel the functional abnormalities? The first anatomical study to investigate this question used high-resolution MR scans and found abnormalities of speech–language areas (Broca’s and Wernicke’s area) (Foundas et al. 2001). In addition, these researchers reported abnormalities in the gyrification pattern. Gyrification is a complex developmental procedure, and abnormalities in this process are an indicator of a developmental disorder.

Decreased white matter tract coherence in the Rolandic operculum

Another recent study investigated the hypothesis that impaired cortical connectivity might underlie timing disturbances between frontal and central brain regions observed in MEG studies (Figure 3). Using a new MRI technique, diffusion tensor imaging (DTI), that allows the assessment of white matter ultrastructure, investigators saw an area of decreased white matter tract coherence in the Rolandic operculum (Sommer et al. 2002). This structure is adjacent to the primary motor representation of tongue, larynx, and pharynx (Martin et al. 2001) and the inferior arcuate fascicle linking temporal and frontal language areas, which both form a temporofrontal language system involved in word perception and production (Price et al. 1996). It is thus conceivable that disturbed signal transmission through fibers passing the left Rolandic operculum impairs the fast sensorimotor integration necessary for fluent speech production.

This theory also explains why the normal temporal pattern of activation between premotor and motor cortex is disturbed (Salmelin et al. 2000) and why, as a consequence, the right hemisphere language areas try to compensate for this deficit (Fox et al. 1996). These new data also provide a theory to explain the mechanism of common fluency-inducing maneuvers like chorus reading, singing, and metronome reading that reduce stuttering instantaneously. All these procedures involve an external signal (i.e., other

readers in chorus reading, the music in singing, and the metronome itself). All these external signals feed into the “speech production system” through the auditory cortex. It is thus possible that this external trigger signal reaches speech-producing central brain areas by circumventing the frontocentral disconnection and is able to resynchronize frontocentral decorrelated activity. In simple terms, these external cues can be seen as an external “pacemaker.”

Dopaminergic System Hyperactivity

Neurochemistry, however, may link stuttering with disorders of a network of structures involved in the control of movement, the basal ganglia. An increase of the neurotransmitter dopamine has been associated with movement disorders such as Tourette syndrome (Comings et al. 1996; Abwender et al. 1998), which is a neurological disorder characterized by repeated and involuntary body movements and vocal sounds (motor and vocal tics). Accordingly, like Tourette syndrome, stuttering improves with antidopaminergic medication, e.g., neuroleptics such as haloperidol, risperidone, and olanzapine (Brady 1991; Lavid et al. 1999; Maguire et al. 2000), and anecdotal reports suggest that it is accentuated or appears under treatment with dopaminergic medication (Koller 1983; Anderson et al. 1999; Shahed and Jankovic 2001). Hence, a hyperactivity of the dopaminergic neurotransmitter system has been hypothesized to contribute to

stuttering (Wu et al. 1995). Although dopamine antagonists have a positive effect on stuttering, they all have side effects that have prevented them from being a first line treatment of stuttering.

Impaired Auditory Feedback Processing

Alterations of auditory feedback (e.g., delayed auditory feedback, frequency altered

feedback), various forms of other auditory stimulation (e.g., chorus reading), and alteration of speech rhythm (e.g., syllable-timed speech) yield a prompt and marked reduction of stuttering frequency, which has raised suspicions of impaired auditory

processing or rhythmic pacemaking in stuttering subjects (Lee 1951; Brady

and Berson 1975; Hall and Jerger 1978; Salmelin et al. 1998). Other groups

have also reported discoordinated and delayed onset of complex articulation

patterns in stuttering subjects (Caruso et al. 1988; van Lieshout et al. 1993).

The assumption that stuttering might be a form of dystonia—involuntary muscle contractions produced by the CNS—specifi c to language production (Kiziltan and Akalin 1996) was not supported by a study on motor cortex excitability (Sommer et al. 2003).

Neurological Theories of Stuttering – Conclusions. Is stuttering neurological disorder?

Ample empirical evidence exists to support the notion that stuttering can involve abnormalities of virtually any or all neural systems involved in speech, with a possible predominance of hypoactivity in the language processing areas and hyperactivity in the premotor and motor areas. In right-handed PWnS the left hemisphere is usually seen as the dominant hemisphere with regard to the cognitive aspects of speech. Indications are that this may not be the case in PWS and that suboptimal functioning of speech-related areas of the left hemisphere, whatever the cause, could lead to a compensatory hyperactivity in the right hemisphere. Preliminary indications are that abnormalities in the order of cerebral processing, as well as discoordination between the subsystems of speech initiation (respiration, phonation and articulation) may also be instrumental in the dysfluency of speech. Abnormalities of either cortical or subcortical systems may underlie the disturbances in coordination between these various systems. Although the implications are not quite clear it can, with a fair amount of certainty, be assumed that the hemispheric lateralisation of PWS differs from that of the rest of the population and that stuttering may perhaps be more prevalent in individuals with right hemispheric dominance. Various approaches try to explain age-dependent recovery from stuttering, but the most exciting explanation is that of delayed cerebral maturation. How this fits in with the other neurological correlates of stuttering is not clear, but the maturation hypothesis of stuttering leaves the door wide open for research of a more pragmatic nature by individuals who do not have high technology at their disposal. Briefly – the stuttering IS neurological disorder!

In addition, it should be stressed that despite confirmation of the involvement of structural and functional abnormalities in dysfluency of speech, the possible contribution of psychological factors and the potential for correction through therapeutic intervention should not be disregarded. This is particularly relevant in view of the influence of early life experience on cerebral structure and function, as well as the fact that cerebral plasticity persists virtually throughout life.

Genetics and Heredity

Presence of affected family members suggests a hereditary component. The concordance rate is about 70% for monozygotic twins (Andrews et al. 1983; Felsenfeld et al. 2000), about 30% for dizygotic twins (Andrews et al. 1983; Felsenfeld et al. 2000), and 18% for siblings of the same sex (Andrews et al. 1983). Given the high recovery rate, it may well be that the group abnormalities observed in adults reflects impaired recovery rather than

the causes of stuttering (Andrews et al. 1983).

Learnt (conditioned) Social Behavior – behavioral learning theory

Other theories regard stuttering as a learned behavior resulting from disadvantageous external, usually parental, reactions to normal childhood dysfluencies (Johnson 1955). While this model has failed to explain the core symptoms of stuttering (Zimmermann et al. 1983), it may well explain secondary symptoms (Andrews et al. 1983), and guided early parental intervention may prevent persistence into adulthood (Onslow et al. 2001).

The Linked Covert Repair Hypothesis Account of Stuttering

Kolk and Postma's (1997) account (called the covert repair hypothesis, CRH) approaches the issue of stuttering primarily from a psycholinguistic perspective. It was developed from Levelt's (1989) well-known model of speech breakdown in fluent speech control, in which speech errors are regarded as providing important evidence about speech control. A diagram of Levelt's model is presented as on the figure below:

The main features to note about the Levelt model follow:

• There is a hierarchical linguistic system, and errors can be made at different points in the hierarchy. Speech errors like “cuff” in “cuff of coffee” (Fromkin, 1971) are indisputably errors. However, Levelt (1983) regards repair events as results of errors in the psycholinguistic system. For instance, a speaker giving directions on how to go from one place to another might give an erroneous set of directions. Assigning these a status of linguistic errors is disputable as they could stem from poor spatial, rather than linguistic, ability. To ensure that linguistic errors are involved, errors are defined here as a phoneme in the wrong position to complete an intended word. According to this view, Fromkin's “cuff” and the words “hissed” and “mistory” in the classic spoonerism “missed my history lesson” are all errors. “Turn left, no, turn right” in a repair and “m.missed” and “hhhistory,” on the other hand, are not errors. A further point to note for later is that errors according to this strict definition are infrequent in speech control; Garnham, Shillcock, Brown, Mill, and Cutler (1981) estimate that these occur in only approximately .01% of words.
• Errors are fed to a monitoring system via two routes—the external, and internal, loops. Both loops send information to the perception system, which decodes the speech. The decoded speech is transmitted to the monitor, which compares the intended message with that which perception indicates has actually been made. If the two correspond, speech has been produced as intended and output can continue. If there is a discrepancy, an error has occurred, speech is interrupted, and the correct message is reinitiated. Evidence from speech repairs has been used as support for both loops: Overt speech repairs such as “to the left of, no, to the right of the curtain” provide support for the external loop. The speaker has produced the word “left” when “right” was intended. The Levelt (1983) account assumed that the speaker hears this, interrupts speech (signified by the comma), and repeats some components that are not essential (“to the,” called a retrace) before making the correction. Using “left” instead of “right” may not be the result of an error in the linguistic system (for the same reason that such “errors” were excluded in the above definition, and, consequently, would have little relevance to the workings of psycholinguistic processes. Events that are taken as evidence for the internal loop are retraces like “to the, to the right of the curtain.” There is no overt error in these repairs; they are called covert repairs. It is possible that they are the results of internal monitoring where an error has been detected, interrupted, and corrected before the error is output.
• Some specification is given about the site of the language–speech interface in this model. A phonetic string is supplied by the linguistic system that is then output through the motor system. Subsequently, this output is detected by the peripheral auditory system and eventually transmitted to the monitor (that detects and interrupts production when an error occurs over the external loop).

Kolk and Postma's (1997) CRH was originally developed from Levelt's account to explain the frequent occurrence of pauses (interruptions) and word repetition (retraces) in stuttered speech. In Levelt's model, these events were seen as a result of errors detected over the internal loop that were repaired covertly. The early version of the CRH account did not explain why PWS should show a higher rate of covert repairs (and, by implication, a higher error rate in linguistic processing) than speakers who do not stutter. This was partly rectified by Kolk and Postma. They used Dell and O'Seaghdha's (1991) spreading activation model to explain how a slow phonological (or, more precisely, phonetic) system leads PWS to make errors (in particular, errors that lead to covert repairs). According to Kolk and Postma, when a speaker intends to say the word “cat” (the target unit), phonetically related competing units are also activated (e.g., “rat”). Dell and O'Seaghdha's model has steps involving lexical activation and phonetic encoding. Kolk and Postma focus on how activation patterns could lead to phonetic errors after lexical selection has taken place. The buildup of activation for the target and competing units follows similar trajectories in early epochs, but later they asymptote at different levels. The trajectories for target units asymptote at a higher level than do those for competing units. At asymptote, the higher activation level of the target unit always indicates what the appropriate word response was. Operating under time pressure (such as when speech has to be produced rapidly) requires a speaker to generate words in the period where activation is still building up. The word response at this point would still be the one with highest activation. However, as the target and competing options have similar activation trajectories during buildup, noise in the activation process can lead to the competing options having highest activation and be triggered (resulting in a speech error) if word selection is made in this time region. Kolk and Postma propose that PWS have slow phonetic systems. The result is, effectively, that the amount of time in the buildup phase is extended. A word response generated at the same time as that of a fluent speaker will be “early” for these speakers and lead to a heightened chance of speech error arising for the same reason as with speech produced by fluent speakers under time pressure. As speech output is made early, responses will mainly involve the internal loop, which explains why the proportion of overt errors is not high in these speakers (Melnick & Conture, 2000; Wolk, Edwards, & Conture, 1993). There will, however, be evidence that a repair is being made based on the occurrence of retraces and pauses.

Thus, the CRH explains whole word repetition and hesitation as due to errors that are detected over the internal loop. Using the terms presented in the introduction, the CRH can be characterized as a linked theory where errors occur in the linguistic system. The second theory, like the CRH, also addresses why whole word repetition and hesitation occur, but it does not include the questionable perceptual monitoring component (operating over either the internal or the external loop), nor does it assume that such repetitions and hesitations are the result of errors made during production. In this model, the principal site of fluency problems (for speakers in general, not just speakers who stutter) is the language–speech interface. The description begins, after some general background, with the account of word repetitions and hesitations, and then the application of the theory to other known characteristics of stuttering is given.

EXPLAN Account of Stuttering

The EXPLAN model (Howell, 2004) argues that speech production involves independent planning and execution processes. Fluency failures such as repetition of prior words, pausing, prolongation and repetition of parts of the current word occur when the word to be produced is not ready (the planning process is not complete) by the time the execution of the previous word is concluded. EXPLAN can explain the behaviour of both fluent speakers and also the speech of speakers who stutter (SWS).

There are two influences that lead to the plan for the current word not being ready in time a) execution time of the prior word and b) planning time of the current word. Rapid execution of a preceding word advances the time at which the current word needs to be ready. Factors that make the current word complex lengthen its planning time and delay when it is ready. Execution time of the previous word is easily measured but an effective measure of word complexity has been harder to obtain. The connectionist models reported here compared two schemes which measure the phonetic complexity of words to see if they could predict which items in a stream of naturalistic speech from SWS were likely to be stuttered. Two multi-layer perceptron models were trained on the same data set of 6743 spontaneously produced words from eight SWS. For one model the words in the training set were represented by index of phonetic complexity (IPC) codes (Jakielski, 1998) and for the other the input was made up of analysis of phonetic structure (ANOphS) (Diment, Howell and Harris, in preparation) codes representing the words. The model was required to output a stuttered or a fluent response depending on the phonetic complexity of the word measured by either the IPC or ANOphS scheme. The models were tested using a further set of 1000 unseen words. While the model trained using the IPC codes could not learn to discriminate between stuttered and fluent items the ANOphS model demonstrated that it could learn the task. Further modelling is planned to test the EXPLAN model in which the ANOphS coding scheme will be used as a metric of phonetic complexity.

Role Avoidance theory

Sheehan (1970) defines stuttering as a disorder of the social presentation of the self. He sees it as essentially a conflict revolving around self and role, and states that therapy should be role specific. He further claims that the stutterer typically experiences no difficulty when alone and that the stuttering behavior requires both a listener and a speaker. The stutterer avoids the role of stutterer. This avoidance creates whole cognitive – emotional subliminal iceberg in the stutterer. According to Sheehan avoidance reduction is the key to stuttering reduction.

Psychoanalytical “Theories”

• Stuttering is the oral conflict between the instinctive need of the stutterer to stay on infantile oral level and his ego need of appropriate behavior. The anxiety in stutterers is due fear of their own autoeroticism” (Coriat, 1931)

• Stuttering is pregenital (anal) conversive (hysteric) neurosis. (Fenichel, 1945)

• Stuttering represents the need of the stutterer to defecate (anal fixation) on his parents (authorities). (Freud…)

• Stuttering is ambivalence stemming from the conflict between obedience, aggression or avoidance. It develops as a result of over demanding, perfectionist parenting style. (Barbara, 1954)

• Stuttering is attempt to avoid ones own verbal aggression toward the others, avoidance of hearting them. Stuttering is keeping ones own mother for oneself. (Goldsmit, 1988)

• Stuttering is expression of the child’s dissatisfaction and feebleness in his attempts to stop the father’s affections toward the mother (during the oedipal phase) (Estienne, 1996)

• Stuttering is unconscious need of speech removal, i.e. infantile oral fixation (Evely, 1982; Dolto, 1988)

• Stuttering is unconscious aggressive act toward the listeners (Fenichel, 1945)

• Stuttering appears because of the ambivalent behavior of the mother – aggressive gestures, interruptive speech, anxiety. The mother is “Stuttering wet-nurse”.

Conclusion and Discussion

As it is clearly seen, the scientific research places stuttering among the neurological disorders. The stuttering brain develops differently in the early childhood years; it processes the speech differently through virtually every brain part, involved in the speech production. The direct conclusion is: STUTTERING PRIMARILY IS NEUROLOGICAL DISORDER. During his social life the stuttering child develops lots of psychological subliminal cognitive schemes that interfere the emotional and social wellbeing. Regarding this, the psychoanalytical “researchers” make the mistake to postulate some emotional causes (most often preposterous) being reason for stuttering. As the scientific research shows, stuttering is pure neurological disorder and imposing some ridiculous “theories” as cause of stuttering includes lots of cognitive distortions in the process of logical thinking and secondly, imposes unneeded guilt on the stuttering mentality and the stuttering image.

On the other hand, psychological factors undoubtedly exist in stutterers. But they are mere consequence, logical conclusion of the neurological speech break down in the social conditions and emotional realization of PWS.

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