Exchange of stuttering from function words to content words with age. (1/165)

Dysfluencies on function words in the speech of people who stutter mainly occur when function words precede, rather than follow, content words (Au-Yeung, Howell, & Pilgrim, 1998). It is hypothesized that such function word dysfluencies occur when the plan for the subsequent content word is not ready for execution. Repetition and hesitation on the function words buys time to complete the plan for the content word. Stuttering arises when speakers abandon the use of this delaying strategy and carry on, attempting production of the subsequent, partly prepared content word. To test these hypotheses, the relationship between dysfluency on function and content words was investigated in the spontaneous speech of 51 people who stutter and 68 people who do not stutter. These participants were subdivided into the following age groups: 2-6-year-olds, 7-9-year-olds, 10-12-year-olds, teenagers (13-18 years), and adults (20-40 years). Very few dysfluencies occurred for either fluency group on function words that occupied a position after a content word. For both fluency groups, dysfluency within each phonological word occurred predominantly on either the function word preceding the content word or on the content word itself, but not both. Fluent speakers had a higher percentage of dysfluency on initial function words than content words. Whether dysfluency occurred on initial function words or content words changed over age groups for speakers who stutter. For the 2-6-year-old speakers that stutter, there was a higher percentage of dysfluencies on initial function words than content words. In subsequent age groups, dysfluency decreased on function words and increased on content words. These data are interpreted as suggesting that fluent speakers use repetition of function words to delay production of the subsequent content words, whereas people who stutter carry on and attempt a content word on the basis of an incomplete plan.  (+info)

Developmental stuttering and Parkinson's disease: the effects of levodopa treatment. (2/165)

The effects of dopamine on developmental stuttering was studied in a 44 year old man with developmental stuttering and Parkinson's disease during three levodopa "on" periods and three "off" periods. When compared with the "off" periods, during the "on"' periods he demonstrated an increase of speech dysfluencies. These findings lend support to the dopamine hypothesis of developmental stuttering.  (+info)

Single word reading in developmental stutterers and fluent speakers. (3/165)

Ten fluent speakers and nine developmental stutterers read isolated nouns aloud in a delayed reading paradigm. Cortical activation sequences were mapped with a whole-head magnetoencephalography system. The stutterers were mostly fluent in this task. Although the overt performance was essentially identical in the two groups, the cortical activation patterns showed clear differences, both in the evoked responses, time-locked to word presentation and mouth movement onset, and in task-related suppression of 20-Hz oscillations. Within the first 400 ms after seeing the word, processing in fluent speakers advanced from the left inferior frontal cortex (articulatory programming) to the left lateral central sulcus and dorsal premotor cortex (motor preparation). This sequence was reversed in the stutterers, who showed an early left motor cortex activation followed by a delayed left inferior frontal signal. Stutterers thus appeared to initiate motor programmes before preparation of the articulatory code. During speech production, the right motor/premotor cortex generated consistent evoked activation in fluent speakers but was silent in stutterers. On the other hand, suppression of motor cortical 20-Hz rhythm, reflecting task-related neuronal processing, occurred bilaterally in both groups. Moreover, the suppression was right-hemisphere dominant in stutterers, as opposed to left-hemisphere dominant in fluent speakers. Accordingly, the right frontal cortex of stutterers was highly active during speech production but did not generate synchronous time-locked responses. The speech-related 20-Hz suppression concentrated in the mouth area in fluent speakers, but was evident in both the hand and mouth areas in stutterers. These findings may reflect imprecise functional connectivity within the right frontal cortex and incomplete segregation between the adjacent hand and mouth motor representations in stutterers during speech production. A network including the left inferior frontal cortex and the right motor/premotor cortex, likely to be relevant in merging linguistic and affective prosody with articulation during fluent speech, thus appears to be partly dysfunctional in developmental stutterers.  (+info)

Stuttering: an update for physicians. (4/165)

Stuttering is a disturbance in the normal fluency and time patterning of speech. Developmental stuttering (DS), with or without associated psychiatric illness, is the most common form and includes all cases with gradual onset in childhood that are not the result of acquired brain damage. Persistent developmental stuttering (PDS) is DS that has not undergone spontaneous or speech-therapy-induced remission. Organic models of DS focus on incomplete lateralization or abnormal cerebral dominance. There is also evidence that DS has a significant genetic component to its cause. Neuroimaging research data and the effectiveness of dopamine receptor antagonists in DS seem to support the theory of a hyperdopaminergic origin. Speech therapy remains the main treatment for DS; however, antidepressants can be useful in selected cases. Risperidone, a serotonin-dopamine antagonist, has been shown to be more effective than placebo in decreasing the severity of stuttering. The long-term efficacy and safety of serotonin-dopamine antagonists in DS deserve further study.  (+info)

Subcortical infarction resulting in acquired stuttering. (5/165)

Stuttering is an uncommon presentation of acute stroke. Reported cases have often been associated with left sided cortical lesions, aphasia, and difficulties with other non-linguistic tests of rhythmic motor control. Three patients with subcortical lesions resulting in stuttering are discussed. In one patient the ability to perform time estimations with a computerised repetitive time estimation task was characterised. One patient had a pontine infarct with clinical evidence of cerebellar dysfunction. A second patient had a left basal ganglionic infarct and a disruption of timing estimation. A third patient had a left subcortical infarct and a mild aphasia. These findings expand the reported distribution of infarction that can result in acquired stuttering. Subcortical mechanisms of speech control and timing may contribute to the pathophysiology of acquired stuttering.  (+info)

Brain correlates of stuttering and syllable production. A PET performance-correlation analysis. (6/165)

To distinguish the neural systems of normal speech from those of stuttering, PET images of brain blood flow were probed (correlated voxel-wise) with per-trial speech-behaviour scores obtained during PET imaging. Two cohorts were studied: 10 right-handed men who stuttered and 10 right-handed, age- and sex-matched non-stuttering controls. Ninety PET blood flow images were obtained in each cohort (nine per subject as three trials of each of three conditions) from which r-value statistical parametric images (SPI inverted question markr inverted question mark) were computed. Brain correlates of stutter rate and syllable rate showed striking differences in both laterality and sign (i.e. positive or negative correlations). Stutter-rate correlates, both positive and negative, were strongly lateralized to the right cerebral and left cerebellar hemispheres. Syllable correlates in both cohorts were bilateral, with a bias towards the left cerebral and right cerebellar hemispheres, in keeping with the left-cerebral dominance for language and motor skills typical of right-handed subjects. For both stutters and syllables, the brain regions that were correlated positively were those of speech production: the mouth representation in the primary motor cortex; the supplementary motor area; the inferior lateral premotor cortex (Broca's area); the anterior insula; and the cerebellum. The principal difference between syllable-rate and stutter-rate positive correlates was hemispheric laterality. A notable exception to this rule was that cerebellar positive correlates for syllable rate were far more extensive in the stuttering cohort than in the control cohort, which suggests a specific role for the cerebellum in enabling fluent utterances in persons who stutter. Stutters were negatively correlated with right-cerebral regions (superior and middle temporal gyrus) associated with auditory perception and processing, regions which were positively correlated with syllables in both the stuttering and control cohorts. These findings support long-held theories that the brain correlates of stuttering are the speech-motor regions of the non-dominant (right) cerebral hemisphere, and extend this theory to include the non-dominant (left) cerebellar hemisphere. The present findings also indicate a specific role of the cerebellum in the fluent utterances of persons who stutter. Support is also offered for theories that implicate auditory processing problems in stuttering.  (+info)

Non-word reading, lexical retrieval and stuttering: comments on Packman, Onslow, Coombes and Goodwin (2001). (7/165)

A recent study by Packman, Onslow, Coombes and Goodwin (2001) employed a non-word-reading paradigm to test the contribution of the lexical retrieval process to stuttering. They consider that, with this material, the lexical retrieval process could not contribute to stuttering and that either anxiety and/or the motor demand of reading are the governing factors. This paper will discuss possible processes underlying non-word reading and it argues that the conclusion arrived at by Packman et al. does not stand up to close scrutiny. In their introduction, the authors acknowledge that the lexicalization process involves retrieval and encoding of words. In a non-word-reading task, the word retrieval component is eliminated. The possibility that the encoding component of the lexicalization process leads to stuttering is, however, completely ignored by the authors when they attribute stuttering to motor demands. As theories put forward by Postma and Kolk (the Covert Repair Hypothesis, 1993) and Howell and Au-Yeung (the EXPLAN theory, 2002) argue heavily for the role of the phonological encoding processes in stuttering, Packman et al.'s work does not evaluate such theories. Theoretical issues aside, Packman et al.'s arguments about reading rate and stuttering rate based on reading time is also questionable.  (+info)

Sociodynamic relationships between children who stutter and their non-stuttering classmates. (8/165)

BACKGROUND: Previous research has indicated that children who stutter are more likely to be bullied and to hold a lower social position than their peers who do not stutter. However, the majority of this research has used data from respondents who were in the educational system more than 20 years ago. The current policy on integration of children with severe disabilities into mainstream education and the increased awareness of bullying in schools would indicate that attitudes toward children who stutter might have changed in the intervening period. METHOD: The study uses a sociometric scale (adapted from Coie, Dodge, & Coppotelli, 1982) to assess children who stutter in classroom groups with fluent peers. The peer relationships between 16 children who stutter and their classmates (403 children in total) were examined. RESULTS: Children who stutter were rejected significantly more often than were their peers and were significantly less likely to be popular. When compared to children who do not stutter, the children who stutter were less likely to be nominated as 'leaders' and were more likely to be nominated to the 'bullied' and 'seeks help' categories. CONCLUSIONS: The changes in integration policy and the implementation of anti-bullying policies in many schools appear to have made little impact on the social status of children who stutter. The incidence of bullying and rejection reported in this study has implications for schools and clinicians.  (+info)