Note
Studied by 6 people
Constitutional Factors in Stuttering
Introduction
Constitutional factors are aspects of a person's makeup that influence stuttering.
Understanding these factors can help in counseling people who stutter and reassuring parents.
Stuttering has a biological basis, but its impact can be overcome.
Many successful people have stuttered (e.g., Emily Blunt, James Earl Jones, Joe Biden).
Research into constitutional factors may lead to new and effective interventions.
A video titled "Process of Research" on LipanCot Connect outlines the stages of research.
This chapter covers heredity, childhood brain injury, trauma, and brain differences related to stuttering.
Figure 2.1 gives an overview of the areas covered.
Hereditary Factors
Traits are often inherited from parents.
Gregor Mendel's pea experiments revealed principles of genetic inheritance, including equal parental contributions and dominant/recessive traits.
Charles Darwin, who likely inherited stuttering, proposed the theory of evolution by natural selection.
Useful traits for survival are passed on to future generations.
Stuttering and Inheritance
The idea that stuttering runs in families has long been recognized.
Some argued that stuttering is due to inherited neurological differences.
Others claimed that critical attitudes toward normal disfluency are passed down, leading to a cycle of fear and hesitations.
Currently, there is broad agreement that stuttering is frequently inherited.
Genes do not work alone; heredity and environment interact with elements of chance.
Example
Tomato plants from the same seed packet were grown in different environments (warm vs. cold).
The environment had a strong effect on their development.
Stuttering Example
A child may inherit genes predisposing them to stutter, but a low-key environment may prevent its development.
Another child with similar genes may stutter in a fast-paced environment.
Approaches to Studying Heredity and Stuttering
Four approaches: family studies, twin studies, adoption studies, and genetic studies.
These methods complement each other, providing converging insights.
Insights are vital in counseling individuals and families.
Studies have become more rigorous over time.
Family Studies
Early studies provided clear evidence of a strong genetic component but had weaknesses.
Weaknesses
Only families with stuttering were studied, without control families.
Subjects were adults recalling family history, excluding those who recovered as children.
Parent reports, rather than observations, were used to determine stuttering.
Early Reports
A Newcastle, England study compared family histories of children who stuttered with those who didn't.
Children who stuttered had more relatives who stuttered.
Males were more likely to stutter, but females who stuttered were more likely to have relatives who stuttered.
Yale University researchers confirmed that males are more vulnerable, and females are more resistant.
These patterns are best explained by an interaction between environment and multiple genes.
University of Illinois Studies
Studied family histories of children newly diagnosed with stuttering.
Found that children who stuttered had more stuttering relatives.
Male and female children had similar chances of having relatives who stuttered.
Recovery is more frequent among females, and persistence tends to run in families.
Persistent and recovered stuttering may be transmitted by the same genes, with additional genetic factors affecting recovery.
Vishwanath et al.
Hypothesized that persistent and recovered stuttering are two genetically different disorders.
Confirmed that stuttering is inherited through a dominant gene.
Found that males are more susceptible, and inheritance is more likely from parents than distant relatives.
Clinical Relevance of Family Studies
Clinicians can ask families about relatives who stuttered and whether they recovered.
Inform parents about the likelihood of inherited stuttering to relieve guilt.
Example of Relief from Understanding Inheritance
A man whose parents stuttered felt comfortable talking about his own stuttering with his son and reassuring him that stuttering was okay; His son grew up with only a mild stutter and no self-consciousness about it.
Predicting Recovery or Persistence
Yeri et al. (1996) found that predictors of recovery include good phonology, language, nonverbal skills, family members' recovery from stuttering, and early age of onset.
Factors that impede recovery may be determined by other genes.
Yeri and Ambrose (1999) expanded this list.
Factors Predicting Recovery
Good phonology, language, and nonverbal skills.
Family members who recovered.
Early age of onset.
Being female.
Decreasing severity and frequency of stuttering.
Currently stuttering less than a year.
Having fewer repetition units and slower repetitions.
Decreasing prolongations and blocks.
Suggestions for Future Family Studies (Yeri et al., 1996)
Look for subgroups of stutterers with different genetic etiologies.
Examine family members who don't stutter to find factors that may resist stuttering.
Search for environmental factors that interact with genetic factors.
Subramanian and Yeri (2006)
Conducted a study of family members, turning up a factor that may have helped them resist stuttering.
Finger tapping task: stutterers, their fluent family members, and a control group were studied.
Stutterers tapped faster than family members or controls in the fast tapping condition, but showed greater variability.
Family members had the slowest tapping rate with little variability.
Resisting speaking faster than their natural rate may help them be fluent.
Nandini Devi et al. (2018)
Studied consanguineous families (parents genetically related) in Tamil Nadu, India.
Prevalence of stuttering was low (0.46%).
Family aggregation of stuttering was higher in families where parents were related.
Twin Studies
Stuttering occurs more often in both members of identical (monozygotic) twin pairs than fraternal (dizygotic) twin pairs.
This supports the hypothesis that stuttering is inherited.
Higher concordance of stuttering in identical twins.
Heredity Does Not Work Alone
Some identical twin pairs are discordant (one twin stutters, the other doesn't).
Genes interact with the environment.
A gene might not express itself in stuttering unless there is prenatal or postnatal stress.
Andrews et al. (1991)
Studied 3,810 twin pairs.
Estimated that 71% of the variance was accounted for by genetic factors, and 29% by the environment.
Felsenfeld et al. (February)
Studied a new sample of 1,567 twin pairs.
Additive genetic effects accounted for 70% of the variance.
Individual's unique environment accounted for 30% of the variance; supports that genes and environment interact.
Oke (2005)
Studied 1,896 twin pairs.
Determined that the proportion of genetic influence on stuttering in males was 80% and 85% in females.
Females' rate of stuttering showed slightly more genetic influence, echoing evidence that females have some resistance to stuttering; more genetic influence is needed for a female to develop stuttering.
Dworzynski et al (02/2007)
Discovered differences between twins who recovered and those who persisted.
Recovered group: 40% concordance for identical twins, 20% for fraternal twins.
Persistent stuttering group: 19% concordance for identical twins, 0% for fraternal twins.
Genetics of persistent stuttering are complex; persistent stuttering may have additional genetic factors.
Van Bechter Velvet et al (02/2010)
Used a very large participant pool of 105,000 twin pairs at age 5.
Parents estimated the frequency of repetitions, prolongations, and blocks in their children's speech.
Concordance for probable stuttering was higher in identical twins.
High non-fluency was also genetically based.
Fagnani et al (02/2011)
Used a large participant pool of 33,317 adults from the Danish twin registry.
Questionnaires ascertained whether they had ever stuttered.
9% of males and 4% of females reported stuttering at some point in their past.
Greater concordance in monozygotic twins.
70% of the variance was due to heredity; 30% was due to environment or environment-gene interaction.
Radzikovsky et al (February)
Self-report from adults in a study of 1,728 twins in Finland.
82% of the variants could be attributed to additive genetic effects, and 18% to non-shared environmental influences.
Frigerio Dominguez and Draina (2017) Assessment
Monozygotic twins consistently display a higher concordance for stuttering than dizygotic twins, indicating strong evidence for a genetic component.
Monozygotic twin concordance is not 1, meaning germline genetic factors do not explain all stuttering; heritability estimates vary, but many produce estimates of high heritability, often exceeding 0.80.
Aside by Bloodstein et al. (2021)
Questioned the assumption that influence on stuttering not accounted for by genetic factors must be attributed to environmental factors.
Identical twins have discordance for traits due to variations in embryo development.
Some variations may be related to epigenetics.
Epigenetics
Non-DNA factors that are inherited and influence the expression of genes' effects on specific behaviors or phenotypes.
Adoption Studies
Difficult to conduct due to birth record access.
Offer larger contrasts in environmental factors.
Bloodstein (1961)
Interviewed 13 adopted stutterers about the presence of stuttering in their adoptive families.
4 of the 13 reported having relatives who stuttered in their adoptive families, higher than expected by chance.
Small sample without data from biological families only supports the possibility of the environmental effect.
Felsenfeld (1997)
Reported preliminary data on adopted children with speech disorders.
History of stuttering in biological families was slightly more predictive than stuttering in the adoptive family.
Genetic inheritance appears to contribute more strongly.
Genes
The basis of inheritance; sequences of DNA that determine traits.
Genes reside on chromosomes, strings of DNA in every cell.
Genetic Linkage Studies
Difficult to understand; a video by The Stuttering Foundation explains Dennis Draina's work in this area.
Genetic lineage refers to the fact that genes related to a disorder may be physically close together on the chromosome when they are inherited.
Genetic linkage analysis compares the chromosomes of family members who have a trait with those who do not.
Stuttering is thought to be polygenic -- the result of more than 1 gene.
Draina and Colleagues at NIH
Examined 68 families in North America and Europe.
Found evidence that genes on chromosome 18 may be related to stuttering in these families.
May be genes that control intercellular communication; disordered intercellular communication may lead to dyscoordinated info for speech production.
Draina and Geneticists in Lahore, Pakistan
Chose Pakistan because tradition encourages marriage within families, producing less genetic variation and greater concentration of genetic disorder.
Kang et al. (02/2010)
Published a study in the New England Journal of Medicine.
Included 123 Pakistani individuals who stuttered and 270 individuals in the US and England who stuttered.
Control group of 372 individuals in these 3 countries who did not stutter.
Mutations of three genes (GNPTAB, GNPTG, and NAGPA) on chromosome 12 were found to be associated with stuttering.
Some individuals showed mutations of gene GNPTAB.
Others had mutations on GNPTAB.
Still others had mutations on NAGPA.
The work of all three genes is related to controlling enzymes in a cell's lysosome structure, the part of a cell involved in recycling cell waste products.
Known genetic disorders (mucolypidosis) of this waste recycling process affect joint, skeletal, and other body components and brain development, resulting in delays in movement coordination; some forms are accompanied by speech problems.
One of the genes, GNPTG, is associated with motor control and emotional regulation by way of the gene's expression in the cerebellum and the hippocampus.
Lee et al. (2011)
Provided evidence that mutations in one of these genes, NAGPA, may cause stuttering.
Effect of the mutations is to diminish enzyme activity in cells.
Not enough is known about how neuronal deficits affect speech to explain how these mutations result in stuttering, but it has been hypothesized that diminished activity related to lysosomal processing may underlie incomplete myelination of white matter tracts important in speech motor control.
Buddha et al. (02/2014)
Through a meta-analysis of many studies of differences in individuals who stutter, they concluded that the diminished activity related to lysosomal processing may underlie incomplete myelination of white matter tracts important in speech motor control.
The incomplete myelination hypothesis will be discussed again when eye present findings on white matter tracts, the brain's connecting pathways.
For more than 70 years, there have been hypotheses that incomplete myelination contributes to stuttering.
Rasa et al (02/2015)
Another gene, AP4E1, was found to be associated with stuttering and also involved in lysosomal processing.
Frigerio Dominguez and Draina (2017)
Because no other neurological deficits appear with stuttering when one of the genes is mutated, the pathology seems to be limited to a small and specialized population of neurons.
Mice that have been given mutations of GNPTAB have shown stuttering-like vocalizations.
Benito Aragon et al (02/2020)
Using neuroimaging and graph theory, suggested that mutations in the gene GNPTAB may be associated with disruption in cortical networks that support auditory motor integration for speech motor control.
Problems in auditory motor integration may be an important element in stuttering.
Auditory motor integration dysfunction is part of the basic neuropathology of stuttering, rather than the result of brain changes caused by years of stuttering.
Genome Wide Association Study
Examine the DNA of a large number of individuals who have a disorder and compare them with the DNA of a large number of individuals who don't have
This comparison is hoped to reveal genetic differences between the two groups to pinpoint genes that may be responsible for the disorder.
Genome wide studies look at large populations and linkage studies look within families.
Kraft (2010)
Conducted a genome-wide association analysis of the genes of 84 persistent stutterers and 107 controls in which the DNA of a population of unrelated individuals is examined.
She scanned the DNA of all of her participants, looking for markers that distinguish the DNA of stuttering participants.
She didn't find a single gene that clearly characterized stuttering.
These findings found (1) neural development (2) neural function and (3) behavior.
Kraft points out that future research should look for combinations of genes that are related to stuttering.
Congenital and Early Childhood Trauma Studies
Alternative causal explanations of stuttering.
May account for individuals with no family history of stuttering.
No Heredity of Stuttering
West et al. (1939)
Examined 204 people who stuttered; 100 reported no family members who stuttered.
85 of these 100 reported congenital factors or early childhood stressors.
Stressors included infectious diseases, nervous system diseases, and injuries prior to stuttering onset.
These factors may have created a trigger for stuttering, but the exact mechanisms are unknown.
Kulos and Webster (1991)
57 of 169 clients reported no family history.
37% of these reported congenital or early childhood factors, while 2.4% of those with family history reported such factors.
Factors included anoxia, premature birth, surgery, head injury, mild cerebral palsy, mild regurgitation, and intense fear.
Story from New York Times (Avi Habib, 2022)
A man named Raul recalled his childhood experiences during a bombing in the Lebanon civil war.
Developed a stutter afterwards, which was likely triggered by the trauma.
Alman Risperd (2007)
Examined 32 individuals who stuttered to look for etiological subgroups.
72% had family histories.
53% had sustained neurological lesions prior to onset.
7 of 9 individuals with no family history reported pre-onset neurological lesions.
Supports the hypothesis that genetics inheritance and brain injury both contribute.
Bob (1968)
Examined a sample of 313 individuals who sustained brain damage at birth or in early childhood.
24% developed stuttering, compared to 5% in the general population.
Indicates that congenital or early childhood brain injury can often result in stuttering.
Sagalowicz and Brown (1991)
Surveyed 600 high school students to ascertain how many had experienced head injury during their childhoods.
Of 92 students who reported head injury, 9 reported having been diagnosed with stuttering.
It was not clear if stuttering appeared after the head injury.
There was a significant relationship between having a head injury and being diagnosed with stuttering, particularly for those children who were unconscious for a period of time after the head injury.
Oscar and Oscar (2019)
Evaluated 64 stuttering children younger than age 18 in Turkey.
21% had family histories.
31.3% had experienced life stressors within a week of stuttering onset, including the death of their mother, birth of a sibling, starting primary school, and moving to a new home.
Diagnosis were made at either a psychiatric clinic or an end clinic.
Similar mechanisms to adult onset stuttering that are often associated with head injury, neurological disease, stress, or psychological trauma.
The same mechanisms may be involved in childhood stuttering in the absence of a family history of stuttering.
Why would some children and adults, but not others, begin to stutter as a result of intense fear or brain injury?
Which brain structures and functions affected by head injury and neurological disease result in stuttering?
How are they similar to and how do they differ from the effects of inheriting a predisposition to stutter?
No Difference in Stuttering Behavior From Family History (Andrews and Harris, 1964, and Kidd et al., 1980)
Janssen et al, 1990 then looked at a wider variety of speech and language-related variables between the 2 groups
They found several significant differences, as well as similarities between the group with family histories of stuttering and the group without such histories.
The groups did not differ significantly in responsiveness to treatment, reading ability, or speech-related anxiety.
Those with family histories of stuttering showed more prolongations and blocks than those with no family history of stuttering.
Those with positive family histories for stuttering showed significantly longer durations of voice segments of speech and significantly greater variability in length of unvoiced segments during fluent speech.
The authors interpreted this finding to suggest that the stutterers with positive family histories were slower and more variable in their fluent speech.
Conclusion
Those with family histories of stuttering have inherited greater neuromotor instability than those without family histories of stuttering, an instability that produces more prolongations and blocks and that may require individual to speak more slowly to maintain fluency.
Those without a family history of stuttering may have a family history of other speech and language disorders.
Brain function and structure
Brain functions and structures are the link between what you've just been reading about, genetic predisposition or childhood trauma, and the behaviors of stuttering that we see in here.
When someone has a genetic predisposition for stuttering or has had childhood trauma, we ask, how does that affect the brain in a way that results in stuttering?
Benito Aragon et al 02/2020 found that the gene GNPTG affect auditory motor integration for speech
Brain function differences
Early research looked at brain function rather than structure due to technology limits.
Cerebral Dominance For Speech
Studies have shown that individuals who stutter have greater activity in their right hemispheres than in their left hemispheres during both fluent and stuttered speaking
Brain of adults who stuttered was often in the same location in the right hemisphere as those active in left hemisphere, known as homologous areas..
This pattern suggests that left hemisphere structures for speech and language in individuals whose stutter may have developed more slowly or differently in ways that contribute to stuttering.
Electroencephalographic studies
Samuel Orton and Lee Edward Travis used EEG to measure brain waves
Their hope was to find proof that the brains of stutterers didn't show the normal left hemisphere dominance during speech and that this difference might account for the mistiming of signals sent from the brain to muscles of the speech production system.
Despite problems, EEG studies have produced interesting findings.
Findings
Studies showed that individuals who stutter tended to have more activity on the right side of the brain during speech than did those who didn't stutter.
These findings suggest that rather than lacking dominance, individuals who stutter may be more likely to have a right hemisphere dominance for speech and language, whereas non-stutterers generally have left hemisphere dominance for speech and language.
Cerebral Blood Flow Studies, A More Detailed Look At Different Areas Of The Brain
Researchers used a radioactive tracer to detect blood flow in the brain
The greater the amount of neural activity in an area, the greater the blood flow in that area, and the greater the amount of radioactivity given off.
Wood et al 1980
Published the first study of CBF in stuttering using only two participants.
Researchers found greater activity in the right hemisphere region corresponding to Broca's area, the right frontal operculum during stuttering before treatment with the drug haloperidol.
After two weeks of treatment with haloperidol, both participants showed that the greater activity had shifted from right to left hemisphere speech areas.
Poole et al 1991
Studied the brains of 20 adults who stuttered using single photon emission computed tomography scan, an improved technology that enabled scientists to view the brain from multiple angles and obtain better images of what was going on.
The principal finding from this study was that the stuttering group showed less left hemispheric dominance compared to controls in areas that are believed to be associated with language processing.
Positron Emission Tomography Studies and Beyond
In 1995, another CBF study took advantage of a new brain imaging tool, positron emission tomography, which allowed researchers to make more accurate inferences about where increased blood flow was occurring in the brain.
Wu et al. 1995
Studied the brains of four adults who stuttered and a controlled group in two conditions - reading aloud alone and reading in unison with someone else (choral reading).
Research revealed that two important speech and language areas of the brain, Broca's area and Wernicke's area, both in the left hemisphere showed decreased activity compared to their normal speaking controls when participants were stuttering under typical speaking conditions compared to when they were fluent during choral reading.
These functions may have been shifted away from Broca's and Wernicke's areas to write hemisphere homologous areas in these stutterers when they were stuttering.
Because choral reading provides external timing cues, it compensated for poorly timed speech, allowing fluency in the use of left hemisphere typical speech structures.
Clear Evidence
Researchers identified that the brains of people who stutter work differently than those of people who don't. Years of previous speculation and studies suggesting anomalous cerebral dominance, inadequate laterality, auditory processing problems, and language dysfunction in stuttering seem to be confirmed.
The anomalies the suggest are organized by whether they are overactivations or underactivations in various areas of the brain, brain changes after stuttering therapy and anomalies in the structure and functions of white matter nerve tracts that convey information.
Brain Overactivation During Stuttering
Certain areas of the brain show higher levels of activation in those who stutter than in controls, sometimes during stuttering and sometimes during fluent speech..
Some overactivations may be important etiological factors, while others may be compensatory.
Overactivation of Right Hemisphere Cortical Areas
Individuals who stutter demonstrate high levels of activity in the right hemisphere, especially when they are stuttering (focus of activity is greatest in right hemisphere structures that are homologous to those in the left hemisphere used by speakers who don't stutter).
Another area in the right hemisphere commonly found to be active during stuttering is the right insula itself.
Braun et al 02/2005
Conducted a meta analysis comparing many brain studies that included people who stuttered and controls.
A major abnormality in those who stutter was a general over activation of right hemisphere areas that are homologous to left hemisphere areas active for speech production.
Overactivity in left hemisphere areas related to motor control of speech compared to nonstuttering peers.
There are two possible explanations for overactivation of right hemisphere structures during stuttering:
During embryonic development, the right side of the brain, instead of the left, becomes wired to be the primary speech and language area. Right hemisphere structures are not generally suited for the rapid processing of signals required for speech. At multiword utterances, stuttering may emerge as they try to produce at faster speech rates. Ken 1984. Malikot 1972
The child who stutters initially tries to use left hemisphere regions for speech and language, but the neural networks do not function adequately and result in stuttering. Then Child's brain begins to use right hemisphere structures in a compensatory way to try to achieve more normal speech; they implore right hemisphere structures to compensate for damaged areas in the left hemisphere. Sommer 02/2002
Supporting Evidence for the 2nd compensation hypothesis:
Activations of right hemisphere sensory areas were negatively correlated with stuttering (these regions became more active as speech became more fluent).
Right hemisphere activations were greater in participants who stuttered moderately compared to those who stuttered severely.
Still Future Research Could Clear Up Which Hypotheses Are Correct In A Specific Patient
Some individuals develop right hemisphere processing for speech and language before they begin to stutter.
Other develop right hemisphere processing after they begin to stutter as a compensatory response.
Still others may, in fact, process speech and language in both hemispheres simultaneously.
Overactivation in Midbrain Areas
Midbrain: situated beneath the cortex and is the top section of the brainstem.
Researchers reported high levels of activity in midbrain structures that may disrupt smooth speech movements.
Some structures of the basal ganglia have been shown to be overactive in stutterers..
A number of neuroscientists developed models of stuttering based on the motion of basal ganglia circuit malfunction.
Basal ganglia play an important role in the corticobasal ganglia, Thalamocortical loop that provides timing signals to the supplementary motor area, SMA of the cortex to initiate motor programs for speech..
In fluent speech, the SMA acts on this timing information from the basal ganglia thalamus to generate the appropriate speech movements for the desired phonemic sequence.
In stuttering, theorists propose that over activation in the production of the neurotransmitter dopamine causes the timing information to be modeled so that the smooth production of syllables is disrupted.
Brain Underactivation During Stuttering
Motor and sensory centers in the brain have been found to be underactive in stuttering.
Underactivation in Speech Motor Areas
During speech production, individuals whose stutter showed decreased activity compared to controls in areas related to using sensory and motor information and planning sequential movements on both sides of the brain.
Watkins et al point out that deficits present serious problems because the left hemisphere deficits some stutterers have has been found to compensate
Underactivation in Auditory Areas
Many brain imaging studies of stuttering have shown a lack of activity in the superior temporal lobe, including auditory association areas.
Thus, asynchrony or timing disturbance that many see as the basis of stuttering is caused by a paucity of signals..
Therapies that emphasize the use of increased explicit attention to their speech by speakers may increase the amount of information available for synchronizing speech by focusing on another feedback modality.
Dysfunction of internal timing cues from the basal ganglia from external timing cues.
Other functions besides monitoring one's own speech may also reside in the under activated regions of the auditory cortex.
Activation of this region of the brain may be a key stage in phonological planning for speech production; a Lack of adequate activation during stuttering may reflect a deficit in the sequence of phonological selection, phonetic planning, and motor execution.
Connectivity Deficits in White Matter Tracts
In a study of adults who stutter, connectivity deficits in white matter tracts were found in the left hemisphere that linked areas and premotor corex.
Heightened functional connectivity for stutterers compared to nonstutterers in the right hemisphere may have been a compensation for left hemisphere deficits.
In one of the first multimodal neuroimaging studies of young children, structural and functional connectivity were compared in white matter tracts in 56 children three nine years old who stuttered versus their fluent peers -- deficiencies in the networks connecting auditory pathways and amblyophthalamocorticoids in children who stuttered were found. Girls who stutter have higher connectivity and auditory motor tracks than boys who stutter
Brain Structure Differences
After the year 2000, research on structural differences in brains of people who stutter started to increase
They examined the brain anatomy of adults who stuttered by measuring the shape, size, and density of speech and language areas.
Findings suggest that sensory, planning, and motor areas in the left hemisphere of these individuals developed differently from those in matched non-stittering individuals.
Wide matter tracts, which convey information from sensory centers in the left hemisphere to motor execution areas of the left hemisphere have been shown to be less dense than those in typical speakers.
Differences
Recovered group compared to those who hadn't recovered into a control group of age-matched children who had never stuttered.
Both recovered and persistent stutterers had reduced volumes of gray matter around Broca's area.
Auditory perception of speech showed reduced volume in bilateral temporal lobe areas.
Persistent stutterers, but not the subgroup who recovered showed less dense white matter tracts connecting areas associated with phonological representations of sounds to speech motor execution areas.
Sikowsky et al (02/2010),
The most robust difference between adults who stutter and those who don't is in left hemisphere white matter fiber tracts that communicate between the inferior parietal cortex, sensory integration in the ventral frontal cortex and motor planning.
Nerve fibers aren't structured as effectively to conduct impulses along the directional flow of the nerve bundle, called reduced connectivity in white matter tracts, which is not as fast as it could be.
Superior Longitudinal Fasciculus
Connects speech output planning areas of the ventral frontal cortex with sensory motor integration areas of the inferior parietal lobe.
Carlin
The basic cause for stuttering is a delay in the myelination of the cortical areas in the brain concerned with speech.
Myelin sheath functions to insulate nerves
Incomplete myelination of some nerves results in slower transmission in those nerves, and bus, where many different nerves are working together in the network the slow transmission in some nerves but not others could result in action that are less well coordinated.
Myelination occurs earlier in girls than in boys, which may help explain the greater persistence of stuttering in boys.
Effect of Reduced Myelination
Increased stuttering during high levels of emotion be the result of disruptions in neurotransmission in poorly myelinated white matter tracts and speech areas of the brain.
Longer sentences spoken more quickly put stress on the left-hemisphere areas responsible for phonological word-storage
Other Studies
Study by was the first to show white matter deficits in many areas of the brain in young children who stutter to suggest what might distinguish recovery from persistence, and to find connectivity differences that distinguish mild and moderate stuttering from severe stuttering
They found that increased connectivity was present in the right rather than left frontal islant track.
Does this mean that the more severely stuttering subjects had left fat areas that function poorly for speech initiation, and they activated right hemisphere areas in an attempt to compensate?
They found that the ventral laryngeal motor cortex neural networks had less connectivity in stuttering subjects compared to fluent subjects as well as less connectivity than the connections in participants experiencing more severe stutters
In particular, white matter integrity was significantly lower in the arcuate fasciculus that connects left temporal parietal junction and posterior temporal gyrus. Deficits in white matter integrity were also found in the corpus callosum and fibers connecting bilateral motor regions in the children who stuttered. Suggested to interfere with integration of sensory feedback and speech movements, as well as limiting the ability of the left and right motor cortices to work together.