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For a long time, stuttering has been misunderstood as a psychological flaw, a bad habit, or a result of parenting styles.1 However, decades of neuroscientific research have fundamentally overturned these notions, clearly defining stuttering as a complex neurodevelopmental disorder with a genetic predisposition.3 From a modern perspective, stuttering is understood not merely as a phenomenon of getting stuck on words, but as a condition with fundamental issues in the timing and connectivity of the neural circuits responsible for planning, initiating, and executing the complex motor sequences required for speech.7 The core of this understanding is that stuttering is a biological phenomenon originating from the structural and functional characteristics of the brain, not a problem of an individual's will or personality.
Historically, the causes of stuttering were attributed to various speculations, such as the forced correction of left-handedness or childhood trauma.1 These misconceptions placed unnecessary guilt and social stigma on individuals who stutter and their families.2 However, advancements in genomic research, brain imaging technology, and neurophysiology have clearly illuminated the neurobiological underpinnings of stuttering, presenting a new paradigm. It is now widely accepted that stuttering originates from the abnormal development and function of specific neural networks in the brain, particularly the left-hemisphere network responsible for language processing and motor control.
This report aims to comprehensively analyze and present the latest scientific understanding of stuttering. To this end, it will first explore the results of large-scale genome studies that have uncovered the genetic architecture of stuttering and the biological reasons for the gender disparity in its incidence. Next, it will delve into the structural and functional characteristics of the brain in people who stutter, as revealed by brain imaging studies, with a particular focus on deficits in white matter connectivity and the dysfunction of the cortico-basal ganglia-thalamo-cortical circuit. The report will also analyze how stuttering interacts with cognitive and emotional functions and the neurobiological mechanisms by which stress and anxiety exacerbate stuttering. It will explain the neurological principles behind the improvement of fluency in specific situations like singing or acting, clarify the impact of a bilingual environment on stuttering, and clearly distinguish the key differences between developmental and neurogenic stuttering. Finally, based on this scientific understanding, the report will highlight the positive changes (neuroplasticity) that speech therapy induces in the brain and conclude by forecasting the potential of future innovative treatment technologies such as pharmacotherapy, neurostimulation, and brain-computer interfaces. Through this process, this report will provide a multidimensional and integrated understanding of stuttering and seek directions for effective, evidence-based intervention strategies.
The most definitive evidence that stuttering has a strong biological basis, which cannot be explained by psychological or environmental factors alone, comes from genetic research. Stuttering tends to run in families, suggesting that genetic predisposition plays a significant role.10 In fact, approximately 70% of people who stutter report a family history of the disorder 11, and twin studies have shown that the genetic contribution to stuttering ranges from 42% to as high as 84%.12 This high heritability supports the view that stuttering is not a mere habit but a distinct biological trait.1
In the past, research was limited to inferring genetic tendencies through family history studies. However, recent dramatic advances in genomic analysis technology have made it possible to directly identify specific genes associated with stuttering. In particular, the Genome-Wide Association Study (GWAS) has marked a turning point in stuttering research. A prime example is a large-scale international collaborative study that utilized DNA data from the genetic analysis company '23andMe' to compare the genomes of about 100,000 individuals with a history of stuttering and over one million individuals without.1 This study identified 48 genes and 57 distinct genetic loci that showed a statistically significant association with stuttering.1 This clearly demonstrates that stuttering is not determined by a single gene but is a polygenic disorder involving the complex interplay of multiple genes.
A particularly noteworthy gene from this study is VRK2.1 This gene is significant because previous studies have reported its association with rhythm sense and the decline of language abilities in Alzheimer's patients.1 This strongly suggests that the genetic predisposition for stuttering is not limited to 'inaccurate pronunciation' but may be genetically linked to a broader brain circuit for temporal information processing and motor control, encompassing musicality, speech, and language. In other words, the genetic vulnerability for stuttering may stem from a deficit in the brain's intrinsic rhythm generation and timing regulation abilities, and this deficit becomes prominently manifested in the process of 'speaking,' which requires the most precise and rapid temporal control.
Furthermore, early genetic studies revealed that variations in genes related to lysosome function (GNPTAB, GNPTG, NAGPA) were associated with some cases of stuttering.14 Lysosomes are organelles that process cellular waste, and problems in their function can affect the health and efficiency of neurons. This implies that subtle inefficiencies in the energy supply or waste removal processes of nerve cells could lead to disruptions in energy-intensive neural activities like speaking.16
Moreover, some of the genetic variations related to stuttering have been found to share genetic similarities with autism spectrum disorder, depression, and musicality.2 This suggests that these conditions and traits may share common neural circuits related to social communication, emotional regulation, and auditory-motor integration, with underlying common genetic factors. Therefore, the anxiety or social withdrawal experienced by people who stutter may not just be a psychological reaction to their speech difficulties but could have deep-seated biological links to emotional disorders like depression. This provides a strong biological rationale for considering emotional and psychological aspects alongside simple speech training in the treatment of stuttering.
One of the most consistent findings in stuttering research is the significant gender difference. In childhood, boys are about twice as likely to stutter as girls, but in adulthood, this ratio widens to 4:1, and in some cases, up to 5:1.1 This large disparity in incidence and natural recovery rates between sexes suggests that differences in male and female neurodevelopmental processes and hormonal environments play a crucial role in the manifestation and persistence of stuttering.
From a neurodevelopmental perspective, girls tend to show faster and more active overall brain development, especially in the left temporal lobe, which is closely related to language function.19 In contrast, boys tend to develop the parietal lobe, associated with spatial perception and motor senses, earlier. Additionally, boys tend to predominantly use the left brain, which is responsible for logical and analytical functions, whereas girls are known to use both hemispheres in a more balanced manner.19 Fluency in speech requires not only the language centers in the left brain but also smooth coordination with the right brain's functions related to prosody and context comprehension. Therefore, if a boy with a genetic predisposition has a relative delay in left brain development or a developmental tendency skewed towards the left brain, he may be at a higher risk of stuttering due to an overload in the complex language processing system.
Sex hormones are identified as a key biological factor influencing these gender differences in neurodevelopment. In particular, the hypothesis has been proposed that exposure to high concentrations of testosterone during the fetal period can delay the development of the left brain, relatively increasing the activity of the right brain, which may increase the risk of neurodevelopmental disorders such as stuttering, autism, and dyslexia.20 Research findings supporting this hypothesis are accumulating. For example, a group of children who stutter had significantly higher blood testosterone levels compared to a group of children who speak fluently, and these testosterone levels showed a significant correlation with the severity of stuttering.18 This suggests that testosterone may have a direct impact not only on the onset of stuttering but also on the severity of its symptoms.
Conversely, the female hormone estrogen is known to play a neuroprotective and organizational role in brain development.24 Estrogen receptors are widely distributed in the hippocampus and cerebral cortex, which are important for language and memory functions, and they promote the growth of nerve cells and the formation of synapses in these areas.25 Therefore, it is presumed that even if females have genetic risk factors, the neuroprotective effects of estrogen may allow their brains to more effectively compensate for or overcome these vulnerabilities, leading to a higher rate of natural recovery.
In conclusion, the male predominance in stuttering can be understood as the result of a complex interaction between genetic predisposition and the hormonal environment. Males, in addition to genetic risk factors, may face a 'double hit' where the development of the left-hemisphere neural network, crucial for language processing, is delayed or stressed by the influence of fetal testosterone. In contrast, females may exhibit greater resilience to the same genetic risks due to a relatively neuroprotective hormonal environment (estrogen). This implies that there are distinct biological pathways for the onset and recovery of stuttering depending on sex, and it raises the need for developing sex-specific prevention and treatment strategies in the future.
Understanding how genetic predispositions affect the brain's structure and function to manifest as stuttering is key to unraveling its neurobiological mechanisms. Over the past two decades, studies using advanced brain imaging technologies like functional magnetic resonance imaging (fMRI) and diffusion tensor imaging (DTI) have revealed that the brains of people who stutter show subtle but consistent differences, both structurally and functionally, compared to the brains of fluent speakers. These differences are not confined to a single brain region but can be summarized as a 'connectivity disorder'—a problem in the extensive neural networks that connect various areas involved in speech.
The brain's white matter consists of bundles of axons that connect neurons, serving as a high-speed highway for transmitting information between different brain regions. Diffusion tensor imaging (DTI), a technique that measures the diffusion direction of water molecules to assess the structural integrity of white matter fiber bundles, has provided crucial evidence in stuttering research.
DTI studies consistently report a reduction in white matter integrity, specifically a decrease in Fractional Anisotropy (FA) values, in people who stutter.29 This white matter deficit is particularly prominent in the left hemisphere, which is crucial for language function. Specifically, a decrease in FA values is consistently observed in the superior longitudinal fasciculus (SLF) and the arcuate fasciculus (AF), which connect the auditory and sensory areas of the occipital lobe with the motor and planning areas of the frontal lobe.16 This neural pathway is essential for the sensorimotor integration process of hearing one's own speech (auditory feedback) and modifying speech plans. The weakened structural connectivity of this pathway means that the rapid and accurate exchange of information between auditory information and motor commands, necessary for fluent speech, is physically hindered.
More importantly, the developmental trajectory of this white matter structure is critical. In children who naturally recover from stuttering, the integrity of these major neural pathways tends to strengthen with age. In contrast, children whose stuttering persists into adulthood show a stagnation or even a decline in the development of these pathways.16 This suggests that whether the white matter development normalizes in early childhood could be a crucial neurobiological indicator for the recovery or persistence of stuttering.
Gray matter is the area where nerve cell bodies are concentrated and where information processing occurs. Studies using Voxel-Based Morphometry (VBM) have reported subtle differences in gray matter volume in the brains of people who stutter. Although results vary somewhat between studies, commonly implicated areas include the left inferior frontal gyrus (including Broca's area) and bilateral temporal lobe regions, with reports of reduced gray matter volume in these areas in children who stutter.29 In adults, there are also reports of increased gray matter volume in some areas, which may be the result of long-term compensatory mechanisms for stuttering.31
Stuttering is understood less as a problem with specific brain regions themselves and more as an issue of communication between them, i.e., functional connectivity. In particular, the dysfunction of the Cortico-Basal Ganglia-Thalamo-Cortical (CBGTC) circuit, which regulates the initiation, sequencing, and timing of voluntary movements, is identified as the core neurophysiological mechanism of stuttering.15
Brain imaging studies consistently show that people who stutter exhibit abnormal neural activity patterns within this circuit during speech.30 The importance of this connectivity became even clearer through studies of neurogenic stuttering, which is acquired due to stroke or trauma. Although the brain damage sites causing neurogenic stuttering were anatomically very diverse, a new analysis technique called lesion network mapping revealed that all damage sites were functionally connected to the same neural network centered on the left putamen.40 The putamen is a key component of the basal ganglia and acts as a gateway for regulating the execution of motor plans.
Crucially, a study of adults with developmental stuttering that began in childhood also showed a significant correlation between the degree of structural change in this left putamen area and the severity of stuttering.40 This strongly suggests that two types of stuttering with different origins (developmental and neurogenic) share a common neural substrate: the dysfunction of the CBGTC circuit centered on the left putamen. Furthermore, cases where deep brain stimulation (DBS) in the basal ganglia for other conditions like Parkinson's disease incidentally induced or alleviated stuttering provide direct evidence that this circuit plays a causal role in regulating speech fluency.15
Fluent speech is a function predominantly led by the left brain. The core of the neurofunctional characteristics of stuttering can be summarized as the hypoactivation of this left hemisphere and the compensatory overactivation of the right hemisphere in response.
Numerous fMRI studies consistently show that during speech, people who stutter have reduced activity in the left hemisphere's language and motor areas, such as the left inferior frontal gyrus and the ventral premotor cortex, compared to fluent speakers.7 This functional deficit is directly linked to the structural deficits in white matter connectivity mentioned earlier. In other words, because the 'hardware' of the brain's neural network connections is weak, the 'software' of neural activity cannot function properly.
The brain mobilizes the opposite side, the right hemisphere's homologous regions, to compensate for this functional deficit in the left hemisphere. As a result, the brains of people who stutter show a characteristic pattern of excessive activation in right hemisphere regions such as the right frontal operculum and the right anterior insula.8
However, this compensatory action of the right hemisphere is a double-edged sword. The right hemisphere tends to perform functions related to the inhibition or stopping of language production rather than its generation. In particular, the overactivation of the right inferior frontal gyrus (right IFG) can act as a 'neural brake,' interfering with the initiation and flow of speech movements.8 This can lead to a 'neural deadlock' where the signal to initiate speech from the left hemisphere clashes with the signal to inhibit it from the right hemisphere. This provides a neurophysiological explanation for the core symptom of stuttering, the 'block,' where the flow of sound and air completely stops. Therefore, the compensatory activation of the right hemisphere is not only an inefficient alternative but can sometimes act as a maladaptive process that worsens stuttering symptoms. Interestingly, successful speech therapy has been shown to induce a reorganization of brain function, reducing this right hemisphere overactivation and normalizing the activity of the left hemisphere language network.38
A prominent hypothesis that explains the dysfunction at the macroscopic network level of the brain at the neurochemical level is the 'dopamine hypothesis.' This hypothesis posits that stuttering is related to a state of overactivation of the dopamine system in the striatum region of the basal ganglia.16
Evidence supporting this hypothesis has been presented from multiple fronts. First, positron emission tomography (PET) studies have shown that people who stutter have an abnormally increased presynaptic dopamine activity.16 Second, because dopamine acts as an inhibitory neurotransmitter in the striatum, excessive dopamine reduces the metabolic activity of the striatum, causing dysfunction in the entire CBGTC circuit.53 This becomes the neurochemical mechanism that causes the 'gateway' of the basal ganglia, responsible for the selection and initiation of motor plans, to malfunction, leading to difficulties in initiating speech (blocks) or timing errors in motor sequences (repetitions, prolongations). Third, the pharmacological evidence is very strong. Dopamine antagonist drugs such as Haloperidol, Risperidone, and Ecopipam significantly reduce stuttering symptoms, while dopamine agonists can worsen them.53 Fourth, stuttering shares similar characteristics (childhood onset, male predominance, exacerbation by stress, etc.) with other motor disorders related to dopamine system abnormalities, such as Tourette's Syndrome, and responds to similar medications.53 All this evidence suggests that dopamine excess is a key neurochemical mechanism that causes dysfunction in the CBGTC circuit, providing a crucial link between macroscopic brain network abnormalities and microscopic synaptic-level imbalances.
Stuttering is not merely a problem confined to the movements of the lips and tongue. It is a phenomenon where high-level cognitive processes and deep emotional experiences are intricately intertwined. The brain of a person who stutter not only shows inefficiency in the neural circuits for fluent speech but also forms a vicious cycle where this inefficiency interacts with other cognitive functions like attention and working memory, and is further amplified by emotional factors such as stress and anxiety.
Executive Functions (EF) refer to a set of higher-order cognitive abilities that control and manage one's thoughts, emotions, and actions for goal-oriented behavior. Key components include working memory, which temporarily stores and manipulates information; inhibitory control, which suppresses unnecessary stimuli or impulses; and attention, which shifts and focuses attention.59 Stuttering research shows a deep connection between these executive functions and speech fluency.
Working memory, especially phonological working memory which processes linguistic information, appears to be relatively weaker in people who stutter. Both children and adults tend to show lower performance on phonological working memory tasks like non-word repetition compared to fluent speakers.60 This implies a reduced efficiency in the cognitive system that temporarily holds and manipulates sound information during the speech planning stage, which can be a direct cause of speech errors or disfluencies.62 Interestingly, some dual-task studies have observed that stuttering decreases when another task that consumes working memory resources is performed simultaneously.67 This supports the hypothesis that hyper-monitoring of one's own speech is a factor in stuttering, and that diverting cognitive resources elsewhere can reduce this excessive monitoring and improve fluency.
Research findings on attention and inhibitory control are somewhat mixed, but overall, children who stutter (CWS) tend to have weaker attentional control and inhibition abilities compared to fluent children.59 Parent-report questionnaires often rate children who stutter as having lower attention spans and higher impulsivity.59 Additionally, about 23% of adult stutterers report a significant number of inattentive traits, a key feature of Attention-Deficit/Hyperactivity Disorder (ADHD), suggesting a possible neurobiological link between the two disorders.72 A recent magnetoencephalography (MEG) study provides more direct evidence, observing an increase in activity in the right pre-supplementary motor area (R-preSMA) just before a block occurs.75 This area is closely related to the 'stop-signal' for response inhibition, suggesting that a strong 'motor inhibition' signal is already being generated in the brain before the block happens.
These differences in executive function may not be separate comorbid conditions but rather different manifestations of the inefficiency of the same neural circuit. The CBGTC circuit, mentioned earlier, plays a key role not only in fluent speech but also in executive functions like inhibitory control and task switching.70 Therefore, the functional inefficiency of this circuit can manifest as stuttering in a speech context and as a decline in executive function in other cognitive task contexts. This explains why linguistically demanding tasks, such as constructing complex sentences or using difficult words, which impose a high cognitive load, particularly exacerbate stuttering. In other words, when additional load is placed on an already near-capacity neural system, the system collapses.
While stress and anxiety do not 'cause' stuttering, there is no doubt that they are the most powerful factors that dramatically 'exacerbate' existing stuttering.6 The relationship between stuttering and anxiety is not one-sided but forms a mutually amplifying vicious cycle. That is, the experience of stuttering causes social anxiety, and this heightened anxiety, in turn, makes stuttering more severe.54 At the center of this vicious cycle is the brain's emotion regulation system, particularly the amygdala.
The amygdala is the brain's threat detection and fear response center. According to fMRI studies, the activity level of the right amygdala in adults who stutter during conversation with others showed a significant positive correlation with the frequency of blocks.77 This suggests that the mere 'anticipation' of negative evaluation or communication failure activates the brain's fear circuit, and this activated emotional circuit directly interferes with the already vulnerable speech motor system.76 Furthermore, people who stutter have been shown to have reduced activity in the prefrontal cortex, which down-regulates amygdala activity, indicating a diminished top-down control over emotions.77
These psychological and neural processes lead to neurochemical changes. Psychological stress promotes the secretion of the stress hormone cortisol, which can increase dopamine release in the striatum of the basal ganglia.80 This provides a direct neurochemical link between stress and the core motor deficit of stuttering. In other words, anxiety about a specific speaking situation (amygdala activation) triggers a stress response, and the resulting increase in dopamine further impairs the function of the basal ganglia, exacerbating the core motor control problem of stuttering.53
In conclusion, a moment of stuttering can be seen as a self-fulfilling neurobiological prophecy created by the interaction of cognitive, emotional, and motor systems. The process is as follows: First, a person who stutters 'anticipates' a difficult word or a specific situation (cognitive event).75 Second, this anticipation triggers anxiety and activates the amygdala (emotional response).77 Third, amygdala activation can trigger a stress response, increasing dopamine levels (neurochemical response) 80, and simultaneously, the anticipation of error activates the excessive inhibitory control network of the R-preSMA (motor inhibition response).75 The combination of excessive dopamine interfering with the basal ganglia's 'go' signal and the R-preSMA sending a strong 'stop' signal creates a neural state where fluent speech initiation is nearly impossible. Ultimately, the speech blocks, which confirms the initial prediction and further strengthens this maladaptive neural pathway for the next speaking situation. This integrated model explains the cognitive, emotional, and motor aspects of the complex disorder of stuttering as one coherent neurobiological vicious cycle.
One of the most interesting and paradoxical features of stuttering is its variability. Most people who stutter experience severe disfluency in certain situations, yet can speak with surprising fluency in others. The phenomenon of stuttering almost disappearing when singing, speaking in unison with others, or acting with a different accent is strong evidence that the essence of stuttering is not a deficit in language ability or the articulatory organs themselves. These phenomena provide important clues for understanding the neurobiological mechanisms of stuttering and show how various modulating factors affect the brain's speech network.
Most people who stutter experience a dramatic reduction or complete disappearance of stuttering when they sing, speak in unison with others (choral speech), imitate another person's voice or accent while acting, or whisper.81 This is not simply due to psychological comfort but occurs because these activities use different neural circuits than normal conversation or bypass the existing faulty circuits.
The effects of these fluency-inducing conditions are like 'naturally occurring experiments' that reaffirm that the core deficit of stuttering is not in the speech organs themselves or in linguistic knowledge, but in the dysfunction of a specific neural circuit responsible for intrinsic rhythm generation and sensorimotor integration for speech motor control.
A common misconception is that being bilingual causes stuttering. To be clear, there is no scientific evidence that learning and using two or more languages itself is a cause of stuttering.88 Bilingualism is an asset with many cognitive and social benefits and should not be considered a risk factor for stuttering.
However, to understand the relationship between a bilingual environment and stuttering, several important points must be distinguished.
In conclusion, a bilingual environment is not a cause of stuttering, and the claim that a second language should be eliminated for a child who has started to stutter is unfounded. On the contrary, this could deprive the child of their linguistic assets and negatively impact their cultural identity.91 What is important is to understand the additional linguistic burden that a child with a predisposition to stuttering may experience and to support them in acquiring both languages in a stress-free environment.
Neurogenic stuttering is a fluency disorder that is acquired later in life following a specific neurological event such as a stroke, traumatic brain injury (TBI), tumor, or neurodegenerative disease.101 It is distinct from developmental stuttering, which begins in childhood without any obvious brain injury. While the two types differ in their cause and some clinical features, recent research suggests they may share a common neural basis.
As mentioned earlier, lesion network mapping studies have shown that neurogenic stuttering caused by brain damage in various locations is commonly associated with dysfunction in a neural network centered on the left putamen.40 The severity of developmental stuttering was also related to structural changes in the same brain region. This is a significant finding suggesting that both disorders may fundamentally stem from the dysfunction of the same motor control circuit in the brain.
Nevertheless, for clinical diagnosis and understanding, it is crucial to clarify the main differences between the two types.
| Feature | Developmental Stuttering | Neurogenic Stuttering |
|---|---|---|
| Onset | Typically gradual onset in childhood, between ages 2-5 1 | Sudden onset after CNS injury/disease, regardless of age 101 |
| Cause | Neurodevelopmental factors; strong genetic predisposition 1 | Acquired factors; stroke, TBI, tumor, neurodegenerative disease 102 |
| Location of Disfluency | Primarily on the first sound/syllable of words; more common on content words (nouns, verbs) 15 | Can occur at any position in a word (initial, medial, final); occurs on both content and function words 101 |
| Secondary Behaviors | Common; facial grimacing, eye blinking, limb movements to push through speech 106 | Rare or absent 101 |
| Anxiety/Awareness | High levels of awareness and anxiety about speaking are common 9 | Often unaware of or unconcerned about their disfluency 101 |
| Fluency-Inducing Conditions | Fluency significantly improves with singing, choral reading, whispering (adaptation effect present) 81 | Disfluency often persists during singing, choral reading (no adaptation effect) 101 |
| Neurological Findings | No obvious brain lesion; subtle differences in white/gray matter and network function 29 | Associated with an identifiable, specific brain lesion 40 |
This comparison provides important clinical guidelines for the differential diagnosis of the two types of stuttering and for establishing treatment plans tailored to their respective characteristics. At the same time, the fact that both disorders share a common neural network once again emphasizes that the core neurobiological mechanism of stuttering lies in a specific motor control circuit of the brain.
The understanding that stuttering is a neurodevelopmental disorder based on the brain's structural and functional characteristics has brought about a fundamental shift in therapeutic approaches. Modern therapy aims not just to correct speaking habits but to induce neuroplasticity—the process of reorganizing and retraining the brain's neural circuits. From behavioral interventions like speech therapy to cognitive approaches like mindfulness, various treatments help to change the brain's maladaptive patterns and build more efficient speech strategies.
Speech therapy is the cornerstone of stuttering treatment, and it is not merely behavioral training but a form of 'applied neuroplasticity' that actively changes brain function.110 Brain imaging studies provide objective evidence of how speech therapy actually reorganizes the brain's activity patterns.
Before treatment, the brain of a person who stutters typically shows a pattern of hypoactivation in the left-hemisphere language-motor areas and compensatory overactivation in the right hemisphere.47 However, after successful fluency shaping therapy, dramatic changes in brain activity are observed. Post-treatment fMRI scans show that the activity in the maladaptively overactivated right-hemisphere regions significantly decreases, while the activity in the previously underactivated left-hemisphere language-motor and auditory areas increases.38
This means that through therapy, the brain has been 'retrained' to reduce its reliance on inefficient right-hemisphere compensatory strategies and to reactivate or use more efficiently the left-hemisphere neural circuits originally responsible for language function.52 In other words, therapy induces the brain to reorganize neural communication in areas closer to the source of the dysfunction, thereby restoring fluency at a more fundamental level. Furthermore, some studies suggest that intensive therapy can also bring about positive changes in the structural integrity of white matter, showing the potential for behavioral training to strengthen the brain's physical connection network.115
The vicious cycle of stuttering involves not only the core motor control problem but also the cognitive and emotional factors that amplify it. Therefore, therapeutic approaches must also consider these multidimensional aspects. Mindfulness-based interventions aim not to 'cure' the motor deficit of stuttering itself, but to change the individual's 'relationship' with stuttering.116
The key mechanisms of mindfulness are as follows:
Clinical studies show that mindfulness meditation has a significant effect on reducing the frequency of stuttering, alleviating anxiety, and improving overall quality of life.116 This emphasizes that stuttering treatment should be a process that changes the individual's internal experience of living with stuttering, beyond just teaching the skills to speak fluently.
In conclusion, the most effective and sustainable therapeutic approach should adopt a dual strategy. One is to directly address the 'bottom-up' deficits of the speech motor system through behavioral therapies like fluency shaping techniques. The other is to manage the 'top-down' regulatory systems such as attention, anticipation, and anxiety through mindfulness or cognitive-behavioral therapy (CBT). Treatment that only addresses motor control may be vulnerable to relapse in emotionally and cognitively stressful situations, and treatment that only addresses anxiety does not solve the fundamental motor timing deficit. Therefore, integrating these two approaches to retrain motor patterns while simultaneously regulating the cognitive-emotional environment surrounding stuttering can lead to the most robust treatment outcomes.
As our understanding of the neurobiological mechanisms of stuttering deepens, the treatment paradigm is shifting from behavioral correction to directly modulating brain circuits. New neurotechnologies such as pharmacology, non-invasive brain stimulation, and real-time brain imaging feedback have the potential to maximize treatment effects by directly intervening in the fundamental neurophysiological causes of stuttering. This signifies a move beyond rehabilitation to an era of neuromodulation.
The 'dopamine excess hypothesis' of stuttering provides the clearest target for drug development. Based on evidence that the dopamine system in the basal ganglia is overactivated, drugs that block dopamine receptors are being studied as treatments for stuttering.53
While drug therapy is not yet a standard treatment for all people who stutter, it holds great potential for its ability to directly correct neurochemical imbalances and could be an important alternative, especially for severe cases of stuttering that do not respond to other treatments.
Non-invasive brain stimulation is a technique that delivers weak electrical or magnetic stimulation to specific areas of the brain through the scalp to modulate the activity of neurons. It can be used to directly correct the dysfunction of brain areas related to stuttering and, when combined with speech therapy, to promote neuroplasticity and enhance treatment effects.
While it is unlikely that current invasive BCIs will be applied to stuttering treatment in the near future, technological advancements in this field could have a significant 'technological spillover' effect on stuttering treatment. In particular, non-invasive BCI technology using electroencephalography (EEG) could be used to detect the brain activity patterns of fluent and disfluent states in real-time.141 In the future, it may be possible to develop a personalized neurofeedback system where a wearable device with built-in EEG sensors detects the characteristic brainwave signals just before a block occurs (e.g., an increase in beta waves in the right supplementary motor area) and sends a subtle tactile or auditory signal to the user, inducing an unconscious shift in brain state to prevent the block. Thus, cutting-edge technologies being developed for other neurological disorders are laying the groundwork for future stuttering treatments.
This report has defined stuttering as a complex neurodevelopmental disorder involving multiple genes and has analyzed its neurobiological mechanisms from a multidimensional perspective. Synthesizing the latest research findings, the core of stuttering can be summarized as follows. First, stuttering is deeply rooted in a genetic predisposition, and this genetic vulnerability leads to inefficiency in the brain's core circuits that regulate the timing and sequencing of speech movements, particularly the cortico-basal ganglia-thalamo-cortical (CBGTC) loop. Second, this dysfunction has a physical basis in the brain's structural differences, such as the reduced integrity of the left-hemisphere white matter tracts connecting language-motor areas. Third, the brain mobilizes the right hemisphere to compensate for these left-hemisphere deficits, but this compensatory action is often inefficient or even results in a maladaptive inhibition of speech. Fourth, at the neurochemical level, the overactivation of the dopamine system in the basal ganglia is a significant factor that causes and exacerbates this network dysfunction.
However, the actual manifestation of stuttering is not determined solely by these core neurophysiological vulnerabilities. It is the final outcome of a complex interaction with top-down regulatory factors such as cognitive load, linguistic complexity, and emotional state. When the burden on executive functions increases, or when the brain's fear circuit is activated by social anxiety, the already unstable speech system crosses a threshold and collapses, resulting in the phenomena we observe as blocks, repetitions, and prolongations.
This integrated model provides important directions for future research and clinical practice. Future research should focus on longitudinal studies in early childhood to track the neurodevelopmental trajectories that distinguish persistence from recovery in stuttering.16 Efforts to identify more genetic risk factors and to elucidate the neurobiological functions of these genes must also continue.16
Clinically, we are now moving into an era of personalized, multi-component treatment that considers individual characteristics. The most effective treatments will likely be those that integrate behavioral approaches like traditional fluency shaping techniques, cognitive-emotional approaches like mindfulness, and neurostimulation technologies to promote neuroplasticity.43 This approach involves retraining motor circuits with behavioral therapy, breaking the vicious cycle with cognitive therapy, and accelerating and consolidating those changes with neuromodulation technology.
In conclusion, the advancement of scientific understanding of stuttering is dispelling the long-held misconceptions and stigma surrounding this disorder. Stuttering is not a matter of will but a matter of the brain, and the brain can change. The progress in neuroscience is not only unraveling the complex puzzle of stuttering but is also heralding an era of more effective, evidence-based, brain-based therapies that can improve the lives of millions of people who stutter worldwide.