from the brains of adults who do not stutter. several neuroimaging studies have emerged to identify areas associated with stuttering. in general, during stuttering, cerebral activities change dramatically in comparison to silent rest or fluent speech between people who stutter and people who do not. there is evidence that people who stutter activate motor programs before the articulatory or linguistic processing is initiated. brain imaging studies have primarily been focused on adults. however, the neurological abnormalities found in adults does not determine whether childhood stuttering caused these abnormalities or whether the abnormalities cause stuttering. studies utilizing positron emission tomography (pet) have found during tasks that invoke disfluent speech, people who stutter show hypoactivity in cortical areas associated with language processing, such as broca's area, but hyperactivity in areas associated with motor function. one such study that evaluated the stutter period found that there was overactivation in the cerebrum and cerebellum, and relative deactivation of the left hemisphere auditory areas and frontal temporal regions. functional magnetic resonance imaging (fmri) has found abnormal activation in the right frontal operculum (rfo), which is an area associated with time-estimation tasks, occasionally incorporated in complex speech. researchers have explored temporal cortical activations by utilizing magnetoencephalography (meg). in single-word-recognition tasks, people who did not stutter showed cortical activation first in occipital areas, then in left inferior-frontal regions such as broca's area, and finally, in motor and premotor cortices. the stutterers also first had cortical activation in the occipital areas but the left inferior-frontal regions were activated only after the motor and premotor cortices were activated. during speech production, people who stutter show overactivity in the anterior insula, cerebellum and bilateral midbrain. they show underactivity in the ventral premotor, rolandic opercular and sensorimotor cortex bilaterally and heschl's gyrus in the left hemisphere. additionally, speech production yields underactivity in cortical motor and premotor areas. abnormal lateralization much evidence from neuroimaging techniques has supported the theory that the right hemisphere of people who stutter interferes with left-hemisphere speech production. in 2008, it was shown that adults who stutter have anatomical differences in gyri within the perisylvian cortex, in frontotemporal areas. a large amount of white matter is found in the right hemisphere of the brain, including the region of the superior temporal gyrus. this was discovered using voxel-based morphometry. on the other hand, lesser amounts of white matter are found in the left inferior arcuate fasciculus connecting the temporal and frontal areas in stuttering adults. as of 2011 it was known that the corpus callosum, which transfers information between the left and right cerebral hemispheres. rostrum, and the anterior mid-body sections were larger in adults who stutter as compared to normally fluent adults. this difference was thought to be due to unusual functions of brain organization in stuttering adults or a result of how the stuttering adults performed language-relevant tasks. furthermore, previous research had found that adults who stutter show cerebral hemispheres that contain uncommon brain proportions and allocations of gray and white matter tissue. there is less coordination between the speech motor and planning regions in the brain's left hemisphere of men and women who stutter, when compared to a non-stuttering control group. anatomical connectivity of the speech motor and planning regions is less vigorous in adults who stutter, especially women. men who stutter seem to have more right-sided motor connectivity. on the other hand, stuttering women have less connectivity with the right motor regions. in non-stuttering, normal speech, pet scans have shown that both hemispheres are active but that the left hemisphere may be more active. by contrast, people who stutter yield more activity on the right hemisphere, suggesting that it might be interfering with left-hemisphere speech production. another comparison of scans anterior forebrain regions are disproportionately active in stuttering subjects, while post-rolandic regions are relatively inactive. bilateral increases and unusual right-left asymmetry has been found in the planum temporale when comparing people who stutter and people who do not. these studies have also found that there are anatomical differences in the rolandic operculum and arcuate fasciculus. in 2019, denis drayna suggested that brain imaging studies of people who stutter do not tell if the differences in the brain anatomy caused stuttering or if they are the effect of stuttering;in the mouse model for stuttering created by drayna and team, they noticed significant similarities between the vocalizations in mice (carrying gnptab mutation) and human stuttering. in 2021, researchers investigated the brain tissue from the mice mutants and reported a significant decrease in the number and density of astrocytes in their corpus callosum. astrocyte is a star-shaped cell in the brain that supports the nerve cells by supplying oxygen and nutrients, and taking away the waste. the corpus callosum enables the communication between the left and right hemispheres of the brain. as of 2020 follow-up experiments with the gnptab mutation introduced to brain cell types showed that the vocalization defects in mice were specific to the loss of astrocytes, and mice did not show stuttering-like vocalization defects when the mutation was engineered to other brain cell types. dopamine recent studies have found that adults who stutter have elevated levels of the neurotransmitter dopamine, and have thus found dopamine antagonists that reduce stuttering (see anti-stuttering medication below). overactivity of the midbrain has been found at the level of the substantia nigra extended to the red nucleus and subthalamic nucleus, which all contribute to the production of dopamine. however, increased dopamine does not imply increased excitatory function since dopamine's effect can be both excitatory or inhibitory depending upon which dopamine receptors (labelled d1–d5) have been stimulated. diagnosis some characteristics of stuttered speech are not as easy for listeners to detect. as a result, diagnosing stuttering requires the skills of a certified speech–language pathologist (slp). diagnosis of stuttering employs information both from direct observation of the individual and information about the individual's background, through a case history. information from both sources should consider things such as age, the various times it has occurred, and other impediments. the slp may collect a case history on the individual through a detailed interview or conversation with the parents (if client is a child). they may also observe parent-child interactions and observe the speech patterns of the child's parents. the overall goal of assessment for the slp will be (1) to determine whether a speech disfluency exists, and (2) assess if its severity warrants concern for further treatment. during direct observation of the client, the slp will observe various aspects of the individual's speech behaviors. in particular, the therapist might test for factors including the types of disfluencies present (using a test such as the disfluency type index (dti)), their frequency and duration (number of iterations, percentage of syllables stuttered (%ss)), and speaking rate (syllables per minute (spm), words per minute (wpm)). they may also test for naturalness and fluency in speaking (naturalness rating scale (nat), test of childhood stuttering (tocs)) and physical concomitants during speech (riley's stuttering severity instrument fourth edition (ssi-4)). they might also employ a test to evaluate the severity of the stuttering and predictions for its course. one such test includes the stuttering prediction instrument for young children (spi), which analyzes the child's case history, part-word repetitions and prolongations, and stuttering frequency in order to determine the severity of the disfluency and its prognosis for chronicity for the future. stuttering is a multifaceted, complex disorder that can impact an individual's life in a variety of ways. children and adults are monitored and evaluated for evidence of possible social, psychological or emotional signs of stress related to their disorder. some common assessments of this type measure factors including: anxiety (endler multidimensional anxiety scales (emas)), attitudes (personal report of communication apprehension (prca)), perceptions of self (self-rating of reactions to speech situations (ssrss)), quality of life (overall assessment of the speaker's experience of stuttering (oases)), behaviors (older adult self-report (oasr)), and mental health (composite international diagnostic interview (cidi)). clinical psychologists with adequate expertise can also diagnose stuttering per the dsm-5 diagnostic codes. the dsm-5 describes childhood-onset fluency disorder (stuttering)" for developmental stuttering, and "adult-onset fluency disorder". however, the specific rationale for this change from the dsm-iv is ill-documented in the apa's published literature, and is felt by some to promote confusion between the very different terms "fluency" and "disfluency". normal disfluency main article: developmental dysfluency preschool aged children often have difficulties with speech concerning motor planning and execution; this often manifests as disfluencies related to speech development (referred to as normal dysfluency or "other disfluencies"). this type of disfluency is a normal part of speech development and temporarily present in preschool aged children who are learning to speak. these normal disfluencies can present as interjections ("um"), multisyllable repetitions ("i want i want to do that"), or revised or abandoned utterances ("i want—hey what's that?"). normal disfluency should be ruled out before diagnosing stuttering. classification developmental stuttering (also known as childhood onset fluency disorder) is stuttering that originates when a child is learning to speak and may persist as the child matures into adulthood. stuttering that persists after the age of seven is classified as persistent stuttering. other much less common causes of stuttering include neurogenic stuttering (stuttering that occurs secondary to brain damage, such as after a stroke) and psychogenic stuttering (stuttering related to a psychological condition). developmental stuttering is typically a developmental disorder beginning in early childhood and continuing into adulthood in at least 20% of affected children. the mean onset of stuttering is 30 months. although there is variability, early stuttering behaviours usually consist of word or syllable repetitions, while secondary behaviours such as tension, avoidance or escape behaviours are absent. most young children are unaware of the interruptions in their speech. with young stutterers, disfluency may be episodic, and periods of stuttering are followed by periods of relatively decreased disfluency. though the rate of early recovery is very high, with time a young person who stutters may transition from easy, relaxed repetition to more tense and effortful stuttering, including blocks and prolongations. some propose that parental reactions may affect the development of a chronic stutter. recommendations to "slow down", "take a breath", "say it again", etc., may increase the child's anxiety and fear, leading to more difficulties with speaking and, in the "cycle of stuttering," to yet more fear, anxiety and expectation of stuttering. with time secondary stuttering, including escape behaviours such as eye blinking and lip movements, may be used, as well as fear and avoidance of sounds, words, people, or speaking situations. eventually, many become fully aware of their disorder and begin to identify themselves as stutterers. with this may come deeper frustration, embarrassment and shame. other, rarer patterns of stuttering development have been described, including sudden onset with the child being unable to speak, despite attempts to do so. the child usually is unable to utter the first sound of a sentence, and shows high levels of awareness and frustration. another variety also begins suddenly with frequent word and phrase repetition, and does not include the development of secondary stuttering behaviours. neurogenic stuttering some stuttering is also believed to be caused by neurophysiology. neurogenic stuttering is a type of fluency disorder in which a person has difficulty in producing speech in a normal, smooth fashion. individuals with fluency disorders may have speech that sounds fragmented or halting, with frequent interruptions and difficulty producing words without effort or struggle. neurogenic stuttering typically appears following some sort of injury or disease to the central nervous system. injuries to the brain and spinal cord, including cortex, subcortex, cerebellum, and even the neural pathway regions. acquired stuttering in rare cases, stuttering may be acquired in adulthood as the result of a neurological event such as a head injury, tumour, stroke, or drug use. the stuttering has different characteristics from its developmental equivalent: it tends to be limited to part-word or sound repetitions, and is associated with a relative lack of anxiety and secondary stuttering behaviors. techniques such as altered auditory feedback (see below), which may promote decreasing disfluency in those with the developmental condition, are not effective with the acquired type. psychogenic stuttering may also arise after a traumatic experience such as a death, the breakup of a relationship or as the psychological reaction to physical trauma. its symptoms tend to be homogeneous: the stuttering is of sudden onset and