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Stuttering Lecture 3: Constitutional Factors in Stuttering
Terms in this set (54)
Stuttering is a learned behavior
Stuttering is a psychological problem caused by anxiety
-but psychological consequences
What evidence points to a physical basis for stuttering?
•Sensory and motor performance
•Genetics and heredity
Disturbance in sensory feedback
•Judging tone duration (how long tone lasts)
•Difficulty screening out background noises
•Delayed auditory feedback (DAF) is very different
-if DAF, they become fluent
-if DAF to person who is fluent, they become disfluent
•Auditory processing --- dichotic listening tasks (for speech) to assess brain dominance
-to understand language
-processing sensory feedback
Dichotic Listening Test
R = right ear
L = left ear
NC = Noncompeting
C = Competing
-information coming into the ears in both competing and no-competing situations
-what did they hear? what words did they remember most?
-stutterers will do better in the left ear than right ear
-right hemisphere is working better for linguistic information, they process it better
-for people who are fluent = right ear
Using linguistic stimuli, most PWS show reversed hemisphere dominance (Left Ear Advantage)
Another Way of Looking at Dichotic Listening
-Listener pays attention to one ear only
-Fluent speakers: R ear/right side dominant. (left hemisphere dominant)
-Stutterers do better with LEFT EAR because right hemisphere is working harder than left.
Another Way of Looking at Dichotic Listening cont.
1. Reaction time (espec. linguistic material) is slower
2. Fluent speech differences (speech is motor task!)
- longer vowel duration, slower transitions, longer VOT, slower articulatory movements with more errors, sound sequencing abnormalities that aren't stuttering
3. Motor control (few differences)
- Finger movement
•Appears to be problem in fine motor skills and NOT learning the sequence of tapping (2018)
-nothing wrong with intelligence or memory
-about motor skill
GENETICS & HEREDITY
Is there a stuttering gene?
•Associated stuttering with genes in chromosomes 1, 7, 9, 12, 13, 15, 16 and 18
•Familial cases show ratio of 1.5 male: 1 female
-For every 1.5 cases male, is 1 female
-Girls at relatively high risk
•No family history, ratio is 7 or 8 males to 1 female
-Girls at relatively low risk
-not a single gene, but number
-girls being effected depended on there being a family history
18 - controls intercellular communication (Shurgart, et al, 2004) - one cell communicating with another
1, 13, 16 - unspecified (Cox & Yairi, 2005)
12, 1 - linked to stuttering (Riaz et al, 2005) - mutations
9 - linked to stuttering incidence
15 - linked to stuttering persistence (Suresh et al, 2006)
Kang & Drayna (2010)
•Based on 2005 study (Riaz et al.)
•Chromosome 12 (87 genes)
-Gene called GNPTAB
-Encodes enzyme which recycles cellular waste
•Subjects -123 Pakistanis with persistent stuttering (some related, some from same families)
•Found mutations in some of those who stutter
•Mutations cause serious organ and brain problems as well as speech (can lead to death if too large)
•But most people don't have this mutation
•Caused a lot of controversy...and interest
-enough to be notable and significant
•Subsequent studies support results (Raza et al., 2015)
Stuttering Mice (Barnes, Wozniak, Gutierrez, Han, Drayna, Holy, 2016)
-altered the GNPTAB gene in mice
-took spectrograms of mice while speaking and compared to typical mike squeaks
-evidence of little repetitions and blocks
Focusing in on Genetics
•In addition to GNPTAB gene, there are associations on:
•12%-20% of persistent stuttering seems related to mutations on one of these four genes
•All four genes related to intracellular trafficking (movement of substances within a cell).
-Transport vesicles take proteins to structures within a cell/recycles cellular waste
-This allows a cell to function well
•Intracellular trafficking deficits connected with some neurological deficits (e.g., Parkinson's disease, Huntington's chorea)
Twins Who Stutter
•Stuttering occurs more often in monozygotic (identical) than dizygotic (fraternal) twins
•But what is inherited?
-not at all genetics
•Heredity does not work alone; genetics explains 69%-82%, environment contributes 31%-18% (all stutterers)
-we can manipulate the environment which has a powerful influence
Genetics & Heredity
•Genetics has role
• Genetic markers (some genes)
-Identify "at risk"
-69% CWS have other family members who stutter (runs in families)
•But understanding of precisely what these associations mean is undetermined
-focus on not psychological or learned
-depending on adult or child
-we can say its brain based
Brain Structure in PWS
o Sensory, planning, motor areas in Left hemisphere developed differently in PWS
-left hemisphere helps you execute motor movements for speech and language
o Compared to Fluent Speakers (FS)
-Tracts in L hemisphere that transmit information from sensory areas (store phonological representations of sounds) to motor execution areas are less dense
-Tracts in R hemisphere are denser
Think-pair-share: What do you think this means for speech?
-motor execution of speech and language will not be as good, not as efficient
-flip flopped to right
Brain Structure in PWS cont.
-CWS: Less volume in gray matter around Broca's area (Beal, 2011; Chang et al., 2008)
-Less connectivity of white matter underlying supramarginal gyrus and left rolandic operculum
Brain Structure in PWS pic
-Less connectivity of white matter underlying supramarginal gyrus and left rolandic operculum
-the structure is different, doesn't mean they are less intelligent
Can normally fluent speech be expected when component parts are abnormal or aren't working properly?
Differences in Brain Structure
•Delay in gray matter development in school-age years among CWS (persistent stutterers)
•Children thus have reduced neural resources for effective processing of speech sounds needed for fluency (they do not have the same brain structure)
Could the eventual development of these structures explain recovery?
-therapy can change brain structure and function
-become more like the brains of those who are fluent
-brain differences disappear when they "recover"
Brain Function in PWS
•Brain works differently during stuttering
-Greater R hemisphere activity than L
•No significant differences when speaking fluently
•Most robust difference between PWS and FS:
-Nerve fibers in L hemisphere between sensory integration area and motor planning area
-Not structured to conduct impulses as fast or efficient
-Impulses are not as efficient
Differences in Brain Function
•Increased motor activity and reduced auditory activity during speech
-Before speech, more activation in motor areas
-Depressed sensory input
•Less L hemi brain activity in phoneme monitoring and less R hemi activity for prosody monitoring
•Atypical activation in left inferior frontal gyrus and right auditory regions
Suggests neural speech production utilized differently in PWS
-people who are fluent have left hemisphere dominance
-people who are disfluent have right hemisphere dominance
Movement Programming for Speech: FS
FS: almost no right-side activity
Movement Programming: PWS
PWS: normal left-side activity; hyperactive right-side activity
DeNil et al, 1995 (images enhanced)
Movement Release: FS
FS: weak activation
-should be quick and gentle, very sensitive!
-as a person moves from one sound to the next
Movement Release: PWS
PWS: overactive; switches hemispheres in stuttered speech (interruption; initiation of program repeated)
-far more than what is needed
-switched hemispheres when stuttering
-cues to release motor movement are messed up
-releases are exaggerated, interrupting the start of a new movement
Motor Control: FS
FS: Stronger activity in left hemisphere
Motor Control: PWS
PWS: Equal activity in hemispheres when stuttering; left side stronger when fluent
-motor control the same in both hemispheres
-speaking fluently: left side is greater
-our therapy will help activate the left side more to create more fluent speech
Movement Coordination: FS
FS: little activation from left
-delicate, fine movement
-don't need overkill to speak
-just enough to move from one sound to next
Movement Coordination: PWS
PWS: left and right sides of cerebellum activated during stuttered speech; impairment of timing and coordination
-with greater intensity
Auditory Monitoring: FS
FS: stronger activation of auditory areas
-really monitoring what is coming in
-aware of mistakes
Auditory Monitoring: PWS
PWS: weak activation
-harder to auditorily monitor
-So it appears that the brain of PWS can work "backward" or is "flip-flopped" (nothing to do with intelligence or memory)
-Are PWS left-brain dominant for language, but using the right-brain for speech?
Speech therapy has been shown to change the brain structures to function like FS !!
Smith & Weber, 2017
However, across the many studies using a variety of experimental and analytic approaches, certain brain areas and neural networks are repeatedly implicated in stuttering in adults:
left premotor and motor areas specialized for speech motor programming and execution, left perisylvian networks underlying auditory and language functions and their interactions with speech motor areas, the interhemispheric connections of the corpus callosum, and basal ganglia-thalamo-cortical loops. The most recent work in young children, while revealing some differences from earlier findings in adults,
also generally implicates the left-dominant, widespread neural network important for the complex integration of neural functions necessary for fluent speech production as a significant factor in early stuttering.
-certain areas are repeatedly implicated
Ongoing Research: Identifying Babies at Risk
-can we identify babies who are going to stutter?
-can we look at their brains?
•Strong research base on lateral brain differences
•But also research suggesting atypical basal ganglia and cerebellar function
-Impaired ability of basal ganglia to produce timing cues for next motor movement initiation (Cunnington et al., 1996; Toyomura et al., 2015)
-some medications affect basal ganglia positively
-gene based defect? not sure
-can predispose, but not a cause of stuttering
Emotional Issues in Stuttering
Anxiety and Autonomic Fear Arousal
•PWS often have "social anxiety"
-Stuttering is not a neurosis
-they learn to be anxious and frightened because negative things have happened
•Don't confuse this with it being a neurological condition.
-Neurosis meaning ≠ neurological meaning
-react to things easily
-from beginning? but still a lot to learn
•CWS: less able to inhibit emotions (though mixed results)
Emotional Issues in Stuttering cont.
•CWS: startle; react to background noise
•Preschoolers more likely to be shy (Tumanova, Woods, & Razza, 2020)
-Less likely to respond to comments
-Latency to respond to comments
-Not know if a result or cause.
The Emotional Reflex
The brain's instinctive reaction to fear - the 'fight or flight' response
-everybody is uncomfortable and frightened about something
How the Brain Functions in Fear
When an alarm is triggered, signals travel via two pathways
-Quick (reflexive) response from threats (jump, feels like your heart is stopping)
-"Prudent" (mediated) action allows assessment (worried, can think of things, have time)
What are examples of each?
-Reflexive: loud noises, stepping on something painful, bugs, something hot
-Mediated response: presentation to class, heights
How the Brain Functions in Fear cont.
-The function of the "reflexive" pathway cannot be diminished
-But the function of the "mediated" pathway can be enhanced and worked with
-A productive avenue in modifying and mitigating the effects of fear of stuttering
Remembering How You Felt
-Thalamus [houses memories] [relays information to cortex]
-Hippocampus [factual memory]
-Amygdala [emotional learning & fear conditioning]
Conditioned response stored in amygdala. If memory retrieved/triggered from amygdala, will get same emotional response
When do we see this clinically?
•When making phone calls...(remember what happened last time)
•Introductions....(having to say their name)
•During an interview or presentation....(they are going to have to remember how they felt)
•Anticipating a feared word....
Clinical Signs of Emotional Involvement (amygdala triggered)
-Fear and its physiologic effects
-Rapid speaking rate
-Abrupt, forceful articulation and voice onsets
-Feared words; circumlocutions, substitutions
-Diminished cognition of speaking process
-Difficulty managing/coordinating breathing
-Hesitations or reluctance to speak
-Resistance in therapy
Consequences of these emotions
• Not aware of specifics of stuttering [Diminished cognition/denial]
• Social withdrawal
• Pre-stuttering symptoms
• Feelings (denial)
• Behaviors and disfluencies
• Access to targets...
• "I forgot to use my targets."
-we are not aware of what is happening with stuttering
-so into fear
-not aware of what is happened with stuttering
How is this information significant?
• To be able to answer patient questions and explain what stuttering is and what it is not.
-not psychological problem!
• To construct a model of stuttering from which you can justify your therapy.
-frame therapy sessions
-understand why you are doing what you do
-differences between PWS versus FS
Could there be different causes of stuttering?
Are there different types or subtypes of stuttering?
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