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Anatomical Locality on Haptic Feedback to Attenuate Stuttering by Travis A. Fortin A thesis submitted to the faculty of The University of Mississippi in partial fulfillment of the requirements of the Sally McDonnell Barksdale Honors College. Oxford May 2016 Approved by Advisor: Dr. Dwight Waddell Reader: Dr. Greg Snyder

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Page 1: thesis.honors.olemiss.eduthesis.honors.olemiss.edu/634/1/Thesis Final Travis .docx  · Web viewAnatomical Locality on Haptic Feedback to Attenuate Stuttering. by. Travis A. Fortin

Anatomical Locality on Haptic Feedback to Attenuate Stuttering

byTravis A. Fortin

A thesis submitted to the faculty of The University of Mississippi in partial fulfillment of the requirements of the Sally McDonnell Barksdale Honors College.

OxfordMay 2016

Approved by

Advisor: Dr. Dwight Waddell

Reader: Dr. Greg Snyder

Reader: Dr. Adam Smith

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©2016Travis A. Fortin

ALL RIGHTS RESERVED

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Acknowledgements

I would first like to thank my partner, Meliah Grant. She was instrumental in this

project through her dedication and willingness to help me in every possible way.

Without her, this project would never have gotten off the ground.

I would also like to thank my advisor, Dr. Waddell, for allowing me to partake in this

project. Without him and his efforts, I would not have been able to pursue an

exploratory research in this field.

I would finally like to thank Dr. Snyder. His expertise and assistance to the project in

its entirety was invaluable. I am most appreciative of his willingness to assist me

and find times that would accommodate both of our busy schedules to meet.

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Abstract

Purpose

The purpose of this study was to investigate whether a change in the location of the

tactile stimulator would alter the instances of stuttering.

Method

Each subject was required to read a randomly assigned 300-syllable passage in each

of the five assigned speaking conditions, which includes the control, fingers, chest,

wrist, and foot.

Results

The stuttering count for each condition was analyzed by two trained research

assistants. The median for the control was 44 syllables, the fingers were 41

syllables, the chest was 35 syllables, the wrist was 44 syllables, and the foot was 23

syllables. An RM-ANOVA was performed after data transformation, and revealed no

clear distinction between any of the speaking conditions, however, an overall

reduction in the distribution of instances of stuttering between the control and foot

of nearly 50%.

Conclusions

The null hypothesis was accepted based on the results, however, the results were

not in line with the data from previous publications. The data suggested that the

foot was a promising location in altering the fluency in those who stutter.

Investigating protocol would be beneficial towards future research.

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Table of Contents

LIST OF FIGURES.......................................................................................................................................vi

LIST OF ABBREVIATIONS.....................................................................................................................vii

INTRODUCTION .........................................................................................................................................1

CHAPTER I: Mirror Neurons and Secondary Speech Signals...................................................6

CHAPTER II: Mechanoreceptors and Vibrotactile Perception................................................9

CHAPTER III: Tactile Information in the Brain...........................................................................15

METHODOLOGY.......................................................................................................................................17

RESULTS......................................................................................................................................................21

DISCUSSION................................................................................................................................................25

CONCLUSION:............................................................................................................................................27

CITATION OF SOURCES.........................................................................................................................28

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List of Figures

Figure 1 Relative Comparison of All Speaking Conditions..........................................22

Figure 2 Relative Comparison of Control v. Foot Speaking Conditions.................23

Figure 3 Estimated Marginal Means Relative to Speaking Conditions…..............24

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List of Abbreviations

CNS central nervous system

FA1 fast-adapting type 1; Meissner corpuscles

FA2 fast-adapting type 2; Pacinian corpuscles

fMRI functional magnetic resonance imaging

GNPTAB N-acetyl-glucosamine-1-phosphate transferase gene

PDS persistent developmental stuttering

PPC posterior parietal cortex

S1 primary somatosensory cortex

S2 secondary somatosensory cortex

SA1 slow-adapting type 1; Merkel discs

SA2 slow-adapting type 2; Ruffini corpuscles

SSS secondary speech signal

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Introduction

Stuttering is behaviorally manifested as an involuntary disruption in the fluency of

speech. The speech of those who stutter is encompasses part-word and whole-word

repetitions, prolongations, and inaudible postural fixations (Bloodstein & Bernstein

Ratner, 2008). In contrary to what is commonly believed by the general public,

stuttering not only includes audible repetitions or exaggeration of sounds or

syllables, but it also includes an inaudible component. The disruptions in speech,

audible and inaudible, may also be accompanied by secondary behaviors that

include eye blinking, head movements, jerking of the jaw (Büchel & Sommer, 2004).

These secondary behaviors are conditioned behaviors that are have been ingrained

into the normal vernacular of individuals who stutter with the unintentional

purpose to mitigate the severity of the stuttering (Ashurst & Wasson, 2011).

Naturally, stuttering and the associated secondary behaviors can typically lead to

increased physiological discomfort just like any other disorder. The psychological

discomfort associated with stuttering such as fear or embarrassment has the

potential to possibility to further increase the degree of stuttering in the individual

(Bloodstein, 2008).

There are roughly 3 million people in the United States and 55 million people

worldwide who have some form of the stuttering disorder. This equates to roughly

1% of the global population being people who stutter (Bloodstein & Bernstein

Ratner, 2008). There is no known disparity in stuttering between people of different

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social classes, however, stuttering can be detrimental to one's advancement in

socioeconomic status (Büchel & Sommer, 2004).

It has been estimated that 5% of all children worldwide will experience some form

of stuttering (Ashurst & Wasson, 2011). Stuttering is thought to equally affect men

and women during early childhood, and is consistent with a ratio of two to one

(Yairi & Ambrose, 1999). Nearly 80% of children who present stutter-like

disfluencies will spontaneously recover (Bloodstein, 2008). Young women have

considerably higher spontaneous recovery rates than do young men. The difference

of spontaneous recovery rates can lead to an even greater disparity between the

gender ratios as children age from their early childhood to adolescence

developmental periods. The male-to-female ratio of those who stutter during

adolescence and adulthood is three to four males to every one female (Büchel &

Sommer, 2004).

Stuttering can be acquired or developmental. Developmental stuttering is the most

common form and typically manifests in children from ages three to eight (Ashurst

& Wasson, 2011). These years are extremely critical in a child’s development of

language and speech; hence, the term developmental is used in the nomenclature.

Persistent developmental stuttering (PDS) is the primary form of stuttering that

chronically affects the majority of the stuttering population. PDS has an incidence

estimated at 1% of the global human population. As an idiopathic disorder, PDS is

likely to manifest before puberty between the ages of two and five (Büchel &

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Sommer, 2004). It receives it name from its nature to not spontaneously resolve,

and is even to resist being permanently corrected by speech therapy. Between men

and women, men are more likely to develop an onset of PDS. Men with this form of

stuttering are much more likely to have children who inherently develop

developmental stuttering. When these men reproduce, they have a 9% chance of

having daughters who will develop developmental stuttering, and they will have a

22% chance of producing a son with developmental stuttering (Kidd, 1980). When

women with PDS reproduce, they have a 17% chance of having daughters who will

develop developmental stuttering, and they will have a 36% chance of producing a

son with developmental stuttering (Kidd, 1980). When compared to neurogenic and

psychogenic stuttering, developmental stuttering is typically more prominent in the

beginning of a word or syllable, long or sentimental words, or complex words

(Karniol, 1995; Natke, Grosser, Sandrieser, & Kalveram, 2002). The accompanying

secondary behaviors are usually exaggerated as well (Prasse & Kikano, 2008)(Costa

& Kroll, 2000).

There are two other forms of stuttering, both of which are of little significance to

this particular study, however, they are both worthy of mention to grasp a better

understanding of the subject matter. The first is neurogenic stuttering, also referred

to as acquired stuttering, manifests after a significant injury to the brain. A

significant injury to the brain can encompass a stroke, hemorrhage, traumatic

injury, or Alzheimer disease (Ashurst & Wasson, 2011). People with neurogenic

stuttering lack the secondary behaviors that can be seen in developmental

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stuttering. The second is the psychogenic form of stuttering. This type of stuttering

one in which a person who stutters will rapidly repeat the initial sounds of a word.

Psychogenic stuttering is most often seen in adults who have had a history of

psychological disorders or emotional trauma (Ashurst & Wasson, 2011).

Although not fully understood, a strong amount of evidence indicates that a genetic

pathology in stuttering is possible (Kang et al., 2010). This genetic basis in

stuttering, more specifically PDS, reveals a correlation to the improper functioning

of the central nervous system (Bloodstein & Bernstein Ratner, 2008). Dysfunction in

the CNS has been thought to be a result of incomplete left lateralization of speech

and other motor processes. Over activation of the right hemisphere during speech

and language production (Fox et al., 2000), reduced metabolic glucose activity in the

left frontal and limbic regions (Wu et al., 1995), and abnormal cerebral laterality

(Foundas et al., 2003) are types of significant neurological activation patterns that

affect adults with PDS. Determined through twin studies, nearly 70% of

developmental stuttering is associated to genetics (Felsenfeld et al., 2000). An

example of a genetic pathology in stuttering has been found in select families in

Pakistan who have a familial linkage to PDS (Kang et al., 2010). The family that had

the most prolific stuttering in the study conducted by Kang et al had a missense

point mutation on chromosome arm 12q in the N-acetyl-glucosamine-1-phosphate

transferase gene (GNPTAB) (Kang et al., 2010). This mutation caused a substitution

of a lysine residue for a glutamic acid residue at position 1200 (Glu1200Lys) in

GlcNAc-phosphotransferase (Kang et al., 2010). They theorized that the mutations

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in their genes such as this one caused a lysosomal malfunction where the efficiency

of lysosomal targeting of enzymes is minimized (Kang et al., 2010).

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Mirror Neurons and Secondary Speech Signals

In contrary to data that indicates a genetic basis to the pathology of stuttering,

management techniques continue to limit themselves to the instruction and

execution of behavioral speech targets (Bloodstein & Bernstein Ratner, 2008),

which results in a high prevalence of therapeutic relapse (Saltuklaroglu &

Kalinowski, 2005). In recent years, research has indicated that there is a link

between gestural perception and production to enhance the fluent speech in people

who stutter (Saltuklaroglu & Kalinowski, 2011). The idea behind the perception-

production link in speech and fluency enhancement lies in the concept of the mirror

system hypothesis (Saltuklaroglu & Kalinowski, 2011). Mirror neurons, which are

primarily thought to be central to behavioral characteristics such as observational

learning and empathy, are involved in processing language (i.e. linguistic gestures),

speech (i.e. linguistic gestures expressed through the vocal tract) (Rizzolatti &

Arbib, 1998), manual and oral activity (Ferrari, Gallese, Rizzolatti, & Fogassi, 2003),

and have been thought to provide a neural substrate for enhanced fluency in people

who stutter through a secondary speech signal (SSS) (Saltuklaroglu & Kalinowski,

2011).

An SSS is the speech feedback of a second gesturally similar and concurrent speech

signal relative to the original spoken speech signal (Kalinowski, Stuart, Rastatter,

Snyder, & Dayalu, 2000). A SSS can be administered several ways (e.g. auditory,

visual, tactile), and has the ability to be used synchronously or asynchronously with

the production of the speaker’s original speech signal (Kalinowski et al., 2000;

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Snyder, Hough, Blanchet, Ivy, & Waddell, 2009; Waddell, Goggans, & Snyder, 2012).

Through the use of perception and production (speech) gestures, researchers are

able to interpret the neural mechanism of fluency enhancement as the engagement

of mirror neuron networks (Saltuklaroglu & Kalinowski, 2011). In a publication,

Mirror neurons as a model for the science and treatment of stuttering, researchers

initiated an exploratory study to test the viability of the mirror neuron system

hypothesis in the fluency enhancement of those who stutter (Snyder, Waddell, &

Blanchet, 2016). The data they collected was interpreted to support the use of the

mirror neuron system hypothesis relative to the study and enhancement of fluent

speech in those who stutter (Snyder et al., 2016). The fluency enhancement in the

study was significant, however, it was suspected that it would not be as profound as

other implementations of an SSS (Bloodstein & Bernstein Ratner, 2008; Kalinowski

et al., 2000; Saltuklaroglu & Kalinowski, 2011; Snyder et al., 2009; Waddell et al.,

2012). The difference exists in that voiceless gestures within the SSS do not improve

fluency as well as voiced gestures within an SSS (Dayalu, Saltuklaroglu, Kalinowski,

Stuart, & Rastatter, 2001). SSS’s perform better when there is more similarity to the

speaker’s primary speech signal (Guntupalli, Nanjundeswaran, Kalinowski, &

Dayalu, 2011). It is suggested that action-understanding networks, which highlight

the role of the basal ganglia and subthalamic networks (Caligiore, Pezzulo, Miall, &

Baldassarre, 2013), are significant in supporting mirror neuron networks relative to

the enhancement of fluent speech in those who stutter (Saltuklaroglu & Kalinowski,

2011). Interestingly, increased activity within the basal ganglia-thalamocortical

network was also found while measuring contingent negative variations in those

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who stutter (Vanhoutte et al., 2015). The activation of this network has been

hypothesized to serve as a successful compensation strategy (Vanhoutte et al.,

2015). The compensation strategy proposed is that people who stutter may attempt

to use the action of stuttered speech as a compensatory behavior to trigger this

alternate premotor network, thereby initiating subsequent gestural productions.

This study was centralized around the concept of using tactile feedback as a means

of an SSS. In SSS’s using tactile feedback, the vocalization produced by those who

stutter was captured by an accelerometer where the signal was processed and then

returned through an output as a mechanical tactile speech feedback to the person’s

skin (Waddell et al., 2012). The results from the publication (Waddell et al., 2012)

determined that the accelerometer-driven tactile feedback minimized stuttering by

up to 80%(Waddell et al., 2012). It was ultimately determined that the self-

generated tactile feedback can significantly increase fluency for people who stutter

(Waddell et al., 2012). Although a different set of hardware was used to process the

vocalization in this particular study, the end result of stimulating the skin through

tactile feedback remained constant.

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Mechanoreceptors and Vibrotactile Perception

Tactile sensation is dependent on the afferent function relaying the sensory

information between the skin and central nervous system (Fromy, Sigaudo-Roussel,

& Saumet, 2008). This involves the cutaneous transducers detecting mechanical

stimuli and the transmission of the sensory stimuli to higher brain structures,

including the efferent function of sensory nerve fibers by releasing

neurotransmitters in the skin (Fromy et al., 2008).

Tactile information is relayed from the peripheral nervous system to the central

nervous system, more specifically, the thalamus in the brain. This pathway

constantly innervates the brain with interaction with the skin. Mechanoreceptive

afferents can process a vast amount of information from tactile stimulation to the

skin, such as force, pressure, and vibration (Johnson, 2001; Knibestöl & Vallbo,

1980). The skin has several different types of mechanoreceptive afferent. They are

differentiated by whether they have glabrous or hairy skin, and whether they have

fast-conducting myelinated axons (30-75 m/s) or slow-conducting unmyelinated

axons (~1 m/s) (Ackerley & Kavounoudias, 2015). Mechanoreceptive afferent are

also differentiated by their ability to adapt to a constant tactile indentation (slow-,

intermediate-, or fast-adapting) (Ackerley & Kavounoudias, 2015). Merkel discs,

Ruffini corpuscles, and Pacinian corpuscles mechanoreceptive afferents, myelinated

hair afferents, field afferents (Vallbo & Johansson, 1984), and C-tactile (CT) afferents

have all been found on hairy skin (Vallbo, Olausson, & Wessberg, 1999). CT

afferents, which are related to the pleasantness of sensation, relay soft touches with

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a delay of >1.5 s before the information is processed in the brain. The delay is a

result of the slow conduction along the unmyelinated axon (Ackerley, Eriksson, &

Wessberg, 2013).

The glabrous skin has four main types of mechanoreceptive afferent, which

specialize in providing information to the central nervous system (Ackerley &

Kavounoudias, 2015). Providing information about cutaneous tension, pressure,

touch, and vibration, they are fast-adapting type 1 (FA1, Meissner corpuscles),

slowly adapting type 1 (SA1, Merkel discs), fast-adapting type 2 (FA2, Pacinian

corpuscles) and slowly adapting type 2 (SA2, Ruffini corpuscles) mechanoreceptive

afferents (Ackerley & Kavounoudias, 2015). Type 1 mechanoreceptive afferents

have small, pointed receptive fields, and type 2 affects have large, branched

receptive fields (Ackerley & Kavounoudias, 2015).

Pacinian corpuscles and Meissner's corpuscles are collectively known as low-

threshold or high-sensitivity mechanoreceptors because they can elicit action

potentials from faint mechanical stimulation to the skin. The Meissner and Pacinian

corpuscles are found in glabrous skin and come with the ability to rapidly adapt to

stimuli. Merkel’s disks and Ruffini’s corpuscles are cutaneous mechanoreceptors

that are slowly adapting.  

Meissner corpuscles are mechanoreceptors that respond to low frequency stimuli.

The Meissner corpuscles are found in the dermal papillae under the epidermis of the

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fingers, palms, and soles. The mechanoreceptors that are found in the most

abundance in glabrous skin are Meissner corpuscles. They are elongated receptors

that are formed by a connective tissue capsule of Schwann cells (Purves et al., 2001).

Afferent nerve fibers that produce fast adapting action potentials from minimal

stimulation to the skin are found in the center of the capsule (Purves et al., 2001).

The densities of Meissner corpuscles are the highest in the fingertips and diminish

in presence from distal to proximal areas (Johansson & Vallbo, 1979). Their afferent

fibers compose around 40% of the sensory innervation in the hand (Purves et al.,

2001). Information is most efficiently transduced at low-frequency vibrations

(Purves et al., 2001).

Pacinian corpuscles are encapsulated endings that are found in the subcutaneous

tissues of the body and are more responsive to high frequency stimuli. The Pacinian

corpuscle is a multi-layered capsule such that the inner core of membrane lamellae

is separated from an outer lamella by fluid. In the center of the capsule, lies one or

more fast adapting afferent axons. Compared to Meissner corpuscles, the Pacinian

corpuscles have a lower response threshold and adapt more rapidly. It has been

noted that the lower response threshold and the ability to adapt more rapidly in

Pacinian corpuscles allow them to discriminate stimuli that produce high-frequency

vibrations on the skin (Purves et al., 2001). Of the cutaneous receptors in the human

hand, the Pacinian corpuscles comprise 10-15% of them. It is speculated that

Pacinian corpuscles found in interosseous membranes detect vibrations transmitted

to the skeleton.

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Located in the epidermis, Merkel’s disks are aligned with the papillae that are

situation just under the dermal ridges. They are densely packed in the external

genitalia, fingertips, and lips. It is estimated that Merkel’s disks make up 25% of the

mechanoreceptors in the hand (Purves et al., 2001). The slowly adapting nerve

fibers in Merkel’s disk experiences a change in shape into a saucer-shaped ending

that is applied to another specialized cell which contains vesicles that excrete

peptides that influence the nerve terminal (Purves et al., 2001). When these

mechanoreceptors are stimulated, the hand feels slight pressure. Merkel’s disks are

responsible in the static discrimination of edges, rough textures, and shapes that are

encountered during everyday life.

The last of the four mechanoreceptors located in the hand are the Ruffini’s

corpuscles. These mechanoreceptors do not elicit a tactile sensation when they

receive an electrical stimulation. They are elongated, spindle-shaped capsular

specializations which are found deep in the skin (Purves et al., 2001). The long axis

of the corpuscle is fashioned in a parallel orientation to the stretch lines in the skin,

thus making the Ruffini’s corpuscle sensitive to the cutaneous stretching produced

by limb movement (Purves et al., 2001). They comprise nearly 20% of the

mechanoreceptors in the human hand.

The human hand is composed of nearly 17,000 myelinated mechanoreceptors

(Johansson & Vallbo, 1979). Of the myelinated mechanoreceptors in the hand, 43%

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are Meissner corpuscles, 25% are Merkel discs, 13% are Pacinian corpuscles, and

19% are Ruffini corpuscles (Johansson & Vallbo, 1979). A high density of

mechanoreceptors allows the hands to effectively sense tactile stimuli and

discriminate between various tactile surfaces. Meissner corpuscles are the densest

in the fingertips, which allow them to have the highest sensitivity of tactile stimuli

and the highest discrimination between tactile surfaces in the hand (Ackerley &

Kavounoudias, 2015).

Vibrotactile Perception in Finger Pulps and in the Sole of the Foot in Healthy Subjects

among Children or Adolescents was a recent publication in 2015 that evaluated the

vibrotactile perception at different frequencies in the fingers and feet of healthy

children and adolescents. The vibrotactile perception thresholds were measured in

the finger pulps of the index and little fingers and at the first and fifth metatarsal

head and at hell in the sole of the foot (Dahlin, Güner, Larsson, & Speidel, 2015). The

results determined that at all three of the examined sites in the sole of the foot had

vibrotactile perception thresholds that increased proportionally with higher

frequencies (Dahlin et al., 2015). The vibrotactile perception thresholds at lower

frequencies were found to be higher in finger pulps, whereas at higher frequencies,

vibrotactile perception thresholds were lower in the finger pulps than in the sole of

the foot (Dahlin et al., 2015). The conclusion determined from this information

provided an inverse relationship between the vibrotactile perception in the sole of

the foot and that of the finger pulps. This means that the tactile perception in the

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sole is superior to the finger pulps at lower frequencies, but inferior at higher

frequencies.

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Tactile Information in the Brain

Upon stimulation of a mechanoreceptor, the first-order neuron outputs the

information to the central nervous system and up the spinal cord. In the spinal cord,

second-order neurons in the dorsal column nuclei transmit projections across the

midline, terminating in the thalamus (Ackerley & Kavounoudias, 2015). Tactile

information is processed and integrated cortically in the somatosensory cortex upon

innervation from third-order neurons originating in the thalamus (Mountcastle,

1957).

The cortical areas related to tactile processing work in a network, which include the

contralateral primary somatosensory cortex (S1), the bilateral secondary

somatosensory cortices (S2), and the contralateral posterior parietal cortex (PPC)

(Ackerley & Kavounoudias, 2015). These cortices are activated by touch, which can

be seen during functional magnetic resonance imaging (fMRI) (Ackerley et al., 2012;

Disbrow, Roberts, & Krubitzer, 2000; Francis et al., 2000).

It is to be believed that incoming tactile information in humans is connected in

parallel rather than in series. The first cortical activity is registered in the

contralateral S1 about 20-30 ms after stimulation to the electrical nerve, and about

90 ms in the contralateral and ipsilateral S2 (Allison, McCarthy, Wood, & Jones,

1991; Wegner, Forss, & Salenius, 2000). Information flows between the S1 and S2.

The S1 tallies the differences in firing between the SA1 afferents in close proximity

and the S2 integrates the information (Hsiao, Johnson, & Twombly, 1993). The S2

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helps discriminate in somatosensory processing, however, somatotopic maps, which

can be found in S1, are absent in the S2 (Ackerley & Kavounoudias, 2015). Tactile

stimulation received on only one side of the body can produce bilateral activations

in the S2 during an fMRI (Disbrow et al., 2000; Ruben et al., 2001).

Third order neurons from the ventral posterolateral nucleus of the thalamus, which

terminate somatotopically, send projections to the S1 (Ackerley & Kavounoudias,

2015). The S1 cortical layer IV is the final destination of the inputs directed to the

thalamus (Ackerley & Kavounoudias, 2015). As a result, neurons from the S1

cortical layer IV project onto nearby cortical areas (Ackerley & Kavounoudias,

2015). The Brodmann area 3B receives the brunt of the thalamic input and is unique

to FA1, SA1, and SA2 afferents in responsivity. The thalamus, which essentially is the

final destination of the tactile stimuli, is the key to relieving the instances of

stuttering in SSS’s. Although the general process of relaying information to the

thalamus is understood, the mechanism explaining how tactile information that is

administered through the use of a SSS affects the instances of stuttering after it

reaches the thalamus is not understood. Therefore, the purpose of this study is to

measure the effects of the tactile feedback on the enhancement of fluency in those

who stutter.

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Methodology

Design and Procedure

The subjects were required to read 300-syllable passages taken from junior high

science textbooks, all of which have been used in previous research (Kalinowski et

al., 2000). All of the trials were conducted in the same room, which was sound-

controlled and quiet. Each subject was required to read a randomly assigned

passaged along with a randomly assigned location. The five speaking conditions

were: (a) collar worn with no tactile stimulator - control, (b) collar worn with tactile

stimulator located between the right index and thumb, (c) collar worn with tactile

stimulator located at the top of the right pectoralis major, (d) collar worn with

tactile stimulator located on the ventral side of the right wrist, (e) collar worn with

tactile stimulator located in the middle of the ventral side of the right foot. During

the trials, subjects were instructed to read the passage aloud in what they

considered a normal tone of voice without using any coping mechanisms. Stuttering

was defined as whole-part and part-word repetitions, sounds or syllable

prolongations, or audible postural fixations (Bloodstein & Bernstein Ratner, 2008).

The stuttered syllables from the read passages were quantified by two trained

research assistants for each condition.

Subjects

The subjects consisted of five right-handed adults who stutter. The degree of

stuttering seen in the subjects ranged from mild to severe, which was informally

determined during the course of data collection. Other than stuttering, the subjects

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reported no diagnosed speech, language, or hearing disorders, and they all had at

least a high school education. Each subject was provided informed consent as

approved by the University’s Institutional Review Board before his or her

participation in the study.

Instrumentation

Amplifiers

After the information received by the transducer collar was processed through a

high-pass filter and a low –pass filter, the signal was then passed through two

amplifiers. The first amplifier was a HP 465A Amplifier, which is a general-purpose

amplifier, and an ideal impedance converter (10 mega-ohms to 50 ohms). The

amplifier was used at a 20-dB gain over a continuous frequency range of 5 cps to 1

megacycle. The second amplifier is an AudioSource AMP 5.3A Monoblock Amplifier.

The specifications of the amplifier include: power output of 250 watts RMS 250

watts RMS (20-20,000 Hz, <0.1% THD at 4 ohms), signal to noise ratio of 95 dB,

damping factor greater than 200 at 4 ohms, balanced input impedance of 20k ohms,

unbalanced input impedance of 10k ohms, and an auto-on input sensitivity of 1V.

Filters

The information received by the transducer collar was passed through a filter. The

filter comprised of a high-pass filter and a low-pass filter. In comparison to the Ole

Miss Stuttering Device, the use of the high-pass and low-pass filters was omitted.

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Oscilloscope

A Tektronix TDS 3012 two-channel color digital phosphor oscilloscope was used to

keep the intensity of the vibration produced by the tactile stimulator relatively

constant. Regulating the intensity was accomplished by keeping the voltage output

under a reading of 10 volts.

Throat Accelerometer

An ACH-0l-03/l0 accelerometer (Measurement Specialties Inc., Hampton, Virginia,

USA) was used to record the vibrations and the movement of the vocal chords from

the subject’s throat on a one-dimensional recording axis orthogonal to the skin

surface. The accelerometer provided the input into the tactile stimulator. It uses a

piezoelectric film as a transducer coupled with a junction gate field-effect transistor

(JFET). The JFET uses a DC power supply, and the piezoelectric transducer behaves

in such a way that allows it to control how much signal needs to sent as an output

through the JFET, depending on the acceleration experienced by the transducer. A

three-stage Sallen–Key high-pass Butterworth filter was used to block frequencies

lower than those produced by the human voice. This filter mitigates the device from

responding to user movement, and only responding to vibrations from vocal input.

The accelerometer directs the electrical signal to an interface. The tactile stimulator

is then innervated by the electrical output given by the interface.

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Transducer collar

The transducer collar is a hemispherical collar that was modified from a hands-free

microphone headset. Being obsolete, the earphones were removed from the collar. A

microphone and a one-dimensional accelerometer were unilaterally mounted in the

earphones stead. These newly added components served as input transducers for

the subject’s vocal activity. The collar could have been worn on either side of the

neck; usually what is most comfortable for the subject. The microphone and

accelerometer rested comfortably against the subject’s thyroid cartilage.

Tactile stimulator

The tactile feedback was provided to the skin through the use of a specialized skin

transducer called an Audiological Engineering Skin transducer (Model VBW32 Skin

Transducer). The intent of the product is to output mechanical vibrations to the

skin. The input to the skin transducer was the electrical signal sent from the input

transducers from the collar. The peak frequency transmitted by this device is 250

Hz. The tactile stimulator was administered to four locations: between the index and

thumb, the top of the pectoralis major, the ventral side of the wrist, and the middle

of the ventral side of the foot. All locations other than the fingers were held in place

with black ACE sports tape with just enough pressure to ensure that the tactile

stimulator was secure.

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Results

For the speaking conditions, each instance of stuttering was counted for each

syllable out of the total 300 syllables in each passage. The stuttering count for each

condition was analyzed without the aid of transformation. The distributions of

stuttering frequency as a function of experimental speaking condition are presented

in Fig. 1. The medians for each of the speaking conditions were all relatively similar.

The median for the control was 44 syllables, the fingers were 41 syllables, the chest

was 35 syllables, the wrist was 44 syllables, and the foot was 23 syllables. Based on

the data presented in Fig. 1, there was no clear distinction between any of the

speaking conditions. The only notable difference in any of the conditions was

between the control and the foot, which can be seen more clearly in Fig. 2. There

was an overall reduction in the distribution of the instances of stuttering of nearly

50%. Their medians differ by 21 syllables.

21

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55555N =

L oc a tion o f Tac ti le S tim u la to r

FootWri stChestFi ngerControl

Num

ber o

f Stu

ttere

d Sy

llabl

es 100

80

60

40

20

0

-20

Stut

tere

d Sy

llabl

es

Location of Tactile Stimulator

Relative Comparison of All Speaking Conditions

Fig. 1

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55N =

L oc a tion o f Tac ti le Stim ula to r

FootControl

Num

ber o

f Stu

ttere

d Sy

llabl

es 80

70

60

50

40

30

20

10

0

Stut

tere

d Sy

llabl

es

Location of Tactile Stimulator

Fig. 2

Relative Comparison of Control v. Foot Speaking Conditions

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Est imated Marg inal MeansRelat ive to Speaking Cond it ion

Spea k ing Co ndition

FootWri stChestFi ngersControl

Aver

age

Num

ber o

f Stu

ttere

d Sy

llabl

es

38

36

34

32

30

28

Fig. 3

Stut

tere

d Sy

llabl

es

Location of Tactile Stimulator

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Discussion

The results obtained through this experiment came as a surprise. Previous

publications have shown that the frequency of overt stuttering can be significantly

reduced through the use of a tactile SSS. More specifically, previous publications

have shown that novel tactile feedback can significantly reduce the instances of

overt stuttering when a tactile stimulator is held between the index finger and the

thumb versus a control of no tactile stimulation (Waddell et al., 2012). The findings

from previous publications related to novel tactile feedback were the foundation for

developing this particular experiment. Unlike the results found in previous

publications, the results in this experiment, however, showed that there was no

difference between the locations of the index finger and thumb versus the control.

The results can only suggest that factors yet to be discovered resulted in the lack of

significance in the data between the control condition and the speaking conditions

using tactile stimulation. A highly unlikely, but possible factor that could have

caused the unfavorable results and the difference between results found in previous

publications using tactile feedback to reduce the instances of stuttering, was that a

different set of equipment was used in providing the tactile stimulation from the

primary speech of those who stutter. This hypothesis is highly unlikely because as

long as tactile feedback is the end result, the path the tactile feedback takes to get to

the skin should not matter. Evidence in the mirror neuron theory suggests that the

absence of clinical instruction may have ultimately caused the unfavorable results

and the difference between the results in previous publications using tactile

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feedback (Snyder et al., 2016). Clinical instruction would have allowed the subjects

to have a unique understanding on how to use tactile feedback though coaching on

how to tune in to the tactile feedback and though more practice with tactile

feedback in general. In essence, the subjects were given a tool without any

knowledge of how to use it.

There were some notable differences between some of the speaking conditions. The

location of the chest proved to be a poor choice for tactile feedback for two reasons.

All patients reported having difficulty feeling the tactile stimulation in the chest,

which was most likely due to the low sensitivity of the skin in the chest. Another

reason why the location of the chest proved to ultimately be ineffective was that the

relative distance between the collar and the tactile feedback stimulator created

interference. In contrast to the chest, the location of the ventral side of the foot

proved to be the most favorable location between the subjects. They reported that

the foot was not only a comfortable location, but that they could feel the tactile

stimulation in the foot the best. Their claims fell in line with the data, where the foot

out preformed all other speaking conditions, which can be seen best in Fig. 2.

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Conclusion

The null hypothesis stated that there was no difference in the reduction of stuttering

between different locations of the tactile stimuli. The null hypothesis was ultimately

accepted based on the results. Even though the trend was small, there was a

reduction in the instances of stuttering clear enough to suggest that unknown

factors may have caused the results to depart from previous publications. The

experiment failed to replicate previous publications due to a departure in previous

procedures with the use of a new apparatus and with the absence of clinical

instruction. A call for more research is necessary to arrive at a definitive answer as

to why data behaved the way that it did.

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