Lecture 2

Question 1

Genes That Have Been
Linked to Stuttering

Answer 1

 Evidence of mutations in three specific genes among
people who stutter
GNPTAB, GNPTG, and NAGPA
 Associated with cellular metabolism
 NAGPA and GNPTAB
Each is associated with neurological development functioning in
 Hippocampus (emotions)
 Cerebellum (motor control)

Question 2

Diathesis-Stress Model

Answer 2

 Diathesis
One’s predisposition or inherited vulnerability to develop a
disorder

 Stress
One’s life experiences
Environment

 Interactions
Environmental factors can affect likelihood of inherited
vulnerabilities being expressed

Question 3

Diathesis-Stress Model
 Implications
Factors that affect the occurrence of stuttering

Answer 3

Stuttering occurs as a result of various factors
 Multiple genetic risk factors
 Multiple environmental factors
Risk factors can be present, but
 If not sufficient in strength, stuttering symptoms may not
be present

Question 4

Dual Premotor Model of Stuttering
How does it work ?

Answer 4

 According to Per Alm (2004, 2005, 2007a),
speech is a sequential motor activity where
each syllable is initiated by a “go signal”
 The basal ganglia sends timing information
to the supplementary motor area and informs
that the previous signal has executed, and
it’s time for the next syllable

Question 5

Dual Premotor Model of Stuttering
(Continued)
 Stuttering and cluttering are cause

Answer 5

 Stuttering and cluttering are caused by
impaired initiation of speech segments by the
medial premotor system
 Cluttering and stuttering are both opposite
systems of the same functions (impaired
initiation in stuttering; premature initiation of
speech segments in cluttering)

Question 6

Dual Premotor Model
of Stuttering (Continued)

two parallel systems for initiating movements and which areas of the brain are responsible for each system

Answer 6

There are two parallel systems for initiating movements:
 Medial system for spontaneous speech (basal ganglia and SMA)
 Lateral system for automatic tasks (the lateral premotor cortex and the cerebellum)

Question 7

Dual Premotor Model of Stuttering
(Continued)
 Abnormal medial system
What does it do?

Answer 7

 Abnormal medial system shifts the
responsibility for speech timing to the lateral
system during specific communicative
conditions, such as choral reading, singing,
metronome, timed-syllable speech

Question 8

Stuttering as a timing disorder
Van Riper and Kent views

Answer 8

Van Riper (1982) viewed stuttering as mis-coordination of the timing patterns
needed for speech.

Kent (1984) viewed stuttering as a temporal programming disorder. The left
hemisphere is superior to the right in processing rapid auditory patterns
(sounds, syllables, words). Right hemisphere is better equipped for longer
temporal durations (prosody).

Kent points out the possible interference with effective function by overactivity
in the right hemisphere caused by emotional arousal.

Question 9

Lateralization Models
Whose model is it ?

Answer 9

Geschwind-Galaburda model (1985)
 A variety of speech-language disturbances (dyslexia, stuttering,
autism) may arise from delays in left hemisphere development during
gestation.
 Such delays lead to inefficient left hemisphere dominance for
language functions. Because of the loading of such disorders in males,
the authors hypothesized a role of fetal exposure to high levels of
testosterone.

Question 10

Neuroanatomical Differences

Answer 10

– Right lateralized asymmetry in inferior parietal cortex (Foundas et al., 2004)

– Atypical morphology in L inferior frontal cortex (Foundas et al., 2001)

– Demyelination of white matter
– Atypical development of left hemisphere associative and commissural
fibers (Cykowski et al. 2010)

– Atypical white matter tract development near tongue and laryngeal
representation in L. sensorimotor cortex (Sommer et al. 2002)

Question 11

Areas/Tracts with Evidence of Abnormal White Matter
Connectivity/Integrity in Speakers Who Stutter

Answer 11

 Ventral premotor area
 Central premotor cortex
 Ventral perisylvian region
 L anterior perisylvian
cortex
 L rolandic operculum
 L and R arcuate
fasciculus
 L and R superior
longitudinal fasciculus
 Corpus callosum
(anterior, posterior, body,
forceps minor)
 L corticospinal tract
 L corticobulbar tract
 R frontal aslant tract
 Cerebellar peduncles

Question 12

Neuroimaging Studies of Brain Activation
During Various Conditions

Answer 12

 Functional effects:
– Speech-motor control/regulation
– Sensorimotor integration
– Speech-motor planning
– Compensation for impairment

Question 13

Neuroimaging Studies of Brain
Activation During Various Conditions
Types of anomalies

Answer 13

 Types of anomalies
Overactivation
Underactivation
Deactivation
Loss of functional connectivity
Asymmetrical lateralization
Male – female differences