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CHAPTER 3. An Historical Perspective of Etiologies.

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Scientists often strive for special status by claiming a unique form of “objectivity” inherent in a supposedly universal procedure called the scientific method. . . . This image may be beguiling, but the claim is chimerical, and ultimately haughty and divisive. For the myth of pure perception raises scientists to a pinnacle above all other struggling intellectuals, who must remain mired in constraints of culture and psyche. (p. 148)

Stephen Jay Gould (1995)

slide3

Slavish adherence to a theoretical protocol and maniacal promotion of a single theoretical approach are utterly in opposition to science. (p. 217) Bruce Wampold (2001)

  • . . . no model or theory will get it right all the time, and in practice, often a single theory (approach) explains only a small amount of the variance in targeted behaviors.” (p.66)

Jill Cockburn (2004)

an historical perspective of etiologies and the zeitgeist
An historical perspective of etiologies . . . and theZEITGEIST
  • “Learning theory seems to suggest that man is basically a ping-pong ball with a memory.”
  • Models of information theory (breakdown theories) suggest that humans are “basically a digital computer constructed by someone who had run out of insulating tape.” (1966, p. 22)
an historical perspective of etiologies and the zeitgeist continued
An historical perspective of etiologies . . . and theZEITGEIST (continued)

“Psychoanalytic theories seem to suggest that man is basically a battlefield. He is in a dark cellar in which a well-bred spinster lady and a sex-crazed monkey are forever engaged in mortal combat, the struggle being refereed by a rather nervous bank clerk.” (1966, p. 21) Don Bannister

so why bother with old or new theories
So why bother with old (or new) theories?
  • Will need an answer (nature v. nurture)
  • Beware of authoritative answers
    • (Ed Conture’s comments, 1990, 2001)
  • Stuttering across time and cultures
  • Your perspective will make a difference to your

client

  • Stereotypes usually negative
    • Anchoring in experience of the fluent speaker
    • Acknowledgement may assist the listener
slide7
Table 3-1Types of theories explaining the onset and development of stuttering described in the following sections.
slide8
Table 3-1Types of theories explaining the onset and development of stuttering described in the following sections. (continued)
emotional psychological views
Emotional/psychological views

Freudian, neo-Freudian

  • Repressed-need hypothesis—stuttering as a symptom
  • The issue is the source/level of the “conflict”
  • Travis, Freund, Glauber, Travis, etc.

Empirical Evidence:

  • Little empirical support—Adams 1993; Yairi 1997
emotional psychological views continued
Emotional/psychological views (continued)

Empirical Evidence (continued):

  • The best research has failed to show that people who stutter, as a group, are more neurotic or have more other psychological disorders than those who do not stutter. We do not think that your child began stuttering because of any serious emotional difficulties. (Yairi & Ambrose, 2005, p. 387)
learning theory
Learning theory

The Diagnsogenic/Semantogenic theory

The diagnosis of stuttering—that is, the decision made by someone that a child is beginning to stutter—is one of the causes of the stuttering problem, and apparently one of the most potent causes. Having labeled the child’s hesitations and repetitions as “stuttering,” the listener—somewhat more often the mother than the father—reacts to them as if they were all that the label implies. (Johnson, 1962, p. 2)

learning theory continued
Learning theory (continued)

Empirical Evidence

  • Many studies showing that earliest stuttering far from normal in both quantity and quality
  • The “Monster” study
behavioral theories
Behavioral theories
  • Classical (respondent) & operant (instrumental) conditioning of behavior
  • Classical models provide better account of onset
  • Operant models offer better account of development
  • Two-Factory Theory—Brutten & Shoemaker (1967)
behavioral theories continued
Behavioral theories (continued)
  • Empirical Evidence
    • Inconsistent results in the laboratory and especially in daily environment (Siegel, 1970)
    • Little explanation of reasons for increases or decreases in fluency
    • Contingent responses most likely highlight or distract, thereby decreasing stuttering
early reports of cerebral asymmetry
Early reports of cerebral asymmetry
  • Orton & Travis in 1920s–30s; handedness etc.
    • Less left-hemi dominance for speech

Wada test, dichotic listening studies, & decreased REA for verbal stimuli

  • EEG studies & ERPs
    • Suppression of neural activity in cortex (right hemi for PWS)
  • Neuroimaging of cortical & subcortical areas
      • Structural: CAT/CT, MRI; X-ray & magnetic properties
      • Functional: RCBF, PET, SPECT, fMRI
structural differences pws nfs
Structural differencesPWS – NFS
  • Both right and left planum temporal larger in PWS
    • Left asymmetry seen in NFS not present
  • Asymmetry for > volume of white (transmission) matter in left hemi for NFS while PWS have more white matter in right hemi.
  • More activity in right frontal operculum (RFO) (BA45) of PWS—possible compensation in this area—rt homologue of Broca’s area
  • Several studies suggesting change to left-hemi activity with fluency enhancing activities and successful treatment—a reorganization of neural functioning.
structural differences pws nfs continued
Structural differences PWS – NFS (continued)
  • A loss, reversal, or reduction of asymmetry between cerebral areas,
  • Aberrant features of white matter tract connectivity and tract size, and
  • Abnormal patterns of perisylvian cortical folding including aberrant sulcal patterns and increased gyrification. (Ingham et al. 2007; p. 63)
functional differences pws nfs
Functional differences PWS – NFS
  • In comparison to fluent speakers, individuals who stutter show overactivation, especially in the right anterior insula (BA 13) as well as the cerebellar vermins and frontal eye fields (BA 8)
  • Anomalous right-dominant lateralization of the above areas
  • Additional motor and nonmotor areas of activation not seen in the fluent speakers
functional differences pws nfs continued
Functional differences PWS – NFS (continued)
  • An absence of auditory activations bilaterally (BA 21/22)
  • A small level of left basal ganglia activation was noted in the fluent speakers (mostly in the putamen) but was not observed in those who stuttered

(Ingham et al., 2007; pp. 59–60)

dual pre motor systems hypothesis p alm 2004 2005
Dual pre-motor systems hypothesis (P. Alm, 2004, 2005)
  • The basal ganglia are subcortical structures in the center of the brain and receive input from many areas of the cerebral cortex and the limbic system
  • The basal ganglia play a key role for the automatization of fast motor sequences; provide timing cues to (SMA) for many activities, including speech
dual pre motor systems hypothesis p alm 2004 2005 continued
Dual pre-motor systems hypothesis (P. Alm, 2004, 2005) (continued)
  • Two premotor pathways—a direct, medial pathway that includes the basal ganglia, limbic system,and the SMA and a lateral, indirect pathway including the lateral premotor cortex and the cerebellum
dual pre motor systems hypothesis p alm 2004 2005 continued1
Dual pre-motor systems hypothesis (P. Alm, 2004, 2005) (continued)
  • The two pathways have different dopamine receptors, with the medialsystem more impaired due to changes in dopamine & greater emotional response via the limbic system
  • A peak in dopamine receptors occurs in the basal ganglia at age 2.5 to 3.0 years. It has also been suggested that the receptors are different in boys.
dual pre motor systems hypothesis p alm 2004 2005 continued2
Dual pre-motor systems hypothesis (P. Alm, 2004, 2005) (continued)

Stuttering occurs when structural or functional anomalies impair the medial system

Fluency-inducing conditions shift speech motor timing to the lateral system, bypassing the instability of the medial system.

the covert repair hypothesis crh kolk postma 1997
The covert repair hypothesis (CRH) (Kolk & Postma, 1997)
  • Via internal monitoring, speakers detect errors in phonological encoding prior to the implementation of articulatory commands
  • Planning of the phonetic sequence is interrupted and the correct plan is reinitiated resulting in a disfluency (for all speakers)
  • It is suggested that PWS possess an abnormally slow rate of phonological encoding requiring more time to activate a target, resulting in a greater chance of error
the covert repair hypothesis crh kolk postma 1997 continued
The covert repair hypothesis (CRH) (Kolk & Postma, 1997) (continued)
  • Detection/repair combined inability to select correct phonological target results in the manifestation of stuttering behavior
  • Some support from several studies including Brocklehurst (2008) who found that CWS have difficulty organizing lexical information
the explan model howell au yeung 2002 howell 2004
The EXPLAN model(Howell & Au-Yeung, 2002; Howell, 2004)
  • Elaborates the CRH with separate linguistic and motor systems
  • System not linked to internal or external monitoring
  • Internal cognitive-linguistic system that covertly plans (PLAN) the syntactic, lexical, phonetic features in serial order
  • Motor process organizes and executes (EX) the output
the explan model howell au yeung 2002 howell 2004 continued
The EXPLAN model(Howell & Au-Yeung, 2002; Howell, 2004) (continued)
  • When linguistic system experiences difficulty generating linguistic sequence the motor system is unable to execute fluent speech
  • PWS have difficulties with motor timing, especially with increased linguistic complexity (some support from studies of motor and syntactical abilities & structural/functional neuroimaging studies)
feedback models fairbanks 1954 mysak 1960
Feedback models(Fairbanks, 1954; Mysak, 1960)
  • Cybernetic & servosystem models of mechanical and biological systems in the 1950s (e.g., Fairbanks, 1954; Mysak, 1960)
  • Interrupted/distorted feedback prevents reduction of error signal to zero
feedback models fairbanks 1954 mysak 1960 continued
Feedback models(Fairbanks, 1954; Mysak, 1960) (continued)
  • Many studies of delayed auditory feedback (DAF)
    • (Black, 1951; Lee, 1951; Neeley, 1961; Yates, 1963)
  • Few theoretical implications but some clinical utility
evidence from the human genome
Evidence from the human genome
  • The human genome is arranged into 24 distinct chromosomes
  • 46 chromosomes with 22 pairs of autosomes and 2 chromosomes that determine sex
    • Females are XX and males are XY
  • Each chromosome contains many genes, each with specific base sequences that encode instructions for making proteins
evidence from the human genome continued
Evidence from the human genome (continued)
  • The human genome is estimated to have 20,000 – 30,000 genes
  • Genotype is determined by the basic DNA of an organism and phenotype provides the outward nature of the organism
  • Monozygotic (MZ) One fertilized egg that develops into two embryos. Dizygotic(DZ) two fertilized eggs that develop separately from two zygotes into two embryos into two embryos.
evidence from the human genome continued1
Evidence from the human genome (continued)
  • Concordance is the occurrence of a trait (e.g., stuttering) in both members of a pair of twins. When this is not the case, the twins are said to be discordant.
  • Stuttering follows familial patterns (Kidd et. al., 1970s)
  • Females who stuttered were likely to have a parent who stuttered 19% of the time; males 67% of the time (Ambrose & Cox, 1997).
evidence from the human genome continued2
Evidence from the human genome (continued)
  • Felsenfeld et al. (2000): 91 twins where one or both stuttered
    • MZ concordant 45% ; DZ concordant 15%
    • 70% of variance for stuttering genetic; 30% environmental
  • Dworznski et al. (2007): longitudinal study of boys & girls, age 2–7; genetic and environmental influence for onset and recovery at rates similar to Felsenfeld
evidence from the human genome continued3
Evidence from the human genome (continued)
  • Yairi & Ambrose (2005): strong family history best predictor of persistence and recovery
  • Marginally significant linkages and relatively low LOD scores to date
    • A desirable threshold for LOD scores is 3.0 (indicating odds of 1,000 to 1)
evidence from the human genome continued4
Evidence from the human genome (continued)
  • Shugart et al. (2004): chromosome 18 (LOD 1.5), (68 families 226 probands of European ancestry)
  • Riaz et al. (2005): chromosomes 1q (LOD 4.61) and 12q (LOD, (46 highly inbred Pakistani families)
  • Viswanath et al. (2004): statistical modeling indicated a significant autosomal major gene interacting with gender and affection status of the parents
evidence from the human genome continued5
Evidence from the human genome (continued)
  • Suresh et al. (2006): females ch 21 (LOD 4.5), males ch 7 (LOD 2.99), ch 7 also linked to specific language impairment and autism
current multifactorial views
Current (multifactorial) views
  • Demands & Capacities

(Starkweather & Gottwald, 1990)

  • A Neurophysiological Model

(De Nil, 1999)

  • A Multifactorial-Dynamic Model

(Smith 1990, 1999; Smith & Kelly, 1997)

demands capacities starkweather gottwald 1990
Demands & capacities (Starkweather & Gottwald, 1990)

Demands:both environmental and internal

Capacities:

Motoric:The ability to initiate and control coarticulatory movements smoothly, rapidly, and with minimal effort

Linguistic:The ability to formulate sentences

Socioemotional:The ability to produce smooth movements when under communicative or emotional stress)

Cognitive:The ability to use metalinguistic skills.

Refer to Figure 3-2 for the Stuttering Diagnostic Space