Dysfluency secondary to CNS damage

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Dysfluency secondary to CNS damage
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Subgroups of acquired fluency disorders

• True neurogenic stuttering is also known as
  acquired or cortical stuttering.
• However, it must be distinguished from other
  fluency disturbances following CNS damage that
  share few features with classic stuttering
• Subgroups include
• Dysarthric disfluency
• Apraxic disfluency
• Disfluency stemming from anomia
• Palilalia

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Dysarthric disfluency

• This category includes Parkinsonian patients, who
  often demonstrate
• Frequent prolongations
• Rapid sound, syllable and word repetitions
• blocking associated with failure to progress to
  the next articulatory target
• Symptoms worsen as the disease progresses (Benke,
  et al., 2000) levodopa treatment may further
  aggravate fluency (Louis, et al., 2001)

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Dysarthria (continued)

• PD may prompt re-emergence of developmental
  stuttering (Shahed Jonkovic, 2001).
• Ataxic dysarthrics may show
• Long prolongations
• Easy repetitions

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Other subgroups

• Apraxic dysfluency apraxic patients often repeat
  initial segments while groping for the
  appropriate target this needs to be
  distinguished from the stuttering behavior of
  perseverative repetitions of the correct target,
  as in true stuttering. Both may be seen in
  apraxia.
• Some people have suggested that the two disorders
  share a common neurological basis.

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Dysfluency stemming from anomia

• Dysfluencies are characterized primarily by
  pausing, articulatory groping, and the
  interjection of filled pauses and/or phrase
  repetitions while searching for lexical targets.
• Usually, other additional aphasic symptoms are
  present
• Wernickes patients may be more prone to this
  pattern of dysfluency than other aphasic
  syndromes.

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Palilalia

• Found in a number of neurological conditions
  (including Parkinsons), speech is characterized
  primarily by
• word and phrase repetitions (NOT) sound or
  syllable repetitions) that may become
  increasingly more rapid, and progressively more
  unintelligible.

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True cortical stuttering

• Quite rare
• Typically documented in the literature through
  isolated case studies
• Patients show true stutter-like symptoms which
  cannot be attributed to neuromotor or language
  planning disturbance

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Causes of cortical stuttering

• Stroke, typically multiple and bilateral events
• However, site of lesion has been reported to be
  extremely variable (Franco, et al., 2000
  including subcortical regions Ciabarra, et al.,
  2000) and occasionally subtle enough to be
  detected only using very sophisticated measures
  (e.g., SPECT, Heuer, et al., 1996).
• This variability has impeded the use of acquired
  stuttering cases to shed light on the underlying
  defect in developmental stuttering.
• Stroke sometimes prompts return of resolved
  developmental stuttering (Mouradian, et al., 2000)

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Causes (continued)

• Penetrating objects and tumors
• Occasionally, there are reports of stuttering
  caused/cured by removal of tumors or invasive
  objects
• CHI these cases typically show
• bilateral involvement
• loss of consciousness after injury
• Development of seizure disorder
• Emergence of stuttering following establishment
  of seizure disorder
• Senile and dialysis dementia

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Drug-induced stuttering

• A wide number of medications have been reported
  to induce disfluency, including some that have
  been shown to marginally increase fluency in
  developmental stuttering (Brady, 1998).
• Similarly, while trials continue to explore the
  use of medication in alleviating stuttering
  (e.g., resperidone, Maguire, et al., 2000)),
  there is some consensus that medications will
  best augment, rather than replace, conventional
  therapy in stuttering treatment.

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Overlap Neurogenic and psychogenic stuttering

• Psychogenic stuttering, while rare, typically
  shows some symptom overlap with neurogenic
  dysfluency
• Patients often show evidence of some degree of
  neurological insult or disease state
• Differential diagnosis is important, and focuses
  on ruling out potential alternative explanations
  for the dysfluency, while gauging pt. profile
  similarity to known neurogenic subgroups (see
  Helm-Estabrooks Hotz (1998) for case study
  example.)

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Features of neurogenic and psychogenic
stuttering (from Manning, 2001)

• NEUROGENIC
• Disfluencies on function as well as content words
• Speaker annoyed but not usually anxious
• Behaviors not solely on initial syllables
• Secondary symptoms not linked to disfluencies
• Lack of adaptation effect
• lack of variability across speaking tasks and
  situations

• PSYCHOGENIC
• Rapid and favorable response to limited treatment
• Bizarre struggle and other signs of anxiety
• Stuttering may be episodic
• Stuttering pattern differs from both
  developmental and neurogenic stuttering

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Treatment

• If stuttering is accompanied by seizure disorder,
  medications to control seizures often ameliorate
  dysfluency
• Remission most often occurs within three months
  persistent cases have less favorable prognosis
• Combination of fluency shaping (emphasis on rate
  and pacing) and stuttering modification (to
  reduce struggle) is most often recommended.
  Limited efficacy data are available.