Advanced Articulation Disorders Chapters 12 & 13

  1. Absence of speech
  2. Speechlessness due to a severe loss of neuromuscular control over speech; usually reserved for dysarthria in its most severe form.
  3. Why can't anarthric individuals speak? 
    How is their language/cognition?
    • Neuromuscular system doesn't permit speech
    • Language and Cognition may be intact
  4. What types of dyarthria are most likely the culprits when a single dysarthria type leads to anarthria?
    • Spastic
    • Hypokinetic
  5. Spastic dysarthria represents the most frequent cause of anarthria in __________ diseases.
  6. Which account for more cases of anarthria:  Mixed type or Single type?
    Mixed type
  7. What is the most frequent cause of anarthria?
  8. Special & dramatic manifestation of anarthria characterized by total immobility of the body except for vertical eye movements and blinking; cognition intact so can communicate with eye movements.
    Locked-in syndrome
  9. Describe the prognosis for an individual with Locked-in syndrome.
    • Poor
    • Dysphagia severe
    • 90% mortality rate / 4 months after onset
    • Pulmonary complications most common cause of death
  10. Long term survival of Locked-in syndrome has improved; People w/ _________ etiologies tend to show earlier/more complete recovery.
  11. What is the leading cause of Locked-in syndrome?
  12. Syndrome characterized by severely reduced voluntary orofacial mobility. (Hypotonic/void appearance)
    Biopercular syndrome
  13. Due to severe dysphagia, pts with biopercular syndrome are at high risk for ________________.
    Aspiration pneumonia
  14. What may be a good mode of communication for a patient with biopercular syndrome?
    • Writing
    • limb movments may be preserved
  15. When biopercular syndrome etiology is _________, the severe dyarthria and dysphagia tend to persist.
  16. Biopercular syndrome is nearly always caused by ________.
  17. Biopercular syndrome frequently occurs after a __________ opercular lesion from which there may be good recovery, followed by a second stroke on the other side.
  18. A patient with biopercular syndrome is likely to have a poor prognosis for recovery for speech, at least when the etiology is __________ or __________.
    • Vascular
    • Degenerative
  19. What type of mutism is primarily seen in children aged 6-9 yrs and nearly always follows surgery to remove large tumors?
    Cerebellar mutism
  20. 29% of patients undergoing sugery to remove cerebellar tumors develop _______ mutism, so the problem is not rare and may be considered the price paid to cure them.
    Transient (not permanent)
  21. When speech re-emerges in a patient with cerebellar mutism, _________ is apparent in 80% or more of the cases.
  22. It's not unusual, in the acute stage, for _____________ to be associated with mutism, but it seldom lasts for more than a few days when caused by stroke but sometimes can persist even in the absence of aphasia & dysarthria.
    Apraxia of speech
  23. Mutism in the acute period following onset of aphasia in __________ is not unusual but persisting mutism, even in people with ____________ is uncommon.
    • Adulthood
    • Global aphasia
  24. Aphasia & AOS acquired in ___________ (stroke/trauma)is often associated with a period of mutism.
  25. What 2 things could persisting mutism raise suspicions about?
    • Aphasia diagnosis inaccuracy
    • Additional problems present (MSDs or nonaphasic cognitive deficits)
  26. State of unarousable unresponsiveness and absence of sleep/wake cycles on EEG.
    • Coma
    • disorders of arousal
  27. Describe a patient's behavior in a coma.
    • Voluntary behavior diminished/absent
    • Eyes closed
    • No purposeful movement
    • Responses are reflexive
  28. What types of damage could a patient in a coma most likely have?
    • Bilateral cerebral hemispheric damage
    • Brainstem injury
    • Both
  29. What are the 2 most common etiologies for coma?
    • TBI
    • Vascular events
  30. Patients in this state fail to show higher level cerebral function, don't exhibit purposeful behavior, are unable to interact, but do maintain wake-sleep cycles.
    Vegetative state
  31. Vegetative state generally follows an initial period of coma when caused by ______, but can occur w/out precedic coma in ___________ & ___________.
    • TBI
    • Metabolic disorders
    • Severe dementia
  32. Describe the neurological pathology associated with patients in a vegetative state.
    • Bilateral cerebral hemispheric pathology
    • Brainstem functions relatively preserved
  33. What type of etologies are associated with vegetative state?
    • Widespread Cortical dysfunction
    • (TBI, anoxia, toxic drugs, Alzheimer's)
  34. Patients in an ___________ state can appear similar to those in a vegetative state; difference may be only one of __________.
    • Apallic state (Coma Vigil)
    • Degree
  35. Referring to the absence of the pallium or grey matter of the cortex.
  36. Patients in this state may respond to painful stimuli, sit as placed, have prominent sucking/grasping reflexes, move/shout spontaneously, visually follow examiner but feeling, thought, and motivation to act are absent.
    Apallic State (Coma Vigil)
  37. Lack of initiative or spontaneity of thought, speech, physical action, and affective expression.
  38. Pathology in the ____________ may lead to abulia.
    Frontal lobes
  39. Form of mutism characterized by a lack of motivation to speak, difficulty initiating and sustaining the cognitive/motor effort required for speech, or an apparent absence of thoughts to be communicated.
    • Akinetic mutism
    • (extreme abulic state)
  40. -Not due to neuromuscular difficulty
    -Sits with eyes open; seemingly alert
    -May follow movement/won't react to it
    -Vegetative jaw/face movements
    -May swallow food if placed in mouth after delay
    -Indifferent/literal/monotonic speech
    • Akinetic mutism
    • (abulic state)
  41. Akinetic mutism is most often associated with what pathology/etiology?
    • Massive Frontal Lobe damage
    • (Stroke, tumor, TBI, encephalitis, A-V malformations, aneurysms, hydrocephalus, and anoxia)
  42. Mutism that occurs as a result of surgery to the part of the brain that connects the two cerebral hemispheres to reduce seizures or remove tumors.
    Mutism following Corpus Callostomy
  43. What mode of communication may be used in a patient with mutism following corpus callostomy?
    • Writing
    • comprehension is spared
  44. What is one of the most common events associated with partial __________ seizures; speech that's in progress at onset of seizure is halted even though conciousness is maintained?
    • Frontal Lobe seizures
    • Speech Arrest (ictal)
  45. __________ can produce sudden speech arrest or uncontrolled vocalization.
  46. Drug-Induce mutism has been reported as a neurotoxic response to immunosupressive drugs that are used following _______________.
    Liver & Heart transplants
  47. Why is rapid identification of speech loss considered important in patients that have received a liver or heart transplant?
    Reducing dose/cessation of offending drug may reverse the problem
  48. Why is recognition of other neurogenic speech disturbances (distinct from MSDs) important?
    • It's important to understanding speech, language, & communication in the brain
    • It has implications for localization and management
  49. What 3 broad anatomic categories of "other neurogenic speech disturbances" were discussed in class?
    • Diverse CNS lesions
    • Left Hemisphere abnormalities
    • Right Hemisphere abnormalities
  50. Dysfluent speech acquired as a direct result of neurologic disease.
    Neurogenic Stuttering (NS)
  51. What is the most frequent dysfluency type for patients with neurogenic stuttering?
    Sound-syllable repetitions (often occuring in initial word position)
  52. In what ways is neurogenic stuttering different than developmental childhood stuttering?
    • Doesn't adapt/improve with tx
    • Not restricted to initial syllables
    • Function and content words are dysfluent
    • No difference bet/spontaneous speech & imitation
    • No significant anxiety/secondary characteristics
  53. What are the two most frequent causes of neurogenic stuttering?
    • Stroke
    • TBI
  54. Neurogenic stuttering tends to be more persistent with _________ or __________ lesions.
    • Multifocal
    • Bilateral
  55. Compulsive repetition of utterances, often in a context of increasing rate and decreasing loudness (associated w/ hypokinetic dysarthria)
  56. What type of dysfluencies are associated with palilalia?
    • Word and Phrase repetitions
    • (sound and syllable repetitions are usually excluded)
  57. Reiterations of those with palilalia occur most often during ____________ and least often during __________.
    • Most--conversation/elicited speech (generally at the end of utterances)
    • Least--reading/automatic responses
  58. What's the pathology and etiologies for palilalia?
    • Bilateral Basal Ganglia pathology (hypokinetic dysarthria)
    • Degenerative diseases, Multiple strokes, Seizures, & Lesions
  59. Is palilalia considered a speech production problem or a language problem?
    Speech production problem
  60. Unsolicited repetition of another's utterances
  61. What's the difference in full-blown echolalia and a less complete form of echolalia?
    • Full blown:  automatic, effortless, compulsive, and parrotlike w/out comprehension of meaning
    • Less complete:  repetition of all or part of what apparently has been understood
  62. Type of echolalia in which portions of speech from TV programs or conversations going on around patient are echoed and have been observed in demented individuals.
    Ambient echolalia
  63. Type of echolalia that contains a self-generated response to an inquiry; part of the inquiry is repeated as part of the response.  This demonstrates that echolalia doesn't always occur in the complete absence of language processing
    Mitigated echolalia
  64. Mitigated echolalia can occur in people with:
    • Dysarthria
    • Apraxia of speech
    • Agrammatism
    • Simplified grammatical structure
  65. Echolalia that is characterized by laborious repetition of portions of statements that precede a self-generated response; affected persons can be aware of the behavior but cannot inhibit it consistently.
    Effortful echolalia
  66. What's the pathology/most common etiology of echolalia?
    • Diffuse or Multifocal Cortical pathology or as a sign of Left Hemisphere disease
    • Stroke (Pick's Alzheimer's etc.)
  67. Is echolalia more strongly tied to disinhibition of lower-level mechanisms or higher-level cognitive deficits?
    • Higher level Cognitive deficits--echolalia
    • Lower-level mechanisms--palilalia
  68. Reduced speed of verbal responding, reduced linguistic & cognitive complexity of content, reduced vocal loudness and completeness of phonation, & flattened prosody. (literal/limited thought/indifference)
    Attenuation of Speech
  69. Inappropriate, involuntary vocalizing (Tourette's, LH & RH lesions, Alzheimer's, etc.)
    Disinhibited vocalization
  70. CNS disturbance of the capacity to interpret/formulate symbols for communicative purposes.
  71. Which modalities of language are affected by aphasia?
    ALL (spoken expression, verbal comprehension, reading, writing, & nonverbal propositional communication)
  72. Aphasia cannot be attributed to __________ impairments of cognitive functions, confusion, or sensory/motor deficits.
  73. Is aphasia a speech disorder or language disorder?
    Language disorder
  74. Damage to what anatomical location is aphasia nearly always the result of?
    Left Hemispheric Perisylvian Language Zone
  75. What is the most common cause of aphasia?
  76. Rare disorder in which the articulatory and prosodic characteristics of the patient's speech are perceived as a foreign accent.
    Foreign Accent Syndrome (FAS)/pseudoforeign accent
  77. Foreign Accent Syndrome is commonly dominated by what speech characteristics?
    • Vowel production abnormalities
    • Prosody
  78. Dialects vary most often by the way the _________ are produced.
  79. In foreign accent syndrome, __________ is the cause in approximately 70% of the time and  _______ in 20% of the cases.  In the majority of the cases, the lesion is in the ______ hemisphere.
    • Stroke
    • CHI
    • Left hemisphere
  80. There's a theory that foreign accent syndrome may be an unusual variant of _________ in which prosodic abnormalities predominate and in which articulatory deficits are relatively confined to distortions of vowels and consonants/ groping for articulatory postures.
    Apraxia of speech
  81. Deficit in the interpretation or production of distinctions in the fundamental frequency durational or amplitude variations in speech that convey emotional tone, emphasis, and certain linguistic information.
  82. Aprosodia refers to deficits specifically associated with ____________ damage, but the production of _________ is complex and not localizable to any single area of the brain.
    • Right hemisphere
    • Prosody
  83. _______________ of prosodic variations can occur in MSDs (hypokinetic dysarthria) and in neurogenic cognitive-affective disorders (e.g. depression).
  84. Patients with ___________ damage can have deficits in the comprehension of prosodic variations (including difficulty identifying and discriminating emotions conveyed by prosody, as well as problems with linguistic prosody that may alter meaning, provide emphatic stress and confey info about sentence type).
    Right Hemisphere
  85. Not all patients with right hemisphere damage have ________ speech characteristics.
Card Set
Advanced Articulation Disorders Chapters 12 & 13
Advanced Articulation Disorders Chapters 12 & 13