Acquired apraxia of speech Flashcards

1
Q

what is AOS?

A

“AoS is broadly defined as an acquired disorder of learned volitional actions associated
with breakdown in the planning or programming of the movements needed for
speech” (Miller and Wambaugh, 2017, p. 493).

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2
Q

AOS is…

A

acquired, affects volitional movements and movements for speech, breakdown is in planning or programming movements needed for speech

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3
Q

AOS is not…

A
  • Developmental (unlike Childhood AOS or developmental verbal dyspraxia)
  • Doesn’t affect reflexive movements like coughing
  • Doesn’t affect non-speech movements like smiling/blowing (if affected called oral apraxia/bucco-facial apraxia)
  • Breakdown not in expressive or receptive language (aphasia) or sensation (dysarthria)
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4
Q

History of apraxia

A
  • Initially for limb movement issues
  • Liepmann (1900a) described a patient who was unable carry out movements, in the absence of any paralysis (weakness) or ataxia (incoordination).
  • This led Liepmann to develop an influential theory about how our brain sends instructions
    to our limbs to carry out movements. When this process is disrupted – the result is an
    “apraxia”.
  • This disorder known as “apraxia” can affect limb movements (as described above); eye movements (“ocular apraxia”); facial movements (“oral/bucco-facial apraxia”, or it can
    affect the ability to carry out movements using objects- known as “ideational apraxia”.
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5
Q

Discriminatory Kernel features (McNeil et al., 1997; 2004; 2009) of AOS

A
  • sound distortions (including disordered substitutions)
  • extended segment durations
  • extended intersegment durations
  • prosodic defecits
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6
Q

sound distortions (including disordered substitutions)

A
  • “Substitutions” = speaker has selected or accessed
    incorrect phonemes and articulated these normally
    (e.g in phonemic paraphasia)
  • “Distortions” = correct phoneme was accessed, but
    articulated in an imprecise or unusual way (e.g. in
    AOS, dysarthria)
  • “Distorted substitutions” = the impression that both
    phoneme selection and articulatory accuracy are
    incorrect – most common error type in AOS
  • Most common distortions in AOS: length, voicing,
    tongue placement
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7
Q

Extended segment* durations + Extended intersegment duration

A
  • “Extended segment durations” = lengthened
    production of consonants and vowels
  • rate of speech is perceived as slower overall
  • “Extended intersegment durations” =
    lengthened pauses between sounds and
    between words
  • speech sounds segmented
  • May also be referred to as “syllabification”
  • May insert “intrusive schwa” in between segments
  • *Segment = smallest unit of sound e.g. consonant or syllable
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8
Q

prosodic deficits

A
  • May see restricted alteration of pitch,
    intonation, loudness – may sound monotonous
  • Slow rate of speech is common – this may be
    due to increased segment and intersegment
    durations
  • Equal lexical stress
  • Individuals with AOS are highly likely to
    produce more equal lexical stress (i.e., overstress the initial weak syllable) in multisyllabic words (Ballard et al., 2016)
  • No longer sound like themselves/unnatural
    sounding
  • Can very occasionally sound like a foreign
    accent (rare)
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9
Q

non-discriminatory features

A
  • articulatory groping
  • perseverative errors
  • increasing errors with word length
  • speech initiation difficulties
  • awareness of errors
  • automatic speech > propositional
  • islands of error-free speech
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10
Q

severity of AOS

A
  • varies from relatively fluent, slow segmented speech with sound errors and disturbed prosody, to complete inability to speak
  • In some cases, the difficulty planning or programming the movements for speech is so severe that it is
    hard for the person to produce any speech sounds, in any context (reading, repeating/imitating,
    spontaneous speech)
  • These clients may sometimes be described as “non-verbal”
  • In other severe cases, a client might be able to produce one or two speech sounds or syllables, (usually
    when imitating the SLT) but have difficulty stringing syllables together to make word
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11
Q

when is it difficult to reliably diagnose AOS?

A

It is difficult to reliably diagnose AOS in a client who has very little speech output, because this does not allow you to observe the core features of AOS. You might reach a tentative diagnosis of “probable” or “suspected” AOS but you may also need to consider other diagnoses such as aphasia. Being unable to produce any verbal output can also be caused by aphasia.

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12
Q

AOS overlap with other disorders

A
  • Almost always co-occurs with aphasia in over 90% of cases
  • Sometimes with dysarthria
  • Makes assessment and diagnosis more tricky
  • Cases of pure AOS are rare; only a handful
    have been described
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13
Q

etiology of AOS

A

Acute AOS
- Primarily caused by stroke – typically left hemisphere; most often frontal and parietal lobes; most often larger strokes
- Can also be caused by head injury (traumatic brain injury or TBI) or a brain tumour/brain surgery

Primary progressive AOS (Josephs et al., 2006):
- Isolated progressive motor speech deficit can be the first sign of a progressive neurodegenerative disease, such as: Cortico-basilar degeneration (CBD); Progressive supranuclear palsy (PSP); Motor neurone disease (MND)/Amyotrophic lateral sclerosis (ALS)

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14
Q

neurobiology of AOS

A

Pinpointing a singular brain region associated with AOS has been controversial, with many different lesion
sites proposed, including: the left insula; Broca’s area/left inferior frontal gyrus; the pre-central gyrus and
post-central gyrus i.e. primary motor and somatosensory areas) and the pre-motor cortex (Basilakos et al.,
2015; Graff-Radford et al., 2014)

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15
Q

why is it difficult to say where AOS lesions occur?

A
  • Our current understanding is that speech is likely organised across a wide network of structures with different roles including: parts of Broca’s area, precentral gyrus, postcentral gyrus, anterior insula, subcortical structures (basal ganglia, cerebellum)
  • Stroke/TBI can affect multiple areas of the brain
  • The organisation of speech in the brain may change after stroke/TBI due to neuroplasticity and cortical reorganisation therefore we don’t know whether different structures have taken over different roles in the person with AOS
  • Moser (2016) reported on 2 people with similar cases of AOS who had very different brain damage locations when brain imaging (MRI scan) was used suggesting there may not be one area specific to AOS
  • Research studies have often used differing diagnostic criteria to identify AOS (due to the controversies about diagnostic symptoms) and this makes it hard to compare and collate results of different experiments
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16
Q

models and theories of AOS

A
  • Van der Merwe 4-stage model
  • DIVA/GODIVA model
17
Q

Van der Merwe (1997)

A

Conceptual-linguistic
- pre-motor stage
- intention to speak
- message constructed: syntax, semantics, morphology
- phonological plan (phonemes)
APHASIA

Motor planning
- strategy of action
- spatial specifications (place and manner)
- temporal specifications (timing)
- core motor plans = goals of movement
AOS

Motor programming
- muscle-specific programmes selected
- spatial and temporal dimensions: tone, direction, force, rate

Execution
DYSARTHRIA

18
Q

What goes wrong with motor planning in AOS?

A
  • We don’t know for definite yet and researchers continue to try to answer this question. There are several possible ways in which motor planning/programming can possibly go wrong after a stroke/TBI which might explain the types of the errors we see in AOS:
  • The brain mis-selects the incorrect motor programme (i.e. the opening or closing settings or sequences for the
    articulators) for the intended production target (e.g. selects the programme for /p/ when the target was /d/)
  • The brain can no longer access stored programmes for the intended target, or the quality of these stored
    programmes has deteriorated
  • There is interference in the brain between competing motor programmes (e.g., competition between the tongue
    tip vs. dorsum raising in target /’take’/  dorsum raising “wins”  may lead to what the listener hears as /‘cake’/
  • The correct programme is selected, but the programme is applied to the wrong articulator (e.g., closing gesture
    applied to tongue dorsum instead of lips for the target /m/ would result in production of /ng/ instead)
  • We also still don’t know what size these programmes in the “speech sound map” are – sound/syllable/word/phrase?
    (Ziegler, et al., 2012)
19
Q
A