Apraxia of Speech Flashcards

1
Q

What is apraxia of speech?

A

“Apraxia is a neurologic speech disorder that reflects an impaired capacity to plan or program sensorimotor commands necessary for directing movements that result in phonetically and prosodically normal speech. It can occur in the absence of physiologic disturbances associated with the dysarthrias and in the absence of disturbance in any component of language.”

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2
Q

Apraxia of speech (AOS) is a problem with

A

the motor programming of speech movements.

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3
Q

Dysarthria is a problem with

A

muscles/movement.

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4
Q

Aphasia is a

A

linguistic/language problem.

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5
Q

In apraxia are the muscles damaged?

A

No

the muscles are OK.

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6
Q

Does Apraxia involve language?

A

No
doesn’t involve language unless it co-occurs with aphasia and dysarthria.
*co-occurrence is common

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7
Q

Does Dysarthria or Apraxia co-occur with aphasia more often?

A

Apraxia co-occurs with aphasia more often than dysarthria

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8
Q

Can Oral or limb apraxia co-occur with apraxia of speech?

A

Yes

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9
Q

Apraxia of Speech is almost always due to what kind of lesion?

A

Left cerebral hemisphere damage

* so helps in localization of the lesion

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10
Q

What are the Steps in speaking? (4)

A
  1. Speaker conceptualizes what is going to be said. This is where the message is determined.
  2. Speaker formulates the message through selecting semantic, syntactic, morphological, phonological structures for the message.
  3. The Motor Speech Programmer programs/plans the movements necessary to produce the needed phonemes. It activates a plan for the motor execution needed.
  4. This program is sent to through the nervous system to produce muscle movement/motor execution
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11
Q

If difficulties occur in the speaker formulating the message through selecting semantic, syntactic, morphological, phonological structures for the message (step 2), the result may be:

A

aphasia

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12
Q

If difficulties occur in the Motor Speech Programmer programs/plans the movements necessary to produce the needed phonemes. It activates a plan for the motor execution needed (step 3), the result may be:

A

apraxia

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13
Q

If difficulties occur with sending the program through the nervous system to produce muscle movement/motor execution (step 4), the result may be:

A

dysarthria

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14
Q

Other names for Apraxia of Speech (AOS) (2):

A
  • speech apraxia

- oral verbal apraxia.

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15
Q

AOS vs Broca’a aphasia:

A

1 AOS is sometimes confused with Broca’s aphasia because the phonologic impairment seen in Broca’s aphasia may be similar to AOS.

2 Broca’s aphasia may include AOS but involves more than AOS.

3 Individuals with AOS do not have linguistic problems that are seen in Broca’s aphasia.

4 The two have similar sites of lesion.

5 Probably some of the speech problems people with Broca’s aphasia have are due to MSP problems and not always linguistic problems

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16
Q

Why do you need to always assess for both Aphasia and Apraxia?

A

Because aphasia and apraxia so often co-occur, always evaluate for both in a client suspected of one or the other.

17
Q

ANATOMY AND BASIC FUNCTIONS OF THE MOTOR SPEECH PROGRAMMER

A
  • The Motor Speech Programmer (MSP) is considered to be responsible for programming speech.
  • It transforms the abstract phonemes to a neural code from which the motor programming can occur.
  • This neural code determines the specific muscle movements needed.
  • It is theorized that the motor speech plans are prepared before the muscle movement begins and that they are held in a buffer area. These plans can be modified before movement begins or during movement. This pre-planning is thought to be what allows us to have rapid speech.
  • You have to have linguistic input in order to know what to organize. This linguistic input to the MSP comes mainly from the perisylvian area in the left hemisphere. This includes the temporoparietal cortex, the insula, and the basal ganglia and thalamus.
18
Q

Some of the specifics of the programming possibly include (we don’t know for sure) (6):

A
  • Duration of movement
  • Amplitude of movement
  • Acceleration
  • Deceleration
  • Time to peak velocity
  • Timing of speech events.
19
Q

Where is the MSP thought to be located?

A

In the left cerebral hemisphere.

It is a theoretical system that involves several interacting structures and pathways in the left cerebrum.

These structures are primarily located in the parietal-frontal and related subcortical circuits.

20
Q

The insula:

A
  • is a cortical brain area that is buried within the lateral (sylvan) cerebral fissure.
  • It is hidden in the folds and can’t be seen unless you separate the temporal and frontal lobes.

(However the latest research done by Dr. Robin and Dr. Wambaugh indicate that the insula might not be involved in apraxia.)

  • The insula (?) is an important area in apraxia in that it is a frequent site of lesion for people with apraxia. It can be the only site of lesion but apraxia can occur without lesions in the insula. (Note that this has recently been questioned.)
21
Q

Specifically the following areas are thought to be primarily involved with the MSP (4):

A

1 Premotor area (see page 46 figure)
2 Parietal lobe somatosensory cortex and supramarginal gyrus
3 The insula (?)
4 The basal ganglia

22
Q

Dr. Don Robin (RIC-UTHSC) has found that Brodman’s area 6:

A
  • is an important area in apraxia and that damage in that area is associated with apraxia
23
Q

Premotor area (see page 46 figure):

A

o In the Pre-motor area, Broca’s area is especially important for apraxia. People with apraxia are most often found to have lesions in Broca’s area.

o Supplemental motor area is not a common site of lesion for apraxia but may be sometimes involved.

o The premotor areas are linked to the basal ganglia and cerebellar circuits for input. They also send connections to the motor area for impulses to be sent on and put into place by the Motor Speech Program.

24
Q

Parietal lobe somatosensory cortex and supramarginal gyrus:

A

are important in integrating sensory information that is needed for skilled motor activity.

25
Q

Why is there a likelihood of having a co-occurrence of apraxia with aphasia?

A

Because these structures are so close together

26
Q

The basal ganglia:

A
  • Is also thought to be important in MSP.

- Lesions in the striatum (putamen and caudate nucleus) are common in people with AOS

27
Q

To recap, the most common sites of lesion in AOS are (3):

A
  • left posterior frontal lobe area (Broca’s)
  • insula (?)
  • basal ganglia
28
Q

Other nonspeech characteristics that may accompany AOS and reflect left hemisphere damage are (3):

A

o Some right-sided weakness and spasticity

o Babinski reflex and hyperactive stretch reflexes

o Sometimes limb apraxia is present and is associated with left hemisphere pathology although it is present in both right and left sides but may be masked on the right side by hemiparesis or hemiplegia. (Note: the MSP is thought to be located in the left hemisphere and thus may influence all motor movement.)

29
Q

ETIOLOGIES of apraxia:

A

1 Anything that causes dominant hemisphere impairment of structures involved in motor planning.

2 Usually not inflammatory or toxic-metabolic diseases because they cause diffuse effects and rarely are associated with AOS. Demyelinating disorders are also not common causes.

3 Degenerative diseases rarely are associated with AOS.

4 Tumors, trauma and stroke (if they affect left hemisphere) are most often associated with AOS, particularly stroke.

30
Q

Patients complaints and perceptions:

A

Can’t pronounce words right – they know what they want to say but the words won’t come out right. They may indicate it worsens in stress.

Patients with AOS alone do not typically have problems with swallowing bc swallowing is a muscular function and apraxia is not a muscular problem. If patients do complain of swallowing, neuromuscular problems may exist which would implicate dysarthria as well as dysphagia.

31
Q

Why must an aphasia exam be conducted to rule out possibility of aphasia?

A

Because AOS and aphasia so often co-occur

32
Q

Clinical findings for oral mechanism exam:

A

o If dysarthria does not co-occur, gag reflex, chewing and swallowing should be WNL. Similarly, there should be no pathological oral reflexes or tongue weakness without dysarthria.

o Because motor programming involves sensory involvement as well as motor, note whether or not oral sensation is impaired.

33
Q

Clinical findings for Nonverbal oral apraxia (NVOA):

A
  • Problems with volitional movements of oral structures while the same movements may be performed involuntarily.
  • It is a fairly common occurrence in patients with AOS.
  • Lesions for NVOA are typically located in left hemisphere.
  • Always assess for NVOA and limb apraxia in an AOS eval. (See Helms-Estabrooks figure.)
34
Q

Clinical findings for Auditory process skills:

A
  • Patients with AOS but DAF (delayed auditory feedback) can cause more severe breakdowns in individuals with AOS and Broca’s aphasia than in normal speakers
35
Q

Clinical findings for Speech:

A

o Use voluntary speech tasks (conversational speech, narratives, reading) to elicit AOS.

o Tasks that require sequencing of various sounds and syllables are especially useful as that is where the person with apraxia will breakdown. Examples of these tasks are Sequential Motion Rates (SMRs) (pu-tu-ku) and multisyllabic words and sentences (e.g. catastrophe, Mississippi, refrigerator, “the municipal judge sentenced the criminal”.

o Have the pt imitate or read words that become increasingly more complex in terms of multisyllables, example - endear, endearing, endearingly. Breakdowns may occur as the word gets more complex.

o Imitation tasks reduce the need for word retrieval or other kinds of word formulation which may be a problem if aphasia co-exists. It is often difficult to tease out whether the problems are related to aphasia or AOS.

o Patients may do OK on those speech tasks which are overlearned/automatic, i.e. counting, days of weeks, familiar phrases, etc. These have become automatic and nonvolitional.

o Listen for false articulatory starts. (start to say a word and realize they did it wrong and they keep trying again and again to get to the correct sound – do not see this with dysarthria)

o Watch for groping of articulators.

o Patients with severe AOS may not be able to do many of these tasks. For these patients, try to elicit any speech response and determine what they can do (e.g. repeat CVC syllables).

o Articulatory distortions

o Rate and prosodic problems are very common in AOS.

o Fluency becomes abnormal as individuals start and stop repetitively in attempts to self-correct and produce words correctly

36
Q

The primary articulation error with apraxia of speech is:

A
  • distortion
  • It may be a perceived substitution but it is actually a distortion.
  • Articulation is a key problem with inconsistent errors occurring. One difference from the paraphasias that occur in aphasia is the articulatory distortions that occur in AOS. In paraphasias, there is usually no distortion. Articulatory problems are greater on blends than single consonants. (Articulation problems typically present as distortions.)
37
Q

The most important diagnostic criteria for AOS (3):

A

o Slowed rate of speech – segmentation of syllables (increased interval time between syllables)

o Sound errors – disotortions, inconsistent, unpredictable

o Prosodic abnormalities

38
Q

For severe AOS speech characteristics:

see pg 320, figure 11-4

A

Because these people often have severe aphasia it is hard to tease out the differences between the effects of aphasia and that of AOS.

A person with severe AOS may not initially be able to phonate and may be mute. This typically doesn’t last too long – most can phonate after 2 weeks.

If muteness lasts longer than 2 weeks, consider another diagnosis such as severe aphasia, anarthria or psychogenic mutism.