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Motor Speech > midterm > Flashcards

midterm Flashcards

1
Q

in what parts of speech are ataxic dysarthria characteristics most evident

A

articulation and prosody

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2
Q

what are the reasons for the characteristics

A

incoordination and reduced muscle tone

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3
Q

identification of ataxic dysarthria can help localize the lesions to….

A

cerebellum or cerebral control circuit

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4
Q

ataxic dysarthria predominantly reflects problems of…

A

motor control

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5
Q

what are purkinje cells

A

inhibitory and sole output neurons of cerebellar cortex

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6
Q

what level of the motor system does the cerebellum infuence? motor or sensory

A

sensory

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7
Q

what are the roles in speech

A
  • reciprocal connections with cerebral cortex
  • auditory and proprioceptive feedback from speech muscles, tendons, and joints
  • reciprocal connections with brainstem component of indirect activation pathway
  • cooperation with the basal ganglia control circuit through loops among the thalamus, cortex, and indirect motor system
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8
Q

what is the function of the cerebellum

A
  • helps time components of movement
  • scales the size of muscle actions
  • coordinates sequences of muscle contraction for skilled motor behavior
  • monitors the adequacy of movement outcomes based on feedback from muscles, tendons and jints, and auditory feedback in speech.
  • makes modifications that smooth the timing and coordination of movement
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9
Q

which part of the cerebellum is used for preparation of speech via the thalamus, SMA, motor cortex, and insula

A

Anterior-superior

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10
Q

which part of the cerebellum is used for speech execution

A

inferior portions

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11
Q

ataxic dysarthria is associated with what part of the cerebellum

A

bilateral cerebellar hemisphere, paravermal, dentate nucleus

*especially assoicated with damage to paramedian regions of superior cerebellar hemispheres

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12
Q

is ataxic dysarthria associated with bilateral or unilateral lesions

A

bilateral

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13
Q

where else can lesions be to cause ataxic dysarthria

A

superior cerebellar peduncle or along the frontopontocerebellar pathways

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14
Q

where are cerebellar lesions when they are focal

A

lateral hemispheres and posteromedial or paravermal

unilateral lesions causing ataxic dysarthria are often on the right

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15
Q

what is the direct activation pathway

A

pyramidal tracts, form part of the UMN. Their activity stimulates the LMN. Includes the corticospinal and corticobulbar tracts. Innervate muscles contralateral from lesion

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16
Q

What is the indirect pathway

A
  • extrapyramidal.
  • synapses occur between corex and brainstem via basal ganglia, cerebellum, reticular formation, vestibular nuclei or red nucleus.
  • Regulate reflexes and maintain posture, tone.
  • primarily inhibitory
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17
Q

what are common clinical signs of cerebellar lesions

A

broad stance and gait

  • truncal instability
  • steps irregularly placed
  • legs overlifted
  • no difference in standing with feet together and eyes open or closed
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18
Q

what is the romberg test

A

stand with feet together. Test steadiness with eyes open and closed

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19
Q

What is titubation

A

rhythmic tremor of body or head that can occur with cerebellar disease
*usually in trunk (rocking) or head (forward back, side to side, or rotary)

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20
Q

What is nystagmus

A

abnormal eye movements (rapid back and forth)

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21
Q

What is ocuardysmetria

A

small rapid eye movements as eyes attempt to fix on a target or to correct for inaccurate fixation

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22
Q

what is pendulousness

A
  • extremity allowed to swing freely in pendular manner has *greater number of oscillations before resting. Function of hypotonia.
  • may also include impaired check and excessive rebound
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23
Q

what is dysmetria

A
  • common sign of cereballar disease

* characterized by overshooting or undershooting target by abnormalities in speed, making the movements look jerky

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24
Q

what is dysdiadochokinesis

A
  • errors in timing and speed of components of a movement
  • manifestation of decomposition of movement (dyssynergia)
  • results in poor coordination
  • tested by alternating alternate movements such as knee pat test
  • poor performance is characterized by abnormalities in rate, rhythm, amplitude, and precision
25
Q

what is ataxia

A

product of dysmetria, dysdiadochokinesis, and decomposition of movement

26
Q

what is decomposition of movement

A

errors in the timing and speed of components of a movement

27
Q

what is intention or kinetic tremor

A

tremor that is apparent during movement

obvious as a target is approximated (terminal tremor)

28
Q

what are other signs with cerebellar disease

A
  • mild facial weakness, lower face
  • occurs frequently with focal cerebellar lesions
  • cognitive disturbances
29
Q

what is cerebellar cognitive affective disorder

A

affective, cognitive, and language deficits in people with cerebellar disease

30
Q

what are common etiologies of ataxic dysarthria

A
  • degenerative disease
  • demylinating disease
  • vascular disorders
  • neoplastic disorders
  • trauma
  • toxic or metabolic conditions
31
Q

what are hereditary ataxias

A

autosomal recessive X linked. Largely confined to cerebellum
when they also affect spinal cord (spinocerebellar
when they affect inferior olive and pontine nuclei(olivopontocerebellar)

32
Q

What is Friedreich’s ataxia

A

degenerative disorder
begins before age 20
limb gait ataxia, dysarthria, absent muscle stretch reflexes in lower limbs, sensory loss, signs of corticospinal tract involvement
may have LMN weakness

33
Q

what is ataxia telangiectasia

A

geneticdisorder

truncal or appendicular ataxia, choreoathetosis, dystonia, sensory loss, and distal muscle atrophy

34
Q

what are primary episodic ataxias

A

intermittent, brief attacks of ataxia
often dysarthria and sometimes other neurologic signs
can be induced by exercise or startle
can be managed pharmacologically

35
Q

what is olivopontocerebellar atrophy

A

degeneration of the pontine, arcuate, and olivary nuclei

36
Q

what demylinating diseases are associated with ataxic dysarthria

A

MS
paroxysimal ataxic dysarthria PAD: brief episodes of ataxic dysarthria in otherwise normal individual. Overbreathing may evoke the paroxysms
Miller Fisher syndrome

37
Q

what is Miller Fisher syndrome

A

subtype of Gullain-Barre

autoimmune acute neuropathy characterized by opthalmoplegia, arefelexia, and ataxia

38
Q

what vascular disorders are associated with ataxic dysarthria

A

aneurysms
AVM
stroke
occurs at posterior inferior cerebellar artery PICA, anterior inferior cerebellar artery AICA, at pons, superior cerebellar artery in midbrain,

39
Q

which artery lesions more common with ataxic dysarthria

A

superior cerebellar artery lesions

40
Q

what is Von Hippel Lindau disease

A

inherited condition that produces tumors in cerebellum. medulla, and spinal cord

41
Q

which tumors are the most risk for ataxic dysarthria

A

midline tumors which can displace portions of the cerebellum

42
Q

what are paraneoplastic disorders

A

autoimmune conditions associated with cancer

43
Q

what type of trauma causes damage to cerebellum

A

anoxia secondary to TBI

rotational injuries associated with TBI

44
Q

what is punch drunk encephalopathy

A

damage by repeated boxing blows to the head

45
Q

what toxic conditions can lead to ataxic dysarthria

A

acute or chronic alcohol abuse creates abnormal stance and gait
neurotoxic levels of drugs such as the anticonvulsant Dilantin, Tegretol, Depakote, and Mysoline
cerebellar dysfunction can develop with severe malnutrition and vitamin deficiencies

46
Q

what are other causes of ataxic dysarthria

A

hypothyroidism
normal pressure hydrocephalus
viral, bacterial, and other infectious processes
heat stroke
lack of proprioceptive input which leads to sensory ataxia

47
Q

what is normal pressure hydrocephalus

A

enlarged ventricles even when CSF pressure is maintained

48
Q

what is the most frequent cause of ataxic dysarthria

A

degenerative diseases most frequent

49
Q

what are patient complaints in ataxic dysarthria

A

slurred speech
inability to coordinate their breathing with speaking
bike cheek or tongue while talking or eating
unexpectedly stumble over words

50
Q

what are nonspeech oral mech findings with ataxic dysarthria

A

nonspeech AMRs of jaw, lips, and tongue may be irregular

51
Q

what are clinical speech findings with ataxic dyssarthria

A

irregular speech AMRs are a distinguishing characteristic

associated impaired coordination or control of movement (sequenced movements give distinctive character)

52
Q

which are the most useful tasks to distinguish ataxic dysarthria characteristics

A

conversational speech, reading, and speech AMRs

repetition of multisyllabic words

53
Q

what are the clusters of deviant demenisions of ataxic dysarthria

A
  • articulator inaccuracy, represented by imprecise consonants, irregular articulatory breakdowns, and vowel distortions
  • prosodic excess, composed of excess and equal stress, prolonged phonemes, prolonged intervals, and slow rate
  • phonatory-prosodic insufficiency, composed of harshness, monopitch, and monoloudness
54
Q

what is scanning

A

isochronous syllable durations that seems to reflect a prolongation of short vocalic elements

55
Q

what is telescoping

A

inconsistent breakdown of articulation in which a syllable or series of syllables are unpredictably run together, giving speech a transient accelerated character

56
Q

what are physiologic respiratory findings for ataxic dysarthria

A

*incoordination between timing of onset of exhalation and phonation, leading to air wastage
*paradoxical movements or abrupt changes in movements of rib cage and abdomen
*irregularities in chest wall movements during sustained vowels and syllable repetition
*tendency to initiate utterances at lower than normal lung volume levels
abnormalities reflect poor coordination of speech breathing and phonatory

57
Q

what are acoustic findings for articulation, rate, and prosody in ataxic dysarthria

A

*slow rate including longer syllable and sentence durations, longer formnt transitions, lengthened consonants clusters and vowel nuclei in syllable and wordslonger VOT

58
Q

what are explanations for slow rate in ataxic dysarthria speakers

A
  • hypotonia which delays generation of muscle force and reduced rate of muscle contraction
  • cerebellar damage that interferes with feedforward motor commands and leads to heavier reliance on cerebral ortex motor control
  • reliance on auditory feedback
  • abnormalities in rhythm on speech AMR tasks

Motor Speech (1 decks)

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