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SPA6233 Motor Speech > Week 1 (A&P Review, Intro Substrates) > Flashcards

Week 1 (A&P Review, Intro Substrates) Flashcards

1
Q

Sensory Cortex: Function and Efferents

A

Fx: somatic sensation, visual stimuli, and movement planning
Efferents: Primary Motor Cortex, Brainstem

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2
Q

Motor Cortex: Function and Efferents

A

Fx: Involved in planning of goal-directed movement.
External target of movement needed.
Efferents to: motor strip, brainstem

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3
Q

Define: motor homonculus

A

cortical map involved in the execution of movement

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4
Q

Function of cingulate gyrus

A

sensorimotor integration

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5
Q

Function of insular cortex (a.k.a. insula)

A

sensory-cued but stereotyped motor behaviors or habits

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6
Q

Define: direct activation pathway

A

Also referred to as the Pyramidal Tract
Has direct connection on the final common pathway
Forms part of the upper motor neuron system
Effect is primarily facilitative – leads to movement – not inhibition of movement

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7
Q

Direct activation is divided into what 2 tracts?

A

Corticospinal and corticobulbar tract

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8
Q

Explain: DAP division into CS and CB tracts

A

Axons descend from the cortex
Terminate in the brainstem/spinal cord
Synapse with cranial/spinal nerves

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9
Q

3 effects of damage to the direct activation pathway

A

Loss or reduction of skilled movement
Normal reflexes
Because CN supply to V, IX, X, XI are bilateral, unilateral UMN lesions are usually minor

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10
Q

Deifne: indirect activation pathway

A

Also referred to as the Extrapyramidal Tract
Has indirect connection on the final common pathway
There are multiple synapses between the origin in the cortex and its arrival and activation of the FCP
Functions for speech poorly understood
This pathway is a source to lower motor neurons, whereas the control circuits are not.

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11
Q

Indirect activation pathway is divided into what 2 tracts?

A

Corticoreticular and corticorubral

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12
Q

Define: corticoreticular

A

cortex to reticular formation

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13
Q

Define: corticorubral

A

cortex to red nucleus

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14
Q

Effects of damage to indirect activation pathway

A

spasticity and hyperreflexia

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15
Q

Explain: corticoreticular tract

A

From cortex to reticular formation (brainstem)
Reticular formation: Set of interconnected nuclei that are located throughout the brain stem
Intermingled with corticospinal and corticobulbar fibers
Descend to midbrain, medulla and pons
Fibers then distributed bilaterally
Mediates ascending sensory information

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16
Q

Corticoreticular tract has ______ and _______ influences

A

facilitatory and inhibitory

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17
Q

explain: facilitatory and inhibitory influences

A

Crucial for regulation of muscle tone

Excites extensor motor neurons and inhibits flexor motor neurons

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18
Q

Explain: corticorubral tract

A

Fibers sent from the cortex to the red nucleus

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19
Q

Explain: 4 important facts about the red nucleus

A

Oval mass of cells in the midbrain
Serves as a relay station between a pathway from the cerebellum to thalamus and cortex
Major influence is on flexor muscle groups in the limbs
Role involved in speech is unclear

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20
Q

Effects of damage to corticorubral tract

A

spasticity and hyperreflexia

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21
Q

5 main points: direct pyramidal tract

A
  1. voluntary
  2. conscious
  3. movements generated by cognitive activity
  4. corticospinal and corticobulbar tract division
  5. damage: loss or reduction of skilled movement. Unilateral: weakness on contralateral side
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22
Q

7 main points: indirect pyramidal tract

A
  1. involuntary
  2. subconscious
  3. Gives the direct pathway a framework to accomplish the skilled movement
  4. Regulates reflexes
  5. Maintain posture, tone
  6. corticoreticular and corticorubral tract division
  7. damage: affect muscle tone and reflexes (spasticity and hyperreflexia)
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23
Q

Define and explain: final common pathway

A

Referred to as lower motor neuron system
Peripheral mechanism through which all motor activity is mediated
Last link in the chain of neural events that lead to movement
Generates activity in skeletal or somatic muscles

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24
Q

The final common pathway includes what 3 things?

A

nuclei/cell bodies of cranial and peripheral nerves; their axons; and neuromuscular junction

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25
Q

Primary cranial and peripheral nerves for: respiration

A
  1. spinal (cervical and thoracic)

2. phrenic nerve, intercostals

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26
Q

Primary cranial and peripheral nerves for: phonation

A

Vagus (CNX)- larynx

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27
Q

Primary cranial and peripheral nerves for: resonance

A

Vagus (x) + (IX and XI) velopharynx and larynx

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28
Q

Primary cranial and peripheral nerves for: articulation

A
  1. trigeminal (CNV)- jaw
  2. facial (CNVII)- face
  3. hypoglossal (CNXII)- tongue
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29
Q

4 subcortical structures

A

caudate, internal capsule, putamen, globus pallidus

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30
Q

Thalamus provides connections to and from

A 
To: Primary Motor cortex
     Premotor cortex
     Supplemental Motor cortex
     Insula
From: Basal Ganglia, Cerebellum, Brainstem
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31
Q

Function of the thalamus

A

relaying sensory and motor signals to the cerebral cortex, regulation of consciousness, sleep, and alertness

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32
Q

Define and explain: control circuits

A

Basal ganglia and cerebellum large collections of nuclei that modify movement on a minute-to-minute basis.
Motor cortex sends information to both
Both send information right back to cortex via thalamus
Do not have direct contact with LMN’s (like the direct and indirect pathways)

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33
Q

Cerebellum output = _________

A

excitatory

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34
Q

Basal ganglia output = __________

A

inhibitory

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35
Q

Effects of balance vs. disturbance of control circuits

A 
balance = smooth coordinated movement
disturbance = movement disorder
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36
Q

Basal ganglia includes what 3 structures?

A

caudate nucleus, putamen, and globus pallidus

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37
Q

Define and explain: basal ganglia control circuit

Balance of what 3 neurotransmitters?

A

Reciprocal connections with diverse areas of the cerebral cortex
Needs a balance of various neurotransmitters: Acetylcholine, Dopamine, and GABA

38
Q

4 functions of the basal ganglia control circuit

A

voluntary movement, motor planning, initiation of movement
Regulates muscle tone
Maintains normal posture and static muscle contraction upon which voluntary , skilled movements are superimposed
Regulates amplitude, velocity, and initiation of movement

39
Q

Define and explain: cerebellar control circuit

A

Most important components of the cerebellum for speech: vermis and cerebellar hemispheres
Imposes control on movement initiated elsewhere
Coordinates timing and sequencing of movement
Helps scale size of muscle actions and maintain steadiness of movement
Major role in error control based on feedback from periphery and knowledge of action goals

40
Q

2 effects of damage to cerebellar control circuit

A

Errors in force, speed, timing, range, and direction of movements
Hypotonicity

41
Q

Define and explain: central pattern generator for respiration

A

There is a rhythmic pattern of neuronal firing for breathing that can occur automatically without voluntary input from the cortex.

42
Q

Define and explain: neural control of breathing

Location of neuron network?

A

A network of neurons located in the medulla of the brainstem control respiration.
Signals from the brainstem travel via peripheral spinal nerves to reach the muscles of the chest wall.
Example: For inspiration, signals are sent through spinal neurons to the diaphragm via the phrenic nerve

43
Q

Explain: opening and closing during Myoelastic Aerodynamic Theory

A 
2.  Aerodynamic:
Opening – Positive pressure 
Closing – Bernoulli effect and elasticity
PTP – Phonation Threshold Pressure
1.  “Myo”
44
Q

3 steps of myoelastic aerodynamic theory

A

1) vocal folds are appropriately positioned (postured) in a closed or semiclosed position
2) Subglottal pressure is built up below the folds
3) folds repeatedly open and close because of repeated pressure build-up, drop, etc.

45
Q

What nerve innervates the larynx?

A

CNX- vagus

46
Q

CNX emerges from the ________

A

medulla

47
Q

2 divisions of the laryngeal nerve. What muscles does each innervate?

A

Recurrent laryngeal nerve
IA, PCA, Thyrovocalis, LCA

Superior laryngeal nerve
Cricothyroid

48
Q

5 reasons we care about motor speech disorders

A 
• Occur frequently 
• Prevalence may increase 
• Can be treated/managed 
• Mayannounce neurologic disease 
• Can inform decisions regarding	the differential	
 diagnosis
49
Q

VDM FNPD Chart: intent to communicate verbally

A

NP: voluntary fronto-limbic system
D: Cognitive/affective disorders

50
Q

VDM FNPD Chart: Linguistic/symbolic planning

A

NP: temporal/parietal area, Broca’s and adjacent areas
D:Aphasia

51
Q

VDM FNPD Chart: Motor Planning

A

NP: Broca’s area; Wernicke’s area; Prefrontal cortex; Area 6; SMA; Areas 5 & 7 (Parietal)
D:Apraxia of Speech

52
Q

VDM FNPD Chart: Motor Programming

A

NP: SMA; Basal ganglia; Lateral Cerebellum; Fronto-limbic system; Motor Cortex
D: Hypokinetic, Hyperkinetic, Ataxic, Spastic Dysarthrias

53
Q

VDM FNPD Chart: Sensation

A

NP: SMA; Cerebellum; Basal ganglia; Motor cortex; Thalamus; Brain Stem; Motor units
D: Flaccid Dysarthria

54
Q

Define: dysarthria official definition

A

“…….a collective name for a group of speech disorders resulting from disturbances in muscular control over the speech mechanism due to damage of the central or peripheral nervous system. It designates problems in oral communication due to paralysis, weakness or incoordination of the speech musculature” (DAB 1969)

55
Q

Define: dysarthria simple definition

A

Disorder of movement due to abnormal neuromuscular execution (speed, strength, range, timing, accuracy)

56
Q

Dysarthria affects what 5 things?

A

respiration, phonation, resonance, articulation and prosody

57
Q

Each different type of dysarthria corresponds to? Each likely having different what?

A

damage to particular part(s) of the nervous system, and underlying neuropathophysiology

58
Q

Each type of dysarthria has different what?

A

auditory perceptual characteristics which can be distinguished clinically

59
Q

Accurate identification of dysarthria has implications for what?

A

localization of brain lesions

60
Q

Accurate description of dysarthria provides what?

A

clues for management

61
Q

3 facts about the motor programming domain

A

“Strategies prescribe the general nature of plans and tactics give them particular specifications in space and time.”
Programs specify muscle tone, movement direction, force, range, and rate as well as mechanical stiffness of the joints
Muscle-specific

62
Q

8 Hypokinetic dysarthria errors

A
  • Monopitch
  • Reduced stress
  • Monoloudness
  • Inappropriate silences
  • Short rushes of speech
  • Variable rate
  • Increase rate -segments
  • Increased rate -overall
63
Q

7 Hyperkinetic dysarthria errors

A

*Prolonged intervals
*Variable rate
*Inappropriate silences
*Excess loudness variations
*Sudden forced expiration or
inspiration
*Voice stoppages
*Transient breathiness

64
Q

Hypokinetic and hyperkinetic errors in motor programming stem from the __________.

A

basal ganglia

65
Q

4 Ataxic dysarthria errors

A
  • Excess & equal stress
  • Irregular articulatory breakdown
  • Distorted vowels
  • Excess loudness variations
66
Q

Ataxic errors in motor programming stem from the ________

A

cerebellum

67
Q

4 Spastic dysarthria errors

A

Imprecise consonants

  • Low pitch
  • Slow rate
  • Strained-strangled quality
68
Q

Spastic dysarthria errors stem from the

A

bilateral UMN

69
Q

1 fact about the execution domain

A

The hierarchy of plans and programs is transformed into non-learned automatic (reflex) motor adjustments

70
Q

5 flaccid dysarthria errors

A
  • Hypernasality
  • Breathiness (continuous)
  • Nasal emission
  • Audible inspiration
  • Short phrases
71
Q

Flaccid dysarthria errors stem from the ________.

A

LMN (lower motor neuron)

72
Q

Apraxia of speech- official definition

A

“Phonetic-motor disturbance of speech production resulting from brain injury reflecting an impaired capacity to accurately or efficiently translate intended phonemes and phoneme sequences into neural commands that generate movements within and among muscles and structures that lead to accurate articulation and prosodically normal speech. In the absence of weakness, slowness, or incoordination when used for reflex or automatic acts.”

73
Q

3 facts: define and explain apraxia of speech

A

Disturbance in the planning of movements for speech.
Can exist independent of language problems
Often coexists with dysarthria and aphasia

74
Q

4 facts about non-verbal oral apraxia (NVOA)

A

1) . Inability to imitate or follow commands to perform volitional movements of speech structures
2) . Substantial proportion of people with AOS exhibit NVOA
3) . Clinical test: cough, click tongue, etc.
4) . Presence of NVOA = failure to respond or effortful groping for correct movements or inconsistent trial-and-error attempts.

75
Q

5 facts about the motor planning domain

A

1) . “Highest” level of the motor hierarchy
2) . Formulating the strategy of action by specifying motor goals
3) . Gradual transformation of symbolic units (phonemes) to a code that can be handled by a motor system
4) . Articulator specific, not muscle-specific
5) . Cannot be disentangled from motor programming “clinically”

76
Q

2 prominent errors in motor planning disorders

A

1) . Slow, struggling speech with distortion and even apparent substitutions
2) . Slowed temporal flow of speech

77
Q

Distribution of neurogenic speech disorders

A

Dysarthria- 53%, Aphasia- 25.8%, Non-aphasic cognitive communication disorders- 16.8%, Apraxia of speech-3.9%

78
Q

Distribution of dysarthrias

A

mixed- 28%, hyperkinetic- 19%, hypokinetic- 9%, ataxic- 9%, spastic- 7%, flaccid-8%, apraxia- 7%, undetermined- 4%, unilateral- 8%

79
Q

Determining the specific pathology depends partly on what?

A

establishing the course or temporal profile of the disease.

80
Q

What are the 3 categories of the development of motor speech disorder symptoms? How much time for each?

A

Acute, within minutes
Subacute, within days
Chronic, within months

81
Q

5 categories of the evolution/course of the disease after symptoms have developed

A

1) . Transient, when symptoms resolve completely after onset
2) . Improving, when severity is reduced but symptoms are not resolved
3) . Progressive, when symptoms continue to progress or new symptoms appear
4) . Exacerbating-remitting, when symptoms develop, then resolve or improve, then recur and worsen, and so on
5) . Stationary (or chronic), when symptoms remain unchanged for an extended period of time

82
Q

2 other facts about motor speech disorders

A

MSDs can appear at any point during the development and evolution of neurologic disease.
Their presence can inform localization and diagnosis.

83
Q

3 things that cause degenerative diseases

A

1) . Gradual decline in neuronal function of unknown cause
2) . In some cases, neurons atrophy and disappear, whereas in others neuronal changes may be more specific (e.g., neurofibrillary tangles in Alzheimer’s disease)
3) . Most oftenchronic, progressive, anddiffuse

84
Q

3 things that can cause inflammatory diseases

A

1) . They are characterized by an inflammatory response to microorganisms, toxic chemicals, or immunologic reactions
2) . The development of clinical signs and symptoms is usuallysubacute
3) . Many inflammatory diseases are progressive and diffusely located

85
Q

2 things that can cause toxic-metabolic diseases

A

1) . Vitamin deficiencies, thyroid hormone deficiency, genetic biochemical disorders, complications of kidney and liver disease, hypoxia, hypoglycemia, hyponatremia, and drug toxicity are examples of toxic and metabolic conditions that can alter neuronal function
2) . Effects are usually diffuse; development and course can beacute, subacute,orchronic.

86
Q

1 thing that causes neuroplastic diseases

A

1). Tumors usually create focal signs and symptoms and arechronicorprogressivein their course.

87
Q

3 things that cause trauma

A

1) . Onset is almost alwaysacute,with maximum damage around the time of onset.
2) . The course is usually one ofimprovementor resolution. Residual focal signs and symptoms tend to reflect areas of severe anatomic damage, as can occur with contusions, lacerations, and hematomas.
3) . Penetrating (focal)vsclosed head injury (CHI; diffuse)

88
Q

1 thing that causes vascular diseases

A

1). Vascular disease is the most common cause of neurologic deficits and, probably, MSDs. The most common cerebrovascular disease isstroke(also calledinfarctandcerebrovascular accident), in which neurons are deprived of oxygen and glucose because of an interruption in blood supply. This deprivation is known asischemia.

89
Q

Speech is a ____________ under sensorimotor control

A

fine motor skill

90
Q

Normal production of speech requires a _______ of respiratory, phonatory, and articulatory events which must occur in a _________________

A

multitude, complex and coordinated manner

91
Q

Motor speech disorders lead to ______________ with breakdown or degradation of the speech signal.

A

dysfunction in the sensorimotor control of speech

92
Q

The proper identification and (therefore) management of motor speech disorders is reliant upon what 4 things?

A

1) . A sound framework of speech sensorimotor control
2) . An understanding of the mechanisms underlying apraxia of speech and dysarthria
3) . Knowledge of the deviant speech characteristics specific to each speech disorder
4) . A well trained ear to perceive discrete perceptual speech changes

SPA6233 Motor Speech (5 decks)

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