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Motor Speech > Dysarthria Types > Flashcards

Dysarthria Types Flashcards

1
Q

Flaccid Dysarthria results from:

A

damage to one or more cranial or spinal nerves (LMN system)

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2
Q

Neurologic basis flaccid

A

Weakness, reduced muscle tone

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3
Q

LMN system also known as

A

final common pathway

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4
Q

6 characteristics of LMN damage

A

weakness, hypotonia, diminished reflexes, atrophy, fasciculations, rapid weakening w/ use and recovery w/ rest

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5
Q

Flaccid caused by anything that damages the _____ of cranial/spinal nerves

A

nuclei, axons, NM junctions

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6
Q

7 etiologies of flaccid

A

NM junction diseases (Myasthenia Gravis), vascular (brainstem stroke), infectious (polio, herpes), demyelinating diseases (Gillain-Barre syndrome), degenerative (ALS, progressive bulbar palsy), physical trauma (surgery), muscle disease (muscular dystrophy), tumor

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7
Q

T/F- It is rare that only CN V is involved in flaccid dysarthriasrsrssssrsss at

A

True

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8
Q

with a CNV lesion, jaw deviates to ___ side

A

weak

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9
Q

CN V Function

A

Motor- jaw

Sensory- midface, inside cheek, front tongue, chin, lower lip

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10
Q

CN VII function

A

motor and sensory (gag) face

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11
Q

Damage to CN VII can affect muscles of entire face _____ to the lesion

A

Ipsilateral

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12
Q

Glossopharyngeal nerve function

A

motor (stylopharyngeus, pharynx muscles); sensory (pharynx and posterior tongue)

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13
Q

CN X pharyngeal branch function

A

constricts pharynx, elevates/retracts palate

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14
Q

CN X superior laryngeal

A

sensory (larynx, epiglottis, base of tongue); motor (inferior constrictor and cricothyroid)

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15
Q

CN X RLN function

A

all intrinsic muscles of larynx; sensory (larynx)

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16
Q

If CNX lesion, palate could hang low on ____

A

side of lesion

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17
Q

Multiple CN lesions is referred to as

A

Bulbar Palsy

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18
Q

Phonotory incompetence (breathy voice, audible inspiration, AND short phrases) only seen in

A

Flaccid

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19
Q

Resonatory incompetence (hypernasality, nasal emission, imprecise consonants, AND short phrases) only seen in

A

Flaccid

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20
Q

BEST distinguishing speech characteristics of Flaccid dysarthria

A 
hypernasality 
nasal emission 
continuous breathiness 
audible inhalation/stridor
short phrases
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21
Q

T/F: Typically, damage to LMN system will result in damage on ipsilateral side of body

A

True

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22
Q

Involvement with which CN would result in jaw deviating to weak side?

A

V

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23
Q

Involvement with which CN would result in an asymmetric smile?

A

VII

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24
Q

Involvement with which CN would result in a breathy voice?

A

X (RLN/SLN)

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25
Q

Involvement with which CN would result in the palate pulling towards the nonparalyzed side upon phonation?

A

X (pharyngeal branch)

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26
Q

Involvement with which CN would result in weakened head turning?

A

XI

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27
Q

Involvement with which CN would result in tongue atrophy/fasciculations?

A

XII

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28
Q

The most common motor neuron disease; affects the bulbar, limb, and respiratory muscles

A

ALS

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29
Q

Characterized by progressive weakness with use and improved function after a period of rest

A

Myasthenia Gravis

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30
Q

A vascular disorder that most commonly impacts IX and X

A

Brainstem stroke

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31
Q

A mostly demyelinating disease that can impact the facial and orofacial muscles and can cause neuromuscular

A

Gullain-Barre syndrome

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32
Q

A type of cranial mononeuropathy that impacts the facial nerve

A

Bell’s Palsy

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33
Q

T/F: If CN XII is damaged, the tongue will deviate to the side contralateral to the damage

A

False

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34
Q

Neurologic basis for spastic

A

weakness and excessive muscle tone (spasticity)

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35
Q

Spasticity

A

slows movement and reduces the range and the force of motion

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36
Q

Patients tend to be ____ in one direction and ____ in the other

A

Spastic; weak

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37
Q

Spastic damage to…

A

BL damage to UMN

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38
Q 
spasticity
weakness
reduce ROM
slow movement 
pathogenic/hyperactive reflexes
emotional liability 
dysphagia
A

Characteristics of BL UMN damage

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39
Q

4 etiologies of spastic

A

Vascular disorder
tumors
TBI
degenerative diseases

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40
Q

low rate
slow, regular AMRs
strained-harsh voice
monopitch/loudness

A

More distinguishing speech characteristics for spastic

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41
Q

The corticobulbar and corticospinal tracts are part of the _____ activation pathway

A

Direct

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42
Q

The direct activation pathway…

A

controls skilled, discrete muscle movements

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43
Q

The indirect activation pathway…

A

maintains muscle tone and posture

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44
Q

T/F: UMN lesions almost always disrupt both the direct and indirect activation pathways

A

True

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45
Q

Portions of which CNs primarily receive contralateral input from the UMNs?

A

Facial, Hypoglossal

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46
Q

T/F: asymmetrical presentation of the lips is a confirmatory sign of spastic dysarthria

A

FALSE

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47
Q

Most common cause of spastic

A

Vascular disorders

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48
Q

T/F: a single lesion in the brainstem can result in spastic dysarthria

A

True

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49
Q

Ataxic dysarthria caused by

A

Damage to cerebellar control circuit

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50
Q

Neurologic basis for ataxic

A

Incoordination (and perhaps reduced muscle tone)

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51
Q

Each cerebellar hemisphere controls movement on the _____ side of the body

A

Ipsilateral

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52
Q

4 primary functions of cerebellum:

A

Timing movement
Scaling size of muscle actions
Coordinating sequences of muscle contractions
Error control

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53
Q

2 Important terms under ataxia

A

Dysmetria and Dysdiadochokinesis

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54
Q

Dysmetria

A

over/undershooting of movement

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55
Q

Dysdiadochokinesis

A

Inability to perform rapid, alternating movements

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56
Q

Characteristics of cerebellar lesions

A 
Ataxia 
Difficulty w/ stance and gait
Intention tremor; titubation 
Abnormal eye movements 
Hypotonia
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57
Q

Titubation

A

a nervous system disorder that causes uncontrollable, rhythmic shaking

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58
Q

Etiologies of ataxic dysarthria

A

Degenerative, vascular, tumors, TBI, toxic/metabolic conditions

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59
Q

Friedreich’s ataxia is a _____ ataxia that affects the ______ in addition to the cerebellum. It usually begins before age ____ and is sometimes mixed with ____.

A

hereditary
spinal tract
20
spastic dysarthria

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60
Q

____ ataxic dysarthria is very suggestive of Multiple Sclerosis

A

Paroxysmal

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61
Q

2 subgroups of speech deviation for ataxic dysarthria

A

Predominant prosodic excess; predominant articulatory inaccuracy

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62
Q 
Excess loudness variations
Irregular artic breakdowns
Irregular AMRs 
Distorted vowels 
Excess & equal stress
Prolonged phonemes 
Trouble coordinating breathing w/ speaking
A

More distinguishing speech characteristics of ataxic

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63
Q

Nonspeech findings consistent with ataxic dysarthria

A

Ataxic gait
Over/under shooting
Intention tremor
Mestagmis (eye movement thng)
Titubation (shaking or swaying of body/head)
Normal symmetry and structures on oral mec

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64
Q

T/F: The cerebellum plays a role in learning and memory

A

True

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65
Q

Most common cause of ataxic dysarthria

A

Degenerative diseases

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66
Q

T/F: Cerebellar damage can impact one’s ability to coordinate breathing and speaking

A

True

67
Q

T/F: Ataxic dysarthria reflects a breakdown in motor control

A

True

68
Q

Hypokinetic dysarthria is caused by damage to

A

Basal Ganglia Control Circuit

69
Q

Neurologic basis for hypokinetic dysarthria

A

Rigidity & reduced ROM

70
Q

Prototypic disease for hypokinetic dysarthria

A

Parkinson’s!

71
Q

PD characteristics

A 
Mask-like face
Asymmetric resting tremor 
Postural instability 
Shuffling steps 
Parkinson's gait 
Slowed movement
Reduced arm swing 
Rigidity 
Freezing
72
Q

Striatum (in BG)’s function

A

Recieves info from cortex, thalamus, and substantia nigra and sends info to substantia nigra and globus pallidus

73
Q

Globus Pallidus (in BG)’s function

A

sends info to thalamus, subthalamic nucleus, red nucleus, and reticular formation

74
Q

Some functions of BG control circuit

A
  • Control postural adjustments during skilled movement
  • Regulates movements for goal-directed activities
  • Assists in motor learning
  • Helps regulate muscle tone
  • Participates in motor programming
  • Contributes to sensory-motor integration
  • Contributes to cognitive and emotional function
75
Q

Normal BG function depends on integrity of connections & proper balance of NTs…

A

Dopamine

Acetylcholine

76
Q

2 main things that happen when damage to BG control circuit

A
  • Reduced movement (hypokinesia)

- Failure to inhibit voluntary movement (hyperkinesia)

77
Q

Etiologies of hypokinetic

A

** PD
vascular (uncommon)
toxic-metabolic (antipsych meds)
infectious conditions

78
Q

Demonstrate many characteristics of PD but they don’t respond to Tx for PD (then they think maybe its Lewy Body dementia, etc.

A

Parkinsonism

79
Q

Parkinson’s Plus Syndromes

A
  • Multiple systems atrophy
  • Progressive supranuclear palsy
  • Corticobasal degeneration
80
Q

T/F: PD is thought to have genetic susceptibility in combination with certain undetermined environmental factors

A

True

81
Q

For PD, cell loss in the _____ and the associated loss of _____ in the striatum is accepted as the primary explanation for motor symptoms

A

Substantia nigra

dopamine

82
Q

4 classic motor signs of PD

A

Tremor
Rigidity
Akinesia
Postural Instability

83
Q

Cognitive changes associated with PD

A

executive dysfunction, problems with working memory, attention, memory, visuospatial…

84
Q

Hypokinetic dysarthria nonspeech oral mec findings

A

Stoic (masked face); symmetrical face, small size of movement; tremor of tongue; movement slow to initiate
Tongue lateralization perceived as fast

85
Q

Most distinguishing speech characteristics hypokinetic

A
  • Reduced loudness
  • Monopitch
  • Monoloudness
  • Reduced stress
  • Inappropriate silences
  • Repeated phonemes
  • Variable rate
  • Short rushes of speech
  • Increased overall rate
86
Q

Respiratory-phonatory in hypokinetic

A

Breathiness, short phrases

87
Q

Articulation in hypokinetic

A

Imprecise

88
Q

T/F: too much dopamine causes the body to make involuntary movements

A

True

89
Q

Hyperkinesia

A

Muscle spasms

90
Q

Which 2 neural structures are damaged in corticobasal degeneration

A
  • Basal Ganglia

- UMNs in cerebral cortex

91
Q

A classic sign of Progressive Supranuclear Palsy (PSP) is

A

Eye movement problems

92
Q

Nonspeech AMRs in pw/ hypokinetic will be

A

fast and reduced in range

93
Q

Hyperkinetic dysarthria is caused by disruptions in

A

Basal Ganglia control circuit

94
Q

Neurologic basis for hyperkinetic dysarthria

A

Involuntary movements that are heterogeneous

95
Q

Many hyperkinesias result from failure of _____ pathways to _____ cortical motor discharges

A

BG-thalamic

inhibit

96
Q

A group of disorders characterized by involuntary movements of muscles

A

Dyskinesia

97
Q

5 types of dyskinesias

A 
Myoclonus
Chorea
Athetosis 
Dystonia 
Tremor
98
Q

Tardive (late onset) dyskinesia results from

A

prolonged use of antipsychotics

99
Q

Single/repetitive involuntary brief jerks of a muscle or group of muscles (rhythmic or non-rhythmic)

A

Myoclonus

100
Q

Rapid, random, purposeless movements that are brief, abrupt, irregular, unpredictable

A

Chorea

101
Q

Relatively slow, writhing movements

A

Athetosis

102
Q

Athetosis is associated with what disease

A

Athentoid Cerebral Palsy

103
Q

Uncontrollable muscle contractions and abnormal postures

A

Dystonia

104
Q

Rhythmic movements of body part (most common involuntary movement)

A

Tremor

105
Q

Hyperkinetic dysarthrias usually the result of ____ rather than structural

A

Neurochemical abnormalities

106
Q

Hyperkinetic Etiologies

A

Degenerative (Huntington’s); Toxic-metabolic conditions (antipsychotic); infectious processes (sydenham’s chorea)

107
Q

Hyperkinetic nonspeech oral mec findings

A

size, strength and symmetry of orofacial muscles normal

  • dysphagia
  • drooling
  • abnormal movements
108
Q

Hyperkinetic respiration/phonation

A
  • sudden forced inspiration/expiration
  • strained-harsh voice
  • voice stoppages
  • excess loudness variations
109
Q

Hyperkinetic Resonance

A

intermittent hypernasality

110
Q

Hyperkinetic articulation

A

irregular artic distortions, slow irregular AMRs, distorted vowels

111
Q

Hyperkinetic prosody

A

inappropriate silences, prolonged phonemes, variable stress/loudness patterns

112
Q

Most common etiology of hyperkinetic dysarthria

A

Toxic-metabolic conditions

113
Q

T/F: pw hyperkinetic dysarthria may exhibit sudden, forced inhalation or exhalation; a finding not usually encountered with any other dysarthria type

A

True

114
Q

Nonspeech AMRs in pw hyperkinetic dysarthria may be

A

slow and irregular

115
Q

T/F: accelerated rate is a characteristic of hyperkinetic

A

FALSE

116
Q

Hiccups and sleep starts are examples of

A

Myoclonus

117
Q

UUMN is caused by damage to

A

the UMNs unilaterally

118
Q

UUMN dysarthria primarily results in a disorder of ____ and to a lesser degree, _____ and ____

A

Articulation

-phonation and prosody

119
Q

The neurologic basis for UUMN dysarthria is

A

weakness and perhaps incoordination

120
Q

UUMN dysarthria often co-occurs with _____ (4)

A

aphasia
RHD
Aprosodia
Apraxia of speech

121
Q

T/F: UUMN dysarthria can be masked and may take a back seat to co-occurring conditions

A

True

122
Q

for UUMN, the bottom of face is affected on one side

A

ok

123
Q

For LMN damage, the whole side of face is affected

A

ok

124
Q

Most common cause of UUMN dysarthria

A

stroke

125
Q

T/F: UUMN dysarthria is NOT from degenerative, inflammatory, toxic-metabolic, or traumatic conditions b/c those produce diffuse effects

A

TRUE

126
Q

Physical findings of UUMN dysarthria

A
  • contralateral lower facial weakness
  • contralateral tongue weakness (25-50%)
  • contralateral hemiparesis/hemiplegia
127
Q

in UUMN dysarthria, if the _______ is spared, you may see a mismatch btw emotional and volitional smiling

A

indirect pathway

128
Q

T/F: you will see a mismatch btw emotional and volitional smiling in Flaccid dysarthia

A

FALSE, only in UUMN dysarthria

129
Q
  • imprecise articulation
  • mildly slow rate
  • irregular articulatory breakdowns
  • slow and sometimes irregular AMRs
  • voice harsh (but should go away)
  • loudness reduced occasionally
A

Primary speech characteristics of UUMN dysarthria

130
Q

UUMN dysarthria is ___ more than moderately severe

A

rarely

131
Q

UUMN dysarthria is almost always accompanied by

A

central facial weakness, and frequently lingual weakness

132
Q

dysphagia and emotional liability occur much more frequently and dramatically in pw _____

A

BL UMN lesions

133
Q

In patients with UUMN dysarthria resulting from damage to the right cortical hemisphere, the tongue will deviate to the ____

A

left side

134
Q

Mixed dysarthrias result from damage to

A

more than one part of the motor system

135
Q

most common etiology for mixed dysarthria

A

Degenerative diseases

136
Q

Common etiologies causing mixed dysarthria

A

ALS, MS, TBI, PSP, Multiple systems atrophy

137
Q

ALS is a degenerative motor neuron disease affecting the ____.

A

UMNs and LMNs

138
Q

What muscles does ALS affect

A

limbs and bulbar

139
Q

Most common presenting symptom of ALS is

A

focal weakness, usually on one of the limbs

140
Q

ALS causes either _____ or ____ dysarthria

A

Flaccid or spastic

usually a mixed flaccid-spastic

141
Q

ALS speech

A

-Imprecise consonants, hypernasality, harshness, slow rate, monopitch, excess equal stress, breathiness

142
Q

Multiple Sclerosis is the most common _____ CNS disease

A

Demyelinating

143
Q

MS affects ____, the brainstem, spinal cord, and optic nerves

A

white matter

144
Q

4 types of MS

A

A. Relapsing-remitting
B- Progressive-relapsing
C- Secondary-progressive
D- Primary-progressive

145
Q

Most common type of MS

A

Secondary progressive

146
Q

MS can produce signs such as

A 
-Gait disturbance 
cerebellar dysfunction 
CN abnormalities
Psychiatric disturbance 
cognitive deficits
dysarthria
147
Q

Dysarthria occurs in ____% of MS cases

A

40-50

148
Q

MS typically causes what kind of dysarthria

A

ataxic, spastic, or mixed spastic-ataxic

149
Q

MS speech characteristics

A
  • impaired control of loudness
  • harshness
  • imprecise artic
  • impaired emphasis
  • impaired control of pitch
150
Q

Types of deficits common after TBI

A

Cognitive
Dysarthria
Dysphagia

151
Q

With TBI, dysarthria occurs in approximately ____ of cases

A

1/3

152
Q

Diffuse or multifocal lesions in TBI can result in virtually _____ of mixed dysarthrias

A

any combo

153
Q

more common TBI caused dysarthrias

A

combos of flaccid, spastic, ataxic, hypokinetic

154
Q

This is associated with cell loss, particularly of structures such as the subthalamic nucleus, substantia nigra, globus pallidus, thalamus, midbrain and cerebellum

A

Progressive Supranuclear Palsy

155
Q

Primary symptoms of Progressive Supranuclear Palsy

A
  • Vertical gaze palsy
  • postural instability
  • Parkinsonian symptoms
156
Q

Progressive Supranuclear Palsy and speech

A

-Dysarthria
-Palilalia and dysfluencies
AOS
-combos of hypokinetic, spastic, and ataxic

157
Q

Vertical gaze palsy

A

peripheral vision isn’t working: they need to turn head to see something

158
Q

PSP versis PD

A

PD: flexed neck posture, expressionless face, hypokinetic

PSP: neck extension, worried face, pseudobulbar affect, hypernasality, nasal emission, excess equal stress, slow rate

159
Q

Multiple Systems Atrophy also called

A

Shy Drager Syndrome

160
Q

A rare and sporadic neurodegenerative condition that affects involuntary functions, including blood pressure, breathing, bladder, and muscle control

A

Multiple Systems Atrophy

161
Q

Multiple Systems Atrophy is a varying combo of

A

parkinsonism, ataxia, spasticity, and autonomic dysfunction

162
Q

2 MSA subtypes:

A

MSA-P (when parkinsonian features predominate)

MSA-C (when cerebellar features predominate)

163
Q

most common etiology for mixed dysarthria is

A

Degenerative disease

164
Q

Speech characterized by imprecise consonants, hypernasality, slow rate, and nasal emissions would likely be a combo of

A

spastic-flaccid

Motor Speech (1 decks)

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