Motor Speech Quiz 1 Questions

Front 1

What is responsible for planning and initiation of fine, voluntary movement for speech?

Back 1

cortex

Front 2

What transmits motor commands?

Back 2

descending pathways & cranial nerves

Front 3

What are the 2 motor control circuits?

Back 3

basal ganglia & cerebellum

Front 4

What are the cortical areas involved in speech motor control?

Back 4

a) motor strip
b) premotor area, supplementary motor area, Broca's area, insula
c) somatosensory cortex & supramarginal gyrus

Front 5

What are the descending pathways?

Back 5

a) corticospinal & corticobulbar
b) extrapyramidal descending pathway (indirect/UMN)
c) final common pathway (FCP)

Front 6

What is the PNS comprised of?

Back 6

a) cranial nerves
b) spinal nerves

Front 7

What is composed of all the remaining nerves of the body and their associated collections of cell bodies (ganglia)?

Back 7

PNS

Front 8

What are the 3 stages of speech motor control?

Back 8

a) speech motor planning
b) speech motor programming
c) speech motor execution

Front 9

What is the formulation of the plan/strategy of action that involves specific motor goals?

Back 9

speech motor planning

Front 10

What is the term used to denote the set of muscle commands that are set before a movement begins & can be delivered without external feedback?

Back 10

speech motor programming

Front 11

What is used to change a motor program as needed, as movement occurs?

Back 11

sensory feedback

Front 12

What is the execution stage that involves the actual physiologic act of muscle contraction allowing movement of the structures involved in speech production?

Back 12

speech motor execution

Front 13

Lesions here are associated with deficits in complex skilled movement. Therefore, patient will have difficulty with coordination of the lip, tongue, and jaw for speech and swallowing

Back 13

primary motor cortex

Front 14

What makes up the descending tracts?

Back 14

corticospinal
corticobulbar
indirect activation pathways

Front 15

Where does the primary motor cortex send information?

Back 15

a) spinal cord - corticospinal tract
b) brain stem - corticobulbar tract

Front 16

What makes up the pyrimidal system?

Back 16

corticospinal & corticobulbar tracts

Front 17

What is are the corticospinal and corticobulbar tracts responsible for?

Back 17

fine, voluntary motor control

Front 18

What is the indirect motor pathway system also called?

Back 18

extrapyrimidal system

Front 19

Damage to the indirect & direct pathways result in ______ syndromes.

Back 19

UMN

Front 20

Which pathway is concerned with voluntary, discrete, skilled movement?

Back 20

corticospinal

Front 21

Which pathway goes from the cortex to voluntary muscles of the head?

Back 21

corticobulbar

Front 22

What is included in the descending tracts (indirect activation systems)?

Back 22

reticulospinal, vestibulospinal, rubrospinal

Front 23

The descending tracts/indirect pathway is largely responsible for...

Back 23

automatic activity in motor function (i.e. posture)

Front 24

Descending/indirect pathways are primarily _____________. Therefore, damage to these systems often results in abnormalities of what things...?

Back 24

inhibitory
muscle tone and/or UMN signs

Front 25

What composes the LMNs?

Back 25

a) sensory receptors & afferent sensory pathways
b) peripheral efferent motor pathways & effector endings
c) spinal cord
d) brain stem & cranial nerves

Front 26

What is diminished/absent tone; muscle will feel soft & flabby?

Back 26

hypotonia

Front 27

What is increased tone; muscle will exhibit spasticity/rigidity?

Back 27

hypertonia

Front 28

What is loss of function, especially loss of voluntary motion?

Back 28

paralysis

Front 29

What means sudden (regular/irregular) contraction of an isolated muscle/muscle group, usually associated with lesions from the cortex to spinal cord?

Back 29

myoclonus

Front 30

Paralysis to one side of the body

Back 30

hemiplegia

Front 31

What are the clinical signs of UMN lesions?

Back 31

a) Babinski sign
b) loss of performance of fine skilled movements

Front 32

What are signs of other descending tracts/indirect activation pathways?

Back 32

a) paralysis (no atrophy)
b) spacticity/hypertonicity
c) exaggerated deep muscle reflexes
d) clasp knife reaction

Front 33

What are clinical signs of LMN lesions?

Back 33

a) flaccid paralysis
b) atrophy
c) fasciculations
d) muscle contractions

Front 34

What are the 12 cranial nerves?

Back 34

Olfactory
Optic
Occulomotor
Trochlear
Trigeminal
Abducens
Facial
Vestibulocochlear
Glossopharyngeal
Vagus
Spinal accessory
Hypoglossal

Front 35

What are the sensory/motor designations of the cranial nerves?

Back 35

Sensory
Sensory
Motor
Motor
Both
Motor
Both
Sensory
Both
Both
Motor
Motor

Front 36

Bilateral connections are present for all cranial motor nuclei except...?

Back 36

lower facial nucles of CN 7
hypoglossal motor nucleus

Front 37

What are the 3 divisions of CN 5?

Back 37

opthalmic
maxillary
mandibular

Front 38

What is the principle sensory nerve for the face & head and the motor nerve for the muscles of mastication?

Back 38

Trigeminal (CN 5)

Front 39

What will be displayed with a UMN lesion affecting CN 5?

Back 39

No significant change in mastication because the masticator nucleus is innervated by both cerebral hemispheres

Front 40

What will be displayed in LMN lesion affecting CN 5?

Back 40

Paralysis & eventual atrophy of the muscles of mastication on the affected side. The mandible will deviate to the affected side.

Front 41

What do the muscles of facial expression mediate?

Back 41

several reflexes initiated by the optic, acoustic, touch, & emotional impulses
a) closing the eye in response to touching the cornea
b) contracting/relaxing stapedius muscle
c) facial expressions of rage/joy

Front 42

If cranial nerves 6 & 7 are not functioning, what does this suggest?

Back 42

a lesion in the pons of the brainstem

Front 43

If CN 7 & 8 are not functioning, what does this suggest?

Back 43

a lesion in the internal acoustic meatus

Front 44

In a UMN lesion, what can we expect with regard to facial expression?

Back 44

loss of voluntary control if only the lower muscles of facial expression CONTRALATERALLY

Front 45

In a LMN lesion, what do we expect with regard to facial expression?

Back 45

all muscles supplied by the nerve are paralyzed ipsilateral to the lesion (same side)

Front 46

What is characterized by LMN paralysis of all the muscles of facial expression on the affected side?

Back 46

Bell's Palsy

Front 47

What are clinical considerations for CN 9 damage?

Back 47

Because of its close proximity to CN 10 & 11 there is rarely an isolated lesion of CN 9.

Front 48

How do we test the integrity of the glossopharyngeal nerve?

Back 48

stroking the pharyngeal wall; absence of the gag reflex may show damage to the nerve

Front 49

What are the nuclei associated with the vagus nerve?

Back 49

1. nucleus ambiguus
2. dorsal motor nucleus
3. spinal trigeminal
4. nucleus solitarius

Front 50

What part of the vagus nerve supplies the pharynx?

Back 50

pharyngeal branch

Front 51

What part of the vagus nerve supplies the cricothyroid which lengthens the vocal folds?

Back 51

superior laryngeal nerve

Front 52

What part of the vagus nerve supplies the rest of the intrinsic muscles of the larynx?

Back 52

recurrent laryngeal

Front 53

What indicates a unilateral lesion of the vagus (LMN lesion)?

Back 53

hoarseness (loss of function of intrinsic muscles of the larynx) & difficulty swallowing

Front 54

What indicates a unilateral lesion of the recurrent laryngeal nerve (LMN lesion)?

Back 54

ipsilateral weakeness/paralysis of VF; results in breathiness

Front 55

What indicates a lesion of the superior laryngeal (LMN lesion)?

Back 55

difficulty with pitch control

Front 56

What sometimes accompanies a complete laryngectomy that often results in a LMN lesion of CN 11 (accessory)?
What does this cause?

Back 56

radical neck surgery

downward & lateral rotation of scapula & shoulder drop

Front 57

What does hypoglossal nerve supply?

Back 57

all the intrinsic & all but one extrincic muscle

Front 58

What are signs of LMN lesion affecting hypoglossal?

Back 58

ipsilateral flaccid paralysis; tongue deviates toward the side of the lesion

Front 59

What are the signs of UMN lesion affecting hypoglossal?

Back 59

no obious effect

Front 60

What are the input & output strutures of the basal ganglia?

Back 60

input: cortex
output: through thalamus back to prefrontal, premotor, & motor cortex

Front 61

Lesions to the _________________ cause motor disturbances such as dyskinesias (involuntary movement).

Back 61

Basal Ganglia

Front 62

What is the afferent portion of the BG?

Back 62

striatum (caudate & putamen)

Front 63

What is the efferent portion of the BG?

Back 63

globus pallidus

Front 64

What is the difference between cerebellum & BG?

Back 64

cerebellum receives direct spinal input & striatum does not; cerebellum influences major descending pathways directly & BG is more closely related to the cerebral cortex

Front 65

What are the similarities between cerebellum & BG?

Back 65

both striatum & cerebellar cortex receive inputs from all areas of the cortex and send output to the motor cortex

Front 66

What is the critical factor in deficits in motor control due to BG dysfunction? What does this depend on?

Back 66

pattern of activity in the globus pallidus, not the amount; depends on the balance between direct & indirect pathways

Front 67

What affects the balance between direct & indirect pathways?

Back 67

dopamine levels (lack impairs initiation of motor programs; excess impairs suppression of unwanted movement)

Front 68

What are the 2 major classes of syndrome linked to B lesions?

Back 68

a) hyperkinetic
b) hypokinetic

Front 69

What is a dystonic syndrome characterized by an excess of spontaneous, aimless, or unintentional movements?

Back 69

hyperkinetic

Front 70

What is hyperkinetic disorder characterized by?

Back 70

a) chorea- rapid, involuntary, purposeless jerks
b) hemiballismus- spontaneous throwing of extremities
c) athetosis- slower, continuous movement of fingers, toes, tongue

Front 71

What is rigid syndrome (i.e. Parkinson's Disease)?

Back 71

hypokinetic

Front 72

What is hypokinetic disorder characterized by?

Back 72

a) akinesia- disinclination to use affected part of body
b) rigidity- resistance to passive movement
c) tremor- involuntary when limb is held at rest

Front 73

What are the 2 major constituents of the subcortical loops of the motor system?

Back 73

BG & cerebellum

Front 74

What is different with respect to lesions in cerebellum & those in the BG?

Back 74

signs of BG lesion appear on contralateral side; signs of cerebellum lesion appear on ipsilateral side

Front 75

What words to control smooth contraction of voluntary muscles & coordinates that contraction with relaxation of muscle antagonists?

Back 75

cerebellum

Front 76

What are the functions of the cerebellum?

Back 76

a) maintain equillibrium
b) coordinate muscle action
c) synergy of muscle action
d) makes sure muscles contract at the right time with the right force
d) influence over postural & voluntary movements

Front 77

What will a cerebellum lesion cause?

Back 77

disturbance of motor function without voluntary paralysis

Front 78

What kinds of disturbances will a patient experience w ith a cerebellum lesion?

Back 78

a) hypotonia
b) gait alterations
c) postural changes
d) dysdiadochokinesis
e) reflex disturbances
f) nystagmus
d) dysarthria

Front 79

What are the different types of dysarthria?

Back 79

Flaccid
Spastic
Ataxic
Hypokinetic
Hyerkinetic
Unilateral UMN
Mixed
Undetermined

Front 80

What is the localization of flaccid dysarthria? What are symptoms?

Back 80

LMN (FCP)
weakness

Front 81

What is the localization & symptoms of spastic dysarthria?

Back 81

bilateral UMN (direct & indirect pathways)
spasticity

Front 82

What is the localization & symptoms of ataxic dysarthria?

Back 82

cerebellum
incoordination

Front 83

What is the localization & symptoms of hypokinetic dysarthria?

Back 83

BG
rigidity/reduced range of movement

Front 84

What is the localization & symptoms of hyperkinetic dysarthria?

Back 84

BG
abnormal movements

Front 85

What is the localization & symptoms of a unilateral UMN dysarthria?

Back 85

UMN
weakness, incoordination, spasticity

Front 86

What is the localization & symptoms of apraxia of speech?

Back 86

left (dominant) hemisphere
motor planning/programming deficits

Front 87

What are the functions, structures, and designations of the FCP?

Back 87

function: stimulates muscle contraction & movement
structures: cranial & spinal nerves
designations: LMN

Front 88

What are the functions, structures, and designations of the direct activation pathway?

Back 88

function: influences consciously controlled, skilled voluntary movement
structures: corticobulbar & corticospinal tracts
designations: UMN

Front 89

What are the functions, structures, and designations of the indirect activation pathway?

Back 89

function: mediates subconscious, automatic muscle activities like posture, tone, & movement to accompany voluntary muscle movement
structures: corticorubral, corticoreticular, rubrospinal, reticulospinal ,vestibulospinal
designations: UMN

Front 90

What are the functions of the BG?

Back 90

function: plan & program postural & supportive components of motor activity

Front 91

What are the functions of the cerebellum?

Back 91

function: integrate & coordinate execution of smooth, directed movements

Front 92

What are distinctive signs of LMN lesions?

Back 92

weakness, diminisehd reflexes, decreased muscle tone, atrophy, fasciculations

Front 93

A neurological motor speech impairment characterized by slow, weak, imprecise and/or uncoordinated movements of the speech musculature

Back 93

dysarthria

Front 94

A motor speech disturbance characterized by a disruption of planning/programming of sequential movement for volitional speech production

Back 94

apraxia

Front 95

What are the differences between UMNs & LMNs?

Back 95

UMNs originate in the motor region of the brainstem; they are NOT responsible for the targeted muscle & DON'T carry info down to the FCP. They work through NT called glutamate. LMNs get impulses from UMNs, work by making use of glutamate to trigger depolarization and allow muscles to contract