Neuro Unit 1

Front 1

Normal speech involves 3 processes:

Back 1

1) Cognitive Linguistic Process
2) Motor Speech Programming
3) Neuromuscular Execution

Front 2

A neurogenic speech disorder resulting from impairment of the capacity to program sensorimotor commands for the positioning and movement of muscles for the volitional production of speech.

Back 2

Apraxia

Front 3

It can occur without significant weakness or neuromuscular slowness, and in the absence of disturbances of conscious thought or language.

Back 3

Apraxia

Front 4

A group of neurological disorders that reflect disturbances in the strength, speed, range, tone, steadiness, timing, or accuracy of movements necessary for prosodically normal, efficient and intelligible speech.

Back 4

Dysarhtiras

Front 5

They result from CNS or PNS conditions that adversely affect respiratory, phonatory, resonatory, or articulatory speech movements.

Back 5

Dysarthrias

Front 6

They are often accompanied by nonspeech impairments

Back 6

Dyasarthrias

Front 7

Can be transient, improving, exacerbating-remitting, progressive, or stationary.

Back 7

Dysarthrias

Front 8

Disorders of speech resulting from neurologic impairment affecting the motor programming or neuromuscular execution of speech

Back 8

Motor Speech Disorders

Front 9

2 types of motor speech disorders

Back 9

1) Apraxia of speech
2) dysarthrias

Front 10

Although we think of MSD as a motor impairment we cannot exclude the role of:

Back 10

tactile, kinesthetic, and proprioceptive sensation in the maintenance of normal speech.

Front 11

Normal speech involves 3 processes:

Back 11

1) Cognitive Linguistic Process
2) Motor Speech Programming
3) Neuromuscular Execution

Front 12

A neurogenic speech disorder resulting from impairment of the capacity to program sensorimotor commands for the positioning and movement of muscles for the volitional production of speech.

Back 12

Apraxia

Front 13

It can occur without significant weakness or neuromuscular slowness, and in the absence of disturbances of conscious thought or language.

Back 13

Apraxia

Front 14

A group of neurological disorders that reflect disturbances in the strength, speed, range, tone, steadiness, timing, or accuracy of movements necessary for prosodically normal, efficient and intelligible speech.

Back 14

Dysarhtiras

Front 15

They result from CNS or PNS conditions that adversely affect respiratory, phonatory, resonatory, or articulatory speech movements.

Back 15

Dysarthrias

Front 16

They are often accompanied by nonspeech impairments

Back 16

Dyasarthrias

Front 17

Can be transient, improving, exacerbating-remitting, progressive, or stationary.

Back 17

Dysarthrias

Front 18

Disorders of speech resulting from neurologic impairment affecting the motor programming or neuromuscular execution of speech

Back 18

Motor Speech Disorders

Front 19

2 types of motor speech disorders

Back 19

1) Apraxia of speech
2) dysarthrias

Front 20

Although we think of MSD as a motor impairment we cannot exclude the role of:

Back 20

tactile, kinesthetic, and proprioceptive sensation in the maintenance of normal speech.

Front 21

Malfunctions in sensorimotor processes from brani damage can contribute to:

Back 21

MSD

Front 22

MSD

Back 22

Motor Speech Disorders

Front 23

Other neurogenic speech disturbances that are not MSD:

Back 23

1) Acquired Stuttering
2) Palilalia
3) Echolalia
4) Mutism
5) Pseudo-Foreign Dialect
6) Affective Communication Disorders altering Prosody

Front 24

Non-neurogenic speech disturbances that are not MSD:

Back 24

1) Psychogenic Disorders
2) Normal Variations in Speech Production

Front 25

After neurologic damage, a number of alterations in communicative ability can occur resulting from linguistic and other cognitive deficits. This makes *this* a challenge.

Back 25

Examination and Diagnosis

Front 26

Mild dysarthria may co-occur with:

Back 26

1) Aphasia, from a stroke in the left hemisphere
2) Right hemisphere communication disorder, from a stroke in the right hemisphere
3) With Apraxia of Speech

Front 27

How dysarthria and aphasia differ

Back 27

1) Dysarthria not a language disorder
2) Lesions that produce aphasia are limited to the cortical language zones and related subcortical connections.
3) Lesions that produce dysarthria occur in a variety of areas in both the CNS and PNS

Front 28

Dysarthria and dementia differ; however:

Back 28

Dementia is seen in later stages of dysarthria groups associated with movement disorders: Parkinson’s disease, Huntington’s chorea, and progressive supranuclear palsy.

Front 29

Dysarthria and confusion differ; however,

Back 29

If the dysarthria occurs as a result of head trauma, confusion may be a co-occurring feature

Front 30

AOS

Back 30

Apraxia of Speech

Front 31

AOS is associated with:

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The LH

Front 32

Dysarthria has this site of lesion.

Back 32

There are many sites associated with dysarthria.

Front 33

Errors of phoneme substitution, abnormal prosody, and initiation difficulty

Back 33

AOS

Front 34

Distortion errors predominate; articulation is imprecise; phonation, resonance, and respiration can be altered.

Back 34

Dysarthria

Front 35

Automatic or involuntary tasks are intact or significantly less impaired (e.g., chewing).

Back 35

AOS

Front 36

A motor production disorder involving abnormalities in movement rates, precision, coordination, and strength; the problems are present all of the time.

Back 36

Dysarthria

Front 37

Great dx indicator for dysarthria

Back 37

Problems are present ALL of the time

Front 38

In AOS, prosodic errors:

Back 38

Reflect the patient's efforts to compensate for or avoid articulation errors.

Front 39

In dysarthria, prosodic errors:

Back 39

Reflect impaired speed, strength, and timing of movements for speech.

Front 40

Dysarthria is present in a number of frequently-occurring:

Back 40

Neurological Diseases

Front 41

This represents a significant proportion of all acquired neurological communication disorders.

Back 41

Dysarthria

Front 42

What are some neurological disorders that often include dysarthria?

Back 42

1) TBI
2) Parkinson's Disease
3) ALS
4) Lacunar Stroke
5) AOS

Front 43

It is likely that many patients for which "swallowing" catches the physician's eye, this will also be an issue.

Back 43

MSDs

Front 44

These are likely underreported, due to swallowing being the paramount issue and saving inpatient care dollars.

Back 44

MSDs

Front 45

Methods for MSD Categorization

Back 45

1) Perceptual
2) Acoustic
3) Physiologic

Front 46

Based on the auditory-perceptual attributes of speech;
most believe the, “gold-standard” for MSD

Back 46

Perceptual methods for categorizing MSD.

Front 47

Valuable in that they can contribute to the acoustic quantification and description of clinically perceived deviant speech (state of the art instrumentation used

Back 47

Acoustic methods for categorizing MSD

Front 48

Rather than focusing on the signal this type of analysis moves “up-stream” toward the source of activity that generates the signal (e.g., muscle contractions, structural movements, etc.)

Back 48

Physiologic methods for categorizing MSD

Front 49

When categorizing age of onset for MSD, what are the two main types?

Back 49

1) Acquired
2) Congenital

Front 50

Courses dysarthria takes:

Back 50

1) Developmental
2) Recovering
3) Stable
4) Degenerative
5) Exacerbating-Remitting

Front 51

An SLP's role in the course of dysarthria include:

Back 51

1) Preventing secondary complications.
2) Educating patients and families
3) Providing augmentative communication options if indicated

Front 52

Sites of Lesions for MSD

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1) Diverse loci
2) Neuromuscular junction
3) PNS and CNS
4) Brainstem
5) Cerebellum
6) Pyramidal and Extra-Pyramidal Pathways
7) Cortex

Front 53

Broad categories of neurologic diagnosis for dysarthria

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1) Vascular
2) Degenerative
3) Inflammatory
4) Nepotistic
5) Toxic-Metabolic
6) Trauma
7) Congenital-Developmental

Front 54

Refers to things that determine the deviant.

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Pathophysiology

Front 55

When categorizing the dysarthrias, these perceptual features will reflect certain abnormalities of speech.

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1) Spasticity
2) Flaccidity
3) Ataxia
4) Tremor
5) Rigidity
6) Various Involuntary Movements

Front 56

Variables related to speech disorders used in categorization.

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1) Speech Components Involved
2) Severity (always relevant to management decisions)
3) Perceptual Characteristics

Front 57

How many types of dysarthria?

Back 57

Six major types

Front 58

Two most recent categories of dysarthria

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1) Unilateral UMN
2) Undetermined

Front 59

Localization of flaccid dysarthria

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LMN (Final common pathway, motor unit)

Front 60

Localization of spastic dysarthria

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Bilateral UMN (direct and indirect activation pathways)

Front 61

Localization of ataxic dysarthria

Back 61

Cerebellum (cerebellar control circuit)

Front 62

Localization of hypokinetic dysarthria

Back 62

BG control circuit (extrapyramidal)

Front 63

Localization of hyperkinetic dysarthria

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BG control circuit (extrapyramidal)

Front 64

Localization of unilateral UMN dysarthria

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Unilateral UMN

Front 65

Localization of mixed dysarthria

Back 65

More than one site

Front 66

Localization of undetermined dysarthria

Back 66

???

Front 67

Localization of AOS

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Left (dominant) hemisphere

Front 68

Neuromater basis of flaccid dysarthria

Back 68

Weakness

Front 69

Neuromater basis of spastic dysarthria

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Spasticity

Front 70

Neuromater basis of ataxic dysarthria

Back 70

Incoordination

Front 71

Neuromater basis of hypokinetic dysarthria

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Rigidity or reduced ROM

Front 72

Neuromater basis of hyperkinetic dysarthria

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Abnormal movements

Front 73

Neuromater basis of unilateral UMN dysarthria

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Weakness, incoordination, or spasticity

Front 74

Neuromater basis of mixed dysarthria

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More than one

Front 75

Neuromater basis of undetermined dysarthria

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???

Front 76

Neuromater basis of AOS

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Motor planning or programming

Front 77

Most common type of MSD

Back 77

Flaccid dysarthria

Front 78

With AOS, this is NOT impaired.

Back 78

Musculature

Front 79

The problem is motor planning.

Back 79

AOS

Front 80

Making the translation between language forms and the movement that occurs to create the sounds understood by the listener.

Back 80

Motor Planning

Front 81

Getting the motor plan into action to lead to actual muscle contractions.

Back 81

Motor Execution

Front 82

Primary perceptual disturbances of AOS

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1) Articulation
2) Rate
3) Prosody
4) Rhythm

Front 83

Articulatory errors in AOS

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Vowel and consonant distortions, but substitutions are also present.

Front 84

Articulation errors are inconsistent.

Back 84

AOS

Front 85

Errors are perceived as approximations of target sounds. Errors increase as words get longer and phonemic complexity increases.

Back 85

AOS

Front 86

Any loss or abnormality of psychological, physiological, or anatomical structure or function

Back 86

Impairment

Front 87

Restriction or lack of the ability to perform an activity in the manner or within the range considered normal for the human being

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Disability

Front 88

A disadvantage for a given individual (resulting from an impairment or a disability) that limits or prevents the fulfillment of a role that is normal (depending on age, sex, social, cultural) for that person.

Back 88

Handicap

Front 89

Standpoints from which a MSD can be viewed.

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1) Basic Scientist (Speech Physiologist
2) Physician (Neurologist)
3) Rehabilitation Specialist
4) Consumer (speaker and family)

Front 90

Overall measures of performance in relationship to normal individuals.

Back 90

Functional Limitations

Front 91

What systems are involved?

Back 91

Impairment (Subsystem)

Front 92

Where is the level of breakdown that causes the functional disorder (can be examined from the cellular level)

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Pathophysiology

Front 93

Given the maximum amount of support, how does the person do in the contexts in which he/she communicates

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Disability (contextual level)

Front 94

Does the MSD prevent the individual from achieving a desired role because of society limitations?

Back 94

Societal Limitation

Front 95

Oral communication includes 4 domains

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1) Cognition
2) Language
3) Motor Planning
4) Speech Executionq

Front 96

Primary motor cortex controls:

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Large, gross movements.

Front 97

Premotor cortex controls:

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Finer movements

Front 98

Functional divisions of motor system organization

Back 98

1. The final common pathway
2. The direct activation pathway
3. The indirect activation pathway
4. The control circuits
5. Conceptual Programming Level (Includes planning and programming processes)

Front 99

This kind of integration is needed for normal movements.

Back 99

Sensorimotor integration

Front 100

Lesions of the sensory portion of the sensorimotor system may result in:

Back 100

Abnormal motor behavior

Front 101

LMN system, aka:

Back 101

Final Common Pathway

Front 102

The peripheral mechanism through which all motor activity is mediated.

Back 102

Final Common Pathway

Front 103

The last link in the chain of neural events that lead to movement”

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Final Common Pathway

Front 104

The LMN pathway generates activity in:

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Skeletal (movement) and somatic (sensation) muscles

Front 105

These types of muscles can be voluntarily controlled.

Back 105

Skeletal muscles

Front 106

A single muscle can do one of three things:

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1) Contract
2) Stretch
3) Relax

Front 107

Complex movements are not completed by:

Back 107

Individual muscles

Front 108

Complex movements occur when single muscles are integrated with the:

Back 108

Actions of larger gruops of contiguous or distant muscles.

Front 109

A collection of striated muscle fibers (cells) that connect to the bony framework of the body may be part of the appendicular or axial skeleton.

Back 109

Skeletal muscle

Front 110

Also called striated muscles

Back 110

Skeletal muscles

Front 111

Another word for LMN

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Alpha Motoneuron

Front 112

Controls the extrafusal muscle fibers.

Back 112

Alpha Motoneuron (LMN)

Front 113

Contractile element in the skeletal muscle to generate force for movement.

Back 113

Extrafusal muscle fibers

Front 114

The alpha motoneuron cell body or nuclei is located in:

Back 114

1) Brainstem
2) Anterior horn of the spinal cord

Front 115

Motor Unit consists of:

Back 115

1) LMN or alphamotoneuron
2) Muscle fibers (cells) it innervates

Front 116

This type of muscle innervation is strongly tied to the direct activation pathways.

Back 116

Skeletal Muscle Innervation

Front 117

Axons leave the brainstem or spinal cord within a:

Back 117

Cranial or spinal nerve

Front 118

The axon travels to specific muscles where it subdivides into any number of terminal branches that make contact with:

Back 118

Muscle Fibers (cells)

Front 119

Each axon in a nerve may innervate several muscle fibers and, conversely, each muscle fiber may receive input from:

Back 119

Branches of several different alpha motor neurons.

Front 120

Force can be increased by:

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1) Temporal summation
2) Spatial summation

Front 121

Increasing the rate of firing of individual motor units

Back 121

Temporal summation

Front 122

Recruiting a greater number of motor units

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Spatial summation

Front 123

Motor unit size is determined by:

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The number of extrafusal muscle fibers innervated by a single motor neuron.

Front 124

The number of muscle fibers per axon is called

Back 124

Innervation ratio

Front 125

Discrete movements have smaller innervation ratios because:

Back 125

There are less muscle fibers innervated by one neuron.

Front 126

Besides extrafusal muscle fiber, what else do LMN (alpha motor neurons) innervate?

Back 126

Interneurons (also called Renshaw cells)

Front 127

These cells are capable of inhibiting alpha motor neurons by providing a negative feedback response tell the LMN to turn off. In turn it can then get ready to fire again.

Back 127

Interneurons or Renshaw Cells

Front 128

These motor neurons are crucial for maintaining muscle tone.

Back 128

Gamma motor neurons

Front 129

The gamma motor neuron has a relationship to alpha motor neurons, and the activities of the direct and indirect activation pathways by way of the:

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Gamma loop, which results in movement control.

Front 130

Results from a mild degree of resistance that occurs when a muscle is stretched.

Back 130

Muscle Tone (response known as stretch reflex).

Front 131

Muscles want to maintain their original length and normal muscle tone. As a result, the muscle never completely:

Back 131

Relaxes...so, in a sense, muscles are always maintained in a state of "readiness" for movement. This sustained nature makes it an ideal support mechanism upon which
quick, unsustained movements may be superimposed.

Front 132

Besides the alpha motor neuron, this is another type of neuron in the motor nerve that is part of the FCP.

Back 132

Gamma motor neuron

Front 133

Interact with the alpha motor neuron to control motor movement.

Back 133

Gamma motor neuron

Front 134

These neurons innervate muscle spindles or intrafusal muscle fibers.

Back 134

Gamma motor neuron

Front 135

Cells located parallel to the extrafusal fibers (cells)

Back 135

Intrafusal muscle fibers

Front 136

Properties of the gamma motor neuron

Back 136

1) Smaller in diameter
2) Slower conducting
3) Strongly influenced by the cerebellum, BG, and the indirect activation system of the CNS.

Front 137

Consists of gamma motor neuron, muscle spindle, stretch receptor and sensory neuron, the LMN, and the extrafusal muscle fibers.

Back 137

Gamma Loop

Front 138

A mechanism through which muscle length adjusts reflexively to the relative length of muscle spindles

Back 138

Gamma Loop

Front 139

Indirect activation pathways of the CNS use this system to present the desired length of the muscle spindle for static postures (example- move hand and hold it in a given position)

Back 139

Gamma Loop

Front 140

Can be used to prepare for and anticipate the degree of muscle contraction required for intended ongoing movement

Back 140

Gamma Loop

Front 141

Extrafusal muscle fibers and muscle spindles are stimulated to contract by:

Back 141

1) Alphamotor neurons
2) Gamma motor neurons

Front 142

When a muscle is stretched by movement, so is the:

Back 142

Spindle

Front 143

The sensory receptor of the spindle sends an afferent message to the spinal cord or brainstem and synapses on the:

Back 143

Alphamotor neuron

Front 144

With the gamma loop, the alphamotor neuron will contract to resist the:

Back 144

Stretch, which gives us muscle tone.

Front 145

The amount (continuation of the gamma loop) changes depending on the:

Back 145

Posture

Front 146

Gamma Motor System Process

Back 146

1) The Gamma Motor euron fires.
2) The muscle spindles contract.
3) The sensory receptor detection in spindles.
4) Impulse triggers through sensory neuron
5) Brainstem or spinal cord receives message
6) Synapse occurs on alphamotor neuron
7) Alpha motor neuron sends message back to extrafusal fibers
8) Contraction occurs until they are the same length as the spindle fibers
9) Sensory receptors say, "Hey, there is no longer a difference."
10) Loop inactivated.

Front 147

Integrates activity from peripheral sensory system and the direct and indirect activation pathway

Back 147

FCP

Front 148

There is a direct relationship between the sensory system and the alpha motoneurons[simple reflex when sensory neuron synapses
directly on alpha motoneuron].

Back 148

Reflex

Front 149

If there is a FCP damage the reflexes can be

Back 149

Weakened or abolished.

Front 150

If there is peripheral sensory pathway damage the reflex may be weakened or abolished by way of the:

Back 150

Removal or weakening of the trigger for the reflex.

Front 151

Damage to a nerve may lead only to weakness or paresis if some but not all of the alpha motoneruons supplying the muscle:

Back 151

Are not damaged

Front 152

Paralysis results if a muscle is deprived of all of its input from:

Back 152

LMNs

Front 153

Loss of muscle bulk when LMN innervation is impaired

Back 153

Atrophy

Front 154

Excess or spontaneous motor unit activity with a lowered firing threshold (discharges) can be seen on the surfaces of the skin as brief localized twitches.

Back 154

Fasciculations

Front 155

Slow repetitive action potentials with resultant regular contractions [cannot be seen through the skin].

Back 155

Fibrillation

Front 156

Final Common Pathway and Speech includes:

Back 156

1) The paired cranial nerves involved in speech supply muscles for
phonation, resonance, articulation, and prosody.
2) The paired spinal nerves that innervate respiration

Front 157

Cranial Nervves

Back 157

OLFACTORY
OPTIC OCULOMOTOR TROCHLEAR TRIGEMINAL ABDUCENS FACIAL
VESTIBULOCOCHLEAR
GLOSSOPHARYNGEAL VEGAS SPINAL ACCESORY HYPOGLOSSAL

Front 158

innervates the muscles of mastication, tensor tympani, and the tensor veli palatini

Back 158

Trigeminal Nerve (Mandibular Branch)

Front 159

Where does the mandibular branch of the trigeminal nerve originate?

Back 159

Midpons

Front 160

LMN lesions of the masticatory nucleus or its axons (CN5), lead to:

Back 160

1) Ipsilateral flaccid paralysis
2) Paresis and atrophy of the muscles on the paralyzed side.
3) Slight jaw deviation toward side of injury; especially noted on jaw protrusion
4) Usually not too big of an impact on speech

Front 161

Bilateral LMN lesions (CN5) severely affect speech and swallowing, due to:

Back 161

1) Difficulty with jaw movement (usually hangs open)
2) Limited ROM

Front 162

Lesions from the motor pathways from the cerebral hemispheres are commona nd referred to as:

Back 162

UMN Lesions

Front 163

UMN lesions usually affect both:

Back 163

Direct and Indirect Pathways

Front 164

Speech Effects from Spasticity:

Back 164

1) Slows Movement
2) Hyperadduction of the VFs during phonation
3) Fairly mild when unilateral
4) When bilateral can be severe including hyperactive reflexes, dysphagia, and disinhibition of the physical expression of emotion (seen in ALS)

Front 165

What types of dysarthria come from spasticity?

Back 165

1) Spastic dysarthria (bilateral)
2) Unilateral UMN Dysarthria

Front 166

Help integrate and control the varied activities of the many structures and pathways in motor performance.

Back 166

Control Circuits

Front 167

Unlike the direct and indirect activation pathways, these do not have direct contact with LMNs.

Back 167

Control circuits

Front 168

Integration and coordination of motor performance are accomplished through activities of:

Back 168

1) BG Circuit
2) Cerebellar Control Circuit

Front 169

Does the basal ganglia directly influence the FCP?

Back 169

No.

Front 170

Skilled movements need to be planned and executed with knowledge about:

Back 170

1) Posture
2) Position in Space
3) Tone
4) Environment

Front 171

The receptive portion of the BG

Back 171

Striatum

Front 172

Receive info from the frontal cortex, the thalamus and hte lower BG areas

Back 172

Striatum

Front 173

The main efferent pathway of the BG

Back 173

Globus Palladus

Front 174

Most info goes back to the thalamus and then back, gets relayed back to cortex as well as other BG areas and the reticular formation.

Back 174

Globus Palladus

Front 175

The BG control circuit consists of many

Back 175

Loops

Front 176

Synaptic transmitter when a neuron's axons terminate in the striatum.

Back 176

Acetylcholine

Front 177

Manufactured in the substantia nigra and transmitted to the striatum where it acts as a neurotransmitter.

Back 177

Dopamine

Front 178

If neurons in substantia nigra are destroyed, this content in the striatum will be reduced.

Back 178

Dopamine

Front 179

Important for regulating muscle tone and maintaining normal posture and statis mucle contraction upon which voluntary, skilled movements are superimposed.

Back 179

BG

Front 180

Important to regulating the amplitude, velocity, and the initiation of movement.

Back 180

BG

Front 181

Can dampen or modulate the movement goals coming out of the cortex.

Back 181

BG

Front 182

The BG usually affects both:

Back 182

Direct and Indirect Pathways

Front 183

BG damage can result in:

Back 183

1) Increased muscle tone
2) Increased resistance t passive movement (rigidity)
3) Slow and stiff movements
4) Initiation or discontinuation of movements can be difficult
5) Reduced ROM
6) Associated with disease of the substantia nigra and deficiency of dopamine.
7) Hypokinetic dysarthria, the most common dysarthria in Parkinson's Disease

Front 184

3 Lobes of Cerebellum

Back 184

1) Flocculonodular
2) Anterior Lobe
3) Posterior Lobe

Front 185

The midportion of the cerebllum

Back 185

Vermis

Front 186

Forms the midline of the anterior and posterior lobe of the cerebellum.

Back 186

Vermis

Front 187

3 structures which allow fibers (axons) to leave the cerebellum

Back 187

1) Inferior cerebellar peduncle
2) Middle cerebellar peduncle
3) Superior cerebellar peduncle

Front 188

Efferent pathway from cerebellum

Back 188

Superior cerebellar peduncle

Front 189

Afferent cerebellar pathway whose fibers decussate in the pons

Back 189

Middle Cerebellar Peduncle

Front 190

Deep Nuclei of the CB

Back 190

1) Dentate
2) Globos
3) Emboliform
4) Fastigal

Front 191

Goes from primary motor cortex and premotor regions to the lateral cerebellum regions via the pontine nuclei.

Back 191

Cortico Cerebellar Pathway

Front 192

Descending corticospinal and corticobulbar fibers to the intermediate aspects of the cerebellar hemispheres then to the deep nuclei of the Cb, to the ventral thalamic nuclei and then back to the primary motor cortex.

Back 192

Cortico Cerebellar Pathway

Front 193

Provides the Cb with immediate information about cortical output regarding intentions of skilled movements.

Back 193

Cortico Cerebellar Pathway

Front 194

inability to stand or sit without swaying or falling

Back 194

Truncal Ataxia

Front 195

Abnormal eye movements

Back 195

Nystagmus

Front 196

Similar to BG because it has a specialized position because specific movement disorders result from damage to it

Back 196

Cerebellar Control Circuit

Front 197

connections to vestibular mechanism for modulating
equilibrium and orientation of the head and eyes.

Back 197

Flocculonodular Lobe of Cerebellum

Front 198

a projection area for spinocerebellar proprioceptive information which helps regulate posture, gait, and truncal tone.

Back 198

Anterior Lobe of Cerebellum

Front 199

Helps coordinate skilled, voluntary muscle activity and
muscle tone.

Back 199

Posterior Lobe

Front 200

Results from reduction in the BG circuits “damping” effect on cortical discharges

Back 200

Hyperkinesia

Front 201

Signifies involuntary, variable, and unpredictable movements. (excessive and unpredictable variation in muscle tone and movement)

Back 201

Hyperkinesia

Front 202

Innervates ipsilateral muscles of facial expression and a small muscle in the middle ear called the stapedius.

Back 202

Facial Nerve

Front 203

This motor nucleus is large and located in the ventrolateral caudal pons.

Back 203

Facial Motor Nucleus

Front 204

Damage to this results in weakness on the entire ipsilateral half of the face (also excessive secretions and loss of taste from anterior 2/3 of tongue).

Back 204

Facial motor nucleus or facial motor nerve fibers

Front 205

When this is damaged, fasciculations can be seen in the perioral area and chin.

Back 205

Facial motor nucleus or the facial motor nerve fibers.

Front 206

Visceral efferent of submandibular and sublingual salivary glands.

Back 206

Facial Nerve VII

Front 207

Excess or spontaneous motor unit activity with a lowered firing threshold (discharges) can be seen on the surfaces of the skin as brief localized twitches.

Back 207

Fasciculations

Front 208

Somatic sensory fibers from skin of outer ear

Back 208

Facial Nerve VII

Front 209

Visceral/Special sensory fibers
from parts of the nasal cavity, soft palate, and taste buds from anterior 2/3 of tongue.

Back 209

Facial Nerve VII

Front 210

Component of the facial nerve that has a clear role in speech (these fibers make up the bulk of the nerve)

Back 210

The motor component

Front 211

Damage to this nerve results in swallowing disorders, since it elevates the pharynx during swallowing. Can also result in excess salivation (posterior 1/3 of tongue taste)

Back 211

Glossopharyngeal

Front 212

Emerges from the lateral aspect of the medulla and branches off three ways.

Back 212

CN X Vagus

Front 213

Responsible for pharyngeal constriction and retraction and elevation of the soft palate during speech and swallowing.

Back 213

Pharyngeal branch of vagus nerve

Front 214

Innervates the palatoglossos of the tongue.

Back 214

Pharyngeal branch of vagus

Front 215

Forms the internal and external laryngeal nerves

Back 215

Superior Laryngeal Branch

Front 216

This laryngeal nerve is pure sensory.

Back 216

Internal laryngeal nerve (of the superior laryngeal branch)

Front 217

Carries sensation from the mucous membrane lining the larynx down to the vocal folds, epiglottis, base of tongue, aryepiglottic folds, and dorsum of the arytenoid cartilage.

Back 217

Internal laryngeal nerve (of the superior laryngeal branch)

Front 218

Transmits sensory information from the muscle spindles and other stretch receptors in the larynx.

Back 218

Internal laryngeal nerve (of the superior laryngeal branch)

Front 219

Supplies the inferior pharyngeal constrictor and the cricothyroid muscle.

Back 219

External laryngeal nerve (of the superior laryngeal branch)

Front 220

It lengthens the vocal folds and is important in pitch adjustments.

Back 220

Cricothyroid muscle (supplied by the external laryngeal nerve of the superior laryngeal branch)

Front 221

This nerve doubles back on itself before reaching the larynx.

Back 221

Recurrent laryngeal nerve branch

Front 222

The right and left recurrent laryngeal nerves take different:

Back 222

Paths.

Front 223

These nerves innervate all of the intrinsic muscles of the larynx except the cricothyroid muscle.

Back 223

Recurrent laryngeal nerve branch

Front 224

This branch has a sensory function of some of the fibers which transmit info from vocal folds and larynx.

Back 224

Recurrent laryngeal nerve banch

Front 225

If there is damage to all branches of CN X, there will be:

Back 225

Weakness of soft palate, pharynx, and larynx.

Front 226

Unilateral lesions of this nerve may affect resonance, voice quality (greatest affected), and swallowing.

Back 226

Unilateral CN X damage

Front 227

Bilateral lesions of this nerve will cause pronounced effects on resonance and phonation (hoarse/harsh vocal quality) with secondary effects on prosody and articulation; swallowing can be severely impaired.

Back 227

Bilateral lesions to CN X.

Front 228

There is a cranial and spinal portion to this nerve.

Back 228

Accessory Nerve (Cranial Nerve XI)

Front 229

Fibers go to uvula, levator veli palatini, and intrinsic laryngeal muscles and these fibers intermingle with fibers from the vagus nerve by joining the jugular ganglion.

Back 229

Cranial portion of accessory nerve

Front 230

Some fibers of this nerve become part of the pharyngeal, superior, and recurrent laryngeal branches of the vagus.

Back 230

Accessory nerve

Front 231

The cell bodies are located in the ventral horn of the first 5-6 cervical segments of the spinal cord

Back 231

Accessory Nerve

Front 232

Innervate the sternocleidomastoid and trapezius muscle.

Back 232

Spinal branch cell bodies

Front 233

Damage here weakens head rotation toward side opposite lesion.

Back 233

Foramen magnum or jugular foramen (accessory nerve)

Front 234

Damage here can reduce the ability to elevate or shrug the shoulders on the side of the lesion.

Back 234

Accessory nerve

Front 235

Innervates IPSILATERAL tongue muscles

Back 235

Hypoglossal

Front 236

Enters tongue from below and supplies all of the intrinsic muscle and all but one of the extrinsic tongue muscles (palatoglossus).

Back 236

Hypoglossal

Front 237

Damage here would cause would cause weakness, atrophy, and/or fasciculations of the ipsilateral tongue.

Back 237

Hypoglossal

Front 238

Damage here would cause the tongue to deviate to the side of weakness during protrusion.

Back 238

Hypoglossal

Front 239

Bilateral lesions of this nerve can cause difficulties with speaking and eating.

Back 239

Hypoglossal

Front 240

These nerves are indirectly involved in voice, resonance, and articulation.

Back 240

Spinal nerves (upper cervical spinal nerves)

Front 241

Directly these nerves control respiratory function.

Back 241

Spinal nerves

Front 242

These nerves control exchanging oxygen and CO2 between the lungs and blood and cells of the body.

Back 242

Spinal nerves

Front 243

LMN serving respiration are spread from the:

Back 243

Cervical through the thoracic divisions of the spinal cord.

Front 244

This type of respiration is what is of concern in speech production.

Back 244

Forced respiration

Front 245

The LMNs supplying the respiratory muscles are also widely distributed and therefore,

Back 245

diffuse impairment is needed to significantly interfere with respiration, especially speech respiration.

Front 246

If respiration is impaired, these can also be affected.

Back 246

Voice function, voice production, loudness, phrase length, and prosody

Front 247

If damage occurs to the 3,4, and 5 cervical segment, paralysis of the this can occur bilaterally and breathing seriously affected.

Back 247

Diaphragm

Front 248

Include neurons that regulate LMNS

Back 248

UMN systems

Front 249

Are controlled directly or indirectly by the cortex, the cerebellum, or basal ganglia.

Back 249

UMN systems

Front 250

These systems are contained entirely in the CNS.

Back 250

UMN systems

Front 251

This system is regulated and/or controlled by UMN systems.

Back 251

LMN system

Front 252

A "peripheral" mechanism through which all motor activity is mediated.

Back 252

LMN

Front 253

Distinctive signs of lesions: loss of skilled movement, hyporeflexia, decreased tone.

Back 253

UMN lesions

Front 254

Distinctive signs of lesions:

Back 254

Weakness of all movements, diminished reflexes, atrophy, decreased tone, and fasciculations.

Front 255

1) Contained entirely within the CNS
2) Regulates LMNs
3) Includes the direct and indirect activation pathways
4) Does not include the Cerebellum or Basal Ganglia control circuits

Back 255

UMN system

Front 256

Has a major influence on the cranial and spinal nerves that form the FCP (LMN) for speech production.

Back 256

Direct Activation Pathway

Front 257

This passage emerges from the cortex and directly connects to cranial and spinal nerves

Back 257

Direct Activation Pathway

Front 258

The DAP effect on the LMN is primarily:

Back 258

Facilitatory

Front 259

Initiates but does not inhibit movement.

Back 259

Facilitatory

Front 260

This pathway allows for finely controlled, discrete movements, which are needed for speech.

Back 260

Direct Activation Pathway

Front 261

2 other names for DAP

Back 261

1) Pyramidal tract
2) Direct motor system

Front 262

2 primary tracts of DAP

Back 262

1) Corticospinal tract
2) Corticobulbar tract

Front 263

This tract influences the activities of the cranial nerves.

Back 263

Corticobulbar tract

Front 264

This tract influences the spinal nerves.

Back 264

Corticospinal tract

Front 265

The pyramidal tract (DAP) forms part of this system.

Back 265

UMN system

Front 266

The DAP originates in the:

Back 266

Cortex of each cerebral hemisphere.

Front 267

The main launching platform of the DAP is the:

Back 267

Primary motor cortex (aka precentral gyrus)

Front 268

1/3 of direct system originates here.

Back 268

Primary motor cortex (precentral gyrus)

Front 269

DAP fibers originate from the primary motor cortex and the:

Back 269

Premotor cortex

Front 270

This is just anterior to the primary motor area in the frontal lobe.

Back 270

Premotor Cortex

Front 271

An area within the premotor cortex that is important for speech.

Back 271

Supplementary Motor Area

Front 272

In the DAP, there are UMN fibers that originate in the postcentral gyrus in the parietal lobe; however, this overlaps some of the:

Back 272

Sensory cortex located in the postcentral gyrus.

Front 273

Postcentral gyrus aka:

Back 273

Secondary motor area

Front 274

Only about 30% of the DAP fibers arise here:

Back 274

Motor cortex

Front 275

This is the cortical focal point of the pyramidal tracts for speech.

Back 275

Motor cortex

Front 276

These muscles are represented in an upside-down fashion along the length of the motor strip.

Back 276

Striated muscles

Front 277

The arm, leg, and foot are located on this portion of the motor strip.

Back 277

Top portion of the strip

Front 278

The face, tongue, and larynx are influenced by neurons on this portion of the motor strip.

Back 278

Lower portion

Front 279

The number of motor neurons devoted to striated muscle is allocated according to the:

Back 279

Degree of fine motor movement involved.

Front 280

The small muscles of the tongue and face are given this type of representation of the motor strip.

Back 280

Large representation (require greater degree of fine motor movement)

Front 281

here groups of neurons that complete a given function are lined up from the surface to the deep structure of a given area of the cortex, which represents functional organization of muscle groups.

Back 281

Cortical columns

Front 282

During electrostimulation study, one of these was stimulated and vocalization, tongue protrusion, and palatal elevation occurred.

Back 282

A particular cortical column

Front 283

The axons from the neuron cell bodies of the DAP, located in the cortex, travel through the:

Back 283

1) Corticobulbar Tracts
2) Corticospinal Tracts

Front 284

The axons travel down the spinal cord and synapse on the anterior horns of the spinal cord areas which serve muscles of respiration.

Back 284

Corticospinal Tracts

Front 285

The axons go to and synapse on the brainstem cranial nerve nuclei for nerves (V, VII, IX, X, XI, and XII)

Back 285

Corticobulbar tracts

Front 286

The corticobulbar and corticospinal tracts (in each hemisphere) are arranged in a fanlike mass of fibers known as the:

Back 286

Corona Radiata

Front 287

The Corona Radiata converges into a compact band called the:

Back 287

Internal Capsule

Front 288

A very important region in the brain where all the motor fibers (axons) descend from where they originate in the cortex.

Back 288

Internal Capsule

Front 289

Contains all the sensory and motor fibers projecting to and from the cortex.

Back 289

Internal Capsule

Front 290

Most of the afferent fibers in the Internal Capsule arise from the:

Back 290

Thalamus

Front 291

Afferent fibers that arise from the thalamus project as *these* to various regions of the cortex.

Back 291

Thalamocortical radiations

Front 292

3 components of internal capsule

Back 292

1) Anterior Limb
2) Posterior Limb
3) Genu

Front 293

This component of the internal capsule contains prefrontal cortico-pontine fibers.

Back 293

Anterior Limb

Front 294

This component of the internal capsule contains corticospinal fibers, fronto-pontine fibers, some cortico-rubral fibers, and some cortico-reticular fibers.

Back 294

Posterior Limb

Front 295

This component of the internal capsule contains cortico-bulbar fibers and cortico-reticular fibers.

Back 295

Genu

Front 296

Lesions in the genu and posterior limb of the IC produce greater speech deficits than the:

Back 296

Anterior Limb

Front 297

In the IC, so many thalamocortical, corticobulbar, and corticospinal fibers occupy a compact area that small lesions can:

Back 297

Produce widespread motor deficits

Front 298

V, VII, and IX are located in the:

Back 298

Pons

Front 299

The DAP of the UMN system primarily innervates LMN on the:

Back 299

Contralateral side of the body

Front 300

UMN DAP innervation of the LMN speech cranial nerves is primarily:

Back 300

Bilateral

Front 301

The tongue (XII) gets mostly contralateral control, but there is some:

Back 301

Bilateral supply

Front 302

From the corticobulbar pathways, the lower face (VII) receives primarily:

Back 302

Contralateral control (but there are significantly fewer ipsilateral fibers)

Front 303

The direct activation pathway is essential to voluntary motor activity especially:

Back 303

1) Conscious
2) Controlled Skilled
3) Discrete and Often Rapid Movements

Front 304

Moves of the DAP UMN system can be triggered by sensory stimuli and:

Back 304

Cognitive activity that invovles planning.

Front 305

Damage to the UMN System can cause loss or reduction of:

Back 305

Voluntary skilled movements.

Front 306

A unilateral UMN system lesion usually results in:

Back 306

Contralateral weakness (but not as profound as in LMN damage(

Front 307

With UMN system damage, these are usually preserved since they occur primarily at the level of the FCP (LMN system)

Back 307

Reflexes

Front 308

Unilateral UMN lesions can produce mild dysarthria from weakness and loss of skilled movements called:

Back 308

Unilateral UMN Dysarthria

Front 309

You can get a unilateral UMN dysarthria resulting in spasticity if this pathway is affected.

Back 309

Indirect pathway (extrapyramidal tract)

Front 310

Bilateral UMN lesions can have mild to devastating effects on speech, as they usually reflect combined effects of dysfunction in these two pathways.

Back 310

1) DAP
2) IAP

Front 311

Bilateral UMN lesions cause this type of dysarthria.

Back 311

Spastic dysarthria

Front 312

This type of dysarthria results from bilateral weakness and loss of skilled movement as well as alterations in muscle tone.

Back 312

Spastic dysarthria

Front 313

The lower part of the face receives unilateral (UMN) projections from the:

Back 313

Contralateral cortex

Front 314

Each side of the upper part of the face receives UMN projections from:

Back 314

Both sides of the cortex (bilateral)

Front 315

Innervates motor neurons of the brainstem.

Back 315

Corticobulbar tract

Front 316

Corticobulbar tract innervation is primarily:

Back 316

Bilateral

Front 317

One important exception to bilateral corticobulbar innervation is this cranial nerve nuclei.

Back 317

Facial VII

Front 318

A unilateral UMN lesion affects muscles in this part of the face.

Back 318

Contralateral lower half of the face with upper facial muscle sparing (can still wrinkle forehead and close the eye)

Front 319

Complete destruction of either the facial nucleus (LMN) or bilateral cortical lesion damage produces:

Back 319

Pseudobulbar palsy

Front 320

Bilateral impairment of the function of the lower cranial nerves resulting in bilateral facial palsy or paralysis.

Back 320

Pseudobulbar palsy

Front 321

Corticobulbar innervation of the cranial nerve nuclei VII is bilateral for the upper face motor neurons but exclusively contralateral for the:

Back 321

Motor neurons of the lower face.

Front 322

LMN lesions of the facial nerve can paralyze muscles on the:

Back 322

Entire ipsilateral side of the face.

Front 323

A unilateral UMN lesion of the facial nerve affects muscles in the:

Back 323

Contralateral lower half of face with upper facial muscle sparing (can still wrinkle forehead and close the eye)

Front 324

Indirect Activation Pathway aka:

Back 324

1) Extrapyramidal Tract
2) Indirect motor system

Front 325

The IAP has multiple synapses between its origin in the cortex and its arrival and activation of the:

Back 325

FCP (LMN)

Front 326

2 Tracts of the IAP

Back 326

1) Corticoreticular Tract
2) Corticorubral Tract

Front 327

These set of nerve axons travel from the cortex (motor, premotor and sensory cortex) to the reticular formation.

Back 327

Corticoreticular Tract

Front 328

This tract's fibers intermingle with the corticospinal and corticobulbar fibers of the DAS and descend to enter the reticular formation in the medulla and pons where they are distributed bilaterally but with a contralateral dominance.

Back 328

Coritcoreticular Tract

Front 329

Besides corticoreticular fibers, there are other fibers coming to and leaving the reticular formation, especially from/to the:

Back 329

Cerebellum

Front 330

Set of fibers which project form the cortex to the red nucleus.

Back 330

Corticorubral Tract

Front 331

Thought of as the "seat of consciousness"

Back 331

Reticular formation

Front 332

A field of scattered cells between large nuclei and fiber tracts in the medulla, pons, and midbrain.

Back 332

Reticular Formation

Front 333

Portions of this excite extensor motor neurons and other parts inhibit flexor motor neurons –this is what leads to muscle tone.

Back 333

Reticular Formation

Front 334

This is heavily involved in sensorimotor integration and has complex effects on the LMNs.

Back 334

Reticular Formation

Front 335

Crucial in the role of muscle tone (its [i.e., corticoreticular tract]) fibers terminate primarily on gamma motor neurons) and is involved in both facilitatory and inhibitory influences of reflex activity, ascending sensory information and cortically induced voluntary movement.

Back 335

Reticular formationm

Front 336

Corticoreticular tract fibers terminate primarily on:

Back 336

Gamma motor neurons

Front 337

Oval mass of cells in the midbrain.

Back 337

Red nucleus

Front 338

These cells receive cortical projections from the corticorubral tract and act as a relay station between a pathway from the cerebellum to the ventrolateral nucleus of the thalamus, and ultimately the cortex.

Back 338

Red nucleus

Front 339

Faciltates flexor and inhibits extensor alpha and gamma motor neurons.

Back 339

Rubrospinal tract

Front 340

This pathway regulates reflexes and maintains posture, tone, and associated activities that provide a framework on which the direct activation pathway can accomplish its skilled, discrete actions.

Back 340

IAP

Front 341

Damage to this pathway causes problems with muscle tone and reflexes. The effects are different for flexor and extensor muscles.

Back 341

IAP

Front 342

Damage to corticoreticular fibers above the midbrain and the red nucleus results in:

Back 342

Increased extensor tone in legs and increased flexor tone in arms. (legs extended and resist flexing or bending; arms bent (flexed) and resist extension.

Front 343

This posturing occurs because all the descending pathways are uninhibited.

Back 343

Decorticate posturing

Front 344

This posturing occurs when there is damage to corticoreticular fibers at the midbrain level below the red nucleus

Back 344

Decerebrate posturing

Front 345

This posturing occurs when there is removed arm flexor excitation and lead to excitation of all extensor muscles and increased extensor tone.

Back 345

Decerebrate posturing

Front 346

Lesions to corticoreticular fibers below the medulla results in a:

Back 346

Loss of all descending input and produce generalized flaccidity in muscles supplied by spinal nerves.

Front 347

Lesions at the level of the brainstem that damage the reticular formation usually result in:

Back 347

Death

Front 348

When the cortical controls are nonfunctional, the unchecked reticular system makes extensor muscles:

Back 348

Hyperexcitable, increasing muscle tone and causing spasticity.

Front 349

Lesions from the motor pathways from the cerebral hemispheres are common and referred to as:

Back 349

UMN lesions

Front 350

UMN lesions usually affect both of these pathways.

Back 350

1) DAP
2) IAP

Front 351

Result in spasticity, increased muscle stretch reflexes (from indirect), and loss of skilled movements (from direct).

Back 351

UMN lesions

Front 352

Speech effects from spasticity:

Back 352

1) Slows movement
2) Hyperadduction of the vocal folds during phonation
3) Fairly mild when unilateral
4) When bilateral, can be severe including hyperactive reflexes, dysphagia, and disinhibition of the physical expression of emotion (seen in ALS)

Front 353

Help integrate and control the varied activities of the many structures and pathways in motor performance.

Back 353

Control Circuits

Front 354

Unlike the direct and indirect activation pathways, control circuits do not have direct contact with the:

Back 354

LMNs

Front 355

Some of these integrate the DAP and IAP.

Back 355

Control Circuits

Front 356

Integration and coordination of motor performance are accomplished through activities of these 2 control circuits:

Back 356

1) BG Circuit
2) Cerebellar Control Circuit

Front 357

The Striatum consists of:

Back 357

1) Caudate Nucleus
2) Putamen

Front 358

The lentiform nucleus consists of:

Back 358

1) Putamen
2) Globus Pallidus

Front 359

2 Clusters of cell bodies anatomically and functionally related to the BG.

Back 359

1) Substantia Nigra
2) Subthalamic Nucleus

Front 360

3 Components of BG

Back 360

1) Caudate Nucleus
2) Putamen
3) Globus Pallidus

Front 361

Have important reciprocal connections with diverse areas of the cerebral cortex and strong functional ties to the exprapyramidal pathway or indirect motor system.
They do not directly influence the FCP.

Back 361

BG

Front 362

Receptive portion of the BG.

Back 362

Striatum

Front 363

The striatum receive info from:

Back 363

1) Frontal cortex
2) Thalamus
3) Lower BG areas

Front 364

Main efferent pathways of the BG.

Back 364

Globus Palladus

Front 365

Most info. goes back to thalamus and then back, gets relayed back to cortex as well as other BG areas and the reticular formation.

Back 365

Globus Paladus

Front 366

BG depends on neurotransmitters and their continued balance
for:

Back 366

Motor Control

Front 367

Synaptic transmitter when a neuron’s axons terminate in the striatum

Back 367

Acetylcholine

Front 368

Manufactured in the substantia nigra and transmitted to the striatum where it acts as a neurotransmitter.

Back 368

Dopamine

Front 369

If neurons in the substantia nigra are destroyed, this content in the striatum will be reduced.

Back 369

Dopamine

Front 370

Chief inhibitory neurotransmitter

Back 370

GABA

Front 371

Plays an important role in regulating neuronal excitability throughout the nervous system.

Back 371

GABA

Front 372

In humans, this neurotransmitter is directly responsible for the regulation of muscle tone.

Back 372

GABA

Front 373

When there is a disruption in the balance of neurotransmitters, this can occur.

Back 373

Movement disorders

Front 374

3 main BG neurotransmitters

Back 374

1) Acetylcholine
2) Dopamine
3) GABA

Front 375

Important to regulating the amplitude, velocity, and the initiation of movement.

Back 375

BG

Front 376

Important for regulating muscle tone and maintaining normal posture and static muscle contraction upon which voluntary, skilled movements are superimposed

Back 376

BG

Front 377

Important to generating motor programs for speech by helping to maintaining a stable musculoskeletal environment.
e.g., restricting jaw movements for speaking.

Back 377

BG

Front 378

Can dampen or modulate the movement goals coming out of the cortex

Back 378

BG

Front 379

BG damage results in:

Back 379

1) Reduced Mobility
2) Involuntary Movements

Front 380

Associated with disease of the substantia nigra and deficiency of dopamine.

Back 380

Hypokinesia

Front 381

Reduced ROM

Back 381

Hypokinesia

Front 382

Increased muscle tone, increased resistance to passive movements (rigidity), slow and stiff movements.

Back 382

Hypokinesia

Front 383

Initiation or discontinuation of movements can be difficult.

Back 383

Hypokinesia

Front 384

Most common dysarthria in Parkinson's Disease

Back 384

Hypokinetic dysarthria

Front 385

Results from reduction in the BG circuits “damping” effect on cortical discharges.

Back 385

Hyperkinesia

Front 386

Signifies involuntary, variable, and unpredictable movements. (excessive and unpredictable variation in muscle tone and movement)

Back 386

Hyperkinesia

Front 387

3 Lobes of Cerebellum

Back 387

1) Flocculonodular
2) Anterior Lobe
3) Posterior Lobe

Front 388

This lobe of Cb has connections to vestibular mechanism for modulating equilibrium and orientation of the head and eyes.

Back 388

Flocculonodular

Front 389

This lobe of the Cb has a projection area for spinocerebellar proprioceptive information which helps regulate posture, gait, and truncal tone.

Back 389

Anterior Lobe

Front 390

This Cb lobe helps coordinate skilled, voluntary muscle activity and muscle tone.

Back 390

Posterior Lobe

Front 391

The midportion of the Cb; forms the midline of the anterior and posterior lobe

Back 391

Vermis

Front 392

There is a left and right Cb hemisphere and each connects to:

Back 392

The contralateral thalamus and cerebral hemisphere.

Front 393

3 Structures which allow fibers (axons) to leave the Cb.

Back 393

1) Inferior cerebellar peduncle
2) Middle cerebellar peduncle
3) Superior cerebellar peduncle

Front 394

Efferent pathway of Cb

Back 394

Superior Cerebellar Peduncle

Front 395

Afferent pathway of Cb whose fibers decussate in the pons.

Back 395

Middle Cerebellar Peduncle

Front 396

Mostly afferent fibers but also some efferent flow to vestibular mechanism and reticular formation from this pathway of Cb.

Back 396

Inferior Cerebellar Peduncle

Front 397

The sole output neuron of the Cb is called the:

Back 397

The Purkinje Cells (found in the middle layer of the cortex)

Front 398

These cells synapse on deep structures where many nuclei are found and it is these deep nuclei that sends axons out of the Cb.

Back 398

Purkinje Cells of Cb

Front 399

4 Deep Nuclei of Cb

Back 399

1) Dentate
2) Globos
3) Emboliform
4) Fastigal

Front 400

This portion of the Cb might be involved in speech because it seems to be active in in initiating movement, executing preplanned motor tasks, and regulating posture.

Back 400

Dentate

Front 401

Goes from primary motor cortex and pre-motor regions to the lateral Cb regions via the pontine nuclei. Its return pathway to the same areas via the deep Cb nuclei and ventral thalamic nuclei.

Back 401

Cortico-Cerebellar Pathway

Front 402

The Cortico-Cerebellar Pathway is an important loop in:

Back 402

Planning and programming learned movements.

Front 403

Descending corticospinal and corticobulbar fibers to the intermediate aspects of the cerebellar hemispheres then to the deep nuclei of the Cb, to the ventral thalamic nuclei and then back to the primary motor cortex.

Back 403

Cortico-Cerebellar Pathway

Front 404

Provides the Cb with immediate information about cortical output regarding intentions of skilled movements.

Back 404

Cortico-Cerebellar Pathway

Front 405

Similar to BG because it has a specialized position because specific movement disorders result from damage to it.

Back 405

Cb Control Circuit

Front 406

Input from the cortex prepares*this* to check adequacy of speech output as feedback from muscles, tendons, joints arrive from the periphery.

Back 406

Cb

Front 407

Inhibits excessive output; helps smooth and coordinate speech movements.

Back 407

Cb

Front 408

Interprets sensory information and integrates it with ongoing input from the cortex about movement goals.

Back 408

Cb

Front 409

Interprets sensory information and integrates it with ongoing input from the cortex about movement goals.

Back 409

Cb

Front 410

Inability to stand or sit without swaying or falling.

Back 410

Truncal Ataxia

Front 411

Abnormal eye movements

Back 411

Nystagmus

Front 412

Damage to Cb causes:

Back 412

1) Truncal ataxia
2) Disturbances in gait
3) Nystagmus

Front 413

Cb posterior lobe lesions cause:

Back 413

1) Limb ataxia and hypotonia
2) Intention tremor
3) Incoordination ipsilateral to side of lesion

Front 414

Speech effects of Cb lesion

Back 414

Ataxic dysarthria

Front 415

Interprets sensory information and integrates it with ongoing input from the cortex about movement goals.

Back 415

Cb

Front 416

The highest level of motor organization.

Back 416

Conceptual programming level

Front 417

Inability to stand or sit without swaying or falling.

Back 417

Truncal Ataxia

Front 418

Establishes the meaning or goals of the speech act and the essentials of the program for achieving them

Back 418

Conceptual programming level

Front 419

Abnormal eye movements

Back 419

Nystagmus

Front 420

Establishes the “idea” or “plan” for activity, specifies movements needed for the plan to be realized.

Back 420

Conceptual programming level

Front 421

Damage to Cb causes:

Back 421

1) Truncal ataxia
2) Disturbances in gait
3) Nystagmus

Front 422

Straddles the boundaries between an internal, nonmotor thought-related processes and a sensorimotor programming process that results in movement.

Back 422

Conceptual programming level

Front 423

Cb posterior lobe lesions cause:

Back 423

1) Limb ataxia and hypotonia
2) Intention tremor
3) Incoordination ipsilateral to side of lesion

Front 424

Speech effects of Cb lesion

Back 424

Ataxic dysarthria

Front 425

The highest level of motor organization.

Back 425

Conceptual programming level

Front 426

Establishes the meaning or goals of the speech act and the essentials of the program for achieving them

Back 426

Conceptual programming level

Front 427

Establishes the “idea” or “plan” for activity, specifies movements needed for the plan to be realized.

Back 427

Conceptual programming level

Front 428

Straddles the boundaries between an internal, nonmotor thought-related processes and a sensorimotor programming process that results in movement.

Back 428

Conceptual programming level

Front 429

Coverings of the CNS

Back 429

Meninges

Front 430

Outermost membrane of CNS

Back 430

Dura Mater

Front 431

LIes beneath the dura and is applied loosely to the surface of the brain.

Back 431

Arachnoid

Front 432

Located between the inner bone of the skull and the dura.

Back 432

Epidural space

Front 433

Directly beneath the dura.

Back 433

Subdural space

Front 434

The subarachnoid space surrounds the brain and spinal cord and is filled with:

Back 434

CSF

Front 435

The subarachnoid space is connected to the interior of the brain through the:

Back 435

Ventricular system

Front 436

Lies dorsal to the 4th ventricle.

Back 436

Cerebellum

Front 437

The spinal cord begins at the:

Back 437

Foramen Magnum

Front 438

The PNS consists of:

Back 438

Cranial and Spinal Nerves

Front 439

Most of the cranial nerves originate in the:

Back 439

Brainstem

Front 440

Cavities that contain CSF.

Back 440

Ventricles

Front 441

CSF is produced by choroid plexuses located in each:

Back 441

Ventricle

Front 442

These two comprise the CSF system.

Back 442

1) Ventricular System
2) Subarachoid Space

Front 443

Primary function is to cushion the CNS against physical trauma and to help maintain a stable environment for neural activity.

Back 443

CSF

Front 444

All blood vessels that supply the brainstem and cerebral hemispheres arise from the:

Back 444

Aortic Arch in the chest

Front 445

Blood enters the brain by way of the:

Back 445

1) Carotid system
2) Vertebrobasilar system

Front 446

The carotid system and the vertebrobasilar system are capable of some communication with each other through connecting channels in the brainstem, known as the:

Back 446

Circle of Willis

Front 447

The internal carotid arteries arise in the neck from the:

Back 447

Common carotid arteries

Front 448

Each internal carotid artery separates at the:

Back 448

Circle of Willis

Front 449

Each internal carotid artery separates at the circle of Willis into the:

Back 449

1) Anterior cerebral artery
2) Middle cerebral artery

Front 450

The anterior cerebral arteries are connected to each other by the:

Back 450

Anterior communicating artery

Front 451

Course upward and supply blood to the superior portion of the frontal and parietal lobes.

Back 451

Anterior cerebral arteries

Front 452

Course laterally and supply blood to most o the lateral surfaces of the cerebral hemispheres and the deep structures of the frontal and parietal lobes.

Back 452

Middle cerebral arteries

Front 453

Disturbances of this artery are a common cause of apraxia of speech.

Back 453

Left middle cerebral artery

Front 454

Vascular disturbances in the left or right carotid artery and in the left or right anterior and middle cerebral arteries can produce:

Back 454

Dysarthrias

Front 455

The paired vertebral arteries enter the brainstem through the foramen magnum and join to form the:

Back 455

Basilar artery

Front 456

Branches from these arteries supply the midbrain, pons, medulla, cerebellum, and portions of the cervical spinal cord.

Back 456

Vertebral arteries

Front 457

These are branches of the vertebrobasilar system

Back 457

Posterior cerebral arteries

Front 458

Supply the occipital lobe, the thalamus, and the inferior and medial portions of the temporal lobe in each hemisphere.

Back 458

Posterior cerebral arteries

Front 459

Vascular disturbances in the vertebrobasilar system often lead to:

Back 459

MSDs

Front 460

Drive all neurologic functions

Back 460

Neurons

Front 461

PNS motor and sensory functions

Back 461

Nerves

Front 462

Communication among groups of neurons

Back 462

Tracts or pathways

Front 463

Between cerebral hemispheres

Back 463

Commisural fibers

Front 464

Within cerebral hemispheres

Back 464

Association fibers

Front 465

Vascular disturbances in the vertebrobasilar system often lead to:

Back 465

MSDs

Front 466

Fibers that run to and from higher and lower centers within CNS

Back 466

Projection fibers

Front 467

Drive all neurologic functions

Back 467

Neurons

Front 468

Surround CNS axons (myelin)

Back 468

Oligodendroglia

Front 469

PNS motor and sensory functions

Back 469

Nerves

Front 470

Surround PNS axons (myelin)

Back 470

Schwann Cells

Front 471

Communication among groups of neurons

Back 471

Tracts or pathways

Front 472

Produce CSF

Back 472

Ependymal Cells of ventricles/choroid plexuses

Front 473

Between cerebral hemispheres

Back 473

Commisural fibers

Front 474

Within cerebral hemispheres

Back 474

Association fibers

Front 475

Fibers that run to and from higher and lower centers within CNS

Back 475

Projection fibers

Front 476

Surround CNS axons (myelin)

Back 476

Oligodendroglia

Front 477

Surround PNS axons (myelin)

Back 477

Schwann Cells

Front 478

Produce CSF

Back 478

Ependymal Cells of ventricles/choroid plexuses

Front 479

Transport substances from blood vessels to neurons.

Back 479

Astrocytes

Front 480

Injest or remove damaged tissue

Back 480

Microglia

Front 481

Cover and bind fibers together in PNS nerves

Back 481

Connective Tissue

Front 482

Supporting cells

Back 482

Glial cells

Front 483

3 parts of a neuron

Back 483

1) Axon
2) Dendrite
3) Cell Body

Front 484

In most instances, the axon and dendrite (or muscle fibers) are separated by a:

Back 484

Synaptic cleft

Front 485

Collection of nerve fibers (axons) bound together by connective tissue.

Back 485

Nerve

Front 486

Groups of fibers that that travel together in the CNS.

Back 486

Tracts

Front 487

Groups of fibers that travel together in the PNS.

Back 487

Nerve

Front 488

The major distinction between PNS nerves and CNS tracts is that CNS tracts transmit impulses to other neurons, whereas PNS nerves transmit impulses from nerves to:

Back 488

End organs, such as muscle.

Front 489

These cell types form the insulation or myelin that surrounds axons in the CNS and PNS.

Back 489

1) Schwann Cells
2) Oligodendroglia

Front 490

Mechanism that prevents the passage of many metabolites from the blood into the brain, thereby protecting it from toxic compounds and variations in blood composition.

Back 490

Blood-brain barrier

Front 491

Line the ventricular system

Back 491

Ependymal cells

Front 492

Form the choroid plexuses

Back 492

Ependymal Cells

Front 493

Scavenger Cells

Back 493

Macrophages

Front 494

Deprivation of oxygen and cessation of oxidative metabolism, as occurs in stroke.

Back 494

Ischemia

Front 495

4 major functional divisions of the 1motor system

Back 495

1) FCP
2) DAP
3) IAP
4) Control Circuits

Front 496

Collection of abnormally formed veins and arteries.

Back 496

Arteriorvenous malformation

Front 497

Stimulates muscle contraction and movement. Other motor divisions must act through it to influence movement.

Back 497

FCP

Front 498

Influences consciously controlled, skilled voluntary movement.

Back 498

DAP

Front 499

Mediates subconscious, automatic muscle activities including posture, muscle tone, and movement that support and accompany voluntary movement.

Back 499

IAP

Front 500

Integration or coordination of sensory information and activities of direct and indirect activation pathways to control movement.

Back 500

Control Circuits

Front 501

Plan and program postural and supportive components of motor activity.

Back 501

BG

Front 502

Integrates and coordinates execution of smooth, directed movements.

Back 502

Cerebellar

Front 503

LMN and the muscle fibers innervated by it are known as a:

Back 503

Motor Unit

Front 504

If you had a right-sided lesion to the mandibular branch of the trigeminal nerve you would have what type of problem?

Back 504

Paralysis or paresis to the muscles of mastication on the right half of the mandible due to LMN damage

Front 505

If you had a lesion to the left motor cortex innervating the right mandible?

Back 505

Probably minimal problems noted due to bilateral innervation (the left motor cortex also sends messages to the ipsilateral mandible. If any problems occurred they would be related to slight weakness and slight reduction in skilled movements. The person’s speech would be probably unimpaired (not much jaw movement is necessary for speech and the left mandible would be normal and compensating).

Front 506

If you had a lesion to the both the left motor cortex and the right motor cortex innervating the mandible?

Back 506

Severe problems because both sides of the jaw would most likely be paralyzed to some extent and the jaw would hang open. Speech would be severely impaired. The problems would related to bilateral weakness, loss of skilled movements and spasticity (because both the direct and indirect pathways would be affected).

Front 507

Purposes of the clinical examination

Back 507

1. To detect or confirm a suspected problem
2. To establish a differential diagnosis
3. To classify within a specific disorder group
4. To establish Implications for localization and Disease Diagnosis
5. To specify severity
6. To establish a prognosis
7. To specify more precisely the treatment focus
8. To establish criteria for treatment termination

Front 508

Components of the clinical examination

Back 508

1) History
2) Physical examination
3) Motor speech examination
4) Disabling aspects of the motor speech disorder

Front 509

A history should include:

Back 509

1) Interview
2) Neurologic Evaluation
3) Medical Data

Front 510

A physical exam should include:

Back 510

1) Cranial nerves
2) Observation
3) Non-speech tasks

Front 511

A motor speech examination should include:

Back 511

Speech Tasks

Front 512

Disabling aspects of motor speech disorders include:

Back 512

1) Perceptual features
2) intelligibility
3) Comprehensibility

Front 513

Clinical measures should be:

Back 513

1) Objective
2) Replicable
3) Understandable

Front 514

Measurement is important to determine:

Back 514

1) If treatment has helped
2) If the problem is getting worse
3) If the disability is being minimized

Front 515

Biographical data that should be gathered:

Back 515

1) Basic biographical data
2) Information that has prognostic significance
3) Other info that can assist in the development of the treatment plan/stimuli.

Front 516

These things have prognostic significance.

Back 516

1) Age
2) Education
3) Pre-morbid handedness
4) Occupational status at onset
5) Pre-morbid intelligence

Front 517

Consider sources of medical data:

Back 517

1) Access records
2) Communicative status of the patient
3) Availability of family as historians

Front 518

What do we need to know about patient's prosthetic/assistive devices?

Back 518

1) Patient's visual acuity, corrected and uncorrected field abnormalities)
2) Auditory functioning (acuity aided or unaided; ear pathologies)
3) Find out if patient wears dentures and determine if he uses them and how they fit

Front 519

What info should you gather from medical chart?

Back 519

1) Basic facts about onset and course of the problem.

2) Information about the etiology of the problem affecting CNS or PNS involvement (trauma, CVA, infection, neoplasm, disease) and familial history of similar disorders).

3) Localizing information.

Front 520

Types of localizing information

Back 520

1) Results of neuroradiological procedures such as MRI, CT Scan, Blood flow, Spinal Tap studies).

2) Past medical history (PMH). Other major medical diagnoses (diabetes, chronic cardiac problems) may impinge upon the patient’s status for evaluation and treatment.

3) Medications: numbers, types, and side effects of any medications the patient takes. These can also affect the patient’s performance in assessment and treatment.

Front 521

Things you look for in the motor speech examination to identify the cause of the problem and to plan interventions.

Back 521

Salient features

Front 522

Six salient features are important to consider in conducing a motor speech examination:

Back 522

1) Strength
2) Speed of movement
3) Range of movement
4) Steadiness
5) Tone
6) Accuracy

Front 523

Muscle weakness is most prominent in this type of dysarthria that affects the final common pathway.

Back 523

Flaccid

Front 524

Weakness can affect all 3 major speech valves:

Back 524

1) laryngeal
2) velopharyngeal
3) articulatory

Front 525

In MSDs muscle strength is usually reduced, often consistently, and sometimes:

Back 525

Progressively

Front 526

Weakness can be present in all components of speech production:

Back 526

1) Respiration
2) Phonation
3) Resonance
4) Articulation
5) Prosody

Front 527

If a muscle is weak, it cannot:

Back 527

Contract to its desired level.

Front 528

Muscles have sufficient strength to perform their normal functions, plus:

Back 528

A reserve of excess strength to handle excess demands.

Front 529

Acoustic feature of flaccid dysarthria:

Back 529

Imprecise consonants

Front 530

How is muscle weakness usually observed at rest?

Back 530

Atrophy

Front 531

This speed of movement is common in MSDs.

Back 531

Slow

Front 532

In MSDs, movements can be slow to:

Back 532

1) Start (lag)
2) Slow in their course
3) Slow to stop or relax

Front 533

Reduced speed can affect all:

Back 533

1) Speech Valves
2) Components of Speech Production

Front 534

Slow movements can occur on single or:

Back 534

Repetitive movements

Front 535

Slow movements particularly affect PROSODY because normal prosody is:

Back 535

Dependent on quick mm. adjustments that affect rate of sound production, pitch, and loudness variability.

Front 536

The effects of reduced speed can be perceived in:

Back 536

1) Speech (slow rate)
2) Visibly seen during speech and oral mech exam (reduced AMRs)
3) Measured physiologically and acoustically

Front 537

Effects of reduced speed are most noticeable in these types of dysarthria.

Back 537

1) Spastic
2) Mixed

Front 538

The distances traveled by speech structures are precise and small and have little:

Back 538

Variation

Front 539

Reduced ROM is common in the context of these rates.

Back 539

1) Normal
2) Excessive
3) Slow

Front 540

Abnormalities of ROM affect prosody resulting in:

Back 540

Excessive or restrictive prosodic variation (excess=stress)

Front 541

Reduced ROM can have effects on all:

Back 541

1) Major speech components
2) Major speech valves

Front 542

This dysarthria is characterized by reduced ROM and excessively rapid rate

Back 542

HYPOkinetic

Front 543

Variability of ROM is common in these types of dysarthria.

Back 543

1) Ataxis
2) HYPERkinetic

Front 544

There are normal very small oscillations of body muscles that occur during rest and oscillations are mostly nonvisible during movement.

Back 544

Steadiness

Front 545

If motor steadiness breaks down in neurologic disease the terms used are “involuntary movements” or:

Back 545

Hyperkinesias

Front 546

Most common involuntary movement.

Back 546

Tremor

Front 547

Consists of alternating, repetitive, relatively rhythmic oscillations of a body
part, ranging in frequency from 3-12 Hz.

Back 547

Tremors

Front 548

This type of tremor occurs at reset:

Back 548

Resting Tremor

Front 549

This type of tremor occurs when a structure is maintained against gravity.

Back 549

Postural Tremor

Front 550

This type of tremor occurs during movement.

Back 550

Action Tremor

Front 551

This type of tremor occurs at the end of a movement.

Back 551

Terminal Tremor

Front 552

4 Types of tremor

Back 552

1) Resting
2) Postural
3) Action
4) Terminal

Front 553

Tremor most often affects this component of speech:

Back 553

Phonation

Front 554

When severe, tremor can affect this type of speech component besides phonation.

Back 554

Prosody

Front 555

The effects of tremor on speech are most easily detected during this speech task:

Back 555

Sustained Vowel Production

Front 556

Types of involuntary movements

Back 556

1) Tremor
2) Dystonia
3) Dyskinesia
4) Chorea
5) Athetosis

Front 557

Involuntary movements can be random and unpredictable, varying in:

Back 557

1) Speed
2) Duration
3) Amplitude

Front 558

Maintained by the gamma loop and indirect activation pathway.

Back 558

Tone

Front 559

In neurological disease, tone can be:

Back 559

Excessive or reduced

Front 560

Effects on tone impacts all:

Back 560

1) Speech valves
2) Components of speech

Front 561

Types of alterations in tone

Back 561

1) Reduced (flaccid)
2) Increased (spastic and hypokinetic)
3) Variable (hyperkinetic)

Front 562

This dysarthria is marked by reduce tone.

Back 562

Flaccid

Front 563

These dysarthrias are marked by increased tone.

Back 563

1) Spastic
2) Hypokinetic

Front 564

This dysarthria is marked by variable tone.

Back 564

Hyperkinetic

Front 565

Accurate speech movements reflect a combination of:

Back 565

1) Precision in tone
2) Strength
3) Speed
4) Range
5) Steadiness
6) Timing of muscle activity

Front 566

Inaccurate movements lead to a variety of speech problems:

Back 566

1) Excessive force and ROM (articulators overshoot targets)
2) Decreased force and ROM (undershoots targets)
3) Poor timing (smoothness may be faulty and rhythm is affected)

Front 567

Inaccurate movements occur at all speech valves and all levels of speech production, but they are generally perceived most easily in:

Back 567

1) Prosody
2) Articulation

Front 568

Inaccurate movements occur in all of the dysarthrias but when it's a timing or coordination problem, it is usually associated with:

Back 568

1) Ataxic Dysarthria
2) AOS
(makes dx difficult)

Front 569

When inaccurate movements are related to random or unpredictable involuntary variations then it usually
reflects:

Back 569

Hyperkinetic Dysarthria

Front 570

The salient features of movement often do this with each other.

Back 570

Interact (e.g., reduced strength often accompanies reduced tone, ROM, accuracy, etc.)

Front 571

Features, other than deviant speech characteristics and salient neuromuscular features, that help confirm the speech diagnosis.

Back 571

Confirmatory Signs

Front 572

Decrease in muscle mass due to disruption/loss of nerve supply or disuse

Back 572

Atrophy

Front 573

Seen in drooping, sagging posture.

Back 573

Reduced Tone

Front 574

Irregular contractions and relaxation’s of muscle unit, appearing as a twitch or ripple

Back 574

Fasciculations

Front 575

Poorly inhibited laughing/crying.

Back 575

Lability

Front 576

How patient walks and sits

Back 576

Gait and Station

Front 577

Strength of cough.

Back 577

Coup de Glotte

Front 578

Confirmatory Signs

Back 578

1) Atrophy
2) Reduced Tone
3) Fasciculations
4) Lability
5) Reduced Normal Reflexes or Increased Pathologic Reflexes
6) Strength of Cough or Coup de Glotte
7) Gait and Station

Front 579

Assessment of MSDs include:

Back 579

1) Nonspeech Exam
2) Speech Exam
3) Reflexes
4) Motor Programming Exam (if applicable, based on 1-3)

Front 580

The nonspeech exam largely involves observations of speech structures at:

Back 580

1) At Rest
2) During sustained postures
3) During movement
4) Reflexes

Front 581

If there is significant groping, you may want to do a:

Back 581

Motor Programming Exam

Front 582

Is intelligibility or comprehensibility the more functional measure?

Back 582

Comprehensibility

Front 583

When doing reading activities, it's important to read things the:

Back 583

Patient is interested in. Will read more like they talk.

Front 584

Kind of a grunt

Back 584

Coup de glotte

Front 585

The thalamus takes in sensory info and:

Back 585

Filters what info goes where.

Front 586

Function of this is a supportive role for the DAP.

Back 586

IAP

Front 587

This pathway regulates reflexes.

Back 587

IAP

Front 588

If the laryngeal valve is affected, there will be:

Back 588

Breathiness

Front 589

If the velopharyngeal valve is affected, you will have:

Back 589

Hyponasality

Front 590

If the articulatory valve is affected, you will have:

Back 590

Imprecise articulation

Front 591

Fasciculations that you can't see:

Back 591

Oscillations

Front 592

AMR

Back 592

Articulatory motion rates

Front 593

SMR

Back 593

Sequential motion rates

Front 594

Dystonias occur during:

Back 594

Contraction movements

Front 595

This involuntary movement occurs during voluntary movement:

Back 595

Dyskinesia

Front 596

This is a type of chorea:

Back 596

Athetosis

Front 597

Ataxic dysarthria and AOS can:

Back 597

Co-occur

Front 598

Result from damage to the motor units of cranial or spinal nerves that serve the speech muscles.

Back 598

Flaccid Dysarthrias

Front 599

The lesion in flaccid dysarthria will always be:

Back 599

somewhere between the
brain stem or spinal cord and the muscles used in speaking.

Front 600

Flaccid dysarthria results from final common pathway involvement and the key characteristic is:

Back 600

Weakness

Front 601

Flaccid dysarthria is associated with damage to the motor units of:

Back 601

Cranial nerves or spinal nerves that serve speech muscles.

Front 602

Lesions that cause dysarthria can occur from vascular problems in the:

Back 602

Vertebrobasilar System

Front 603

Flaccid dysarthria can be caused by any process that damages the:

Back 603

Motor Unit

Front 604

Refers to any disease involving the nerve, regardless of cause, but usually of an inflammatory etiology.

Back 604

Neuropathy

Front 605

Flaccid dysarthria results from damage to this pathway.

Back 605

Final Common Pathway

Front 606

With flaccid dysarthria, these types of movements are ffected.

Back 606

1) Reflexive
2) Automatic
3) Voluntary

Front 607

Most often, however, flaccid dysarthria (when non-progressive) results from strokes and trauma affecting the posterior fossa level structures (brain stem, medulla, pons) damaging several cranial nerves, resulting in a condition called:

Back 607

Bulbar Palsy.

Front 608

When non-progressive, flaccid dysarthria can range from very severe (all cranial nerves affected) to very mild (a single cranial nerve affected). In the former case augmentative communication may be required; in the latter case, treatment may be:

Back 608

Rehabilitative, behavioral, compensatory, or prosthetic.

Front 609

Primary finding and nearly everything we hear in flaccid dysarthria can be traced to:

Back 609

Weakness or reduced strength or force of muscle contraction.

Front 610

Produced by damage to the direct and indirect
activation pathways of the CNS, bilaterally.

Back 610

Spastic Dysarthria

Front 611

A unilateral CVA cannot cause this type of dysarthria.

Back 611

Spastic Dysarthria

Front 612

Most people with this reflect decreased skilled movement and weakness from direct activation pathway damage and increased muscle tone and spasticity from indirect activation pathway damage.

Back 612

Spastic paralysis

Front 613

A combination of hyperactivity of stretch reflexes and increased muscles tone.

Back 613

Spasticity

Front 614

Repetitive reflex contraction when mm. is under tension

Back 614

Clonus

Front 615

Clinical features associated with DAP damage:

Back 615

1) weakness: more pronounced in distal then proximal mm; positive Babinski reflex = extension of great toe; fanning of other toes reflecting release of reflex from inhibition of CNS (normal in infants);
2) pathological oral reflexes: suck, snout, jaw jerk

Front 616

Clinical features associated with IAP damage:

Back 616

1) In general “positive signs” or over activity such as increased m. tone, spasticity, and hyperactive reflexes. Positive sign is something that appears that is not supposed to be there after a lesion. Negative sign is something that is supposed to be there disappears after a lesion.
2) Spasticity = a combination of hyperactivity of stretch reflexes and increased muscles tone.
3) Clonus: repetitive reflex contraction when mm. is under tension

Front 617

Patient complains that my speech is slow and it's effortful to talk.

Back 617

SD

Front 618

You learn the most about SD from these tasks:

Back 618

1) Conversation
2) AMRs
3) Vowel prolongation

Front 619

Characteristics of SD

Back 619

1) Slow speech
2) Effortful speech
3) Fatigue with speaking
4) "Nasal" speech
5) Intelligibility is a problem
6) Deviant speech characteristics are not described by going through the cranial nerves because SD is associated with impaired movement patterns rather than weakness of individual mm.

Front 620

Non-speech characteristics of SD:

Back 620

1) Difficulty controlling emotional expression
2) Dysphagia -- careful swallowing, trouble chewing meat, drooling
3) Pseudobulbar affect -- emotional state doesn’t match expression
4) Weak face, tongue ROM reduced with weakness, AMRs are slow
with reduced range but usually rhythmic
5) Hyperactive gag
6) Pathologic oral reflexes – sucking, snout and jaw jerk

Front 621

Emotional state doesn't match expression.

Back 621

Pseudobulbar affect

Front 622

Pathologic oral reflexes:

Back 622

1) Sucking
2) Snout
(also absence of jaw jerk)

Front 623

Spastic dysarthria is often accompanied by cognitive disturbances that may include:

Back 623

1) Dementia
2) Cognitive-communication deficits associated with RHD, TBI, and aphasia.

Front 624

Therapy for SD:

Back 624

1) Address posture, breath control
2) Evaluation for palatal lift 3) Therapy for easy onset, voice control
4) Muscle tone reduction, strength training, phonemic practice

Front 625

Pseudobulbar affect and drooling are associated more with:

Back 625

SD

Front 626

Phonation typically has a tight, strained strangled vocal quality.

Back 626

SD

Front 627

The hypernasality that may be present in spastic dysarthria is usually not as severe as that heard in:

Back 627

Flaccid dysarthria

Front 628

Two features of SD help distinguish it from other MSDs:

Back 628

1) Strained-harsh/strangled voice quality
2) Slow speech rate -- slow, yet regular AMRs

Front 629

Abnormal speech characteristics clusters:

Back 629

DAB Clusters

Front 630

DAB Clusters related to SD:

Back 630

1) Prosodic excess (relates to slowness of individual and repetitive movements)
2) Articulatory-resonatory incompetence (effects of reduced range and force of articulatory movements of lips tongue, jaw, and face) and velopharyngeal movements.
3) Prosodic insufficiency (attributable to reduced vocal
characteristics)
4) Phonatory stenosis (trying to produce voice through a narrowed glottis)

Front 631

DAB Cluster
1) Excess and equal stress (excess stress on unstressed parts of speech)
2) Slow rate (rate of speech abnormally slow)

Back 631

Prosodic Excess

Front 632

DAB Cluster
1) imprecise consonants (consonants lack precision; slurring, inadequate sharpness, distortions, and lack of crispness; clumsiness going from one consonant sound to another. THIS is a common characteristic of the dysarthrias.
2) Distorted vowels (vowels sound distorted throughout their duration)
3) Hypernasality

Back 632

Articulatory-resonatory incompetence (effects of reduced range and force of articulatory movements of lips tongue, jaw, and face) and velopharyngeal movements.

Front 633

DAB Cluster
1) monopitch
2) monoloudness
3) reduced stress (reduction of proper stress or emphasis
patterns)
4) short phrases

Back 633

Prosodic insufficiency (attributable to reduced vocal
characteristics)

Front 634

DAB Cluster
1). low pitch
2) harshness
3) strained-strangled voice  4) pitch breaks
5) short phrases
6) slow rate

Back 634

Phonatory stenosis (trying to produce voice through a narrowed glottis)

Front 635

This type of dysarthria is often seen with hypotonia and reduced or absent reflexes.

Back 635

Flaccid

Front 636

DAB Clusters
1) Phonatory Incompetence (incompetence at laryngeal valve including inadequate VF adduction and abduction)
2) Resonatory Incompetence (weakness at the laryngeal valve)
3) Phonatory-Prosodic Insufficiency (hypotonia in all laryngeal muscles)

Back 636

Flaccid

Front 637

This DAB cluster involves:
1) breathy voice
2) audible inspiration
3) short phrases

Back 637

Phonatory Incompetence

Front 638

This DAB cluster involves:
1) hypernasality
2) nasal emission
3) Imprecise consonants
4) short phrases

Back 638

Resonatory Incompetence

Front 639

This DAB cluster involves:
1) harsh voice
2) monopitch
3) monoloudness

Back 639

Phonatory-Prosodic Insufficiency

Front 640

How does a brainstem stroke cause dysarthria?

Back 640

Disrupts bloodflow to cell bodies in the LMN

Front 641

How does a tumor cause dysarthria?

Back 641

Compresses a cranial nerve

Front 642

How would a viral/bacterial infection cause dysarthria?

Back 642

Damage the tissue of the nerve

Front 643

How would physical trauma cause dysarthria?

Back 643

Fractured bone compresses or cuts the nerve

Front 644

How would a surgical accident cause dysarthria?

Back 644

Slip of scalpel, sever or nick a nerve

Front 645

Types of neuromuscular junction disease:

Back 645

1) Myasthenia Gravis
2) Botulism

Front 646

Types of vascular disorders:

Back 646

1) Brainstem Stroke
2) Sarcoidosis

Front 647

Types of infectious processes:

Back 647

1) Polio
2) Herpes Zoster
3) Collet-Sicard Syndrome

Front 648

Demyelinating disease

Back 648

Guillain-Barre

Front 649

Muscle Disease

Back 649

Muscular Dystrophy

Front 650

Anatomic anomalies example

Back 650

Arnold-Chiari malformation

Front 651

Degenerative diseases

Back 651

1) Progressive bulbar palsy
2) ALS

Front 652

Etiologies of Flaccid Dysarthria

Back 652

1) Neuromuscular junction disease
2) Vascular disorders
3) Infectious processes
4) Demyelinating
5) Anatomic Anomalies
6) Degenerative Disease
7) Other (radiation therapy, cranial mononeuropathyies)
8) Surgical trauma
5) Muscle Disease

Front 653

A chronic auto-immune disease that affects the neuromuscular junction.

Back 653

Myasthenia Gravis

Front 654

Its major characteristic is an abnormally rapid weakening of voluntary muscles with use and especially during stress testing and improvement with rest.

Back 654

Myasthenia Gravis

Front 655

Its thought that antibodies destroy ACh receptors on muscle, making it less responsive to the ACh that triggers m. contraction.

Back 655

Myasthenia Gravis

Front 656

Myasthenia gravis occurs most often after age 50 and is often accompanied by:

Back 656

1) Ptosis (drooping of the eyelid)
2) weakness of the facial muscles of mastication
3) Flaccid dysarthria
4) Dysphagia

Front 657

How is MG treated?

Back 657

Surgery and hormone replacement

Front 658

A disorder of unknown cause often preceded by a
viral infection. Characterized by acute or subacute onset of PNS dysfunction and felt to result from demyleninzation of peripheral and cranial nerves. Proximal muscles of mastication are affected more severely than distal muscles.

Back 658

Guillain-Barre Syndrome

Front 659

Facial, oropharyngeal, and ocular muscles are affected first and more than half of these patients have facial weakness, dysphagia, and flaccid dysarthria. Recovery is rapid and complete sometimes,but some patients are left with permanent weakness.

Back 659

Guillain-Barre Syndrome

Front 660

A viral disease that affects LMN cell bodies in the lumbar and cervical regions of the spinal cord.

Back 660

Polio

Front 661

Those who developed polio before the vaccine was invented are showing signs of developing insidious onset of progressive weakness in later life. This is called:

Back 661

Post-polio syndrome. Can affect speech and swallowing.

Front 662

A disorder of volitional movement involving errors in rate, range, force and direction of movement

Back 662

Ataxic Dysarthria

Front 663

Overshoots spatial targets

Back 663

Ataxic Dysarthria

Front 664

Rhythmic ataxic movement

Back 664

Intention tremor

Front 665

Associated with damage to the cerebellar control circuit.

Back 665

Ataxic Dysarthria

Front 666

Ataxic dysarthria is evident in:

Back 666

1) Articulation
2) Prosody

Front 667

Ataxic dysarthria reflects a breakdown in:

Back 667

1) Motor organization
2) Motor control

Front 668

When you listen to a person with ataxic dysarthria, the impression is NOT one of underlying weakness, but an activity that is:

Back 668

Poorly coordinated.

Front 669

With this, you can sometimes hear explosive loudness and poorly modulated pitch.

Back 669

Ataxic dysarthria

Front 670

Located in the posterior fossa of the brain behind the pons and the medulla.

Back 670

Cerebellum

Front 671

Lesions in ataxic dysarthria are usually:

Back 671

1) Bilateral
2) In the vermis
3) Diffuse or generalized

Front 672

The cerebellum makes sure that movement occurs in a:

Back 672

Smooth and coordinated fashion

Front 673

The cerebellum receives info from the cortex about:

Back 673

Intended movements that it wishes to accomplish.

Front 674

This type of dysarthria occurs from damage to cerebellar control circuit.

Back 674

Ataxic dysarthria

Front 675

Rhythmic tremor of body or head

Back 675

Titubations

Front 676

Decreased resistance of passive movement

Back 676

Hypotonia

Front 677

Movement errors can be seen in:

Back 677

1) Force
2) Speed
3) Range
4) Direction
5) Timing

Front 678

Disturbance in controlling aim or range of movement
(overshoot/undershoot)

Back 678

Dysmetria

Front 679

Decomposition of movement

Back 679

Dysdiadochokinesis

Front 680

Ataxic movements are:

Back 680

Halting, imprecise, jerky, poorly coordinated, reduced speed and lacking fluidity of movement

Front 681

Clinical findings of ataxic dysarthria:

Back 681

1) Difficulties with standing or walking
2) Titubations
3) Nystagmus
4) Hypotonia
5) Movement Errors
6) Dysmetria
7) Dysdiadochokinesis
8) Ataxic movements
9) Intention or kinetic tremor, typically seen as target is approximated.

Front 682

Degenerative etiologies of ataxic dysarthria:

Back 682

1) Friedrichs Ataxia
2) Olivopontinecerebellar atrophy (OPCA)
3) Paroxysmal ataxic dysarthria (PAD)

Front 683

Types of etiologies of ataxic dysarthria.

Back 683

1) Degenerative
2) Vascular
3) Neoplastic Disorders
4) Trauma

Front 684

Broad based stance and instability, frequent falls.

Back 684

Ataxia

Front 685

Inborn error of metabolism; starts before adolescence and evolves to incapacitation and death over a course of about 20 years.

Back 685

Friedrichs Ataxia

Front 686

Falls into a group of heterogeneous conditions involving multiple systems atrophy.

Back 686

OPCA

Front 687

A condition reflected by brief episodes of ataxic dysarthria.

Back 687

PAD

Front 688

It's primarily spinocerebellar in characteristics. (However, often extrapyramidal and LMN problems can be observed;
2) Associated with skeletal deformities).
3) There is no medical treatment.

Back 688

Friedrichs ataxia

Front 689

Associated with degeneration of the pontine and olivary nuclei in the pons, the middle cerebellar peduncles, and the cerebellum.

Back 689

OPCA

Front 690

1) Can have few to hundreds of episodes per day lasting 5-30 seconds.
2) Medical treatment: Tegretol

Back 690

PAD

Front 691

Therapy for Ataxic Dysarthria

Back 691

1) Increase breath control, slow and controlled respiration, speak immediately on exhalation, stop phonation early
2) reciting syllables to a metronome, finger or hand tapping, cued reading material, chunking of phrases
3) Increase volume control, medical evaluation & intervention for vocal tremor
4) Muscle force training, phonemic practice, intelligibility drills, exaggerated consonants
5) contrastive stress drills, pitch range exercises, intonation profiles, chunking utterances into syntactic units

Front 692

DAB Clusters involved in Ataxic Dysarthria

Back 692

1) Articulatory Inaccuracy
2) Prosodic Excess
3) Phonatory-prosodic insufficiency

Front 693

DAB cluster marked by harshness, monopitch, monoloudness.

Back 693

Phonatory-prosodic insufficiency

Front 694

DAB cluster marked by excess and equal stress, prolonged phonemes, prolonged intervals, slow rate.

Back 694

Prosodic excess

Front 695

DAB cluster marked by imprecise consonants, irregular articulatory breakdowns, vowel
distortions.

Back 695

Articulatory inaccuracy

Front 696

Best tasks to hear ataxic dysarthria:

Back 696

1) Conversational speech/reading/speech AMRs
2) Repetition of sentences with multisyllabic words may promote prosodic and irregular articulatory breakdowns.
3) Irregular speech AMRs are a distinguishing characteristic of ataxic dysarthria.

Front 697

Patient complains of slurred speech (drunken quality), difficulty coordinating breathing with speech, bite cheeks or tongue while talking, stumble over words.

Back 697

Ataxic Dysarthria

Front 698

Tumors within the cerebellum or those exerting mass effects of the cerebellum can lead to cerebellar signs, including ataxic dysarthria.

Back 698

Neoplastic disorders

Front 699

Lesions secondary to aneurysms, arteriovenous malformations (AVMs) hemorrhage, or blockages in the vertebrobasilar system, particularly its lateral regions.

Back 699

Vascular etiologies of ataxic dysarhtira

Front 700

1) TBI associated with limb ataxia and dysarthria.
2) Punch drunk encephalopathy - dementia puglistica seen in boxers who have sustained repeated blows to the head and cerebral injuries.

Back 700

Trauma that cause ataxic dysarthria

Front 701

Clinical findings of ataxic dysarthria:

Back 701

1) Oral-mech exam is often normal (non-speech AMRS jaw, lips, and tongue may be irregular (lateral wiggling of tongue or retraction and pursing).
2) Irregular speech AMRs
3) May have associated cognitive deficits

Front 702

With ataxic dysarthria, impaired prosody reflects the decomposition of movement and timing associated with:

Back 702

Cerebellar movement

Front 703

Where we see trouble with prosody in ataxic dysarthria:

Back 703

1) Stress patterns (convict vs. convict), phrase stress (hot dog vs. hot dog)
2) Sentence stress "The Couple came to the Party"
3) emphatic or contrastive stress: Jay in not involved in the Red Zinger bicycle race (factual) versus Jay is not ...... (but somebody is).

Front 704

Paths are:

Back 704

Functional

Front 705

Tracts are:

Back 705

Based on location