Measures of Tongue Function: Normative Data & Clinical ...



| |ICCD 2016 |

| |Iowa Conference on Communicative |

| |Disorders |

| |Cedar Falls, Iowa |

|[differential diagnosis of Motor Speech Disorders] |

| |

| |

Motor Speech Disorders

The evolution of a classification system

Prior to the classification system first introduced by Darley, Aronson, & Brown (1969), the dysarthrias were considered a single diagnosis.

The implication was that this diagnosis had homogeneous features.

Distinctions were made between dysarthria and aphasia, even dysarthria and apraxia of speech.

Parallels

Autism

No longer really considered a unitary diagnosis

Autism spectrum

Further definition

Asberger’s Syndrome

Differential diagnosis

Evolution of a discipline

A need to better understand and define clinical populations.

Evaluation

More accurate diagnosis

Treatment

Guide our treatment decisions

Darley, Aronson, & Brown

Pivotal articles (1969)

“Motor Speech Disorders” text (1975)

Defined and identified the dysarthrias

Initial sample = 212 patients

Lesion site

Perceptual characteristics

Motor characteristics

Benefits & Drawbacks

Assists with confirmation of lesion site

Can rule out other potential diagnoses

Clinical “shorthand”

Similar to aphasia syndromes

Guides treatment decisions

Understanding the underlying pathology results in selecting the appropriate treatment

Reliability has been questioned

Corresponding lesion data

Clinical knowledge

Not confirmed empirically

Take home message…

Clinically useful

Evolution continues

Our understanding of neuropathology will never be static

New discoveries

New procedures

For now, the system is a useful one that will continue to be refined

Hyperkinetic

Myriad of movement disorders

The Dysarthrias

“A collective name for a group of neurologic speech disorders resulting from abnormalities in the strength, speed, range, steadiness, tone, or accuracy of movements required for control of the respiratory, phonatory, resonatory, articulatory, and prosodic aspects of speech production. The responsible pathophysiologic disturbances are due to central or peripheral nervous system abnormalities and most often reflect weakness; spasticity; incoordination; involuntary movements; or excessive, reduced or variable muscle tone.”

(Duffy, 2013 p. 4)

Prevalence of MSD

Based on a sample > 14, 000 people referred for a speech/language evaluation at Mayo Clinic from 1993-2008

Other neurologic speech disorders - 0.4%

Apraxia of Speech – 3.9%

Nonaphasic cognitive-communication disorders – 16.8 %

Aphasia – 25.8%

Dysarthria – 53%

Definition revisited:

Key features of the dysarthrias

Neurologic basis

Disorder of movement

Categorized based on

Lesion

Physical characteristics (OME findings)

Speech characteristics

| | | | |

|DYSARTHRIA |Lesion |Physical signs |Speech |

| | | | |

|FLACCID | | | |

| | | | |

|SPASTIC | | | |

| | | | |

|ATAXIC | | | |

|HYPOKINETIC | | | |

| | | | |

|HYPERKINETIC | | | |

| | | | |

|MIXED | | | |

| | | | |

Flaccid Dysarthria

Results from injury/damage to cranial and/or spinal nerves

Final common pathway

Lower motor neuron

Reflexive, automatic, and voluntary activities are ALL affected when the lesion resides in the FCP.

Can impact all subsystems of speech

Primary characteristics can be traced to weakness

Which of the Cranial and/or spinal nerves might be implicated?

Etiologies

Surgical

Nonsurgical

Neuropathies

Tumor/Neoplasm

Myasthenia gravis

Degenerative

Vascular

Anatomic malformation

Demyelinating

Other

Lesion analysis

Trigeminal

Innervation properties

Three branches (sensory)

Motor component

Signs

Sensory loss

Jaw deviation (unilateral)

Jaw may hang open (bilateral)

How do you test?

Speech signs

Imprecision in connected speech

Most affected with bilateral lesions

Facial

Innervation properties

Sensory

Motor

Which would be most devastating to speech?

Signs

Facial droop

Drooling (possibly)

Pocketing

Testing

Speech signs

Imprecision in connected speech

Related to facial weakness

What sounds would be most affected?

Glossopharyngeal

Innervation properties

Sensory

Motor

Signs

Testing

Speech signs

Vagus

Innervation properties

Sensory

Motor

Signs

Velar signs

Testing

Speech signs

Phonation

Respiration

Resonance

Spinal Accessory

Innervation properties

Motor

Signs

Shoulder weakness

Testing

Speech signs

Hypoglossal

Innervation properties

Motor

Signs

Tongue deviation

Atrophy

Testing

Speech signs

Imprecision with articulation

Compensation with the mandible

Spinal nerve lesions

Damage to spinal nerves C-1 through C-5

Primary damage to respiration

How does that interfere with speech?

Signs

Rapid/shallow breathing

Exaggerated thoracic expansion

Flaccid dysarthria related to isolated damage to spinal nerve lesions is rare

Primary Characteristics

Weakness

Hypotonia and reduced reflexes

Fasciculations and fibrillations

Darley, Aronson & Brown (1969)

Hypernasality

Articulatory Imprecision

Breathiness

Monopitch

VPI

Audible inspiration

Harsh vocal quality

Short phrases

Monoloudness

***********************************************************************************

Spastic Dysarthria

Secondary to damage of the direct and indirect pathways of the CNS (UMN system)

Direct pathway

Pyramidal tract

Corticobulbar tracts

Interacts with cranial nerves

Corticospinal tracts

Interacts with spinal nerves

Facilitatory action

Leads to skilled discrete movements

Indirect pathway

Extramyramidal

Regulates reflexes, maintains posture, tone

Inhibatory nature

Clinical Characteristics

Difficulty with fine, discrete movements

Initially decreased tone

Weakness

Develops into increased tone, spasticity

Those muscles utilized in fine movements most affected

Decreased reflexes initially, then more pronounced

Babinski sign

Oral motor reflexes

Suck

Snout

Jaw jerk

Etiologies

Vascular

Brainstem stroke

Bilateral effects

Cerebral stroke can’t have the same impact, unless there is previous damage, or perhaps midline shift/compression from a hemorrhagic stroke

Lacunar infarcts

Multi-infarct dementia

Not a common problem with DAT

Inflammatory

Leukoencephalitis

Degenerative disease

Primary lateral sclerosis

Traumatic Brain Injury

Multiple Sclerosis

Neoplasm

Oral Mechanism

Dysphagia

Drooling

Pseudobulbar affect

Normal jaw strength

Facial movements may be slow then move into excess/extreme

Hyperactive reflexes

Speech Characteristics

Impairments noticed most by looking at muscle movement rather than isolated muscles

?« speed

?«range

?«force

?ªmuscle tone

Darley, Aronson, & Brown (1969a)

Imprecise artic

Monopitch

?« stress

Harshness

Monoloudness

Low pitch

Slow rate

Hypernasality

Strained-strangled quality

Short phrases

Distorted vowels

Pitch breaks

Breathy quality

Excess and equal stress

***********************************************************************************

Ataxic Dysarthria

Cerebellum

Two cerebellar hemispheres

Vermis

Ipsilateral contribution

Unlike the cerebral hemispheres which have contralateral contributions

With median lesions, effects may be bilateral

How does the “circuit” function?

The “circuit”

Notice of movement-cerebral hemispheres

Monitors the movement via feedback from the muscles/joints that conduct the movement.

Regulates movement in an ongoing fashion based on both ends of this circuit.

Clinical Characteristics

Ataxic dysarthria typically manifests with diffuse cerebellar damage

Any signs/symptoms from unilateral lesions tend to improve rapidly

Disordered gait

Truncal instability, titubation

Rotated head postures

Occular motor abnormalities

Ataxic dysarthria

Etiologies

Degenerative Diseases

Hereditary Ataxias

Multiple Sclerosis

Paroxysmal Ataxic Dysarthria

Vascular Disorders

Aneurysms

AVMs

Occlusion in the vertebrobasilar system

Neoplasm

Trauma

Toxic/metabolic conditions

Alcoholic cerebellar degeneration

Severe malnutrition

Vitamin deficiencies

Pharmacological

Antiseizure drugs

Lithium

Valium

Hypothyroidism

Normal Pressure Hydrocephalus

Oral Mechanism

Most aspects of the OME can be entirely normal

Size

Strength

Symmetry

Face, jaw, tongue, palate

Rest, and during sustained postures

Gag

Reflexive swallow

OME abnormalities

Irregular AMRs

Observe the regularity of movement of the tongue, lips, and jaw

AMRs and connected speech

Systemic problem

Affects the entire system rather than isolated impairment from muscles/muscle groups

Speech

Imprecision with artic

Irregular artic breakdown

Distorted vowels

Excess and/or equal stress

Prolonged phonemes/pauses

Slow rate

Harshness

Monopitch

Monoloudness

Reduced/irregular breathgroups

Darley, Aronson, & Brown 1969

Artic imprecision

Excess/equal stress

Irregular artic breakdowns

Distorted vowels

Harsh quality

Prolonged phonemes

Prolonged intervals

Monopitch

Monoloudness

Slow rate

Loudness variations

Voice tremor

***********************************************************************************

Hypokinetic Dysarthria

Pathology of the basal ganglia control circuit

Rigidity

Reduced force/range

Decreased mobility a/o range lead to the name “hypokinetic”

The only dysarthria which has

“rapid” speech rate as one of the perceptual characteristics.

Depletion or reduction of the neurotransmitter, dopamine.

Parkinson’s disease that best reflects hypokinetic dysarthria.

Basal Ganglia Control Circuit

Functions

Regulate muscle tone

Movements that support goal directed activity

Postural adjustments

Adjust movements to the environment

Assists in learning new movements

Damage results in reduced movement a/o a failure to inhibit involuntary movement

Hypokinetic dysarthria most reflects reduced movement

Clinical Characteristics

Resting tremor

4-7 Hz

Limbs

Pill-rolling

Jaw, lips, and tongue

Rigidity

Resistance to passive stretch

Decreased movement

Bradykinesia/Akinesia

Slow movement

Freezing

Shuffling gait

Micrographia

Masked facies

Reduction in:

Arm movement while walking

Gestures

Blinking

Head movement

Swallowing frequency

Loss of postural reflexes

Reduced “righting” response

Stooped posture

Difficulty initiating movment

While lying down

Sitting to standing

Etiologies

Damage to the basal ganglia

Degenerative

Vascular

Traumatic

Inflammatory

Neoplastic

Toxic

Metabolic diseases

Oral Mechanism

Immediate revealing features

Masked facies

Flat affect

Respiratory signs

Infrequent swallowing

May result in drooling

Size, strength, and symmetry may be normal

AMRs may be slowly initiated a/o rapid and restricted in range

Speech Characteristics

Monopitch

Monoloudness

Reduced intensity

Breathy quality

Reduced stress

Short phrases

Variable rate

Short rushes of speech

Imprecise consonants

***********************************************************************************

Hyperkinetic Dysarthria

Another dysarthria type that manifests secondary to damage to the basal ganglia control circuit

May effect all or isolated speech subsystems.

Involuntary movement is the hallmark feature

Rhythmic

Irregular

Fast

slow

Abnormal

What constitutes abnormal?

Involuntary movements when steadiness is expected

Hyper-in this case does not mean fast

Excessive, extra

Many forms

Classified based on speed and periodicity

Classification

Dyskinesia

Myoclonus

Tics

Chorea

Ballism

Athetosis

Dystonia

Spasm

Tremor

Etiologies

Degenerative

Vascular

Traumatic

Inflammatory

Toxic

Metabolic disease

***********************************************************************************

Mixed Dysarthrias

Mixed dysarthrias

Combination of dysarthrias

Two or more

Diffuse damage

Etiologies

Degenerative

ALS

MS

PSP

Toxic metabolic

Wilson’s disease

Hepatocerebral degeneration

Hypoxic encephalopathy

Vascular Disorders

Trauma

Neoplasm

Infectious diseases

***********************************************************************************

Apraxia of Speech

“A neurologic speech disorder that reflexts an impaired capacity to plan or program sensori-motor commands necessary for directing movements that result in honetically and prosodically normal speech. It can occur in the absence of physiologic disturbances associated with the dysarthrias and in the agsence of disturbance in any component of language.”

(Duffy, 2013, p. 4)

Apraxia of speech is secondary to a disturbance of the motor programming system.

Central impairment

Can occur without muscle impairment

Normal function is apparent

High variability

The motor speech programmer executes the motor movements/sequences necessary to convey language

Speech ‘vs’ Language

Primarily left hemisphere lesions

Motor speech area

Brocca’s area

Supplementary motor cortex

Insula

Variability in lesion locations

Dronkers, 1993

Etiologies

AOS is secondary to primarily focal lesions

vascular

Tumors

Focal/discrete trauma

Surgical

Other

Degenerative conditions

Occasionally have focal effects

Clinical Characteristics

May exhibit right sided weakness

May also have sensory deficits

Hyperactive reflexes

Limb apraxia

Concomitant aphasia

Brocca’s type

Can exist in a “pure” form

Few documented cases

Assessment findings

Oral mechanism

May have rt. weakness

May result in dysarthria that is not the same as AOS

Nonverbal oral motor apraxia

Difficulty performing oral tasks.

Sequential AMRs

Most sensitive task to the effects of AOS.

Specific Speech Characteristics

Slow rate

Prolonged consonants/vowels

Many pauses

Inter/intrasegmental

Disruptions in prosody

Equal stress

Decreased pitch/intonation contours

False starts

Effortful/laborious speech

Repetitions

***********************************************************************************

Factors that influence speech production

Walking

Injurious Falls

One-third of Americans aged 65+ fall each year.

Every 14 seconds, an older adult is treated in the E.R. for a fall, every 29 minutes an older adult dies after a fall.

Annually, falls result in more than 2.4 million injuries in emergency departments, resulting in over 772,000 hospitalizations and over 21,700 deaths.

In 2012, the costs related to falls was over $36 billion, with an expectation to reach over 59 billion annually by 2020.

Aging

Affects gait patterns

Change in skeletal structure

Reduced muscle mass/strength

Results in a higher incidence of neuropathology.

Often with deleterious cognitive and motor effects.

Increasing incidence of falls

Fear of falling

Multitasking

Bombarded today by competing stimuli

Cell phones

Talking or texting

Music

Environment

Walking while talking

Sharing tasks may become more difficult when systems become compromised.

Statement of the Problem

Injurious falls are a major medical concern.

Individuals with neurologic compromise may be at a greater risk.

There are known factors that contribute to fall risk.

Physical decline

Cognitive decline

Pharmacological effects

Environmental factors

What other factors may be influential?

Cognitive load…

GAITRite™ System

Analysis of gait conducted using the GAITRite™ System

14’ portable carpet

16,128 embedded sensors to capture footfalls instantly

Measures include temporal and spatial parameters

Procedures

Each of the groups completed the following:

Montreal Cognitive Assessment

Beck Depression Index

Gait Measures

Baseline (walking, no talking)

Low load (counting by ones)

Medium load (subtracting by 3s)

Originating number varied/attempt

High load (alpha-numeric sequence)

D-7, E-8, F-9…

Gait conditions were counterbalanced to account for order effect.

Each walk was completed twice to control for learning

The average was used for analysis.

Dependent measures

Functional ambulation profile (FAP)

Ratio of step length to leg length to step time; FAP score is derived from a formula that includes several critical gait parameters found to be highly related to fall risk. (Nelson et. al, 1999)

Velocity

Centimeters/second

Stride length

Centimeters

Double support time

The percentage of time per ambulation cycle with both feet on the ground.

Parkinson and Healthy Elderly

Twenty six participants with Parkinson Disease: Peak medication time

Age: Mean = 67.44 (41-91)

Hoehn & Yahr Stage:

22-Stage 2, 3-Stage 3, 1-Stage 4

Thirteen healthy elderly participants

Age: Mean – 68.07

Matched for education level

No significant differences across groups

Stride length or Velocity

Data were collapsed and a condition effect was revealed Baseline > High load

A significant difference and interaction was revealed for Double Support

The healthy adult group significantly increased their Double Support time

The group with PD did not

High vs. Low Medication State

We recruited the same twenty six participants several months later. We asked that they be within 30 minutes of their next medication administration. The same procedures were followed, and we added the Functional Ambulation Profile (FAP) score as a predictor of fall risk.

No differences between conditions or High/Low medication states

Step velocity

Step length

Double support

FAP

Dopaminergic replacement medication did not alleviate the effect of cognitive load.

These results were shared at the World Congress on Parkinson Disease in Paris 2009

Current Study

A double blind, randomized control study to investigate the effects of cognitive enhancing medication on performance in individuals with Parkinson disease.

Participants were randomly assigned to a drug (Rasagiline vs. Placebo). 

Prior to taking the drug, baseline measures were collected on all experimental tasks (Pre-treatment).

Gait

Additional measures 

After 30 days, participants received an increased dose

Participants receiving Rasagiline were given a higher dosage for the next 30 days.

Participants receiving the placebo received additional placebo tablets.

After 60 days, final data collection occurred (Post-treatment).

Gait

Additional measures 

Walking while talking

Individuals with neurological compromise are at an increased risk for falls during the multitask of talking while walking.

Automatic speech doesn’t carry as great a risk.

Increased cognitive load will have deleterious effects especially in high fall risk conditions

Low light

Descending stairs

Giving directions

Mental calculations

Tracking conditions

Obstacles

Environmental variations

Cranial Nerve Information Sheet

|Cranial Nerve |Type |Function |

|I – Olfactory |Sensory |Smell |

|II – Optic |Sensory |Vision |

|III - Oculomotor |Motor |Eye movement |

|IV - Trochlear |Motor |Eye movement (superior oblique) |

|V - Trigeminal |Sensory |Facial sensation – 3 branches |

| | |Opthalamic |

| | |Maxillary |

| | |Mandibular |

| | |Anterior tongue sensation |

| |Motor |Muscles of mastication |

|VI - Abducens |Motor |Eye Movement - lateral rectus |

|VII - Facial |Sensory |Taste - anterior 2/3 tongue |

| |Motor |Facial expression |

|VIII - Vestibulocochlear |Sensory |Hearing |

| | |Balance |

|IX - Glossopharyngeal |Sensory |Pharyngeal sensation |

| |Motor |Pharyngeal muscles |

|X - Vagus |Sensory |Pharynx, larynx, esophagus |

| |Motor |Muscles of palate, pharynx, and larynx |

|XI- Spinal Accessory |Motor |Shoulder, head movement |

|XII - Hypoglossal |Motor |Tongue movement |

For the purpose of screening, the functions listed above are the primary functions of the cranial nerves. This is not meant to serve as an exhaustive list of cranial nerve functions.

© Stierwalt, J.A.G., (2003) Cranial Nerve Information Sheet

Cranial Nerve Screening

|Cranial Nerve |Function |Screening Task |

|I – Olfactory |Sensory - Smell |odors |

|II – Optic |Sensory - Vision |vision chart/acuity |

|III- Oculomotor |Motor – Eye movement |"follow the moving finger" |

|IV - Trochlear |Motor – Eye movement (superior oblique) |look at the nose |

|V - Trigeminal |Sensory - facial sensation/anterior tongue |Have the individual close their eyes: touch |

| | |the face |

| |Motor - muscles of mastication |Palpate muscles that clench the teeth |

|VI - Abducens |Motor - lateral rectus |look to the side |

|VII - Facial |Sensory - taste |sweet, sour, bitter, salt |

| |Motor - facial expression |smile, raise the eyebrows |

|VIII - Vestibulocochlear |Sensory - hearing |a tuning fork |

| |balance |look for vertigo |

|IX - Glossopharyngeal |Sensory - pharynx sensation |gag reflex |

| |Motor – pharyngeal muscles |gag reflex |

|X - Vagus |Sensory –pharynx, larynx, esophagus |Check phonation |

| |Motor - muscles of palate, pharynx, and larynx|Assess vocal quality |

|XI- Spinal Accessory |Motor – Shoulder, head movement |shoulder shrug and/or turning the head to |

| | |resistance |

|XII - Hypoglossal |Motor - tongue movement |Assess tongue movement |

© 2003 Julie A.G. Stierwalt, Ph.D.

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