Medical Speech Pathology

Curiosity, Dialogue, and Knowledge

Introduction to Dysarthria


Includes the bulbar palsies (old term).

An impulse for movement must eventually pass along a final common path to the muscle.

The LMN & the muscle fibers that it innervates are known as the motor unit, which is the final common pathway from the CNS to the muscles.

If the LMN or its nerve is damaged, all types of movement: voluntary, automatic, or reflexive, are impaired.

The result is flaccidity, hypotonia, hyporeflexia, muscle atrophy, & muscle fasciculations.

Facial palsy

Caused by damage to the LMN of CN VII or the nerve itself.

Skin sensation on the affected side is spared because it is controlled by sensory portion of the trigeminal.

The affected side sags.

The eye on the affected side has trouble closing (tears a lot).

Diagnostically, you can always tell the affected side because the tip of the nose & mouth are pulled towards the unaffected side.

Unilateral facial palsy – trouble pursing the lips, & with symmetrical retraction or spreading of the lips & problems firming that cheek. Intraoral air pressure may suffer. Air will escape between the lips on the affected side.

Damage is almost always unilateral.

Bilateral damage causes a transverse smile: upside down smile, sides of mouth are pulled down, unable to pucker or retract the lips, unable to increase intraoral air pressure for plosives.

Mastication palsy

Damage to the LMN of CN V or to the nerve itself (mixed nerve) results in mastication palsy.

If damage occurs to the motor nerve, then sensation is spared.

If damage occurs at the level of the brainstem to the LMN, often sensation is also affected because the motor neuron & the sensory neuron are very close together on the brainstem.

If unilateral, there is no effect on speech because the weak side of the jaw is held up by the unaffected strong side. You can talk with your jaw shut.

If bilateral, the jaw hangs open.

The Major problem of mastication palsy is chewing and swallowing .

Hypoglossal palsy

Damage to LMN of CN XII or the nerve itself results in hypoglossal palsy.

Affected side of the tongue will be flaccid, hypotonic, looks shrunken (b/c of atrophy).

That atrophy will cause rolls in the tongue on the affected side.

It’s easy to see fasciculations (twitching uncontrollably) on the affected side.

On protrusion, the tongue will deviate to the affected side.

Unilateral – fairly mild to moderate effects on speech. It’s fairly easy to teach someone to compensate.

Dysphagia is likely an issue if ½ of tongue is weak.

Could be bilateral – caused by tumors or bilateral stroke.

Can’t protrude tongue much past the teeth.

Very restricted tongue movement – speech, chewing & swallowing are very difficult.

Pharyngolaryngeal palsy

Damage to the LMN of CN X or the nerve itself.

2 types of vagal lesions: high and low.

A high vagal lesion involves the LMN of CN X or damage to the vagus nerve before it innervates the soft palate; ½ of the soft palate will be flaccid & hypotonic. The uvula/soft palate is pulled up & over towards the unaffected side.

Because CN X also innervates the larynx, there will also be poor innervation to 1 of the vocal folds via recurrent & superior laryngeal nerves (which branch off of the vagus), 1 vocal fold will be flaccid. Unilateral vocal fold paralysis will be present. Breathy & hypernasal voice quality will also be noted.

Low vagal lesion – the soft palate will be spared but there will be unilateral vocal fold paralysis. Damage is below the level of the soft palate, below the level of the pharyngeal branch of the Vagus.

Recurrent Laryngeal branch – the Vagus on the right comes off of the brainstem, runs down the neck, into the chest, wraps around the subclavian artery, comes back up the neck & innervates the vocal fold on that side.

The superior laryngeal nerve on the right has a very direct route: branches off of the vagus, into the larynx.

Recurrent On the left – the vagus exits the CNS, comes down the neck much further into the chest, where it wraps around the aorta of the heart, comes back up the chest & neck into the left vocal fold.

A common side effect of heart surgery is a weakened voice because the recurrent laryngeal nerve is stretched, compressed by edema, or severed.

Generalized bulbar palsy

When 2 or more bulbar palsies exist

Very common


Caused by damage to the UMN or the primary motor strips or damage to their axons or tracts.

Tends to affect larger groups of muscles.

The affected muscles (in spite of having too much tone) are weak & move very sluggishly with a great deal of effort.

True spastic dysarthria is associated primarily with spastic cerebral palsy.

If the spasticity is unilateral to the articulators, speech isn’t horribly affected.

Speech will be slow, imprecise, & because ½ of soft palate is sluggish, that person will sometimes sound hypernasal or hyponasal.

Pseudobulbar Palsy (CNs that support speech – Hypoglossal, Facial, Vagus, & Trigeminal)

Only affects the articulatory muscles

The result of bilateral damage to the Corticobulbar tracts.

The larynx, soft palate, lips, face & tongue are all hypertonic (spastic).

Because the whole face is bilaterally spastic, it is very difficult to show any facial expression (mask-like face).

Patients tend to have a hard time gathering & swallowing saliva – they tend to drool.

Articulation is slow, imprecise, & distorted.

Very hypernasal

Voice is very tight & strained sounding (vocal folds are very tightly adducted).

Patients have inappropriate infantile oral reflexes.

Patients have a lot of swallowing problems.

Hallmark sign: emotional lability – will laugh & cry for no apparent reason & are very embarrassed by it. They don’t laugh & cry appropriately because cortex is unable to inhibit those behaviors

Tends to occur in the older population

Ataxic dysarthria

Disorder of the cerebellum

In addition to speech problems: intention tremors, decomposition of movement (robotic arm movement), dysmetria – (unable to judge how far away/close an object is)

Incoordination of respiration, phonation, articulation, & resonance

The hallmark symptom: variability of articulatory errors.

Not easy to address because it is so variable.

If caused by a degenerative (progressive) disease of the cerebellum, not only ataxic dysarthria, but also increasing cognitive problems.

Also, will have problems with appropriate prosody in speech.

Problems coordinating pitch, intensity, & pause changes.

Hypokinetic dysarthria

Problems involving the extrapyramidal system – basal ganglia & substantia nigra.

Most common example is Parkinson’s disease.

Hypo in this case refers to slowness of movement.

Parkinson’s has a typically slow onset & progression.

Patient’s have a hard time getting a movement started then have a hard time stopping it – Parkinsonian shuffle.

Mask-like face due to fact that they are unable to move their face easily to show emotion.

Speech is very monotone.

Weak phonation.

Speech is characterized by a lot of hesitations, followed by quick bursts of rapid speech.

Speech is sometimes characterized by perseveration of speech sounds or words – can sound like a clonic type stuttering block.

If the tremoring is severe/unable to be controlled by dopamine, will perform stereotaxic surgery on the thalamus – go to a particular set of neurons in the thalamus & they destroy that collection of neurons. Often the severity is reduced to the point it can be controlled by medication.


Problems typically result in 2 or more separate types of dysarthria:

ALS – Lou Gehrig’s disease – (amyotrophic lateral sclerosis)

Caused by progressive deterioration of both the upper & lower motor neurons

Both spastic & flaccid symptoms, typically with 1 predominating

Can have flaccidity of the articulatory musculature & in other parts of the body can have spasticity

ALS is Progressive & fatal.  There is no known cause or cure,  and no effective treatments (try to treat symptoms).

Typically, individuals have about 7 years from the time they are diagnosed until they die -some only have 3 years (depends on how long a diagnosis took).

No effect on cognition.

Eventually the person ends up completely paralyzed, unable to move anything voluntarily.

The last part of the body with which they have voluntary movement is typically the eyes.

As a SLP, your responsibilities change as the disease progresses

Try to keep them speaking as intelligibly as possible for as long as possible

Speech will eventually fail them – job changes to AAC.

Swallowing becomes a major issue, eventually they will need a PEG tube.

MS Multiple Sclerosis

Typically has an onset in the 30’s or 40’s (can have teen onset).

The cause is unknown.

Portions of myelin are attacked repeatedly causing that portion of myelin to become inflamed & to impede transmission of both efferent motor signals (if attacking motor axons or motor nerve) and/or afferent sensory symptoms. As the myelin is repeatedly attacked, it will eventually die & be replaced by scar tissue (hardening). That hardening is called sclerosis – when it occurs in 2 or more places it is called multiple sclerosis.

Drugs can help alleviate the symptoms but there is no cure.

Difficult to diagnose.

Does not show up on MRIs until that myelin is sclerotic (begins to really harden).

Symptoms involve – spasticity, flaccidity, ataxia, sensory symptoms – based upon where the myelin is attacked & what nerves or axons are affected.

2 major types

1. Relapsing Remitting

Everything is fine, then all of a sudden they have an attack – causes very abrupt disability, then it plateaus, and then all of the symptoms resolve.

Have another attack – a relapse with even worse disability, then a plateau, then it resolves & everything is ok

Myelin is not attacked severely enough to cause permanent damage

Never goes away but symptoms can get better

Drugs are pretty good

Subtype: Progressive relapsing remitting

Disability happens, gets worse, plateaus, improves somewhat, then there is another attack (worse than before)

This has a stepwise function over time of increasing disability.

There is remittance, but it never goes back to normal.

2. Primary Progressive

Keeps getting worse over time

– Secondary Progressive

Improves a little and then gets worse.

Also there are combinations of types

If there is a complaint of double vision, red flag.

50% have speech/language problems as a result.

Cognition is usually spared.

Wilson’s disease

Genetic metabolic disorder – the body is unable to metabolize copper. Copper is stored in the body – typically in the cornea & iris – look for a cooper ring in the eyes.

Also, it’s stored in the UMNs of the PMS, in the basal ganglia & in the cerebellum.

Results in spastic, ataxic & hypokinetic symptoms – they will have all three.

Impedes function of UMNs in the PMS (spasticity or hyperreflexia).

Impedes function of basal ganglia (ataxia or tremors).

Impedes function on the cerebellum (hypokinesia or bradykinesia).

Blood Supply

For the brain, there are two large vertebral arteries – the internal and external carotid arteries (you have left and right carotid). These join together & become the huge basilar artery. It comes into the brain through the magnum foramen.

On the bottom of brain is large artery called the Circle of Willis. This brings blood to the left & right hemispheres.

Superior Cerebellar Artery (SCA) – goes to the cerebellum.

Posterior Cerebral Artery (PCA) – goes to the hemispheres.

Left and Right Middle Cerebral Arteries are of critical importance, because the left MCA, which takes arterial blood to the left hemisphere, is called the artery of aphasia. Damage to the left MCA is what results in aphasia. A stroke of the right MCA may result in the aprosodias.

Anterior cerebral arteries (left and right) take arterial blood to the frontal portion of both hemispheres.

Middle cerebral arteries are responsible for blood supply to the middle portions of each hemisphere.

Posterior Cerebral arteries are responsible for blood supply to the rear portions of both hemispheres.

All have branches that take blood all over each hemisphere.

Depending upon which branch of the left MCA is blocked or bleeding, determines what type of aphasia you have.

Strokes are caused by three different types of arterial problems:

1. Thrombosis-blockage of the artery, typically caused by build-up over the years of fatty deposits inside the artery, which fills the artery, and blocks the blood from getting past it.

2. Embolism-occurs when bacteria or a piece of fatty deposit breaks off and travels with the arterial blood up the artery. The clot becomes stuck and you can’t get any blood past that point and have a stroke. If the clot goes to the carotid, vertebral, or basilar artery – it will result in stroke.

3. Hemorrhage- a bleed. A branch of an artery bursts.

Aneurysm is a type of hemorrhage caused by a congenital weakening of an arterial wall. The arterial wall becomes thinner and thinner and begins to balloon out. There are no symptoms until it bursts or presses on a critical area.

-These all will result in aphasias if it involves the left MCA or any of its branches, some go to Broca’s, some to Wernicke’s, and some the cortex in between.

CVAs (cerebrovascular accidents/strokes)

After age 55 incidence of stroke doubles every ten years.

Broca’s aphasia as result of stroke is more common in younger patients (60’s).

Wernicke’s aphasia as result of stroke is more common in older patients (70-75’s).

The prevalence of Wernicke’s and Global Aphasia is higher in women than men.


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