Neuroanatomy of UMN

and LMN Motor

Speech Disorders
ASHA Presentation
November 19, 2009
Susan T. Jackson
 Disorders Causing UMN and LMN
Speech Disorders
z Stroke (UMN, LMN)
z ALS (UMN and LMN)
z CP (UMN, LMN)
z Tumor (UMN, LMN)
z Trauma (UMN, LMN)
z MS (UMN, LMN)
z Wilson’s disease (UMN)
http://www.ninds.nih.gov/disorders/wilsons/wilsons.htm
z Myasthenia Gravis (LMN)
http://www.ninds.nih.gov/disorders/myasthenia_gravis/myasthenia_gravis.htm
z Bell’s palsy (LMN)
z Guillain-Barré Syndrome (LMN)
http://www.ninds.nih.gov/disorders/gbs/gbs.htm
Dysarthrias that Result from
UMN and/or LMN Damage
z Spastic dysarthria
z Stroke, CP, tumor, trauma, encephalitis

z Flaccid dysarthria
z Stroke, CP, tumor, trauma, Bell’s palsy, Myasthenia
Gravis, Guillain-Barré Syndrome
z Mixed spastic-flaccid dysarthria
z Stroke, trauma, ALS

z Mixed spastic-ataxic-hypokinetic
z Wilson’s disease

z Variable (spastic-ataxic-flaccid)
z MS
Nerve Fibers
z Three types: commissural, association, projection
z These fibers are white matter, and they are bundles
of axons
z Commissural fibers – connect the two cerebral
hemispheres. The corpus callosum is the largest,
and is the main conveyor of inter-hemispheric info.
z Association fibers – connect areas of the brain
within the same hemisphere. Long association
fibers are known as fasciculi. Fasciculi are large
bundles of axons. There are three major fasciculi,
but we’ll mention one – the arcuate fasciculus. It
connects Broca’s area with Wernicke’s area, and
lies one inch below the cortex.
z Projection fibers - connect areas of the cortex with
lower levels of the nervous system
Projection Fibers
z Efferent projection fibers are motor (they carry info
from the cortex)
z Afferent fibers are sensory (they carry info to the
cortex)
z Efferent motor fibers originate in the pre-central
gyrus and in the area of the frontal lobe anterior to
the pre-central gyrus. They innervate cranial nerve
nuclei in the brainstem or cells in the spinal cord.
z Afferent sensory projection fibers originate in
sensory receptor cells and their destination is the
post-central gyrus
Lobes of the Brain
Projection Fibers

z We will concentrate on the efferent motor fibers

z Four major divisions of the motor system have
been identified
z 1) the final common pathway (lower motor neuron
system)
z 2) the direct activation pathway (upper motor neuron
system or pyramidal tract)
z 3) the indirect activation pathway (extrapyramidal tract
– direct contact with LMNs)
z 4) the control circuits (basal ganglia and cerebellum –
no direct contact with LMNs)
z UMNs are part of the CNS, and LMNs are part of
the PNS.
Projection Fibers
z UMNs originate in the motor cortex and synapse
onto cranial nerve nuclei in the contralateral
brainstem (corticobulbar tract) or onto cells in
the contralateral spinal cord (corticospinal tract)
z LMNs originate in the cranial nerve nuclei (in
which case they are known as cranial nerves) or
in cells in the spinal cord (in which case they are
known as spinal nerves). They synapse onto
muscles. The junction between the LMN and
the muscle is known as the motor end plate.
z Cranial nerves innervate muscles of the head
and neck, whereas spinal nerves innervate
muscles of the limbs and trunk
UMNs and LMNs
Corticospinal Tract
z Main pathway for nearly all voluntary muscle
activity
z Comprised of UMNs
z It’s a bundle of axons, which changes names as
it courses from cortex to muscles (corona
radiata, posterior limb of the internal capsule,
basis pedunculi)
z This is a crossed pathway. At the level of the
pyramids in the medulla, approx. 80-90% of the
fibers in the tract cross to the other side of the
brainstem; therefore, they descend in the
opposite side of the spinal cord from where they
originated.
Corticospinal Tract
z Movement of one side of the body is controlled
by the contralateral (opposite) side of the brain
z Although the UMNs that originate in the pre-
central gyrus are responsible for the initiation of
voluntary motor activity, the UMNs that originate
in the frontal lobe anterior to the pre-central
gyrus do not initiate impulses. In fact, they act
as suppressors or inhibitors of the LMNs. They
prevent the LMNs from overdischarging in
response to stimuli. If these inhibitory fibers are
damaged, you end up with spasticity.
Corticobulbar Tract
z Is comprised of UMNs
z Originates in the motor cortex (lower third)
z Crosses to the opposite side of the brain at
various levels of the brainstem (midbrain, pons,
medulla)
z Innervates cranial nerve nuclei at various levels
of the brainstem
z Corticobulbar projections to most cranial nerve
nuclei is bilateral, but corticobulbar projections to
some cranial nerve nuclei is contralateral only
Bilateral Innervation of Cranial
Nerve Nuclei
Contralateral Innervation of
Cranial Nerve Nuclei
 Projection Fibers
z Thus, if UMNs are damaged, you get spasticity as
well as not being able to initiate skilled motor
movements
z Spasticity = increased muscle tone. A Babinski sign
signals the presence of UMN damage. Reflexes are
exaggerated.
z If LMNs are damaged, you end up with flaccid
paralysis
z Flaccidity = decreased muscle tone. Atrophy of
muscles. Reflexes are diminished or absent.
Bilateral Cortical (UMN)
Lesions – Spastic Dysarthria

z Bilateral UMN lesions are likely to produce

chronic dysarthria
z The following can cause spastic dysarthria:
stroke, CP, severe brain injuries, MS,
encephalitis, and extensive brain tumors
z Blood supply disruption – carotid artery system
(e.g., MCA, ACA)
z Spastic dysarthria is also called pseudobulbar
dysarthria
Bilateral Cortical Lesions –
Spastic Dysarthria
z Strained-strangled phonation – associated
with hyperadduction of the true and false
vocal cords, and is characterized
aerodynamically by elevated laryngeal
airway resistance and subglottal pressure,
and by reduced laryngeal airflow
z Velopharyngeal dysfunction includes
increased pharyngeal constriction; slow,
sluggish velopharyngeal movement; and
incomplete VP closure
z Imprecise articulation
 Unilateral UNM Lesions –
Flaccid Dysarthria
z Dysarthria in unilateral stroke is typically mild and
temporary, and may co-exist with and be masked by
aphasia or AOS
z Imprecise consonant production was by far the most
deviant speech feature in a retrospective study of 56
people with unilateral UMN dysarthria. Slow speaking
and reduced oral movement rates were also found.
z Physical findings of unilateral lower facial weakness
and unilateral lingual weakness * (talk about why later)
z Less common was vocal harshness and hypernasality.
The neurologic bases of the phonatory and
velopharyngeal features are unclear.
Unilateral and Bilateral LMN
Damage: Flaccid Dysarthria
z The LMNs to which we are referring are cranial
nerves
z Damage to one cranial nerve can result in flaccid
dysarthria
z Damage to multiple cranial nerves can result in
flaccid dysarthria
z The symptoms of flaccid dysarthria vary depending
on which cranial nerves are damaged, and whether
the damage is unilateral or bilateral
z The following can cause flaccid dysarthria: stroke,
CP, trauma, tumor, ALS, MG, Bell’s palsy, Guillain
Barré
Lesions in the Area of Vertebrobasilar
Circulation – Flaccid Dysarthria
z Infarcts in the areas of the brain supplied by the
vertebrobasilar system are less common than
cortical infarcts, accounting for all CVAs
z Brainstem strokes may result in flaccid paralysis
of the speech muscles
z Two major muscular abnormalities are
weakness and hypotonia – seen in all
movements of affected muscles (reflexive,
automatic, or voluntary)
z The salient perceptual speech characteristics
are marked hypernasality coupled with nasal
emission of air, continuous breathiness during
phonation, and audible inhalation (stridor on
inhalation)
Cranial Nerves
z There are 12 pairs of cranial nerves
z Cranial nerves are LMNs that originate in the cranial
nerve nuclei (various levels of the brainstem)
z Some cranial nerves are motor only, some are
sensory only, and some are motor and sensory
z The cranial nerves innervate the muscles of the jaw,
face (including lips), pharynx, larynx, soft palate,
tongue, and neck
z The muscles affected are ipsilesional (i.e., the R
cranial nerves innervate the R side of the body, and
the L cranial nerves innervate the L side of the
body)
Cranial Nerves
z Six pairs of cranial nerves are important for speech
z V – Trigeminal (sensory and motor)

z VII – Facial (sensory and motor)

z IX- Glossopharyngeal (sensory and motor)

z X – Vagus (sensory and motor)

z XI – Accessory (motor)

z XII – Hypoglossal (motor)

z Since most cranial nerve nuclei receive bilateral

UMN innervation, unilateral UMN damage does not
have a major deleterious effect on speech (with a
few exceptions)
Trigeminal Nerve (V)

z The trigeminal motor nucleus receives bilateral UMN

input
z The sensory fibers have 3 main branches
(ophthalmic, maxillary, mandibular)
z Motor to:
z jaw (masseter, lateral and medial pterygoids)

z temple (temporalis)

z soft palate (tensor veli palatini)

z larynx (mylohyoid and anterior belly of the

digastric – both extrinsic muscles of the larynx)
z middle ear (tensor tympani)
 Trigeminal Nerve (V)
z Functions
z Cutaneous sensations (touch, pain, temperature) and
proprioceptive sensations (awareness of posture and muscle
movements) from the head, face, oral and nasal cavities,
sinuses, teeth, anterior 2/3 of the tongue, anterior ½ of the
pinna, external auditory meatus, and external surface of the TM
z Mastication (jaw opening and closing, lateral movements of
chewing)
z Articulation (jaw opening and closing)

z Flattening and tensing of the soft palate (which brings the soft
palate to one side and prevents food from entering the nasal
pharynx)
z Prevents damage to the inner ear hair cells from loud noises
when tensor tympani muscle contracts
z Opens the eustachian tube
Trigeminal Nerve (V): Testing
z Inspect the masseter and temporalis bulk
z Palpate the masseter when the person bites
z Observe the position of the jaw when the person
is at rest
z Ask the person to open and close the mouth
z Evaluate the strength of jaw closure
z Ask the person to move the jaw from side to side
z Attempt to elicit the jaw jerk reflex (physician)
z Test sensation by touching the person’s face
with a cotton swab and asking if the person felt it
z Ask the person about facial pain
 Trigeminal Nerve (V)
z Behaviors that Suggest Unilateral LMN Damage
z Deviation of the jaw to the side of the lesion and an
inability to force the jaw to the side opposite the
lesion
z Mildly reduced strength of the masticator muscles on
the same side as the lesion
z Reduced bulk of masseter and temporalis muscles
(atrophy) on the side of the lesion
z No major effects on speech

z Ipsilateral loss of sensation to face, oral and nasal

cavities, and other areas served by CN V
z Trigeminal neuralgia (pain) on the same side of the
face as the affected CN V
 Trigeminal Nerve (V)
z Behaviors that Suggest Bilateral LMN Damage
z The jaw hangs open and cannot be closed, or
moves slowly and with limited range
z Reduced bulk (atrophy) of masseter and
temporalis muscles on both sides of the face
z Articulation is affected in a major way (labial and
lingual articulatory movements are not accurate
in place or manner)
z Bilateral loss of sensation to face, oral and nasal
cavities, and other areas served by CN V
z Trigeminal neuralgia (pain) on both sides of the
face
Trigeminal Nerve (V)
z Behaviors that Suggest Unilateral UMN Damage
(Input to CN V)
z No real effect on speech because CN V receives
bilateral UMN input
z Behaviors that Suggest Bilateral UMN Damage
(Input to CN V)
z Limitation of jaw movement (opening and closing);
mandible hangs low
z Exaggerated jaw jerk reflex

z Articulation is affected in a major way (vowels and

labial and lingual consonants)
 Facial Nerve (VII)
z The motor cranial nerve nucleus that innervates the
upper 1/3 of the face receives bilateral UMN input
z The motor cranial nerve nucleus that innervates the
lower 2/3 of the face receives primarily contralateral
(unilateral) UMN input
z Motor to:
z Muscles of facial expression (orbicularis oculi,
zygomatic, biccinator, orbicularis oris, platysma)
z Middle ear (Stapedius)

z Larynx (stylohyoid, posterior belly of the digastric –

both are extrinsic muscles of the larynx)
z Sensory to:
z Sublingual, submandibular, and lacrimal glands

z Taste receptors on the anterior 2/3 of the tongue

Facial Nerve (VII)
z Functions
z All movements of facial expression (e.g., wrinkle
forehead, close eyes tightly, pull back corners of
mouth)
z Guards the middle ear by innervating the
stapedius muscle, which acts to dampen
excessive movement of the ossicles in the
presence of a loud noise
z Taste on the anterior 2/3 of the tongue
 Facial Nerve (VII): Testing
z Observe the person’s face at rest and note the symmetry
z Ask the person to look up at the ceiling and note
wrinkling of the forehead
z Ask the person to close his/her eyes tightly and note
wrinkling around the eyes
z Ask the person to smile and note the symmetry
z Ask the person to pucker his/her lips and note the
symmetry
z Ask the person to fill his/her cheeks with air, gently press
on the cheeks, and note whether the person can
maintain a lip seal
z Does the person report that sounds are uncomfortably
loud?
 Facial Nerve (VII)
z Behaviors that Suggest Unilateral LMN Damage
z The entire side of the face ipsilateral to the lesion droops (e.g.,
forehead has no wrinkles, difficult to close eye, corner of mouth
droops, flattened nasolabial fold). If the right CN VII is damaged,
the right side of the face is affected. If the left CN VII is damaged,
the left side of the face is affected.
z Atrophy of the muscles on the side of the face ipsilateral to the
lesion
z Fasciculations of the peri-oral area and chin on the side of the face
ipsilateral to the lesion
z Speech is not negatively affected to any great extent. There may
be some mild articulatory imprecision.
z Ordinary sounds may be perceived as uncomfortably loud on the
side ipsilateral to the lesion (hyperacusis)
z Loss of taste from the anterior 2/3 of the tongue on the side of the
tongue ispilateral to the lesion
Facial Nerve (VII)
z http://www.uptodate.com/patients/content/ima
ges/neuropix/Bells_palsy_photos.jpg
z http://thebarefootkitchenwitch.typepad.com/th
e_barefoot_kitchen_witc/images/2008/02/24/
palsy.jpg
z http://www.egms.de/figures/journals/cto/2005
-4/cto000016.f4.png
z http://www.ninds.nih.gov/disorders/bells/bells.
htm
Bell’s Palsy in an Adult
Bell’s Palsy in a Child
 Facial Nerve (VII)
z Behaviors that Suggest Bilateral LMN Damage
z Both sides of the face are affected as
described above
z Hearing is affected bilaterally as described
above
z Taste is affected bilaterally as described
above
z Major difficulty producing labial and
labiodental sounds
z http://www.biomedcentral.com/1472-6815/4/3
z http://scienceblogs.com/purepedantry/2007/05/mobius_s
yndrome.php
z http://www.ninds.nih.gov/disorders/mobius/moebius.htm
Bilateral Facial Weakness
Before Tx for Herpes Zoster After Treatment
Mobius Syndrome
Pre-surgery Post-surgery
 Facial Nerve (VII)
z Behaviors that Suggest Unilateral UMN Damage (Input
to CN VII)
z The lower 2/3 of the face on the side contralateral to
the lesion will be affected (flattened nasolabial fold,
corner of mouth droops)
z Little effect on speech

z Behaviors that Suggest Bilateral UMN Damage (Input to

CN VII)
z Paralysis of the upper and lower facial muscles on
both sides of the face
z Preservation of emotional expression even though
there is paralysis of voluntary movements of the facial
muscles
z Major difficulty producing labial and labiodental
sounds
Vagus Nerve (X)
z Motor to:
z Cardiac muscles

z Smooth muscles of the esophagus, stomach, and intestine

z Muscles of the pharynx and larynx

z Muscles of the soft palate

z Palatoglossal muscle of the tongue

z Sensory to:
z Mucosa of the pharynx

z Inferior surface of the epiglottis

z Trachea, bronchi, esophagus, stomach, intestines

z Mediates pain input and stretch afferent feedback from

pharyngeal and laryngeal muscles
z The nucleus ambiguus of CN X receives bilateral innervation
Vagus Nerve (X)
z Functions
z Regulation of cardiovascular, respiratory, and
gastrointestinal functions
z Taste sensation from the pharyngeal area
z Controls muscles of the larynx, pharynx, and soft
palate for phonation, swallowing, and resonance,
and for opening the respiratory pathway
z Motor fibers originate from the posterior 2/3
of the nucleus ambiguus. These fibers give
rise to the pharyngeal nerve, the superior
laryngeal nerve, and the recurrent laryngeal
nerve (all branches of CN X).
 Vagus Nerve (X)
z Pharyngeal nerve
z Supplies the three pharyngeal constrictor muscles

z Supplies all soft palate muscles except the tensor veli

palatini
z Superior laryngeal nerve
z Supplies the cricothyroid muscle (an intrinsic muscle of
the larynx that lengthens the vocal folds for pitch
adjustments)
z Sensory to the mucous membrane as far down as the
vocal cords
z Recurrent laryngeal nerve
z Supplies all RIML (remaining intrinsic muscles of the
larynx)
z The left and right recurrent laryngeal nerves take different
paths. The L hooks under the aortic arch near the heart.
Recurrent Laryngeal Nerve
Vagus Nerve (X): Testing
z Observe the soft palate at rest and when the
person says, “Ah” (multiple short productions)
z Elicit a gag reflex
z Laryngoscopy to visualize the vocal folds
z Ask the person to phonate and prolong a vowel
sound
z Ask the person to raise and lower the pitch of a
prolonged vowel or sing up and down a scale
z Listen to the person during conversation
z Ask the person to count to 300 (speech stress
test)
 Vagus Nerve (X)
z Behaviors that Suggest Unilateral LMN Damage
z Palate droops on side ipsilateral to lesion; mild hypernasality

z http://www.scielo.br/img/revistas/anp/v64n3a/a15fig01.gif

z Vocal fold is paralyzed on same side as lesion; breathy

and/or hoarse voice; diplophonia
z Weak pharynx on same side as lesion; swallowing difficulty

z Behaviors that Suggest Bilateral LMN Damage

z This state of affairs is often not compatible with life
(respiratory centers in this area of the brainstem)
z Palate droops bilaterally; severe hypernasality

z Bilateral vocal fold paralysis (flaccid); severe breathy voice;

inhalatory stridor
z Weak pharynx bilaterally; severe swallowing difficulty
Unilateral Palatal Droop
 Unilateral VF Paralysis
(Damage to CN X)

Abducted Position Adducted Position

(R L) (R L)
Vagus Nerve (X)
z Behaviors that Suggest Unilateral UMN Damage (Input
to CN X)
z minimal to no effect on phonation, resonance, or
swallowing because of bilateral innervation
z Harsh voice quality

z Behaviors that Suggest Bilateral UMN Damage (Input to

CN X)
z Paralysis of vocal folds in the paramedian position;
spasticity of VFs
z Strained-strangled phonation, hypernasality

z Swallowing difficulty
 Hypoglossal Nerve (XII)
z The nucleus of CN XII receives bilateral innervation with
one exception: the cells serving the genioglossus muscle
(the largest muscle of the tongue – protrudes and retracts
tongue, and elevates hyoid bone) receive only
contralateral UMN input
z CN XII innervates all intrinsic muscles of the tongue and
3/4 extrinsic muscles of the tongue (genioglossus,
hypoglossus, styloglossus)
z Functions: all movements of the tongue
z Shortening, concaving, narrowing, elongating, flattening

z Protrusion, drawing the tongue upward and backward,

retraction and depression
z The genioglossus participates in phonation (it elevates the
hyoid bone)
Hypoglossal Nerve (XII): Testing

z Observe the tongue at rest

z Ask the person to stick out the tongue
z Ask the person to move the tongue from side
to side
z Ask the person to elevate and lower the
tongue tip
z Ask the person to protrude and retract the
tongue
z Ask the person to lick his/her lips
 Hypoglossal Nerve (XII)
z Behaviors that Suggest Unilateral LMN Damage
z Atrophy, weakness, and fasciculations of the
tongue on the same side as the lesion
z Tongue deviates to side of lesion (weak side
of tongue) on protrusion
z Mild imprecise articulation (can be isolated to
lingual phonemes)
z May have difficulty moving food around in the
mouth
z http://www.ispub.com/ostia/index.php?xmlFilePath=journ
als/ijhns/vol1n1/tapia.xml
Unilateral Tongue Weakness
Figure 1: The tongue deviation to the dennervated
side during tongue protrusion and atrophy on the
same side.
Unilateral Tongue Weakness
Figure 12: Typical picture of a unilateral hypoglossal
paralysis. The deviation of the protruded tongue to the
affected side is visible. This is caused by the greater
innervation of the uninvolved side.
Hypoglossal Nerve (XII)
z Behaviors that Suggest Bilateral LMN Damage
z Bilateral atrophy, weakness, and
fasciculations of the tongue
z No tongue deviation, but tongue protrusion
may be limited or nonexistent
z Mild – severe imprecise articulation (can be
isolated to lingual phonemes)
z Severe difficulty in swallowing and eating

z Alterations in resonance
Hypoglossal Nerve (XII)
z Behaviors that Suggest Unilateral UMN Damage
(Input to CN XII)
z Some weakness of the tongue on the side
opposite the lesion
z Tongue deviates to side opposite the lesion
(weak side of tongue) on protrusion
z Mild articulatory imprecision

z Behaviors that Suggest Bilateral UMN Damage

(Input to CN XII)
z Bilateral tongue weakness

z Mild-severe articulatory imprecision

References
z Duffy, J.R. (2005). Motor speech disorders,
2nd edition. Elsevier Mosby, St. Louis, MO.
z Duffy, J.R. (1995). Motor speech disorders.
Mosby, St. Louis, MO.
z Yorkston, K.M., Beukelman, D.R., Strand,
E.A., & Bell, K.R. (1999). PRO-ED, Austin,
TX.