1. Cranial Nerves BLOCK 3 – 2011-12
Robert R. Terreberry, PhD
Room 142 Ph

2. Cranial Nerves CN I Olfactory ----------- CN II Optic -----------
CN III Oculomotor Midbrain
CN IV Trochlear Midbrain
CN V Trigeminal Pons
CN VI Abducens Pons
CN VII Facial Pons
CN VIII Vestibulocochlear Pons
CN IX Glossopharyngeal Medulla
CN X Vagus Medulla
CN XI Spinal accessory Medulla
CN XII Hypoglossal Medulla
All part of the PNS
1 and 2 are not part of the brainstem at all

3. Spinal Cord / BS Changes
Brainstem
Alar plates  dorsal horns
Basal plates  ventral horns
In the brainstem, Alar plates move laterally  4th ventricle open up basal are medial therefore  sensory tends to be more lateral than motor nuclei
A.Embryologic development of functional cell columns
1.Spinal cord
a. Alar plate - becomes the dorsal horn. Neurons are termed nuclei of termination, and are classified as general somatic afferents (GSA) or general visceral afferents (GVA).
b. Basal plate - becomes the ventral horn. Neurons are known as nuclei of origin, and axons of these motor neurons leave the spinal cord as ventral roots. These neurons are classified as general somatic efferents (GSE) or general visceral efferents (GVE).
2. Brainstem
a. Alar plate - gives rise to nuclei of termination of cranial nerves. In addition to GSA and GVA classifications, there are special visceral afferents (SVA) and special sensory afferents (SSA) as well.
b.Basal plate – gives rise to the motor nuclei of cranial nerves. GSE cell columns provide motor innervation to skeletal muscle of somite (myotomal) origin. Cranial nerves III, IV, VI, and XII are comprised of GSE neurons.
Special visceral efferent (SVE) cell columns are unique to the brainstem, and are not present in most of the spinal cord. These SVE cell columns provide motor innervation to skeletal muscle of somites that migrated into branchial arches. Cranial nerves V, VII, IX, X and XI have SVE component
GVE cell columns give rise to preganglionic, parasympathetic fibers. Cranial nerves III, VII, IX, and X have GVE components

4. CN Functional Components
4 sensory routes (GSA, GVA, SSA, SVA ), 3 motor routes (GSE, GVE, SVE)
- Lets you know in general where cranial nuclei should be

5. CN Functional
Columns
S.L.
4th
VENTRICLE
GSE
GVE
SVE
GVA
SVA
SSA
GSA
Discontinuous aspects of functional columns (gaps)
Basic pattern is fairly constant btwn brainstem

6. CN Nuclei

7. Cranial Nerves CN I Olfactory SSA CN II Optic SSA
CN III Oculomotor GSE, GVE
CN IV Trochlear GSE
CN V Trigeminal SVE, GSA
CN VI Abducens GSE
CN VII Facial SVE, GVE, GSA, SVA
CN VIII Vestibulocochlear SSA
CN IX Glossopharyngeal SVE, GVE, GSA, SVA
CN X Vagus SVE, GVE, GSA, GVA, SVA
CN XI Spinal accessory SVE
CN XII Hypoglossal GSE
Not all cranial nerves have all functional characteristics
Concentrate on mainly on motor aspects of cranial nerves
1,2,8  strictly sensory (SSA)
3, 7, 9, 10 – Parasympathetic system (GVE)
4, 6, 12 – purely GSE  skeletal muscle
5, 7, 9, 10, 11 – innervate muscles from pharangeal arches (SVE)
Trigeminal (5) – main sensation from head (GSA)
Facial – main motor to face
7, 9, 10 – SVA = taste (7 = anterior 2/3 of tounge,9 posterior 1/3 of tounge, 10 – epiglottis)

8. Cranial Nerves CN I Olfactory SSA CN II Optic SSA
CN III Oculomotor GSE, GVE
CN IV Trochlear GSE
CN V Trigeminal SVE, GSA
CN VI Abducens GSE
CN VII Facial SVE, GVE, GSA, SVA
CN VIII Vestibulocochlear SSA
CN IX Glossopharyngeal SVE, GVE, GSA, SVA
CN X Vagus SVE, GVE, GSA, GVA, SVA
CN XI Spinal accessory SVE
CN XII Hypoglossal GSE
All of the motor components
General vs special – arbitrary designation, because both innervate skeletal muscle, just know that SVE comes from pharangeal arches with developmental
Skeletal muscle is voluntary, you have absolute control over all of the nerves that have the GVE and SVE component. The voluntary movement comes from a stimulus from cerebral cortex in order to get this voluntary response
All of these cranial nerves that are motor  influenced by cerebral cortex
All of these neurons that have lower motor neurons if GSE and SVE (axons leave, become part of the peripheral nerve go out and innervate something)  originally came from corticobulbar (aka corticonuclear) system  in brainstem and then you have fibers that project out to individual nerves
Terreberry’s notes:
B.Cranial nerve connections
Sensory nuclei
The sensory components of cranial nerves I, II and VIII will be covered in later lectures.
Only the sensory aspects of the trigeminal nerve will be covered in detail in this lecture.
Motor nuclei
Afferent input comes from cerebral cortex and other subcortical centers for voluntary and involuntary control of motor output, from reticular formation, and from sensory nuclei for reflexes.
Efferent projections are to autonomic ganglia and skeletal muscle.

9. Corticobulbar Projections
No CBs for CN III, IV or VI - through PPRF in pons
Most of them are bilateral
Two exceptions:
Face
Hypoglossal system (12)
CN 3, 4, and 6 = control extraoccular muscles (eyes can voluntarly move eyes R or L without moving your head, moving by medial and lateral rectus)
Controlled by frontal eye fields, not the primary motor cortex through the corticobulbar system
Therefore, if you had a stroke in the primary motor cortex, your eyes not really effected b/c they do not run through this. You can still see a pt move their eyes when stroking out a lot of times b/c of this
Frontal eye fields = broadman’s area 8
paramedian pontiene reticular formation = PPRF
Trigeminal system for example  muscles of mastication is protected if you lesion one side because it is bilateral
That is why there are bilateral systems to protect really impt functions (you can’t chew and you die)
Ex. Low facial is not super impt= makes you smile  not survival where as upper facial is impt for closing your eyes so that is bilateral  needed for survial
Things that are required for survival are usually bilateral
9 and 10 – swallowing
Hypoglosseal = tounge (not conserved if one side lesion
EXCEPTIONS for bilateral face and tounge is not all bilateral
Terreberry’s notes:
C. Corticobulbar (corticonuclear) projections – from the cerebral cortex to brainstem (bulbar) nuclei.
1.Corticobulbar projections arise from neurons in the premotor (Area 6), primary motor (Area 4) and somatosensory (Areas 3,1,2 and 5 & 7)) cortices.
2.These projections affect voluntary control of the muscles innervated by these brainstem nuclei.
3.These projections are primarily bilateral with two important exceptions
a. Innervation of the muscles of facial expression
b.Innervation of tongue muscles

10. CN III GSE LR6(SO4)3 GVE Sphincter pupillae, ciliary muscles EW
III Nucleus
GSE LR6(SO4)3
GVE Sphincter pupillae, ciliary muscles
At superior colliculi level, nuclei located just off the midline
Goes through the two cerebral peduncles  btwn superior cerebellar and posterior cerebral arteries
Seen at the caudal end of the midbrain  two compents:
GSE = LR6 (lateral rectus – abducens n) SO4 (superior oblique – trochlear n)  the rest of the ocular muscles (3) are by occularmotor
GVE = Sphincter pupillae (makes pupil smaller, decrease the amt of light entering the retina), ciliary muscles(maintain shape of lens  contract removes fibers off lens and allows lens to fatten up = get thicker)
NO direct corticobulbar for this system
GSE = occularmotor nucleus (III nucleus)
GVE = Edinger-Westphal nucleus
Entirely ipsilateral system
R nuclei = R eye, L nuclei = left eye
Terreberry’s notes:
GSE motor component
Located in the midbrain
Axons of these lower motor neurons exit the oculomotor nucleus to enter the ipsilateral oculomotor nerve
Innervate ipsilateral extraocular muscles
Superior rectus, inferior rectus, medial rectus, inferior oblique, and levator palpebrae superioris.
NOTE:There are no direct corticobulbar projections to the brainstem motor nuclei of CN III, IV, and VI. The cerebral cortex influences these cranial nerve nuclei through connections with the “gaze” (PPRF) centers. More later in Block
GVE motor component
Preganglionic, parasympathetics in Edinger-Westphal nucleus (located dorsal to the rostral portion of the oculomotor nucleus) exit the brainstem with GSE fibers.
They synapse on postganglionic neurons in the ciliary ganglion in the orbit.
Postganglionic fibers innervate the sphincter pupillae and ciliary muscles that function to constrict the pupil and change lens shape for accommodation.
No direct CBs

11. Pupillary Light Reflex
Reflexes associated with CN III
Pupillary light reflex
A bright light shown into one eye  goes into pretectum ipsilaterally  goes bilaterally to both Edinger-Westphal nucleus  goes to ciliary ganglion in the orbit  Should result in bilateral constriction of the pupils = protective reflex
This happens even if you shine the light in one eye
You have to test both eyes to make sure that you don’t get just one eye restricted
The eye you shine the light in: if constricts that is a direct response
The eye that you didn’t shine the light in: consensual response
Accommodation reflex  near reflex (focus from distant to near)
This involves the occularmotor nucleus (nucleus III), the pathway is not as clearly known, but it is a visual stimulus
You can test this by bringing an object from a far distance to a very close distance to a pt
Three actions occur to change the focus from a distant object to a near object and allow this visual stimulus to accommodate correctly:
GSE  You eyes have to come in, so the medial recti muscles contract (eyes converge  cross eyed)
GVE  Sphincter pupillae muscles contract causing pupils to constrict (light decreases)
GVE  Ciliary muscles contract which causes a decrease in tension of the ligaments attached to the lens, resulting in the lens becoming more round (lens gets thicker)

12. CN III Lesion
Right CN III nerve or nucleus lesion  ipsilateral system (right eye is faulty)
If you lesion CN 3, only two muscles working = LR and SO (b/c not innervated by CN 3) (again this is an ipsilateral system) The parasympathetic system is completely lost (no EW either) 
Ptosis – drooping eyelid due to denervation of levator palpebrae superioris muscle
Cannot open eye b/c it droops
Lateral strabismus – affected eye is abducted and inferiorly rotated due to the unopposed actions of lateral rectus and superior oblique muscles
Mydriasis (pupillary dilatation) – affected eye is dilated due to denervation of sphincter pupillae muscle, and therefore, unopposed sympathetic activity.
Loss of pupillary light reflex and accommodation reflex due to denervation of sphincter pupillae muscle
Inability to laterally gaze to the side opposite the lesion without diplopia due to denervation of medial rectus muscle

13. CN IV GSE LR6(SO4)3 IV Nucleus No direct CBs
Only nerve to come out of the inferior aspect of brainstem
In the cut, fibers are dark, nuclei do not stain. (interior to inferior colliculi)
Superior oblique only
No corticobulbar
Trochlear nucleus (should see one on each side, you just can’t see it in this cut)  it is located just off the midline
Contralateral system
R nucleui  control SO in L eye
Terreberry’s notes:
GSE motor component
Located in the midbrain
axons of these lower motor neurons decussate and exit the brainstem on its dorsal surface
Innervate the contralateral superior oblique muscle
NOTE: There are no direct corticobulbar projections to the brainstem motor nuclei of CN III, IV, and VI. The cerebral cortex influences these cranial nerve nuclei through connections with the “gaze” (PPRF) centers. More later in Block
No direct CBs

14. CN IV Lesion Right CN IV nerve or left nucleus lesion
If lesion the CNIV nucleus then get a contralateral effect. However, if you lesion the nerve you get ipsilateral findings. The findings will be the same no matter where you lesion in terms of how the pt will present
Eye on R is somewhat elevated and maybe pulled in just a little bit (SO moves the eye out and down normally, and so if you take that away  moves up and out)
Terreberry’s notes:
Lesions of CN IV (either the lower motor neurons or the nerve)
Isolated lesions are uncommon
Affected eye is somewhat elevated at rest due to the unopposed action of the inferior oblique muscle, and the patient will experience diplopia in the vertical plane.
NOTE: To clinically test the integrity of CN IV and the superior oblique muscle, have the patient look medially and then inferiorly. This will isolate the action of superior oblique muscle from the other extraocular muscles

15. CN V GSA Face, scalp, nasal/oral cavities, dura
Main S
Motor
GSA Face, scalp, nasal/oral cavities, dura
SVE Muscles of mastication
Responsible for proprioception, tactile, pain, and temp
Comes out at mid pons level and goes through middle cerebellar peduncle
Several brainstem nuclei are associated with this nerve
Sensory (comes from alar plate) GSA (Face, scalp, nasal/oral cavities, dura)
Chief (main/principal) sensory nucleus
Two other sensory nuclei associated with the trigeminal nucleus (you can’t see them on this section)
Spinal trigeminal nucleus and tract
Mesencephalic nucleus and tract
Motor (SVE) for mastication/chewing
Motor nucleus of the trigeminal nerve
Terreberry’s notes
Trigeminal nerve is responsible for the transmission of vibration, touch, conscious and unconscious proprioceptive, pain and temperature sensations from the head, and also the motor innervation of the muscles of mastication (temporalis, masseter, medial and lateral pterygoid muscles) and several other small muscles in the head (tensor tympani, tensor veli palatini, anterior belly of the digastric and the mylohyoid muscle)
Bilateral CBs

16. Trigeminal Nuclei GSA SVE Terreberry’s notes: GSA sensory component
General sensations of the face, oral and nasal cavities, dura mater and proprioception for associated muscles
Functions like the dorsal columns, anterolateral system and spinocerebellar tracts for the rest of the body
Nuclei associated with GSA activity
Three nuclei form an almost continuous column of cells from the cervical spinal cord to the midbrain
Spinal trigeminal nucleus and spinal trigeminal tract
Located in lateral tegmentum of medulla and caudal pons
Nucleus is considered to be the rostral continuation of the substantia gelatinosa of the dorsal horn, while the tract is considered to be the rostral continuation of Lissauer’s tract
Concerned with pain and temperature and crude touch information from the head
Functionally analogous to the anterolateral system
Chief (main/principal) sensory nucleus
Located in the dorsolateral pontine tegmentum at midpontine level, lateral to the fibers of the trigeminal nerve
Concerned with fine touch, 2-point discrimination, vibratory and conscious proprioception information from the head
Functionally analogous to the dorsal column-medial lemniscal system
Mesencephalic nucleus
Located in the rostral pons and caudal midbrain adjacent to the periaqueductal gray
Concerned with unconscious proprioception information from the head
Functionally analogous to the spinocerebellar system
SVE motor component
Motor nucleus of the trigeminal nerve
Located in the dorsolateral pontine tegmentum at mid-pontine level, medial to the fibers of the trigeminal nerve and the chief sensory nucleus
Motor innervation of the muscles of mastication and several other small muscles in the head (tensor tympani, tensor veli palatini, anterior belly of the digastric and the mylohyoid muscle) [Derivatives of embryologic Branchial Arch I]
Corticobulbar projections to the trigeminal motor nucleus are bilaterally equal
Lesion of trigeminal motor component (either the lower motor neurons or the nerve) – with paralysis of muscles of mastication, the jaw will protrude to the side of the lesion due to unopposed action of healthy pterygoids on the opposite side. The jaw-jerk reflex will be absent due to paralysis of these muscles

17. KNOW:
Spinal CN5 – pain and temp (STT)
Chief CN5 – DC stuff (conscious proprioception, vibration, 2 pt, touch
GSA  Goes to postcentral gyrus  medial gyri (HAL) (how info gets to the cortex from the peripheral)

18. Trigeminal Dermatomal Distribution
Non-overlapping dermatomes, unlike spinal nerves
Opthalmic division = V1 (pink), maxillary division = V2 (yellow), and mandibular division = V3 (green)

19. Trigeminal Corticobulbars
Bilateral innervation for muscles of mastication
Each motor nucleus for CN5 on either side gets innervation from both an ipsilateral and contralateral motor cortex

20. Trigeminal Corticobulbars Lesion
MOTOR CORTEX
(FACE AREA)
MOTOR V
NUC.
Corticobulbar projections lost
Shows what happen if you have a lesion to the motor cortex. The motor nuclei of the ipsilateral side of the lesion will only be minimally affected because of the supply from the contralateral side as well. Therefore, the overall ability to chew is not impaired, and only minimally impaired on the ipsilateral side to the lesion

21. Corneal Reflex
Touch cornea  ipsilateral spinal trigeminal nucleus  pain/temp system
However when you touch your eye with a cotton swab, its not very painful. However, still goes to the pain and temp system b/c the cornea is extremely sensitive, so anything coming towards the eye is perceived as being dangerous
Spinal thalamic nucleus then distributes information bilaterally to the VII motor nuclei  orbicularis oculi = close your eyes (ipsilateral / direct response and contralatera/ consensual response)
test both eyes
Terreberry’s notes:
Corneal (blink) reflex – unilateral stimulation of the cornea (pain) results in reflex blinking and eye closure.
a. Afferent limb – ophthalmic division of CN V1 to the spinal trigeminal nucleus
b. Central connections – bilateral projections to the facial motor nuclei
c. Efferent limb – facial nerves to orbicularis oculi muscles
d. Direct response – stimulated eye closes
e. Consensual response – non-stimulated eye closes

22. Lacrimal Reflex
Not usually test in the clinic b/c make tears roll down pts face  just ask if eyes are dry
Every time you put contacts In  override this reflex
Terreberry’s notes:
Lacrimal (tear) reflex – unilateral stimulation of the cornea (pain) results in tear production
a. Afferent limb – ophthalmic division of CN V to the spinal trigeminal nucleus
b. Central connections – bilateral projections to superior salivatory nuclei (preganglionic parasympathetic (GVE) neurons) in the pons
c. Efferent limb – facial nerves to pterygopalatine ganglion, via the greater petrosal nerve, to the lacrimal gland for tear production

23. Trigeminal System Lesions
Peripheral nerve lesions
All sensations lost in distribution of division involved
Unilateral motor nucleus lesion
Ipsilateral loss of muscles of mastication (LMN)
However, the motor nucleus is bilateral so the effects are minimal even on the ipsilateral side to the lesion

24. Trigeminal System Lesions
Unilateral spinal V nucleus lesion
Ipsilateral loss of pain and temperature sense
Unilateral chief V nucleus lesion
Ipsilateral loss of discriminative senses (touch, 2-pt, vibration, proprioception)
Unilateral VTTT, VPM, internal capsule or Area 3,1,2 lesion
Contralateral loss of all modalities
Contralateral loss above the cortibulbar tracts, so anything from a nucleus down will be ipsilateral, but then above that into the thalamus area and such you’re going to decussate at some point and everything shows a contralateral effect if above the nuclei is lesioned.

25. CN VI GSE LR6(SO4)3 VI Nucleus No direct CBs
Comes out along pondomedullary junction
Lateral rectus only
No direct CB (uses PPRF) (so a lesion to the primary motor cortex will not effect this)
Nucleus near the 4th ventricular space (just off the midline)
Ipsilateral system
Terreberry’s notes:
GSE motor component
Located in the caudal pons
Axons of these lower motor neurons exit the brainstem at the pontomedullary junction.
Innervate ipsilateral lateral rectus muscle
NOTE: There are no direct corticobulbar projections to the brainstem motor nuclei of CN III, IV, and VI. The cerebral cortex influences these cranial nerve nuclei through connections with the “gaze” (PPRF) centers. More later in Block
No direct CBs

26. CN VI Lesion Right CN VI nerve lesion Right CN VI nucleus lesion
Lesion of right CN VI nerve = R eye - Medial strabismus – affected ipsilateral eye is adducted due to the unopposed action of medial rectus muscle
lesion of the right CN VI nucleus- Inability to laterally gaze to the side of the lesion without diplopia. Individual cannot abduct the effected eye past the midpoint
NOTE: a lesion of the abducens nucleus (lower motor neurons) in the pons will always affect the ipsilateral PPRF. So, a central lesion of CN VI will result in a gaze preference away from the side of the lesion due to PPRF involvement because the ipsilateral eye does the same, where as the contralateral eye will now not be able to adduct past the midpoint
- Get lesion of PPRF (effects contralateral eye) and lesion of nucleus (effects ipsilateral eye) (why this causes both a direct and consensual response)

27. CN VII GSA Skin around ear, EAM SVA Anterior 2/3 tongue
SVE Muscles facial expression
GVE Lacrimal, submandibular, sublingual glands, nasal/oral mucosa
Facial
Motor
Nucleus
Medial to 8, lateral to 6
Course of axon, course around 6, goes up, and then back around
GSA: Skin around ear, external auditory meatus
SVA: Anterior 2/3 tongue
Terreberry’s notes:
SVE motor component
Located in the caudal pons
Axons of these lower motor neurons exit the facial motor nucleus to enter the ipsilateral motor root of the facial nerve
Innervation is to the muscles of facial expression, stapedius, stylohyoid, and posterior belly of the digastric muscles
Within the pons, the facial motor nucleus is subdivided so that innervation to upper facial muscles (superior to and including orbicularis oculi muscles) is from bilateral corticobulbar projections. Innervation to lower facial muscles is from contralateral corticobulbar projections only.
GVE motor component
Preganglionic, parasympathetics are located in the superior salivatory nucleus in the pons
Axons leave this nucleus to enter the ipsilateral facial nerve
Postganglionic neurons are located in the pterygopalatine and submandibular ganglia
Innervation is to the mucous glands of the oral and nasal cavities, lacrimal gland, and the submandibular and sublingual salivary glands.

28. Facial Nerve Corticobulbars Bilateral CBs Upper
Contralateral CBs Lower
In regards to the SVE component of CN 7
 exception to bilateral corticobulbar system
Want to test upper and lower half of face  have pt close eyes and mouth
For eye portion, corticobulbar = bilateral where mouth = contralateral only

29. CN VII
Lesions b c
Upper motor neuron lesion in B – contralateral lower face weakness only
Lower motor neuron lesion in C (nerve or nucleus)– complete ipsilateral loss
(pics are backwards in regards to lesion for C)
Terreberry’s notes:
Lesions of CN VII
(c)Lower motor neuron lesions (of either the facial motor nucleus or the facial n) result in complete (upper and lower face) ipsilateral facial flaccid paralysis. Fasciculations may be present.
(b) Upper motor neuron lesions of corticobulbar projections to the facial motor nucleus result in;
Paresis (weakness) of the contralateral lower face only
Disuse atrophy over time
No fasciculations
NOTE: Because the upper face muscles are bilaterally innervated, a patient with a unilateral cortical lesion will still be able to wrinkle their brow and close their eyes. Because lower face muscles are not bilaterally innervated, a patient with a unilateral cortical lesion cannot smile on the side of the face contralateral to the lesion. However, if the same patient is told a joke that they find funny, they can smile bilaterally! There are poorly understood projections from the hypothalamus and limbic system involved in an emotional, descending pathway.

30. CN VIII
Cochlear
Nuclei
SSA Hearing
Vestibulocochlear nerve

31. CN VIII SSA Balance, equilibrium Vestibular Nuclei
Vestibulocochlear nerve

32. of Solitary Tract (NTS)
CN IX
Nucleus
of Solitary Tract (NTS)
Nucleus
Ambiguus
GSA Misc ear, pharynx
SVA Posterior 1/3 tongue
SVE Stylopharyngeus
GVE Parotid gland
Don’t test motor side of 9 to investigate it (SVE, GVE)
SVA, GSA = NTS = Nucleus of the solitary tract, made of afferent nuclei (visceral sensory fibers = solitary tract). This is the major visceral sensory nucleus of the brainstem (from 7, 9, and 10)
Nucleus ambiguus = efferent fibers (9 and 10); laryngeal and pharyngeal muscles
Gag reflex = 9 and 10 (in on 9 (afferent) , out on 10 (efferent) )
Terreberry’s notes:
SVE motor component
Located in the nucleus ambiguus in the medulla
Axons of these lower motor neurons enter the ipsilateral glossopharyngeal nerve
Innervation is to the stylopharyngeus muscle
Corticobulbar projections are bilateral.
GVE motor component
Preganglionic, parasympathetic neurons located in the inferior salivatory nucleus enter the ipsilateral glossopharyngeal nerve
Course through the tympanic plexus and lesser petrosal nerve to the otic ganglion in the infratemporal fossa
Postganglionics join the auriculotemporal branch of the mandibular nerve and provide secretomotor innervation to the parotid gland.
Lesions of CN IX – (either the lower motor neurons or the nerve)- isolated lesions are extremely rare.
It is difficult to test stylopharyngeus muscle alone.
Lesion of the nerve or the inferior salivatory nucleus would cause a loss of parotid gland secretions.
Testing the integrity of CN IX is usually done by checking the afferent components (gag reflex).
Afferent limb of gag reflex is carried in CN IX
Efferent limb of gag reflex is carried in CN X
Bilateral CBs

33. CN X GVA Thorax / abdomen viscera SVA Epiglottis GSA Ear, TM, dura
NTS
Dorsal Motor
Nucleus of Vagus
Nucleus
Ambiguus
GVA Thorax / abdomen viscera
SVA Epiglottis
GSA Ear, TM, dura
GVE Paras to thorax / abdomen viscera
SVE Pharynx, larynx
“wandering nerve”
Dorsal motor nucleus of vagus = major parasympathetic nucleus of the brain (contains preganglionic parasympathetic fibers that go to thorax and abdomen)
Nucleus ambiguus  efferent fibers to heart, thorax, and neck
TM = tympanic membrane
Open mouth say ahhhh  soft palate should elevate, uvula (hangs in back of throat)
If issue  soft palate on side of lesion sags, and uvula points towards opposite side of the lesion
Gag reflex  no gag (in on 9, out on 10), so this with sagging palate = vagus
Terreberry’s notes:
SVE motor component
Located in the nucleus ambiguus
Axons of these lower motor neurons enter the ipsilateral vagus nerve
Innervation is to the soft palate and, in conjunction with fibers of cn xi, muscles of pharynx and larynx, including the vocal cords.
Corticobulbar projections are bilateral.
GVE motor component
Preganglionic, parasympathetic neurons located in the dorsal motor nucleus of the vagus in the medulla enter the ipsilateral vagus nerve
Postganglionic neurons are located in ganglia in the pharynx, larynx, thoracic and abdominal viscera.
Innervation is to mucous membranes of the pharynx and larynx, and to smooth muscle and glands of thoracic and abdominal viscera.
NOTE: The efferent limb of the carotid sinus reflex for controlling heart rate is carried by GVE fibers of neurons in the nucleus ambiguus.
Lesions of CN X – (either the lower motor neurons or the nerve)- usually occur in conjunction with CN IX lesions, due to their close proximity to each other.
Unilateral lesion of CN X
Ipsilateral paralysis of soft palate; droops ipsilaterally, and does not rise in phonation. Possible deviation of uvula to the intact side upon phonation (inconstant sign).
Ipsilateral vocal cord palsy, due to loss of SVE fibers to larynx. Hoarseness and coughing are temporary signs, as the contralateral vocal cord will adapt over time.
Visceral signs of a unilateral lesion are generally negligible because of bilateral distribution of vagal fibers in the periphery.
Bilateral lesion of CN X
Vocal cord paralysis may lead to death by asphyxiation.
Lesions involving GVE fibers within nucleus ambiguus may accelerate the heart rate to the point of death.
Upper motor neuron lesions of corticobulbar projections to nucleus ambiguus are difficult to detect due to bilateral innervation.
Bilateral CBs

34. CN XI SVE Trapezius and SCM Bilateral CBs
Shoulder on same side depressed, and test of sternoclinomastoid. When contracts turn head to opposite side and up, have pt try to turn head against resistance  it will be weak
(L lesion, head turns to R, chin will go to side of lesion)
Terreberry’s notes:
A. SVE motor component
located in the ventral horn of the spinal cord at C1–C5 levels
axons of these lower motor neurons enter the ipsilateral spinal accessory nerve
Rootlets emerge from the lateral aspect of the spinal cord between dorsal and ventral roots, and then join to form a common trunk lateral to the spinal cord.
The nerve enters the skull via foramen magnum, and exits through the jugular foramen.
Innervation is to ipsilateral sternocleidomastoid and trapezius muscles
Lesions of CN XI
Ipsilateral shoulder sag and inability to elevate the upper limb above the horizontal plane due to loss of trapezius muscle
Plegia when pointing the chin away from the side of the lesion, especially against resistance.
Chin points to the side of the lesion due to the loss of sternocleidomastoid m and the unopposed action of intact contralateral sternocleidomastoid muscle
Bilateral CBs

35. CN XII
Hypoglossal
Nucleus
GSE Intrinsic and all extrinsic tongue muscles except palatoglossus
Contralateral only
Terreberry’s notes:
GSE motor component
Located in the hypoglossal nucleus in the medulla
Axons of these lower motor neurons enter the ipsilateral hypoglossal nerve
Innervation is to ipsilateral intrinsic and extrinsic muscles of tongue (except for palatoglossus – CN X)
Corticobulbar projections are contralateral
Contralateral CBs

36. CN XII Corticobulbars Contralateral CBs
Left tract damage right half of tounge
Right half damaged left half of tounge
1.Lower motor neuron lesions (either the lower motor neurons or the nerve) –
a.Paralysis of ipsilateral tongue muscles
b.Deviation of the tongue to the side of the lesion due to the unopposed action of intact genioglossus (assisted by geniohyoid) muscle
c.Atrophy of ipsilateral muscles
d.Fasciculations ipsilateral to the lesion.
2.Upper motor neuron lesions of corticobulbar to contralateral hypoglossal nucleus results in:
a.Contralateral paresis in tongue muscles
b.Deviation of the tongue to the side opposite the lesion due to the unopposed action of intact genioglossus muscle
c.Disuse atrophy over time.
d.No fasciculations.

37. CN XII Lesions Contra UMN lesion OR Ipsi LMN lesion Contralateral CBs
If L contract all by itself  tounge goes to R
If contract and same time  tounge stick out
R cortex lesion  L nucleus can’t get signal  right nucleus predominates  tounge goes to L (the side of weakness) Vs
Lesion of L nucleus, L is weak,  side of weakness therefore tounge goes to L
The touge does not always point to the side of the lesion, but always points to the side of weakness (contralateral if UMN weakness, and ipsilateral if LMN weakness)
TOUNGE ALWAYS GOES TOWARDS SIDE OF WEAKNESS
Contralateral CBs
NORMAL

38. Alternating Hemiplegias
Classic brainstem = alternating hemiplegias (half weak)
Have one in medulla, pons, and midbrain
Due to stroke
Get upper motor neurons symptoms  Corticospinal system of the body
Get Lower motor neurons symptoms cranial NS (for whatever the nerve innervates)
Terreberry’s notes:
This is the hallmark of brainstem lesions, and involves cranial nerves (nuclei in the brainstem or the fibers of the n) and the corticospinal tract where they course in close proximity to one another in the brainstem.
NOTE: Certain brainstem lesions will also result in crossed sensory findings for the body vs. the head. Alternating (dissociated) sensory findings for the body (excluding the head) are the hallmark of spinal cord lesions.
A. Alternating hemiplegias – involves a lesion of a cranial n and the corticospinal tract. Usually associated with paramedian lesions that interrupt the corticospinal tract and a cranial n that is exiting the brainstem at that level.
Ipsilateral LMN signs for the cranial nerve
Contralateral UMN signs for the corticospinal tract.

39. Alternating Hemiplegias Contra UMN Signs Paresis (generalized)
Increased DTRs
Increased muscle tone
Spasticity
Babinski sign present
Clonus may be present
Disuse atrophy
Alternating oculomotor hemiplegia
Also known as “Weber’s syndrome”
Associated with infarct of the basal branch of the posterior cerebral a, and involves the medial portion of the ventral midbrain.
LMN signs for ipsilateral oculomotor nerve
Contralateral UMN signs for the ipsilateral corticospinal tract (rostral to the decussation).

40. Alternating Hemiplegias Contra UMN Signs Paresis (generalized)
Increased DTRs
Increased muscle tone
Spasticity
Babinski sign present
Clonus may be present
Disuse atrophy
Alternating abducens hemiplegia
Associated with infarct of the pontine branches of the basilar a, and involves the medial portion of the ventral caudal pons.
LMN signs for ipsilateral abducens nerve
Contralateral UMN signs for the ipsilateral corticospinal tract (rostral to the decussation).

41. Alternating Hemiplegias Contra UMN Signs Paresis (generalized)
Increased DTRs
Increased muscle tone
Spasticity
Babinski sign present
Clonus may be present
Disuse atrophy
Alternating hypoglossal hemiplegia
Also known as “medial medullary syndrome”
Associated with infarct of the paramedian branch of the anterior spinal a., and involves the medial portion of the ventral medulla.
LMN signs for ipsilateral hypoglossal nerve
Contralateral UMN signs for the ipsilateral corticospinal tract (rostral to the decussation).
Contralateral loss of tactile sensation and conscious proprioception due to loss of ipsilateral medial lemniscus.

42. Questions??