Approach to CN9, CN10, CN11, CN12 Palsy

Question 1

CN 9 - glossopharyngeal nerve (mixed)

Answer 1

Innervations
1. Stylopharyngeus muscle: raises pharynx and larynx during swallowing
2. Sensory: posterior one-third of tongue, tonsils and pharynx
3. Parasympathetic: saliva production (parotid gland)

Pathway
1. Medulla (nuclei)
2. Exits via jugular foramen (along CN 9, 10, 11)

Defects
1. Loss of taste and sensation on the posterior 1/3 of the tongue, upper pharynx, tonsils.
2. Loss of gag reflex (afferent).
3. Dysphagia
4. Loss of carotid sinus reflex (labile BP)
5. Dry mouth (xerostomia)
6. Glossopharyngeal neuralgia: Paroxysmal severe pain in the throat, ear, back of tongue, triggered by swallowing or talking.

Question 2

CN 10 - vagus nerve (mixed)

Answer 2

Innervations
1 Motor: soft palate and pharynx for phonation and swallowing
2. Sensory: external ear, larynx and pharynx
3. Parasympathetic: reduces heart rate, stimulates peristalsis

Pathway
1. Medulla (nuclei)
2. Exits via jugular foramen (along CN 9, 10, 11)

Deficits
A. Unilateral:
1. Uvula deviation away from the lesion
2. Palatal droop on the affected side,
3. Hoarseness/breathy voice
4. Dysphagia
5. Loss of gag reflex (efferent)

B. Bilateral:
1. Severe dysphagia, choking, nasal regurgitation,
2. Bilateral vocal cord paralysis (stridor)
3. Autonomic dysfunction (worse in brainstem lesion).

Question 3

CN 11 - accessory nerve (motor)

Answer 3

Innervations
1. Laryngeal/pharyngeal muscles
2. Sternocleidomastoid (SCM) and trapezius muscles

Pathway
1A. Cranial nerve root - medulla (nucleus ambiguus)
1B. C1-C5/6 Spinal Cord (spinal accessory nucleus)
2. Spinal root ascends through foramen magnum, joins with cranial root then exits skull via jugular foramen

Deficits
1. Head turning weakness away from the side of the lesion (SCM)
2. Shoulder shrug weakness on the affected side (trapezius).
3. Shoulder droop on the affected side.
4. Winging of the scapula on arm abduction > 90 degrees
5. SCM and Trapezius muscles atrophy.
6. Shoulder pain or discomfort

Question 4

CN 12 - hypoglossal nerve (motor)

Answer 4

Innervations
1. Intrinsic and extrinsic tongue muscles
- Intrinsic: tongue shape
- Extrinsic: genioglossus (protrusion), hyoglossus (depression), styloglossus (retraction/elevation)

Pathway
1. Medulla (hypoglossal nucleus)
2. Exits via hypoglossal canal

Deficits
1. Tongue protrusion - deviation towards the side of the lesion
2. Atrophy of affected side of the tongue.
(Be aware of pseudobulbar palsy - deviation way from side of lesion)
3. Fasciculations on the affected side.
4. Dysarthria, thick or slurred speech.
5. Oral dysphagia - difficulty manipulating food bolus within mouth

Question 5

Testing of bulbar cranial nerves

Answer 5

Testing of CN9 and CN10 is combined
1. Palatal and uvula deviation
- Open mouth, say “ahhhh”
2. Gag reflex (not usually tested in PACES)
- Tongue depressor gently and deliberately touch pharyngeal wall or either side tonsillar pillars (test both sides)
- Patient will gag (elevate and constrict phayngeal muscles, elevate soft palate, retract tongue)

Testing of CN11
1. Sternocleidomastoid muscle
- Turn your head to one side then the other, palpate SCM muscles
2. Shoulder shrug - trapezius
- Shrug shoulders, push down against them

Testing of CN12
1. Tongue deviation
- Stick out your tongue
2. Tongue weakness
- Push tongue against cheeks

Question 6

Bulbar palsy is a lower motor neuron lesion of cranial nerves from medulla oblongata bulb involving CN 9, 10, 11, 12.

There is direct damage to nerve nuclei in brainstem or peripheral nerves resulting in denervation of supplied muscle.

Causes:
1. Motor neuron disease - ALS, PBP
2. Guillain-Barre syndrome
3. Myasthenia gravis
4. Brainstem stroke or tumour (Wallenberg)
5. Kennedy’s disease (SMA, bular muscular atrophy)
6. Infections (polio, diphtheria)

Question 7

Pseudobulbar palsy is caused by bilateral damage to UMN over corticobulbar tracts.

Corticobulbar tracts descend from cerebral cortex and synapse onto LMNs in brainstem nuclei.

Almost all bulbar muscles receive bilateral UMN innervation (thus bilateral lesion to cause pseudobulbar palsy)
(Exception lower face, tongue)

Causes:
1. Bilateral strokes (cortical, subcortical, pons/midbrain stroke)
2. Motor neuron disease (mixed UMN/LMN)
3. Multiple sclerosis
4. Traumatic brain injury
5. Progressive supranuclear palsy
6. Central pontine myelinosis
7. Brain tumour affecting bilateral pathways

Question 8

Differences between bulbar palsy and pseudobulbar palsy

Answer 8

Question 9

Clinical features of bulbar palsy (LMNL)

Answer 9

1. Dysphagia and nasal regurgitation
2. Dysarthria - flaccid, slurred, hypernasal
3. Dysphonia
4. Tongue wasting and fasciculation
5. Soft palate weakness (on saying “aaah”)
6. Reduced/absent gag reflex
7. Absent jaw jerk

Question 10

Clinical features of pseudobulbar palsy (UMNL)

Answer 10

1. Dysphagia
2. Dysarthria - spastic, slow strained speech, poor articulation
3. Stiff, spastic, slow moving tongue
4. Sluggish palate
5. Hyperactive gag reflex
6. Brisk jaw jerk
7. Pseudobulbar affect (emotional lability) - uncontrollable laughing/crying