Lecture 7 - Cranial Nerves l-Vl Flashcards
What do CN’s supply, where are they located & what system are they apart of?
What are the 4 types of fibres that they carry?
- Supply tissues & structures of H&N including sense organs. Nuclei located within the brainstem, part of the PNS.
1) Mixed (sensory + motor)
2) Sensory only
3) Motor only
4) Parasympathetic
What are the general 3 areas where lesions can occur affecting CN’s and the structures they innervate?
1) The brainstem (where nuclei is located)
2) The CN during its route outside of the CNS
3) The tracts within forebrain that communicate with CN’s (e.g.: from PMC on contralateral side)
Where are each of the 12 CN’s located? (Use 2, 2, 4, 4)
2 - from the forebrain (olfactory & optic)
2 - from the midbrain (oculomotor & trochlear)
4 - from the pons (trigeminal, abducens, facial, vestibulocochlear)
4 - from the medulla (glossopharyngeal, vagus, accessory, hypoglossal)
How is CN l (olfactory) function tested?
What is the most common cause of lesions/malfunction?
Describe the course of the olfactory nerve
- Not routinely tested, ask if sense of smell is gone (if tested, 1 nostril at a time). No smell = Anosmia
- Most common cause is URT infection, but also head/facial impact or anterior cranial fossae tumours.
- Olfactory nerves travel through cribriform plate perforations in anterior fossae to reach nasal cavity (now olfactory bulb). Past olfactory bulb known as olfactory tract received by temporal lobe.
How is CNll (optic) function tested?
What are the most common cause of CNll lesions?
- Test pupillary light reflex, visual acuity (Snellen chart), visual fields or check appearance of CNll with ophthalmoscope
- Any disease involving CNll, e.g.: optic neuritis or anterior ischaemic optic neuropathy (see papilloedema (optic disc swelling) on ophthalmoscope due to raised ICP)
Describe the course of the visual pathway from the retina to the primary visual cortex in the occipital lobe?
- Rods & cones communicate with retinal ganglion cells which come together to form optic nerves.
- Optic nerves exit orbit via optic canal, fibres merge and cross at the optic chiasm
- This forms optic tract which carries information from both eyes on both sides
- Optic radiation communicates with the primary visual cortex in occipital lobe
How do different lesions within visual pathway affect vision?
What can compress the optic chiasm and cause bitemporal hemianopia?
- Different lesions give different patterns of visual loss
- Pituitary tumours compress optic chiasm, giving bilateral visual symptoms
What fibres does CNlll (oculomotor) carry & what are their target tissues?
How is CNlll function tested?
What are the examination signs of a CNlll lesion?
- Carries motor & parasympathetic fibres. Innervates 4 of the 6 extra-ocular muscles, levator palpebrae superioris & sphincter papillae
- Infect resting eye gaze, eye movements, eyelid position & pupillary light reflex
- Ptosis (droopy eyelid), “down & out eye”, pupil may or may not be dilated depending on cause
What are the 2 main categories of causes for CN lll lesions?
Which of these involves the pupil?
1) Microvascular ischaemic (pupil sparing) - blood vessels affected due to diabetes/hypertension.
2) Compressive (pupil involving) - aneurysm of posterior communicating artery, head injury or tentorial herniation (free edge squeezing nerve) secondary to raised ICP
Explain why microvascular causes of CN lll lesions spare the pupil but compressive causes do not
- Microvascular diseases typically affect vasa nevorum, put parasympathetic fibres have back up supply from pial blood vessels so pupil not affected.
- Compressive causes affect pial blood vessels as well, so pupil will be involved
What type of fibre does CN lV (trochlea) carry & what muscle does it supply?
How in function tested & what are symptoms of CN lV lesions?
What are the common causes of CN lV lesions?
- Motor only to the superior oblique muscle of the eye
- Inspect resting gaze/eye movements, lesions cause diplopia (double vision), abnormal eye position (eye moves upwards) & head tilt (to compensate)
- Microvascular ischaemia (diabetes/hypertension), trauma (even minor) or tumours
What type of fibre does CN Vl (abducens) carry & which muscle does it supply?
How is function tested & what are signs of a lesion?
What are the common causes of CN Vl lesions?
- Motor, supplying lateral rectus muscle only
- Resting gaze & eye movements, diplopia, abnormal eye position & inability to move affected eye laterally
- Microvascular ischemia (hypertension/diabetes), head injury, tumour, raised ICP
Why is the abducens nerve vulnerable to increased ICP?
- Arises from lower part of pons (ponso-medullary junction) and must rise steeply to enter the cavernous sinus, before entering the orbit through the superior orbital fissure
- If ICP is increased things are pushed downwards, stretching the nerve
CN’s lll, lV & Vl all supply eye muscles, what is the common location in their routes?
- All exit brainstem from slightly different levels
- All pass through the cavernous sinus
- All enter the orbit via the SOF (just underneath lesser wing of sphenoid)
What fibres does the CN V (trigeminal) carry & what are the target tissues?
What are the signs of CN V lesions?
What are some causes of CN V lesions?
- Motor & general sensory, innervates muscles of mastication, corneal reflex & supplies sensory innervation to Va, Vb & Vc divisions
- Sensory deficits in dermatomal regions, weakness of muscles of mastication & abnormal corneal reflex
- Trigeminal herpes zoster (e.g.: shingles), trigeminal neuralgia, orbital/mandibular fractures & posterior cranial fossae fractures
What pathways do the individual divisons of the trigeminal nerve take?
- Va & Vb both pass through cavernous sinus
- Va passes through S.O.F
- Vb passes through foramen rotundum
- Vc passes through foramen ovale
