Cranial Nerves Flashcards
Causes of Optic Neuropathy
If <50, most likely demyelinating cause (e.g. MS, NMO)
If > 50, most likely ischaemic cause e.g. GCA
Inflammatory Causes
- Sarcoidosis, vasculitides
Infective Causes
- Syphilis, TB, lyme disease
Compressive Causes
- Tumours (e.g. Optic glioma), dysthyroid eye disease, pituitary tumour
B12 Deficiency
Toxic Causes
- Methanol, Ethambutol
Optic Neuropathy - Features
Subacute loss of vision
- Usually painless
Reduced visual acuity, especially central
Afferent pupillary defect
Pale optic disc +/- cupping
Function of CNIII
CN III = oculumotor nerve
Controls 4 of the 6 extraocular muscles
(MR, IO, SR and IR)
Pupil constriction and accommodation (parasymp)
Eyelid opening (levator palpebrae)
Features of a Compressive (“Complete”) CN III Palsy
Complete ptosis
Pupil on affected side dilated and non reactive to light
Eye on affecting side “down & out”
{Why?
- Parasympathetic fibres responsible for pupillary response are on outside of nerve and most superficial = affected by compression!}
Features of a “Medical” CN III Palsy
(Partial)
Complete/partial ptosis
Pupil on affected side is normal and reacts to light
Eye “down and out”
Parasympathetic nerve fibres on CNIII have different blood supply
Medical causes of a CN III palsy
Diabetes Mellitus
MS
Vasculitides
Amyloidosis
Ischaemic stroke
- If also has contralateral hemiparesis = Weber’s (midbrain stroke)
Investigating CN III palsy
Key Qs - is it compressive? are there other palsies present?
COMPRESSIVE LESION
- Urgent MRI/MRA/CT angiogram
- Neurosurgical input
Rx depends on lesion found
SOLITARY PUPIL SPARING CN III PALSY
- Cardiovascular work up = ECG, BP, glucose, Hb1AC, lipids
- Optimise CVD RFs
- If not resolved in 3 months or no obvious CVD RFs = vasculitis screen and MRI (?MS)
Differentials for Ptosis
UNILATERAL PTOSIS
CN III palsy
Horner’s syndrome (constricted pupil)
BILATERAL PTOSIS
Myasthenia gravis (usually bilateral, fatiguability)
Myotonic dystrophy (usually bilateral)
Congenital
Miller- Fischer
Function of CN IV
= Trochlear nerve
Controls Superior Oblique extraocular muscle (SO4) = depression, intorsion and adduction of the eye
Longest intracranial nerve
Features of CN IV Palsy
Affected eye is “upwards and outwards”
Head tilt away from affected side
Defective downward gaze = vertical diplopia (exacerbated by walking downstairs/reading)
Failure of intorsion
- “Follow my finger” as you draw an upwards arc from pts ear to nose
Function of CN VI
= Abducens palsy
Controls Lateral Rectus muscle (LR6) = ABduction
Adbucens nucleus = in pons
Features of CN VI palsy
Affected eye rests in adduction
Inability to abduct affected eye
Horizontal diplopia
Internuclear Ophthalmoplegia
Due to damage to medial longitudinal fasciculus (MLF)
= connection between nuclei of CN III and VI
Can be demyelinating, ischaemic, neoplastic or inflammatory lesion in pons/midbrain
FEATURES
- Inability to adduct affected eye (ipsilateral)
- Nystagmus in contralateral eye when trying to look to affected side
Function of CN V
= Trigeminal nerve
Facial sensation
Muscles of mastication
Corneal reflex
Function of CN VII
= Facial Nerve
“Face, ears, taste, tears”
- Muscles of facial expression
- Stapedius (loud noises)
- Anterior 2/3 of tongue
- Lacrimal and salivary glands
Features of CN VII Palsy
Facial muscle weakness
- Forehead sparing if UMN
Bell’s phenomenon
= eye rolls upwards when trying to close eye (LMN)
Reduced sense of taste
Sensitive to loud noises (hyperacusis!)
Causes of LMN CN VII Palsy
Idiopathic (Bell’s palsy)
Ramsay Hunt Syndrome (Herpes zoster)
Diabetes
Infection - HIV, lyme disease, TB
Sarcoidosis
Vasculitides
Space Occupying lesion
- Acoustic neuroma
- CPA tumour
- Parotid tumour
GBS
Causes of UMN CN VII Palsy
Lesion of CN VII nucleus e.g. stroke, MS, space occupying lesion
Is a UMN facial nerve palsy or LMN facial nerve palsy “forehead sparing”?
UMN is forehead sparing
- CN VII nucleus for upper face receives input from both cerebral hemispheres
Bell’s Palsy
Idiopathic facial nerve palsy
LMN
Increased risk if
- HTN, diabetes, pregnant, FHx, black/hispanic ethnicity
FEATURES
- Rapid onset <72 hours
- Facial muscle weakness (NO forehead sparing)
- Facial/ear/postauricular pain
Difficulty chewing
Change in taste sensation
Incomplete eye closure
Bell’s phenomenon
Hyperacusis
MANAGEMENT
Prednisolone e.g. 60mg for 5 days
Eye care e.g. tape, drops
If untreated 15% have permanent facial weakness
Red flag features in Bell’s Palsy
UMN features e.g. ataxia, limb weakness
Painful facial paralysis
Suspicious head and neck lesion
Unilateral hearing loss (?involvement of CN VIII)
Bilateral
No improvement after 3 weeks
Recurrent
Systemically unwell
Function of CN VIII
= Vestibulocochlear nerve
Hearing and balance
Function of CN IX
= Glossopharyngeal nerve
Posterior 1/3 of tongue taste
Pharyngeal muscles
(Muscles of swallowing and speech)
Function of CN X
= Vagus nerve
Provides motor innervation to the majority of the muscles of the pharynx, soft palate and larynx
(Muscles of swallowing)
Innervates the smooth muscle of the trachea, bronchi and gastro-intestinal tract and regulates heart rhythm
Function of CN XI
= Accessory Nerve
Sternocleidomastoid and trapezius muscle movement
= turning head and shrugging shoulders
Function of CN XII
= Hypoglossal nerve
Motor innervation of the vast majority of the muscles of the tongue
- Tongue deviates towards side of lesion
