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Neurology= Clinical Medicine > Cranial Nerve Disorders > Flashcards

Cranial Nerve Disorders Flashcards

1
Q

How many cranial nerves are there?

A

12 pairs

4 cr nerves above the pons-4 in the pons and 4 below.

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2
Q

4 medial structures

A
  1. motor nuclei 3/4/6/12
  2. motor tract = pyramidal tract
  3. MLF
  4. medial lemnicus
    basilar and vertebral
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3
Q

4 lateral structures

A

1-Symapthetics)
(2-spinothalamic)
(3- spinocerebellar)
(4- sensory nuc. Of cranial nerve V)

Post. Cerebral Art/Sup cerebellar Art/Anterior. Inferior cerebellar Art/ Post. Inferior cerebellar artery

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4
Q

Cranial Nerve 1

A

origin= olfactory tracts

descends into nares through cribiform plate

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5
Q

What is cranial nerve 1 associated with?

A

smell and most of taste
is easily damaged with trauma
will decrease with age

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6
Q

Cranial Nerve 2

A

vision

uni or bilateral

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7
Q

Unilateral issues with cranial nerve 2–> look for?

A

Unilateral ddx- refraction: test with pin hole
Media contact lens/cornea/eye lens /vitreous
Retinal/Macular: respects a horizontal meridian or + amsler grid which reviews the center 10 degrees of vision
Optic nerve –afferent pupillary defect (APD)=Marcus Gunn pupil/red desaturation/acuity loss
Functional
Amblyopia

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8
Q

Bilateral loss with cranial nerve 2–> look for?

A

Bilateral loss is chiasmal/optic tract/lateral geniculate/optic radiation/occiput
Rules: Field defects are more congruous the more posterior
: visual acuity is spared in far posterior lesions
: vascular retinal lesions tend to show field defects top or bottom –respecting a horizontal meridian chiasmal and posterior lesions cause R/L defects respecting a vertical meridian

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9
Q

Optic Neuritis (6)

A

“Pt sees nothing—Practitioner sees nothing”’
If at nerve head- disc edema (field defect+)
If retrobulbar-nl disc on exam (field defect +)
Can be painful- most are Fast onset hrs/day
18 % progress to MS
No etiology-immune mediated-treated with IV not oral steroids-usually unilateral-many resolve with no tx-
Atypical if :age >50,disc pallor at presentation, painless, slow progression over weeks, systemic symptoms (fever, malaise, wt loss etc.)

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10
Q

Diplopia rules for cranial nerve 3-4-6

A

Diplopia study is best done with an eye model or picture of globe and muscles insertion
Head trauma can cause dysfunction of any of these nerves (3-4-6) and 6 is most common
Ischemia is most likely (microvascular) in older age groups and pain can be a big problem

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11
Q

Cranial Nerve 3 anatomy

A

midbrain nucleus (Medial divides into 1/2) –Runs 4 ocular muscles and parasympathetics and levaltor palpebri

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12
Q

Most common and most deadly for cranial nerve 3

A

Most common “Pupillary Sparing Diabetic Third”
Most deadly- PCOM (posterior communicating artery) aneurysm pressure “Blown pupil and the Lid is down”
Can be more painful ischemic than compressive
Given third nerve weakness the lateral rectus rules—Eye is Abducted

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13
Q

what are you thinking with Cranial nerve 4 dysfunction?

A

Vertical diplopia – likely from a 4th nerve ischemia or trauma—tumor less common

Beware of myasthenia which can present with dysfunction of one muscle however!
Thyroid disease also can present with one muscle defective early-can mimic 3/4/6

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14
Q

Cranial nerve 5 (3)

A

Lateral rectus function
Long course lends to problems from trauma and tumors and intracranial pressure
Common pressure issues with #6 happen with Idiopathic intracranial hypertension- bending over and getting up/low csf pressure arising from supine

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15
Q

Cranial nerve 5 common disturbance

A
  1. Trigeminal neuralgia- unilateral in most-idiopathic in most- trigger points common-any division or all-
  2. zoster V1 is most intense
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16
Q

Treatment for trigeminal neuralgia

A

Tx gamma knife and Jenetta proceedure-lancinating pain- refractory to narcotics
rx anticonvulsants

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17
Q

Treatment for zoster

A

acyclovir

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18
Q

Cranial Nerve 7

A 
Facial motor function
Most common disorder Bell’s Palsy
Onset facial numbness common
Abrupt facial weakness incl forehead
treat with steroids
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19
Q

CPA tumor

A

freq meningioma /epidermoid/acoustic
Best physical sign is loss of corneal reflex V-1
loss of hearing– crn 8

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20
Q

Cranial Nerve 8

A

Auditory and starting in Middle ear
Hearing/tinnitus from cochlea
Balance from Semicircular canals

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21
Q

Cranial nerve 9 & 10

A

Motor and Sensory to throat

Glossopharyngeal neuralgia

22
Q

Cranial nerve 11

A

Runs the Trapezius
Unilateral defect with neck surgery/trauma (Hod carrier )
uncommon

23
Q

Cranial nerve 12

A

Tongue motor
Sensory is CN V3
Genioglosssus protrudes the tongue
Atrophy occurs with motor neuron disease
deviates to the side of the stroke/lesions

24
Q

CN 1- Olfactory 3 MC causes

A 
Anosmia – Loss of sense of smell
Most common causes:
Trauma (shearing of “bulb”)
Olfactory groove Meningioma - surgical
Neurodegenerative Disease
25
Q

CN 1- Olfactory Clinical Presentation

A

Usually presents as loss of taste

Loss of smell picked up on examination

26
Q

CN 1- Olfactory- Neurodegenerative Disease

A

Alzheimer’s & Parkinson’s – early symptom / sign – loss of smell -? Predictor of impending disease??
Insufficient data to use this as a reliable predictor
Tx: address underlying cause if possible.

27
Q

CN II- Optic Nerve= Optic Neuritis clinical presentation (6)

A

Sudden onset of ocular pain (severe)
Followed by decreased central vision or central vision loss
Most common women 25 – 45 yrs. old
Idiopathic in nature or demyelinating disease
Presence of a RAPD (Relative Afferent Pupillary Defect) – Marcus Gunn Pupil
Usually resolves spontaneously

28
Q

Optic Neuritis treatment

A

Steroids sometimes used
W/U Pt for demyelinating disease (MS)
MRI looking for white matter lesions
10 – 20% chance of occurring again or in other eye

29
Q

2 Types of Ischemic optic neuropathy

A

Arteritic – secondary to Temporal Arteritis

Non-arteritic – secondary to cerebrovascular disease

30
Q

Vitamin B12 Deficiency (4)

A

Characterized by cognitive changes
Change in level of consciousness
Inattention, confusion, somnolence, apathy
Ocular finding is BILATERAL optic neuropathy – loss of central vision – greater loss of color than black and white vision.

31
Q

Ischemic optic neuropathy- Arteritic

A

Temporal Arteritis / Vasculitis
Complication of DM, HTN, or increased cholesterol
Causes visual loss – less common

32
Q

Ischemic optic neuropathy- NON Arteritic

A 
Usually painless and temporary visual loss
RAPD present
Disc is usually hyperemic (reddened) 
Flame hemorrhages may be present
Symptoms usually improve spontaneously
33
Q

What does Horners syndrome result from

A

Results from loss of sympathetic innervation of the eye
Classic symptoms: ptosis, miosis (small pupil), anhidrosis (lack of sweating) on ipsilateral face
Many different causes possible
Often results in anisocoria

34
Q

How to diagnose/ treat horners syndrome?

A

MRI usually helpful

Treat the causal lesion if possible

35
Q

3rd occular nerve palsy

A

controls pupil constriction, superior and inferior gaze and medial (nasal) gaze. III Nerve palsy = dilated non-reactive pupil

36
Q

6th occular nerve palsy

A

controls lateral (temporal) gaze

37
Q

4th occular nerve palsy

A

hard to see on exam (pts will note diplopia when looking downward)

38
Q

Internuclear Ophthalmoplegia

A

Often associated w/MS
Localizes lesion to the Medial Longitudinal Fasciculus (MLF)
Pt has WEAK adduction of affected eye (cannot gaze nasally) with abduction nystagmus of the contralateral eye
pt can converge**

39
Q

Trigeminal Neuralgia

A

Sudden, severe, unilateral lancinating facial pain
Most common in V2 and V3 branches (cheek / chin)
Pain can be spontaneous or triggered (so called trigger zones)
Touching the face, washing, shaving, chewing, talking, even wind/breeze on the face can trigger
Common after 50

40
Q

Medical Treatment for Trigeminal Neuralgia

A

aimed at controlling attacks with a minimum of side effects
Anti-epileptic meds w/analgesic properties
Carbamazepine was first line – newer agents used now like:
Gabapentin, Baclofen, Na Valproate, Oxcarbazepine, Topiramate

41
Q

Surgical Treatment for Trigeminal Neuralgia

A

initiated only if medical treatments fail
Gamma Knife Radiosurgery (GKRS) – produces controlled injury of the trigeminal nerve (knock out pain fibers but preserve sensation)
Percutaneous procedures i.e., thermal rhizotomy, balloon compression of the nerve

42
Q

2 common facial nerve problems

A

bells palsy

ramsey hunt syndrome

43
Q

Bells palsy

A

Unilateral facial weakness
Affects upper and lower face
Facial weakness of lower face = central facial weakness (typical of stroke)
Facial weakness of upper and lower is peripheral weakness seen in BP – can’t close eye
Facial sensation (CN V) is spared

44
Q

Treatment and Diagnose for bells palsy

A

Diagnosis: Hx & PE (some have day or two of auricular pain prior to BP)
Tx: corticosteroids, anti-virals (i.e. acyclovir)

45
Q

Prognosis of bells palsy

A

majority of pts have full resolution but could take weeks or months – some have a degree of residual weakness

46
Q

Ramsey Hunt Syndrome

A

RHS is caused by Varicella Zoster virus of the geniculate ganglion – results in Facial Nerve palsy
Geniculate ganglion is neurons in the facial nerve found in the facial canal.
Sensory fibers of the facial nerve so RHS frequently affects taste

47
Q

Ramsey Hunt Syndrome Treatment

A

Corticosteroids
Acyclovir for certain w/RHS
Most pts recover fully but some residual symptoms can remain

48
Q

2 component of the acoustic nerve

A

auditory nerve

vestibular nerve

49
Q

Acoustic Neuroma/ Vestibular Schwannoma

A

Benign tumor of the vestibular portion of the Acoustic (VIIIth nerve)
Increased incidence in pts with neurofibromatosis

50
Q

presentation of acoustic neuroma

A

ipsilateral hearing loss, vertigo and tinnitus
Because of proximity of CN VII many pts will have an ipsilateral facial weakness
MRI can localize tumor to the CP angle in the posterior fossa of the brain

51
Q

treatment of acoustic neuroma

A

surgery is the only significant Tx approach

Neurosurgery and ENT team to remove tumor from cerebello-pontine angle

Neurology= Clinical Medicine (6 decks)

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