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NOP > CRANIAL NERVES > Flashcards

CRANIAL NERVES Flashcards

1
Q

causes of anosmia

A

• Head injury (cribriform plate) → ipsilateral anosmia
• Tumours in the frontal, temporal lobes
• Parkinsons disease
• Rare congenital:
o Congenital anosmia secondary to cleft palate in males
o Familial dysautonomia
o Turner syndrome
o Kallmann syndrome: hypogonadothropic hypogonadism

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2
Q

eye examination sequence

A

EYE EXAMINATION (II,III, IV, VI)

  1. Inspection:
  2. Visual acuity each eye separately: ●Snellen ●Close distance
  3. Colour vision
  4. Visual fields: ● with both eyes open: sensory lesions above thalamus (cortical) produce CONTRALATERAL inattention ●individual eye’s fields ●blind spot
    a. Visual field are described from patient’s point of view
  5. Eye movements: ●H-test
  6. Pupils
    a. Accommodation
    b. Light reflex
    c. Fundoscopy
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3
Q

pupillary reflex arc

A
  • Aff: light perception: CNII
  • Eff: pupillary constriction – PNS ofCNIII
  • bypasses lateral geniculate body & the cortex
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4
Q

does pupillary light reflex pass through lateral geniculate body and the cortex?

A

no, bypasses it

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5
Q

corneal reflex ars

A
  • Aff: corneal sensation – Vi

* Eff: blinking – CNVII

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6
Q

gag reflex

A
  • Aff: laryngeal sensation – CNIX

* Eff: gag – CNX

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7
Q

qccommodation reaction pathw

A

Aff: frontal lobes, ●Eff: PNS of CNIII

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8
Q

on general inspection of eyes

A

● Ptosis: complete/partial
!!Ptosis is NOT a feature of CNVII palsy – in facial nerve palsy the eye doesn’t close
● Ocular deviation
● Pupils: shape, regularity, size, asymmetry
● Proptosis

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9
Q

how to measure visual acuity and troubleshooting

A 
Always inspect with glasses or through pinhole – any uncorrected visual loss can then be assumed to be neurological rather than refractive
If cannot read any letters: 
● CF (count fingers 1m), 
● HM (hand movements 30cm), 
● PL (perception of light)
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10
Q

abnormal eye position in CNIII palsy

A

eye is down and out position on primary gaze. Limited movement in all directions except abduction, associated may be ptosis and pupil dilatation

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11
Q

eye position in CNIV pal

A

affected eye cannot look down and in

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12
Q

what movement affected by CNVI palsy

A

limited abduction

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13
Q

Voluntary eye movements (saccadic) initiated in …

A

frontal eye fields

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14
Q

pursuit is controlled by

A

occipital lobe

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15
Q

vestibulo-ocular reflex is controlled

A

in the cerebellum

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16
Q

converge is controlled in

A

????

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17
Q

which reaction is stronger: pupillary to light or to accommodation?

A

to accommodation

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18
Q

Weakness of the extraocular muscles results in double vision in which direction

A

in the direction od movement of that muscle

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19
Q

in double vision, which image arises from the affected eye

A

the outer image is from the affected eye

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20
Q

DDx ptosis

A
  1. congenital
  2. \horner’s (always PARTIAL ptosis)
  3. CNIII palsy (usually complete)
  4. Myasthenia Gravis (usually complete)
  5. Myopathy
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21
Q

eye movements in the internuclear ophthalmoplegia

possible ddx in uni or bi-lateral ION

A

caused by a lesion in the medial longitudinal fasciculus. May be damaged by demyelination (MS)
(usually bilateral) or vascular disease (uniloateral). Produces horizontal diplopia and reduces adduction on the side of the lesion and nystagmus on the contralateral abducting eye.

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22
Q

in internuclear ophthalmoplegia, can the eyes move medially (adduction) when converging?

A

YES, convergence is preserved

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23
Q

jerky VERTICAL NYSTAGMUS is due to…

A

brinstem leasion.
if upbeat : lesion in the midbrain or floor of 4th ventricle
downbeat nystagmus : foramne magnugm lesion, phenytoin or alscohol also

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24
Q

what do you need to do when examining the pupils?

A

● Symmetry of pupils, regularity of shape
● Direct reflex + Consensual reflex when the patient is looking into the distance
If no response from shining a light into the eye, but there is normal response on accommodation – this is AFFERENT papillary defect, indicates significant optic nerve disease.
● Accommodative reflex
● Exclude RAPD (swinging light) – partial CNII damage → intensity and speed of reflex are ↓

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25
Q

what is the likely cause of intact accommodation with absent light

A

Argyll Robertson pupils (pupils small and irregular) in diabetes and neurosyphilis.

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26
Q

a larger, regular, reacting sluggishly to accommodation but NO direct or consesual response to lpupil is…

A

holmes-aldie pupil

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27
Q

ophthalmoscope: what lens to use if the pt is shortsighted

A

(-) anticlockwise (red)

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28
Q

ophthalmoscope: what lens to use if the pt is farsighted

A

clockwise Green (+)

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29
Q

where is the optic disc in relation to the macula\?

A

optic disc is 15degrees medial to hte macula

30
Q

background diabetic retinopathy appearane

A

dot blood haemorrhages
miscroaneurysms
soft exudates

31
Q

pre-proliferative diabetic retinopathy appearance

A

hard exudates
intraretinal microvascular abnormalities
cotton wool spots

32
Q

proliferative diabetic retinopathy appearnce

A

neovascularisation on the disc or in the retine

33
Q

hypertensive retinopathy features

A 
AV nipping
silver wiring
flame shaped haemorrhages
exudates
cotton wool spots
blurred disc margin
34
Q

central renal artery occlusion appearance

A

retinal pallor,
affects all four quadrants
cherry-red spots
central retinal vein occluson appearance

35
Q

central retinal vein occluson appearance

A

dialted tortuous veins, widespread haemorrhage

cotton wool spots

36
Q

causes of CNIII palsy

A 
SURGICAL
•	Generally affect the pupil
•	Posterior communicating artery aneurysm
•	SOL  in midbrain/sphenoid wing near cavernous sinus
•	Haemorrhage
MEDICAL
•	Often pupil is unaffected
•	Causes of mononeuritis multiplex (MM)
•	Demyelination	
•	Infarction
37
Q

causes of VI palsy

A
  • Causes of MM
  • Vascular lesion
  • Malignancy
  • Demyeliantion
  • Infection – lyme disease, syphilis
  • Raised ICP
  • Wernickes encephalopathy can cause palsy bilaterally
38
Q

causes of internuclear ophthalmoplegia

A

MS

vascular disease/event

39
Q

afferent pupillary defect meaning and DDx

A
  • Pupil unreactive to light (direct reflex is absent)
  • Consensual reflex is absent
  • Indicates a complete optic nerve lesion - causes dilated pupil
40
Q

RAPD meaning (pathology) and D

A
  • Incomplete damage to one optic nerve
  • Direct and indirect reflexes are intact in each eye but differ in relative strength
  • When light is swung from one eye to the other, the affected eye dilates slightly when illuminated and constricts when unaffected eye is illuminated (consensual stronger than direct reflex in affected)
41
Q

sparing of the pupil in CNIII palsy: ddx and pathology

A

PNS fibres undamaged (run in a discrete bundle on the surface of the nerve). Diabetic CNIII infarction is usually painless and pupil sparing, unlike compression by a PCA aneurysm

42
Q

complete external ophthalmoplegia ddx

A

COMPLETE EXTERNAL OPHTHALMOPLEGIA: immobile eye when III, IV, VI nerves are paralysed at the orbital apex or within the cavernous sinus (thrombosis or meningioma).

43
Q

CNV lesion findings

A

o Complete lesion causes unilateral sensory loss on the face, anterior 2/3 of tongue and buccal mucosa. Jaw deviated to the side of lesion when opened.
note that the angle of jaw is supplied by C1
and teh V1 goes up on the top of the head all the way to the vertex

44
Q

CNVII lesions findings

A

o weakness/palsy of facial expression mu
o Loss of taste from anterior 2/3 of tongue (via chorda tympani)
o Hyperacusis (supplies stapedius muscle)
o The upper face receives bilateral supranuclear innervation

45
Q

o UMN lesions in facial palsy: findings

A

o UMN lesions cause weakness of the lower part of the face contralaterally. Frontalis is spared, brow furrowing is spared

46
Q

LMN lesions in facial palsy: findi

A

o LMN lesions cause ipsilateral weakness of all facial muscles: angle of mouth falls, unilateral dribbling develops. Cornea may be damaged if the lid does not close.

47
Q

combination of • Unilateral III, IV, V and VI involvement possible ddx

A

lesion in cavernous sinus

48
Q

combination of unilateral V, VII, VIII involvement ddx

A

cerebellopontine angle lesion (usually a tumour)

49
Q

unilateral IX, X, XI involvement ddx

A

jugular foramen lesion

50
Q

combined bilateral X, XI, XII ddx

A

bulbar palsy if LMN Sx are present, pseudobulbar if UMN signs are present

51
Q

weakness of the eye and facial muscles that worsens with repeated contractions possible ddx

A

myasthenia

52
Q

what is acoustic neuroma

A

Schwann cell-derived tumours that commonly arise from the vestibular portion of CNVIII. >90% are unilateral. Bilateral in NF2

53
Q

aetiology and risk factors for acoustic neuroma

A
  1. NF2
  2. Exposure to loud noise
  3. Childhood exposure to low-dose radiation
54
Q

features of acoustic neuroma (findingS)

A

Symptoms of CN compression by tumour
CNVIII: hearing loss, tinnitus, unsteadiness while walking
CNV: facial numbness, parasthesia, pain (17%)
CNVII: facial weakness (6%)
With tumour progression → compression of CPA → ipsilateral ataxia + nystagmus
Compression of the lower CNs (IX, X, XI) → dysphagia, dysarthria
Look for Sx of neurofibromatosis

55
Q

management of acousti

A

Mx: surgery to prevent further disability, does not restore hearing. Three approaches: retromastoid suboccipital, translabyrinthine and middle fossa
Radiation: for small <3cm neuromas and if unfit for surgery

56
Q

bells palsy aetiology and features

A

Lyme disease and HIV seroconversion may cause that. Bell’s phenomenon: upward conjugate eye movement when eyes are closed.
• Profound unilateral facial weakness.
• Develops over 24-48h
• Pain behind the ear on onset
• Difficulty closing the eye
• Slurred speech, losing food from the corner of the mouth
• Reduced taste
• Hyperacusis
• Tx: steroids (prednisolone 10d) and antivirals (acyclovir)
• 75% improve spontaneously in 6mo
• 25% develop synkinesis, crocodile tears

57
Q

CN IX anatomy

A

exits the skull through jugular foramen with CN X and CN XI

58
Q

lesions of CN IX cau

A
  1. Loss of gag reflex (interrupted afferent limb)
  2. Hypersensitive carotid sinus reflex (syncope)
  3. Loss of general sensation in the pharynx, back of the tongue
  4. Loss of taste from posterior 1/3 tongue
  5. Glossopharyngeal neuralgia: stabbing pain in the root of the tongue
59
Q

CN X lesions cause

A
  • Ipsilateral paralysis of the soft palate, pharynx, larynx → dysphonia, dyspnoea, dysarthria, dysphagia
  • Anaesthesia of pharynx+larynx → unilateral loss of cough reflex
  • Aortic aneurysm and tumours of neck/thorax frequently compress the nerve
  • Complete laryngeal paralysis if bilateral can cause asphyxia and death
  • Oculocardiac reflex: pressure on the eyes slows the heart rate (aff CN V1, eff CN X)
60
Q

how to inspect cranials controling the mouth

A

Soft palate movement (IX, X)
o “say ahh”
Mention gag reflex
Mention swallow test

Tongue movement (XII)
o Wiggle the tongue from side to side
o Stick your tongue straight out (will deviate towards the site of lesion)
o Power (push against cheek)

61
Q

features of Horners syndrome

A

Features:

b. Miosis
c. Partial ptodid
d. Enophthalmos
e. Hemifacial loss of sweating

62
Q

ddx for weakness of 1 or two muscles unilaterallly

A

a. Look for parotid enlargement or surgical scar over parotid
b. Usually due to aberrant reinnervation

63
Q

ddx for bilateral

A

a. Myotonic dystrophy: frontal balding, furrowed brow, haggard face, thin neck and myotonia
b. Myasthenia gravis
c. Ocular myopathy - ophthalmoplegia, facial weakness, furrowed brow
d. Bilateral Horner‘s – with intrinsic cord lesions eg syringomyelia
e. Syphillis

64
Q

characteristics of normal pressure hyd

A
  1. Dementia.
  2. Urinary incontinence.
  3. Gait abnormalities.
  4. Dementia may improve with ventricular shunting.
  5. How is NPH diagnosed?
    By brain imaging (CT or MRI). The radiologic hallmark: ventriculomegaly out of proportion to cerebral atrophy. Ventriculomegaly that results from cerebral atrophy. In a patient with a gait apraxia and ventricles that are too big for her or his brain, the response to treatment with gait
    improvement is the ultimate diagnostic test.
65
Q

via CN XI, Ipsilateral cerebral hemisphere supplies what?

A

Ipsilateral cerebral hemisphere supplies the contralateral trapezius and ipsilateral SCM.thus a single UMN lesion gives bilateral signs.

66
Q

if you find Unilateral weakness of SCM + trapezius:

A

peripheral accessory palsy. Look for ipsilateral IX and X lesions: ? jugular foramen lesion (glomus tumour or neurofibroma)

67
Q

If you find weakness of ipsilateral SCM and contralateral trapezius:

A

UMN weakness on SCM side

68
Q

Bilateral wasting and weakness of SCM: ddx

A

myopathy or MND(look for bulbar abnormalities)

69
Q

Small tongue with fasciculations: ddx

A

BILATERAL LMN lesions, MND (progressive bulbar palsy type_, syringobulbia

70
Q

Small tongue with recude speed of movements ddx

A

bilateral UMN (look for jaw jerk, labile emotions): pseudobulbar palsy

71
Q

Tongue deviates to one With unilateral wasting + fasciculations =

A 
towards lesion
unilateral LMN (rare|)
72
Q

tongue deviates to one side with normal bulk

A 
unilateral UMN (common): stroke
towards lesion

NOP (24 decks)

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