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CRANIAL NERVES Flashcards

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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
what is the likely cause of intact accommodation with absent light
Argyll Robertson pupils (pupils small and irregular) in diabetes and neurosyphilis.
26
a larger, regular, reacting sluggishly to accommodation but NO direct or consesual response to lpupil is...
holmes-aldie pupil
27
ophthalmoscope: what lens to use if the pt is shortsighted
(-) anticlockwise (red)
28
ophthalmoscope: what lens to use if the pt is farsighted
clockwise Green (+)
29
where is the optic disc in relation to the macula\?
optic disc is 15degrees medial to hte macula
30
background diabetic retinopathy appearane
dot blood haemorrhages miscroaneurysms soft exudates
31
pre-proliferative diabetic retinopathy appearance
hard exudates intraretinal microvascular abnormalities cotton wool spots
32
proliferative diabetic retinopathy appearnce
neovascularisation on the disc or in the retine
33
hypertensive retinopathy features
``` AV nipping silver wiring flame shaped haemorrhages exudates cotton wool spots blurred disc margin ```
34
central renal artery occlusion appearance
retinal pallor, affects all four quadrants cherry-red spots central retinal vein occluson appearance
35
central retinal vein occluson appearance
dialted tortuous veins, widespread haemorrhage | cotton wool spots
36
causes of CNIII palsy
``` 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
causes of VI palsy
* Causes of MM * Vascular lesion * Malignancy * Demyeliantion * Infection – lyme disease, syphilis * Raised ICP * Wernickes encephalopathy can cause palsy bilaterally
38
causes of internuclear ophthalmoplegia
MS | vascular disease/event
39
afferent pupillary defect meaning and DDx
* Pupil unreactive to light (direct reflex is absent) * Consensual reflex is absent * Indicates a complete optic nerve lesion - causes dilated pupil
40
RAPD meaning (pathology) and D
* 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
sparing of the pupil in CNIII palsy: ddx and pathology
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
complete external ophthalmoplegia ddx
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
CNV lesion findings
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
CNVII lesions findings
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
o UMN lesions in facial palsy: findings
o UMN lesions cause weakness of the lower part of the face contralaterally. Frontalis is spared, brow furrowing is spared
46
LMN lesions in facial palsy: findi
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
combination of • Unilateral III, IV, V and VI involvement possible ddx
lesion in cavernous sinus
48
combination of unilateral V, VII, VIII involvement ddx
cerebellopontine angle lesion (usually a tumour)
49
unilateral IX, X, XI involvement ddx
jugular foramen lesion
50
combined bilateral X, XI, XII ddx
bulbar palsy if LMN Sx are present, pseudobulbar if UMN signs are present
51
weakness of the eye and facial muscles that worsens with repeated contractions possible ddx
myasthenia
52
what is acoustic neuroma
Schwann cell-derived tumours that commonly arise from the vestibular portion of CNVIII. >90% are unilateral. Bilateral in NF2
53
aetiology and risk factors for acoustic neuroma
1. NF2 2. Exposure to loud noise 3. Childhood exposure to low-dose radiation
54
features of acoustic neuroma (findingS)
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
management of acousti
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
bells palsy aetiology and features
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
CN IX anatomy
exits the skull through jugular foramen with CN X and CN XI
58
lesions of CN IX cau
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
CN X lesions cause
* 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
how to inspect cranials controling the mouth
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
features of Horners syndrome
Features: b. Miosis c. Partial ptodid d. Enophthalmos e. Hemifacial loss of sweating
62
ddx for weakness of 1 or two muscles unilaterallly
a. Look for parotid enlargement or surgical scar over parotid b. Usually due to aberrant reinnervation
63
ddx for bilateral
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
characteristics of normal pressure hyd
1. Dementia. 2. Urinary incontinence. 3. Gait abnormalities. 4. Dementia may improve with ventricular shunting. 67. 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
via CN XI, Ipsilateral cerebral hemisphere supplies what?
Ipsilateral cerebral hemisphere supplies the contralateral trapezius and ipsilateral SCM.thus a single UMN lesion gives bilateral signs.
66
if you find Unilateral weakness of SCM + trapezius:
peripheral accessory palsy. Look for ipsilateral IX and X lesions: ? jugular foramen lesion (glomus tumour or neurofibroma)
67
If you find weakness of ipsilateral SCM and contralateral trapezius:
UMN weakness on SCM side
68
Bilateral wasting and weakness of SCM: ddx
myopathy or MND(look for bulbar abnormalities)
69
Small tongue with fasciculations: ddx
BILATERAL LMN lesions, MND (progressive bulbar palsy type_, syringobulbia
70
Small tongue with recude speed of movements ddx
bilateral UMN (look for jaw jerk, labile emotions): pseudobulbar palsy
71
Tongue deviates to one With unilateral wasting + fasciculations =
``` towards lesion unilateral LMN (rare|) ```
72
tongue deviates to one side with normal bulk
``` unilateral UMN (common): stroke towards lesion ```

NOP (24 decks)

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