Examination

Question 1

Equipment required in a cranial nerve examination?

Answer 1

Pen torch
Snellen chart
Ishihara plates
Ophthalmoscope and mydriatic eye drops (if necessary)
Cotton wool
Neuro-tip
Tuning fork (512hz)
Glass of water

Question 2

Clinical signs suggestive of neurological pathology upon general inspection of the patient?

Answer 2

Speech abnormalities: may indicate glossopharyngeal or vagus nerve pathology
Facial asymmetry: suggestive of facial nerve palsy
Eyelid abnormalities: Ptosis may indicate oculomotor nerve pathology
Pupillary abnormality: madras is occurs in oculomotor nerve palsy
Strabismus: may indicate oculomotor, trochlear or abducens nerve palsy
Limbs: soacisity, weakness, wasting, tremor, fasiculation

Question 3

Objects or equipment to take note of upon general inspection of the patient in a cranial nerve examination?

Answer 3

Walking aids: gait issues - Parkinson’s, stroke, cerebellar disease, myasthenia graves
Hearing aids: often worn by patients with vestibulocochlear nerve issues (e.g. Ménères disease)
Visual aids: the use of visual prisms or occludes may indicated underlying strabismus (oculomotor, abducens or trochlear nerve palsy)
Prescriptions

Question 4

What is CN I and how is it assessed?

Answer 4

Olfactory nerve, transmits sensory information about orders to eh CNS where they are perceived as smell (no motor component)

Ask patient about recent changes to their sense of smell

Question 5

Causes of anosmia?

Answer 5

Mucous blockage of the nose
Head trauma resulting in shearing of CN I
Genetics - congenital
Parkinson’s disease
COVID-19 infection

Question 6

What is CN II and it’s role?

Answer 6

Optic nerve, transmits sensory visual information from the RETINA to the BRin

Question 7

How to assess pupils in a cranial nerve examination?

Answer 7

Assess size: normal pupil size varies between individuals, depends on lighting conditions, and are usually smaller in infancy and larger in adolescence

Assess shape: should be round, abnormal shares can be congenital or due to pathology (such as posterior synechiae seen in uveitis)

Assess pupil symmetry: Anisocoria can be longstanding and non-pathological but can also be due to pathology such as CN III palsy (large) or Horners syndrome (small and reactive). If the difference is more pronounced in bright light this suggests the large pupil is abnormal (ie. CN III palsy) and in the dark suggests smaller pupil is abnormal (Horners syndrome)

Pupillary reflexs — direct and consensual, swinging light test, accommodation reflex

Colour vision using Ishiara plates

Question 8

How to assess visual acuity in a cranial nerve examination?

Answer 8

Snellen chart at 6m, with glasses if patient wears them.
Test one eye at a time, ask patient to read to lowest line and record (ie. 6/6, 6/60) including UA/PH
See if pinhole improves vision (suggests reparative component)
If unable to read to top line, reduce distance to 3m and 1m if required. If still unable use CF and PL/NPL (see if pt can detect light from a pen torch shone into each eye)

Question 9

If visual acuity is found to be reduced, what might the potential causes be?

Answer 9

Refractive errors
Amblyopia
Ocular media opacities (cataract, corneal scarring)
Retinal diseases - ARMD
Optic nerve CN II pathology - optic neuritis
Lesions in higher visual pathways

Question 10

How to assess pupillary reflexes?

Answer 10

Patient is seated in a dimly lit room

Direct: shine pen torch into the patients pupil and observe for restriction in the ipsilateral eye - normal: constriction

Indirect: shine pen torch into the patients pupil and observe for restriction in the contralateral eye - normal: constriction

Swingling light test: Move the pen torch rapidly between the two pupils to check of a relative afferent pupillary defect

Accommodation reflex: ask patient to focus on a distant objects, place your finger approximately 20-30cm in front of their eyes, and ask them to switch there gaze to your finger. Observe the pupils for constriction and convergence bilaterally (normal reflex)

Question 11

Which nerve is responsible for the afferent limb of the pupillary light reflex and how is it assessed?

Answer 11

CN II, optic nerve.
Shining light into the eye and observing for ipsilateral constriction which should be present if the nerve is functioning correctly

Question 12

Which nerve is responsible for the efferent limbs of the pupillary light reflex and how is it assessed?

Answer 12

CN III, oculomotor

Motor output: transmitted from the PRETEXTAL NUCLEUS to the EDINGER WESTOHAL NUCLEI on BOTH SIDES of the brain
Each EDINGER WESTOHAL nucleus gives rise to efferent nerve fibres which travel in the oculomotor nerve to innervate the ciliary sphincter and enable pupillary constriction
Shine light into the eye and observe for contralateral pupil constriction which should be present if the limbs are intact

Question 13

Relative afferent pupillary defect (Marcus-Gunn pupil) O/E

Answer 13

Normally light shone into either eye should constrict both pupils equally (due to the dual efferent pathways).
When the afferent limb in one of the optic nerves is damaged, partially or completely, both pupils will constrict less when light is shone into the affected eye compared to the healthy eye.
The pupils appear to relatively dilate when swinging the torch from the healthy to the affected eye.
This is termed a relative afferent pupil are defect

Question 14

Why might a relative afferent pupillary defect be found on examination?

Answer 14

Significant retinal damage in the affected eye secondary to central retinal artery or vein occlusion and large retinal detectatchment
Significant optic neuropathy such as optic neuritis, unilateral advanced glaucoma and compression secondary to tumour or abscess

Question 15

Unilateral efferent defect O/E

Answer 15

Ipsilateral pupil is dilated and non-responsive to light entering the eye due to loss of coil Larry sphincter function
The consensual light reflex in the unaffected eye would still be present as the afferent Kathy way for the affected eye and efferent pathway of the unaffected eye remain intact

Question 16

When assessing the cranial nerves colour vision deficiencies may be found using Ishihara plates, asking the patient to identify the number on each (with glasses if they wear them) to assess contrast sensitivity. What might cause colour vision deficiencies?

Answer 16

Optic neuritis (typically reduction in red colour vision)
Vitamin A deficiency
Chronic solvent exposure

Question 17

How to assess for visual neglect?

Answer 17

At 1m away from the patient ask them to Ramona focused on a fixed point on your face (e.g. nose) and to state if they see your left right or both hands moving. Hold hands out laterally with each occupying one side of the patients visual field. Take turns wiggiling each finger to see if or can identify which is moving and wiggle both simultaneously to see if the patient is able to correctly identify this - often patients with visual neglects will only report the hand moving in the unaffected visual field (ie, ipsilateral to the primary brain lesion)

Question 18

How to assess visual fields?

Answer 18

1. Sit directly opposite the patient, at a distance of around 1 metre.
2. Ask the patient to cover one eye with their hand.
3. If the patient covers their right eye, you should cover your left eye (mirroring the patient).
4. Ask the patient to focus on part of your face (e.g. nose) and not move their head or eyes during the assessment. You should do the same and focus your gaze on the patient’s face.
5. As a screen for central visual field loss or distortion, ask the patient if any part of your face is missing or distorted. A formal assessment can be completed with an Amsler chart.
6. Position the hatpin (or another visual target such as your finger) at an equal distance between you and the patient (this is essential for the assessment to work).
7. Assess the patient’s peripheral visual field by comparing to your own and using the target. Start from the periphery and slowly move the target towards the centre, asking the patient to report when they first see it. If you are able to see the target but the patient cannot, this would suggest the patient has a reduced visual field.
8. Repeat this process for each visual field quadrant, then repeat the entire process for the other eye.
9. Document your findings.

Question 19

Types of visual field defects

Answer 19

Bitemporal heminopia: tunnel vision, occurs typically as a result of optic chiasm compression by a tumour (pituitary adenoma, craniopharyngioma)
Homonymous field defects: same side of the visual field in each eye and are commonly attributed to stroke, tumour, abscess (I.e. pathology affecting visual pathways posterior to the optic chiasm) heminopia if half field and quadrantanopia if quarter.
Scotoma: area of absent or reduced vision surrounded by areas of normal vision, can be caused by demyelinating disease and diabetic maculopathy
Monocular vision loss: total loss in one eye secondary to optic nerve pathology (anterior ischaemic optic neuropathy) or ocular disease (e.g.central retinal artery occlusion, total retinal detachment)

Question 20

How to assess a blind spot?

Answer 20

1. Sit directly opposite the patient, at a distance of around 1 metre.
2. Ask the patient to cover one eye with their hand.
3. If the patient covers their right eye, you should cover your left eye (mirroring the patient).
4. Ask the patient to focus on part of your face (e.g. nose) and not move their head or eyes during the assessment. You should do the same and focus your gaze on the patient’s face.
5. Using a red hatpin (or alternatively, a cotton bud stained with fluorescein/pen with a red base) start by identifying and assessing the patient’s blind spot in comparison to the size of your own. The red hatpin needs to be positioned at an equal distance between you and the patient for this to work.
6. Ask the patient to say when the red part of the hatpin disappears, whilst continuing to focus on the same point on your face.
7. With the red hatpin positioned equidistant between you and the patient, slowly move it laterally until the patient reports the disappearance of the top of the hatpin. The blind spot is normally found just temporal to central vision at eye level. The disappearance of the hatpin should occur at a similar point for you and the patient.
8. After the hatpin has disappeared for the patient, continue to move it laterally and ask the patient to let you know when they can see it again. The point at which the patient reports the hatpin re-appearing should be similar to the point at which it re-appears for you (presuming the patient and you have a normal blind spot).
9. You can further assess the superior and inferior borders of the blind spot using the same process.

Question 21

What does an extensor plantar suggest?

Answer 21

UMN problem

Question 22

What does a Horners syndrome suggest in terms of aetiology?

Answer 22

Problem with ipsilateral sympathetic pathway

Question 23

Hemiplegic gait

Answer 23

Abduction and circumduction of the affected limb

UMN lesion affecting the leg

Question 24

Spastic gait

Answer 24

Sissoring gait found in spastic paraplegia

Question 25

Steppage gait?

Answer 25

In patients with footdrop and high stepping gait lifts the foot to avoid catching the toes.

Can be bilateral

Question 26

Ataxic gait

Answer 26

Road based, uncoordinated, unsteady gait

Characteristic of cerbellar syndromes of where there is loss of propioception

Question 27

Upgoing toe?

Answer 27

UMN

Question 28

Waddling gait

Answer 28

In muscular dtstophy weakness of the trunk and pelvis result in an exaggerated lumbar lordsis and tilting of the pelvis towards the no weight bearing side with each step

Question 29

Stamping gait

Answer 29

Loss or proprioception the gait is ataxic with the advancing leg lifted too high and brought down with a solid stamp

Question 30

Parkinsonian Gait

Answer 30

Forward flexed, shuffling gait with reduced arm swing

Question 31

Antalgic gait

Answer 31

If there is pain on weight bearing in one leg the step on the side is short, the foot brought down gingerly and then the step completed as quickly as possible resulting in a limp

Question 32

Upper motor neuron signs?

Answer 32

Increased tone
Clonus
Weakness (or mild clumsiness if subtle)
Brisk tendon reflexes
Extensor plantars

Question 33

Lower motor neuron signs

Answer 33

Wasting
Fasiculation
Reduced tone
Reduxced or absent tendon reflexes
Flexor plantars

Question 34

Distribution of sensory disturbance

Answer 34

Peripheral
- Roots
- Peripheral neuropathy
Spinal Cord tracts
- Dorsal columns
- Lateral spinothalamic tracts
Central

Question 35

DANISH - components of cerebellar examination

Answer 35

D – Dysdiadochokinesia
A – Ataxic gait (ask the patient to walk heel-to-toe)
N – Nystagmus (see below for more detail)
I – Intention tremor
S – Speech (slurred)
H – Heel-shin test

Answer 36

Unilateral horizontal nystagmus is more likely to be a peripheral cause. Bilateral or vertical nystagmus suggests a central cause.