Neurology Flashcards
What are the cranial nerve syndromes and what nerves are involved in each?
Cavernous sinus syndrome:
- Unilateral CN3, 4, 5(1,2) and 6
Cerebellar pontine angle syndrome:
- Unilateral CN5, 6, 7, 8 (usually due to a tumour in the cerebellar pontine angle)
Jugluar foramenal lesion:
- Unilateral CN9, 10, 11 (Dif from bulbar plasy because it is unilateral)
What causes Cavernous sinus syndrome?
Caused by lesions that affect the cavernous sinus such as:
-> Vascular / thrombotic: VTE cavernous sinus, ICA aneurysm
-> Neoplastic
-> Infection of the cavernous sinus
-> Inflammation from another etiology
Presentation of cavernous sinus thrombosis /syndrome?
Presentation (not all must be present):
- Ipsilateral proptosis (only found in thrombosis, due to congestion of the blood and fluid in the orbit from venous obstruction)
- Chemosis secondary to proptosis
- complex opthalmoplegia from LMN lesion or from congestion and phsysical restriction of the EOMs (similar to graves eye disease)
- Horners syndrome
- Trigeminal sensory loss in V1 and 2
Presentation of cerebello-pontine angle syndrome?
What is the most common cause of cerebello-pontine angle syndrome and what are some differentials in this aetiology?
Hearing loss, Tinitus, vertigo (CN 8)
Unilateral facial weakness (CN 7)
Loss of facial sensation / facial pain and muscles of mastication (CN5)
Diplopia (CN6)
Most common cause is tumour
Most common tumour is acoustic neuroma (CN8 tumour), but can also be meningioma or other tumours
- Because acoustic neuroma is most common cause, pt will present with vestigular and cochlear symptoms +/- additional CN5,6,7 symptoms
What is bruns-Cushing nystagmus and where does it localise to?
Bruns-cushing nystagmus localises to teh cerebelo-pontine angle
It is the combination of a gaze paretic slow beating large amplitude nystagmus, and a contralateral gaze evoked fast beating nystagmus
What is gaze paretic and gaze evoke nystagmus?
Gaze paretic nystagmus is a type of gaze evoked nystagmus
Gaze evokes nystagmus is nystagmus that is only present when pt is not in neutral position (ie they are attempting gaze)
- Gaze paretic nystagmus means the pt is unable to hold the gaze position (they have beats of nystagmus to the gaze position but overall the eye tend to the neurtal position)
What causes jugular foraemen syndrome? How does it present?
Main cause is vascular :
- Vascular:
-> Internal jugular thrombosis
-> Mass effect from aneurysm of extracranial internal carotid
-> Jugular diverticulum
Other causes include inflammatory, infectious, neoplastic
Presentation is usually hoarsness of voice / dysphonia, often with persistent unilateral periauricular pain and headache
- Hoarse voice and unilateral palate paralysis (uvula dieviation) due to CN 10 Vagus paralysis
- Ipsilateral loss of gag reflex and posterior aspect of tongue due to CN 9 palsy
- Unilateral difficulty with trap and SCM due to CN11 affected
Where do the 12 cranial nerves roughly emerge? (relative the the midbrain, pons and medulla)
CN1 and 2 are direct from cerebrum
CN3,4 from midbrain
CN5,6,7,8 from pons
CN9,10,11,12 from medulla
What are the localizing forms of nystagmus?
There are localization and non localizing nystagmus.
Non localizing is most common and includes:
- Gaze evoked nystagmus ie horizontal beating gaze evokes, vertical gaze evoked
If you see localizing type of nystagmus you know there must be a lesion at the area the nystagmus localises to:
- Primary position (D)own beating - (C)ervicomedulary junction
- Primary position (U)p beating - (V)ermis of cerebellum
- (C)onvergence retraction nystagmus - (D)osal midbrain
- (S)ee saw nystagmus - (T)hird ventricular or parasella region
- Periodic alternating nystagmus (PAN): spontaneously and periodically direction in primary position - Cerebellum
- Rebound nystagmus (like PAN but alternates with gaze)
- Bruns-Cuhsing - CPA lesion usually tumour
What lesion would cause a see saw nystagmus?
This is a localizing nystagmus in hte primary position
It is due to lesion in the sellar and parasellar region ie a tumor
- often associated with bitemporal hemianopia from optic chiasm compression from this lesion
What lesion would cause a convergence retraction nystagmus?
Dorsal midbrain syndrome is a collection of signs that include convergence retraction nystagmus.
Other main sign is light, near dissociation due to dirupted afferent pathways at teh dorsal midbrain (efferent is still good because edinger westphal nucleus is not affected)
Dorsal midbrain lesion:
- Neoplastic ie pineal region mass
- Vascular ie stroke
- Demyelination ie MS
Look from side to see retraction. look from front to see convergence in neutral and upward position
What lesions would cause PAN?
PAN can be congenital or acquired.
Localities to the cerebellum or posterior fossa, but doesnt localize more then that (ie etiology of issue)
Rx is baclofen for all causes
What is the most common lesion that would lead to primary position downbeat nystagmus?
This is a localizing form of nystagmus, localizes to the cervicomedulary junction
It is worse on downward gaze (alexanders law) and especially down and lateral gaze
Causes:
- The most common structural cause is an arnold chiari malformation
- Demyelination ie MS
- Vascular ie infarction
What is the most common cause of primary gaze upbeat nystagmus?
This is a localising form of nystagmus and classically localises to the cerebellar vermis.
Can also be due to lesion anywhere in the brain stem (midbrain, pons and medulla)
In other words, the lesion is in the posterior fossa somewhere. Causes include:
- Neoplastic
- Vascular ie stroke, haemorhage
- Demyelination ie MS
- Nutritional or etoh (wernickes encephalopathy mainly)
- Paraneoplastic
- Autoimmunity
Signs of CN3 palsy? Causes of CN3 palsy?
- Unilateral complete or partial ptosis - CN3 controls levator palpebrae superioris
- Dilated pupil, imparied reativity
- Down and out eye in primary position (exotropic and hypotropic)
(Note, not all these signs may be present because may have only divisional involvement rather than whole occulomotor nerve involvement. Ie superior division involvement would only cause ptosis and hypotropia)
Causes:
- Isolated third nerve:
-> Vascular: posterior communicating artery aneurysm (PCOM), stroke
-> Neoplastic
-> demyelination
-> infectious
-> inflammatory
- Can also be due to cavernous sinus syndrome if combined with other CN palsies
What is the significance of pupiliary involvment in thrid nerve palsy?
The inner most fibers of the occumormotor nerve are the motor fibers. the outermost control the pupil
- Therefore if teh cause is ichemic, it will affect the inner most fibers first causing CN 3 palsy that is pupil sparing
- If cause is compressive ie PCOM aneurysm then then outer most fibers will be affected causing dilation of CN palsy with pupil involvement
How is the eye covering test useful in diagnosing opthalmoplegias?
If pt with a opthalmoplegia is asked to focus on a point, they will do so with their non affected eye and try to do so with their affected eye. Because there is a palsy, their affected eye will often not be exactly the same in position as the unaffected eye.
When you cover an eye and ask the patient to look at a certain point, they will focus on the point with the eye that is not covered.
If they have a third nerve palsy, if their affected eye is covered then they will focus on the point with their normal eye and the affected eye will drift into deviated position. Then when their affected eye is uncovered it will try to move back to the gaze position to focus on the point. This movement when uncovered demonstrates the extent of deviation.
Similarly, if unaffected eye is covered then the pt will attempt to focus on point with affected eye. In doing so the unaffected eye will become significantly dieviated such that when it is now uncovered and moves back into position the extent of dieviation is demonatrated.
This meas that the primary dieviation is less than the secondary dieviation which can help indicate which eye is affected.
What are the differentials of exotropia in the primary position? What else should you check if you see exotropia?
Thrid nerve palsy
- May also deep slight depression of the eye (exotropia and hypotropia), ptosis and dilated pupil
Other causes will not cause ptosis or cause pupiliary defects. These include:
- INO
- MG
- Decompensated childhood exotropia
What are the differentials for ptosis? What else should you check if you see ptosis?
If see ptosis need to check for third nerve palsy by assessing EOM and pupil
Other causes include MG, also need to assess EOM because MG associated opthalmoplegias
Need to check for horners syndrome with contriced pupil, anhydrosis
Other cause is levator muscle dehissence (isolated ptosis)
What are the differentials for dilated pupil? What else should you check?
Physiologic aniscoria
- will react and accommodate equally
- Only small difference
Adie’s tonic pupil (idioopathic pathology of teh cilliary ganglion)
- Tonically dilated pupil that reacts slowly to light but accommodates well (light-near disassociation)
Iris pathology
- Test on slit lamp examination
Pharmacological dilation
Need to check for ptosis, and EOM which will be involved to some degree in third nerve palsy. If there is only pupil involved then not going to be third nerve palsy
What is light- near dissacociation? what is it caused by?
It is when the eye doesnt contrict to light well, but accomodates normally
- Usually these should be about the same (ie not dissacociated)
It can be due to afferent disease or efferent disease
- Afferent disease
-> bilateral light blindness (cannot be assessed with RAPD because defect is symetrical and bilateral)
-> dorsal midbrain syndrome from mass or syphilus (called argyle ribinson pupil if this is the cause here)
- Eferent disease
-> Idiopathic cilliary ganglion disease is called Adie’s pupil
What is the only cranial nerve that crosses before traveling to peripheries? What is the implication of this?
CN4. Exits nucleus and crosses before traveling to peripheries
Therefore trauma or mass efect lesions at dorsal midbrain can impact on both causing bilateral CN4 palsy
What is the primary action of CN4?
Only inervates the superior oblique muscles. therefore will always present with blurred vision, eye pain and diplopia as presenting symptoms
Primary action of muscle is intorsion of the eye (in primary position). In some positions it has depression action as well
Approach to Dx CN4 palsy on examination?
Inspection:
- Primary position may see slight hypertropia in the affected eye. But also may be normal
Eye movements:
- Grossly may appear normal so have to look closely
- Hypertropia will be worst when affected eye is adducting (look for this with horizontal movements alone)
- Then test depression in adducted position for both eyes. relative hypertropia will be greatest in the affected eye when it attempts to depress in the adducted position
Special tests
- Covering test: will see affected eye hypertropia and exotropia that corrects when affected eye is uncovered (primary dieviation). May see larger secondary deviation in unaffected eye
- Covering test in lateral gaze:
-> the primary and secondary dieviation will be accentuated when the affected eye is made to adduct (ie looking away from the lesion)
- Eye cover test on head tilt test - pt tilts head towards the lesion (this means the pt has to intort the eye which they cant do with a CN4 palsy). Eye covering test in this position will also accentuate the primary and secondary dieviation
