posterior fossa pathology Flashcards
what happens to facial weakness in UMN lesion
opposite side lower half of face is weak. sparing of frontalis, preserved brow furrowing, eye closure and blinking unaffected
what happens to facial weakness in LMN lesion
ipsilateral weakness of all facial expression. angle of mouth falls, frowning and eye closure are weak. impaired taste sensation
what is the commonest cause UMN lesion leading to facial weakness
stroke with contralat hemiplegia
what happens if the facial nerve is damaged in the pons
loops around CN6 leading to lateral rectus palsy with unilat LMN weakness
what can cause facial weakness in the pons
tumour eg glioma, MS, infarction
what can be compressed with facial nerve in the cerebellopontine angle
5,6,8.
what can cause facial weakness in the cerebellopontine angle
acoustic neuroma, meningioma, mets
causes of facial nerve weakness in the petrous temporal bone
bells palsy, trauma, middle ear infection, herpes zoster
signs of damage at the petrous temporal bone
loss taste in ant 2/3 tongue. hyperacusis
what is Bells palsy
acute facial palsy thought to be due to viral infection causing swelling of the facial nerve in the tight petrous temporal bone facial canal
symptoms Bells palsy
unilateral LMN weakness developing over 24-48 hours, sometimes lost/altered sensation on the tongue, hyperacusis. pain behind ear common at onset
what does it mean if other cranial nerves are involved (if suspecting Bells palsy)
its not bells palsy
what can cause Bells palsy
Lyme disease in endemic areas, HIV seroconversion in Africa
treatment Bells
early corticosteroids- prednisolone 1mg/kg for 7 days. acyclovir and valaciclovir can be given in combination
come complications Bells
if cant blink can get exposure keratitis- lubricating eye drops. if severe weakness and cant close eye- need ophthal assessment. aberrant reinnervation of facial muscles eg twitching- late complication
prognosis Bells
good, 85% completely recover in 3-8 weeks even without specific treatment. rarely recurs
what may be helpful if recovery is not complete in Bells
cosmetic surgery
what does the trigeminal nerve do
mostly sensory but motor muscles of mastication
what happens in a 5th nerve lesion
unilateral sensory loss on the face. disminution of corneal reflex is an early sign
causes trigeminal lesion
brainstem- infarction, demyelination; CPA- acoustic neuroma, meningioma; tumour, infection
main risk factor for trigeminal neuralgia
hypertension. typically occurs 60-70+
what are the causes
ectatic vascular loop. in younger patients can be MS, CPA tumours
features trigeminal neuralgia
paroxysms of knife like or electric shock like pain which lasts seconds. in the distribution of the 5th nerve
which branch of V does trigeminal neuralgia commence
V3- mandibular. can spread to V2 maxillary and occasionally V1 ophthalmic
when would the TN be bilateral
demyelination. rare
what can stimulate TN
washing, shaving, cold wind, chewing
treatment TN
carbamazepine 600-1200mg a day. alternative- lamotrigine3, gabapentin, oxcarbazine
if medical treatment is not tolerated what can be used to treat TN
surgery- percutaneous radiofrequency selective ablation of trigeminal ganglion or microvascular decompressin of the nerve in post fossa
what does the oculomotor supply
superior, inferior and medial recti, inferior olique, levator palpabrae superioris (lifts eyelid), parasympathetic constriction of the pupil
causes of oculomotor lesion
aneurysm in posterior communicating artery, infarction of 3rd nerve(diaebetes, atheroma), coning temporal lobe, midbrain tumour or infarction
signs complete 3rd lesion
unilateral complete ptosis (weakness levator), down and out (unopposed lateral rectus and superior oblique), fixed and dilated pupil
which type of 3rd nerve lesion causes painless and pupil sparing
diabetic infarction. posterior communicating aneurysm causes it to be painful and doesn’t spare the pupil
what way does the eye go in 6th nerve palsy
inwards (esotropia), cant fully abduct
what happens to the eye in trochlear palsy
torsional diplopia- 2 objects at an angle when attempting to look down so head tilts away from that side
what does the trochlear supply
superior oblique
what does the abducens supply
lateral rectus
what is BPPV due to
loose otoliths in the semicircular canal
signs BPPV
precipitated by head movements- position, turning in bed, sitting up. sudden onset seconds-minds. less severe on repeated movement- fatigue
what can BPPV sometimes follow
vestibular neuritis, head injury, ear infection
diagnosis BPPV
hallpike manoeuvre. sit up then lie down and support head turn towards affected side. nystagmus with a latent interval
how is BPPV treated
Epley manoeuvre- shift otoliths
DDX BPPV
cerebellar mass but there may be nystagmus and vertigo immediately- no latent interval. also doesn’t fatigue
vertigo that lasts secs-mins
BPPV
vertigo that lasts mins-hours
menieres
vertigo that lasts hours-days
labyrinthine or central pathology
symptoms with menieres
episodic rotatory vertigo 30 mins-hours. sensorineural hearing loss, fullness in affected ear, loss of balance, tinnitus, vomiting
what can be used in treatment Menieres
betahistine prochlorperazine. vestibular sedatives- cinnazine. chemical labyrinthectomy using ototoxic- gentamicin
how long should vestibular sedatives be use for
cease within 2 weeks as can cause parkinsonian side effects
what is the main sign of vertigo
nystagmus
what symptoms would be accompanying vertigo in peripheral (vestibular) vertigo
tinnitus, deafness
what symptoms would be accompanying vertigo in central vertigo
diplopia, weakness, cerebellar signs
central causes of vertigo
brainstem pathology. infarction eg in lateral medullary syndrome; demyelination; posterior fossa ass lesions; migraine; CPA mass lesions; drugs
investigations in vertigo
examine eye movements, assess heaing, head impulse (thrust) test, Hallpike, caloric testing (labyrinthine function), pure tone audiogram, MRI is central cause suspected
what is vestibular neuronitis
isolated vertigo with nystagmus. vomiting, days-weeks, self limiting rarely recurs. can be followed by BPPV. deafness absent. vestibular sedatives used
if vomiting isn’t a prominent feature is it central or peripheral
central
what is the head impulse test
to check vestibular ocular reflex. high velocity head turns fixating on target look for catch up (overt) saccade. if abnormal the fixation is lost and then catch up
what are the 2 phases of nystagmus and what do they mean
fast- direction of the beat. slow- eye catching up
what does the fast phase nystagmus show in central
ipsilateral lesion. shows contralat in perhipheral
what direction can central nystagmus be
horizontal, vertical or mixed
what is the effect of visual fixation in both types nystagmuc
no effect on central, suppresses nystamus in peripheral
what is the effect of head shaking on central and peripheral nystagmus
reverses direction in central, increases intensity but no change in direction in peripheral
type of nystagmus in central
jerk or pendular (jerk only in peripheral)
difference between dysphasia and dysarthria
dysphasia- problem with language and speech. dysarthria- problem in speech but language is in tact (disordered articulation, slurred speech)
drugs that can cause vertigo
gentamicin, metronidazole, diuretics, co trimaxole
what is Menieres due to
dilatation endolymphatic spaces of membranous labyrinth
what is a positive Rombergs
balance worse when eyes are shut- impaired JPS or vestibular input
what is a positive Unterbergers
march up and down on the spot with arms stretched out in front and eyes closed if >45 degree turn in
treatment menieres
prochlorperazine, betahistine
what is acute vestibular failure
follows a febrile illness in adults- sudden vertigo, vomiting, exacerbated by head movement. try cyclizine
