MRCP revision battle 32.1: Deafness: Rinnes and Webers

Final day in the hat trick of eyes and neurology battles...


MRCP revision battle 32.1: Deafness: Rinnes and Webers
MRCP revision battle 32.2: Tinnitus
MRCP revision battle 32.3: TIA
MRCP revision battle 32.4: Epilepsy
MRCP revision battle 32.5: Macular degeneration
MRCP revision battle 32.6: Glaucoma
MRCP revision battle 32.7: Autonomic neuropathy



MRCP revision battle 32.1: Deafness: Rinnes and Webers

Hearing loss and Rinne and Weber's tests are MRCP favourites.


Remember there are 2 types of deafness:

• conductive deafness
• ear wax
• otosclerosis
• otitis media
• glue ear
• sensorineural deafness
• acoustic neuroma
• Pagets
• MS
• CVA
• Menieres
• head trauma
• noise exposure
• drugs
• aminoglycosides (gentamycin)
• furosemide
• lead

Tests are done with a 256- 512 Hz tuning fork





Rinne's test:

• hold vibrating tuning fork next to ear meatus, then place on mastoid
• ask which is louder
• air conduction (AC) > bone conduction (BC) = normal, or, if hearing is decreased, suggests sensorineural loss
• BC>AC = conductive deafness = Rinne negative
• Remember as: ALS (like the course) - air loudest: sensorineural.  

Weber's test:

• hold vibrating tuning fork on forehead
• ask which side it is heard loudest in
• in sensorineural loss it laterals to the unaffected side
• in conductive loss it laterals to the affected side
• midline if normal, or bilateral sensorineural loss
• Remember as: SUCA - sensorineural unaffected, conductive affected.

Next up - a spot of tinnitus...

MRCP revision battle 32.2: Tinnitus

Tinnitus is ringing/buzzing in ears.


Causes include:

• eax
• viral infections
• presbyacusis
• head injury
• Menieres
• drugs
• aspirin
• furosemide
• gentamycin

Pulsatile tinnitus may indicate carotid artery stenosis or dissection



Now on to the meatier topic of TIAs...

MRCP revision battle 32.4: Epilepsy

Epilepsy is defined as a recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifest as seizures (OHCM definition)



Epileptic seizures are subdivided into:

• partial seizures = features come from one part of the brain
• simple partial = consciousness not impaired
• complex partial = consciousness impaired - usually temporal lobe, aura may preceed and automatisms may feature
• generalised seizures = features not localisable to one part of the brain
• absence = petit mal = brief <10 second pauses - 3Hz spikes
• atonic = becomes flaccid
• tonic-clonic - classic stiffening and jerking
• myoclonic

Treatment is usually started after the second seizure.   It would be started after the first if any of the following conditions apply:

• neurological deficit
• structural abnormality
• EEG unequivocal
• pt/family/carers keen for treatment

First line treatment depends on the seizure type:

• generalised
• 1st line: sodium valproate
• 2nd line: lamotrigine
• partial
• 1st line: carbamezepine
• 2nd line: sodium valproate
• absence
• sodium valproate or ethosuximide
• note that carbamazepine may worsen absence seizures

Remember that both sodium valproate and lamotrigine are associated with Steven Johnson syndrome.




Cannot drive until seizure-free for 1 yr, or 3 yrs of night time only seizures.
HGV drivers need to be off meds and seizure-free for 10 yrs.



If a pt has no seizures for 2 yrs, you may consider stopping meds over 2-3 months.


On to battle 32.5...

MRCP revision battle 32.3: TIA

TIA (=transient ischaemic attack) = sudden onset of focal CNS phenomena which last <24 hours.  Caused by temporary occlusion of part of the cerebral circulation.



Causes of TIAs:

• thromboembolism
• chiefly from carotids
• may be from heart - AF, mural thrombus etc)
• hyperviscosity
• myeloma
• polycythaemia
• sickle cells
• very high white cells

Management depends on the ABCD2 score, which is calculated as shown below:

• age >60 : 1 point
• BP greater or equal to 140/90 : 1 point
• clinically:
• unilateral weakness : 2 points
• speech disturbance without weakness : 1 point
• duration
• >60 mins : 2 points
• 10 - 59 mins : 1 point
• diabetes : 1 point

ABCD2 score of 4 or more, or crescendo TIAs (=2 or more in one week):

• specialist review within 24 hrs
• start 300mg aspirin OD

ABCD2 score of 3 or below, or symptoms >1 week ago:

• specialist review within a week
• start 300mg aspirin od

After specialist review, usually 75mg aspirin OD and dipyridamol OD for 2 yrs.
If pt is aspirin intolerant, prescribe monotherapy of clopidogrel.




If assessed to be a candidate for carotid endarterectomy, imaging should be performed within 1 week of symptom onset and if carotid stenosis of:

• 50–99% according to NASCET criteria, or 
• 70–99% according to ECST criteria 

carotid endarterectomy should be performed within 2 weeks of symptom onset.



Remember pt must inform DVLA and no driving for 1 month (car) or 1 yr (lorry).  This increases to 3 months for car if multiple TIAs.



Of course other risk factors (hypertension, alcohol, smoking, etc etc etc) should also be addressed.




Differentials for TIA may include:

• migraine
• epilepsy
• hypoglycaemia
• malignant hypertension 
• MS

Lets move on to tackle epilepsy...

MRCP revision battle 32.5: Macular degeneration

Macular degeneration is the commonest cause of blindness in the UK.


There are 2 types:

• dry 
• drusen - yellow spots in Bruchs membrane
• wet
• choroidal neovascularisation
• worse prognosis

Below is an image of dry macular degeneration showing drusen.  To link to an image of wet macular degeneration click here

Risk factors for macular degeneration are:

• age >60
• female
• smoking
• caucasian
• family history

Treatment - there is no cure:

• high dose beta caratene - but may increase risk of lung cancer in smokers
• vitamin C and E - but vit E may increase risk of heart failure
• zinc
• for wet:
• photocoagulation
• anti VEGF
• Ranibizumab
• photodynamic therapy

Keeping on eyes, next up is glaucoma...

MRCP revision battle 32.6: Glaucoma

Glaucoma is damage to the optic nerve, generally due to increase in intra-ocular pressure.


There are 2 types of glaucoma:

1. acute = closed angle glaucoma
2. chronic = open angle glaucoma

Acute closed angle glaucoma

Acute closed angle glaucoma presents as:

• pain
• decreased visual acuity
• worsening of pain with mydriasis
• hard, red eye
• halos around lights
• semi-dilated, non-reactive pupil
• pt systemically unwell

Risk factors for closed angle glaucoma include hypermetropia and pupillary dilation.


Management is:

• urgent opthalmic review
• IV acetazolamide (a carbonic anhydrase inhibitor; decreases aqueous secretions)
• topical pilocarpine (constricts pupil)

Open angle glaucoma


This affects 2% of over 40s.


Risk factors include:

• family history
• black
• myopia
• hypertension
• diabetes

Features include:

• peripheral field loss
• decreased visual acuity
• optic disc cupping

Treatments include:

• eye drops (beta blockers or prostaglandins)
• possibly surgery.

Now to our final battle of the day, autonomic neuropathy

MRCP revision battle 32.7: Autonomic neuropathy

Autonomic neuropathy is characterised by:

• postural hypotension
• erectile dysfunction
• constipation or diarrhoea
• urinary retention
• inability to sweat
• loss of decreased heart rate on deep breathing
• Horners
• Holmes-Adie pupil

Causes:

• endocrine
• diabetes
• infective
• HIV
• syphilis
• leprosy
• autoimmune
• SLE
• other
• GBS
• MSA
• parkinson's disease
• liver/renal failure.

Treatment is symptomatic; remember fludrocortisone as an option for severe postural hypotension.


On that list-intensive battle lets retire for the day.