Sunday, 17 October 2010

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

  • 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.