Thursday 4 November 2010

MRCP revision battle 42.1: Bell's Palsy

Yet another assault on the neurology knowledge-mountain with 7 neurology-focused battles...

MRCP revision battle 42.1: Bell's palsy
MRCP revision battle 42.2: Mononeuropathies
MRCP revision battle 42.3: Carpal tunnel syndrome
MRCP revision battle 42.4: Diabetic neuropathy
MRCP revision battle 42.5: Nystagmus
MRCP revision battle 42.6: Miosis
MRCP revision battle 42.7: Picks Disease

MRCP revision battle 42.1: Bell's palsy

Bell's palsy is an acute, unilateral, idiopathic facial nerve paralysis.

It affects LMN.

Classical features are:
  • sudden onset unilateral facial weakness
  • numbness/pain behind ipsilateral ear
  • absent taste from anterior 2/3rds of tongue
  • dry eyes
  • hypersensitivity to sound

Treatment is prednisolone for 10 days.
Some evidence suggests giving aciclovir as varicella zoster antibodies are often raised.
The eye should be protected - artificial tears, taping of eye at night, ?tarsorrhaphy.

Most cases fully recover; 15% will have a prolonged or incomplete recovery.
Some subsquently suffer from 'crocodile tears' = eating stimulates unilateral lacrimination instead of salivation.

Now on to some more mononeuropathies...

MRCP revision battle 42.2: Mononeuropathies

Mononeuropathies are lesions of individual nerves.  The main causes of mononeuropathies are trauma or entrapment.

If 2 or more nerves are affected it is called mononeuritis multiplex. Causes may be remembered by the mnemonic DRAWS PLC:
  • diabetes
  • rheumatoid
  • amyloid
  • wegeners
  • sarcoid/SLE
  • PAN
  • leprosy/lyme disease
  • carcinomatosis/churg strauss

Important individual mononeuropathies to be familiar with include:

Key nerves of the arm: RUM - radial nerve C5-T1, ulnar never C6-T1 and median nerve C7-T1

Radial Nerve
  • Origin: C5-T1
  • Route: radial groove in humerus then anterior to the lateral epicondyle
  • Sensory supply: lateral 3.5 fingers in back of hand; only small area at base of thumb unique
  • Motor supply: tricipes and extensors of wrist/fingers plus suppinators
  • Classical presentation: 'Saturday night paralysis' - fall asleep with arm across back of chair, compress radial nerve in its groove and bruise it so awake with wrist drop.

Ulnar Nerve
  • Origin: C6-T1
  • Route: posteriomedial aspect of humerus then adjacent to ulna.  Runs superficial to flexor retinaculum into hand.
  • Sensory supply: medial 1.5 fingers
  • Motor supply: interossei, hypothenar eminence, medial 2 lumbicals
  • Classical presentation: claw hand/unable to cross fingers 

Median Nerve
  • Origin: C7-T1
  • Route: medially, goes through carpal tunnel
  • Sensory supply: lateral 3.5 fingers palmar aspect of hand plus nail beds of these fingers
  • Motor supply: pronator, LOAF = 1st and 2nd lumbricals, opponens pollicis, abductor pollicis brevis, flexor pollicis brevis (=thenar enimence)
  • Classical presentation: carpal tunnel syndrome 

Carpal Tunnel Syndrome is so common it deserves its very own battle...

MRCP revision battle 42.3: Carpal tunnel syndrome

Carpal tunnel syndrome is a mononeuropathy of the median nerve at the carpal tunnel = space under the transverse carpal ligament and above the carpal bones.

It is the commonest mononeuropathy.

Classical presentation is pain in hand and arm with paraesthesia in thumb, index and middle fingers.  The pain is often worse at night and is relieved by dangling the hand out of bed and shaking it.

'Bedside tests' include:
  • Phalen's test = maximal wrist flexion ('praying') for 1 minute recreates symptoms
  • Tinel's test = tapping over nerve at wrist recreates symptoms
(I remember which way round these tests go by thinking 't for tapping, t for tinel)

Associations with carpal tunnel syndrome include:
  • diabetes
  • acromegaly
  • hypothyroidism
  • pregnancy
  • RA

 Management may be conservative, spliting, steroid injections or surgery.

Now on to some diabetic neuropathy...

MRCP revision battle 42.4: Diabetic neuropathy

Diabetics may suffer from several different types of neuropathy.

1. Diabetic sensory neuropathy

The classic diabetic neuropathy is sensory neuropathy.  This causes a distal numbness ('glove and stocking') with tingling and pain.  

  • 1st line: TCA
  • 2nd line: gabapentin, pregabalin

2. Diabetic amyotrophy

Diabetic amyotrophy is sometimes known as proximal diabetic neuropathy.  This causes painful wasting of the quadriceps.   It is thought to be caused by occlusion of the vasa nervorum of the proximal lumbar plexus.  There is loss of the knee reflexes.

3. Autonomic neuropathy

If you need a recap refer back to revision battle 32.7

4. Mononeuritis multiplex

Particularly of CN III and VI.

Next up... a bit of nystagmus...

MRCP revision battle 42.5: Nystagmus

Nystagmus is involuntary, jerky eye movements.  

Nystagmus at the extremes of gaze is normal.

Horizontal nystagmus may be due to:
  • vestibular lesions - acutely the nystagmus is away from the affected side
  • cerebellar lesions - tends to be fast nystagmus and towards the affected side
  • MS - suspect if nystagmus is more in the eye which is abducting
  • benign positional vertigo - suspect if nystagmus varies with head position
  • peripheral lesion - suspect if also tinnitus/other signs

Down beat nystagmus is associated with:
  • Arnold Chiari malformations
  • Syringobulbia  (not sure what these are? revise battle 11.3!)

Upbeat nystagmus is associated with:
  • cerebellar vermis lesions
  • organophosphate poisoning

Sticking with eyes we're now going to consider miosis....

MRCP revision battle 42.6: Miosis

Miosis is a small pupil.

Causes of miosis include:

(my personal mnemonic for miosis: AAA pooch)
  • age
  • Argyll Robertson pupil
  • antipsychotics
  • pontine haemorrhage
  • pilocarpine
  • opiods
  • organophosphates
  • cluster headache
  • Horners

On to Pick's disease....

MRCP revision battle 42.7: Picks Disease

Pick's disease is the eponym for frontotemporal dementia.

It presents as loss of inhibition, socially unacceptable behavior, loss of empathy and compulsive behaviour.  There may also be loss of language skills.

Memory and spatial skills remain intact.

Pathophysiologically there are tau-positive inclusions.

There is no cure.