Diseases of Peripheral Nerves

Question 1

Clinical assessment of the motor unit (RAT).

Answer 1

decreased spinal Reflexes.
denervation Atrophy of the muscles.
decreased muscle Tone.
*can present at different severity levels.

Question 2

Tests for neuromuscular diseases?

Answer 2

Electrodiagnostic studies.
- quite complicated to perform.
- can detect denervation signs.
– as abnormal activity in the muscle.
- can measure how impulse travels along nerve by measurement of nerve conduction velocity.
– can detect where main problem lies to see where to go next w/ dx.
- can detect NM end plate dz by evaluating muscle contraction over time following a stimulus.
Often need biopsy of nerve and muscle e.g. inflammatory dz.
Blood test - CK and AST – muscle enzymes which indicate muscle damage when high.

Question 3

1. Generalised diseases causing acute loss of reflexes followed by muscle atrophy.
2. Focal diseases causing acute loss of reflexes followed by muscle atrophy.

Answer 3

1. Polyradiculoneuritis.
   Ddx:
   - Fulminant myasthenia gravis.
   - Botulism.
   - Tick paralysis (Not UK).
2. Brachial plexus avulsion.
   Tail pull injury.

Question 4

1. What is polyradiculoneuritis and signalment for it, effects, progression, symmetry, pain?
2. Dx of polyradiculoneuritis.

Answer 4

1. Acute immune mediated dz that predominantly attacks axons on dogs.
   It affects the pelvic limbs first, then thoracic limbs.
   Affects middle aged dogs of any breed but terriers are predisposed.
   Progress over 5-7d then static to improving.
   Usually symmetrical and non-painful.
2. Rule out metabolic differentials and myasthenia gravis.
   Thoracic rads (no megaoesophagus associated w/ myasthenia gravis).
   - Hx any regurgitation etc.
   Electrodiagnostics = diffuse axonal disease (more localised to nerve roots).
   CSF sampling - elevated protein w/ normal cell count.

Question 5

1. Tx for polyradiculoneuritis.
2. Px of polyradiculoneuritis?

Answer 5

1. Supportive:
   - NO steroids as may make worse as make more prone to severe infections and muscle catabolism.
   - physiotherapy to prevent muscle contractures.
2. V good - most dogs recover to walk but may remain slightly atrophied; takes 1-3months so give them time!

Question 6

1. Brachial plexus avulsion Dx.
2. Progression of brachial plexus avulsion.
3. Tx of brachial plexus avulsion.
4. Main differential of brachial plexus avulsion in cats?
5. What syndrome can be associated w/ brachial plexus avulsion and why?

Answer 6

1. Hx of trauma, scratches, wound.
   X rays, CT to rule out concurrent fractures.
   Electrodiagnostics - abnormal after 4-5d.
   - may choose to measure at beginning as baseline to gauge recovery of patient later on.
2. Static or improving.
3. Physiotherapy, amputation if self trauma due to no feeling of the limb (non painful).
4. Thromboembolism.
5. Horner’s syndrome.
   Trauma site at spinal cord closely associated w/ T1-T3 (C6 where root of brachial plexus comes out of spinal cord)

Question 7

Horner’s syndrome associated with brachial plexus avulsion (BPA).

Answer 7

BPA causes tearing and damage to spinal nerves at around level C6-T2 of spinal cord.
Nerves that provide sympathetic innervation to the eye arise at this level of the spinal cord too.
So damage at this level of the spinal cord sometimes causes compromised innervation and therefore ipsilateral Horner’s Syndrome.

Question 8

1. Tail pull injury spp. typically affected.
2. Tail pull injury clinical signs.
3. Tail pull injury Dx.
4. Px of tail pull injury.
5. Tx of tail pull injury?

Answer 8

1. Cats.
2. Flaccid tail.
   +/- flaccid anus.
   +/- urinary incontinence.
   +/- sciatic nerve deficits if more cranial or more severe.
3. Hx and CE.
   Radiographs - for fracture/luxation.
4. Px fair to guarded.
   - can gauge recovery of the animal by monitoring tail base sensation at ~5d post trauma.
   - 4-8w expected for bladder function to return to normal.
5. Bladder management!
   +/- tail amputation.
   - consider if do not regain mobility of tail.

Question 9

1. Diseases that can cause generalised loss of muscle mass as a predominant clinical sign.
2. Diseases that can cause focal loss of muscle mass as a predominant clinical sign.

Answer 9

1. Polymyositis.
   Congenital myopathy (likely in young animals).
   Ddx: systemic dz.
   - e.g. PLE/PLN causing cachexia.
2. Nerve sheath tumour.
   Bilateral loss of muscle in the head:
   - think masticatory myositis.
   Unilateral loss of muscle mass in the head:
   - think nerve sheath tumour.

Question 10

Polymyositis aetiology.

Answer 10

Mostly immune-mediated.
- very frequently masticatory myositis rather than generalised.
– >6months old.
Then infectious.
- most commonly neospora (young dog), which can also cause radiculoneuritis and myositis
Then paraneoplastic.
- very rarely.
- expected more in older dogs.

Question 11

Dx of polymyositis causes.

Answer 11

Serology for neospora, toxoplasma, masticatory muscle myositis (of antibodies against these fibres).
Biopsy of muscle.
Other blood testing for extremely increased AST and CK.
- 10x baseline for myositis and 10,000x baseline for myopathy.

Question 12

Polymyositis localisation.

Answer 12

Muscle atrophy and exercise intolerance.
Reflexes and responses are reserved.
May only affect pharynx, causing dysphagia/regurgitation - Vislas.

Question 13

Does polymyositis cause pain?

Answer 13

Not a typical feature but can be seen.
Remember to palpate muscles to establish if painful.

Question 14

1. Brachial plexus tumour diagnosis.
2. Tx of brachial plexus tumour.
3. Px of brachial plexus tumour?

Answer 14

1. Hx (insidious onset) + CE.
   - lameness, then pain, then muscle loss, then loss of reflexes.
   MRI better than CT - visualise enlargement of the nerves.
   Electrodiagnostics - abnormal.
   Biopsy is definitive.
   - difficult to access as complex structures surrounding.
   - can cause iatrogenic damage.
2. Sx - remove tumour +/- amputation (px can be much improved).
   Palliative w/o sx - may not be ethical due to level of pain.
3. Px guarded.
   - months to years.

Question 15

Causes of insidious onset fatigue +/- loss of reflexes and muscle mass.

Answer 15

Exercise induced weakness.
- myasthenia gravis.
- Ddx = CR diseases.
- Ddx = metabolic diseases.
Progressive (weeks to months) weakness.
- degenerative polyneuropathy.

Question 16

Myasthenia gravis clinical signs.

Answer 16

Stiff gait.
Weakness more notable on exercise.
Megaoesophagus - regurgitation.
Progressively weakening patellar reflex over 10 mins.

Question 17

Dx myasthenia gravis.

Answer 17

Hx and clinical signs.
- insidious onset of signs.
- may be acute/fulminant.
– px even poorer.
Assess exercise tolerance.
Assess reflexes over time.
Thoracic radiographs.
- for megaoesophagus.
- to look at mediastinum to assess for a mass that may be triggering antibodies against acetylcholine.
Rule out metabolic differentials.
Neostigmine (Tensilon) test / Acetylcholine receptor antibody titre / electrodiagnostics.

Question 18

1. Treatment of myasthenia gravis.
2. Px of myasthenia gravis?

Answer 18

1. Acetylcholinesterase inhibitors (pyridostigmine).
   +/- immune suppression.
   Postural feeding (Bailey’s chair).
2. Guarded.
   - death usually caused by megaoesophagus complications incl. aspiration pneumonia.

Question 19

Dx of of degenerative polyneuropathy.

Answer 19

Rule out metabolic differentials.
Electrodiagnostics - supportive.
Nerve biopsy - often see mild changes.
Genetic testing.
Signs of sciatic nerve defects?
Signs of recurrent laryngeal nerve deficits?
- more obvious as progresses.

Question 20

Px and tx of degenerative polyneuropathy?

Answer 20

Guarded to poor over months/years.
Monitor and assess QoL.
May remain static for a long period.
Supportive tx.
- steroids – important to definitively diagnose as can make worse in some cases of other dz.

Question 21

Idiopathic facial nerve paralysis:
- signalment.
- onset.
- progression.
- symmetry.
- pain.
- tx?

Answer 21

Adult dogs.
Peracute.
Improvement after weeks/months.
Asymmetrical.
Non painful.
Supportive tx.
- tear replacement in cases where tear production is affected.
– to reduce risk of KCS.

Question 21

1. Acute cranial neuropathies.
2. Chronic progressive cranial neuropathies.

Answer 21

1. Idiopathic facial nerve paralysis.
   Idiopathic peripheral vestibular syndrome.
   Idiopathic trigeminal neuritis.
   Otitis media/interna (only one that is not idiopathic).
   Idiopathic Horner syndrome.
2. Nerve sheath tumour.

Question 22

1. Dx of idiopathic peripheral vestibular syndrome.
2. Px of idiopathic peripheral vestibular syndrome.
3. Tx of idiopathic vestibular syndrome?

Answer 22

1. Normal clinical and otological exam.
   MRI and CSF - largely unremarkable. Geriatric signalment.
   Localise central or peripheral.
   - peripheral better outcomes.
2. 2/3 resolve.
   Marked improvement over 72hrs.
   Most common differential for peripheral vestibular disease so avoid euthanasia.
3. Supportive.
   NO STEROIDS.

Question 23

1. Idiopathic peripheral vestibular syndrome localisation.
2. Signalment for idiopathic vestibular syndrome?
3. Onset/chronology of idiopathic peripheral vestibular syndrome?
   - progression?
   - symmetry?
   - pain?

Answer 23

1. CN VIII (head tilt, ataxia, nystagmus) +/- CN VII +/- Horner syndrome.
2. Older dogs ++.
3. Peracute.
   - improves in days/weeks.
   - asymmetrical.
   - non painful.

Question 24

Non-idiopathic peripheral vestibular syndrome.

Answer 24

Ddx = otitis media/interna. - otological exam. - +/- MRI/CT/myringotomy. = (neoplasia). = (trauma). In dogs, idiopathic more commonly than otitis. In cats otitis (polyps) more commonly than idiopathic.