Peripheral nervous system diseases 1

Question 1

PNS components

Answer 1

 Ventral roots
 Spinal nerve
 Peripheral nerve
 NMJ
 Muscle

Question 2

Peripheral nervous system or
Neuromuscular diseases categories

Answer 2

1. Peripheral nerve
2. Neuromuscular junction
3. Skeletal muscle

Question 3

Peripheral nerve disease (neuropathy)
- what we see?

Answer 3

 Reflexes: Decreased / absent
 Reduced / absent muscle tone
 CNs: can be affected
 Neurogenic muscle atrophy

Question 4

Neuromuscular junction disease
(junctionopathy)
- what we see?

Answer 4

 Reflexes: Normal / Decreased / Absent
 Diffuse clinical signs vs focal
 Exercise-induced weakness (MG)
 CNs: can be affected
 E.g. Myasthenia gravis, botulism

Question 5

Muscle disease (myopathy)
- what we see?

Answer 5

 Reflexes: Usually normal
 Focal vs Diffuse (exercise intolerance)
 Severe muscle atrophy
 Muscle pain possible
 CNs: usually normal (masticatory ms atrophy)
 E.g. Polymyositis, masticatory muscle myositis

Question 6

Mono-neuropathies:
- what can be affected

Answer 6

 One nerve affected
> E.g. facial paralysis, radial nerve trauma…
 A group of adjacent nerves affected
> E.g. brachial plexus avulsion

Question 7

Poly-neuropathies:
- what can be affected?

Answer 7

 All limbs affected
 Cranial nerves can be affected
 E.g. coonhound paralysis

Question 8

main causes of mononeuropathies

Answer 8

Traumatic
 Brachial plexus avulsion
 Radial nerve, sciatic nerve damage
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Neoplastic
 Peripheral nerve sheath tumor (PNST)
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Others
 Ischemic neuromyopathy, foraminal IVDH,
inflammatory (abscess, brachial plexus neuritis)

Question 9

Brachial plexus avulsion
- what does it cause? how common?
- what can cause it?

Answer 9

 Most common cause of acute thoracic limb
monoparesis / monoplegia
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 Causes:
◦ Abduction and simultaneous caudal displacement TL
◦ Road traffic accidents, falls from a height

Question 10

Brachial plexus avulsion
 Pathogenesis:

Answer 10

◦ Traction nerves brachial plexus (C6-T2)
◦ Avulsion nerve roots from spinal cord
> Ventral roots more affected (C6-T2)

Question 11

Brachial plexus avulsion: Clinical signs

Answer 11

 Acute monoparesis / monoplegia TL
> LMN: C6-T2
 Dragging, knuckling, unable to bear weight
 Absent proprioception
 Decreased/absent spinal reflexes TL
 Hypotonia, neurogenic atrophy
 It is NOT a painful disease!
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Horner’s syndrome (T1-T3)
 Usually partial: Miosis
 Protrusion 3rd eyelid
 Enophtalmos
 Ptosis
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Absent ipsilateral cutaneous trunci (C8-T1)

Question 12

Brachial plexus avulsion: Treatment

Answer 12

Supportive:
◦ Prevent contractures, abrasive lesions (dragging)
◦ Keep limb clean and dry
◦ Covering foot with boots, bandages
◦ Treating any wound
◦ Physical therapy

Question 13

Brachial plexus avulsion: Prognosis

Answer 13

Best predictor: DEEP PAIN
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◦ Preserved: Recommend supportive treatment
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◦ Absent: Few chances of recovery
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◦ If no improvement during first 2 months: Recovery is unlikely
> Consider AMPUTATION (self-mutilation)

Question 14

Atrophy supra/infraspinosus corresponds to what spinal segments?

Answer 14

 C5-C7 (suprascapular nerve)

Question 15

Cutaneous trunci: what spinal segments?

Answer 15

 C8-T1

Question 16

Peripheral nerve sheath tumor (PNST)
- Origin
- areas affected
- spread

Answer 16

 Origin: Cells surrounding axons in the PNS
 Any peripheral nerve or nerve root
 Common: C6-T2, CN V (trigeminal)
 Slow spread:
◦ Proximally and distally along the nerve
◦ May invade the vertebral canal

Question 17

PNST C6-T2: Clinical signs

Answer 17

Lameness vs monoparesis TL:
◦ Unilateral, chronic, progressive
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Neurologic dysfunction:
◦ Can take weeks-months before is noticed!
◦ LMN
◦ Absent cutaneous trunci (C8-T1): ipsilateral
◦ Horner’s syndrome (T1-T3): ipsilateral
◦ Rarely on axillary palpation: pain, detectable mass

Question 18

PNST CN V – Trigeminal nerve is affected - signs

Answer 18

 Unilateral atrophy masticatory muscles (acute)

Question 19

Polyneuropathies
- what does this mean?
- clinical signs?

Answer 19

Multiple peripheral nerves dysfunction
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Clinical signs:
◦ Tetraparesis / tetraplegia (flaccid)
◦ Decreased / absent spinal reflexes
◦ Neurogenic atrophy, unable to lift the head
◦ CNs:
> CN X: dysphonia/aphonia, megaesophagus
> CN VII: facial paralysis

Question 20

Polyneuropathies: Causes
- acute and chronic

Answer 20

ACUTE
 Acute idiopathic polyradiculoneuritis
> “Coonhound paralysis”
 DxD: Botulism/Tick paralysis/Acute fulminating MG
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CHRONIC
 Multitude reported
> Inherited / Degenerative (breed-related)
> Acquired (progressive)

Question 21

Polyneuropathies: Chronic
- possible causes we see: infectious, metabolic, neoplasia

Answer 21

• Neospora, Toxoplasma
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  Endocrine:
• Hypothyroidism
• Diabetes mellitus
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  Paraneoplasitc:
• Insulinoma
• Malignant neoplasias

Question 22

Acute idiopathic polyradiculoneuritis
- what is this?
- who gets it?
- pathogenesis
- anatomy affected

Answer 22

 “Coonhound paralysis” (CHP)
 Most common in dogs
 Immune-mediated
> Contact with raccoon saliva (1-2w before)
> Post-vaccination
> AIP vs CHP: Same syndrome!
=> CHP: trigger identified
=> AIP: trigger unidentified
 Ventral roots / proximal nerve portion

Question 23

Acute idiopathic polyradiculoneuritis:
Clinical signs

Answer 23

• Rapid generalized LMN paresis (flaccid)
  ◦ Tetraparesis
  ◦ Decreased reflexes
  ◦ Decreased muscle tone
• PLs and progress to TLs (sometimes opposite)
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  Variable severity:
   Tetraparesis / tetraplegia
   Respiratory paralysis (Life-threatening)
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  CNs:
  1.CN X (dysphonia/aphonia) : common
  2.CN VII (facial paresis): occasionally
   Usually able to urinate/defecate, eat/drink

Question 24

Acute canine polyradiculoneuritis:
 Course of the disease:

Answer 24

1. Initially progressive
    Up to 5-10d post-onset
2. Stable
    Usually 2-3w (up to 4-6m)
3. Slow recovery
    Weeks-months (usually complete)

Question 25

Acute canine polyradiculoneuritis:
Diagnosis

Answer 25

 History
> Raccon contact, vaccination
 CS
> Acute, progressive, generalized LMN
 Rule-out other causes:
> CBC, biochem profile, UA
> Thoracic radiographs, abdominal Ux
 Support diagnosis:
> Electrodiagnosis: EMG, NCV…
> Muscle / nerve biopsies

Question 26

Acute canine polyradiculoneuritis:
Treatment

Answer 26

 Supportive care:
> Frequent turning, padding…
 Physiotherapy
 Monitoring respiratory function
 Do NOT use corticosteroids!

Question 27

Myasthenia gravis
- what is it? forms?
- what do we see?

Answer 27

Transmission failure of ACh at the NMJ:
 Congenital form
 Acquired form
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EXERCISE-INDUCED WEAKNESS
◦ Normal neurologic examination prior to induction of
exercise-induced weakness
◦ Normal spinal reflexes

Question 28

Myasthenia gravis
- who gets it?
- species, age

Answer 28

 Dogs > cats
 Age:
> Bimodal
> 4m-4y vs 9y-13y

Question 29

Myasthenia gravis
 Pathogenesis:

Answer 29

1. Congenital MG: failure of receptors, uncommon
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2. Acquired MG:
    Autoimmune: Ab anti-AchR (nicotinic)
    Association with thymoma
    Focal vs generalized clinical syndromes

Question 30

Myasthenia gravis: Diagnosis

Answer 30

ACh receptor antibody concentration
 GOLD STANDARD
 High sensitivity (98%) and specificity
 Negative in congenital MG
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Thoracic radiographs:
◦ MEGAESOPHAGUS
◦ Aspiration pneumonia
◦ Cranial thoracic mass
(thymoma)
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Edrophonium chloride test (Tensilon):
 Ultra-short-acting treatment (anti-AChE)
 Dramatic increase in muscle strength
 Frequent false positives and negatives
 Supports presumptive diagnosis
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CBC, biochem profile, UA:
◦ Unremarkable

Question 31

Myasthenia gravis: Treatment

Answer 31

Anticholinesterase drugs (anti-AChE)
 Pyridostigmine (0.5-2 mg/kg q8h PO)
 Neostigmine (0.04 mg/kg q6h IM)
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Supportive treatment:
 Aspiration pneumonia, gastrostomy tube, respiratory support
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Prognosis:
 Guarded
 High incidence aspiration pneumonia (megaesophagus)