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Spine / lower motor neuron Flashcards

1
Q

What is the mechanism (presynaptic / postsynaptic) of lower motor neuron dysfunction for tick paralysis / elapid snake envenomation / botulism / myasthenia gravis

A
  • Tick paralysis: pre-synaptic -> inhibits depolarization in distal motor neurons + inhibitis release of ACh at the NMJ
  • Elapid snake envenomation: pre-synaptic (phospholipase A2 -> prevents release of ACh) and post-synaptic (ACh receptor antagonist)
  • Botulism: pre-synaptic -> inhibits ACh release (blocks ACh vesicular fusion with terminal membrane)
  • Myasthenia gravis: post-synaptic -> destruction / blockade of ACh receptors at NMJ
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2
Q

What are the 2 toxins produced by Clostridium tetani? Which one is responsible for the clinical signs of tetanus

A
  • Tetanolysin: causes local tissue damage and helps proliferation of C tetani in wounds
  • Tetanospasmin: responsible of neuro signs
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3
Q

Explain the pathogenesis of tetanus

A
  • Contamination of a wound by spores of Clostridium tetani
  • Spores proliferate under anaerobic conditions in the wound and secrete tetanolysin and tetanospasmin
  • Tetanospasmin is internalized in axons and transported retrograde in motor, then sensory and autonomic neurons (peripheral -> spinal cord -> brain)
  • Tetanospasmin inhibits neurotransmitter release by inactivating synaptobrevin. Mostly affects inhibitory neurons (release of GABA and glycine) -> disinhibited neuronal activity in motoneurons first then autonomic neurons
  • Binding of toxin is irreversible -> need to build new neurons
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4
Q

What is the resistance of cats to tetanus compared to dogs

A

10 times more resistant
(and dogs are 600 times more resistant than horses)

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5
Q

What are possible autonomic signs of tetanus

A
  • Bradycardia, tachycardia, arrhythmias (disinhibited parasympathetic or sympathetic stimulation)
  • Hypertension
  • Hypoperfusion from vasoconstriction
  • Salivation
  • Increased bronchial secretions
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6
Q

What is the delay between wound infection and development of clinical signs in tetanus? Over how long do clinical signs typically get worse? By how long is improvement expected?

A
  • Usually 5-12 days before development of signs (up to 4 weeks)
  • Progression over a median of 4 days (up to 14 days)
  • Improvement expected within 5-12 days
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7
Q

What is the recommended dose of equine tetanus antitoxin for dogs and cats? For how long will the antitoxin persist in circulation?

A

100-1000 U/kg (max 20000 U/kg) IV preferably or IM or SQ

Persists for 14 days ->do not repeat dose!

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8
Q

What is the serum total magnesium goal in patients with tetanus treated with MgSO4

A

2-4 mmol/L

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9
Q

Describe the tetanus severity classification system

A
  • Class I: only facial signs
  • Class II: generalized rigidity and dysphagia (with or without facial signs)
  • Class III: class I and/or class II signs + recumbency and/or seizures
  • Class IV: class I and/or II and/or III signs + abnormal HR, RR, and/or BP

Survival 100% for class I and class II, 58% for class III-IV

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10
Q

What is the main prognostic indicator in tetanus in dogs

A

Autonomic dysfunction (associated with mortality)

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11
Q

What cells are damaged in the Schiff-Sherington posture

A

Border cells
(inhibitory to thoracic limb motor tone)

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12
Q

What reflexes are most affected by spinal shock? What is the usual delay before reflexes are re-established?

A

Withdrawal reflexes > patellar reflexes

Usually come back in 2h (patellar) to 12h (withdrawal)

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13
Q

What are the chances of return to ambulation for dogs with spinal trauma with loss of nociception

A

12%

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14
Q

True or false: Orthogonal spinal radiographs (lateral and VD) should be obtained in case of suspicion of vertebral fracture / luxation

A

Only if you can take a horizontal beam radiograph.
The patient should never be turned if there is suspicion of fracture / luxation

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15
Q

What are the chances of recovery (partial or full) for dogs with thoracolumbar IVDD with nociception / without nociception

A
  • With nociception -> 50-100% with medical management, 95-97% with surgical management
  • Without nociception -> <5-7% with medical management, 25-75% with surgical management
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16
Q

What are the most common bacteria involved in diskospondylitis

A
  • Staphylococcus spp
  • Brucella spp
  • Streptococcus spp
  • E Coli

Less common:
- Bordetella spp
- E faecalis
- Pseudomonas aeruginosa

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17
Q

What radiographic changes are associated with diskospondylitis

A
  • Collapse of the intervertebral disk space
  • Bone lysis centered at the vertebral endplates
  • Sclerosis
  • Spondylosis
  • Possible secondary fractures / luxations
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18
Q

What fungal agent can cause diskospondylitis

A

Aspergillus (systemic aspergillosis)

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19
Q

What is the average duration of treatment for diskospondylitis

A

1 year (at least 4-6 months)

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20
Q

What are the most commonly affected sites in diskospondylitis

A

L7-S1, T13-L1, L1-L2, L2-L3

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21
Q

What is a recommended first-line empiric antibiotic for diskospondylitis

A

Cephalexin

(Clavamox ok too)

22
Q

What is the prevalence of progressive myelomalacia in dogs with IVDD

A

2% overall, 10-15% in dogs without nociception

23
Q

Name causes of focal neuromuscular disease

A
  1. Neuropathy:
    - Traumatic (brachial plexus avulsion, sciatic nerve injury, caudal nerve injury)
    - Ischemic neuromyopathy (aortic thrombus)
  2. Junctionopathy
    - Focal myasthenia gavis
  3. Myopathy
    - Inflammatory (masticatory myositis, extraocular myositis)
    - Trauma (direct trauma, compartment syndrome)
    - Ischemic neuromyopathy (aortic thrombus)
  4. Neoplasia
    - Peripheral nerve sheath tumor
    - Lymphoma
    - Peripheral meningioma
24
Q

Name causes of generalized neuromuscular disease

A
  1. Neuropathy
    - Polyradiculoneuritis
    - Degenerative (inherited polyneuropathy, lysosomal storage disease)
    - Metabolic (diabetic polyneuropathy, hypothyroid neuropathy, hyperinsulinism)
    - Paraneoplastic
    - Infectious (Toxoplasma, Neospora)
    - Toxin (heavy metals, organophosphates)
    - Drugs (vincristine, vinblastine, cisplatin)
  2. Junctionopathy
    - Myasthenia gravis
    - Toxin (botulism, tick paralysis, Black widow spider, organophosphates, blue-green algae, etc.)
    - Drugs (aminoglycosides, ampicillin, ciprofloxacin, imipenem, phenothiazines, tetracyclines, anti-arrhythmics)
  3. Myopathy
    - Metabolic (hypoK, hypo- / hyper-adrenocorticism, hypothyroidism, mitochondrial myopathy)
    - Inflammatory (immune-mediated polymyositis)
    - Infectious (Toxoplasma, Neospora, Babesia, Leishmania, Clostridium, Lepto)
    - Degenerative / inherited
25
Which antibiotics can cause dysfunction of the neuromuscular junction
- Aminoglycosides ++ - Ampicillin - Tetracyclines - Ciprofloxacin - Imipenem
26
What are the 4 main causes of acute generalized neuromuscular weakness
- Botulism - Tick paralysis - Polyradiculoneuritis - Fulminant myasthenia gravis
27
What is the pathogenesis of polyradiculoneuritis
Immune-mediated reaction (cell-mediated and humoral with antiglioside antibodies) against ventral nerve roots of spinal nerves -> demyelination, axonal degeneration Usually follows a trigger factor (respiratory or GI infection, Toxo infection, surgery, raccoon saliva exposure, etc)
28
Among tick paralysis, botulism, MG, and polyradiculoneuritis, which one(s) cause(s); - autonomic dysfunction - marked cranial nerve deficits - ascending paralysis - abnormal CSF
1. Autonomic dysfunction: - Botulism (megaesophagus, urine retention / incontinence, altered HR) - Tick paralysis (Australian ticks: megaesophagus, urine retention /incontinence, diastolic dysfunction with severe CHF) - MG only megaesophagus 2. Marked cranial nerve deficits: - Botulism (most severe) - Tick paralysis (Australian ticks) (MG and polyradiculoneuritis can cause some facial paresis) 3. Ascending paralysis: - Polyradiculoneuritis - Tick paralysis 4. Abnormal CSF: - Polyradiculoneuritis (increased protein with normal cell count, more evident on lumbar sample)
29
What is the treatment for polyradiculoneuritis
None except supportive care Can do plasmapheresis or give human IV Ig to allow faster recovery
30
What ticks cause tick paralysis in Australia / North America
- Australia: Ixodes holocyclus or Ixodes cornuatus - North America: Dermacentor andersoni, Dermacentor variabilis
31
What is the pathogenesis of tick paralysis
Release of neurotoxin in the host while the tick is feeding (through tick's saliva) -> blockage of iCa influx in pre-synaptic neuron -> impaired ACh release at the NMJ Holocyclotoxin (from Australian ticks) also targets autonomic nerves -> autonomic imbalance with sympathetic overdrive
32
What is the treatment for tick paralysis
- Removal of tick - Tick antitoxin serum in Australia
33
What is the pathogenesis of botulism
Ingestion of a preformed botulinum neurotoxin (formed by C botulinum) usually in spoiled food -> binds neuronal surface receptors -> internalized -> cleavage of SNARE proteins -> prevents fusion of synaptic vesicles with presynaptic membrane so prevents release of ACh in NMJ
34
What serotypes of botulinum neurotoxin cause botulism in cats and dogs
BoNT-C mostly (2 cases reported with BoNT-D)
35
Can antitoxin serum be used for botulism
No because human serum is only available for neurotoxins A, B, and E (and dogs are mostly affected by C +/- D) There is one equine heptavalent antitoxin for humans - but not approved for use in veterinary medicine and high risk of anaphylaxis
36
Indicate what part of the neuromuscular system is affected in polyradiculoneuritis / botulism / tick paralysis / myasthenia gravis
- Polyradiculoneuritis: neuron (nerve roots) - Botulism: pre-synaptic - Tick paralysis: pre-synaptic - MG: post-synaptic
37
What is the pathogenesis of myasthenia gravis
Production of auto-antibodies against the ACh receptor of the post-synaptic membrane of the NMJ
38
What can be used for a cholinesterase inhibitor challenge for suspected MG? What are the risks?
- Edrophonium 0.1-0.2 mg/kg IV in dogs (or 025-0.5 mg/cat) - OR neostigmine 40 mcg/kg IM or 20 mcg/kg IV Risks: increased respiratory secretions, bradycardia, salivation, diarrhea, bronchospasm
39
What is the treatment for myasthenia gravis
- Cholinesterase inhibitors: pyridostigmine 0.5-3 mg/kg in dogs / 0.25 mg/kg in cats (or 0.01-0.03 mg/kg/h IV) or neostigmine 0.04 mg/kg IM q6h - Immunosuppression is controversial, to be avoided in case of aspiration pneumonia - Can consider TPE / human IV Ig for fulminant form
40
Indicate which diseases among polyradiculoneuritis, MG, botulism, and tick paralysis have the longest expected duration of clinical signs
- Polyradiculoneuritis = 3-6 weeks (recovery can take months) - Botulism = 2-3 weeks (needs to produce new SNARE proteins) - Tick paralysis = within a few hours of tick removal for American tick, a few days for Australian despite antitoxin - MG = variable depending on treatment used and response
41
Name 3 possible causes of respiratory distress in dogs with tick paralysis
- Respiratory paralysis - Cardiogenic pulmonary edema (diastolic dysfunction) - Aspiration pneumonia
42
What is the confirmatory diagnostic test for MG
Titers of antibodies against ACh receptor (dog: >0.6 nmol/L, cats: >0.3 nmol/L) Some dogs can be seronegative if have a form of MG directed against other components of the NMJ (eg. MUSK protein in the muscle)
43
What are 2 underlying causes of MG in cats
- Thymoma (55% of cats with MG have a mediastinal mass) - Thiourylene medication (methimazole)
44
List 3 types of congenital myasthenic syndromes
- Pre-synaptic = mutation in choline acetyltransferase gene (no ACh production) - Synaptic = acetylcholinesterase deficiency - Post-synaptic = primary deficiency in ACh receptor
45
What is the classification of MG in dogs and cats
Focal / generalized / fulminant + subclasses based on underlying cause (see picture)
46
Mechanism of action of magnesium in tetanus
Non-specific calcium channel blocker. At the neuromuscular junction, magnesium decreases calcium entry into presynaptic terminals resulting in decreased ACh release. In addition, it decreases the sensitivity of postsynaptic motor endplates to ACh with the net result of muscle relaxation.
47
2 factors that have been associated with poor outcome in tetanus
- Respiratory complications - Presence of autonomic signs
48
Which enzyme catalyzes the formation of ACh from acetyl coenzyme A (CoA) and choline in the presynaptic terminal?
Choline acetyltransferase
49
What is the mechanism of action of neostigmine?
Acetylcholinesterase inhibitor Block the degradation of ACh, prolong its action at the muscle end plate, and increase the size of end plate potential
50
Which of the lower motor neuron diseases does not impact autonomic function?
Polyradiculoneuritis (coonhound paralysis)
51
What is the risk of cholinesterase inhibitors?
Cholinergic crisis
52
True or false: patients can have spontaneous immune remission of myasthenia gravis
True - in generalized non-thymoma associated MG for dogs and cats

Neuro (4 decks)

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