Chapter 27 - Lower motor neuron disease Flashcards
What composes the ‘‘motor unit’’?
A motor unit is composed of lower motor neuron, the neuromuscular junctions and the muscle fibers they innervate
Where are the lower motor neuron cell bodies located?
The lower motor neuron cell bodies are located in cranial nerve nuclei and ventral horn grey matter of the spinal cord
What neurotransmitter is released into the neuromuscular junctions and what receptor does it bind to on the postsynaptic membrane?
Acetylcholine (ACh) is released from vesicles within the axon terminal into the synaptic cleft and binds to nicotinic ACh receptors on the postsynaptic membrane.
Give examples of LMN junctionopathy
- Myasthenia gravis
- Botulism
- Tick paralysis
- Black widow spider
- Pesticides (organophosphates, carbamates)
- Drugs (aminoglycosides, ampicillin, tetracyclines, ciprofloxacine, imipenem, phenothiazines, antiarrhythmics)
Which one of these four diseases does not affect the autonomic function? Polyradiculoneuritis, tick paralysis, botulism, fulminant myasthenia gravis
Polyradiculoneuritis
The others may cause megaesophagus, urinary incontinence /retention (except MG), cardiovascular dysfunction (except MG)
Which one of these four diseases may be associated with some spinal pain? Polyradiculoneuritis, tick paralysis, botulism, fulminant myasthenia gravis
Polyradiculoneuritis
Which one of these four diseases has a decremental response to repetitive nerve stimulation? Normal or incremental response?
Polyradiculoneuritis, tick paralysis, botulism, fulminant myasthenia gravis
Decremental response to repetitive nerve stimulation: Fulminant myasthenia gravis
Normal or incremental response to repetitive nerve stimulation: Botulism
What is the underlying cause for acute polyradiculoneuritis?
Immune-mediated disease
In case of acute polyradiculoneuritis, where are the lesions?
The immune reaction targets primarily ventral (motor) nerve roots of spinal nerves
How long does it take for acute polyradiculoneuritis to reach the maximal dysfunction?
3-10 days
What is the prognosis of acute polyradiculoneuritis?
With adequate supportive care, most dogs make a full recovery, though the most severely affected may take 4-6 months and may have mild residual neurological deficits
What ticks can cause tick paralysis?
Ixodes (holocyclus or cornuatus), or Dermacentor (andersoni or variabilis)
What are the mechanisms leading to LMN clinical signs in case of tick paralysis (pathophysiology)?
The tick salivary neurotoxin (holocyclotoxin) is thought to impair ACh release at the neuromuscular junction by blocking Ca2+ influx at the axon terminal.
Holocyclotoxin also impairs ACh at autonomic synapses, resulting in autonomic imbalance (cardiac diastolic dysfunction, left-sided congestive heart failure, bladder dysfunction, pupillary dilation, megaesophagus)
T/F: Female only cause tick paralysis
T
What are the mechanisms leading to LMN clinical signs in case of botulism (pathophysiology)?
Botulinum neurotoxin is produced by G+ anaerobic Clostridium botulinum and rapidly and irreversibly binds to neuronal surface receptors on nerve terminals, is internalized, and prevents synaptic release of ACh at the neuromuscular junction, causing flaccid paralysis.
As ACh release is also inhibited at autonomic synapses, signs of autonomic dysfunction may be seen.
