Term
| A dog presents with a 5 day history of progressive difficult walking. His head is down, no reflexes/withdrawal, and showing signs of LMN in all four legs. He has pressure sores and bite wounds around his nose. 24 hours later the dog develops diaphragm paresis. What is the most likely differential? |
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Definition
| Acute Canine Polyradiculoneuritis (ACP), also known as Coonhound Paralysis |
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Term
| What are the most common causes of ACP? |
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Definition
Similar to Guillan Barre syndrome:
1. Campylobacter jejuni infection
2. Post-rabies or influenza vaccine |
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Term
| What is the pathogenesis of ACP? |
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Definition
| Immune mediated mechanism; production of autoantibodies against axon and myelin |
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Term
| What nerve roots develop the most severe pathology in ACP? |
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Definition
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Term
| What nerve roots are essentially spared in ACP? What clinical sign does this lead to? |
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Definition
Dorsal (sensory)
An animal with severe paresis or plegia will still have preservation of pain sensation or even hyperethesia |
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Term
| What spinal cord sections are most severely involved in ACP? |
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Definition
| Lumbar and sacral nerve roots |
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Term
| What is the general progression of ACP? |
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Definition
Clinical signs develop after 7-14 of raccoon or vaccine exposure
- Initial stiff gait
- Rapid progression to LMN tetraparesis/plegia
-Pelvic limbs first, then thoracic |
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Term
| What characteristic of ACP progression is important to keep in mind when seeing a dog in the clinic? |
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Definition
| The progressive phase is 5-7 days, and they will usually get WORSE before they get better |
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Term
| What very common clinical sign for ACP is caused by dysphonia? |
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Definition
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Term
| What clinical sign may you see in a severe case of ACP? |
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Definition
| Paralysis of diaphragm and intercostal muscles |
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Term
| What are the 3 major differences in clinical signs that help distinguish ACP from other LMN diseases? |
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Definition
1. No smooth muscle/autonomic involvement
2. No megaesophagus
3. No cranial nerve dysfunction |
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Term
| How long will it take a dog with ACP to recover, and what is this related to? |
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Definition
Can take between 2 weeks and 6 months, depending on degree of axonal involvement:
- Demyelination is quick to improve
- Axon degeneration takes more time |
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Term
| What is the diagonstic approach for ACP? |
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Definition
Presumptive based on history and neuro exam.
- Lumbar CSF will show increased protein
- Cisternal CSF will be normal |
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Term
| What is the treatment for ACP? |
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Definition
| Supportive care: monitor for respiratory compromise, hand feed, IV fluids, intensive physical therapy |
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Term
| What is the indication for steroids when treating ACP? |
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Definition
| CONTRAindicated - can potentiate muscle weakness and cause other adverse affects |
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Term
| Do dogs develop immunity to ACP? |
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Definition
| No - next bouts are often worse |
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Term
| What is the prognosis for ACP? |
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Definition
| Most recover fully but can take up 2 weeks to 6 months. Severe cases may have residual side-effects, often becomes "financial disease" for owners. |
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Term
| A 5 year old thoroughbred presents with a 2 day history of reluctance to walk, diffuse weakness in all 4 limbs, trouble swallowing, and muscle tremors. What is the likely differential? |
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Definition
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Term
| What are the 3 routes of botulism infection? |
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Definition
Due to ingestion of neurotoxin Clostridum botulinum:
1. Ingestion of pre-formed food (carrion, spoiled)
2. Wound botulism
3. Toxicoinfections (Shaker foals, human infants consuming raw honey) |
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Term
| What is the pathogenesis for botulism? |
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Definition
| Toxin enters nervous system at nerve endings, inhibits transmission of action potential at the NMJ. Prevents ACh release from pre-synaptic terminals. |
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Term
| What are common clinical signs of botulism? |
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Definition
Depends on toxin ingested and species
1. Mild weakness to tetraplegia
2. Dysphonia
3. Evidence of smooth m./autonomic/CN dysfunction: Megaesophagus, dysphagia, mydriasis, decreased PLRs |
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Term
| How does botulism contrast to ACP? |
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Definition
ACP - NO smooth m. involvement, no megaesophagus, no CN involvemnt
Botulism - Flaccid paralysis of smooth AND striated m., megaesophagus, CN dysfunction |
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Term
| What is the gold standard for botulism? Is it commonly used? |
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Definition
| Identificaton of toxin in ingesta, or by neutralization test in small rodents -- NOT commonly used |
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Term
| What is the common diagnostic approach for botulism? |
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Definition
| History, thoracic radiographs (megaesoph, aspiration pneumonia) |
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Term
| What is the treatment for botulism? |
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Definition
| Supportive care: Prevent aspiration pneumonia, bladder care, physical therapy, prevention of pressure sores. Antitoxin not usually used for small animals, may be used for equine. |
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Term
| Why is botulism not treated with antibiotics? |
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Definition
| The animals are not infected with bacteria, in most cases it is an ingested toxin. May be used in the case of wound botulism to prevent infections. |
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Term
| An 8 year old maltese presents with 1 day history of progressive weakness, flaccid paralysis/paresis in all 4 limbs, nociception intact. A tick is removed and she walks within 24 hours. WHAT COULD IT BE |
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Definition
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Term
|
Definition
| Salivary neurotoxin secreted by attached female ticks |
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Term
| Pathogenesis of tick paralysis? |
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Definition
| Females releases neurotoxin, at NMJ, toxin interferes with function of calcium in the release of Ach from the axon terminal (pre-synaptic) |
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Term
| Clinical signs of tick paralysis? |
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Definition
Occur 5-9 days after attachment
Rapid onset LMN paresis starting in pelvic limbs
Animals recumbent in 24-72 hours |
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Term
| Common cause of death in tick paralysis? |
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Definition
| If tick is not removed, death occurs in 1-5 days as a result of respiratory paralysis |
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Term
| Clinical signs that differentiate tick paralysis from other LMN diseases? |
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Definition
No cranial involvement
No megaesophagus
Recovery 24 hours after tick removal |
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Term
| Diagnosis of tick paralysis? |
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Definition
| History of tick exposure, identification of attached tick |
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Term
| Why do you not use doxycycline to treat tick paralysis? |
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Definition
| It is caused by a neurotoxin, not bacterial infection |
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Term
| A 2 year old Newfoundalnd has a 3 day history of being down in pelvic limbs. Non-ataxic tetraparesis, drooling. Within 2 hours of administering an anticholinesterase agent, he is walking again. Differential? |
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Definition
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Term
| What are the two forms of MG? Which is more common |
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Definition
Congenital
Acquired - Most common |
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Term
| Pathogenesis of acquired MG? |
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Definition
| Auto-antibody mediated destruction of Ach receptors at the NMJ, results in muscle weakness and fatigability. Binding of autoantibodies to post-synaptic AchR leads to compliment-mediated destruction of the AchR. Clinical signs present when there are an inadequate number of AchR to bind Ach in the NMJ. |
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Term
| What breeds of dogs and cats are most commonly affected by acquired MG? |
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Definition
MOST COMMON neuromusc disease diagnosed in dogs.
Golden, German shepherd, German short haired pointer.
Familial acquired form in Newfies and Great Danes.
Less common in cats - Abyssinians and Somalis |
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Term
| What are the 3 clinical syndromes of acquired MG? |
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Definition
1. Generalized - most common in vet med
2. Focal - common in human med
3. Fulminating |
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Term
| Clinical signs of generalized MG? |
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Definition
1. Neurologically normal at rest
2. Paresis in pelvic limbs after activity, progresses to thoracic if activity continued
3. Regurgitation (passive -- vomiting is active)
4. Normal spinal reflexes
5. Drooling, eyelid and lip paresis |
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Term
| Most common clinical signs of generalized MG in dogs versus cats? |
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Definition
Dogs - Megaesophagus (84%), Thymoma (3%)
Cats - Thymoma more common than megaesophagus (benign thyroid tumor)
May also see ventroflexion of neck in cats |
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Term
| Where does focal MG occur? |
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Definition
Single muscle groups innervated by cranial nerves.
Most common site is esophagus
Can also be larynx or pharynx (change in bark/meow, dysphagia) |
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Term
| What is the incidence of focal MG in vet med? |
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Definition
| Underdiagnosed - usually attributed to idiopathic megaesophagus or unexplained dysphagia |
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Term
| What are the clinical signs of fulminating MG? |
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Definition
SEVERE form:
1. Sudden onset of megaesoph, severe regurgitation
2. Rapid tetraparesis
3. Loss of spinal reflexes
4. Can progress to ventilatory failure
5. Common in conjuction with thymomas
6. HIGH mortality
7. 16% of MG cases |
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Term
| What is a main differentiation between generalized and fulminating MG? |
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Definition
Generalized - Spinal reflexes are normal
Fulminating - Loss of spinal reflexes |
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Term
| What tests do you use to diagnose acquired MG? |
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Definition
1. Tensilon response test (acetylcholinesterase inhibitor), but high false pos & neg
2. AchR autoantibody test - gold standard
3. Thoracic rads
4. Abdominal US |
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Term
| What are the methods of treatment for acquired MG? |
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Definition
1. Anticholinesterase agents (symptomatic) - pyridostigmine (oral), neostigmine (inject)
2. Immunosuppressive meds - but corticosteroids may exacerbate weakness and aspiration pneumonia
3. Manage aspiration pneumonia and esophagitis
4. Nutrition - May need parenteral nutrition or PEG tube |
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Term
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Definition
Autosomal recessive trait - common in jack russels, springer spaniels, smooth fox terriers.
Defect in AchR - no autoimmune component |
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Term
| How do you diagnose congenital MG? |
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Definition
1. Edrophonium chloride test- same issue with high false pos and neg
2. Quantification of AchRs based on muscle biopsy specimens
3. AchR autoantibody test will be negative
4. Response to pyridostigmine = variable |
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