ClinNeuro- Motor Unit Disorders

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  1. 5 components of the LMN.
    ventral motor neuron body (in ventral grey column of spinal cord), nerve root, peripheral nerve, neuromuscular junction, muscle itself
  2. Animals with diffuse motor unit disease will have the appearance of...
    LMN signs in all four limbs.
  3. History of an animal with diffuse neuromuscular disease. (6)
    regurgitation (passive regurg), voice change, dysphagia, urinary/fecal incontinence, exposure to wildlife or ticks, recent surgery/wound
  4. Clinical manifestations of diffuse neuromuscular disease. (7)
    [all manifestations of weakness] short stride, absence of ataxia, trembling, bunny hopping in pelvic limbs, crouched (due to weakness), "elephant on a beach ball", ventral neck flexion (cats!)
  5. What specific diseases can present with diffuse LMN disease? (4)
    acute canine polyradiculoneuritis (Coonhound paralysis), botulism, tick paralysis, myasthenia gravis
  6. What are common historical components associated with acute canine polyradiculoneuritis (ACP)? (5)
    contact with raccoon saliva, post-rabies vaccine, URI, GI infection, [Campylobacter jejuni in people- boards Q]
  7. Describe the pathogenesis of ACP.
    immune-mediated attack on axons and myelin in the ventral motor nerve root due to molecular mimicry b/w bacterial LPS
  8. With ACP, there is absence of ____________, but _____________ is preserved.
    motor function; pain sensation
  9. Describe clinical signs of ACP. (3)
    initially short stilted gait in pelvic limbs that rapidly progresses to tetraparesis/plegia, dysphonia
  10. How long is the progressive phase of ACP?
    5-7 days (reliably- when they get worse every day...before they get better)
  11. With ACP, there is NO _________________ INVOLVEMENT. [**VERY IMPORTANT**]
    smooth muscle or autonomic
  12. The most severe cases of ACP result in...
    paralysis of the diaphragm and intercostal muscles, which has respiratory implications.
  13. Things that DO NOT occur with ACP. (5)
    NO smooth mm. or autonomic involvement, NO cranial nerve deficits, NO sensory loss, NO incontinence, NO megaesophagus
  14. What might you find on lumbar CSF tap of a dog with ACP?
    normal cell count but often increased protein
  15. How do you treat ACP?
    supportive care (monitor respirations, hand feeding, IV fluids, intense PT, prevent pressure sores)
  16. What should you AVOID using in dogs with ACP?
    steroids (even though it's immune-mediated...steroids don't work here)
  17. How long is the improvement phase of ACP?
    2 weeks to 6 months, depending on how much damage there is to axons (just myelin involvement--> rapid recovery; significant degeneration of axons--> longer recovery)
  18. Can dogs develop immunity to ACP?
  19. What causes botulism?
    ingestion of Clostridium botulinum neurotoxins (spoiled food), wound botulism
  20. ________ are extremely resistant to botulism toxin.
  21. Describe the pathogenesis of botulism.
    toxin enters nerve endings and inhibits transmission at the neuromuscular junction (prevents Ach release from presynaptic terminal), leading to flaccid paralysis of smooth and striated muscle
  22. What muscles are affected by botulinum toxin?
    smooth AND striated
  23. Clinical signs associated with botulism. (5)
    mild weakness to tetraplegia, dysphonia, megaesophagus, cranial nerve dysfunction (decreased pupillary light reflexes, dysphagia)
  24. What do you look for on radiographs of an animal that has botulism? (3)
    megaesophagus, aspiration pneumonia, ileus (gas-distended loops of bowel)
  25. How do you make a definitive diagnosis of botulism? (2)
    identification of toxin in ingesta or by neutralization test in small rodents
  26. Why don't you treat botulism with antibiotics?
    b/c disease is caused by the toxin, NOT the bacteria
  27. How do you treat botulism? (1)
    supportive care (prevent aspiration pneumonia, bladder care, PT, prevent pressure sores)
  28. How long is recovery phase in botulism?
    1-3 weeks (once new docking proteins are manufactured)
  29. What causes tick paralysis?
    salivary neurotoxin secreted by attached female ticks
  30. What ticks are associated with tick paralysis?
    Dermacentor variablis and andersoni (U.S.) [Ixodes in Australia]
  31. Describe the pathogenesis of tick paralysis.
    toxin interferes with Ca2+ at NMJ and prevents release of Ach from the pre-synaptic terminal
  32. How long is the progressive phase of tick paralysis?
    24-72 hours (much more rapid than coonhound paralysis)
  33. What does NOT occur with tick paralysis? (2)
    no cranial nerve deficits, no megaesophagus
  34. How do you treat tick paralysis?
    remove the tick and recovery within 24-72 hrs
  35. What is the most common form of myasthenia gravis?
  36. With tick paralysis, there is absent _____________, but _____________ is intact.
    motor function; pain sensation
  37. Describe the pathogenesis of acquired myasthenia gravis.
    auto-antibody mediated destruction of Ach receptors at the NMJ
  38. What are the 3 clinical syndromes associated with acquired myasthenia gravis?
    generalized (most common-affects all skeletal muscles), focal (single muscle group), fulminating (rapid onset severe form of generalized)
  39. Describe clinical presentation of generalized myasthenia gravis. (6)
    neurologically normal during periods of rest, paresis after activity, regurgitation, normal spinal reflexes, megaesophagus (esp. in dogs), drooling/eyelid and lip paresis
  40. What is an important differentiating factor b/w myasthenia gravis and tick paralysis/coonhound paralysis/botulism?
    with MG, spinal reflexes are normal
  41. __________ is often associated with acquired myasthenia gravis (esp. fulminating form), especially in cats.
    Thymoma (thymus tumor)
  42. What is the most common form of focal myasthenia gravis?
  43. How do you presumptively diagnose acquired myasthenia gravis?
    Tensilon response test- give tensilon and if animal immediately improves, + for MG
  44. Tensilon is a(n) ______________.
    acetylcholinesterase inhibitor
  45. Why is the tensilon response test NOT a gold standard test for diagnosing MG?
    high false negative and false positive rate
  46. How do you definitively diagnose acquired myasthenia gravis?
    test for antibodies against Ach receptors (do not perform this test after steroids...will give false negative)
  47. What are the 2 modalities of treatment for acquired MG?
    acetylcholinesterase inhibitors, immunosuppressive drugs
  48. What acetylcholinesterase inhibitors are used to treat MG? (2)
    • Pyridostigmine (Mestinon)- oral
    • Neostigmine- injectable
  49. What immunosuppressive drugs are often given to treat MG? (2)
    Mycophenelate, Cyclosporine (b/c corticosteroids may excerabate weakness, aspiration pneumonia)
  50. Describe congenital MG.
    defect in Ach receptor (NOT AUTOIMMUNE)
  51. What breeds have the autosomal recessive trait for congenital MG? (3)
    jack russel terriers, springer spaniels, fox terriers
  52. How do you definitively diagnose congenital MG?
    quantification of Ach receptors based on muscle biopsy specimen (Ach receptor antibody test will ALWAYS be negative b/c it is not autoimmune)
Card Set:
ClinNeuro- Motor Unit Disorders
2015-11-30 15:40:51
vetmed clinneuro

vetmed clinneuro
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