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clinical neuro > Neuromuscluar Disease > Flashcards

Neuromuscluar Disease Flashcards

1
Q

The motor unit consists of what 3 things?

A

Lower motor neuron, neuromuscular junction, and muscle

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2
Q

What are common LMN signs?

A
  • Paresis to plegia
  • Muscle atrophy
  • Poor/loss of mm tone
  • Weakness to loss of reflexes
  • Exercise intolerance
  • Paretic, stiff gait
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3
Q

T or F: with LMN Disease, you will typically see ataxia

A

False; typically LMN disease has MOTOR manifestations and doesn’t affect your sensory tracts

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4
Q

What is polyradiculoneuritis?

A
  • Also known as coonhound paralysis (Guillan-Barre syndrome in people)
  • Multiple root inflammatory dz that causes acute, ascending flaccid paralysis (LOSS of reflexes and tone, motor, not sensory > atrophy)
  • CN deficits often seen (VII, gag)
  • May require ventilation, supportive care
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5
Q

If you have the demyelinating version of polyradiculoneuritis, what is your prognosis?

A
  • Rapid recovery - can get distal atonal degeneration
  • Mildly delayed NCV
  • Root and proximal nerve disorder - abnormal F waves
  • Albuminocytologic dissociation on CSF (high protein in the face of a low cell count)
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6
Q

What are your differential causes for polyneuropathy?

A
  • Degenerative
  • Paraneoplastic
  • Endocrine
  • Genetic/heritable
  • Infectious
  • Toxic: Vincristine
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7
Q

Describe clinical signs of degenerative polyneuropathies

A
  • Typically in Labs <10 yrs
  • Laryngeal paresis/paralysis
  • Dysphonia
  • Esophageal dysfunction
  • Paresis, worse in pelvic limbs
  • Abnormal gait
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8
Q

What is sciatic release and what condition might you see this with?

A

Sciatic nerve is dysfunctional and cannot counter the femoral nerve’s effects, so patient will appear to lack sciatic tone and soldier step with degenerative polyneuropathies

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9
Q

What are 3 endocrine polyneuropathies?

A

Paraneoplastic - insulinoma

Hypothyroidism

Diabetic neuropathy - feline

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10
Q

Leonbergers are unique with their polyneuropathy cause, what makes them different?

A

Their degenerative polyneuropathies have a familial component - there’s a genetic test to determine if they have it

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11
Q

What types of ticks cause tick paralysis and what is the mechanism behind it?

A
  • Dermacentor and Amblyomma
  • Ixodes, Argasid in Australia - MUCH worse - need antitoxin
  • Causes presynaptic neuromuscular blockade
    • dogs flaccid 5-9 days after tick attaches (cats resistant)
    • +/- megaesophagus
  • Tx with Frontline
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12
Q

What is the MOA of tetanus?

A
  • Clostridium tetani produces tetanospasmin - must be cleaved to be activated and internalized
  • Tetanospasmin absorbed at the NMJ and travels retrograde to SC
  • Inhibits glycine/GABA at the spinal cord leading to hyperactive alpha motor neurons and constant muscle contraction
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13
Q

What are the clinical signs of tetanus?

A
  • 5-10 days after infection
  • Increased tone, stiffness, risus sardonicus, trismus (active contraction of jaw), elevated tail, sawhorse stance
  • External stimuli may exacerbate spasticity
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14
Q

What is your treatment for tetanus?

A
  • Vaccination - tetanus toxoid (horses)
  • Neutralize circulating toxin - antitoxin
  • Abx and wound debridement
    • it all started with a bacterial infection
  • Sedatives
  • Supportive care
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15
Q

What other things can cause tetany?

A
  • Hyperexcitability of the membrane due to electrolyte imbalance
    • Na, K, Ca, Cl
    • Hypocalcemia
    • HypoMg
  • Strychnine
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16
Q

What are the effects of botulism and how does it get into the system?

A
  • Clostridium botulinum cause presynaptic neuromuscular blockade when animal ingests the preformed toxin (types A-H, C most common)
  • toxin is imported, then blocks presynaptic ACh release from the nerve terminal
17
Q

What are the clinical signs of botulism and how does one diagnose it?

A

CS:

  • 12hrs - 6d
  • Progressive
  • symmetric ascending paresis/paralysis
  • Reflexes and tone are lost
  • CN VII, megaesophagus, decr gag and jaw tone
  • +/- mydriasis, KCS, constipation, urinary retention

Dx: detection of organism in ingesta, serum, vomit, neutralization in rodents, in vitro measuring toxin antigenicity

18
Q

What is your prognosis for botulism and why does it take this long?

A
  • Improvement in 1-3 weeks
  • must regenerate new motor endplates (2-4 mo in mammals)
19
Q

What are the effects of congenital myasthenia gravis and what breed typically get it?

A
  • Rare condition in Jack and Parsons Russell terriers that have signs from birth and generalized weakness due to insufficient receptors
  • CS: neg AChRAb titer
20
Q

What is the MOA of acquired myasthenia gravis?

A

Autoantibodies against nicotinic acetylcholine receptors on the post-synaptic membrane

  • Your receptor is blocked, causing muscle weakness
21
Q

What are the three forms of acquired myasthenia gravis?

A
  1. Focal - typically esophageal mm weakness (only in dogs!, cats have smooth mm)
  2. Generalized - exercise intolerance
  3. Fulminant - 1/4 of the generalized patients, grave prognosis
22
Q

What are the clinical signs of myasthenia gravis?

A
  • Exercise intolerance - progressively stiff, stilted gait, crab-walking, crouched
  • Postural reactions should be intact
  • Reflexes present, though withdrawals can tire
  • No CN deficits - can have weak gag, ptyalism, ptosis
  • Megaesophagus
23
Q

Acquired myasthenia gravis has a bimodal distribution, what two groups does it tend to affect?

A
  1. <5 yr old - immune mediated
  2. <7 yr old - para/pre-neoplastic
  • treat/remove primary source to make tx easier
24
Q

How do you diagnose myasthenia gravis?

A
  • Tensilon test: edrophonium, ultra-short acting AChE inhibitor
  • ACh receptor Ab titer - gold standard (dog or cat)
  • Electrodiagnostics - respective nerve stimulation (RNS): positive decrement
25
Q

What are the treatments for myasthenia gravis?

A
  • AChE inhibitor - incr ACh at the NMJ
  • Immunosuppression - stops Ab production
  • Tx underlying dz - eliminates trigger
26
Q

What are your differentials for causes of generalized myopathy?

A
  • Immune-mediated
  • Infectious - Neospora caninum, Hepatozoon americanum
  • Preneoplastic - lymphoma
  • Dermatomyositis
  • Congenital - muscular dystrophies
27
Q

What are the clinical signs of generalized polymyositis and what breeds are commonly represented?

A
  • CS: Generalized weakness, stilted gaits, dysphagia, muscle atrophy, myalgia is rare
    • do NOT lose reflexes
  • Boxers (preneoplastic) and Newfies (breed specific)
28
Q

What is mastication myositis and how do you diagnose it?

A
  • Get neutrophilic inflammation of Type 2M and Type 1 variant muscle fibers
  • VERY painful > autoantibodies to type 2M fiber, ONLY expressed in masticatory muscles!
  • Dx with serum 2M antibody - very sensitive/specific
29
Q

What are the clinical signs of masticatory myositis?

A

Acute: pain on opening mouth, mild exophthalmia

Chronic: masticatory muscle atrophy, non-painful inability to open mouth, fibrosis of masticatory muscles

30
Q

How do you treat masticatory myositis?

A

Early and aggressive tx - immunosuppression

If chronic and severe atrophy and trismus, consider muscle biopsy for prognosis

31
Q

What are the effects of extraocular myositis and how is it treated?

A

Animals can become effectively blind due to inflamed extraocular muscles; treated the same way as masticatory myositis

32
Q

How does one get polymyositis from Neospora caninum and what are the effects?

A

Prenatal exposure

  • CS: polyradiculoneuritis and polymyositis - encephalomyelitis, muscle atrophy, contracture of PLs
33
Q

What are examples of endocrine myopathies and what fibers are most affected?

A
  • Hypothyroidism - dogs
  • Hyperthyroidism - cats
  • Glucocorticoid excess (endogenous/exogenous) - dogs
  • Electrolyte abnormalities

*Type 2 myofibers more effected

34
Q

What are the two most common feline myopathies and what are the signs?

A
  1. Hyperthyroidism
  • paresis
  • ventroflexion
  • tremors
  • abnormal gait
  • T3 and T4 effects on sarcoplasm
  1. Toxoplasma gondii - brain and systemic infection
35
Q

What is the effect of coral snake envenomation on the muscles?

A
  • Venom components:
    • Postsynaptic alpha neurotoxins
    • neuromuscular blockade
  • Generalized LMN weakness - resp paralysis
36
Q

What are 3 congenital myopathies?

A
  • Muscular dystrophy - Golden retrievers
  • Myotonia congenital - mini Schnauzers
  • Hyperkalemia periodic paralysis (HYPP) - quarter horses
37
Q

What is myoclonus and what is it commonly seen with?

A

Sudden contraction-relaxation muscles, commonly seen with distemper

clinical neuro (7 decks)

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