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Neurology > Neuromuscular disease > Flashcards

Neuromuscular disease Flashcards

1
Q

What is the typical history seen with neuromuscular disease?

A
  • Weakness
  • Difficulty rising
  • Exercise intolerance
  • Altered voice
  • Change in musculature
  • Regurgitation
  • Lameness, pain
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2
Q

What might be seen on physical exam in an animal presenting with neuromuscular disease?

A
  • Gait abnormalities (paresis, ataxia)
  • Muscle loss
  • Altered respiratory effort or inspiratory stridor
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3
Q

What might be seen on neurological exam an animal presenting with neuromuscular disease?

A
  • Tetraparesis +/- proprioceptive ataxia
  • Muscle atrophy/pain
  • Reduced spinal reflexes and muscle tone
  • May see sensory deficits or self-mutilation
  • BUT if you see paresis without ataxia, it’s likely to be muscular in origin
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4
Q

What clinical signs are seen in autonomic neuropathy?

A
  • Dilated pupils
  • Decreased tear production
  • Hyposalivation
  • Bradycardia
  • Constipation
  • Urinary retention
  • Reduced perianal reflex
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5
Q

What gait abnormalities can be seen in neuromuscular disease?

A
  • Paresis +/- ataxia
  • Frequent sitting down
  • Exercise intolerance
  • Low head carriage
  • Choppy and stilted gait (hypometria)
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6
Q

What does electrophysiology tell you about a lesion?

A

Localization and may support suspected diagnosis eg. see abnormal repetitive nerve stimulation in MG

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7
Q

What diagnostics can you use for neuromuscular disease?

A
  1. Biochem + Haem + Urinalysis = checking Creatinine kinase activity and Glucose, electrolytes, cholesterol
  2. Imaging - Neoplasia
  3. Serological tests- Neospora, Toxoplasma
  4. Endocrine testing - HypoT4, Hyperadrenocorticism
  5. AChR ab, Edrophonium response test - myasthenia gravis
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8
Q

What is a normal EMG (electromyogram)?

A

It is silent and a fat signal

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9
Q

What are fibrillation potentials in an EMG?

A

They are spontaneous action potentials of single myofibers, biphasic
Can be due to denervation or inflammation

Sounds like frying eggs/wrinkling of tissue paper/rain on a tin roof

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10
Q

What are positive sharp waves in an EMG?

A

Positive deflection followed by shallow, negative deflection; spontaneous action potentials of single myofibers.
Can be due to denervation

Sounds like a race car driving by

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11
Q

What are complex repetitive discharges?

A

Due to many myofibers firing in near synchrony
Polyphasic and serrated, usually uniform shape

Sounds like a machine gun

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12
Q

What is a myotonic potential?

A

Due to independent repetitive discharges of singled, injured myofibers
unusual
Frequency and amplitude waxing and waning

Sounds like a revving motorcycle or chainsaw

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13
Q

Are electrodiagnostics useful?

A 
Yes
They provide definitive evidence of neuromuscular dysfunction
Localization (nerve vs muscle)
Extent and severity
Treatment monitoring
Prognosis
Which muscles/nerves are affected
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14
Q

What are the components of the neuromuscular system?

A
  1. Neuromuscular junction
  2. Peripheral nerve
  3. Muscle
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15
Q

What is the signalment of immune-mediated myasthenia gravis?

A
  • Older than 3 months, any age

- Breed: GSD, Lab, Golden Retrievers

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16
Q

What are the three forms of immune-mediated myasthenia gravis?

A
  1. Focal MG with megaesophagus/regurgitation (30%)
  2. Generalized MG exercise intolerance with megaesophagus (60%)
  3. Fulminating form (come into the clinic flat and depressed)
17
Q

What is the pathophysiology of immune-mediated myasthenia gravis?

A

Ach receptor reduction due to autoantibodies

18
Q

How is immune-mediated myasthenia gravis diagnosed?

A
  • Edrophonium chloride (tensilon test)
  • Serology
  • Check for paraneoplastic disease (thymoma)
19
Q

What is the treatment and prognosis of immune-mediated myasthenia gravis?

A
  • Pyridostygmine (start low and increase dose)
  • Immunomodulatory drugs (?)
  • Relatively fair prognosis
20
Q

What is the signalment of congenital myasthenia gravis?

A
  • 6 to 8 weeks old

- Breed: Jack Russel Terrier, Springer spaniels, mini dachshund

21
Q

What is the pathophysiology of congenital myasthenia gravis?

A

Decrease of AChR

22
Q

How is congenital myasthenia gravis diagnosed?

A
  • Tensilon test (edrophonium chloride)

- Muscule biopsy of intercostal muscles

23
Q

What is the treatment of congenital myasthenia gravis?

A

Pyridostygmine

24
Q

What are equine botulism outbreaks associated with?

A

Contaminated feed

25
Q

What are the three clinical forms of botulism?

A
  1. Ingested toxin (outbreaks); only form reported in the UK
  2. Toxico-infectious: spores ingested, organism proliferates in the intestine (young foals)
  3. Wound botulism (very rare): organism proliferates and produces toxin in wounds
26
Q

How is botulism diagnosed?

A
  • Characteristic clinical signs and history of exposure to silage eg. flaccid tongue, paresis
  • MOST clinicians consider reduction in tongue tone as the most characteristic sign - not be able to move tongue back in when pulled out
  • Rule out differentials
27
Q

What is the treatment for botulism?

A
  • Antiserum containing antibody to toxin B, C, and D (available in US)
  • Broad spec antibiotics (for pneumonia, avoid procaine and aminoglycosides)
  • Fluid therapy
  • Nutrition
  • Management of recumbent horse
28
Q

What is the prognosis of botulism?

A

Guarded unless caught early

29
Q

What is typically seen in motor neuropathic syndrome?

A

LMN signs

30
Q

What is typically seen in sensory neuropathic syndrome?

A
  • Hypoalgesia
  • Hypoaesthesia
  • CP deficits
  • Self mutilation
  • Reduced reflexes
  • NO atrophy
31
Q

What is typically seen in autonomic neuropathic syndrome?

A
  • Pupillary changes
  • Decreased tear production and salivation
  • Bradycardia
32
Q

What is seen with myopathic syndrome?

A
  • Paresis
  • Exercise intolerance
  • Stiff, stilted gait
  • Muscle atrophy or hypertrophy
  • Muscle pain on palpation
33
Q

What is myasthenia gravis?

A

Exercise induced paresis, megaoesophagus

34
Q

What is clinical signs can you see with botulism?

A

Mild paresis to tetraplegia

LMN signs

35
Q

What are the two types of Myasthenia gravis?

A
  1. Acquired: Immune-mediated MG

2. Congenital MG

36
Q

How does botulism cause its clinical signs?

A

toxin irreversibly blocks the release of acetylcholine at the neuromuscular junction
Cl botulinum found ubiquitously in soil

37
Q

What peripheral neuropathies can occur in large animals in regards with post parurition?

A

Calves - femoral nerve paresis

Cows and horses - obturator nerve

Neurology (13 decks)

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