Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y4 SA - Neurology > Neuromuscular disorders > Flashcards

Neuromuscular disorders Flashcards

1
Q

List the non-specific signs of generalised neuromuscular disease

A
  • Tetraparesis and exercise intolerance
  • Stiff/stilted gait with reduced stride length, bunny hopping
  • Narrow based stance
  • Tremors/fasciculations
  • Regurgitation/altered oesophageal motility
  • Dysphonia (disorders of the voice)
  • Reduced reflexes and tone
  • Muscle atrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe a ‘typical neuromuscular gait’

A

Short strided, appears stiff/lame, difficulty supporting weight, bunny hopping, sensation/proprioception is usually normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does a junctionopathy present?

A
  • Generalised
  • Classically exercise intolerance with fatigue
  • Normal sensory function
  • Often intact tendon reflexes unless severe weakness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the generalised clinical signs of a myopathy?

A
  • Atrophy or hypertrophy
  • Specific features: dimple contractures (myotonia); myalgia; restricted joint movement (contracture)
  • Normal sensory function
  • Often normal tendon reflexes but exceptions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Name 3 causes of junctionpathies

A

Myasthenia gravis
Botulism
Organophosphate toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name 2 causes of myopathies

A
  1. Polymyositis - immune mediated or infectious
  2. Electrolyte abnormalities - Addisons, Hypokalaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What neuropathies present with chronic and progressive neuromuscular signs?

A
  • Inflammatory/infectious e.g. Protozoal, Viral
  • Toxic e.g. lead
  • Metabolic e.g. Diabetes, Cushings, Hypothyroidism
  • Idiopathic
  • Degenerative
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which myopathies present with chronic and progressive neuromuscular signs?

A
  • Inflammatory polymyositis
  • Infectious polymyositis
  • Metabolic/endocrine
  • Paraneoplastic
  • Degenerative e.g. muscular dystrophies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

List the initial tests for neuromuscular diseases

A
  • Haem/biochem
  • Urinalysis
  • Chest radiographs
  • Abdo imaging
  • Endocrine tests
  • Serology/PCR
  • Genetic testing
  • CSF
  • Biopsies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Increases levels of … in blood indicate muscle damage?

A

Creatinine kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Increased levels of … in urine indicate muscle damage?

A

Myoglobinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which 2 conditions linked to neuromuscular disease could be observed on chest radiographs?

A

Megaoesophagus
Aspiration pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where would you take a muscle biopsy?

A
  • Area where muscle fibres are oriented in a single direction
  • Distant from tendons and aponeuroses
  • Disease requirements (e.g. congenital myasthenia gravis biopsy motor point or whole muscle for quantification)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which muscle is a masticatory muscle biopsy taken from?

A

Temporalis muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is polyradiculoneuritis?

A

Inflammation of nerves and roots
- Recent association with Campylobacter and raw feeding
- Most pathology is in ventral spinal roots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Polyradiculoneuritis is predisposed in which breed?

A

Bengal cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does polyradiculoneuritis present?

A
  • Acute onset, rapidly progressive
  • Tetra/paraparesis
  • Flaccid, markedly reduced motor function (inc. absent reflexes)
  • Can affect respiratory muscles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is polyradiculoneuritis diagnosed?

A

CS
History
CSF analysis
Electrophysiology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the natural disease progression of polyradiculoneuritis

A
  • Inflammation is of short duration
  • Recovery depends on severity of damage
  • Remyelination over days-weeks
  • More prolonged if axonal damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is polyradiculoneuritis treated?

A

Supportive
- Recumbency care
- Physiotherapy
- May have to consider ventilatory support

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is myasthenia gravis?

A

Reduced neuromuscular transmission - grave muscle weakness

22
Q

What are the two types of myasthenia gravia?

A

Congenital – genetic defect
Acquired: immune-mediated

23
Q

How does acquired myasthenia gravis present in dogs?

A
  • Generalised (most common)
  • Fulminant: acute onset, rapidly progressive
  • Focal (~40%): facial, pharyngeal, laryngeal
  • Megaoesophagus in ~90% of cases
24
Q

How does acquired myasthenia gravis present in cats?

A
  • Abyssinians predisposed
  • Generalised in 90%
  • Megaoesophagus less likely (15%)
  • Cranial mediastinal mass (thymoma) in ~26-52%
  • Can arise in cats on thiourylene medication for hyperthyroidism
25
Q

How is myasthenia gravis diagnosed?

A
  • Clinical signs
  • nAChR Ab test is gold standard (small percentage of false –ves)
  • Electrodiagnostic tests (repetitive nerve stimulation)
  • Response to cholinesterase inhibitor (edrophonium or neostigmine)
26
Q

How is myasthenia gravis treated?

A
  • Anti-cholinesterase: Pyridostigmine p/o or neostigmine i/m
  • Supportive: postural feeding for megaoesophagus
27
Q

Which Clostridial disease causes neuromuscular disease?

A

Clostridium botulinum

28
Q

How does infection with clostridium botulinum occur?

A
  • Ingestion of contaminated food - esp. animal carcasses
  • Rare in dogs and cats
  • Toxin is absorbed from the gut
29
Q

What is the main effect of exotoxin from clostridium botulinum?

A

Acts to block vesicle fusion with the presynaptic membrane and ACh release

30
Q

Describe the clinical signs of clostridium botulinum infection

A
  1. Nicotinic ACh synapses (junctionopathy) = Acute onset rapidly progressive tetraparesis (2-3 d). May affect cranial nerves: jaw tone, facial paralysis, gag reflex, megaoesophagus. May affect respiratory muscles

2.Muscarinic ACh synapses (dysautonomia) = Urinary dysfunction, GI dysmotility, mydriasis, reduced tear production

31
Q

How is clostridium botulinum diagnosed?

A
  • Clinical signs
  • Electrophysiology
  • Demonstrate: Toxin (feed, faeces) – usually not possible
  • Serology (retrospective exposure)
32
Q

How is botulism treated?

A

Supportive care:
- Bladder management
- Recumbency care
- Megaoesophagus management
- Physiotherapy

33
Q

Who is most commonly affected by immune mediated polymyositis

A

More common in dogs than cats, particularly large breeds - Newfoundland, Boxer, GSD, Labrador, Golden retriever

34
Q

What are the clinical signs of immune mediated polymyositis?

A
  • Pyrexia, stiffness, non-ambulatory tetraparesis, reluctance to move, lowered head carriage, myalgia, muscle swelling
  • Generalised weakness, muscle atrophy, exercise intolerance, fatigue
    +/- oesophageal involvement – regurgitation
35
Q

How is immune mediated polymyositis diagnosed?

A
  • H+B: Inflammatory leucogram, elevated CK/AST (acute typically +++)
  • Electrodiagnostics: marked EMG abnormalities, normal MNCV
  • Muscle biopsy for diagnosis
  • Rule out infectious diseases and tumours
36
Q

How is immune mediated polymyositis treated?

A

Prednisolone

37
Q

What is the cause of infectious myositis?

A

Protozoal - Neospora caninum/Toxoplasma gondii

38
Q

What are the clinical signs of neosporosis in puppies?

A
  • Radiculoneuritis and polymyositis
  • Pelvic limb hyperextension (usually starts in one limb and progresses to other)
  • Ascending paralysis of pelvic limbs with muscle contracture and arthrogryposis
39
Q

How is neosporosis diagnosed?

A

Clinical signs, CK/AST, EMG, biopsy
SEROLOGY
PCR on CSF, blood

40
Q

How is neosporosis treated?

A

Clindamycin/TMPS + pyrimethamine

41
Q

In which breed is there a juvenile form of masticatory myositis?

A

CKCS

42
Q

What are the clinical signs of masticatory myositis?

A

Swollen/painful MM, exophthalmos
Trismus (pain/fibrosis), MM atrophy

43
Q

How is masticatory myositis treated?

A

Prednisolone +/- other IM drugs
Physiotherapy

44
Q

Is trigeminal neuritis more commonly seen in dogs or cats?

A

Dogs

45
Q

What is trigeminal neuritis?

A

Inflammation throughout trigeminal nerves including ganglia bilaterally
Demyelination>axon degeneration

46
Q

What are the clinical signs of trigeminal neuritis?

A
  • Acute onset paresis/plegia of masticatory muscles -> dropped jaw
  • Normal gag and tongue tone and movements (Horner’s or facial paresis can be seen)
  • Sensory deficits in ~30% of cases
  • Masticatory muscle atrophy
47
Q

How is trigeminal neuritis diagnosed?

A

MRI: swollen, inflamed nerves
CSF

48
Q

How is trigeminal neuritis treated?

A

Resolves usually within 3 weeks
Supportive care

49
Q

What are the cases of unilateral temporal muscle atrophy?

A

~50% of cases due to trigeminal nerve sheath tumour
~25% due to other neoplasia
Other possibilities – infectious/inflammatory, idiopathic, traumatic

50
Q

What are the clinical signs of unilateral temporal muscle atrophy?

A
  • Neurogenic atrophy of masticatory muscles, otherwise may be normal at onset
  • May be abnormal sensation (face rubbing, absent palpebral and corneal reflexes)
  • Progression to involve other cranial nerve and brainstem functions if neoplastic

Y4 SA - Neurology (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions