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Year 4 Small Animal Studies > Neurology: Neuromuscular Disorders > Flashcards

Neurology: Neuromuscular Disorders Flashcards

1
Q

How are neuromuscular diseases located?

A
  • Cranial nerve reflexes
  • Gait and postural reactions
  • Muscle bulk and tone

Spinal reflexes
* Peripheral sensory
* Central
* peripheral motor

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2
Q

What are pitfalls of neuromuscular lesion location?

A

multiple lesions
spinal shock

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3
Q

What are non-specific signs of generalised neuromuscular disease?

A
  • Tetraparesis and excercise intolerance/collapse
  • Stiff-stilted gait with reduced stride length, bunny hopping, fatigue
  • Narrow based-stance
  • Tremors/fasiculations
  • Regurgitation/altered oesophageal motility
  • Myalgia
  • Dysphonia
  • Reduced reflexes and tone
  • Muscle atrophy
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4
Q

What clinical signs are specific to neuropathy?

A
  • Cranial/spinal nerves
  • Mono/multiple/generalised
  • Motor ± sensory defecits
  • Severe flaccid paresis
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5
Q

What are clinical signs implying junctionopathy?

A
  • Generalised
  • Classically excercise intolerance with fatigue
  • Normal sensory function
  • Often intact tendon refelxes
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6
Q

What are clinical signs of myopathy?

A
  • Generalised or focal
  • Atrophy or hypertrophy
  • Specific: dimple contractions, myalgia, restricted joint movement
  • Normal sensory function
  • Often normal tendon reflex
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7
Q

What are the DDXs for acute onset generalised neuromuscular:
neuropathy, junctionopathy and myopathy?

A

Neuropathy
* Polyradiculoneuritis

Junctionopathy
* Myaesthenia gravis
* Botulism
* Organophosphate toxicity

Myopathy
* Polymyositis
* Immune mediated or infectious
* Electrolyte abnormalities
* Addisons
* Hypokalaemia

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8
Q

What are causes of chronic neuromuscular neuropathy, junctionopathy, and myopathy?

A

Neuropathy
* Infectious- polyradiculoneuritis, protozoal
* Toxic- lead
* Metabolic, diabetes mellitus, cushings, hypothyroidism
* Idiopathic- distal denervating disease
* Degen/inherited

Junctionopathy- congenital/acquired myasthenia gravis

Myopathy
* Inflammatory polymyostitis
* Infectious polymyositis
* Metabolic/Endocinre- hypothyroid, cushings
* Paraneoplastic
* Degen/inherited

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9
Q

What can cause bilateral and unilateral focal neuropathy?

What can cause a focal myopathy?

A

Bilateral- multiple
* infectious- neospora
* inflammatory- trigeminal
* vascular

Unilateral
* trauma
* inflammatory/infectious
* metabolic
* neoplastic

Focal myopathy
* Traumatic contractures
* Infectious/inflammatory/neoplastic

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10
Q

What are the initial tests for neuromuscular disease

A
  • Haematology
  • Biochem- electtrolytes, glucose, cholesterol, CK
  • Urinalysis- myoglobinuria
  • Chest rads- megaoesophagus, aspiration pneumonia
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11
Q

What further tests can be used for neuromuscular disease?

A
  • Abdominal imaging
  • Endocrine- T4, TSH, ACTH stim
  • Serology
  • Disease specific auto abs
  • Lactate and pyruvate- mitochondrial dysfunction
  • CSF- nerve roots, central involvment
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12
Q

What is the purpose of electrodiagnostic testing?

A
  • Definitive evidence of dysfunction
  • Localisation
  • Extent and severity
  • Prognosis/monitor

Electromyography- extracelluar recordings from myofibres, normal muscle silent

Nerve conduction studies- evaluate amplitude, latency and velocity of waveforms

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13
Q
  1. How are muscle/nerve biopsies processed?
  2. What muscle and where?
A
  1. Formalin-fixed
  2. Affected- lateral tricep, biceps femoris, vstus lateralis, cranial tibial
    Area where muscle fibres in single orientation, distant from tendons
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14
Q

Describe a masticatory muscle biopsy?

A
  • Identify temporalis dorsal to zyomatic arch
  • Clip and prep
  • Incise skin and frontal muscle
  • Tempral has white, shiny aponeurosis
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15
Q

How can nerve biopsy be done?

A

Muscle biopsy
* denervation changes
* intrafasicular nerve branches

Fasicular nerve biopsy
* Axon strucutre and density
* Myelin sheath thickness integrity
* Schwann cells, support tissues

Common- cranial tibial muscle

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16
Q
  1. What is can cause polyradiculoneuritis?
  2. Where is most affected usually?
  3. How does it present?
A
  1. Inflammation of nerve and roots
    * idiopathic/vaccine (rabies)
    * Campylobacter and raw feeding
    * Breed- bengal cats
    * Demyelination- in severe forms

2) Ventral spinal roots- usually pure motor defeicits
3) Acute, rapid progression
* Tetra/paraparesis to non ambulatory paresis/plegia
* Flaccid
* can affect respiratory muscles

17
Q

How is polyradiculoneuritis diagnosed?
How is it treated?

A

Diagnosis- clinical signs, history, electrophysiology and CSF analysis
Inflammation is of short progression, recovery depends on severity of damage

Treatment- supportive, physio

18
Q

What causes myasthenia gravis?

A
  • Congenital- genetic defect
  • Acquired- immune- mediated (ab target nACH receptors)
19
Q

How does myasthenia gravis present in cats and dogs?

A

Dogs- usualy generalised, can be focal (facial, pharyngeal), megaoesophagus in nearly all

Cats- usually generalised, megaoesophagus less likely, cranial mediastinal mass (thymoma)

20
Q

How is myasthenia gravis diagnosed?

A

Clinical signs
* nAchR Ab test gold standard
* Electroiagnostic tests
* Response to cholinesterase

21
Q

How is myasthenia gravis treated?

A
  • Anti-cholinesterase
  • Immunosuppresison
  • Thymectomy
  • Suppotive- postural feeding

Prognosis- guarded to poor, appears to be self-limiting

22
Q

What causes botulism?
What are the clinical signs?

A
  • Exotoxin produced by clostridium botulinum
  • Acts to block vesicle fusion with the presynaptic membrane and ACh release

Clinical signs
* Nicotinic Ach synapses (junctionopathy)- acute onset, rapidly progressive tetraparesis
* Muscarinic ACh synapses- dysautonomia- urinary dysfunction, GI dismotility, mydriasis, reduced tear production

23
Q

How is botulism diagnosed and treated?

A

Diagnosis
* clinical signs
* demonstrate- toxin, serology

Treatment
* supportive- bladder managment, recumbency care, megaoesopgagus managment
* physio

Prognosis- depends on severity of clinical signs

24
Q

What is immune mediated polymyositis?

A
  • Autoimmune condition usually idiopathic- can be immune diseae or neoplasia
  • More common in dogs

CS- acute or chonic
* Pyrexia, stiffness, non-ambulatory, tetraparesis, reluctance to move
* Generalise weakness- atrophy

25
Q

How is immune mediated polymyositis diagnosed and treated?

A
  • Haem and biochem- inflammatory leucogram, CK
  • Electro- EMG abnormalities
  • Muscle biopsy

Tx- prednisolone

26
Q
  1. What cause infectious myostitis?
  2. What are the clinical signs of neosporsosis in puppies?
  3. How is it diagnosed?
  4. How is it treated?
A
  1. Protozoal-neospora/toxoplasma
  2. Radiculoneuritis, polymyositis, pelvic limb hyperextension, ascending limb paralysis
  3. Clinical signs- CK/AST, EMG, biopsy, serology, PCR
  4. Clincamycin/trimethroptim

Poor prognosis with contractures

27
Q
  1. What causes masticatory myositis?
  2. How does it present?
  3. How is it diagnosed and treated?
A
  1. Dogs- antibodies to 2M myosin isoform, juvenile form in CKCS
  2. Acute/chronic- swollen/painful MM, exophthalmos, trismus, MM atrophy
  3. Imaging, CK, 2M antibodies
    TX- prednisiolone
28
Q
  1. What causes trigeminal neuritis?
  2. What are the clinical signs?
  3. How is it diagnosed and treated?
A
  1. Inflammation throughout trigeminal nerves, demyelination
  2. Acute onset paresis/plegia of masticatory muslces- dropped jaw, normal gag anf tongue tone, sensory defecits, masticatory muscle atrophy
  3. DX- MRI-swollen, inflammed nerves, CSF
    TX- resolves in 3 weeks
29
Q

What can cause unilateral temporal muscle atrophy?

How is it treated?

A

Trigeminal sheath tumour or other neoplasia- MRI diagnosis

TNST treatment- radiotherapy, prednisolone

30
Q

What are the different types of traumatic neuropathies?

A

Neuropraxia- temporary nerve damage- no disruption of the nerve or myelin sheath
Axonotmesis- disruption of the axon but intact basal lamina and myelin sheath
Neurotmesis- partial or complete transection of the nerve, partial recovery possible but inlikely

31
Q

How does brachial plexus avulsion present?

A

C6-T2
* Monoparesis, cutaneous trunci absent ipsilaterally
* Cranial/caudal/complete
* Radial function necessary for gait
* Poor prognosis

32
Q

What are the signs of a tail pull injury?

A
  • Urinary function affected
  • Perineal sensation and anal tone
  • Tail base sensation
33
Q

What are neurological defecits of neurological defects?

A
  • Partial/complete plexus involvment
  • Monoparesis-plegia
  • Progression to myelopathy
  • Palpable mass

Chronic progressive thoracic limb, pain, muscle atrophy

Year 4 Small Animal Studies (97 decks)

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