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Neurology > PNS Diseases > Flashcards

PNS Diseases Flashcards

1
Q

Onset of disuse atrophy

A
  • Evolve more slowly, less severe
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2
Q

Onset of neurogenic atrophy

A
  • Fast and severe
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3
Q

Onset of primary myopathic atrophy

A
  • Variable
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4
Q

Pudendal nerve function

A
  • Contract external anal sphincter and external urethral sphincter (skeletal)
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5
Q

Pelvic nerve function

A
  • Contract detrusor muscle of bladder (smooth)
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6
Q

Which spinal cord segments do both the pudendal and pelvic nerve come from?

A
  • S1-S3
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7
Q

What makes up the LMN unit?

Which are parts of the PNS?

A
  • SPinal cord segments (C6-T2, L4-S1)
  • Peripheral nerves (afferent/efferent)*
  • Neuromuscular junction*
  • Muscle (effector organ)*
  • = part of the PNS
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8
Q

What are the top 5 spinal diseases that can impact the spinal cord segments C6-T2 or L4-sacrum?

A
  • Trauma
  • Tumor
  • IVDD
  • Meningitis/myelitis
  • DIscospondylitis
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9
Q

Degenerative/inherited diseases of PNS

A
  • Neuropathy

- Myopathy

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10
Q

Metabolic diseases of PNS

A
  • Diabetic neuropathy
  • Hyperadrenocorticism myopathy
  • Hypothyroidism neuropathy and myopathy
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11
Q

Neoplastic diseases of PNS

A
  • Nerve sheath tumor

- Lymphoma

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12
Q

Infectious inflammatory dz of PNS

A
  • Toxoplasma

- Neospora

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13
Q

Non-infectious inflammatory dz of PNS

A
  • Polyradiculoneuritis
  • Extraocular polymyositis
  • Myasthenia gravis
  • Masticatory muscle myositis
  • Trigeminal neuritis
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14
Q

Traumatic dz of PNS

A
  • Brachial plexus avulsion
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15
Q

Toxic dz of PNS

A
  • Tick paralysis
  • Botulism
  • Chronic organophosphates incats
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16
Q

Vascular dz of PNS

A
  • Aortic thromboembolism
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17
Q

Localization:

Unable to walk

Yesterday started having difficulty moving in the pelvic limbs; today he also has problems in the thoracic limbs; also seems painful everywhere

A
  • Diffuse LMN

- C6-T2 peripherally in thoracic limbs and L4-S1 peripherally in pelvic limbs

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18
Q

Top 3 diffuse LMN diseases

A
  1. Tick paralysis
  2. Botulism
  3. Polyradiculoneuritis (AKA Coonhound paralysis)
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19
Q

Which tick causes tick paralysis in North America?

A
  • Dermacentor variabilis or andersoni
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20
Q

Which tick causes tick paralysis in Australia?

A
  • Ixodes
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21
Q

Where does the toxin in tick paralysis come from, and what does it do?

A
  • Toxin in tick saliva

- Prevents release of ACh from NMJ

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22
Q

Timeline of tick paralysis

A
  • Feed 5-10 days
  • Ascending paresis
  • Flaccid paralysis of all limbs within 12-72 hours
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23
Q

Diagnosis of tick paralysis

A
  • Based on finding ticks and response to therapy once the tick is removed
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24
Q

How soon after tick is removed can tick paralysis resolve?

A
  • 12-48 hours after
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25
Q

Do cats get tick paralysis?

A
  • They tend to be quite resistant
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26
Q

Australian form of tick paralysis

A
  • Much more severe
  • Autonomic signs
  • Respiratory failure and death
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27
Q

Botulism - typical history?

A
  • Young dogs getting into carcasses tends to be where you see this
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28
Q

What is the toxin in botulism?

A
  • Exotoxin (type C1)
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29
Q

Etiology of botulism

A
  • Clostridium botulinum (gram + anaerobe)
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30
Q

Typical route of botulism

A
  • Typically from eating preformed toxin from decaying flesh or spoiled foods
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31
Q

Botulinum exotoxin pathophysiology

A
  • Toxin blocks presynaptic release of Acetylcholine from the Neuromuscular junction
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32
Q

Clinical signs of botulism

  • Onset
  • Unique features
A
  • CS usually within 12-72 hours of ingestion
  • Pelvic paresis –> flaccid paralysis of all limbs
  • CN involvement is common** (megaesophagus, facial paralysis, gag, decreased jaw tone)
  • Occasional autonomic nervous system signs (brady or tachycardia, mydriasis with decreased PLR, urinary retention, constipation)
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33
Q

Which CN signs can be seen with botulism, and which CN are responsible?

A
  • Megaesophagus (CN10)
  • Facial paralysis (CN7)
  • Decreased gag (CN 9 & 10)
  • Decreased jaw tone (CN5)
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34
Q

Treatment for botulism

A
  • SUpportive treatment, usually no immunity to future episodes
  • Prevention is key
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35
Q

Botulism in cats

A
  • Only one report of naturally occurring botulism in cats
36
Q

Polyradiculitis etiology

A
  • initially due to exposure to raccoon saliva

- Has been documented in dogs without raccoon exposure

37
Q

Pathophysiology of polyradiculoneuritis

A
  • Inflammation of the nerve roots (ventral) that’s suspected to be autoimmune
38
Q

Clinical signs of polyradiculoneuritis

A
  • Pelvic limb paresis –> flaccid nonambulatory tetraparesis or tetraplegia within 10 days
  • Hyperesthetic to minimal pressure (most likely due to inflammation of the nerve roots)
  • TYPICALLY no CN deficits but can see facial nerve/muscle weakness and dysphonia (voice change)
39
Q

Treatment for polyradiculoneuritis

A
  • Supportive care
40
Q

How long can recovery take for polyradiculoneuritis?

A
  • 6-8 weeks to several months
41
Q

How common is polyradiculoneuritis in cats?

A
  • Rare
42
Q

What do you worry about with ascending LMN paralysis?

A
  • Eventually worry about paralysis of the diaphragm

- C7, C6, C5 keep the diaphragm alive!

43
Q

Indications that mechanical ventilation may be required?

A
  • Abdominal breathing
  • Respiratory muscle paralysis
  • Hypoventilating (high CO2) (can measure with capnograph and CO2 level)
  • Ventilator
44
Q

Prognosis if mechanical ventilation is required (for botulism, polyradiculoneuritis, or tick paralysis)

A

Poor

45
Q

Neurolocalization:

Short strided gait that worsens with exercise

  • Weakened palpebral reflex
  • No other neurologic abnormalities
  • Regurgitation
A
  • Neuromuscular junction

- Note: often do not have CP deficits

46
Q

Describe neuromuscular junction function

A
  • Action potential comes in
  • Opens calcium channels leading to calcium influx
  • release of acetylcholine in the NMJ and get postsynaptic membranes
  • Sodium potassium channels
  • Once acetylcholine binds, sodium goes in, and potassium goes out so the muscles have an action potential
47
Q

What are the two types of myasthenia gravis?

A
  • Congenital vs acquired
48
Q

Congenital myasthenia gravis?

A
  • Lack of Acetylcholine receptors
49
Q

Acquired myasthenia graivs

A
  • Due to acetylcholine receptor ANTIBODY
50
Q

What are the three subsets of acquired myasthenia gravis?

A
  1. Focal - 40% dogs, 15% cats (just megaesophagus or facial weakness)
  2. Generalized - appendicular weakness
  3. Acute fulminating - Severe, rapidly progressing form of generalized MG, recumbent, 15%
51
Q

Clinical signs of acquired myasthenia gravis

A
  1. Appendicular muscle weakness (short choppy gait, worsens with exercise, improves with rest, typically normal CPs when supporting weight)
  2. Facial muscle weakness (decrease palpebral reflex, 36% in dogs, 60% in cats)
  3. Esophageal muscle weakness –> megaesophagus (84% dogs, 40% cats) –> aspiration pneumonia
  4. Laryngeal muscle weakness (laryngeal paralysis and stridor)
  5. Pharyngeal muscle weakness –> dysphagia
  6. Neck muscle weakness –> ventral neck flexion (cats)
52
Q

Radiographic signs of megaesophagus

A
  • Large dilated esophagus
53
Q

How do you diagnose myasthenia gravis?

A
  • Tensilon test
54
Q

Describe the procedure for the tensilon test?

A
  • Exercise the patient to point of collapse
  • 0.1 mg/kg IV of Edrophonium
  • Should see clinical improvement in gait and palpebral reflex within 30-60 sec
  • Effect lasts 5-10 minutes
55
Q

Mechanism of edrophonium

A
  • Anti-acetylcholinesterase –> increase ACh at the NMJ
56
Q

Signs of overdose with edrophonium

A
  • Cholinergic crisis - SLUD, muscle weakness, respiratory paralysis
  • Endotracheal tube, ambu bag, atropine available in case of overdose
  • Not a definitive diagnosis for myasthenia gravis
57
Q

Definitive diagnosis of congenital myasthenia gravis

A
  • Muscle biopsy to evaluate amount of ACh receptors
58
Q

Definitive diagnosis of acquired myasthenia gravis

A
  • ACh receptor antibody titer
59
Q

Treatment for acquired MG

  • which drugs, and how long to treat for?
A
  • Anticholinesterase therapy until Ab negative
  • Oral anticholinesterase is pyridostigmine
  • IV anticholinesterase is neostigmine
  • Feed elevated if megaesophagus
  • Appropriate antibiotics if aspiration pneumonia
  • Treat underlying disease
60
Q

Immunomodulatory therapy for acquired MG

A
  • Prednisone
  • Try to avoid due to aspiration pneumonia

Prednisone can also worsen neurologic weakness

61
Q

What other diseases can be associated with acquired MG?

A
  • Hypothyroidism
  • Other autoimmune diseases (masticatory myositis, meningitis, polymyositis, dysautonomia)
  • Thymomas (3% in dogs, 20% in cats)
  • Cutaneous lymphoma
  • Cholangiocellular carcinoma
  • anal sac adenocarcinoma
  • Osteosarcoma
  • Methimazole therapy in cats
62
Q

Prognosis for acquired MG

A
  • Remission in 88.7% at average of 6.4 months after diagnosis without prednisone therapy
  • Mortality is highest within the first 2 months
  • Worse with megaesophagus and aspiration pneumonia
63
Q

Neuroanatomical localization:

Right front monoparesis

Decreased withdrawal reflex to the right front limb

Severe muscle atrophy to the proximal muscles of the right front limb

A
  • C6-T2 nerve roots or nerves (one sided)
64
Q

Dfdx for nerve sheath tumors

A
  • Schwannomas
  • Neurofibromas
  • Neurofibrosarcomas
  • Other dfdx lymphosarcoma (cats)
65
Q

Prognosis for nerve sheath tumor in cats

A
  • Peripehral in the limb –> curative with amputation
  • Root level –> guarded (<3 months) even with surgery and radiation therapy
  • Important to refer early on
66
Q

Diagnosis of nerve sheath tumor

A
  • MRI
67
Q

Neurolocalization:

Left front monoplegia

Absent withdrawal reflex

No deep pain

Chewing at the antebrachium

A

LMN to left thoracic limb –> Left C6-T2 nerve roots and/or nerves

68
Q

How can brachial plexus avulsion occur?

A
  • Traumatic abduction of the thoracic limb at the level of the spinal cord
69
Q

Underlying pathophysiology with brachial plexus avulsion

A
  • C6-T2 nerve rootlets stretched or avulsed from the spinal cord
  • Partial or complete (more common)
  • Motor (ventral) vs sensory (dorsal) nerve roots
70
Q

Which nerve roots are more commonly avulsed with brachial plexus avulsion?

A
  • Motor more common (ventral)
71
Q

Clinical signs with brachial plexus avulsion

A
  • Usually non-painful

- Self-mutilate with loss of sensation

72
Q

Prognostic indicators with brachial plexus avulsion

A
  • Lack deep pain –> poor prognosis –> amputation

- preservation of return of triceps function (radial nerve) –> good prognosis

73
Q

Treatment for Brachial plexus avulsion

A
  • Physical therapy and time
  • If they can support weight but are knuckling you could do arthrodesis and help them not get sores or drag
  • Sometimes they get better on their own
74
Q

Underlying defect in diabetic neuropathy

A
  • Demyelination (abnormal schwann cells) and axonal loss
75
Q

3 underlying components with diabetic neuropathy

A
  1. Vascular compromise
  2. Metabolic disturbance (increased polyol pathway due to increased glucose –> increased sorbitol –> Na/K pump malfunction and build-up of free radicals leading to oxidative damage)
  3. Immune mediated
76
Q

Clinical signs of diabetic neruopathy

A
  • Dropped hocks and pelvic limbs

- Sciatic neuropathy

77
Q

Dfdx for diabetic neuropathy

A
  • Orthopedic (calcanean tendon)
  • gastrocnemius muscle ruptures
  • Sciatic neuropathy
78
Q

Trismus

A
  • Lock jaw
79
Q

What disease should you immediately think of with lock jaw?

A
  • Masticatory myositis

- Also think tetanus

80
Q

What’s the clinical difference between masticatory myositis and Trigeminal neuritis?

A
  • masticatory myositis is locked jaw and more guarded prognosis
  • Trigeminal neuritis is dropped jaw and good prognosis (temporal muscle atrophy)
81
Q

Clinical signs with masticatory myositis

A
  • Swollen, painful masseter/temporalis muscles
  • +/- exophthalmos
  • Later on severe masseter and temporalis muscle atrophy
82
Q

How common is masticatory myositis in cats?

A

Rare

83
Q

Diagnosis of masticatory myositis

A
  • Autoimmune disease so looking for 2M antibody titer (muscles of mastication)
  • Elevated CK (nonspecific)
  • Muscle biopsy to help prognosticate
84
Q

Which diagnostic for masticatory myositis can give you the best prognostic indicators?

A
  • Muscle biopsy
85
Q

Treatment for masticatory myositis?

A
  • ASAP, before fibrosis sets in
  • Immunosuppressive dose of pred until clinical signs and CK are normal, then SLOWLY taper over months
  • Relapse if not treated long enough
  • Muscle atrophy may persist

Neurology (14 decks)

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