PNS Diseases Flashcards
1
Q
Onset of disuse atrophy
A
- Evolve more slowly, less severe
2
Q
Onset of neurogenic atrophy
A
- Fast and severe
3
Q
Onset of primary myopathic atrophy
A
- Variable
4
Q
Pudendal nerve function
A
- Contract external anal sphincter and external urethral sphincter (skeletal)
5
Q
Pelvic nerve function
A
- Contract detrusor muscle of bladder (smooth)
6
Q
Which spinal cord segments do both the pudendal and pelvic nerve come from?
A
- S1-S3
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
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
9
Q
Degenerative/inherited diseases of PNS
A
- Neuropathy
- Myopathy
10
Q
Metabolic diseases of PNS
A
- Diabetic neuropathy
- Hyperadrenocorticism myopathy
- Hypothyroidism neuropathy and myopathy
11
Q
Neoplastic diseases of PNS
A
- Nerve sheath tumor
- Lymphoma
12
Q
Infectious inflammatory dz of PNS
A
- Toxoplasma
- Neospora
13
Q
Non-infectious inflammatory dz of PNS
A
- Polyradiculoneuritis
- Extraocular polymyositis
- Myasthenia gravis
- Masticatory muscle myositis
- Trigeminal neuritis
14
Q
Traumatic dz of PNS
A
- Brachial plexus avulsion
15
Q
Toxic dz of PNS
A
- Tick paralysis
- Botulism
- Chronic organophosphates incats
16
Q
Vascular dz of PNS
A
- Aortic thromboembolism
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
18
Q
Top 3 diffuse LMN diseases
A
- Tick paralysis
- Botulism
- Polyradiculoneuritis (AKA Coonhound paralysis)
19
Q
Which tick causes tick paralysis in North America?
A
- Dermacentor variabilis or andersoni
20
Q
Which tick causes tick paralysis in Australia?
A
- Ixodes
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
22
Q
Timeline of tick paralysis
A
- Feed 5-10 days
- Ascending paresis
- Flaccid paralysis of all limbs within 12-72 hours
23
Q
Diagnosis of tick paralysis
A
- Based on finding ticks and response to therapy once the tick is removed
24
Q
How soon after tick is removed can tick paralysis resolve?
A
- 12-48 hours after
25
Do cats get tick paralysis?
- They tend to be quite resistant
26
Australian form of tick paralysis
- Much more severe
- Autonomic signs
- Respiratory failure and death
27
Botulism - typical history?
- Young dogs getting into carcasses tends to be where you see this
28
What is the toxin in botulism?
- Exotoxin (type C1)
29
Etiology of botulism
- Clostridium botulinum (gram + anaerobe)
30
Typical route of botulism
- Typically from eating preformed toxin from decaying flesh or spoiled foods
31
Botulinum exotoxin pathophysiology
- Toxin blocks presynaptic release of Acetylcholine from the Neuromuscular junction
32
Clinical signs of botulism
- Onset
- Unique features
- 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)
33
Which CN signs can be seen with botulism, and which CN are responsible?
- Megaesophagus (CN10)
- Facial paralysis (CN7)
- Decreased gag (CN 9 & 10)
- Decreased jaw tone (CN5)
34
Treatment for botulism
- SUpportive treatment, usually no immunity to future episodes
- Prevention is key
35
Botulism in cats
- Only one report of naturally occurring botulism in cats
36
Polyradiculitis etiology
- initially due to exposure to raccoon saliva
| - Has been documented in dogs without raccoon exposure
37
Pathophysiology of polyradiculoneuritis
- Inflammation of the nerve roots (ventral) that's suspected to be autoimmune
38
Clinical signs of polyradiculoneuritis
- 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
Treatment for polyradiculoneuritis
- Supportive care
40
How long can recovery take for polyradiculoneuritis?
- 6-8 weeks to several months
41
How common is polyradiculoneuritis in cats?
- Rare
42
What do you worry about with ascending LMN paralysis?
- Eventually worry about paralysis of the diaphragm
| - C7, C6, C5 keep the diaphragm alive!
43
Indications that mechanical ventilation may be required?
- Abdominal breathing
- Respiratory muscle paralysis
- Hypoventilating (high CO2) (can measure with capnograph and CO2 level)
- Ventilator
44
Prognosis if mechanical ventilation is required (for botulism, polyradiculoneuritis, or tick paralysis)
Poor
45
Neurolocalization:
Short strided gait that worsens with exercise
- Weakened palpebral reflex
- No other neurologic abnormalities
- Regurgitation
- Neuromuscular junction
| - Note: often do not have CP deficits
46
Describe neuromuscular junction function
- 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
What are the two types of myasthenia gravis?
- Congenital vs acquired
48
Congenital myasthenia gravis?
- Lack of Acetylcholine receptors
49
Acquired myasthenia graivs
- Due to acetylcholine receptor ANTIBODY
50
What are the three subsets of acquired myasthenia gravis?
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
Clinical signs of acquired myasthenia gravis
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
Radiographic signs of megaesophagus
- Large dilated esophagus
53
How do you diagnose myasthenia gravis?
- Tensilon test
54
Describe the procedure for the tensilon test?
- 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
Mechanism of edrophonium
- Anti-acetylcholinesterase --> increase ACh at the NMJ
56
Signs of overdose with edrophonium
- 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
Definitive diagnosis of congenital myasthenia gravis
- Muscle biopsy to evaluate amount of ACh receptors
58
Definitive diagnosis of acquired myasthenia gravis
- ACh receptor antibody titer
59
Treatment for acquired MG
- which drugs, and how long to treat for?
- 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
Immunomodulatory therapy for acquired MG
- Prednisone
- Try to avoid due to aspiration pneumonia
Prednisone can also worsen neurologic weakness
61
What other diseases can be associated with acquired MG?
- 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
Prognosis for acquired MG
- 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
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
- C6-T2 nerve roots or nerves (one sided)
64
Dfdx for nerve sheath tumors
- Schwannomas
- Neurofibromas
- Neurofibrosarcomas
- Other dfdx lymphosarcoma (cats)
65
Prognosis for nerve sheath tumor in cats
- Peripehral in the limb --> curative with amputation
- Root level --> guarded (<3 months) even with surgery and radiation therapy
- Important to refer early on
66
Diagnosis of nerve sheath tumor
- MRI
67
Neurolocalization:
Left front monoplegia
Absent withdrawal reflex
No deep pain
Chewing at the antebrachium
LMN to left thoracic limb --> Left C6-T2 nerve roots and/or nerves
68
How can brachial plexus avulsion occur?
- Traumatic abduction of the thoracic limb at the level of the spinal cord
69
Underlying pathophysiology with brachial plexus avulsion
- C6-T2 nerve rootlets stretched or avulsed from the spinal cord
- Partial or complete (more common)
- Motor (ventral) vs sensory (dorsal) nerve roots
70
Which nerve roots are more commonly avulsed with brachial plexus avulsion?
- Motor more common (ventral)
71
Clinical signs with brachial plexus avulsion
- Usually non-painful
| - Self-mutilate with loss of sensation
72
Prognostic indicators with brachial plexus avulsion
- Lack deep pain --> poor prognosis --> amputation
| - preservation of return of triceps function (radial nerve) --> good prognosis
73
Treatment for Brachial plexus avulsion
- 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
Underlying defect in diabetic neuropathy
- Demyelination (abnormal schwann cells) and axonal loss
75
3 underlying components with diabetic neuropathy
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
Clinical signs of diabetic neruopathy
- Dropped hocks and pelvic limbs
| - Sciatic neuropathy
77
Dfdx for diabetic neuropathy
- Orthopedic (calcanean tendon)
- gastrocnemius muscle ruptures
- Sciatic neuropathy
78
Trismus
- Lock jaw
79
What disease should you immediately think of with lock jaw?
- Masticatory myositis
| - Also think tetanus
80
What's the clinical difference between masticatory myositis and Trigeminal neuritis?
- masticatory myositis is locked jaw and more guarded prognosis
- Trigeminal neuritis is dropped jaw and good prognosis (temporal muscle atrophy)
81
Clinical signs with masticatory myositis
- Swollen, painful masseter/temporalis muscles
- +/- exophthalmos
- Later on severe masseter and temporalis muscle atrophy
82
How common is masticatory myositis in cats?
Rare
83
Diagnosis of masticatory myositis
- Autoimmune disease so looking for 2M antibody titer (muscles of mastication)
- Elevated CK (nonspecific)
- Muscle biopsy to help prognosticate
84
Which diagnostic for masticatory myositis can give you the best prognostic indicators?
- Muscle biopsy
85
Treatment for masticatory myositis?
- 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
