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SAM 1 > Neurology 3 > Flashcards

Neurology 3 Flashcards

1
Q

What 5 things can occur to cause tetraparesis/tetraplegia?

A
  1. Diskospondylitis
  2. Neoplasia
  3. Fractures
  4. Luxations
  5. FCE
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2
Q

Spinal cord lesions between C1-T2: Cervical disc disease

A
  • Type I–explosive
    • 75% chondrodystrophics and Poodles C3-C4
    • 25% large breeds (labs, GSD, rott, dob) C5/C7
  • Type II
    • Dobes/rott at C6/C7 – wobblers
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3
Q

What are the signs of cervical disc disease (C1-T2)?

A
  • 8yrs (2-16)–neck pain (90%); 45% acute
  • Won’t move head–brain fine, hyperreflexia
  • Tetraparesis–64% - rear worse
  • Hemiparesis and tetraplegia (3%)–rare
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4
Q

How do you diagnose cervical disc disease?

A

Myelogram, calcified discs on rads (can find old calcified discs that aren’t causing the current problem, however–need myelogram to confirm)

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5
Q

What is the treatment for cervical disc disease?

A
  • No deficits–cage rest
    • Give time for annulus to repair itself
  • NSAIDs/pred
    • NSAIDs don’t work very well
    • Only use pred when animal is in pain–will slow healing
    • Can add diazepam on top of pred as musc. relaxant
  • Up to 33% recur
  • No improvement/neuro signs = surgery
    • 8% recur, 99% walk unassisted
    • Much faster recovery than back surgery
    • Can fenestrate vertebral body on both sides to lessen chance of recurrence
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6
Q

Cervical spondylomyelopathy

A
  • Canine wobblers
  • Cervical malformation-malarticulation syndrome
  • Caudal cervical spondylopathy, etc x 14
  • Spinal cord compression - esp. > C5/6
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7
Q

What are some specific causes of cervical spondylomyelopathy?

A
  • Stenosis–craniodorsal ridge
    • Problem with development, often in Dobermans (most Dob’s have some degree of stenosis)
    • Front of vertebra grows more than back–> tipping
  • Osteophytes from malformed articular processes
    • Instability from vertebrae –> joints move side-to-side –> ligaments tear from bone –> pressure on spinal cord –> dysfunction
  • Hansen type II disk: increased lig. flavum
    • Dob’s have thicker discs and stenosis –> greater risk
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8
Q

Etiology of cervical spondylomyelopathy?

A
  • Genetics (dob’s, great danes)
  • Congenital stenosis/lig laxity
  • Rapid growth, over-nutrition
  • Abnormal stresses/straint, joint motility/symmetry, cartilage
  • Calcitonin
  • Static and/or dynamic compression
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9
Q

What are the signs of cervical spondylomyelopathy?

A
  • Great danes 3-18mo: congenital spinosis
  • Dobes 5-8 yrs: older–cartilage changes
  • Head guarding (won’t move head side-to-side)
  • Pelvic signs esp. paresis
    • Wobbling, scuffing
    • Hypermetria of hind limbs (long strides)
    • Front legs can also be affected but might look normal compared to back legs–why postural rxns important
  • Thoracic limbs
    • Dysmetria, mild CP def.–stiff gait
    • Atrophy infra-/supraspinatus, w/drawal
      • Can w/draw carpus, can flex elbow; might not be able to operate shoulder
    • Neck pain (15%)–nerve roots
    • Front legs can become pigeon-toed
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10
Q

How do you diagnose cervical spondylomyelopathy?

A
  • Rads, myelogram (much better)
    • Tipping
    • Stenosis
    • Rounding
    • Dec. disc spaces
      • Degeneration in articular facets
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11
Q

What will be seen on the myelogram/MRI of a dog with cervical spondylomyelopathy?

A
  • MRI more helpful when have mult. lesions–will show sc edema
  • Dorsal comp–lig flavum
  • Ventral comp–disc
  • Lateral comp–artic facets
  • Vertebral tipping–>lesions disappear
  • Single <50%
  • Multiple <80%
  • Traction rads
    • No standards, hit or miss, can’t really estimate improvement
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12
Q

Cervical sponylomyelopathy treatment/prognosis?

A
  • Varies–each case is different
  • Medical
    • Palliative–40, 30, 20
    • Condition is progressive
  • Surgery
    • Decompression
    • Distraction-stabilization
  • About 1/2 will get better, ~30% will stay the same, and ~20-30% will get worse
    • Can’t guarantee surgery will help–can try cage rest first
  • Dorsal approach much more difficult w/ more complications than ventral–dogs tend to worsen after sx
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13
Q

What drugs are used for a UMN bladder in dogs with cervical spondylomyelopathy? LMN bladder?

A
  • UMN bladder
    • Phenoxybenzamine–musc. relaxant
    • Prazosin tamsulosin
    • Valium/dantrolene
  • LMN bladder
    • Phenylpropanolamine
    • Bethanecol
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14
Q

Prognosis of cervical spondylomyelopathy

A
  • Disc only = good
  • Tetra- = poor
  • Guarded in others
  • Surgery–80-90% success (?)
  • Recurrence/domino 20-40%, 2-3yr
    • Must warn owners of more surgery and nursing care
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15
Q

Atlanto-axial subluxation

A
  • Spinal cord compression due to dorsal displacement of the axis
  • Large breeds–trauma
  • Small breeds–lack of development
    • Toy breed dogs: see progressive tetraparesis
    • Ligaments can rupture –> spinal cord crushed –> death
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16
Q

What is the best diagnosis for atlanto-axial subluxation?

A
  • Don’t manipulate the neck!!
  • Rads best–vd esp. for absence
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17
Q

Signs of atlant-axial subluxation

A
  • Congenital
    • Toy/mini breeds
    • 6-18 ms (dd cerv discs)
  • Neck pain to tetraplegia (resp paralysis)
    • Insidious in onset + progressive
  • Large breeds: trauma
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18
Q

What is the treatment for atlanto-axial subluxation?

A
  • Hemilaminectomy + wiring/screwing
    • 30% failure rate–bones aren’t very strong + small breeds
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19
Q

Caudal occipital malformation syndrome: tell me all the things

A
  • Chiari 1 malformation syndrome
  • Malform caudal occip bone–crowding in caudal fossa
  • Signs 3-6 yrs (from 6m)
  • Neck/face scratching
  • CP deficits
  • Vestibular signs
  • Spinal hyperesthesia
  • Gabapentin and pred
  • FMD–foramen magnum decompression
    • 70% successful
    • Recurrence 20-40%
20
Q

Muscle and end-plate conditions: general

A
  • Myopathies
    • Weakness (exercise)
    • Stilted stiff gate (short strides)
    • Sometimes pain, CPK
    • Normal CP and reflexes except flexor withdrawal reflex
21
Q

What are the main causes of inflammatory myopathies?

A
  • Infectious (20%)
    • Toxoplasma
    • Neosporum
    • Lyme
    • Hepatozoan
  • FeLV, FIV
22
Q

Canine idiopathic polymyositis–all ze thingzzz

A
  • Normal neuro exam except for flexor withdrawal reflex
  • Immune mediated
    • Large, mature, acute or chronic
    • Weakness/stiff/rapid fatigue/atrophy
    • Some have pyrexia, pain, regurge, bark, dysphagia
  • Patterns of necrosis–lots of lymphs and neutrophils
  • Prednisone +/- azathioprine
  • 25% recover; 50% lifelong
  • Biopsy for definitive diagnosis (take multiple since patchy)
23
Q

Masticatory muscle myositis

A
  • 2M fibers–large breeds, < 4yr
  • Waxing and waning
    • Painful swollen muscles
    • Pseudotrismus
    • Fever
    • Inn
    • Chronic–atrophy
24
Q

How do you diagnose masticatory muscle myositis? What’s the treatment?

A
  • Biopsy/serology
  • Prednisone–good response, even chronics
    • Taper dose slowly
    • With azathioprine–steroid sparing
25
Q

Extraocular myositis–all the things

A
  • Diagnose with biopsy/ultrasound
  • Not very common, tend to be in golden retrievers (young)
  • Autoimmune
  • Eyes bulge out due to muscles being inflamed
  • Pred–resolves in weeks
    • Some need chronic pred
26
Q

Exertional myopathy

A
  • Post exercise
  • Massive CPK
  • Renal failure (myoglobin gets blocked up in kidneys)
  • Hypokalemia (cats)
    • CRF
    • Acid diets
    • Conn’s
    • Hyperthyroid
  • Oral supplementation
  • Normal neuro exam–normal reflexes, just have exreme muscle weakness/exhaustion
  • Can sometimes get hyperalosteronism (ext. rare)
27
Q

Feline idiopathic inflamatory myopathy

A
  • Cat with droopy head, everything else normal
  • Diagnosis of exclusion
  • Usually improve with immunosuppressive dose of pred
    • 10mg/day w/ no side effects
28
Q

Limber tail

A
  • Paralyzed tail after long day of working/running after long period of inactivity
  • Usually gets better w/o treatment
29
Q

What are the 4 degenerative/developmental myopathies?

A
  1. Dystrophic myopathies
  2. Non-dystrophic myopathies
  3. Metabolic myopathies
  4. Miscellaneous conditions
    1. Myotonia
    2. Dermatomyositis
30
Q

Dystrophic myopathies

A
  • Molecule on outside that binds actin to myosin
  • Alpha-2 laminin deficiency
    • Dystrophin normally surrounds muscle –> patchy instead –> muscle doesn’t contract properly –> tears; Ca leaks in, etc.
  • Look normal at birth, develop strange gait
  • Progressive til ~6mo, then relatively stable til ~2yrs
    • Heart is then affected –> death
31
Q

Non-dystrophic myopathies

A
  • Central core-like
  • Nemaline rod
  • Congenital degenerative myopathies
    • Probably genetic–labs, great danes
    • Entire litters affected
  • Start seeing muscle wasting, degeneration
32
Q

Metabolic myopathies

A
  • Hypo- hyperthyroid–lack of metabolism in muscles
  • Hyperadrenocorticism
    • Overproduce glucocorticoids –> tear into muscles
    • Dogs usually brought in for PU/PD
  • Enzyme deficiencies
    • ​Glycogen storage disease
    • Phosphofructokinase deficiency
  • Exercise induced collapse (EIC) in labradors (< 3yrs)
    • < 1% population; working dogs/pets
    • Rocking horse gait (LMN in hind limbs)
    • Limp, 5-25 min. recovery (get better w/ rest)
    • Metabolic cocktail
    • Phenobarb
    • Dynamin gene (DNM1)–neuromuscular transition
33
Q

Myotonia

A
  • Chows, Westies, Danes, cats, fainting goats
  • Cl channelopathy
  • Dimpling
    • Tap muscles–> contract and forms dimple that slowly disappears
    • Can check on tongue
  • Stiff gait, CP slow
  • Reflexes chronic
34
Q

Dermatomyositis

A
  • Sheep dogs, collie breeds
  • Skin lesions 2-6m then weakness
  • megaesophagus
  • Resolves or chronic wax/wane.
  • Pentoxifylline–makes RBCs more bendy
  • Autoimmune disease, damage to capillaries; usually goes away w/in a year
35
Q

Feline hyperesthesia syndrome

Inclusion body myopathy

A
  • Multifactorial condition
  • 5-8 yr pure breeds
  • Intermittent twitching, grooming, agitation (self-trauma), vocalizing, running, aggression
  • Allergies, SC lesions, myositis, behavior, seizures
  • Can respond to pred
    • If doesn’t respond, can try phenobarb
  • Inclusion body myopathy
    • Muscle cells degenerate
      • Protein from cell breakdown cause hypersensitivity rxn
    • No treatment/cure–>only gets worse
36
Q

Myasthenia gravis

A
  • Congenital–Jack russels, foxies (rare, musc. weakness)
  • Acquired–autoantibodies to AchR
    • Stops receptors from working–> weakness
37
Q

What are the 3 forms of myasthenia gravis? How do they differ?

A
  • Classically–weak following exercise
    • Look normal, get weaker and weaker until eventually collapse from exercise
    • Tensalon esterase inhibitor
      • Given IV, stops breakdown of Ach–> dog fine in about 15 min
  • Focal–36% (esoph, face, pharynx, larynx)
    • Skeletal muscles fine; localized
    • Sign: regurgitation
  • Generalized muscle involvement + weakness
    • Acute fulminating 16%
      • Not assoc. w/ exercise–weak all the time plus severe megaesophagus (–> severe regurg.)
      • Die of resp. failure
    • Chronic generalized 48%
      • 80% megaesophagus (clinical sign = regurg)
      • 50% exercise-induced
  • Antibody test exists
38
Q

Tests/treatment/prognosis for masthenia gravis?

A
  • Cats–rare, generalized, thymoma (26%)
    • Weak with exercise
  • Tensilon test–anticholinesterase (only picks up ~1/4 of dogs with it)
    • AchR antibody test/immune complex
  • Support (gastrostomy + cisapride)
    • Increased tone of esoph. sphincter
    • Can get muscle atrophy (disuse)
    • Pyridostigmine–play w/ dose to avoid PNS acitivity
      • +/- prednisolone (aza/cyclo)–avoid if poss.; start w/ low dose (will worsen pneumonia and musc. weakness)
      • +/- thymectomy–thymoma
      • Poor drug response
  • Prognosis: 6 months, resolution in 90%
    • Bad–congenital + fulminant
    • Vaccine–anergy (overwhelm immune system)
39
Q

Botulism

A
  • Dogs-outbreaks when hunted animals aren’t bled out properly
  • Blocks Ach presynaptically
  • Tetraparesis, cranial nerves, esophagus, parasympathetic and sympathetic signs
  • Respiration
  • Slow improvement over 2-3 weeks
    • Need major physiotherapy–turn often
  • Exotoxin in feces/serum
  • Antisera (not effective after), support, neostig
  • If have LMN on all 4 limbs–think of things working on outside peripheral nerves
40
Q

Tick paralysis

A
  • Toxins–Dermacentor + Ixodes + 58 species
  • Unpredictable
  • Block nerve conduction or decrease Ach
    • Stop AP’s–> stop Ach from being released
  • Not all ticks/dogs
  • Can be relatively acute progression
  • Hard to differentiate from botulism–must find the tick
41
Q

What are the major signs of tick paralysis?

A
  • Tetraparesis - plegia
  • LMN signs (all 4 limgs)
  • Cranial nerves, sensation, continence spared
  • Recovery after tick removed
    • Check ext. ear canal/interdigital spaces
  • *Botulism suspect–make sure aren’t any ticks
42
Q

Tetanus

A
  • Dogs–rarely cats–anaerobic wounds
  • Often only affects one limb
  • Puncture wounds where there’s no blood supply
    • Toxin enters wound –> enters nerves –> spinal cord –> animal becomes stiff
  • Sardonic–facial expression of skepticism/disdain
43
Q

What is the diagnosis and treatment of tetanus?

A
  • Diagnosis–clinical signs
  • Treatment
    • Temperature
    • Antitoxin IV (not useful)
    • Pen/peroxide (if find the wound)
    • Val/ace/pent
    • Muscle relaxants***
    • Turn regularly, give fluids, etc. for maintenance
    • Feeding tubes; hernias
  • Slow improvement, sometimes have deficits later on due to nerve damage
44
Q

Acute canine polyradiculoneuritis

A
  • AKA Coonhound paralysis
  • Inflammation/demyelination ventral roots
  • Raccoon saliva/viruses/drugs–hapten
  • Ascending LMN paralysis and tetraplesia
    • Start going off back legs, then front w/in 24 hours
  • Cranial nerves + sensory + continence spared
    • ​Looks like tick paralysis and botulism–treatment the same
  • Pred not helpful–demyelination only there for a few hours, then just left with the damage
45
Q

What is the recovery/treatment/prognosis of acute canine polyradiculoneuritis?

A
  • Spontaneous recovery–weeks to months
  • Diagnosis–clinical signs + EMG (not normally done–would need to biopsy nerve roots)
  • Glucocorticoids don’t help
    • Inflammation is gone relatively quickly and animal heals itself–adding steroids would only slow down healing process (w/ PU/PD, immunosuppression)
  • Supportive therapy
46
Q

Protozoal polyradiculoneurititis

A
  • Toxo/Neosporum caninum
  • Transplancental–subclinical
    • Prog post paresis
  • Serology?
    • Organisms - biopsy
    • TMS–pyrimeth or clindamycin
  • Prog. dependent on contracture
47
Q

Miscellaneous neuropathies

A
  • Diabetic
  • Hypothyroid
  • Trigeminal/brachial plexus neuritis
    • Masticating muscles
  • Paraneoplastic
  • Idiopathic facial nerve
  • Venom
  • Salinomycin (used in chickens to kill coccidia)
  • Inherited/familial neuropathies

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