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Small Animal Final Year > Neurodegenerative Disease > Flashcards

Neurodegenerative Disease Flashcards

1
Q

Define spondylosis

A

•Descriptive term for the production of new bone

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2
Q

Is spondylosis diagnostically significant?

A
  • Usually an incidental finding
  • Can cause problems if extensive, or impinging upon neural structures
  • May indicate that other problems are present
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3
Q

Define discospondylitis

A

•Infectious inflammation within the intervertebral disc (abscess in the disc)

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4
Q

What is the clinical presentation of Discospondylitis?

A

–Chronic, progressive

–Pain (localisable to site)

–Variable paresis (rarely paralysis)

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5
Q

How do you diagnose discospondylitis?

A

–Radiography

  • Destructive changes in vertebral body
  • Loss of definition of vertebral body end plates
  • May take weeks for changes to become apparent (ie radiography may be negative)

–Advanced imaging

–Culture –blood/urine

  • UTI
  • Bacteraemia
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6
Q

How can you treat discospondylitis?

A

–6 weeks of an appropriate antibiotic

  • Hence urine/blood culture
  • Broad spectrum antibiotic

–Monitor on clinical signs and radiography

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7
Q

What are the 2 parts of the intevertebral disc? What are they made up of?

A
  • Annulus fibrosus
    • Fibrocartilage
  • Nucleus pulposus
    • Collagenous protein
    • Non-collagenous protein
    • Proteoglycan
    • Glycoproteins
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8
Q

What are the 2 kind of breed affected by the age related changed of intevertebral disc disease?

A

Chondrodystophic

  • Queen Anne legs (legs with both a concave and convex component)
  • Dachshund, pug, spaniels, basset, beagle, JRT …

non chondrodystrophic

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9
Q

What is the pathophysiology of IVDD?

A

Progressive changes with age within the
nucleus pulposus
• Resulting in changes in physical properties
of the disc
• In chondrodsytrophic breeds these
changes start earlier (from 1 year of age)
and differ in nature
• Degenerate – dehydrate the disc. Change
the disc to a hard rather than jelly. Which
normally shock absorbs and allows
movement. Failure of the disc

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10
Q

Name 2 other terms for intervertebral disc failure(4)

A
  • Slipped disc (lay term)
  • Intervertebral disc prolapse (means both of the next 2 terms)
  • Intervertebral disc extrusion
  • Intervertebral disc protrusion
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11
Q

What are the incidences of:

A) Type 1 disc? Why?

B) Type 2 disc?

A

A) Type I discs: Chondrodystrophic breeds

Dachshund breed incidence 10%

(62% in some families)

Prone to type one! Because the way they degenerate the NP degeerates and can calcify

B) Type II discs: non-chondrodystrophic breeds

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12
Q

How can we diagnose disc extrusion?

A

•Clinical picture

–Compress spinal cord and you will see paresis. The severity of compression will decide the clinical signs

–Extrusion – depends how aggressive it happens. Can get oedema and brusining in S. Depend how much nucleus comes out? Do we just bruise or compress?

–PAIN!!!!!+/- paresis +/- paralysis

•Radiography

–Pretty useless doesn’t give too much info just its there

•Advanced imaging

  • Myelography
  • CT
  • MRI
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13
Q

What are the clinical presentations of disc extrusion?

E.g. acut? Chronic? Progess? Stable?

A

•Acute vs Chronic

–Acute – explode

–Chronic – degeneration

•Progressive vs stable

–Progress if it will continue to buldge

–Stable – once extruded it will stay there

•Pain to ataxia to paralysis

–PAIN IS MOST COMMON

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14
Q

How do you treat acute pathology:

A) Compression?

B) Concussion?

A

Compression – relieve by removing the compression agent

Concussion - leave allow bruising to go down

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15
Q

How long does spinal cord pathophysiology continue for?

A

•Pathology continues over 24-48 hours following acute concussive injury

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16
Q

What can we do for conservative therapy in disc extrusion?

How long for?

A
  • Cage rest
  • Bladder management
  • Good nursing
  • Physiotherapy
  • Analgesia
  • May need to continue for 4 weeks, but should see some improvement within 2 weeks
17
Q

Should we give steroids to acute spinal injury?

A
18
Q

What are the signs of cervical IVDD?

A

all 4 legs affected

19
Q

What are the signs of thoracolumbar IVDD?

A

Hindlimbs affected

20
Q

What is the progression of CDRM/DM? When does it happen? Who does it happen in?

Chronic degenerative radiculomyelopathy (CDRM) Non-painful

Degenerative myelopathy (DM)

A
  • Progressive degenerative pathology affecting the spinal cord. TL then progresses to the C region.
  • Commonest in the aged GSD
  • 6-9 years of age. 9 months from when they go wobbly to when they get PTS.
  • Clinical picture of progressive hindlimb ataxia–> paresis and eventually they become non-ambulatory
  • Become non-ambulatory
  • Eventually affects forelimbs
  • 9 month progression
  • Diagnosis by exclusion
  • (? Over diagnosed)
  • No effective treatment
  • Some palliation with physiotherapy meaning they can walk for longer so slows down clinical picture not the pathological process
  • Now DNA genetic test becoming available but not diagnostic
  • Common d/dx is chronic protrusion of disc.
21
Q

What are the signs of CDRM/DM?

A
  • Clinical picture of progressive hindlimb ataxia
  • Become non-ambulatory
  • Eventually affects forelimbs

–Then affects respiratory

•9 month progression

22
Q

How can we diagnose CDRM/DM?

A

By exclusion common ddx is chronic disc protusion

23
Q

How can we treat CDRM/DM?

A
  • No effective treatment
  • Some palliation with physiotherapy
24
Q

What is a differential of CDRM/DM? How do we distinguish?

A

•Protusive IDDV is a DDx

–Not uncommon to have 5 protrusive disc so the only confirmation is surgery which can make then worse

25
Q

How can we treat age related brain atrophy?

A

•Dietary alteration

–Hills BD

–Aktivait

  • Drug therapy – selegiline
  • Treatment combined with behavioural therapy
26
Q

What happens with lysosomal storage disorders?

A
  • A diverse group of inherited disorders of metabolism
  • Enzyme deficiencies within specific intracellular metabolic pathways
  • All the metabolites cant go to the step that is blocked and cant go alternative path so will accumulate. Only thing they can do is put in lysosome. Eventually so many.
  • Result in the accumulation of abnormal metabolites within cells which eventually becomes toxic
  • Manifest in cells which cant replicate themselves. E.g. neurones and there are no ways to regenerate
27
Q

L-2-hydroxyglutaric aciduria:

A) How does a dog get it?

B) What are the signs?

C) How can we eradicate?

D) Where is it common?

A

A) Inherit

B) Progressive mental retardation seizures tremor or stiffness at exercise

C) DNA testing and breeding

D) Staffie

28
Q

What is the problem here?

A

Radiographic appearance
L6-L7 L7-S1
Bridge of bone joining

29
Q

What is the issue?

A

Lost end plate definition

Something is destroying this

Neoplasia Vs infection

Not neoplasia – Bone based neoplasia DOESN’T cross the joint. Has to metastasis. So destruction of the adjacent end plate cannot. Destroy end plate think neoplasia. Destro 2 adjacent neoplasia

30
Q

What can be seen here?

A

Extrusion – extrude nuclear pulposus out – compressing the spinal cord

31
Q

What is the issue here?

A

Protrusion (tread on doughnut) – buldges. Firbous tissue

32
Q

What do these show in terms of hanen classification?

A

A) Type 1 - extrusion

B) Normal

C) Type 2 - protrusion

33
Q

Where do type 1 and type 2 IVDDs occur?

A

Small Animal Final Year (317 decks)

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