Spinal disease Flashcards

1
Q

Describe grades 1 to 5 of spinal disease

A

1 = no deficits, just pain
2 = paresis, ambulatory
3 = paresis, non-ambulatory
4 = paralysis
5 = no pain sensation

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2
Q

What questions should be asked to obtain details about spinal disease?

A

Signalment (age and breed)
Duration of the clinical signs
Speed on onset (acute vs. chronic)
Progressive or not
Pain

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3
Q

How is a lesion localised to C1-C5?

A

Normal to increased reflexes in the TLs
Normal to increased reflexes in the PLs

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4
Q

How is a lesion localised to C6-T2?

A

Reduced reflexes in the TLs
Normal to increased reflexes in the PLs

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5
Q

How is a lesion localised to C3-L3?

A

Normal reflexes in the TLs
Normal to increased reflexes in the PLs

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6
Q

How is a lesion localised to L4-S3?

A

Normal reflexes in TLs
Reduced reflexes in PLS

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7
Q

List the DDx for spinal disease

A
  • Ischaemic myelopathies
  • Steroid responsive meningitis-arteritis (SRMA); meningomyelitis of unknown origin (MUOs); discospondylitis; Toxoplasmosis, Neosporosis; FIP, FeLV
  • Fractures and luxations
  • Spinal/vertebral neoplasia
  • IVDD type I and II
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8
Q

What are the DDx for peracute onset of spinal disease?

A

Vascular:
- Fibrocartilaginous embolism (dogs)
- Stroke (cats)
Trauma:
- Acute non-compressive annulus pulposus extrusion (ANNPE)
- Fractures/luxations

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9
Q

What is an ischaemic myopathy?

A

Blood supply to spinal cord interrupted - Area of ischemia and necrosis in the spinal cord

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10
Q

What are the clinical signs of an ischaemic myopathy?

A
  • Peracute onset, non-painful; signs often very lateralised
  • One side worse than another
  • Usually at exercise
  • Fibrocartilage from nucleus pulposus embolises in spinal cord vasculature – Fibrocartilagenous embolism (FCE)
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11
Q

What is acute non-compressive nucleus pulposus extrusion?

A

High velocity/low volume; traumatic disc extrusion
- Following traumatic events (RTA, fall from height) or just exercise
- Acute onset, non-painful, non-progressive
- Herniated nucleus pulposus is non-mineralised, causing mainly cord contusion with minimal compression

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12
Q

Describe the pathological changes that occur during acute non-compressive nucleus pulposus extrusion?

A
  • Disc is put under pressure
  • Jelly like material changes for mineralised material
  • Fibrocartilage weakens
  • Can get hernitation of the disk material which pushes onto the spinal cord
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13
Q

What is not indicated for treatment of fibrocartilaginous embolism and traumatic disc disease?

A

Surgery - nothing to remove or stabilise

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14
Q

What is indicated for treatment of fibrocartilaginous embolism and traumatic disc disease?

A

Supportive care and physiotherapy
Median time to ambulation ~2wks
Time to maximal recovery ~3m

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15
Q

Name 3 causes of fractures/luxations of the spine

A

RTA, bite wounds, falling from height

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16
Q

How are fractures/luxations of the spine diagnosed?

A

Careful neurological examination
Thoracic and abdominal radiographs
Survey lateral radiographs of spine
Orthogonal views essential
CT/MRI may be helpful

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17
Q

Describe the initial treatment of fractures/luxations of the spine

A

Stabilise trauma patient and analgesia

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18
Q

Compare conservative vs surgical treatment for fractures/luxations of the spine

A

Use 3 compartment rule → if unstable surgery or splint
Decompression if fragments compressing spinal cord
If transporting patient → splint

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19
Q

Describe the prognosis for fractures/luxations of the spine

A
  • Lack of deep pain perception → < 5% (usually associated with spinal cord laceration)
  • Severe vertebral displacement, other injuries, weight and age, time to referral
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20
Q

List the DDx for acute/subacute onset presentation of spinal disease

A

IVDD type I (extrusion)
Infectious/inflammatory
- SRMA
- Discospondylitis
- Spinal MUO (meningomyelitis)

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21
Q

Describe intervertebral disc degeneration in chondrodystrophic breeds

A

Short legged dogs
- During first 2 years of life
- Chondroid metamorphosis
- IVD dehydrates and nucleus is invaded by hyaline cartilage, nucleus can mineralise

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22
Q

Describe intervertebral disc degeneration in non-chondrodystrophic breeds

A

After middle age
Fibroid metamorphosis
IVD dehydrates and nucleus is invaded by fibrocartilage, mineralisation less common

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23
Q

Describe intervertebral disc degeneration type I

A

Extrusion
- Herniation of nucleus pulposus through annular fibres and extrusion of the nuclear material into the spinal canal
- 3-6y chondrodystrophic and 6-8y non- chondrodystrophic breeds
- Peracute/acute onset, progressive
- Typically painful

24
Q

Describe intervertebral disc degeneration type II

A

Protrusion
- Annular protrusion caused by shifting of central nuclear material, commonly associated with fibroid disc degeneration
- Older, non-chondrodystrophic breeds
- Slowly progressive, chronic onset
- Spinal pain may or may not be present
- Typically less severe signs
- Wont be off limbs

25
How is IVDD treated?
Conservative - Strict rest for 4-6 weeks - Analgesia Surgical
26
When is surgery for IVDD indicated?
- Severe neurological deficits (grades 3-5) - Severe or recurrent pain - Lack of improvement with rest
27
Steroid responsive meningitis-arteritis is the most common cause of?
Neck pain in young dogs (6-18mo)
28
What is steroid responsive meningitis-arteritis?
Immune mediated sterile meningitis Causes pyrexia of unknown origin
29
What are the clinical signs of steroid responsive meningitis-arteritis?
Lethargy, anorexia and fever Cervical rigidity and spinal pain Often concurrent IMPA
30
How is steroid responsive meningitis-arteritis diagnosed?
CSF analysis - Neutrophilic pleocytosis in acute form - Mononuclear pleocytosis in chronic form +/- spinal radiographs, CT, MRI
31
How is steroid responsive meningitis-arteritis treated?
Corticosteroids for 6-9m (+/- azathioprine or ciclosporin) Monitoring with repeated CSF analysis or CRP Very good although potential for relapse
32
What is the main DDx of Steroid responsive meningitis-arteritis?
Discospondylitis
33
What is discospondylitis?
Infection of IVD and adjacent vertebrae, most common at L7-S1 Marked spinal pain, ~30% systemic signs of illness
34
How is discospondylitis diagnosed?
1. Imaging - radiography (2-4 weeks); MRI or CT - Narrowing of IVD space - Roughening of endplates - Proliferation of adjacent bone 2. Bacteriology - blood, urine, CSF, IVD
35
How is discospondylitis treated?
Antibiotics for at least 8 weeks Analgesia
36
What is meningomyelitis of unknown origin?
(Sub)acute, progressive, can be asymmetrical, can be painful Often multifocal (sometimes affects brain) Care as same breeds and often similar presentation to IVDD
37
How is meningomyelitis of unknown origin diagnosed?
MRI – variable findings CSF – mononuclear or mixed pleocytosis
38
How is meningomyelitis of unknown origin treated?
Corticosteroids +/- other immunosuppressive drugs
39
List the DDx for chronic onset presentation of spinal disease
1. Neoplasia 2. Degenerative - IVDD type II (protrusion), CSM, LSDS, DM 3. Anomalous - Spinal malformations, CM/SM,AA instability (if congenital)
40
What are the main features of spinal neoplasia?
Chronic Progressive Painful
41
Describe the 3 locations of spinal neoplasia
1. Extradural: primary vertebral, metastatic, lymphoma 2. Intradural extramedullary: meningioma, nephroblastomas, nerve sheath, metastatic 3. Intradural intramedullary: gliomas, ependymomas, metastatic
42
How is spinal neoplasia treated?
Decompressive surgery Radiation Palliative
43
'Wobblers' is the term given for which disease?
Cervical spondylomyelopathy
44
How does Cervical spondylomyelopathy present?
Short stilted gait and muscle atrophy in thoracic limbs Dobermann - associated with disc protrusion Great Dane - young age, bony compressions
45
Describe the 5 multifactorial causes of cervical spondylomyelopathy
1. Protrusion of IVD (type II IVDD) 2. Hypertrophy of ligamentum flavum and dorsal longitudinal ligament 3. Hypertrophy of synovial membrane 4. Stenosis of spinal canal 5. Degenerative joint disease of facets
46
How is cervical spondylomyelopathy treated?
Conservative treatment = anti-inflammatories, rest Surgical treatment - Decompression vs. distraction-stabilisation - ~80% success independent on technique
47
List the clinical signs of lumbosacral degenerative stenosis
- Reluctance to exercise, rise, jump into car, do stairs - Lameness – nerve root signature (L7) - Lumbosacral pain - Monoparesis/paraparesis - Proprioceptive deficits, reduced withdrawal reflex, muscle atrophy - Urinary and/or faecal incontinence
48
How is lumbosacral degenerative stenosis treated?
Conservative treatment = Anti-inflammatories, gabapentin Surgical treatment - Dorsal laminectomy - Dorsal fusion-fixation - Foraminotomy
49
Describe the signs and features of degenerative myelopathy
Insidious, progressive ataxia and paresis of pelvic limbs, ultimately leading to paralysis (over 6-18m) - Typically T3-L3 myelopathy - Usually asymmetrical - Not painful - Diagnosis of exclusion; genetic test - No treatment but physiotherapy prolongs QOL
50
Atlantoaxial (AA) instability most commonly present in which patients?
Young dogs,Toy breeds
51
How does Atlantoaxial (AA) instability present?
- Acute or chronic, often waxing /waning - Associated with aplasia/hypoplasia of dens in Toy breeds and sometimes with trauma - Neck pain - Ataxia or tetraparesis
52
How is Atlantoaxial (AA) instability treated?
Conservative splint for 6-12 weeks: ~60% success Surgical (ventral stabilisation)
53
Chiari-like malformation are seen in which breed?
CKCS
54
What are Chiari-like malformation?
Mismatch between caudal fossa volume and its contents (cerebellum and brainstem) with caudal displacement of the cerebellum through foramen magnum Hydromyelia – dilatation of central canal Syringomyelia – fluid filled cavitation Syringohydromyelia - both
55
What are the signs of Chiari-like malformation?
Neck pain Neck scratching – “air guitar” Torticollis/scoliosis Thoracic limb weakness and atrophy
56
Describe medical management of Chiari-like malformation?
Gabapentin (pregabalin), amantidine NSAIDs Furosemide, omeprazole, acetazolamide Corticosteroids, paracetamol, opioids…