Myelopathies Flashcards
grey matter is made of what? where in the CNS do we find it? what are the types of neurons?
neuronal cell bodies
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* Sensory neurons
> Dorsal root ganglion / dorsal horn
* Interneurons
* LMNs
> Ventral horn
> To muscles
Spinal cord: Anatomy
- at what vertebra does it terminate in large vs small dogs? cats?
◦ Large-breed dogs > L6 vertebra
◦ Small-breed dogs > L7 vertebra
◦ Cats > L7-S1vertebrae
- Spinal cord divided in segments:
(dog numbers) - how do spinal cord segments line up with vertebra
◦ 8 cervical
◦ 13 thoracic
◦ 7 lumbar
◦ 3 sacral
◦ ≥ 2 caudal
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note spinal segment numbers switch from exiting cranial to vertebral body to caudal at C8
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Segments NOT always lie in the same number vertebra
Most segments are cranial to vertebra Lesion localization: SEGMENTS
issues that affect gait (and posture)
- Ataxia
- Proprioceptive (spinal)
- Vestibular
- Cerebellar - Paresis (weakness)
- motor function - Lameness
Proprioceptive ataxia - what structures might we have issues with?
Sensory function:
1. Receptors (proprioceptors): Joints, tendons, muscles
2. Ascending proprioceptive tracts
3. To cerebral cortex (conscious perception)
Motor function
- what neurons are involved?
- deficits?
◦ Control activity muscles (brain to muscles)
◦ Required to move limbs (muscle contraction)
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Requires 2 neurons:
UMN
LMN
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◦ Deficit: PARESIS (weakness)
UMN and LMN - where are the cell bodies and axons? what do they do?
UMN
◦ Cell body: Brain
◦ Axons: descending WM
◦ “UMN tells LMNs what to do” (descending inhibition)
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LMN
◦ Cell body: ventral horn GM, brainstem nuclei
◦ Axon: PNS to muscle
◦ Responsible for the reflex motor activity (patellar reflex)
Paresis/paralysis - what is this? where might lesions be?
- Lost of voluntary motor function (weakness)
> Lesion affecting UMN or LMN - PARESIS: Partial loss
- PARALYSIS (-plegia): Complete absence
Monoparesis / Monoplegia
Paraparesis / Paraplegia > back limbs
Tetraparesis /Tetraplegia
Hemiparesis / Hemiplegia > both limbs on same side
UMN lesion clinical signs
Paresis (weakness)
Loss of descending inhibition
Spastic paresis / paralysis
Spinal reflexes: normal or increased
Increased muscle tone
Disuse muscle atrophy
Usually associated to proprioceptive ataxia
LMN lesion clinical signs
Paresis (weakness)
Flaccid paresis / paralysis
Spinal reflexes: decreased / absent
Decreased muscle tone
Neurogenic muscle atrophy
LMNs for limbs are in what regions
◦ Thoracic limbs: C6-T2 (cervical intumescence) ◦ Pelvic limbs: L4-S3 (lumbosacral intumescence)
Lesion localization: Spinal cord
Functional classification: (segments)
C1-C5
C6-T2
T3-L3
L4-S3
C1-C5 lesion signs
◦ Tetraparesis / tetraplegia
◦ Proprioceptive def 4 limbs
◦ UMN deficit for 4 limbs (spastic)
◦ Reflexes: normal/increased
C6-T2 lesion signs
◦ Tetraparesis / tetraplegia
◦ Proprioceptive def 4 limbs
◦ LMN deficit TLs (flaccid):
> Decreased/absent reflexes TLs
◦ UMN deficit PLs (spastic):
> Normal/increased reflexes PLs
T3-L3 lesion signs
◦ Paraparesis / paraplegia
◦ Normal TLs
◦ Proprioceptive def PLs
◦ UMN deficit PLs (spastic)
◦ Reflexes PLs: normal/increased
L4-S3 lesion signs
- Paraparesis / Paraplegia
- Normal TLs
- Proprioceptive def PLs
- LMN deficit PLs (flaccid)
- Reflexes PLs: decreased /absent
Classification or myelopathies
Lesion localization
Extradural
Intradural-extramedullary
Intramedullary
Clinical signs spinal cord compression
- order that signs appear?
- Back/neck pain
- Proprioceptive ataxia / deficits
- Paresis
- Paralysis, incontinence
- Loss of nociception
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improve in opposite direction
important rule out for neurodisease when we see weakness, pain
IMPORTANT! Rule out orthopedic disease
(bilateral cruciate rupture, long bone fractures, polyarthritis)
acute causes of myelopathies
- FCEM
- Spinal trauma
- Intervertebral disc herniation (IVDH): extrusion
intervertebral disc anatomy
a. Annulus fibrosus > outer layers
> type I collagen surrounding the nucleus pulposus in approximately 15-20 layer
b. Nucleus pulposus > inner, gelatinous material
Intervertebral disc herniation type
Extrusion - acute: nucleus pulosus breaks though annulus fibrosus, impinges on spinal cord
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Protrusion - chronic: annulus collagen over the years loses its consistency and the disc slowly loses its shape and impinges on the spinal cord
IVDH: extrusion
- pathogenesis
Chondroid degeneration nucleus pulposus
> (nucleus pulposus) becomes hard
HANSEN TYPE 1 DEGENERATION
Extrusion of mineralized nucleus pulposus into the vertebral canal
IVDH extrusion:
clinical signs
who gets this?
location?
Acute, progressive
Chondrodystrophic breeds (small breeds)
◦ Dachshund, Beagle, Cocker Spaniel, Shih tzu…
◦ But may occur in any breed!
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Age
◦ Peak 3-6 years-old (rare < 2y)
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Location:
◦ Caudal thoracic-lumbar: T11-L3 (T12-13,T13-L1)
◦ Cervical
◦ Very uncommon T1-T10 > Intercapital ligament stabilizes
IVDH extrusion: clinical signs
- severity depends on what?
- Location
Thoraco-lumbar often more severe than cervical
Paraparesis / paraplegia vs only cervical pain Less epidural space TL vs cervical spinal canal - Intensity, size, onset, and time since extrusion
IVDH extrusion: diagnosis
Spinal radiographs: very limited information
Myelogram
CT, CT-myelogram
MRI > good for viewing soft tissue
IVDH extrusion: treatment options, indications? when is it an emergency? success rate?
Surgical vs conservative (medical)
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Surgical:
- manually remove compressive material
◦ Decompressive techniques
◦ Thoraco-lumbar: Hemilaminectomy, pediculectomy
◦ Cervical: Ventral slot
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Indications surgical treatment:
Severe or recurrent pain
Neurological deficits
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SURGICAL EMERGENCY:
◦ Absent deep pain
◦ Obvious quick deterioration
◦ Cervical:Tetraplegia
◦ Thoraco-lumbar: Non-ambulatory
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Conservative:
1. FOCUS:
Strict cage confinement: 3-4 weeks
2. Combined or not with Pain killers:
Opioids, NSAIDs, steroids
3. Indications:
First episode of pain without deficits (or mild)
4. Success: 50%; common recurrences
IVDH extrusion: treatment 0 what should we not do?
- NEVER NSAIDs + Steroids!
- NEVER anti-inflammatory without cage rest:
> Increase activity - more pressure disc - more extrusion
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Steroids in acute spinal cord injury? > controversial
IVDH extrusion: prognosis
Depends on presence of deep pain as in any spinal cord injury.
◦ Deep pain:
Present: > 90% chances
Absent: Guarded to poor (≤ 50%?)
Fibrocartilaginous embolic myelopathy
- how can it arise?
Vascular disease: Infarct
Spinal cord ischemia
Embolism spinal cord vessel
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Embolus:
Identical to nucleus pulposus
Theories entry disc material into spinal cord vascular system
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artery or vein in spainal cord is block by fibrinocartilaginous material
> histologically looks like nucelus pulposis, but we dont know for sure what is going on here
FCEM:
- breeds?
- history?
- locations?
Breed:
◦ Non-chondrodystrophic large breed dogs
◦ Miniature Schnauzer
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History
◦ Crying out during mild exercise or traumatic event just before
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Thoracolumbar vs cervical
FCEM: Clinical signs
Presentation:
◦ Acute / hyperacute onset
◦ Non-progressive
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Asymmetrical CS > due to the fact that an infarct on the eg. left side will only affect left side of spinal cord
Non-painful
FCEM: Diagnosis
History, signalment, clinical signs
Rule-out other myelopathies
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MRI
◦ Intramedullary
◦ Focal
◦ Asymmetrical
FCEM
- Treatment, prognosis
Treatment:
- Supportive therapy
- Physical therapy
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Prognosis:
◦ Deep pain presence = better prognosis
◦ Many recover function…but not completely
◦ Better if some recovery within 2 weeks
