Spinal Cord Disease - Chronic & Progressive Flashcards

1
Q

what are differentials for chronic, progressive myelopathies

A
  1. IVDD type II
  2. degenerative myelopathy
  3. diseases of instability (LSS, CSM, AAI)
  4. anomalous (CJA, vertebral malformations, constrictive myelopathies)
  5. spinal cord neoplasia
  6. +/- spondylosis deformans
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2
Q

IVDH type II description

A

disc herniation with annulus fibrosis PROTRUSION into the spinal cord area

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3
Q

IVDH type II pathogenesis

A

fibrous degeneration –> weakening of dorsal annulus –> partial disc protrusion forming dome shaped mass –> compression of spinal cord

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4
Q

IVDH type II signalment

A

breeds: non-chondrodystrophic, large breeds
age: older

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5
Q

IVDH type II clinical signs

A
  • hyperesthesia
  • paresis
  • paralysis
  • CP deficits w/ intact reflexes
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6
Q

IVDH type II diagnosis

A
  1. radiographs
  2. myelography
  3. MRI - hypo intensity in spinal canal compressing cord

use history to differentiate from type I

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7
Q

IVDH type II treatment

A

conservative: activity restriction, pain medications

surgical: decompression (hemilaminectomy)

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8
Q

degenerative myelopathy (DM)

A

slow, progressive degeneration of the spinal cord

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9
Q

DM signalment

A

breeds: GSDs, boxers, bay retrievers, corgis, ridgebacks
age: older (~9 years)

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10
Q

DM pathogenesis

A

mutation in SOD I –> amyotrophic lateral sclerosis (ALS)

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11
Q

DM clinical signs

A
  • NO hyperesthesia
  • progressive PL weakness
  • non-ambulatory within 6 months to 1 year of onset

early:
- asymmetric paresis
- general CP ataxia in PLs
- T3-L3 myelopathy signs

late:
- LMN paraplegia to tetraplegia
- TL weakness
- flaccid weakness
- PL muscle atrophy
- dysphagia
- respiratory distress

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12
Q

DM diagnosis

A

diagnosis of exclusion
- no significant findings on MRI, normal CSF
- histopathology is definitive but rarely done

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13
Q

DM treatment

A

none - elect euthanasia once progressed

poor prognosis

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14
Q

what are the diseases of instability

A
  • degenerative lumbosacral stenosis (LSS)
  • caudal cervical spondylomyelopathy (CSM)
  • atlantoaxial instability (AAI)
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15
Q

lumbosacral stenosis (LSS)

A

degenerative narrowing of the intervertebral foramen (similar to IVDH type II)

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16
Q

LSS signalment

A

breed: medium to large
age: middle aged (~7 years)

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17
Q

LSS clinical signs

A
  • lumbosacral hyperesthesia
  • hunched posture
  • muscle atrophy
  • CP deficits in pelvic limbs
  • reduced flexor and perineal reflexes
  • normal to pseudo-hyperreflexia patellar reflex
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18
Q

LSS diagnosis

A
  1. radiographs - severe calcifications
  2. CT/MRI
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19
Q

LSS treatment

A

conservative: weight loss, activity restriction, corticosteroid injections, NSAIDs
surgical: decompression and stabilization (hemi)

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20
Q

caudal cervical spondylomyelopathy (CSM)

A

lesion in C6-T2 (cervical intumescence) causing narrowing of the spinal canal and spinal cord compression

two types:
- osseous
- disc associated

21
Q

CSM clinical signs

A
  • ambulatory tetraparesis
  • thoracic: LMN signs –> choppy thoracic limb gait
  • pelvic: UMN signs –> long tract signs (long stride gait)
  • CP ataxia
  • +/- cervical pain
22
Q

osseous CSM signalment

A

breed: giant (Great Danes, mastiffs)
age: young (1-2 years)

caused by rapid growth –> osseous proliferation –> stenosis of canal

23
Q

disc associated CSM signalment

A

breed: large (dobermans)
age: middle to older (>5-6 years)

caused by conformation (spinal instability) –> type II IVDD + ligamentous hypertrophy + joint capsule proliferation

24
Q

CSM diagnosis

A
  1. myelogram
  2. MRI/CT
25
Q

CSM treatment

A

conservative: activity restriction, chest harness, weight loss, pain management

surgical: spinal distraction + stabilization OR decompression

26
Q

atlantoaxial instability (AAI)

A

subluxation of the atlanto-axial joint caused by multiple congenital abnormalities –> instability –> over flexion and dorsal subluxation of axis

can be congenital or acquired
- most common: dens hypoplasia or aplasia

27
Q

AAI signalment

A

breed: toy breeds
age: young

28
Q

AAI clinical signs

A
  • cervical hyperesthesia
  • CP ataxia
  • tetraparesis to plegia
29
Q

AAI diagnosis

A
  1. radiographs
  2. CT/MRI
30
Q

AAI treatment

A

conservative: pain management, corticosteroids, immobilization of C spine, strict rest

surgical: dorsal vs ventral stabilization w/ screws or pins and cement

31
Q

cranio-cervical junction anomalies (CJAs)

A

caudal occipital malformations (COMs) such as chiari like malformations leading to cerebellar dysfunction

congenital anomalies leading to overcrowding, compression of cerebellum +/- herniation, kinking of medulla, and CSF flow disruption

32
Q

CJA signalment

A

breeds: small (CKCS)
age: young to middle (~3-6 years)

33
Q

CJA clinical signs

A
  • hyperesthesia in head/neck
  • cervical localization (paresis to plegia in all 4 limbs)
  • ataxia
  • pruritus of face/head
  • CN VII paralysis/paresis
  • hypoglossal nerve deficits
  • syringomyelia
34
Q

syringomyelia

A

fluid accumulation within the spinal cord parenchyma caused by CJA disrupting the normal CSF flow in the subarachnoid space

35
Q

CJA diagnosis

A

MRI - visualize attenuation/obliteration of dorsal SAS

36
Q

CJA treatment

A

conservative: pain management, decrease CSF production/inflammation (corticosteroids), AEDs if seizing

surgical: foramen magnum decompression

37
Q

vertebral malformations

A

errors in embryonic/fetal vertebral center of ossification and/or fusion leading to hemi or butterfly vertebrae

can be incidental but some are clinical

38
Q

vertebral malformation diagnosis

A

most are SUBCLINICAL

  1. radiographs
  2. CT/MRI (check for compressive lesions if clinical)
39
Q

vertebral malformation treatment

A

conservative: NSAIDs or steroids

surgical: in situ hybridization, decompression

40
Q

constrictive myelopathies

A

articular process dysplasia

congenital anomalies that affect either the caudal articular facet (aplasia, hypoplasia, hyperplasia) leading to secondary constrictive fibrosis of the spinal cord

41
Q

constrictive myelopathy signalment

A

breed: pugs
age: variable; 2-11 years

42
Q

constrictive myelopathy pathogenesis

A

malformation caudal to T10 –> loss of an articular process in T10 to L3 causing chronic micromotions –> fibrosis and adhesions to spinal cord –> secondary parenchymal changes of the spinal cord and meninges –> constrictive myelopathy

43
Q

constrictive myelopathy clinical signs

A
  • NO hyperesthesia
  • paraparesis
  • paraplegia

chronic progression of paresis/plegia

44
Q

constrictive myelopathy treatment

A

conservative vs surgical (decompression + stabilization)

45
Q

spina bifida

A

congenital bone malformation of unknown etiology

causes incomplete closure of caudal neuropore –> neural tube defects –> incomplete closure or fusion of dorsal vertebral arches

46
Q

vertebral and spinal cord primary neoplasia

A

extradural: most aggressive
- osteosarcoma
- plasma cell tumor
- multiple myeloma

intradural-extramedullary: slow growth/progression
- meningioma

intramedullary: least painful
- glioma
- ependymoma

47
Q

vertebral and spinal cord secondary neoplasia

A

lymphoma (extradural)

cats - FeLV is risk factor for lymphoma

48
Q

vertebral and spinal cord neoplasia diagnosis and treatment

A

dx: MRI or CT
tx: surgical resection, radiation, chemotherapy