Spinal Cord Disease - Chronic & Progressive Flashcards
what are differentials for chronic, progressive myelopathies
- IVDD type II
- degenerative myelopathy
- diseases of instability (LSS, CSM, AAI)
- anomalous (CJA, vertebral malformations, constrictive myelopathies)
- spinal cord neoplasia
- +/- spondylosis deformans
IVDH type II description
disc herniation with annulus fibrosis PROTRUSION into the spinal cord area
IVDH type II pathogenesis
fibrous degeneration –> weakening of dorsal annulus –> partial disc protrusion forming dome shaped mass –> compression of spinal cord
IVDH type II signalment
breeds: non-chondrodystrophic, large breeds
age: older
IVDH type II clinical signs
- hyperesthesia
- paresis
- paralysis
- CP deficits w/ intact reflexes
IVDH type II diagnosis
- radiographs
- myelography
- MRI - hypo intensity in spinal canal compressing cord
use history to differentiate from type I
IVDH type II treatment
conservative: activity restriction, pain medications
surgical: decompression (hemilaminectomy)
degenerative myelopathy (DM)
slow, progressive degeneration of the spinal cord
DM signalment
breeds: GSDs, boxers, bay retrievers, corgis, ridgebacks
age: older (~9 years)
DM pathogenesis
mutation in SOD I –> amyotrophic lateral sclerosis (ALS)
DM clinical signs
- 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
DM diagnosis
diagnosis of exclusion
- no significant findings on MRI, normal CSF
- histopathology is definitive but rarely done
DM treatment
none - elect euthanasia once progressed
poor prognosis
what are the diseases of instability
- degenerative lumbosacral stenosis (LSS)
- caudal cervical spondylomyelopathy (CSM)
- atlantoaxial instability (AAI)
lumbosacral stenosis (LSS)
degenerative narrowing of the intervertebral foramen (similar to IVDH type II)
LSS signalment
breed: medium to large
age: middle aged (~7 years)
LSS clinical signs
- lumbosacral hyperesthesia
- hunched posture
- muscle atrophy
- CP deficits in pelvic limbs
- reduced flexor and perineal reflexes
- normal to pseudo-hyperreflexia patellar reflex
LSS diagnosis
- radiographs - severe calcifications
- CT/MRI
LSS treatment
conservative: weight loss, activity restriction, corticosteroid injections, NSAIDs
surgical: decompression and stabilization (hemi)
caudal cervical spondylomyelopathy (CSM)
lesion in C6-T2 (cervical intumescence) causing narrowing of the spinal canal and spinal cord compression
two types:
- osseous
- disc associated
CSM clinical signs
- ambulatory tetraparesis
- thoracic: LMN signs –> choppy thoracic limb gait
- pelvic: UMN signs –> long tract signs (long stride gait)
- CP ataxia
- +/- cervical pain
osseous CSM signalment
breed: giant (Great Danes, mastiffs)
age: young (1-2 years)
caused by rapid growth –> osseous proliferation –> stenosis of canal
disc associated CSM signalment
breed: large (dobermans)
age: middle to older (>5-6 years)
caused by conformation (spinal instability) –> type II IVDD + ligamentous hypertrophy + joint capsule proliferation
CSM diagnosis
- myelogram
- MRI/CT
CSM treatment
conservative: activity restriction, chest harness, weight loss, pain management
surgical: spinal distraction + stabilization OR decompression
atlantoaxial instability (AAI)
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
AAI signalment
breed: toy breeds
age: young
AAI clinical signs
- cervical hyperesthesia
- CP ataxia
- tetraparesis to plegia
AAI diagnosis
- radiographs
- CT/MRI
AAI treatment
conservative: pain management, corticosteroids, immobilization of C spine, strict rest
surgical: dorsal vs ventral stabilization w/ screws or pins and cement
cranio-cervical junction anomalies (CJAs)
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
CJA signalment
breeds: small (CKCS)
age: young to middle (~3-6 years)
CJA clinical signs
- 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
syringomyelia
fluid accumulation within the spinal cord parenchyma caused by CJA disrupting the normal CSF flow in the subarachnoid space
CJA diagnosis
MRI - visualize attenuation/obliteration of dorsal SAS
CJA treatment
conservative: pain management, decrease CSF production/inflammation (corticosteroids), AEDs if seizing
surgical: foramen magnum decompression
vertebral malformations
errors in embryonic/fetal vertebral center of ossification and/or fusion leading to hemi or butterfly vertebrae
can be incidental but some are clinical
vertebral malformation diagnosis
most are SUBCLINICAL
- radiographs
- CT/MRI (check for compressive lesions if clinical)
vertebral malformation treatment
conservative: NSAIDs or steroids
surgical: in situ hybridization, decompression
constrictive myelopathies
articular process dysplasia
congenital anomalies that affect either the caudal articular facet (aplasia, hypoplasia, hyperplasia) leading to secondary constrictive fibrosis of the spinal cord
constrictive myelopathy signalment
breed: pugs
age: variable; 2-11 years
constrictive myelopathy pathogenesis
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
constrictive myelopathy clinical signs
- NO hyperesthesia
- paraparesis
- paraplegia
chronic progression of paresis/plegia
constrictive myelopathy treatment
conservative vs surgical (decompression + stabilization)
spina bifida
congenital bone malformation of unknown etiology
causes incomplete closure of caudal neuropore –> neural tube defects –> incomplete closure or fusion of dorsal vertebral arches
vertebral and spinal cord primary neoplasia
extradural: most aggressive
- osteosarcoma
- plasma cell tumor
- multiple myeloma
intradural-extramedullary: slow growth/progression
- meningioma
intramedullary: least painful
- glioma
- ependymoma
vertebral and spinal cord secondary neoplasia
lymphoma (extradural)
cats - FeLV is risk factor for lymphoma
vertebral and spinal cord neoplasia diagnosis and treatment
dx: MRI or CT
tx: surgical resection, radiation, chemotherapy
