Spinal Cord/Cauda Equine Diseases Flashcards
who are the 2 classic examples of breeds affected by cervical spondylomyelopathy/Wobblers?
- danes
-tend to be younger
-osseous-associated: articular processes, cranial-mid cervical
-cranial cervical (C1-C5) - dobies;
-tend to be older
-disc associated
-caudal cervical (C5-C7)
what are the 3 key players of cervical spondylomyelopathy/Wobblers?
- dorsal: ligamentum flavum
- dorsolateral: articular processes
- ventral: IVD, dorsal longitudinal ligament, vertebral body
describe pathology of osseous associated cervical sponylomyelopathy
in YOUNG GREAT DANES
congenital malformation of the cervical vertebrae resulting in stenosis of the vertebral canal; deformation of vertebral arch (dorsal), vertebral pedicle and articular processes (dorsolaterally), all of which result in stenosis of the canal within the body of the vertebra
most commonly C3-C7!!
describe pathology of disc associated cervical spondylomyelopathy
MIDDLE to OLDER DOBERMANS
cervical vertebral instability and chronic degenerative disc disease (IVD);
a result of a degenerative disc that causes collapse of the IVD space; will see hypertrophy/hyperplasia of the dorsal annulus fibrosis
the dorsal longitudinal ligament becomes a passive player, as it will buckle, further compressing the spinal cord with dorsal EXTENSION of the neck
compression is seen ventrally; most commonly C5-C6 and C6-C7
give signalment of cervical spondylomyelopathy
- large to giant breeds
- doberman: middle to older, caudal cervical (avg. 6.8 years)
- great dane: young, mid-caudal cervical, stenosis (avg. 3.8 years)
describe diagnostics of cervical spondylomyelopathy
- MRI: gold standard!
-identify spinal cord compression, degenerative changes to spinal cord parenchyma (gliosis) - plain radiographs: use to exclude other pathologies but not diagnostic
-presence or absence of radiographic findings does NOT correlate with presence and degree of compression
describe treatment/prognosis of cervical spondylomyelopathy
- conservative: (same conservative tx for all neuro things)
-corticosteroids OR NSAIDs
-exercise restriction (at least 4 weeks)
-analgesics: gabapentin - surgical: decompressive surgeries are only options for spinal cord
-hesitate if a lot of gliosis (might not be reversible)
-ventral slot +/- add screws in vertebral bodies and acrylic to hold in neutral position/prevent joint movement hoping for a bony ankylosis over time to create stimulus for fibrosis
-+/- efficacy because may put more stress on vertebrae cranial and cause them to have pathology - variable prognosis: months to years
-no difference between conservative versus surgical
-survival times mean/median (approx 3-4 years)
describe degenerative lumbosacral stenosis
- compression of nervous tissue structures at LS articulation
-cauda equina (L7, S1-S3, and cadual nerves) - L7 nerve root is most commonly affected
describe most common culprit for degenerative lumbosacral stenosis
- german shepherd (or any large breed)
- middle to older aged
describe clinical signs of degenerative lumbosacral stenosis
variable!
1. pain is most common
2. pelvic limb paresis: unilateral or bilateral, seen as difficulty rising, climbing stairs, or nonspecific lameness
3. lack of tail tone
4. urinary/fecal incontinence
5. pseudohyperreflexia: lack of caudal thigh muscles to inhibit the “kick” of patellar reflex, so looks like crazy patellar! but will lack withdrawal!
6. gait:
-crouched stance
-overflexion of hock, stifle, and CF joints
-short strided
7. reflex eval:
-hyporeflexia in region of sciatic: decreased withdrawal and/or inability to flex tarsus
-reduced muscle mass (esp caudal thigh)
-reduced/absent: anal tone, perineral reflex, tail tone, nociception of tail
-hyperesthesia on palpation of spinous processes of verterbral canal over lumbosacral region
-may elicit pain on extension of coxofemoral joint and tail extension
-RULE OUT MSK (hip dysplasia, stifle/CCLD
describe the etiology of degenerative lumbosacral stenosis
initiated by degeneration (Hansen type II) of discs between L7-S1, leading to protrusion of the dorsal annulus, causing ventral compression of the L7 and sacral nerve roots
over time this results in
1. sclerosis and osteophyte production of the end plates and hypertrophy of the longitudinal ligament (contributes to ventral compression)
- degenerative osteoarthritis and joint capsule hypertrophy of articular processes, eventual collapse/narrowing of disc space with subluxation of articular processes (dorsal lateral compression)
- hypertrophy of the ligamentum flavum (dorsal compression)
describe diagnosis of degeneratice limbosacral stenosis?
- plain radiographs:
-DJD articular processes
-subluxation
-ventral spondylosis
-providence evidence but not definitive, and to differentiate from orthopedic disease!! - MRI: same idea as dynamic/doberman cervical spondylomyelosis (signs do not correlate with imaging features)
describe treatment/prognosis of degenerative lumbosacral stenosis
- conservative: can apply steroids via epidural! to avoid systemic side effects
-effective for 50% - surgical:
laminectomy and discectomy +/- stabilization with screws and acrylic
-approx 60-80% improve with sx - variable prognosis
describe the history and clinical signs and signalment of degenerative myelopathy
history:
1. slow, insidious onset (6-18 months)
2. chronic progressive
3. non-painful paraparesis
clinical signs:
1. slowly progressing paraparesis
2. T3-L3 myelopathy
3. occasional loss of patellar reflex
4. NO hyperesthesia (standout feature of DM versus compressive disorders like neoplasia and type II IVDD)
signalment:
1. highest incidence in boxer, then german shepherd, corgis rly only small breed affected with much significance
-any large breed dog
2. middle to older but really just older age
-older than 5 years, mean 9 years
describe pathology of degenerative myelopathy
diffuse loss of myelin and loss of axons in the white matter throughout the spinal cord
describe diagnosis of degenerative myelopathy (4 plus a bonus 5th)
- signalment
- clinical signs
-6-12 months: UMN paresis and GP ataxia
-9-18 months: LMN paresis to paraplegia - exclusion:
-normal MRI
-+/- increased protein lumbar CSF
-not respond to OA treatment - histopathology (post mortem); definitive but when dead so :|
- DM testing- Missouri
-controversial genetic testing
-just one more piece of evidence though, not definitive diagnosis
-we’re not sure what to do with the test result yet though (not tested on for class)
describe treatment and prognosis of degenerative myelopathy
treatment:
1. none proven
2. controlled exercise to help with concurrent OA and maybe keep walking longer
prognosis:
1. poor long term
2. euthanized within 6-12 months
describe etiology of subarachnoid diverticulum/constrictive myelopathy
blind ended dilation of the subarachnoid space that results in compression of the spinal cord
-NOT CYSTS; no epithelial lining and NOT an enclosed space
describe signalment of subarachnoid diverticulum/constrictive myelopathy
- middle to older pug; no gender predisposition
- middle aged french bulldogs
- young rottweilers (<2 years)
describe clinical signs and differential diagnoses of subarachnoid diverticulum/constrictive myelopathy
pugs:
1. progress very slowly (months to years)
2. GP ataxia and UMN paraparesis (T3-L3 myelopathy, nonpainful)
3. fecal incontinence (likely due to lack of sensory information getting to brain in time, so reflex part takes over and they go in the house)
4. low tail carriage
rottweilers:
1. more commonly C2-C3
2. often identified in conjunction with fibrosis of meninges that results in circumferential constriction of the spinal cord just caudal to the diverticulum
differentials:
1. IVDD: type II/chronic hansen
2. degenerative myelopathy
3. neoplasia
describe diagnostics and treatment/prognosis of subarachnoid diverticulum
diagnostics:
1. rads of vertebral column
2. MRI: onion bulb/scallion of subarachnoid space; diverticulum of CSF within subarachnoid space
-results in fibrosis/constriction of leptomeninges
-definitive diagnostic tool!
treatment:
1. often irreversible, esp if gliosis
-can try anti-inflammatories but not really helpful
2. surgery:
-short term improvement but most deteriorate back to where they began in a year so discuss with owners if surgery is worth it (not a fix)
describe the clinical signs and signalment of chiari-like malformation/caudal occipital malformation
clinical signs:
1. cervical pain- most common
2. tetraparesis (C1-C5 vs C6-T2) depending on lesion location
-+/- cranial nerve dysfunction: facial and vestibular
3. unusual neurological signs
-scratching at the neck and ears but phantom scratching (foot doesn’t touch skin)
4. scoliosis
signalment:
1. cavalier king charles spaniel!! most common
2. any toy breed though
describe the pathophysiology of caudal occipital malformation
- obstruction of CSF flow out of the foramen magnum causes syrinx formation in the spinal cord
-syrinx is buildup of fluid within spinal cord - scoliosis: dissection of syrinx through dorsal grey matter takes out sensory stuff on one side, animal turns to the other direction
- scratching: also due to same reason as scoliosis
describe diagnosis of caudal occipital malformation
- MRI is the only way to diagnose!!
-approx 70% of cavalier king charles spaniels have some degree of abnormality
describe treatment of caudal occipital malformation
- medical: try first!
-decrease CSF flow/production: omeprazole, acetozolamide
-symptomatic: pain control if painful or scratching (gabapentin, pregabalin) - surgery:
-remove the obstruction
-re-establish CSF
-procedures: foramen magnum decompression, dorsal laminectomy C1, durotomy
describe prognosis of caudal occipital malformation
- medical therapy: unknown/variable
- surgery: 60-80% improvement with a good possibility of recurrence
describe the anatomy of the atlanto-axial region
- joint between C1 and C2
- dens: ventral process of C2, separate ossification center (sometimes never ossifies!); ligaments attach here
- 4 ligaments:
-transverse
-alar
-apical (2)
describe signalment and clinical signs and diagnostics of atlanto-axial subluxation
signalment:
1. toy breeds: yorkie!, chihuahua, poodle, pomeranian
2. no sex predilections
3. young age of onset (6 months to 2 years)
-not enough time to have a degenerate nucleus that herniated
4. usually present after a little bit of trauma (jump off, bump into; lack of ossification allows rupture of ligaments or breaking of dens)
-but can be due to congenital causes as well (MOST COMMON congenital but trauma injures what little was still holding the joint in alignment)
clinical signs: relatively sudden
1. cervical pain
2. C1-C6 myelopathy
diagnostics:
1. plain radiographs! definitive!
-lateral view most important
describe treatment and prognosis of atlanto-axial subluxation
treatment:
1. surgical: preferred
-dorsal fixation
-ventral fixation
- medical:
-cervical splinting to allow for some fibrosis/scar tissue to form and strengthen the joint
-cage rest
-anti-inflammatories and analgesics as needed)
-big babushka wrap, some dogs don’t tolerate, but good less expensive option
prognosis:
1. independent of fixation: 60-80% improvement
2. depends on
-age: better when younger
-neurologic status
describe congenital malformations (2)
- anomalies of vertebra or spinal cord
-usually incidental findings with no clinical signs - vertebral abnormalities:
-pugs, bulldogs, boston terriers
-hemivertebrae
-block vertebrae
-manx cat: sacrocaudal dysgenesis (we bred for it, oops) - most common presentation: Spina Bifida L7/meningomyelocele
-LMN S1-S3
-when palpate spine, finger goes into a divot
-tipoff is: “can’t housebreak puppy”
what are the first diagnostic steps when you suspect neoplasia? (older dog, chronic progression
- radiographs of vertebral column
-most common neoplasms to affect the spinal cord are vertebral/bone - radiographs of thorax (3 view)
-assess for metastasis - minimum database (CBC, chem, +/- urinalysis)
work most common to least common, outside to inside
describe signalment, clinical signs, diagnosis, and treatment of osteosarcoma
signalment:
1. older, large breed dogs (7-8 years)
clinical signs:
1. variable (progressive myelopathy to acute or subacute development of spinal cord dysfunction)
-rapid onset would suggest pathologic fractures or cancerous vertebrae
2. acute to progressive
3. painful: spinal hyperesthesia is a prominent clinical sign that can precede onset of proprioceptive or motor deficits
4. neuro deficits
diagnosis:
1. plain radiographs: lysis of vertebra would make you suspicious of
2. MRI
3. biopsy: definitive
treatment:
1. radiation seems to be most effective but despite treatment MST is approx 4 months
describe meningioma; including signalment, history/clinical signs. diagnosis, and treatment
the most common tumor that arises from nervous tissue affecting the spinal cord; typically intradural/extramedullary; cells of origin are in the arachnoid layer; cranial cervical spinal cord most commonly affected
signalment: oder dogs (6-9 years); large dogs more common, no gender predilection
history/clinical signs:
1. chronic, progressive myelopathy
2. clinical signs may be steroid responsive at onset but responsiveness declines with time
3. spinal hyperesthesia may be seen prior to onset of proprioceptive and voluntary motor deficits
diagnosis: MRI
treatment/prognosis:
1. surgical resection and/or radiation therapy
2. variable prognosis based on severity and surgical resection
describe diagnostic steps when see monoparesis
- neurological exam!!
- minimum database
-CBC, chem, UA +/- specialized testing based on results - serological tests
- electrophysiology: microscopic evaluation
describe neoplastic nerve sheath tumors
- nerve sheath neoplasms
-unsure of cell of origin - most cases malignant
- behave like sarcomas: locally aggressive, rarely metastasize
signalment:
older dogs (8-9 years) no breed or sex
history:
chronic, progressive, unilateral limb lameness
clinical signs:
1. unilateral lameness
2. pain in axilla (50%)
3. varying degrees of paresis
4. peripheral vs. spinal cord (C6-T2 myelopathy)
5. lame gait but normal ortho exam
diagnosis:
1. strong clinical suspicion: old dog, progressive lame, can’t find ortho disease
-often severe muscle atrophy in affected limb
2. electrodiagnostics: help support that is a neuro issue; maps out distribution
3. MRI
treatment:
1. surgery:
-amputation: can you get high enough to control?
-laminectomy
2. radiation
prognosis:
1. peripheral group: dies of other disease
2. plexus group:
-MST 11 months
-disease free. interval 6 months
3. root group:
-MST 5 months
-DFI 1 month
describe nephroblastoma
- nephrologic tumor in meninges in young dogs!
- come in with T3-L3 myelopathy
- RARE
describe lymphoma; give signalment, history/clinical signs, diagnosis, and treatment/prognosis
most common spinal cord tumor of cats!; typically extradural, can cause compressive myelopathy
signalment:
1. median age 2-3 years
2. likely bimodal: young cats with FeLV or older cats without FeLV
history/clinical signs:
1. more commonly in thoracolumbar region than cervical
2. insidious onset, commonly T3-L3 or vary by location
3. rapidly progressive neoplasm so some can have more acute and rapid onset
diagnosis: most are FeLV positive, have leukemic bone marrow, and multicentric neoplasia
-FeLV testing, bone marrow, and spinal cord imaging
treatment/prognosis:
1. chemo +/- radiation therapy
2. prognosis is poor; most euthanized within 3 months due to progressive or concurrent disease
describe discospondylitis pathology
- infection (likely hematogenous spread) of intervertebral disc and adjacent endplates
- blood supply to vertebral body ends in capillary beds in region of end plates; disc gets nutrients by diffusion through end plates; blood flow is slow so infection can settle
- most common source of infection is UTI
-but could also be skin, heart valves, mouth - etiology:
-bacteria: STAPH, strep, E.coli, klebsiella
-brucella (ZOONOTIC = ALWAYS TEST FOR IF DOG)
-fungal: apergillus (common in german shepherds and young dogs with IgA deficiency)
describe signalment and clinical signs of discospondylitis
signalment:
1. medium to giant breed
2. young to middle age
3. more males than females
clinical signs/history:
1. can occur for days to weeks prior to presentation
2. approx 80% show pain on palpation of vertebral column (spinal hyperesthesia might be ONLY sign)
3. systemic signs of illness: fever, lethargy in 30-50% (this is the only spinal cord disorder that may result in systemic signs of illness)
4. lack of fever does NOT rule out disco!
describe diagnosis, treatment, and prognosis of discospondylitis
diagnosis:
1. plain radiographs-end plate lysis
-narrow disc space followed by lysis followed by sclerosis from inside to outside
2. CT/MRI
3. CBC, chem, urinalysis, urine culture
4. BRUCELLA TEST, fungal testing
treatment:
1. antimicrobials (8-12 weeks): ideally based on culture and sensitivity
-for staph: cephalosporins and potentiated penicillins (amoxicillin/clavulonic acid)
-for brucella: tetracycline and aminoglycosides
2. cage rest
3. analgesics
-NSAIDs or opioids
prognosis:
1. good!
2. worse if serve neuro deficits, resistant bacteria (brucella), or fungal infections
describe traumatic spinal fractures/luxations; include signalment and history
most occur at the junction of relatively stable and mobile portions of the vertebral column
1. thoracolumbar junction
2. lumbosacral junction
3. sacrococcygeal junction
-cervical: C1 and C2 most commonly affected
signalment and history:
1. most common is HBC
2. median age is 2 years; no gender predilection
3. sacrococcygeal luxations are more common in cats
describe diagnosis and treatment/prognosis of traumatic spinal fractures/luxations
diagnosis:
1. combo of history, neuro exam, and rads
2. MRI and/or CT are used to assess the spinal cord and plan for surgical intervention
treatment/prognosis:
1. heavily dependent on the patient!
-without nociception = functionally transected spinal cord and likely also structurally transected = grave prognosis
-normal nociception: fair to good
- medical:
-stable fractures: prolonged cage rest +/- external fixation
-physical therapy
-bladder management
-careful! stable fx can destabilize in the first several days after traumatic even = clinical signs days after trauma - surgical:
-when under gen anesthesia epaxial muscles relax and can further destabilize a fracture
-recommended if severe neuro dysfunction, mod to severe displaced vertebral fx/lux, deteriorating neuro status, evidence of spinal cord compression on myelogram
describe sacrococcygeal luxation
- junction between stable sacrum and flexible lumbar vertebral canal
- tail pull injuries, usually with a history of trauma (HBC)
- common in cats
clinical signs:
1. consistent with cauda equine syndrome
2. paresis/paralysis of the tail with varying degrees of fecal/urinary incontinence, reduced/absent perineal sensation, paraparesis
3. most able to ambulate but incontinence is a severe problem and leads to euthanasia
treatment/prognosis
1. conservative: cage rest
2. surgical: tail amputation
prognosis:
1. anal tone and perineal sensation present: excellent chance of return to continence
2. reduced anal tone and perineal sensation: 75%
3. no anal tone and perineal sensation: 50%
-if unable to urinate normally within 1 month of injury, functional recovery is unlikely
describe fibrocartilaginous embolic myelopathy (FCEM); include signalment
- common syndrome of ACUTE spinal cord ischemia/infarcation caused by embolization of the arterial and/or venous blood supply to an area of the spinal cord; embolism may originate from nucleus pulposus (is fibrous)
signalment:
1. usually nonchondrodystrophic dogs of large and giant breeds
2. increased incidence in some smaller nonchondro breeds: mini schnauzer
3. cats rarely affected
4. age of onset variable but more commonly young to middle aged adults
describe clinical signs of FCEM (4)
- peracute to acute onset
- nonprogressive, nonpainful, often asymmetric neurologic deficits
- owners often observe affected dog cry out in apparent pain during exercise or shortly before the onset of neuro dysfunction, however dogs usually not painful by time present to vet
- signs vary based on location and severity of injury
-seems to be a predilection to cervicothoracic and lumbosacral intumescences
describe diagnosis, treatment, and prognosis of FCEM
diagnosis:
1. history, signalment, clinical signs, exclusion of other causes of acute myelopathy
2. radiographs bc history indicates potential trauma but are NORMAL
3. MRI: most accurate but still presumptive!!
-hyperintense lesions within spinal cord on T2-weighted images
-occasionally can see degen changes in nucleus pulposus of adjacent IVDs
4. CSF analysis may be normal, show increased protein, and/or xanthochromia (evidence of hemorrhage)
treatment:
supportive care: physical therapy +/- bladder management
prognosis:
-variable depending on severity of infarct
-good for dogs that regain functional status within the first 2 weeks
-negative indicators: loss of nociception and LMN signs
