Alphabet Soup Myelopathies
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Presenter: Dr. Christina Scanlon, DVM, DACVIM (Neurology) Title: Alphabet Soup Myelopathies Description: This course will cover signalment, clinical signs, confirmatory diagnostics, and therapies for myelopathic diseases different from the most common IVDD cases. This lecture will help you recognize cases that are more likely to be FCE or ANNPE based on presentation and will discuss recommended testing, prognoses, and therapies. The presentation will also cover one case of a slightly different myelopathy that is less commonly seen overall. Learning Objectives: - To be able to recognize clinical signs and signalment for FCE and ANNPE - To understand imaging characteristics and differences between FCE and ANNPE - To understand prognostic indicators and recommended therapies for FCE and ANNPE
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Alphabet Soup Myelopathies
- 1. WWW.UVSONLINE.COM ALPHABET SOUP MYELOPATHIES 7/25/2022 INSERT YOUR PRESENTATION HERE Christina Scanlon, DVM, DACVIM (Neurology)
- 2. WWW.UVSONLINE.COM OUTLINE 7/25/2022 INSERT YOUR PRESENTATION HERE • IVDD Review • Degenerative Myelopathy Review •Steroid Responsive Meningitis and Arteritis Review •The acute ER setting questions • Then the good stuff - FCE vs. ANNPE •Imaging characteristics •Prognostic indicators •For fun - HNPE case (if time allows)
- 3. WWW.UVSONLINE.COM INTERVERTEBRAL DISC DISEASE 7/25/2022 INSERT YOUR PRESENTATION HERE
- 4. WWW.UVSONLINE.COM 1. Dachshund 2. Dachshund 3. Dachshund 4. Beagles 5. Frenchies 6. Shih Tzu 7. Any chondrodystrophoid dog 8. Any breed realistically PREDISPOSED BREEDS 7/25/2022 INSERT YOUR PRESENTATION HERE
- 5. WWW.UVSONLINE.COM BIGGEST OFFENDER 7/25/2022 INSERT YOUR PRESENTATION HERE
- 6. WWW.UVSONLINE.COM C1-C5 -All 4 limbs affected, reflexes intact C6-T2 (cervical intumescence)- All 4 limbs affected, reflexes diminished in the front, normal in the hind T3-L3 -Hind limbs affected, normal reflexes L4-S3(Lumbar intumescence)- Hind limbs affected. Reflexes diminished. SPINAL CORD SEGMENTS 7/25/2022 INSERT YOUR PRESENTATION HERE
- 7. WWW.UVSONLINE.COM THINGS TO ASK ON EMERGENCY 7/25/2022 INSERT YOUR PRESENTATION HERE •When did this occur/How long has this been going on? •Abnormal prior to non-ambulatory status? •How long? •Has there been any prior treatments? •What medications? •How long? •Painful? •Known trauma? •Previous episodes? •Crate rest? • But seriously...STRICT crate rest???
- 8. WWW.UVSONLINE.COM MOST COMMONLY AFFECTED SITES 7/25/2022 INSERT YOUR PRESENTATION HERE Thoracolumbar = T11-L1 Cervical = C2-3 and C4-5
- 9. WWW.UVSONLINE.COM • Severe T3-L3 injury • Loss of inhibitory signals from “border cells” • These cells live at L1-5 and travel cranially through the entire T3-L3 spinal column • Provide inhibition to the extensors of the thoracic limbs • Decreased inhibition = increased extensor tone. • Can be confusing to localize SCHIFF SHERRINGTON 7/25/2022 INSERT YOUR PRESENTATION HERE
- 10. WWW.UVSONLINE.COM SPINAL RADIOGRAPHS? 7/25/2022 INSERT YOUR PRESENTATION HERE •Not super helpful for IVDD •Shows mineralized discs •Fractures/luxations •Might show bony neoplasia •Might show discospondylitis •Collapsed disc spaces and evidence of mineralized discs • Can allow suspicion, but cannot definitively determine site
- 11. WWW.UVSONLINE.COM CT scan - Who? • Chondrodystrophic dogs are more likely to have mineralized discs MRI - Who? • Everyone - most sensitive for IVDH • Chondrodystrophic dogs that are old or not first time offenders • Small dogs that are predisposed to inflammatory disease (ie: MUE) ADVANCED IMAGING 7/25/2022 INSERT YOUR PRESENTATION HERE
- 12. WWW.UVSONLINE.COM STATISTICS 7/25/2022 INSERT YOUR PRESENTATION HERE Ambulation Status Medical management Surgical Management Deep pain positive (ambulatory or non- ambulatory) 50-75% success 90-95% success Plegic, deep pain negative <5% success 50% success ***Once deep pain negative = 10% chance of myelomalacia
- 13. WWW.UVSONLINE.COM HOW TO CHECK DEEP PAIN 7/25/2022 INSERT YOUR PRESENTATION HERE Motor = deep pain is positive = no need to test deep pain. Withdrawal reflex does not = deep pain positive Positive reactions •Turn abruptly toward you or try and bite •Vocalizing reliably while testing •If severely affected = listen for heart rate elevation while testing
- 14. WWW.UVSONLINE.COM MYELOMALACIA 7/25/2022 INSERT YOUR PRESENTATION HERE •Spinal cord softening •Really only concerned if deep pain negative •10% chance • How to monitor • Temperature changes • Uncontrolled pain despite medication • Ascending neuro signs • Descending neuro signs • Respiratory compromise =put on a resp watch day 1
- 15. WWW.UVSONLINE.COM • If ambulatory • Monitor for worsening neurologic signs • Pain management • Incision • If non-ambulatory • Plegic = monitor deep pain status • Plegic and deep pain negative = monitor for myelomalacia • Bladder management EXTREMELY important • Recumbency care and skin monitoring (ie: urine scald) • Same as above POST OPERATIVE MANAGEMENT 7/25/2022 INSERT YOUR PRESENTATION HERE
- 16. WWW.UVSONLINE.COM BLADDER MANAGEMENT 7/25/2022 INSERT YOUR PRESENTATION HERE •Urinary catheter? • Who? • Already at increased risk of UTIs • Urine cultures are important •Manual expression • Risk of rupture •UMN bladder? • Prazosin, phenoxybenzamine • Skeletal muscle relaxants (diazepam, methocarbamol, etc) •LMN bladder • Bethanechol (+/- prazosin)
- 17. WWW.UVSONLINE.COM NSAIDS VS. STEROIDS 7/25/2022 INSERT YOUR PRESENTATION HERE •No evidence of one proven to be better than the other •Consider co-morbidities •If one is not working, wash out and try the other •However ***PLEASE avoid starting steroids prior to work***
- 18. WWW.UVSONLINE.COM Whenever an owner may want a work up Acute progression Non-ambulatory Failure of medical management WHEN TO REFER 7/25/2022 INSERT YOUR PRESENTATION HERE
- 19. WWW.UVSONLINE.COM • Slowly progressive T3-L3 myelopathy • Symmetric? • Non-painful • Normal MRI • Genetic testing available (SOD1) • Boxers, GSD, Welsh Corgi • Older patients >8 years of age • Tx = Rehab +/- a cart until euthanasia • Poor long term prognosis DEGENERATIVE MYELOPATHY 7/25/2022 INSERT YOUR PRESENTATION HERE
- 21. WWW.UVSONLINE.COM SRMA Boxers, Beagles, Labs, Bernese Mountain Dogs YOUNG Relapsing fever Neutrophilia Neck pain NORMAL neurologic examination* STEROID RESPONSIVE MENINGITIS AND ARTERITIS 7/25/2022 INSERT YOUR PRESENTATION HERE
- 22. WWW.UVSONLINE.COM MRI? CSF – severe neutrophilic pleocytosis and elevated microprotein Serum c- reactive protein? +/- infectious disease testing +/- CSF culture DIAGNOSTICS 7/25/2022 INSERT YOUR PRESENTATION HERE
- 23. WWW.UVSONLINE.COM HISTOPATHOLOGY 7/25/2022 INSERT YOUR PRESENTATION HERE Vandevelde pg 73
- 24. WWW.UVSONLINE.COM Immunosuppression Prednisone Atopica Mycophenolate Often weaned over 3-6 months Management of secondary infections TREATMENT 7/25/2022 INSERT YOUR PRESENTATION HERE
- 25. WWW.UVSONLINE.COM •Young adults •Larger breeds •Non-chondrodystrophoid •Asymmetric clinicalsigns •Non-painful >24h-48h FIBROCARTILAGENOUS EMBOLISM – SIGNALMENT 7/25/2022 INSERT YOUR PRESENTATION HERE
- 26. WWW.UVSONLINE.COM Typically T3-L3 Except – euthanasia bias – intumescences more common Cats? Asymmetric Spinal shock? Incontinence PRESENTING SIGNS 7/25/2022 INSERT YOUR PRESENTATION HERE
- 28. WWW.UVSONLINE.COM THE THEORIES 7/25/2022 INSERT YOUR PRESENTATION HERE Wilfried-Mai pg 566 1: Direct hit of spinal arteries 2: Newly formed inflammatory arteries 3: Embryonic remnant 4: Sinusoidal vessel of bone marrow
- 29. WWW.UVSONLINE.COM CAREFUL LOCALIZATION 7/25/2022 INSERT YOUR PRESENTATION HERE
- 30. WWW.UVSONLINE.COM HISTOPATHOLOGY 7/25/2022 INSERT YOUR PRESENTATION HERE Delahunta - Highlighting here that these are often markedly asymmetric presenting cases Vandevelde
- 31. WWW.UVSONLINE.COM • Focal • Sharply demarcated • Intramedullary • Lateralized usually • Predominantly grey matter FCE ON MRI 7/25/2022 INSERT YOUR PRESENTATION HERE
- 33. WWW.UVSONLINE.COM ACUTE NON-COMPRESSIVE NUCLEUS PULPOSUS EXTRUSION (ANNPE) 7/25/2022 INSERT YOUR PRESENTATION HERE •High velocity, low volume •Concussive injury •Generally non-painful >24h •Other names: Type 3 IVDD, ANDE, Missile Disk
- 34. WWW.UVSONLINE.COM Typically C1-C5 Border Collies Asymmetric Painful? PRESENTING SIGNS 7/25/2022 INSERT YOUR PRESENTATION HERE
- 35. WWW.UVSONLINE.COM ANNPE ON MRI 7/25/2022 INSERT YOUR PRESENTATION HERE •Focal •Overlying an intervertebral disk •Shorter than1 vertebral length •Oftenlateralized •Disruption epiduralspace
- 36. WWW.UVSONLINE.COM Wilfried Mai pg 442 7/25/2022 INSERT YOUR PRESENTATION HERE
- 37. WWW.UVSONLINE.COM TO TAP OR NOT TO TAP? 7/25/2022 INSERT YOUR PRESENTATION HERE •May not be helpful •May cause confusion •Can have elevated TNCC and protein
- 38. WWW.UVSONLINE.COM HOW TO TELL THE DIFFERENCE 7/25/2022 INSERT YOUR PRESENTATION HERE •Cross sectional imaging “diagnostic” features •More difficult to distinguish between the two •Post mortem exam is the only way
- 40. WWW.UVSONLINE.COM PROGNOSIS FOR BOTH FCE AND ANNPE 7/25/2022 INSERT YOUR PRESENTATION HERE 75-85% return to ambulation Typically within 3 weeks Permanent deficits = 50% Negative prognostic = absent nociception
- 41. WWW.UVSONLINE.COM MORE PROGNOSTIC INDICATORS 7/25/2022 INSERT YOUR PRESENTATION HERE
- 42. WWW.UVSONLINE.COM ACUTE, COMPRESSIVE, HYDRATED NUCLEUS PULPOSUS EXTRUSION 7/25/2022 INSERT YOUR PRESENTATION HERE •Extrusion of “semi-normal” nucleus pulposus •Chondrodystrophic and non-chondrodystrophic •Older dogs •Severe, symmetric signs •“Seagull” appearance •Most often non-painful •Cervical >TL
- 44. WWW.UVSONLINE.COM ANNPE VS. HNPE 7/25/2022 INSERT YOUR PRESENTATION HERE •Both considered non to semi degenerate disc extrusion •Conservative therapy vs. surgery •Rehab
- 45. WWW.UVSONLINE.COM HNPE CASE EXAMPLE 7/25/2022 INSERT YOUR PRESENTATION HERE
- 46. WWW.UVSONLINE.COM 2 WEEKS POST OP HEMI FOR T11-12 HNPE 7/25/2022 INSERT YOUR PRESENTATION HERE
- 47. WWW.UVSONLINE.COM 4 WEEKS POST OP 7/25/2022 INSERT YOUR PRESENTATION HERE
- 48. WWW.UVSONLINE.COM 6 WEEK POST OP 7/25/2022 INSERT YOUR PRESENTATION HERE
- 49. WWW.UVSONLINE.COM RESOURCES 7/25/2022 INSERT YOUR PRESENTATION HERE •Bartholomew, K. A., Stover, K. E., Olby, N. J., & Moore, S. A. (2016). Clinical characteristics of canine fibrocartilaginous embolic myelopathy (FCE): a systematic review of 393 cases (1973–2013). Veterinary Record, 179(25), 650–650. doi: 10.1136/vr.103863 •Borlace, T., Gutierrez-Quintana, R., Taylor-Brown, F. E., & Decker, S. D. (2017). Comparison of medical and surgical treatment for acute cervical compressive hydrated nucleus pulposus extrusion in dogs. Veterinary Record, 181(23), 625–625. doi: 10.1136/vr.104528 •Decker, S. D., & Fenn, J. (2018). Acute Herniation of Nondegenerate Nucleus Pulposus. Veterinary Clinics of North America: Small Animal Practice, 48(1), 95–109. doi: 10.1016/j.cvsm.2017.08.004 •Fenn, J., Drees, R., Volk, H. A., & Decker, S. D. (2015). Inter- And Intraobserver Agreement For Diagnosing Presumptive Ischemic Myelopathy And Acute Noncompressive Nucleus Pulposus Extrusion In Dogs Using Magnetic Resonance Imaging. Veterinary Radiology & Ultrasound, 57(1), 33– 40. doi: 10.1111/vru.12289 •Kortum, A., & Freeman, P. (2018). Fibrocartilaginous embolism and marked cerebrospinal fluid pleocytosis in a dog. Veterinary Record Case Reports, 6(2). doi: 10.1136/vetreccr-2018-000608 •Lahunta, A. D., Glass, E., & Kent, M. (2015). Veterinary neuroanatomy and clinical neurology. St. Louis, MO: Elsevier. •Risio, L. D. (2015). A Review of Fibrocartilaginous Embolic Myelopathy and Different Types of Peracute Non-Compressive Intervertebral Disk Extrusions in Dogs and Cats. Frontiers in Veterinary Science, 2. doi: 10.3389/fvets.2015.00024 •Mai, Wilfried. Diagnostic MRI in Dogs and Cats. CRC Press, 2018.
- 50. WWW.UVSONLINE.COM MY NUGGETS 7/25/2022 INSERT YOUR PRESENTATION HERE
- 51. WWW.UVSONLINE.COM INTENTION TREMORS GALORE 7/25/2022 INSERT YOUR PRESENTATION HERE
Editor's Notes
- Type 1 = acute onset. Usually associated with high activity, followed by crying out. Bursting through the annulus fibrosus to release dehydrated nucleus pulposus into the spinal canal. Pebble in the shoe. Surgery is indicated. Painful. Type II = slow progression, chronic in nature, slow development of clinical signs. Bulging of the annulus fibrosis causing compression. Sometimes surgery can be helpful if severely compressive disc is evident. Painful. Extrusion vs. protrusion - small chondrodystropic dogs are predisposed to type 1, larger breeds (ie: GSD, Boxers, Labs, etc) tend to get type 2
- We’ve all seen this guy. It is important to note that this is typically a genetic predisposition from degeneration/dehydration of the discs. So sometimes, it can be an extremely well conditioned pet and owners did not see any event prior to their presentation. I tell people that just like you or I, it can even be as simple as sneezing too hard. I don’t know how many of you have delt with herniated discs yourselves or back pain in general, and while I don’t wish that pain on anyone, it is amazing how simple it can be to injure yourself to a crippling degree. Sometimes we just do not know the inciting incident.
- With L4-S3 – also can see flaccid tail tone, reduce anal tone (MUST do a rectal), reduce perineal reflex. Panniculus SHOULD be intact. Do not get confused with spinal shock or Schiff Sherrington (more to come)
- Timing of things is really important to determine true emergencies and those that need surgery immediately How many times do we see “emergencies” that have actually been going on for 3 weeks. It is important to know drugs dog is on and when last received (ie: steroids, pain meds or sedatives that could alter exam at ER). HISTORY HISTORY HISTORY – I can’t express enough how important this is. I’ve lost count at how many “down dog” consults/transfers I have received that end up being a non-neuro related disease – thinks like bilateral cruciates, hemoabdomen, bloat/GDV, fractures, IMPA, panosteitis, HOD, etc.
- T3-L3 region is most common anatomic location for IVDD and T12-13 and T13-1 are most common sites Of the cervical sites, these are most common (beagles may be over-represented) - everyone knows the Beagle screams French bulldogs like to herniate discs in the lumbar region more so than dachs
- Border cells live at L1-L5 and travel cranially to provide inhibition to thoracic limbs at the level of the cervical intumescence Most evident in lateral recumbency Important to test reflexes. If truly poor reflexes, that would indicate a LMN deficit to TLs from a C6-T2 myelopathy, and should theoretically have reduced tone to TLs. Try bending limb a little manually and pinching a toe at that time to override some of increased tone.
- I don’t often waste money for these as we will still want advanced imaging in most cases. If it is a known trauma, older patient, or non-chondrodystrophic dog, not wrong to do. I typically save rads for cxr prior to anesthesia for imaging/sx, esp if it is a chondrodystrophic, young adult and otherwise healthy dog
- MRI is gold standard, however, we will do CT for dogs that are more likely to have mineralized discs – ie young/adult and otherwise healthy dachs and beagles Those that are predisposed to other diseases such as Frenchies, Boxers, Maltese, etc, we typically prioritize and MRI in hopes of not mixing disease within the soft tissue of the CNS
- If they are feeling any foot or tail, statistics are the same for deep pain positive group We are no longer quoting the 48h rule. This has since been disproven, and we are seeing that paraplegia time frame does not necessarily mean they are unlikely to recover if down over 48h. However, that being said, certainly the sooner to imaging/surgery, the better in those cases.
- Deep pain is the last thing to leave. Therefore, in the acute setting, if they have any motor (not necessarily walking), you do not need to test deep pain, because it is still present. Local reflex vs. nociception = difference between withdrawal reflex Important not to test deep pain repeatedly and multiple times daily (usually we test once to twice daily) as you can desensitize them and make it harder to interpret. Especially if it has been going on for a while before referral to a neurologist. If we are unable to reliably interpret deep pain sensation, then we are having a significantly different discussion with owners about overall outcome, and this can change whether or not owners will pursue further imaging/sx.
- Frenchies seem to be over-represented (more likely to develop hemorrhagic myelomalacia than Dachs). Temp changes - hypo/hyperthermia Ascending signs = ascending panniculus, new TL deficits, resp compromise (Day 1 resp watch) Descending signs - new urinary/fecal incontinence, no anal/tail tone, no perineal reflex That is why daily neuro exams are important Does it stop? - Potentially, but often so painful and risk of ascending until respiratory compromise, we often recommend euth as soon as suspected Those that are walking on day way, and then plegic deep pain negative, I still warn owners of myelomalacia, even if deep pain positive prior to sx. The ones that go down very fast, even with rapid/aggressive therapy, they may still go towards myelomalacia despite everything we do. Nothing is worse than telling an owner who did everything they were supposed to, that their pet now should be euthanized. Definitely something to discuss with them. Even before transfer, ESPECIALLY if sending them far for a referral and they are deep pain negative or had rapid progression.
- Incisional infection rate is less than 1%, however, it can happen. Warning owners about keeping it dry, don’t let them scratch at it, no creams/salves over it, don’t let other house mates groom it, etc. Mentioning some of this stuff because there are certainly cases where owners want to do everything, but become financially constrained for continued hosp and go home for management at home and with rDVM Similarly, some of this nursing care is helpful for causes with other spinal cord diseases (ie: FCE, ANNPE, etc)
- Increased risks of UTIs = increased risk resistance if not managed appropriately = CULTURES Save for large down dogs that are hard to get outside frequently, obese dogs that are hard to express, or mean dogs that are difficult/intolerant of expression Prazosin = alpha antagonist - works at IUS. Phenoxy (non-selective) alpha antagonist Skeletals = work at EUS Bethanechol = parasympathomimetic (non-selective muscarinic agonist) = works at detrusor to help with contraction. Dangerous for rupture if not sure if LMN bladder, we often use in combo with prazosin → very frustrating at home for owners bc leaking urine constantly. Need to warn of this and importance of keeping clean/dry to avoid urine scald. No DIAPERS!
- Co morbidities - already cushinoid, renal or liver dz, already has UTI? If start steroids and they actually have inflam dz, you may have caused false neg diagnostics. Recommend holding steroids for cases that absolutely will not work up further Steroids if non-ambulatory, may be tough for owner with PU/PD, possible exacerbation of increased risk UTI
- Mutation of superoxide dismutase 1 - Shows if they have the gene mutation and are affected/at risk, but cannot make definitive dx prior to histopathology Diagnosis of exclusion and read in light of exam, signalment, and all other diagnostics. Histo = fiber loss and non-inflammatory axonal degeneration secondary to demyelination- generally most severe in mid-caudal thoracic spine Will eventually progress to paraplegic and eventually, quadriplegia - then we worry about respiratory fatigue
- This shows a special stain of what happens to the myelin – DM is a demyelinating disease. Myelin with this special stain (luxol fast blue), should stain myelin, blue. As you can imagine, all of the white matter, surrounding the butterfly in the middle, should contain mostly blue stained myelin. There is massive loss of the blue staining myelin (can compare to dark blue surrounding peripheral nerves).
- These guys are often neurologically normal with a pretty significant neutrophilia, chronic/relapsing fever, and neck pain Usually young dogs (typically, less than 2y old), medium to large breed dogs. In the chronic cases, there can be some paresis or ataxia and there are rare reports of severe myelopathy and even brainstem signs in cases with hyperacute symptoms and extramedullary hemorrhage We discuss CRP in neuro for a number of diseases. In theory, CRP can be elevated in a large assortment of inflammatory diseases. However, worth testing initially in these cases and again at 3 mo of treatment. Those with normal CRP at 3mo of treatment are much less likely to show relapse. It can be used in these cases, as a marker of when it should be ok to start weaning pred – in general, relapse can be seen in about 20% (up to 50% in some sorces) of cases.
- With NONdegenerate - neutrophilic pleocytosis, can consider possible bacterial meningitis = not wrong to consider culture in these cases, but often – if it looks like a duck? CSF can look tubid/cloudy, have hemorrhage or be xanthochromic (bilirubin in it = yellow looking) MRI – If young, adult, just neck pain, fever, and leukocytosis with neutrophilia, we will consider just doing CSF tap without MRI, but ideally, we like to document that we are not missing something else (while considering things we might miss – MUE, which we may treat similarly anyway vs. cancer vs. infectious)
- Histologically – Suppurative inflammation of the meninges especially of the cord Subacute – mononuclear infiltrates dominant and meningeal fibrosis is apparent Necrotizing arteritis (immune complex type) of the spinal arteries (fig below) Occasional meningeal hemorrhage Chronic changes = sub-intimal proliferation of spindle cells and stenosis May have extension into cerebral meninges, choroid plexus and periventricular tissues Mechanism = excessive IgA production as a result of immune dysregulation with a skewed Th2 response
- It is possible that even up to 45% of patients will have concurrent IMPA, luckily, they are treated similarly Often there is rapid response to prednisone. Some patients can be treated with immunosuppressive pred for 3-6 months and then be weaned off Potentially up to 20-50% will have relapse and require secondary immunosuppression and a more long course of therapy. Maybe even life long This is where CRP may be helpful. Less likely to relapse if CRP is normal at the end of 3mo of tx If not resolving or relapse = add secondary immunosuppressive. Any immunosuppression = risks of secondary opportunistic infections. UTIs and some form of dermatitis or pyoderma are what I often see. If living/treating in SW and mid west to SoCal areas, have to consider secondary fungal infections if lesions are noted. Less so here.
- Labs, large to giant mix breeds (labs, boxers, GSD, Collie), reported in mini Schnauzer as well as most common small breed (rule out hyperlipid) Peracute symptoms - can progress up to 48 hours, but usually stabilize within 24h Typically after strenuous activity, often vocalization is reported at initial event
- Most common T3-L3 region (vs. cervical in cats) Multifocal signs in few, mostly T3-caudal (suspect secondary to spinal shock - severe TL injury = depressed reflexes loss of descending facilitatory input to motor neurons = hyperpolarization and transient reduced excitability leading to flaccid paralysis and diminished reflexes caudally - usually resolves in 24 hours) FCE for those that made it to histo- most commonly at C6-T2 and L4-S3, but ante-mortem, most common is T3-L3 and L-S3.
- Piece of fibrocartilage (presumably from nucleus pulposus- Batholomew 2016) is lodged into vasculature of the spine causing ischemia - exact manner as to how it enters vasculature is not known.
- Wilfried - Pathophys for why FCE happens is not known. Theories 1: Direct penetration of spinal arteries by degen disc material 2. Penetration of degen disc material to newly formed inflammatory arteries forming for bc of disc degen 3. Penetration of embryonic remnant vessel within the nucleus pulposus 4. Penetration of sinusoidal vessels of bone marrow.
- Delahunta pg 254 and 110 Need to think of clinical signs and consider spinal shock vs. truly multifocal and is multifocal from myelomalacia, or showering of emboli.
- Left side shows typical H&E staining in which the emboli stains similarly to cartilage. Middle pic shows special stain (alcian-blue stain) that stains fibrocartilage bright blue. Can see the cartilage lodged in a blood vessel of the cord. De Risio - 2015 - Distribution of lesion is generally the territory supplied by embolized vessel and usually asymmetric. Grey matter is often more severely affected than white. As expected with an ischemic event - margins are often well differentiated. Usually ischemic lesion overall, but can have hemorrhage. Can see a lot of this on the right sided photo although it is affecting a larger area of both grey/white matter here
- Hyper to normal gray matter on T2 and FLAIR iso or hypo, hypo to normal on T1. Post contrast T1 may show mild and heterogenous enhancement (on 5th to 7th day post injury) Intramedullary T2 length is generally longer than 1 vertebral length. Possible to be normal if 24-72h after onset (Wilfried Mai) MRI Myelogram (above from wilfried mai pg 569) shows attenuation of dorsal and ventral CSF column to indicate swelling.
- Risio 2015 - Intramedullary hyperintensity above C6 in an English Bull Terrier - left sided intramedullary hyperintensity. No signal changes or extraneous material in epidural space or obvious loss T2 signal of disc (big thing in this image bc could be confused for ANNPE)
- Explosive extrusion of NP causing concussion with no residual compression Similar signalment and symptoms, although may present older than those with FCE, and more likely to vocalize at initial injury and potentially have spinal hyperesthesia in early <24h period.
- ANNPE more commonly C1-C5 compared to FCE T3-S3 and border collies are overrepresented (De Decker 2018) Possibly more often painful on initial injury (20-60% of dogs) than FCE - Risio 2015
- Risio 2015 - No significant compression (sx not indicated), overlying disc, decreased disc space and T2 signal of NP Affects both white and grey matter (Wilfried Mai) Rent in the dorsal annulus (gradient echo) for ANNPE- Wifried Mai Directly over IVD, T2 loss of signal of disc space, less than 1 vertebral length
- Notice reduced volume and T2 hyper at disc space directly below intramedullary hyperintensity. Less than 1 vertebral body. Also has T2 hyperintense tract noted through the cord (arrow) and disruption of epidural fat. Both white and grey matter affected.
- Abnormal CSF is not overly surprising - Disruption of BBB, proinflammatory response, even malacia etc Potentially allow for confusion and even mistake of treating for MUE when not actually the case. Need to take clinical history, breed, and exam into account for treatment of these cases. Case report 2018 - Kortum = acute onset with progression in hosp to plegia DPN. MRI suspicious for FCE. Max cross-sectional area of intramedullary hyperintensity was 54% (not 90 or higher as previously thought to correlate with outcome). Found neutrophilic pleocytosis (200+/uL and protein of 8+mg/dl) = started tx for MUE. Dog progressed and was euthanized. Necropsy confirmed FCE with myelomalacia (not surprising for values that high with malacia, but also started unnecessary treatments)
- ANNPE dx criteria - Disrupted epidural fat over IVD space, minimal compressive extruded disc material (how to know for sure if disc?), narrowed IVD space, loss of volume of nucleus pulposus of the IVD Risio 2015 - Lateralization in about 50-90% in FCE (greater variety), approx 60% ANNPE, and usually significant asymmetry on exam. Lateralization in cats with FCE is about 60% and almost all of FEW reports of cats with ANNPE. Most common in cervical spine in cats with FCE/ANNPE (much less lit out there for this).
- A - ANNPE (over the disc space, loss of T2 signal in disc space) B - FCE (long distance intramedullary change) C - Case with intraobserver disagreement
- Prognosis good to excellent (85%) recovery to ambulation, usually within 3 weeks. Permanent deficits are common (50%), and urinary/fecal incontinence can be permanent even if return to ambulation Nociception absent at diagnosis = worse prognosis (maybe biased due to limited follow up in severe case). However, cases in this study not confirmed definitively as post mortem not available in cases still alive.
- Overall – successful outcome in >75% of cases Risio 2015 - Table suggestive of unsuccessful outcomes - From a study of 50 dogs comparing MRI findings and long term follow up - FCE -looking at a ratio btw length of intramedullary hyperintensity on sag T2 and length of either C6 or L2 (if >2 = 100% sensitive for unsuccessful outcome) and a maximal cross sectional area of lesion (largest region of legion) as a percentage of spinal cord at that level (>67% = 100% sensitive for unsuccessful outcome) Wilfried May- Also noted, that T2* presence of hypointensity within the cord (suggesting hemorrhage) may be associated with a poor outcome. Important to note that overall, ANNPE may have 5x more likely chance for continued incontinence compared to FCE – Vet Rec Dec 2017, although, this is the opposite of what was found in JAVMA Oct 2016 (regarding T3-L3 lesions).
- Was originally thought to be like discal cysts in ppl - people, discal cysts always occur at the thoracolumbar level and no cervical lesions. Pathogeneses suggested = resorption of pre-existing herniation and hematoma associated with a disc prolapse, or fluid exiting from a degenerated and protruded disc which incites a cyst-like pseudomembrane formation. These in animals have since been evaluated and shown to be non to semi degen disc material with no membrane. So more appropriate to call a NP extrusion. Vet Surg 2017 Seagull sign bc of dorsal longitudinal ligament
- Vet Rec Dec 2017 While some studies are biased in the sense that those that are brought to surgery, tend to present with a more severe grade of neuro dysfunction, in this retro study (although small numbers – 16 sx, 18 med) did not have a sig difference in neuro grade, and no sig difference in overall outcome. Similar findings with TL cases (JVIM Jan 2018) – 1 case in this paper was rescanned 4 days later and showed resolution of HNPE on MRI (post mortem scan) I approach these as offering the client a few options – monitor for a few days and if no improve (or worse), consider sx, vs. bite the bullet and do sx now. Offers options for clients with cost constraints as it is very reasonable to consider that the patient may improve on their own over time. Still, it is challenging to see para/tetraplegia and elect to treat conservatively and monitor, however, cases still have been shown to improve with medical management in that state (even a few of my own).
- Decker/Fenn 2018 - Previously thought to be similar to human discal cyst, but histo does show evidence of material most consistent with NP material and no evidence of cyst wall Usually older dogs with severe, symmetric signs not associated with activity (unlike FCE/ANNPE) Generally non-painful (but can be) and more severely neurologically affected in comparison to - typical type I IVDD, and despite severe neuro signs, good outcomes and full recovery has been reported with sx and medical manage Looks like relatively normal/hydrated disc on MRI (vs. “partially degenerate), directly over disc space allowing symmetric/ventral compression (maybe looks seagull bc of intact dorsal longitudinal lig). Variable degrees of contrast enhancement as well as T2 intramedullary hyperintensity Consensus for ANNPE is conservative management +/- rehab, but ideal treatment for HNPE is not yet known. Most studies have shown that those that are selected for surgery tend to be severely neurologically affected and/or those that are really painful Most common sites = C4-5 then C3-4 and C5-6 (Wilfried Mai)
- Notice on right (T2) there is hyperintense material and on left (T1) is is hypointense, indicating there is a fluid component to the material. NOT super compressive left T11-12 hemi - Acutely paraplegic, deep pain intact, seemed painful (but aggressive so hard to tell). Outside for 30 seconds, screeched and paraplegic Decided to move forward with surgery bc of severity of neuro signs. Lots of gelatinous material oozed out of canal. Remained deep pain positive and had been receiving integrative. Improved to paraparesis prior to discharge, and noted to be weakly ambulatory a month after surgery. Would he have improved without surgery? No one knows. Also, now looking back on this case, the limited amount of compression further leads to suspicion that most the injury here was more concussive rather than compressive (but I was left in charge to make the decision as a resident, panicked, and cut it).