FCE

[Guest guest]

I have often asked these very same questions. There are a few neurosurgeons on

the list, perhaps they could chime in with some answers?

>

> Hello to all, I'm a new member and a spinal surgeon (for humans).

> Trying to understand the Dx of FCE. In humans, we recognize embolic

> events to the brain frequently but embolic disease to the cord is

> extremely rare. Can anyone explain the pathophysiogy of how the

> fibrocartilagenous debris finds it way to the cord vasculature? Is

> there any disagreement regarding the validity of the Dx? Thank you

>

[Guest guest]

So I'll at least partially stick my neck out here....but I am not a neurosurgeon and would love to hear what they have to say!

In terms of the diagnosis of FCE:

Usually spinal pain is not present, or only present for about 24 hours after the acute event. If CSF is normal / has mildly increased protein (to rule out meningitis and most LSA that might not be revealed on imaging), and no compressive lesion is present on MRI, then we are left with either a type III disk or an FCE, of which neither are surgical. Sometimes cord edema can be seen on MRI at the site.

In terms of the pathophysiology:

Fibrocartilaginous material is found in the arterioles and veins in the spinal cord causing an ischemic myelopathy. (This is where I hope the neuro folks will chime in:) We think the material originates from the intervertebral disks, enters a venous plexus, and finds it's way to an a/v anastamosis: then on to either an arteriole or vein. I think there are a few other theories out there, but that is the one I hear the most.

Prognosis is worse if the embolis is thought to occur at either intumescence. T3-L3 is the best prognosis of the bunch.

Hope that helps..

We just got one in yesterday, that I started working on today!

Subject: Re: FCETo: VetRehab Date: Saturday, March 17, 2012, 8:46 PM

I have often asked these very same questions. There are a few neurosurgeons on the list, perhaps they could chime in with some answers?>> Hello to all, I'm a new member and a spinal surgeon (for humans). > Trying to understand the Dx of FCE. In humans, we recognize embolic > events to the brain frequently but embolic disease to the cord is > extremely rare. Can anyone explain the pathophysiogy of how the > fibrocartilagenous debris finds it way to the cord vasculature? Is > there any disagreement regarding the validity of the Dx? Thank you>

[Guest guest]

Good explanation! This is something we see more commonly in large breed, young,

active dogs (and min schnauzers!) they are often doing something active at the

time of the occurrence - classic example is jumping for a frisbee. They are

acutely affected and usually non-ambulatory. This can occur anywhere in the

spinal cord (cervical, thoracic and lumbar regions). Typically, is seems that

there is a " showering of emboli " - we can see multifocal signs - changes in

panniculus, LMN bladder and very lateralized signs. The patients are often

non-painful and can improve very quickly. For the ones that are severely

affected (non-ambulatory) we recommend imaging +/- CSF analysis to rule out a

surgical disease - because they can present the same way! The CSF can be normal

- but also we can see a neutrophilic pleocytosis (sometimes marked). Dogs with

LMN signs tend to have a longer recovery...and as with any myelopathy - patients

with alterations in pain perception (especially when the intumescence is

affected) tend to have a more guarded prognosis. Here is a bit from DeLahunta's

book... Hope this helps!

Kube, DVM

DACVIM (Neurology)

" FCEM is a spinal cord lesion that is common in dogs but is uncommon in other

species of domestic animals.* It is most common in young adult dogs of the

larger breeds but it can occur as young as 3 months of age and it is common in

the miniature schnauzer, Labrador retriever, and boxer breeds, in our

experience. The clinical signs are peracute in onset and usually stabilize

within 24 hours. Rarely, clinical signs may progress for 48 hours. Following

that, there is no further progression or there is improvement, depending on the

degree of ischemia or infarction that has occurred. The source of the

fibrocartilage is assumed to be the intervertebral disk that is undergoing

degeneration. This embolic fibrocartilage has the same collagen type that is

found in the nucleus pulposus. How this degenerate fibrocartilage gains access

to the spinal cord vasculature remains speculative. These emboli are more common

in small arteries but also can be found in veins. Arteriovenous anastomoses do

occur in the blood supply of the spinal cord and have been implicated in the

distribution of the emboli. Protrusion of degenerate disk material into the

adjacent ventral internal vertebral venous plexus has occasionally been observed

at necropsy. It has been suggested that the normally avascular intervertebral

disk is invaded by new growth of arteries when degeneration occurs in the

annulus fibrosis and this is a route for these emboli to enter the arterial

vasculature. We find this mechanism difficult to accept. In humans, degenerate

intervertebral disk material can protrude into the adjacent vertebral body where

there is ready access to the blood vessels in the marrow of the vertebra. One

route of venous drainage from this marrow is into the ventral internal vertebral

venous plexus within the vertebral canal. These intramedullary protrusions are

referred to as Schmorl nodes. They are rare, or at least rarely identified in

dogs, which may be because of dogs' quadruped posture and the thick layer of

cortical bone that is adjacent to the intervertebral disk. Reverse venous blood

flow may be involved in the distribution of these emboli. Whenever an animal

strains by contracting its trunk muscles with the glottis closed, the increased

pressure in the thorax and abdomen interferes with the venous return to the

heart and forces the venous blood into the vertebral venous plexus. This is the

Valsalva maneuver, and it may play a role in the ability of these emboli to gain

access to the spinal cord vasculature. The involvement of the intervertebral

disk as the source of these emboli is also supported by the observation that

these lesions occur primarily in the spinal cord. One report of brainstem

lesions with fibrocartilaginous emboli indicated a possible source of emboli

from cervical intervertebral disks.5 Magnetic resonance (MR) imaging often shows

intervertebral disk degeneration at the level of the FCEM lesion in the spinal

cord. These FCEM lesions can be unilateral or bilateral at any level of the

spinal cord, and they affect various combinations of the gray and white

matter. The lesions are usually limited to a few adjacent spinal cord segments.

There are many examples in the following case examples that involve the various

regions of the spinal cord. Caudal brainstem signs are rare and probably are

associated with emboli arising from the cervical intervertebral disks.

Because of the extensive collateral circulation to the spinal cord (Fig. 10-4),

multiple blood vessels must be compromised to cause the degree of infarction and

severe clinical signs seen in dogs similar to Brittney. This suggests that a

sudden shower of emboli must occur at one time. At necropsy, these emboli can be

found in many blood vessels in or near the lesions. Usually, this shower affects

the blood vessels to a few adjacent spinal cord segments and the associated

lesions often are scattered and asymmetric within these segments. Thus, the

clinical signs are usually focal and often asymmetric, as seen in Brittney. FCEM

may be much more common than we realize and not be extensive enough to cause

clinical signs or cause only transient clinical signs. Most veterinarians have

had the experience of being called by a distraught owner who has just found

their pet dog collapsed and unable to stand, but by the time the dog arrives at

the hospital for examination, the dog is walking normally. We believe that some

of these transient episodes of collapse may be due to transient spinal cord

ischemia caused by FCEM.

Many dogs in which you make this clinical diagnosis will recover spontaneously.

This is more common in dogs with paresis and ataxia due to interruption of the

UMN and GP pathways. The more severe the involvement of the gray matter in the

intumescences, the more guarded the prognosis. As a rule of thumb, if there are

no signs of improvement in 10 to 14 days after the onset of clinical signs, it

is unlikely that any recovery will occur. In a few patients, after an initial

mild improvement, there may be a period of weeks before they rapidly regain the

ability to walk. We

usually tell owners that it may take up to 10 weeks before final improvement

occurs.

An interesting observation is that FCEM is very rare in the chondrodystrophic

breeds in which the chondroid metaplastic form of intervertebral disk

degeneration is so common. FCEM also is observed in dogs as young as 3 months of

age in which you do not expect intervertebral disk degeneration to occur. In

these young dogs, the source of cartilage may be the vertebral growth plates.

Often, there is an associated history of mild trauma such as a sudden fall or

vigorous playing and jumping as with catching a frisbee. This relationship

between young age and vigorous handling is associated with FCEM in young feeder

pigs; it occurs during their transportation in crowded trucks. "

> >

> > Hello to all, I'm a new member and a spinal surgeon (for humans).

> > Trying to understand the Dx of FCE. In humans, we recognize embolic

> > events to the brain frequently but embolic disease to the cord is

> > extremely rare. Can anyone explain the pathophysiogy of how the

> > fibrocartilagenous debris finds it way to the cord vasculature? Is

> > there any disagreement regarding the validity of the Dx? Thank you

> >

>

[Guest guest]

Hi All

I have a breeder client of irish Wolfhounds and there seems to be a predisposition of IW puppies at around 8-12 weeks of age. Any ideas? They have classic FCE signs and tend to get better although a few have longterm deficits.

My question is- if the thought is degenerative cartilage- why is it so common in young dogs??

Re: FCE

Good explanation! This is something we see more commonly in large breed, young, active dogs (and min schnauzers!) they are often doing something active at the time of the occurrence - classic example is jumping for a frisbee. They are acutely affected and usually non-ambulatory. This can occur anywhere in the spinal cord (cervical, thoracic and lumbar regions). Typically, is seems that there is a "showering of emboli" - we can see multifocal signs - changes in panniculus, LMN bladder and very lateralized signs. The patients are often non-painful and can improve very quickly. For the ones that are severely affected (non-ambulatory) we recommend imaging +/- CSF analysis to rule out a surgical disease - because they can present the same way! The CSF can be normal - but also we can see a neutrophilic pleocytosis (sometimes marked). Dogs with LMN signs tend to have a longer recovery...and as with any myelopathy - patients with alterations in pain perception (especially when the intumescence is affected) tend to have a more guarded prognosis. Here is a bit from DeLahunta's book... Hope this helps! Kube, DVMDACVIM (Neurology)"FCEM is a spinal cord lesion that is common in dogs but is uncommon in other species of domestic animals.* It is most common in young adult dogs of the larger breeds but it can occur as young as 3 months of age and it is common in the miniature schnauzer, Labrador retriever, and boxer breeds, in our experience. The clinical signs are peracute in onset and usually stabilize within 24 hours. Rarely, clinical signs may progress for 48 hours. Following that, there is no further progression or there is improvement, depending on the degree of ischemia or infarction that has occurred. The source of the fibrocartilage is assumed to be the intervertebral disk that is undergoing degeneration. This embolic fibrocartilage has the same collagen type that is found in the nucleus pulposus. How this degenerate fibrocartilage gains access to the spinal cord vasculature remains speculative. These emboli are more common in small arteries but also can be found in veins. Arteriovenous anastomoses do occur in the blood supply of the spinal cord and have been implicated in the distribution of the emboli. Protrusion of degenerate disk material into the adjacent ventral internal vertebral venous plexus has occasionally been observed at necropsy. It has been suggested that the normally avascular intervertebral disk is invaded by new growth of arteries when degeneration occurs in the annulus fibrosis and this is a route for these emboli to enter the arterial vasculature. We find this mechanism difficult to accept. In humans, degenerate intervertebral disk material can protrude into the adjacent vertebral body where there is ready access to the blood vessels in the marrow of the vertebra. One route of venous drainage from this marrow is into the ventral internal vertebral venous plexus within the vertebral canal. These intramedullary protrusions are referred to as Schmorl nodes. They are rare, or at least rarely identified in dogs, which may be because of dogs' quadruped posture and the thick layer of cortical bone that is adjacent to the intervertebral disk. Reverse venous blood flow may be involved in the distribution of these emboli. Whenever an animal strains by contracting its trunk muscles with the glottis closed, the increased pressure in the thorax and abdomen interferes with the venous return to the heart and forces the venous blood into the vertebral venous plexus. This is the Valsalva maneuver, and it may play a role in the ability of these emboli to gain access to the spinal cord vasculature. The involvement of the intervertebral disk as the source of these emboli is also supported by the observation that these lesions occur primarily in the spinal cord. One report of brainstem lesions with fibrocartilaginous emboli indicated a possible source of emboli from cervical intervertebral disks.5 Magnetic resonance (MR) imaging often shows intervertebral disk degeneration at the level of the FCEM lesion in the spinal cord. These FCEM lesions can be unilateral or bilateral at any level of the spinal cord, and they affect various combinations of the gray and whitematter. The lesions are usually limited to a few adjacent spinal cord segments. There are many examples in the following case examples that involve the various regions of the spinal cord. Caudal brainstem signs are rare and probably are associated with emboli arising from the cervical intervertebral disks.Because of the extensive collateral circulation to the spinal cord (Fig. 10-4), multiple blood vessels must be compromised to cause the degree of infarction and severe clinical signs seen in dogs similar to Brittney. This suggests that a sudden shower of emboli must occur at one time. At necropsy, these emboli can be found in many blood vessels in or near the lesions. Usually, this shower affects the blood vessels to a few adjacent spinal cord segments and the associated lesions often are scattered and asymmetric within these segments. Thus, the clinical signs are usually focal and often asymmetric, as seen in Brittney. FCEM may be much more common than we realize and not be extensive enough to cause clinical signs or cause only transient clinical signs. Most veterinarians have had the experience of being called by a distraught owner who has just found their pet dog collapsed and unable to stand, but by the time the dog arrives at the hospital for examination, the dog is walking normally. We believe that some of these transient episodes of collapse may be due to transient spinal cord ischemia caused by FCEM.Many dogs in which you make this clinical diagnosis will recover spontaneously. This is more common in dogs with paresis and ataxia due to interruption of the UMN and GP pathways. The more severe the involvement of the gray matter in the intumescences, the more guarded the prognosis. As a rule of thumb, if there are no signs of improvement in 10 to 14 days after the onset of clinical signs, it is unlikely that any recovery will occur. In a few patients, after an initial mild improvement, there may be a period of weeks before they rapidly regain the ability to walk. Weusually tell owners that it may take up to 10 weeks before final improvement occurs.An interesting observation is that FCEM is very rare in the chondrodystrophic breeds in which the chondroid metaplastic form of intervertebral disk degeneration is so common. FCEM also is observed in dogs as young as 3 months of age in which you do not expect intervertebral disk degeneration to occur. In these young dogs, the source of cartilage may be the vertebral growth plates. Often, there is an associated history of mild trauma such as a sudden fall or vigorous playing and jumping as with catching a frisbee. This relationship between young age and vigorous handling is associated with FCEM in young feeder pigs; it occurs during their transportation in crowded trucks."> >> > Hello to all, I'm a new member and a spinal surgeon (for humans). > > Trying to understand the Dx of FCE. In humans, we recognize embolic > > events to the brain frequently but embolic disease to the cord is > > extremely rare. Can anyone explain the pathophysiogy of how the > > fibrocartilagenous debris finds it way to the cord vasculature? Is > > there any disagreement regarding the validity of the Dx? Thank you> >>

[Guest guest]

>

> My question is- if the thought is degenerative cartilage- why is it so common

in young dogs??

>

" FCEM also is observed in dogs as young as 3 months of age in which you do not

expect intervertebral disk degeneration to occur. In these young dogs, the

source of cartilage may be the vertebral growth plates. " from the DeLahunta

ref.

Vet Q. 2000 Jul;22(3):154-6.

Fibrocartilaginous embolism of the spinal cord (FCE) in juvenile Irish

Wolfhounds.

Junker K, van den Ingh TS, Bossard MM, van Nes JJ.

SourceDepartment of Veterinary Pathology, Faculty of Veterinary Medicine,

Utrecht University, The Netherlands.

Abstract

This study describes the occurrence of fibrocartilaginous embolism of the spinal

cord (FCE) in eight juvenile Irish Wolfhounds that were presented within a

period of 16 months (1996-1997). The dogs, seven males and one female between

eight and 13 weeks of age, were presented because of an acute onset of abnormal

locomotion. Five dogs were euthanized and FCE was diagnosed by the

histomorphological presence of focal myelomalacia and Alcian

blue-positive-nucleus-pulposus material in the spinal cord vasculature. Three

dogs, which were thought to have FCE because of their clinical symptoms,

improved with partial or almost complete return to normal locomotion. Although

the observed high incidence may be a coincidence, oral information from breeders

and lay reports of similar cases in journals for dog breeders from various

countries suggest that FCE is a common disorder in young Irish Wolfhounds.

Marti Drum DVM, PhD, CCRP, CERP

Clinical Assistant Professor

Small Animal Physical Rehabilitation

University of Tennessee

C247 Veterinary Teaching Hospital

Knoxville, TN 37996

(o)

(f)

mdrum@...

" The most exciting phrase to hear in science,

the one that heralds the most discoveries,

is not 'Eureka!' (I found it!),

but 'That's funny...' "

-Isaac Asimov

[Guest guest]

Hello - I'm looking for additional suggestions and ideas. I have started working

with a MRI confirmed FCE at L3-4 in a 45# 7 yr old Border Collie. She is

bilaterally paretic, however, the right leg appears to be improving whereas the

left leg is showing little movement. In the UWTM she will move her right leg

forward and place her foot appropriately, but I continue to do pattern walking

with the left foot. I have been doing E-stim on bilateral quads/hams and gluts

for 10 min each. I use 120Hz, 300mcs, 3s ramp, 15s on, 15s off, and a setting of

3-4. I am able to get a tetanic muscle contraction of the hams only and not

consistently. Ideas? I have started doing acupuncture btw the toes of both rear

feet daily. For exercises I have been doing assisted standing, assisted

sit-to-stands, and standing over a peanut. She hates withdrawal flexor reflex. I

have been seeing her for 1 week on a daily basis. Thank you for any other ideas!

Christie Carlo, DVM, CCRT

[Guest guest]

Hi Christie, how long had she been down when you saw her? I love FCE's, don't give up... Continue daily reflex/pattern walking with both legs In the treadmill. Massage shoulders, neck and back as theses guys get super tight, I do daily laser and daily acupuncture if owners can afford it all... 90% or better success rate for return to mostly normal! I also do lots of stimulation with sensory Input like cold and hot on feet, stand/ balance exercises on gravel, astroturf or other odd surface. In my experience you have about 2 weeks to hit her hard, then you will see more gradual improvement after that... Good luck! Pam Nichols DVM, CCRPSent from my iPadDr. Pam Nichols cell office

Hello - I'm looking for additional suggestions and ideas. I have started working with a MRI confirmed FCE at L3-4 in a 45# 7 yr old Border Collie. She is bilaterally paretic, however, the right leg appears to be improving whereas the left leg is showing little movement. In the UWTM she will move her right leg forward and place her foot appropriately, but I continue to do pattern walking with the left foot. I have been doing E-stim on bilateral quads/hams and gluts for 10 min each. I use 120Hz, 300mcs, 3s ramp, 15s on, 15s off, and a setting of 3-4. I am able to get a tetanic muscle contraction of the hams only and not consistently. Ideas? I have started doing acupuncture btw the toes of both rear feet daily. For exercises I have been doing assisted standing, assisted sit-to-stands, and standing over a peanut. She hates withdrawal flexor reflex. I have been seeing her for 1 week on a daily basis. Thank you for any other ideas!

Christie Carlo, DVM, CCRT

[Guest guest]

Isn’t this the season for FCE? I know I have 6 on my service

right now… I remember reading a study many, many moons ago saying early Fall

was more the time to see FCE’s than any other time of the year. Maybe I’m

making that up or just heard that somewhere… Anyhoo, I find all are a little different, as far as rate of recovery, but as Pam said, most

improve to functional status and fairly quickly (2-3 weeks) if not in just a

few days. I have one right now I’m re-teaching jumping to(2 months post FCE). I never use e-stim

or LASER on mine though. I only do therapeutic exercise and focus on functional

movement(s). Sit to stands, side bend exercises and some treadmill exercise if

they can be successful in the actions. Later in the game off-balance props can

be added when more challenges are needed.

-Robby J Porter IIICertified Canine Rehabilitation PractitionerLouisiana Veterinary Referral CenterAnimal Rehabilitation CenterMandeville, LA70448Main Hospital: ext. 208lavrc.comtwitter.com/LAVRCfacebook.com/LAVRCyoutube.com/user/LAVRCfacebook.com/louisianaCOP*********************************************************************************************************This document, and any attached information is proprietary, privileged and confidential property of the Louisiana Veterinary Referral Center (LAVRC) under applicable law and is intended exclusively for business use by all LAVRC employees and

intended recipients with a legitimate LAVRC business need. The reproduction, dissemination, distribution and/or disclosure by unintended recipients is unauthorized, strictly prohibited and may be unlawful (Privileged and confidential pursuant to La. R.S. 13:3715.3).If you have received this transmission in error, please immediately reply to the sender and delete this information from your system. To: "VetRehab "

<VetRehab > Cc: "VetRehab " <VetRehab > Sent: Thursday, August 9, 2012 5:18 PM Subject: Re: FCE

Hi Christie, how long had she been down when you saw her? I love FCE's, don't give up... Continue daily reflex/pattern walking with both legs In the treadmill. Massage shoulders, neck and back as theses guys get super tight, I do daily laser and daily acupuncture if owners can afford it all... 90% or better success rate for return to mostly normal! I also do lots of stimulation with sensory Input like cold and hot on feet, stand/ balance exercises on gravel, astroturf or other odd surface. In my experience you have about 2 weeks to hit her hard, then you will see more gradual improvement after that... Good luck! Pam Nichols DVM, CCRPSent from my iPadDr. Pam Nichols cell office

Hello - I'm looking for additional suggestions and ideas. I have started working with a MRI confirmed FCE at L3-4 in a 45# 7 yr old Border Collie. She is bilaterally paretic, however, the right leg appears to be improving whereas the left leg is showing little movement. In the UWTM she will move her right leg forward and place her foot appropriately, but I continue to do pattern walking with the left foot. I have been doing E-stim on bilateral quads/hams and gluts for 10 min each. I use 120Hz, 300mcs, 3s ramp, 15s on, 15s off, and a setting of 3-4. I am able to get a tetanic muscle contraction of the hams only and not consistently. Ideas? I have started doing acupuncture btw the toes of both rear feet daily. For exercises I have been doing assisted standing, assisted sit-to-stands, and standing over a peanut. She hates withdrawal flexor reflex. I have been seeing her for 1 week on a daily basis. Thank you for any other ideas!

Christie Carlo, DVM, CCRT

[Guest guest]

Thanks Pam. I saw her for the first time about 5 days after the initial insult. I have been seeing her daily for the last week and see some improvement. I'll add some of the stimulation that you are suggesting to her feet, but have already been doing the rest. I just tend to be impatient and want to see her being able to move that left leg and walking on her right within the next week. Thanks for the help.

-- Christie Carlo, DVM, CCRTCertified Canine Rehabilitation TherapistSecretary for American Association of Rehabilitation VeterinariansAvondale Veterinary Healthcare Complex

(fax)

[Guest guest]

Thanks Pam. I saw her for the first time about 5 days after the initial insult.

I have been seeing her daily for the last week and see some improvement. I'll

add some of the stimulation that you are suggesting to her feet, but have

already been doing the rest. I just tend to be impatient and want to see her

being able to move that left leg and walking on her right within the next week.

Thanks for the help.

Christie Carlo, DVM ,CCRT

>

> > Hello - I'm looking for additional suggestions and ideas. I have started

working with a MRI confirmed FCE at L3-4 in a 45# 7 yr old Border Collie. She is

bilaterally paretic, however, the right leg appears to be improving whereas the

left leg is showing little movement. In the UWTM she will move her right leg

forward and place her foot appropriately, but I continue to do pattern walking

with the left foot. I have been doing E-stim on bilateral quads/hams and gluts

for 10 min each. I use 120Hz, 300mcs, 3s ramp, 15s on, 15s off, and a setting of

3-4. I am able to get a tetanic muscle contraction of the hams only and not

consistently. Ideas? I have started doing acupuncture btw the toes of both rear

feet daily. For exercises I have been doing assisted standing, assisted

sit-to-stands, and standing over a peanut. She hates withdrawal flexor reflex. I

have been seeing her for 1 week on a daily basis. Thank you for any other ideas!

> >

> > Christie Carlo, DVM, CCRT

> >

> >

>