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View Full Version : Transcription of Selected Speaker Notes from AVMA - Dr. Dewey



Pat
14th August 2010, 05:23 AM
Have finally transcribed selected speaker notes verbatim. Complete speaker notes consist of three and a half typed pages. I'll follow with some of my notes from the session. Then I'll do the same for Dr. Shores' session. Glad I'm a good typist!

Pat


Selected verbatim text from Dr. Dewey’s speaker notes follows. I’ll put parentheses around my paraphrasing of his notes within the body. Multiple periods (…….) indicate that I have omitted some text. I have attempted to report the most important points while not violating copyright. When he uses ( ) I have substituted commas in order that anything in parentheses is my paraphrasing.

“Although only recently described in dogs, this is a very common neurologic disorder in this species…..almost exclusive to small breed dogs….with the CKCS being the most over-represented. The problem in the CKCS breed can be aptly described as a genetic crisis with an estimate of up to 95% of the population having some form of the disorder.”

“There is recent evidence that CM involves a malformation of the entire skull with the intracranial volume being too small to accommodate the intracranial contents. The vast majority of dogs with CM have SM, usually in the cervical spinal cord…..progressive alterations in pressure dynamics between the intracranial and spinal compartments are believed to be responsible for the development of clinical signs of CM/SM.”

“The intramedullary pulse pressure theory is currently the most accepted explanation for the formation of SM cavities in CM/SM…..(then he explains “Venturi effect” with distension, cavity formation, and filling of syrinx with “extracellular fluid” and the “suction effect.”)

“The typical age range at presentation appears to have changed over time, with many dogs developing clinical signs within the first year of life……most dogs present by the time they are 4 years old….dogs that are presented at less than 2 often have more severe clinical signs than older dogs….we have seen an increasing number of younger patients less than one year of age….whether this trend reflects an increasing severity of the disorder with subsequent generations, increased awareness of the veterinary community and hence earlier diagnosis, or a combination of these two factors is unknown.”

(He goes on to describe symptoms – nothing that we haven’t heard before.) “It is important to realize that, especially in the CKCS breed, other conditions may account for some of the clinical signs.” (Goes on to describe PSOM, idiopathic epilepsy, congenital deafness, disk extrusion, inflammatory brain disease – all in CKCS.) “….it may be difficult to discern if the CM/SM is the main problem, contributory, or an incidental finding.”

(He goes on to describe MRI and MRI findings. Nothing new.) “Recently, the width of cervical syrinxes as measured on axial MR images was positively correlated with presence of pain in CKCS dogs with CM/SM.”

“Treatment of CM/SM can be divided into medical and surgical therapy.” (He then reports on human surgical treatment and success/failure rates.) “Medical therapy for dogs with CM/SM generally falls into three categories: analgesic drugs, drugs that decrease CSF production, and corticosteroid therapy.” (Talks about gabapentin and pregabalin….they are using pregabalin more now….it has a longer half-life…7 hrs versus 3-4 hrs and appears to be more potent….says he’s had success with tramadol…..talks about CSF reducing drugs – says all information is anecdotal….said during his talk when I asked that he doesn’t think CSF reducing drugs actually do anything….goes on to cover corticosteroids….says dose should be moved to every other day therapy within a month if at all possible….I certainly agree with that!)

“The preferred surgical procedure for treatment of CM/SM in dogs is FMD. However, surgical success in dogs appears to be less predictable than that reported for people. In one report, the success rate, resolved or improved, was 81.25%. Unfortunately, there was a 25% re-operative rate due to scar tissue formation in this study. This report also found an inverse relationship between the length of time clinical signs were present prior to surgical intervention and the extent of post-operative improvement. In another report, the ultimate surgical failure for FMD in CKCS dogs was near 50% with long-term, >1 year, follow-up. In most cases, clinical signs of pain are routinely relieved with surgery, but scratching activity tends to persist.” (Then he describes his titanium mesh cranioplasty.) “So far, the author and colleagues have operated over (sic) 100 dogs with this procedure. Although results are preliminary, the cranioplasty procedure appears to have substantially decreased the re-operation rate for this disorder in dogs. There is recent evidence that the malformation in CKCS dogs is not restricted to the caudal fossa, and that the disease may represent a relative volume deficiency of the entire intracranial compartment. If this is correct, part of the reason for surgical failure in these dogs may be due to inadequate decompression with a suboccipital approach.”

“There is little information regarding the prognosis for CM/SM in dogs. Most dogs with CM/SM will respond favorably to medical therapy, although in many cases this response is temporary. In one group of 10 CM/SM dogs treated medically, 5 dogs (50%) were euthanized within 2-3 years due to disease progression and diminished responsiveness to therapy. In another report, 5 of 14 dogs, 36%, with the disorder treated medically were eventually euthanized due to disease progression.” (note from Pat – these studies obviously have a TINY number of participants) “Although the surgical success rate is generally favorable for CM/SM in dogs in the short-term, the recurrence rate due to excessive post-operative scar tissue formation is unacceptably high. Hopefully, refinements in surgical technique, such as cranioplasty, will ameliorate this problem. In general, the overall prognosis for CM/SM in dogs is guarded to good for sustained improvement of clinical signs.”

------------------------------------------------------

My personal notes from his session:

15 attendees, including myself.

40% of CM/SM dogs have cerebellar herniation.

He suspects CM/SM genes were in the longer-muzzled dogs used as foundation stock in CKCS.

He reported a sweet story about a dog that was going to be euthanized by owner that he took home. Didn’t tell what happened or how dog is now.

Says new theory is that entire skull is too small, not just the back of skull. Global squishing of the brain.

70-95% of CKCS are affected. 40% asymptomatic. Can be a devastating disorder.

Syrinx usually starts at C2.

Screening tools – BAER may be too sensitive. Working on thermography. “You have a Cavalier, you have CM.” We need a screening test that will tell if dog is symptomatic. “You have two cups of coffee before you do surgery….not one and not three.”

Old theory – Assume fluid CSF; water hammer/suck effect; perivascular space, piston, slosh.

New theory – Not true (that it’s CSF fluid); intramedulliary (sp?) pulse pressure; venturi effect, vascular, probably interstitial fluid, not CSF, goes through constriction at C-2, pull venturi, extra-cellular fluid. Less of a reason to use proton pump inhibitor or furosemide (I raised my hand and asked that question); don’t think they work very well anyway.

Described “Beezer Squeezer” (named after a grade school teacher he had) – asymptomatic dogs are not really asymptomatic because they will scream if you pinch the back of the neck hard and pinch the skull hard right above zygomatic arch. (Note from Pat – don’t try this at home. Dr. Shores said the same thing when I told him what Dr. Dewey said about this. Of course I rushed home and started smishing my two Cavaliers’ heads and necks but I had no idea exactly where or how hard to squeeze. My 8 year old Cavalier seemed to flinch, and I lost my nerve and stopped as I was afraid to know. My 1 year old looked at me like I was nuts which encouraged me to squeeze harder. No reaction. I probably should not be reporting this, but I am. Karlin can remove or not.)

Went on to discuss strabismus, scoliosis, torticolis, now seeing younger dogs. No thoracolumbar syrinx present without cervical syrinx. T2 weighted mid-saggital view, CT scan. Rule out concurrent brain disorders. Lyrica probably better than gabapentin. Half life 7 hrs versus 3-4 hours. ½ dose for cats (cats? Cats have CM/SM???? Edited to add that he was probably just saying that they also use these drugs for various disorders in cats) Medical therapy successful short term. 50% euthanized after two years. 36% euthanized after 1.7 yrs. 80% surgeries are successful; 25-50% relapse – scar tissue. Titanium mesh cranioplasty. Use titanium so that you can do future MRIs. Results – improvement similar. Stay in hospital longer. 7% re-operation rate; plate loosened, scar tissue. 80% improvement with some medication. Occasional secondary lesions. Shunting makes little sense. Wider decompression might not be crazy, now that we know it is a global skull problem.

Future direction – wider decompression, other concurrent malformation. Supratentorial (sp?) decompression in addition to FMD. (He mimed cutting out a hole in the top of the skull. Made the hair on my arms stand up in reaction to that plus FMD!!!) He uses glue – no staples, no sutures.

End of notes. Took two hours to transcribe this. Not sure if I’ll do Dr. Shores tonight.

Bet
14th August 2010, 02:07 PM
Pat,

Thanks so much for this, am I right in thinking that Dr Dewey mentioned that CKCS is the most over- represented Breed with this Problem,and that it it is a Genetic Crisis for Cavaliers and that up to 95 % of the Cavalier Population have some form of SM.

I think Dr Dewey also said that there is a New Theory ,that the Cavaliers' Skull is too Small,not just the Back of the Skull.

Could this possibly link in with the Cavaliers' Skulls being Bred Smaller than they were 20 years ago.

For me this is Depressing Information about the Cavaliers' SM Problem.

Will there be now Many Cavalier Carriers with the SM Gene/Genes, as well as many Cavalier Carriers with the MVD Gene/Genes/

Bet

Karlin
14th August 2010, 02:45 PM
Thank you so much for posting this, Pat. There is so much here–I want to take some time to digest it. Some is old, some is new. I really think a broader comparison of treatment methods needs to be done–Clare herself noted she was taking a small cluster of dogs for an examination of post treatment progression, and this has now become an argument for doing surgery… yet I know Clare herself is far more conservative about proceeding with surgery.

One thing I find quite interesting is that 7% figure for plates and screws coming loose–that's a pretty significant number. Also very interesting, his comments on doing a wider decompression.

Anyway lots to think about. One idea you might want to consider is voice software! I am using it now to post this message. I write all my stories for work using it, and I can tell you one way in which it is worth every cent is when you are transcribing notes because you can just lean back in your chair, put your feet up on the desk and read them! A small amount of cleanup work needs to be done but you can transcribe something amazingly fast and it's actually fun rather than tedious. The Dragon products for PCs are excellent–I use MacSpeech, which uses the Dragon speech engine. I would say it is about 98% accurate but you need a fairly decent computer (something sold within the last few years that will have reasonable chip speed and memory).

Pat
14th August 2010, 05:45 PM
One thing I find quite interesting is that 7% figure for plates and screws coming loose–that's a pretty significant number. Also very interesting, his comments on doing a wider decompression.

I think that what he actually said is that there is a 7% re-operation rate - for various reasons including the mesh becoming loose and shifting and scar tissue and possibly other reasons that he didn't mention. So I don't think we can assume that 7% of the cases have screws coming loose. (Gee, that gives a whole new meaning to that phrase "he has a screw coming loose.")

His comments on wider decompression have opened a whole new world of thought for me. It sounds horrific and incredibly sad to me to think that this defect is so serious that we have to decompress more than one area of the skull to achieve a reasonable level of comfort for these sweet dogs. Some time back I ridiculed what I thought was that incredibly stupid "exploding brains" comment. At AVMA it occurred to me that this might not be the fantasy that I assumed it to be.

My personal belief is that surgery is in its infancy and that ten, fifteen years out it may be routine and different.

Also, American (mostly male, highly intelligent, driven to succeed) neurologists like to do surgery (I'm not saying they are wrong; I have no idea) - we are action-oriented, creative problem-solving people (and I am a female!). As you'll see in my Shores report, he said that "this is not a medically managed disease, it's a surgically managed disease." And it makes sense that you can't "fix" a squished brain without relieving the pressure.

But we have other aspects that merit careful consideration. As example, I've always said that I would never do valve replacement surgery (if it were routinely available) on any of mine with MVD for multiple reasons - including the trauma of open-heart surgery needed at a time when the dog has a good quality of life. (To be successful, valve replacement surgery must be done before the heart is significantly damaged.) Also, we've come a very long way in improving medical management of MVD. My caveat is that I've learned never to say "never" so my views on valve replacement surgery could change in ten years.

Pat

RodRussell
14th August 2010, 05:49 PM
Thanks, very much, Pat. There is a lot in his notes this is not what I would call "Breaking News". He is re-hashing the last couple of years' worth of research papers. But his audience, for the most part, would be general practititioners, and they need to be brought up to date on what has been reported by others.

He does show how what has been published recently can have future consequences. For instance, he said:


Says new theory is that entire skull is too small, not just the back of skull. Global squishing of the brain.

... Wider decompression might not be crazy, now that we know it is a global skull problem.

Future direction – wider decompression, other concurrent malformation. Supratentorial (sp?) decompression in addition to FMD. (He mimed cutting out a hole in the top of the skull. Made the hair on my arms stand up in reaction to that plus FMD!!!) He uses glue – no staples, no sutures.

We know about the recently reported theory that:

"It is hypothesised that through the miniaturisation process of other small dogs, both the cranium and brain are proportionately smaller but in CKCS only the cranium has reduced in volume, hence why there is a higher incidence of CM in CKCS than other small breeds. Cavalier King Charles spaniels also had a greater percentage of their cranial fossa filled with parenchyma (cranial fossa parenchyma percentage) compared with small breeds and Labradors which had a similar percentage. Overcrowding in CKCS might therefore occur due to a mismatch in volumes in both the caudal fossa and cranial fossa of the skull, suggesting the cranial fossa is also involved in the pathophysiology of CM."
--Comparison of cerebral cranium volumes between cavalier King Charles spaniels with Chiari-like malformation, small breed dogs and Labradors. H. R. Cross, R. Cappello, and C. Rusbridge. J Small Anim. Pract. 2009 Aug; 50 ( 8 ) : 399-405.

Perhaps his suggestion of wider decompression is a result of this report. I don't even want to think about how to protect a wider hole in the skull.



He suspects CM/SM genes were in the longer-muzzled dogs used as foundation stock in CKCS.

I'd love to know more about this suspicion. I think most of us have assumed it is the snub-nosed ancestors who where the culprits.


Old theory – Assume fluid CSF; water hammer/suck effect; perivascular space, piston, slosh.

New theory – Not true (that it’s CSF fluid); intramedulliary (sp?) pulse pressure; venturi effect, vascular, probably interstitial fluid, not CSF, goes through constriction at C-2, pull venturi, extra-cellular fluid. Less of a reason to use proton pump inhibitor or furosemide (I raised my hand and asked that question); don’t think they work very well anyway.

What's up with this??? I may be missing the nuances in recent reports, but they appear to me to confirm the major role of CSF and the piston theory. For instance:

"Obstruction to flow at the foramen magnum is common in Cavalier King Charles Spaniels and CSF flow pattern and velocity are related to the presence of syringomyelia."
--Characteristics of Cerebrospinal Fluid Flow in Cavalier King Charles Spaniels Analyzed Using Phase Velocity Cine Magnetic Resonance Imaging. Sofia Cerda-Gonzalez, Natasha J. Olby, Richard Broadstone, Susan Mccullough, Jason A. Osborne. Vet. Rad. & Ultrasound, Sep/Oct 2009, 50(5):467-476.

and

"The association between ventricle and syrinx dimensions supports the theory that SM development is the result of altered cerebrospinal fluid dynamics."
--Relationship of brain parenchyma within the caudal cranial fossa and ventricle size to syringomyelia in cavalier King Charles spaniels. C. J. Driver, C. Rusbridge, H. R. Cross, I. McGonnell, and H. A. Volk. J Small Anim. Pract.; July 2010; 51(7):382-386.


No thoracolumbar syrinx present without cervical syrinx.

This supports the value of the mini-scan.


Titanium mesh cranioplasty. ... 7% re-operation rate; plate loosened, scar tissue. 80% improvement with some medication. Occasional secondary lesions.

Only 7% sounds pretty good to me.


Shunting makes little sense.

Geoff Skerritt has been performing shuntings. Does he still do this?

Pat
14th August 2010, 06:15 PM
am I right in thinking that Dr Dewey mentioned that CKCS is the most over- represented Breed with this Problem,and that it it is a Genetic Crisis for Cavaliers and that up to 95 % of the Cavalier Population have some form of SM.

I think Dr Dewey also said that there is a New Theory ,that the Cavaliers' Skull is too Small,not just the Back of the Skull.

Could this possibly link in with the Cavaliers' Skulls being Bred Smaller than they were 20 years ago.

Will there be now Many Cavalier Carriers with the SM Gene/Genes, as well as many Cavalier Carriers with the MVD Gene/Genes/

Be sure to read all the info in total carefully rather than picking out one or two comments. His written speaker notes said that up to 95% of Cavaliers have Chiari-like Malformation. He said to us in his verbal presentation that 70-95% of CKCS are affected. 40% asymptomatic. My understanding is that it's a big number, but I wouldn't try to pin down an exact figure. And we don't have to pin down an exact figure to be motivated enough to work on this problem. So I'd not like to see arguments in various places on the exact figure.

Yes, Dr. Dewey and Dr. Shores both said that there is overall global compression of the brain. My understanding is that they both believe that the genes have always been in the breed and that there are various reasons for the current situation - genes expressing themselves in more serious presentation (widespread breeding of certain Cavaliers that we didn't know had a particularly "bad" combination of the genes responsible) and wider recognition and understanding of the problem so more frequent and accurate diagnosis. Dr. Dewey specifically mentioned that he thought the genes were in the longer-muzzled dogs that were foundation stock.

I personally believe (and this is a very simplistic statement from a person who does not have a deep understanding of genetics) that every Cavalier carries genes for CM and for MVD and the expression and severity of the diseases is controlled by the individual combination of genes along with some environmental triggers.

Pat

Karlin
14th August 2010, 06:28 PM
Pat, thanks for the clarification on the 7%–much appreciated!

Rod, I asked Clare about that comment on the long muzzled dogs, and she wouldn't agree with that perspective. I am not sure if that is because of the point they are at with the genome research, but I would guess it would be connected to the current body of work coming from several breeds that seems to indicate breeding for smaller dogs and shorter muzzles seems to affect the skull area end how the brain sits in the skull. There is also some work from Dr. Marino on how changes to the front of the skull affects other areas of the skull. This is always the frustration of reading a paper or a talk–it makes you want to ask more questions than are answered!


He is re-hashing the last couple of years' worth of research papers. But his audience, for the most part, would be general practititioners, and they need to be brought up to date on what has been reported by others.

Yes, I agree and wouldn't have meant to indicate from any comments I made that this wouldn't have been exactly what needed to be done in this kind of talk. What is depressing is that there seems to be so little knowledge of the condition, the research, and how fortunate the opportunity was at that conference to hear these leading researchers and practitioners speak about this increasingly widespread condition. It really does not speak much to vets staying on top of current developments in their field if they haven't been aware of this issue, especially with Cavaliers shooting up the breed popularity list done annually by the AKC.

One thing is for sure–the low attendance by US vets gives the lie to some who have insisted that vets all know about SM these days, overdiagnose and are constantly referring dogs to neurologists because they think they have SM when actually they have something else. I don't know of a single neurologist who gets a shower of referrals from vets for this condition, not in the UK and not in the US. And needless to say, there also is not a long queue of pet owners and breeders forming who thought their dog had SM and find that it does not. If there were a general level of awareness about this condition, the sessions would have been full of vets wanting to learn more at the very least about what to look for before referring a dog to a neurologist. it really makes me so exasperated that so many of this breed are going to suffer because their vets have no idea what they're looking at and keep prescribing for allergies and ear mites and slipped discs. :( Too many suffer too long already because of this, and too many reach a point where they get beyond having the option of having the surgery, if that were to have been a consideration.

The Irish Medical Journal carried an article about SM in Cavaliers about 18 months ago and that probably did more to raise awareness than anything else. I am totally sympathetic to the fact that vets are general practitioners but at the same time it does not bode well for the breed getting the care it needs when it does have this horrible problem.

Rod, thanks for pointing out the connection between the location of syrinxes and the usefulness of the mini scan -- it certainly does validate that this cost-saving approach still gives excellent results for breeders looking for grades on their dogs.

Geoff Skerritt does still do shunts, but as of two years ago he was doing a lot of decompressions as well, which was a big shift in perspective for him as he never did them before -- as far as I know. When he did Leo's last MRI, he told me that if I wanted to opt for surgery, a shunt would not be of help, but the decompression likely would be.

Bet
14th August 2010, 06:50 PM
Thanks, very much, Pat. There is a lot in his notes this is not what I would call "Breaking News". He is re-hashing the last couple of years' worth of research papers. But his audience, for the most part, would be general practititioners, and they need to be brought up to date on what has been reported by others.

He does show how what has been published recently can have future conesquences. For instance, he said:



We know about the recently reported theory that:

"It is hypothesised that through the miniaturisation process of other small dogs, both the cranium and brain are proportionately smaller but in CKCS only the cranium has reduced in volume, hence why there is a higher incidence of CM in CKCS than other small breeds. Cavalier King Charles spaniels also had a greater percentage of their cranial fossa filled with parenchyma (cranial fossa parenchyma percentage) compared with small breeds and Labradors which had a similar percentage. Overcrowding in CKCS might therefore occur due to a mismatch in volumes in both the caudal fossa and cranial fossa of the skull, suggesting the cranial fossa is also involved in the pathophysiology of CM."
--Comparison of cerebral cranium volumes between cavalier King Charles spaniels with Chiari-like malformation, small breed dogs and Labradors. H. R. Cross, R. Cappello, and C. Rusbridge. J Small Anim. Pract. 2009 Aug; 50(8):399-405.

Perhaps his suggestion of wider decompression is a result of this report. I don't even want to think about how to protect a wider hole in the skull.




I'd love to know more about this suspicion. I think most of us have assumed it is the snub-nosed ancestors who where the culprits.



What's up with this??? I may be missing the nuances in recent reports, but they appear to me to confirm the major role of CSF and the piston theory. For instance:

"Obstruction to flow at the foramen magnum is common in Cavalier King Charles Spaniels and CSF flow pattern and velocity are related to the presence of syringomyelia."
--Characteristics of Cerebrospinal Fluid Flow in Cavalier King Charles Spaniels Analyzed Using Phase Velocity Cine Magnetic Resonance Imaging. Sofia Cerda-Gonzalez, Natasha J. Olby, Richard Broadstone, Susan Mccullough, Jason A. Osborne. Vet. Rad. & Ultrasound, Sep/Oct 2009, 50(5):467-476.

and

"The association between ventricle and syrinx dimensions supports the theory that SM development is the result of altered cerebrospinal fluid dynamics."
--Relationship of brain parenchyma within the caudal cranial fossa and ventricle size to syringomyelia in cavalier King Charles spaniels. C. J. Driver, C. Rusbridge, H. R. Cross, I. McGonnell, and H. A. Volk. J Small Anim. Pract.; July 2010; 51(7):382-386.



This supports the value of the mini-scan.



Only 7% sounds pretty good to me.



Geoff Skerritt has been performing shuntings. Does he still do this?

Transcription of Selected Speaker Notes from AVMA -Dr Dewey


Could I just mention that what I cannot understand is,if the if the Cavaliers' CM/SM Problem came from Ancestors when the Cavalier Breed originated, in the late 1920's and 1930's, how is it that over all that time the Cavaliers were not affected with the Symptoms of SM that is afflicting them to-day.

I have mentioned before about collecting the Ages of Long Lived Cavaliers and as a result of this have spoken on the Phone to many Cavalier Breeders ,some who were even around in the 1950's ,and not once was it ever mentioned that the Cavaliers were showing the Distressing Symptoms that the Cavaliers are showing to-day who have this Horrible Disease.

The Heart Trouble ,yes, but not any other Weird Disease.

O.K, some might say that the Vets only had the use of MRI Scanners since I believe from the mid 1990's, and that there could have been Cavaliers with SM since the 1930's,and it would not have been known about, but why were those Cavaliers not being affected to the extent that they are being to-day by SM.

What has happened to bring it to the Fore in the Cavalier Breed in the Past 20 or so years,?

There was Half Brother to Half Sister matings taking place in Cavaliers in the early 1980's,and that was the time when it was beginning to be noticed that the Cavalers were being Bred with Smaller Heads.

Is this linked to their SM Problem?

Did the SM Gene/Genes meet up around then and cause SM.?

I just don't know .

But the questioned has to be asked , why was the SM Problem as wide-spread as it is in the Breed as it is to-day and was not giving cause for concern in the past 70 years.

Bet

Pat
14th August 2010, 07:07 PM
Couple of quick comments:

I, too, was quite disappointed with the number of attendees in both sessions. But in defense of GP vets, it was a huge struggle even for me to select which sessions to attend (and I attended 25 total in three days). If there is a session by the top liver guru or top kidney guru in the country, you're going to want to attend that one because of the huge potential that you'll need to know that info for a large population of your practice. And remember there were sessions on dogs AND cats, and some sessions covered diseases for both. For almost every time slot, there was more than one session that I wanted to attend. I'm kicking myself because I was not able to attend even one GI session, and now I have a personal need to know about differential diagnoses of chronic diarrhea. But they had to run multiple concurrent sessions or the convention would have lasted weeks instead of days. Hopefully the attendees are reading all of the speaker notes (as I am) and are sharing them with others in their practice. But we definitely picked up more gems of wisdom if we heard the speaker as well as read his/her notes.

Rod - I owe you some private correspondence. I'm not ignoring you nor have I forgotten - work has been brutal. I'm about to go into office to work 8 hrs today and about the same hours tomorrow. I'll write you later today.
Yes, I agree with your "not much breaking news" comment although there were a few things that were new to me. In contrast, almost everything he said was "breaking news" to the GP vet attendees. I've tried really hard to be an accurate reporter and not put my own interpretation on the info.

Rod, you said "I don't even want to think about how to protect a wider hole in the skull." Yeah, no sh___, that was why I said the hair on my arms stood up when he discussed wider decompression.

I can't comment on the syrinx formation theories - I was writing furiously and trying to understand the physics (not my area of knowledge, I was an English/psychology major) but I was interested because of the potential non-effectiveness of some of the drugs used. And indeed, I was bold enough to interrupt him and ask the question about the drugs. So my notes consist of those key words without totally understanding how they fit together and what they mean.

Pat

Pat
14th August 2010, 07:35 PM
Bet, my very first Cavalier was born in 1982 - almost 30 years ago.

She could not be walked on a lead at all, ever - she would air-scratch and bunny hop continuously. It got much worse as she got older. (She lived to be 14 1/2.) I thought it was a weird personality quirk. I have a huge fenced yard, so it was rarely necessary to walk her on a lead, and we just lived with that quirk. If she had pain or other symptoms, I wasn't smart enough to recognize it. If she were in my home today, I'd be doing far more to figure out what was going on with her. I would have her MRI'd. We didn't have a clue back then. Most of us with long histories in the breed can report similar incidents now in hindsight. I never reported it to anyone at the time, as I thought it had no meaning.

If my girl's genes were passed down to our current Cavaliers, mixed in with those genes from other similar Cavaliers that also had subtle or unexpressed symptoms, could not those subsequent gene combinations have resulted in Cavaliers with more "concentrated" and more serious combinations of "bad" genes? And these Cavaliers have more serious symptoms than my girl with the quirky behavior? And add in the influence of some popular sires that unfortunately had a more serious mix of "bad" genes? My suspicion is that this is what happened to bring us where we are today.

Pat

RodRussell
14th August 2010, 08:16 PM
Pat, I agree with Karlin about using Dragon to dictate your transcriptions. It is not perfect, but it seems to be updated about once a year, and it really does work nearly all of the time. However, I defy Dragon to get "intramedulliary" right.

Blondiemonster
14th August 2010, 08:20 PM
Thank you so much for this info! I'm a newbie but learn new stuff on this SM forum every day....

Pat
14th August 2010, 08:39 PM
Pat, I agree with Karlin about using Dragon to dictate your transcriptions. It is not perfect, but it seems to be updated about once a year, and it really does work nearly all of the time. However, I defy Dragon to get "intramedulliary" right.

Let's see........

1. Need new roof - $5k
2. Currently washing dishes by hand - new dishwasher $1k
3. A/C in both cars not working well - $2k to replace both compressors
4. Really want a digital refractometer to measure canine USG at home - $300

List could go on and on......Voice recognition software to help with hobby - not gonna happen!

Pat

anniemac
14th August 2010, 09:30 PM
Thanks Pat for this information. I am glad there are people who are relaying this information because I still have so much to learn. I am impressed with your note taking. Since Ella was diagnosed, Claire Rusbridge has been a celebrity along with Dr. Shores, Dr. Dewey and Dr. Marino. Hearing Dr. Dewey and Dr. Marino speak would have been great. I think of anyone who actually gets to talk to these highly intellegent people as being so lucky. I am not the best with explaining things but I am interested in all of this information and thanks for telling it to people like me, who could not attend. Also sometimes reading journals and notes from neurologists can be difficult for someone like me so I am glad to know I can ask questions and get a better understanding of things.

Thank you

PS. I really wanted to go to LIVS for Ella's surgery at first from all of the things I read about Dr. Dewey but distance, work etc. was not an option. I know one thing someone told me that I could do was to educate vets. Seeing from the attendees, that might be a point. More vets should be familiar with this I guess.

Kate H
14th August 2010, 11:07 PM
Thanks very much for the notes, Pat. I was particularly interested in Dr Dewey's poor opinion of the value of CSF inhibitors such as furosemide. My Oliver has always been mildly light phobic, and had a really nasty episode last summer of pain in his eyes, which the neurologist attributed to his dilated ventricles pressing on the nerves behind the eyes. He has been on 40mg of furosemide a day for about a year and there is a noticeable reduction in his light sensitivity, and in spite of a lot of strong sunlight this year he hasn't had another bad episode (though I am more careful to keep him out of strong light) - this due, presumably, to a reduction in the fluid in his ventricles. I'm hoping to have him (mini)scanned again later this year, partly to see what his small syrinx is doing, but mainly to see whether there has been a reduction in the CSF in his ventricles. For him at least, CSF reduction seems to be effective.

Kate, Oliver and Aled

RodRussell
15th August 2010, 01:54 AM
Let's see........

... 4. Really want a digital refractometer to measure canine USG at home - $300

Geez, you don't have one of those yet?

lovecavaliers
15th August 2010, 03:13 AM
Thanks Pat for providing this information, I can't wait to read your transciption of Dr. Shores' talk.
Thank you again for transcribing, you provided invaluable information for the many pet owners like myself.

Pat
15th August 2010, 03:22 AM
Geez, you don't have one of those yet?

Nope, and here is a link.

http://secure.sciencecompany.com/Urine-Specific-Gravity-Refractometer-PAL-10-S-P14643C688.aspx

Kidney failure can first be detected by a first morning urine specific gravity reading. Number should be above 1.030 for normal kidney functioning in canines. Problems are detected in the urine long before they are detected in blood chemistry or by symptoms. Having one of these at home would be a huge benefit, esp. in a home full of seniors!

Pat

Cathy T
15th August 2010, 04:33 AM
Mind boggling information for a pretty naive pet owner!! I am so grateful for this board and the knowledgeable people we can turn to for help when we need it....outside of our vets. I was impressed with my vet's knowledge of SM (a new vet I'm seeing) and his comment "I just wonder how many Cavaliers I have treated in the past 25 years for alleregies and ear infections having no idea this is what was going on". Completely understand what you said about the number of topics to choose from and which would be the most advantageous for vets to attend to help the most number of clients. Thankfully you chose this one :)

Bet
15th August 2010, 11:04 AM
Bet, my very first Cavalier was born in 1982 - almost 30 years ago.

She could not be walked on a lead at all, ever - she would air-scratch and bunny hop continuously. It got much worse as she got older. (She lived to be 14 1/2.) I thought it was a weird personality quirk. I have a huge fenced yard, so it was rarely necessary to walk her on a lead, and we just lived with that quirk. If she had pain or other symptoms, I wasn't smart enough to recognize it. If she were in my home today, I'd be doing far more to figure out what was going on with her. I would have her MRI'd. We didn't have a clue back then. Most of us with long histories in the breed can report similar incidents now in hindsight. I never reported it to anyone at the time, as I thought it had no meaning.

If my girl's genes were passed down to our current Cavaliers, mixed in with those genes from other similar Cavaliers that also had subtle or unexpressed symptoms, could not those subsequent gene combinations have resulted in Cavaliers with more "concentrated" and more serious combinations of "bad" genes? And these Cavaliers have more serious symptoms than my girl with the quirky behavior? And add in the influence of some popular sires that unfortunately had a more serious mix of "bad" genes? My suspicion is that this is what happened to bring us where we are today.

Pat


Transcription of Selected Speaker Notes from AVMA-Dr Dewey

Thanks Pat for commenting on my Post, if I could mention that the Cavalier you mentioned is just about the time when the In-Breeding in some Cavaliers was taking place here in Britain, Half Brother to Half Sister Matings, and the Cavalier Heads were beginnimg to be getting Bred Smaller.

This close Breeding that I mentioned was on top of all the In-Breeding that had taken place before in the Cavalier Breed ,even in the 1970's there was still Mother to Son and Father to Daughter Matings happening. The SM Researchers are convinced that In-Breeding is Linked to SM

So maybe by the early 1980's the SM Genes had come to-gether , but I just can't understand why the Cavalier Breeders that I spoke with as far back as the 1950's never mentioned about seeing this Problem, it was'nt just the Top Cavalier Breeders I was speaking to, but ordinary Cavalier Pet Owners like my-self when I was collecting the ages of Long Lived Cavaliers.That is all I can go on,

This is the difference between the Cavaliers ' MVD and SM Problems, there is Positive Evidence about the MVD trouble in the Cavalier Breed from those days , there were Cavaliers dying between 7-8 years of age from Heart Trouble, but no Positive Evidence about SM.

But the Cavaliers are where they are now with this Insidious Disease, what has really shook me is to know that there are Nuts being used to keep what-ever in Place, did I read right ,that some can become loose.

The sooner the SM Gene/Genes are found the better.

Bet

daffymum
15th August 2010, 05:32 PM
Thank you so much Pat for this notes, It helped me to understand the disease more and keep me informed with the current up to date situation. I check the forum every day hoping for a major breakthrough in medical or surgical management of this dreadful disease.

I have been thinking about surgery for my Daffy (5 years old Cavalier)and I will discuss with Clare when I see her in September.

ppotterfield
17th August 2010, 05:50 PM
Thank you, Pat, for sharing. Your time and patience in typing up your notes has been a help to many of us.