WAS YOUR GSD TESTED WITH DR CLEMMONS DM FLASH TEST? - Page 1

If so, can you please let me know if your dog tested positive or negative, and if your dog subsequently went on to develop DM? Since it has been so many years, I am gathering information and data, in relation to those GSDS tested with the Flash Test. So far, the test has proved to be very accurate for our breed, from the data I have gathered, but I would like to hear from a wider audience. Thanks :) Some people have chosen to contact me privately, and I have just made a facebook page to reach those I have not been able to reach, thus far. You can PM me, post it here, or post it on the facebook page https://www.facebook.com/pages/DR-Clemmons-DM-Flash-Test-in-German-Shepherds-Results/1446771572288897

I had my male GSD tested in 2008 by Clemmons when the dog was 5.5 years old. The test came back negative. And although he has shown dome DN symptoms since then, he is now 12.5 years old, such as rear foot dragging, I do not think it is DM since he is still able to run the blinds in IPO and goes for a 2 mile walk every day and can go up and down stairs. If it is DM, it is certainly very mild. I have not had him retested but have had vets check his gaiting and basic diagnosis has been spinal arthritis, etc.

No way would this dog be walking or doing any activities if it was DM. Thank you for letting me know. I think follow up is as important as the testing, and enough time has gone by to begin gathering results. I appreciate your feedback :)

12.5 in dog years is over 100 in human years. 
how many 100 year old humans cannot walk?
while we like to attribute DM to many different symptoms, sometimes its disk problems, arthritis issues, or general old age. 
the only way to completely confirm DM is a necropsy after death. 

12 in dog years is not over 100 in human years. Depending on which age calculator you feel like using, it's anywhere from mid 60's to late 70's. Old, but not that old. 

could be cauda equina, tick disease, polymstosis, a tumor, even thyroid can cause hind end weakness.... There are many many things...the list goes on and on...

Marjorie, where can you get this test done?  I've had mixed results from OFA and Animal Genetics.  

Thanks

Judy

 

It cannot be done, anymore, Judy. The OFA DM DNA Test shut this test down, basically ran it out of business. I am just trying to gather data, since it has been such a long time since it was done. Many years have passed- enough to see if it stood the test of time. Thus far, I have found no errors.. That is probably because it tested for GSDM, not the DM of other breeds. It involved an allelle specific to GSDS, only.

12/6/2011

The web site at UF will be closed shortly, so the link may go bad. It will come back on an educational, commercial site a bit later. I still believe the web should be for free real education, but I guess I got outvoted! The rule is only that it be free and that it is still best to link. Here is what we tell people who inquire of us about GSDM...

Unfortunately, we cannot offer the DM Flash test at this time except for research purposes. We have included information about the test and our typical workup for informational purposes as the information is still correct. 

New information is that we may have a genetic test for the disease. We can run the test for people, knowing that it may be negative in a number of suspect cases, since up to 75% of those with clinical signs actually do not have GSDM. Your veterinarian can help you with this by collecting the blood and arranging to send it to us. We will provide the results within 2 weeks. We still feel it should not be the sole diagnostic run for the disease, but it may go a long way toward confirming the presence of GSDM.

The DM Flash test is not a good screening test for this reason…there are too many false positive results due to a high incidence of the change in the breed while only a limited (10-20%) of the positives get the disease. However, that said, it does say that the risk of developing GSDM is 12 times higher in dogs who are positive on the DM Flash test than in dogs who are negative. A negative test suggests there is a 99% chance the dog will not get GSDM. However, a positive test in normal dogs has only an 11% predictive value.

In dogs with clinical signs of possible DM, the DM Flash test is a good diagnostic test. It is 96% sensitive and 99% specific and is generally going to separate those who have GSDM from those who do not have it (only some other neurologic disease). It still does not replace other tests since there may be more than one disease, but it probably is sufficient to confirm the diagnosis of GSDM and move the patient to the “probably GSDM” category. What this means is that a positive DM Flash test means there is less than a 1% chance the dog does not have DM as part of the clinical picture, while a negative DM Flash test means that there is a 4% chance that the dog may still have GSDM even though the test was negative. With a negative result, only additional tests can be sure that GSDM is part of the disease process or whether another disease is more likely.

So, while 91% of the proportional risk of developing GSDM is accounted by having a positive DM Flash test (genetics accounts for most of the reason the patient gets GSDM). A positive test in a normal dog does not mean they will inevitably get GSDM; just that they are at a greater risk. A negative test means it is highly unlikely that the dog will get GSDM, but not impossible. That is about as good as any test. Those who test positive are the ones who should be watched and extra care taken with. We may ultimately find out what other factors influence the genetics to lead to GSDM and then we might be able to prevent the disease from happening. For now, all you can say is there is a risk of developing GSDM and that might be a reason to alter breeding, but only if other things are factored in as well.

Like families of MS patients, there is a risk that others might get MS because of increased genetic risk. In dogs other than German Shepherds, the DM Flash test may mean the same, but we do not have enough data to say that. As such, we would cautiously recommend that other diagnostics be performed in order to be sure the results are accurate. While we expect that the results of the DM Flash test to be similar in other breeds, only more numbers of patients and studies on randomly-sampled dogs from that breed will answer that question.

Thank you for taking the time to email us about our program on German Shepherd Dog Myelopathy (GSDM). We have studied this disease over the last 30 years and continue to do so. Our current program is unique and designed to improve the diagnosis of GSDM and offer a sensible treatment for GSDM based upon what we know of the underlying cause of the disease. Unfortunately, we cannot answer specific questions about patients that we have not seen. The Internet is not sufficient to establish a valid client-patient-veterinarian relationship. We have offered our web pages (http://neuro.vetmed.ufl.edu/neuro/DM_Web/DMofGS.htm) as a guide and educational resource for people who think their animal is affected with GSDM. There is a lot of mis-information on the Internet, we have tried to provide some sense to that. The information on our web site is what we can currently offer and recommend to those patients we have not seen. Our web site is where you can start. Yes, we have looked at many treatments for GSDM, but what is on the web site is what we have found to help most of the GSDM patients we see. Older versions of our information have been replicated at other sites on the Internet. Our pages are officially what we recommend and do. From our work and the genetic data available on GSDM, we believe the evidence says that GSDM is an animal model of Primary Progressive Multiple Sclerosis in human beings. So, at least, we think we know what GSDM is when we separate those who do have it from those who do not.

Part of our program is the diagnosis of the condition. Unfortunately, it is correct that the only current method to be absolutely sure is with a necropsy, which does not help patients before death. We have established criteria that help us make accurate diagnosis. I think that we do better than what has been reported by some authors. Only 25% of the patients enrolled in their study were found to have the disease. The complicating factors which confused the diagnosis in that study would have been found by our criteria. So, what do we do. Basically, they are routine clinical test, but applied in a specific sequence to help us find out all of the patient's problems. First, is the clinical examination. That includes looking at who the patient is. If the patient is a German Shepherd, then there is a higher probability that a chronic progressive spinal cord problem might be do to GSDM. If it is not a German Shepherd, it may have a myelopathy, but it may be from another cause. We are not sure that the disease in the Corgi or in the Boxer is related to the disease in the German Shepherd. On the other hand, we can distinguish the disease that Corgis, Boxers and Rhodesian Ridgebacks get from GSDM based upon genetic aspects that these breeds have that related to their form of DM. Since these diseases are genetically different, applying our treatment to these breeds may not do any good. The second criterion is based upon the EMG (electromyogram) which evaluates the muscle-nerve connection. The EMG and all peripheral tests of neuromuscular function are normal in uncomplicated GSDM. On the other hand, the spinal cord evoked potential evaluated over C1 is abnormal in GSDM. This indicates that there are problems in the white matter of the spinal cord. We also look at the difference between the cerebrospinal fluid (CSF) collected from the cisterna magnum and the lumbar cistern. The latter shows elevations of CSF protein without concurrent increases in CSF cell counts. While many of these proteins are inflammatory in nature, one of the ones that can be measured easily is CSF cholinesterase. The CSF cholinesterase is elevated in the lumbar CSF (above 300 IU/ml) in most cases. Unfortunately, this change is not specific for GSDM, only for inflammation (GSDM is one of the inflammatory disease of the spinal cord). Titers for infectious diseases are normal or, at least, do not indicate another disease process. Finally, we look at special imaging to evaluate the structure of the spinal column and whether there is evidence of spinal cord compression from some disease process. This does not rule-out GSDM, rather imaging rules-in complications. The former criteria are what help diagnose GSDM: the clinical picture, the EMG with spinal evoked potential, and the CSF analysis with cholinesterase. The imaging only looks for a surgical disease (or its absence). Depending upon the condition and clinical signs, we do myelography plus or minus CT scan or MRI scans to help us determine whether there is a local compressive disease.

Not every neurologist does the tests that we do. That might be why we have success, since we know better what we are treating and also whether to treat a surgical problem or not. On the other hand, there are other approaches to this disease and you will need to follow what is recommended by those who have seen your dog. You should, at least, see a neurologist and let them help you find out what they can for your dog. Remember that without the proper tests, it is a guess as to what is wrong. You can search for the closest neurologist at http://www.acvim.org/. 

The other part of our program is the treatment outlined on our web site. It includes exercise, diet, supplements and medications. Each of these has an impact upon health and upon the disease. The components of the treatment work together to reduce the progression of GSDM. They target the processes which we have uncovered as the causes of the pathologic changes we see. We have seen few side-effects (mostly GI upset) in the patients we diagnose and treat. There are things which can happen as rare occurrences when using any drug. If they complications resolve on stopping the drug and return on re-introduction, then it is probably drug related. If your veterinarians feel there is a problem, then the medications should be stopped until it is determined whether they are the cause or not. Many times it is discovered that some other disease is present rather than the medications. All of the medications have been used in dogs for many years (not just for treating GSDM) so they are not new. Only the application is new. N-acetylcysteine is the newest and we have used it for over 10 years. On the other hand, we do not like to use medications unless we know what we are treating. So, we do not treat without reaching a diagnosis. The 2 parts of our program, diagnosis and treatment, work together. We diagnose early and treat early, which is why we have success. In the past, most patients progressed to posterior paralysis in 3-6 months. This would progress to all 4 legs in another 3-6 months with death from brainstem failure (in those patients allowed to progress that far without intervention) 9-18 months from the first diagnosis of GSDM. That has changed now. In our hands, most GSDM patients will remain functional for 12 months, while many outlive their disease.

If dogs respond well to the therapy, they should continue on it potentially for life. However, if their condition is stable for several months (at least 6 months), then decreasing the medication (aminocaproic acid and acetylcysteine) to 2 twice a day on days given can be attempted. If this works as well as 3 times a day and they remain stable for another 6 months, then the dose can be reduced to daily. Some cases may be able to maintain with diet and supplements alone, but most cases will require continuous medication.

We apologize that we cannot help you more. Certainly, we are happy to see patients at the Veterinary Medical Center at the University of Florida (number below) by appointment. If that is not possible, then follow the course that makes sense to you and your veterinary team. They have seen your dog and know it far more than we can via the Internet. We hope that you receive the care and treatment that you need.

RM Clemmons, DVM, PhD, CVA, CVFT

Former CAPT, USPHSR

Aso Prof of Neurology & Neurosurgery

SACS/University of Florida

2015 SW 16th Ave

Gainesville, FL 32608

A friend had a young GSD with symptoms that suggested early onset DM. The Flash test was positive, the OFA test said he was a carrier. He later had extensive surgery for spinal issues and a hip replacement. He is now almost 9, doing well. When he dies I don't know if his owner will have a PM done to determine if he actually had DM or if the cauda equina  and the HD were the causes of all his early lameness.

Another friend had a male that was clinically diagnosed with DM by a veterinary school. The OFA tested him at risk, the Flash test negative. When he died she was so distraught that the last thing she wanted to do was have him autopsied, so add another ? to the mix. He was sired by a GSL that sired other GSD's with suspected DM and one confirmed at necropsy. As far as I know,  he himself was never tested, but all of his progeny on the OFA database were either carriers or at risk. Ditto for another frequently used ASL stud, not tested, no clear progeny out of maybe 10, 12 that were tested using the OFA scheme.

My own female tested a carrier - the OFA scheme- as did her sire. Her grandsire tested at risk and was eventually put down due to what appeared to be DM. I do not know if he was autopsied. For those reasons, after her DM status was known, she was bred to a clear. There were only 2 puppies, both tested carriers so they too are only bred to clears.

I don't think it's right for the breed to try to undermine any research of DM in the GSD.  If the Flash test were still available, I'd use that in addition to the OFA test. It's up to each breeder how they feel about testing for DM and how they use the results. Some won't do it, other will. Doesn't mean that either is right, wrong, more righteous or more ethical than the other.

Without necropsies, there can never  be a definitive answer to the accuracy of either of these tests. Most people are not going to have necropsies done. I haven't owned a GSD with suspected DM, but I did have a GSD that had cancer and chemo and by the time that ordeal was finished, I was so depressed that the last thing I'd have wanted was to have him autopsided. I suspect some owners of DM suspects feel the same.

Once again, consider having your GSD's DNA banked so it can be used in the future. They ask health questions on their applications form and then ask that owners notify them of any changes to the dog's health so their profiles can be updated and their DNA possislby used for future resarch on that particular disease. When one of my GSD's was banked, she was healthy. At 10 years she was diagnosed with metastic breast cancer, so that information was submitted and added to her health history. All it takes is a cheek swab or blood sample. Why not?

http://www.caninehealthinfo.org/chic_dnabankapp_main.pdf