-------- Original Message --------
Date: Mon, 26 Jun 2006
Hello Dr. Clemmons:
The quote below is from your 1998 Report found on the Internet:
"Recently, we have treated one of our long-standing patients with a new drug used for the treatment of rheumatoid arthritis." The drug is not identified.
My 11 ½ year old male GSD has been getting N-Acetylcysteine, Aminocaproic acid and Antiox-QCB for the past 30 months under the diagnosis of DM by Dr. Beverly Brimacomb in Highland City, Florida. Our dog went down over a day’s time in his worst effect left rear leg on June 1, 2006. Unfortunately, his progression down has continued over the past 25 days until he is now not able to use either of his rear legs. The prescribed treatment above does not now seem to have any effect in slowing this progression. He is also being cared for by Dr. Xie at U.F. in the area of TCVM on a long term basis and has been seen by Dr. Chrisman.
I would like to have the name of the drug you discussed in the above published report to give to Dr. Brimacomb so she can determine if we might try it on our dog as, more or less, a last resort to offer him some help.
Dr. Clemmons answer:
-------- Original Message --------
Subject: RE: Tigger
Date: Mon, 26 Jun 2006
From: R.M. Clemmons, DVM, PhD
Acute changes are not consistent with GSDM….
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. You can download a form and more information at http://neuro.vetmed.ufl.edu/DM_Flash_test_web/ and follow the instruction.
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.
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. So, 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 Teaching Hospital (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.
Best wishes for health and long life,
R.M. Clemmons, DVM, PhD
CAPT, IRC, USPHS
Associate Professor of Neurology & Neurosurgery
Certified in Veterinary Acupuncture
U. F. College of Veterinary Medicine
My response to his one line response:
-------- Response Message --------
Subject: Re: Tigger
Date: Mon, 26 Jun 2006
To: R.M. Clemmons, DVM, PhD
I assume you are very busy so I didn't want to complicate the previous e-mail with additional facts about our GSD but we did have your genetic Flash Test for DM in GSDs done on Tigger on 09-04-05. To all the surprise of the veterinarians associated with treating him, it unexpectedly came back with NEGATIVE results. Since his clinical signs have been so classic to DM, it was assumed that the test was done with laboratory error and could not be valid. Our veterinarian sees no sign of IVDD and says that any existence of spinal meoplasia would have shown up serious manner within the 30 months Tigger has had waxing and waning clinical symptoms of DM. All this leaves us with a dog now in weakening condition with the next step toward helping him unknown.
Also, as far as acute being atypical of GSDM progression: A possible reason is that on May 23, 2006 we were forced to do surgery on his left front foot to remove a painful deformed nail. We took great pains to make this event as stress free as possible and he did well for one week. On May 30, 2006, the day before he went down, he had acupuncture with electrical stimulation for an extended time. Also that day stitches were out of his surgery so three staples were put in without pre-numbing - a painful/stressful event. Any or all this could account for his acutely losing his walking ability the next day.
I would like to get that drug information so that Dr. Brimacomb can look into the specific matter of possible treatment. She is a very busy veterinarian and just doesn't have the time I have to take these steps.
We would appreciate any assistance you can give our veterinarian in this matter.
Note: This second e-mail remains unanswered to date: 08-02-06