06/23/2015
Just a reminder it is Myelopathy Season in the South
DEGENERATIVE MYELOPAHTY:
Degenerative Myelopathy (DM) was first described as a specific degenerative neurologic disease in 1973. Since then, much has been done to understand the processes involved in the disease and into the treatment of DM. Hopefully, this will help you understand the problem and to explain further the steps that can be taken to help dogs afflicted with DM.
The age at onset is 5 to 14 years, which corresponds to the third to sixth decades of human life. Although a few cases have been reported in other large breeds of dogs, the disease appears with relative frequency only in the German Shepherd breed, suggesting that there is a genetic predisposition for German Shepherd dogs (GSD) in developing DM. The work presented here and by others on the nature of DM has been performed in the German Shepherd breed. Care must be taken in extrapolating this information to other breeds of dogs. It is currently not known whether the exact condition exists in other breeds of dogs. Many dogs may experience a spinal cord disease (myelopathy) which is chronic and progressive (degenerative); but, unless they are caused by the same immune-related disease which characterizes DM of GSD, the treatments described herein may be ineffectual.
The gross pathologic examination of dogs with DM generally is not contributory toward the diagnosis. The striking features being the reduction of rear limb and caudal axial musculature. The microscopic neural tissue lesions consist of widespread demyelination of the spinal cord, with the greatest concentration of lesions in the thoracolumbar spinal cord region. In severely involved areas, there is also a reduced number of axons, an increased number of astroglial cells and an increased density of small vascular elements. In the thoracic spinal cord, nearly all funiculi are vacuolated. Similar lesions are occasionally seen scattered throughout the white matter of the brains from some dogs, as well. Many patients have evidence of plasma cell infiltrates in the kidneys on throughout the gastrointestinal tract, providing a hint to the underlying immune disorder causing DM.
I have studied this disease over the last 37 years and continue to do so. The 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. From that 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 the 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 where only 25% of the patients enrolled in the study were found to have the disease. The complicating factors which confused the diagnosis in that study would have been found by our diagnostic 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 due 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 and Boxers 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.
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.
TCM Diagnosis and Treatment:
From a TCVM perspective, GSDM and probably BM are wei syndromes. Most of the patients we evaluate are combined Qi and yin deficient. Of course, there is a spectrum and we, therefore, need to assess each patient to find their pattern. Dr. Xie’s formulas appear to help several; but, in general, acupuncture and herbs are palliative and designed to improve quality of life rather than to achieve a cure. Cures seem to put the diagnosis in question; whereas we do see dogs that outlive GSDM. If the standard TCVM therapies do not work, the formulas that I prefer to use in GSDM and BM patients (both diseases are closer from TCVM pattern diagnosis than Western diagnosis) are Hu Qian Tang and Di Huang Yin Zi Tang. These are available from Jing Tang.
Wei Zheng (flaccidity syndrome) in Western medicine is any disorder of the PNS (Peripheral Nervous System) that may cause weakness or numbness, such as MS (multiple sclerosis or spinal & muscular disorders). This leads of flaccidity of muscles, paralysis, hemiplegia, and muscular atrophy of the limbs. TCVM patterns include excess and deficiency causes, but those that we tend to see in DM patients are chronic deficiencies. The root cause of these problems lies in Kidney Jing deficiency, since the problems are now known to have a genetic basis (even though they take years to develop). Generally, the patterns recognized are:
1. Spleen/Kidney Qi Deficiency; 2) Qi & Yin Deficiency; and 3) Yin & Yang Deficiency. This is also the apparent order in which the signs progress to an extent as well.
Deficiency of Qi: Signs include muscular flaccidity or atrophy of the limbs with motor impairment, marked by lassitude, listlessness, short breath, weak voice, sweating on slight exertion, dizziness, palpitation, pale-wet tongue, and weak pulses.
Deficiency of Qi & Yin: Signs are mostly seen in elderly people. Typically symptoms are muscular flaccidity of the limbs come on slowly, a mild to moderate amount of motor weakness in the legs, accompanied with soreness and weakness of the loin and knees, dizziness and blurring of vision, impotence or seminal emission, red-dry tongue, and thready-rapid pulse.
Deficiency of Yin & Yang: Signs are a combination of the aforementioned processes with the addition of cold signs. The tongue may be pale or red while the pulses are deep and weak.
Local AP points: Hua Tuo Jia Ji, GV-14, Bai Hui
Special AP points: BL-62, BL-64, SI-3, Er Yan, Lie Feng
TCM herbal:
Hu Qian Wan:
English Name Latin Name Actions
Bai Shao Yao Paeonia Nourish Blood
Chen Pi Citrus Move Qi and Relieve Pain
Gan Jiang Zingiberis Strengthen Stomach and Promote Appetite
Gui Ban Plastrum Nourish Yin, anchors Yang, tonify Blood, Nourish Heart
Huang Bai Phellodendron Clear Heat, Nourish Yin
Niu Xi Achyranthes Strengthens the Kidney and Benefit the Knees
Shu Di Huang Rehmannia Nourish Yin, Blood and Jing
Suo Yang Cynomorium Tonify Yang and Jing, Nourish Blood, Strengthen Sinews
Zhi Mu Anemarrhena Nourish Yin, Clear Heat
Di Huang Yin Zi:
English Name Latin Name Actions
Ba Ji Tian Morinda Tonify Kidney, Strengthen Yang
Fan Shi Hu Descurainiae Herba Nourish Yin, Clear Deficient Heat, Nourish Stomach Yin
Fu Ling Poria Drain Damp, Strengthen Spleen
Fu Zi Aconite Warm Spleen
Mai Men D**g Ophiopogon Nourish Yin
Rou Cong Rong Cistanche Salsa Caulis Tonify Kidney, Strengthen Yang
Rou Gui Cinnamomum Tonify Kidney Yang
Shan Zhu Yu Cornus Nourish Yin
Shi Chang Pu Acorus Open Orifices, Transform Phlegm, Calm Spirit, Harmonize Middle Burner
Shu Di Huang Rehmannia Nourish Blood and Yin
Wu Wei Zi Schisandra Consolidate and Nourish Lung Yin
Yuan Zhi Polygala Calm Spirit, Quiet Heart, Clear Orifices