A 31 year old female aquatic animal trainer presented to me 6 months ago. She had been referred by another patient. She complained of headache, dizziness, fatigue, muscle weakness, a loss of balance, tingling and numbness, blurred vision, decreased coordination, episodes of confusion, brain fog, anxiety, irritability, palpitations and episodes of random sweats and chills. The headaches were particularly bad. They were daily, felt like pressure in the front of her head and interfered with sleep.
All the symptoms were new. The symptoms were getting worse. About 2 months before she suffered a closed head injury and a concussion. She had been butted in the head by a dolphin. Initially, I filed this part of the history away and focused on the Lyme evaluation.
Let me insert that she had previously seen numerous physicians including a neurologist. A Brain MRI was negative. No diagnosis or therapy had been suggested.
She tested positive for Lyme disease and seemed to be a fairly typical case. She had a lot of muscle weakness and poor endurance with a loss of strength. The sweating pattern suggested a typical Babesia co-infection syndrome. Treatment with antibiotics produced slow and steady improvement. Antimicrobial therapy included Amoxicillin, Biaxin, Flagyl and Mepron. After several months the improvement was incremental but slow. She was unable to work and was concerned that she might be disabled for an extended period of time. I felt that she was doing fairly well. It would take time; she would eventually be able to return to work. It is impossible to predict how long it will take for a particular patient to get better. Nonetheless, every time I see a patient for follow up I review the initial, presenting symptoms: which symptoms have improved and which have not. About 6 weeks ago I noted that the headaches were quite disabling and had not improved to any significant extent. The headaches had a migraine like quality. Empirically, I prescribed a migraine preventing medicine, Topomax.
When I was her last week I was surprised by her dramatic improvement. The Topamax made a huge difference. The headaches resolved, her sleep improved and virtually all the other symptoms disappeared as well. It was a rather amazing transformation. She had scheduled her return to work- full time.
In retrospect her case looks a bit different. I still believe she suffers with chronic Lyme disease, but this may not have been her main problem. Her illness was triggered by a closed head injury and a concussion. Patients can suffer with a post-concussion syndrome which can persist for many months.
Headaches which resemble migraines and all the other presenting neurological symptoms can be seen in post-concussion syndromes. I have seen many such patients over the years. They frequently experience dizziness, balance issues, visual changes, mood swings, memory loss, brain fog and even bouts of frank confusion or disorientation. All of these symptoms dovetail nicely with many of those associated with typical neuro-Lyme- and this patient's initial list of symptoms.
The connection between fibromyalgia and sleep problems has been well known for decades. Patients deprived of deep sleep, stage 4 delta sleep, all develop a fibromyalgia like syndrome after a period of several weeks, as has been experimentally shown.
The improvement in muscle symptoms could be related to the improvement in sleep that she was experiencing. Perhaps the restoration of brain function caused the marked improvement in muscle symptoms by some other mechanism.
Asymptomatic, persistent Lyme infection be transformed into an active process by another illness, usually an infectious illness. I have seen this many times. In this case I suspect that the neurological injury triggered by the concussion and the associated sleep deprivation, created an environment permitting activation of Lyme- and perhaps Babesia.
Friday, January 30, 2009
Wednesday, January 28, 2009
Thinking about thinking
After two years of oral antibiotic therapy this 55 year old female with chronic Lyme disease is doing great- or is she? Her stamina is now great. The annoying numbness and tingling is a thing of the past. She is free from joint pains- after many long years. The sweats the chills, the low grade fevers are all gone. The brain "fog" is gone. She is functioning well as a teacher, well, sort of. She used to be a lot sharper. She used to be organized. Now she is scattered brained. She looses things and she looses her train of thought. The word retrieval issue still drives her mad. When she finally pulls up the word she was searching for it is hours later. She is not herself. The cognitive symptoms were clearly worse at the start. Things steadily improved but they have reached a plateau and not budged for over 6 months. The Lyme diagnosis seems pretty clear, she has been seropositive several times at IgeneX and at Labcorp. She has been empirically treated for Babesia and other co-infections. To look at her- one might envision a picture of restored health and vitality.
Ia she the best she can be? Is there a next step? If so, what is the next step?
Many LLMDS would be happpy with her progress, rightly so, and tell her to give it time. Perhaps in another year or two things will get back to normal. Or perhaps she would be told- as long as things stay the same and don't get any worse then it is best to leave things alone.
Per the title of the post, I find myself thinking about (her) thinking. Objective measurements may be hard to come by. I ordered a SPECT scan and an MRI. For the sake of this excercize, we will assume that they will both be normal. She would easily pass any pen and paper neurocognitive assessment. What is at stake is her subjective sense of her global cognitive functioning- pre-Lyme, her memory of her memory as it were.
This is a very gray area within another very gray area.
I think that a course of Rocephin should be tried. I have seen it work.
Ia she the best she can be? Is there a next step? If so, what is the next step?
Many LLMDS would be happpy with her progress, rightly so, and tell her to give it time. Perhaps in another year or two things will get back to normal. Or perhaps she would be told- as long as things stay the same and don't get any worse then it is best to leave things alone.
Per the title of the post, I find myself thinking about (her) thinking. Objective measurements may be hard to come by. I ordered a SPECT scan and an MRI. For the sake of this excercize, we will assume that they will both be normal. She would easily pass any pen and paper neurocognitive assessment. What is at stake is her subjective sense of her global cognitive functioning- pre-Lyme, her memory of her memory as it were.
This is a very gray area within another very gray area.
I think that a course of Rocephin should be tried. I have seen it work.
Tuesday, January 27, 2009
Hard to catch?
Many have characterized the IDSA and ILADS dispute with the simple dichotomy: Hard to catch easy to cure, versus easy to catch hard to cure. A snappy little sound bite.
I saw one of my delightful patients today. He is a 23 year old male with cerebral palsy. He has been quadriplegic since birth. He has minimal use of his left hand and motors around the house with an electric wheel chair. He suffers with severe cognitive impairments. He rarely leaves the house and never goes anywhere without his elderly grandmother. He lives in an apartment complex. One year ago he had several tick bites. His grandmother thought it was from the mulching of the trees around the entrance to his apartment complex. He is difficult to communicate with because of his handicaps.
Nonetheless, his care giver could easily see a change in his demeanor. He became sullen, less mobile and in general, appeared uncomfortable. His lab tests were positive for Lyme disease by CDC surveillance criteria. He was treated with two months of antibiotics and got better. Two months later he was ill again. He had malaise, low grade fevers, decreased mobility and a change once more, in his normally cheerful demeanor. After 3 additional months of antibiotic therapy he became well and he remains well to this day.
This young man lives in an apartment with his elderly grandmother. He is permanently confined to a wheel chair. For all intents and purposes, he virtually never leaves his home and he certainly never goes outside to enjoy bucolic scenery. He developed classic Lyme disease with positive CDC serology.
The disease is hard to catch???
We can deal with easy to cure another day.
I saw one of my delightful patients today. He is a 23 year old male with cerebral palsy. He has been quadriplegic since birth. He has minimal use of his left hand and motors around the house with an electric wheel chair. He suffers with severe cognitive impairments. He rarely leaves the house and never goes anywhere without his elderly grandmother. He lives in an apartment complex. One year ago he had several tick bites. His grandmother thought it was from the mulching of the trees around the entrance to his apartment complex. He is difficult to communicate with because of his handicaps.
Nonetheless, his care giver could easily see a change in his demeanor. He became sullen, less mobile and in general, appeared uncomfortable. His lab tests were positive for Lyme disease by CDC surveillance criteria. He was treated with two months of antibiotics and got better. Two months later he was ill again. He had malaise, low grade fevers, decreased mobility and a change once more, in his normally cheerful demeanor. After 3 additional months of antibiotic therapy he became well and he remains well to this day.
This young man lives in an apartment with his elderly grandmother. He is permanently confined to a wheel chair. For all intents and purposes, he virtually never leaves his home and he certainly never goes outside to enjoy bucolic scenery. He developed classic Lyme disease with positive CDC serology.
The disease is hard to catch???
We can deal with easy to cure another day.
MS? Take another look
This 40 year old woman saw a neurologist only once. She did have tingling on the right side of her face. At that point the neurologist stopped asking questions. He ordered am MRI. But she also had headache, joint pains (multiple and diffuse), cognitive issues and floaters. She spent a lot of time outdoors. The neurologist had no interest in this litany. Her neurological exam showed a typical pattern of sensory peripheral neuropathy, not the central nervous system findings one would expect to see in MS. I do not know what he found when he examined the patient.
The neurologist diagnosed MS. A brain MRI showed periventricular and subcortical white mattter disease. The radiology reports reads "While these are nonspecific these lesions are suspicious for demylinating plaques. Clinical correlation is needed to exclude......Lyme disease......"
These findings MRI findings are fairly classic as seen with MS. The neurologist informed the patient that she had MS. Not quite convinced, the patient sought my attention, seeking another opinion.
Again- MS cannot be diagnosed by MRI findings. There are diagnostic criteria listed in many text books. Per Harrison's Textbook of Medicine, 16th edition, page 2464:
There are 5 specific criteria listed. MRI findings are not a prominent aspect of the criteria. The fifth criteria is clear: "The patient's neurological condition could not better be attributed to another disease."
My history and exam pointed to Lyme disease- not MS: See criteria #5.
During a 6 month process of treatment, other symptoms became manifest. The patient had soaking sweats. She had profound fatigue, which increased with antibiotic therapy- a Herx response. She had muscle pains, diffuse numbness and tingling of the extremities, muscle twitching, tinnitus, floaters and sleep difficulties.
The cognitive difficulties were typical of what I have seen in numerous chronic Lyme patients. The patient had "brain fog," word retrieval difficulties, short term memory loss, slow cognitive processing and new ADD like symptoms- difficulty concentrating.
After 5 months of treatment which has focused on Lyme and Babesia she is feeling 80% better.
She never agreed to have labs run through a specialty lab. A limited Lyme WB showed a 23 IgM band. She has had alterations in vitamin D and high complement levels. Her CRP has remained very elevated. Let me comment on the Western Blot. There is much literature demonstrating the existence of sero-negative Lyme disease. This is denied by the IDSA- even though many of their physicians have authored and published papers in the past refuting their current stance. The 23 band is specific for Osp C. This is a specific antigen, outer surface protein C, which many consider diagnostic Bb- the Lyme bacteria, even in the absence of other bands. In truth, there are no universally accepted Western Blot criteria for the diagnosis of Lyme exposure. What exists is an assortment of surveillance criteria and individual guidelines espoused by a variety of physicians and laboratories familiar with the disease. The diagnosis is not cut and dried or black and white; and the treatment is murkier yet by many orders of magnitude. Perhaps as someone said in reference to Lyme and its controversies: "It is an exercise of nailing jello to the wall." This is true, but we still have to deal with the jello!
I ask physicians to try to do a better job, to keep an open mind- and to consider the fact that those of us who see patients in the northeast US and mid-atlantic region are operating in a Lyme endemic region. I also ask physicians to keep in mind that Lyme has aptly earned the title: "The great imitator." Patients with complex, multi-system complaints cannot be diagnosed with a single imaging study. The basic tools of history and examination are as essential now as they were 100 years ago. Something was ingrained into my mind by one of my mentors early in my medical training, something which has held me in good stead for all these years: Rule one- treat the patient, not the lab.
The neurologist diagnosed MS. A brain MRI showed periventricular and subcortical white mattter disease. The radiology reports reads "While these are nonspecific these lesions are suspicious for demylinating plaques. Clinical correlation is needed to exclude......Lyme disease......"
These findings MRI findings are fairly classic as seen with MS. The neurologist informed the patient that she had MS. Not quite convinced, the patient sought my attention, seeking another opinion.
Again- MS cannot be diagnosed by MRI findings. There are diagnostic criteria listed in many text books. Per Harrison's Textbook of Medicine, 16th edition, page 2464:
There are 5 specific criteria listed. MRI findings are not a prominent aspect of the criteria. The fifth criteria is clear: "The patient's neurological condition could not better be attributed to another disease."
My history and exam pointed to Lyme disease- not MS: See criteria #5.
During a 6 month process of treatment, other symptoms became manifest. The patient had soaking sweats. She had profound fatigue, which increased with antibiotic therapy- a Herx response. She had muscle pains, diffuse numbness and tingling of the extremities, muscle twitching, tinnitus, floaters and sleep difficulties.
The cognitive difficulties were typical of what I have seen in numerous chronic Lyme patients. The patient had "brain fog," word retrieval difficulties, short term memory loss, slow cognitive processing and new ADD like symptoms- difficulty concentrating.
After 5 months of treatment which has focused on Lyme and Babesia she is feeling 80% better.
She never agreed to have labs run through a specialty lab. A limited Lyme WB showed a 23 IgM band. She has had alterations in vitamin D and high complement levels. Her CRP has remained very elevated. Let me comment on the Western Blot. There is much literature demonstrating the existence of sero-negative Lyme disease. This is denied by the IDSA- even though many of their physicians have authored and published papers in the past refuting their current stance. The 23 band is specific for Osp C. This is a specific antigen, outer surface protein C, which many consider diagnostic Bb- the Lyme bacteria, even in the absence of other bands. In truth, there are no universally accepted Western Blot criteria for the diagnosis of Lyme exposure. What exists is an assortment of surveillance criteria and individual guidelines espoused by a variety of physicians and laboratories familiar with the disease. The diagnosis is not cut and dried or black and white; and the treatment is murkier yet by many orders of magnitude. Perhaps as someone said in reference to Lyme and its controversies: "It is an exercise of nailing jello to the wall." This is true, but we still have to deal with the jello!
I ask physicians to try to do a better job, to keep an open mind- and to consider the fact that those of us who see patients in the northeast US and mid-atlantic region are operating in a Lyme endemic region. I also ask physicians to keep in mind that Lyme has aptly earned the title: "The great imitator." Patients with complex, multi-system complaints cannot be diagnosed with a single imaging study. The basic tools of history and examination are as essential now as they were 100 years ago. Something was ingrained into my mind by one of my mentors early in my medical training, something which has held me in good stead for all these years: Rule one- treat the patient, not the lab.
Friday, January 23, 2009
Lyme and the CDC: A tangled web
A 50 year old male came into my office in March 2007 to inquire about Lyme disease. He had been referred by anther patient. He had previously been diagnosed with fibromyalgia, depression and other ailments. He is an outdoors man and recalls many tick bites over a period of many years. His illness became pronounced in 1994, but in retrospect had been ongoing for at least 20 years.
He complained of arthritis, sleep problems, severe cognitive impairments, weakness, a loss of coordination, a loss of balance and diffuse muscle pains and restless leg syndrome.
His previous physician had treated him with the antidepressants Wellbutrin and Elavil. His examination showed evidence of sensory peripheral neuropathy. Initial screening blood work was normal. His "Western Blot" for Lyme with a "mill" lab showed a single IgG band in the 58 position.
A brain MRI showed white matter disease. Based on my experience with many similar patients, I felt he had chronic Lyme disease and presumptive neuroborreliosis. The medical literature is replete with information regarding many well documented cases of seronegative Lyme disease. Today's IDSA/CDC crowd makes that claim that not only is seronegative Lyme virtually non-existent, but seropositivity is narrowly defined by the two step ELIZA/Western Blot test. History has been re-written. The CDC has repeatedly stated that this test is for surveillance/epidemiological purposes, not diagnostic.
This patient had a good clinical response to oral antibiotics. Virtually all of his presenting symptoms improved- except the cognitive impairments. These were marked and threatening his professional and personal life. He had short term memory loss, word finding difficulties, episodes of confusion and disorientation and an inability to concentrate. His depression and mood swings were marked.
By February 2008 he was about 50% better overall. Cognitive symptoms had not improved. A Lyme Western Blot performed at IgeneX showed positivity at bands: 18,34,39,41. He was CDC and IgeneX positive. I have found no literature which discusses the issue of Lyme seroconversion. This phenomenon is well known to physicians who treat Lyme disease. It is not discussed by the CDC or in IDSA guidelines. The CDC still maintains that a positive test is based on the two tier test or now- a Western blot showing 5/10 IgG WB bands. Those of us who treat chronic Lyme know three things: The two tier test is inaccurate, A direct Western Blot which incorporates IgG is unhelpful since the vast majority of seropositive patients have IgM responses only and many patients who test positive for Lyme only do so after Herx responses folowing antibiotic therapy. The IDSA does not address the existence of Lyme related Herx responses. IDSA physicians I have spoken with claim that seroconversion has no meaning; they believe it represents a false positive response. It is also trying(to say the least) that the CDC has failed to inform laboratories and physicians what a positive Lyme CDC test means- despite congressional instruction to do so in 2002- signed into law by President Bush. At the present time, every mainstream infectious disease specialist, neurologist and rheumatologist I interact with has mistaken beliefs about the meaning and use of this test. Furthermore, they believe that my interpretations of Lyme tests are tantamount to quackery.
A SPECT scan from June 2008 showed decrease perfusion to the frontal and parietal lobes in the brain. The Lyme denialist camp has claimed that SPECT scans have no validity. This denial is made in the face of evidence based data from Columbia University. This patient received a 5 month course of intravenous antibiotics, ultimately including Zithromax and Flagyl added to Rocephin.
His response was nothing short of spectacular. All of his symptoms, virtually 100% are gone. His mentation is perfect. He has not functioned physically or mentally this well in over 20 years. He is weaning of his antidepressants. His mood is normal.
His remission is maintained with oral antibiotics.
He complained of arthritis, sleep problems, severe cognitive impairments, weakness, a loss of coordination, a loss of balance and diffuse muscle pains and restless leg syndrome.
His previous physician had treated him with the antidepressants Wellbutrin and Elavil. His examination showed evidence of sensory peripheral neuropathy. Initial screening blood work was normal. His "Western Blot" for Lyme with a "mill" lab showed a single IgG band in the 58 position.
A brain MRI showed white matter disease. Based on my experience with many similar patients, I felt he had chronic Lyme disease and presumptive neuroborreliosis. The medical literature is replete with information regarding many well documented cases of seronegative Lyme disease. Today's IDSA/CDC crowd makes that claim that not only is seronegative Lyme virtually non-existent, but seropositivity is narrowly defined by the two step ELIZA/Western Blot test. History has been re-written. The CDC has repeatedly stated that this test is for surveillance/epidemiological purposes, not diagnostic.
This patient had a good clinical response to oral antibiotics. Virtually all of his presenting symptoms improved- except the cognitive impairments. These were marked and threatening his professional and personal life. He had short term memory loss, word finding difficulties, episodes of confusion and disorientation and an inability to concentrate. His depression and mood swings were marked.
By February 2008 he was about 50% better overall. Cognitive symptoms had not improved. A Lyme Western Blot performed at IgeneX showed positivity at bands: 18,34,39,41. He was CDC and IgeneX positive. I have found no literature which discusses the issue of Lyme seroconversion. This phenomenon is well known to physicians who treat Lyme disease. It is not discussed by the CDC or in IDSA guidelines. The CDC still maintains that a positive test is based on the two tier test or now- a Western blot showing 5/10 IgG WB bands. Those of us who treat chronic Lyme know three things: The two tier test is inaccurate, A direct Western Blot which incorporates IgG is unhelpful since the vast majority of seropositive patients have IgM responses only and many patients who test positive for Lyme only do so after Herx responses folowing antibiotic therapy. The IDSA does not address the existence of Lyme related Herx responses. IDSA physicians I have spoken with claim that seroconversion has no meaning; they believe it represents a false positive response. It is also trying(to say the least) that the CDC has failed to inform laboratories and physicians what a positive Lyme CDC test means- despite congressional instruction to do so in 2002- signed into law by President Bush. At the present time, every mainstream infectious disease specialist, neurologist and rheumatologist I interact with has mistaken beliefs about the meaning and use of this test. Furthermore, they believe that my interpretations of Lyme tests are tantamount to quackery.
A SPECT scan from June 2008 showed decrease perfusion to the frontal and parietal lobes in the brain. The Lyme denialist camp has claimed that SPECT scans have no validity. This denial is made in the face of evidence based data from Columbia University. This patient received a 5 month course of intravenous antibiotics, ultimately including Zithromax and Flagyl added to Rocephin.
His response was nothing short of spectacular. All of his symptoms, virtually 100% are gone. His mentation is perfect. He has not functioned physically or mentally this well in over 20 years. He is weaning of his antidepressants. His mood is normal.
His remission is maintained with oral antibiotics.
Thursday, January 22, 2009
Lyme and CIDP
I have been treating a 45 year old male for several months. He has been sick for a very long time. He is seropositive for Lyme disease and Babesia. He has complained of searing total body pain, joint pain and cognitive difficulties for several years. he had become disabled. I tried treating him with a variety of oral and IV medications, with poor results. It has been a frustrating case and I have tried many different strategies. Finally he called me telling me that he had sudden weakness affecting his lower limbs and he was unable to stand. He went to the Hospital and was diagnosed with Guillan Barre syndrome. He was treated with plasmamapharesis. He had a reasonably positive response. He was able to walk but he was still in severe pain and had total body weakness. He was discharged to a rehabilitation facility before returning to see me in the office. I took another look at him. The diffuse, searing neuropathic pain had been ongoing for years. He had weakness of his legs- but there was also weakness of his arms. He had a diffuse loss of sensation to sharp touch in a diffuse pattern. His pain was also very diffuse. His deep tendon reflexes were diminished. He had evidence of mild muscle atrophy diffusely. The neurologist at the hospital had been dismissive. It was Guillan Barre syndrome. Both his intense pain and Lyme disease were dismissed. Unfortunately, my patients frequently get substandard care when they are admitted to the hospital: " Oh no- not another one of so and so's patients."
Guillan Barre is an acute syndrome. It is associated with an ascending neuropathy. This patient had a chronic neuropathy with an acute exacerbation. The plasmapheresis had bought him a little relief, but not much. I am a family doctor- not a neurologist. But it became clear to me what was going on with this patient. He has CIDP- chronic inflammatory demyelinating poly-neuropathy. The disease is a cousin of Guillan Barre, but it is different. It is a chronic disease. It is an autoimmune disease of the peripheral nervous system. Auto-antibodies attack the lipoprotein coat of peripheral neurons, causing diffuse demyelination of the motor and sensory peripheral nerves. In this case, I believe it was Lyme mediated- at least in part. Every time I had prescribed antibiotics for Lyme I only made matters worse. killing Lyme led to increased antigen presentation- feeding a malfunctioning immune response- cranking out noxious auto-antibodies. This is consistent with my model of how Lyme and other germs provide fuel for an autoimmune process. While many believe that autoimmunity is self perpetuating once it begins; it has been my experience that a reduction in germ load can frequently help quiet down the process.
A diffuse loss of myelin of sensory nerves could easily explain his uncontrollable pain. Similarly, the loss of myelin of motor nerves could easily explain the diminished reflexes, weakness and atrophy.
I temporized his therapy with intramuscular injections of steroids while introducing heomeopathic doses of Minocycline. I referred him to a neurologist- whom I believe will do a more thorough evaluation. EMG and NCV studies should confirm the diagnosis.
I also referred him to a hematologist whom I believe will soon start IViG therapy.
Physicians who treat Lyme disease you must be well versed in all of the autoimmune syndromes of the nervous system; It is clear that Lyme can be associated with any one of them.
The widely held injunction prohibiting the use of steroids is not necessarily the case with severe autoimmune disease. Plasmapheresis and IViG are not always practical. The main problem in this patient is not Lyme infection- it is autoimmune disease. A focus only on Lyme wold be a disservice to my patient. I also believe that a focus which excludes Lyme disease would also be a disservice. In my mind, it makes sense to temper steroid therapy with low doses of antibiotics. But of course this is theoretical and speculative. At least I now think we are headed in the right direction.
Guillan Barre is an acute syndrome. It is associated with an ascending neuropathy. This patient had a chronic neuropathy with an acute exacerbation. The plasmapheresis had bought him a little relief, but not much. I am a family doctor- not a neurologist. But it became clear to me what was going on with this patient. He has CIDP- chronic inflammatory demyelinating poly-neuropathy. The disease is a cousin of Guillan Barre, but it is different. It is a chronic disease. It is an autoimmune disease of the peripheral nervous system. Auto-antibodies attack the lipoprotein coat of peripheral neurons, causing diffuse demyelination of the motor and sensory peripheral nerves. In this case, I believe it was Lyme mediated- at least in part. Every time I had prescribed antibiotics for Lyme I only made matters worse. killing Lyme led to increased antigen presentation- feeding a malfunctioning immune response- cranking out noxious auto-antibodies. This is consistent with my model of how Lyme and other germs provide fuel for an autoimmune process. While many believe that autoimmunity is self perpetuating once it begins; it has been my experience that a reduction in germ load can frequently help quiet down the process.
A diffuse loss of myelin of sensory nerves could easily explain his uncontrollable pain. Similarly, the loss of myelin of motor nerves could easily explain the diminished reflexes, weakness and atrophy.
I temporized his therapy with intramuscular injections of steroids while introducing heomeopathic doses of Minocycline. I referred him to a neurologist- whom I believe will do a more thorough evaluation. EMG and NCV studies should confirm the diagnosis.
I also referred him to a hematologist whom I believe will soon start IViG therapy.
Physicians who treat Lyme disease you must be well versed in all of the autoimmune syndromes of the nervous system; It is clear that Lyme can be associated with any one of them.
The widely held injunction prohibiting the use of steroids is not necessarily the case with severe autoimmune disease. Plasmapheresis and IViG are not always practical. The main problem in this patient is not Lyme infection- it is autoimmune disease. A focus only on Lyme wold be a disservice to my patient. I also believe that a focus which excludes Lyme disease would also be a disservice. In my mind, it makes sense to temper steroid therapy with low doses of antibiotics. But of course this is theoretical and speculative. At least I now think we are headed in the right direction.
Wednesday, January 21, 2009
History lessons
I appreciate the comments of my readers. No, I am not suffering like Semmelweis. And I am not fighting the struggle alone.
In 1847 Viennese Physician Semmelweis was ridiculed for suggesting that attending OB physicians wash their hands between patients. He was subsequently called the "Savior of mothers," when deaths from "childbed fever" plummeted.
In 1862 Pasteur suggested the germ theory of disease. His ideas were met with ridicule for years to come.
In 1979 and 1981 Warren and Marshall discovered a bacteria in the stomach. They suggested that the bacteria (Helicobacter pylori) was pathogenic- and that it was associated with peptic ulcers amongst other things. Colleagues, who knew better, dismissed these ideas as nonsense.
Of course, all of these paradigm shattering physicians and scientists, who advanced our knowledge and medical practice in quantum leaps, are now highly revered heroes of history.
After years of rebuke, Warren and Marshall were given long overdue credit; they were awarded the Nobel Prize for Medicine in 2005.
The question is: Are the "Lyme Wars" just another iteration of the paradigm wars described by Thomas Kuhn in his famous essay "The Structure of Scientific Revolutions?" Or, is this particular process different, in some fundamental- perhaps Orwellian way? This is a debate I will not enter.
Many others have vivisected the Klempner study and other purported pillars of the IDSA view point. The notion that this single- highly flawed study should be allowed to discredit the work of hundreds of scientists and physicians is mind boggling, to say the least. As I have noted in the past, it is difficult to wed medicine and science. The practice of medicine has always given equal weight to the art and the science of medicine. Bench top, basic science research is clear. The basic scientific facts as they have been uncovered, offer unwavering support for our contentions. Clinical science is murky at best and is always open to criticism.
This blog is not science. It is a collection of fact, theory and clinical vignettes sent out into the ether of cyberspace, perhaps the equivalent of a modern day message in a bottle. I suppose my motive is similar to that of any other author who scribbles a note on a piece of paper and then sends it out adrift in the sea; perhaps by chance, It will be found, read by the right person- and make a difference.
It seems clear to me that documentaries, books and scientific assemblies offering compelling, and at times horrifying information, have thus far failed to scratch the armor coat of the other side.
I do believe that history is critical. We must never forget its lessons, as we move forward each day, with the knowledge that we are doing the best that we can.
I will veer off the subject of my blog for a moment. I am awestruck and brought to tears of joy at this incomprehensible moment in history. I could never imagined that I would live to see the prophetic vision of one of my personal heroes, Martin Luther King, become reality, as I now watch a black American take the highest office in the land, perhaps the world.
As always, the people can make a difference. The medical community will not accept the truths of Lyme disease until it is forced down their throats by a grass roots movement coming not from doctors like myself, but from ordinary people- like you.
In 1847 Viennese Physician Semmelweis was ridiculed for suggesting that attending OB physicians wash their hands between patients. He was subsequently called the "Savior of mothers," when deaths from "childbed fever" plummeted.
In 1862 Pasteur suggested the germ theory of disease. His ideas were met with ridicule for years to come.
In 1979 and 1981 Warren and Marshall discovered a bacteria in the stomach. They suggested that the bacteria (Helicobacter pylori) was pathogenic- and that it was associated with peptic ulcers amongst other things. Colleagues, who knew better, dismissed these ideas as nonsense.
Of course, all of these paradigm shattering physicians and scientists, who advanced our knowledge and medical practice in quantum leaps, are now highly revered heroes of history.
After years of rebuke, Warren and Marshall were given long overdue credit; they were awarded the Nobel Prize for Medicine in 2005.
The question is: Are the "Lyme Wars" just another iteration of the paradigm wars described by Thomas Kuhn in his famous essay "The Structure of Scientific Revolutions?" Or, is this particular process different, in some fundamental- perhaps Orwellian way? This is a debate I will not enter.
Many others have vivisected the Klempner study and other purported pillars of the IDSA view point. The notion that this single- highly flawed study should be allowed to discredit the work of hundreds of scientists and physicians is mind boggling, to say the least. As I have noted in the past, it is difficult to wed medicine and science. The practice of medicine has always given equal weight to the art and the science of medicine. Bench top, basic science research is clear. The basic scientific facts as they have been uncovered, offer unwavering support for our contentions. Clinical science is murky at best and is always open to criticism.
This blog is not science. It is a collection of fact, theory and clinical vignettes sent out into the ether of cyberspace, perhaps the equivalent of a modern day message in a bottle. I suppose my motive is similar to that of any other author who scribbles a note on a piece of paper and then sends it out adrift in the sea; perhaps by chance, It will be found, read by the right person- and make a difference.
It seems clear to me that documentaries, books and scientific assemblies offering compelling, and at times horrifying information, have thus far failed to scratch the armor coat of the other side.
I do believe that history is critical. We must never forget its lessons, as we move forward each day, with the knowledge that we are doing the best that we can.
I will veer off the subject of my blog for a moment. I am awestruck and brought to tears of joy at this incomprehensible moment in history. I could never imagined that I would live to see the prophetic vision of one of my personal heroes, Martin Luther King, become reality, as I now watch a black American take the highest office in the land, perhaps the world.
As always, the people can make a difference. The medical community will not accept the truths of Lyme disease until it is forced down their throats by a grass roots movement coming not from doctors like myself, but from ordinary people- like you.
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