EMG and IVIG

The diagnosis of chronic Lyme disease is more often than not accompanied by a subjective complain of numbess and tingling, often accompanied by weakness, dizzininess, loss of balance and other neurological complaints. The examination frequently demonstrates a lack of sensation to vibration, pin-prick or temperature in a distal, "stocking/glove" distribution, as well as muscle weakness. The workup for this scenario should include "electro-diagnostic" testing (EMG/NCV - electromyogram and nerve conduction velocity testing), which can demonstrate the presence of a peripheral neuropathy, axonal or demyelinating. If this is negative, a skin biopsy may show the presence of a small fiber neuropathy. These findings may be of profound clinical consequences.

Numerous patients come to mind. One patient, a 55 year old dog groomer came in for the treatment of chronic Lyme disease. He had been sick for years and only getting sicker. His major initail concerns were, progressive fatigue, overall aching of both muscles and joints and increasing forgetfulness/brain fog. He was not significantly bothered by the lack of sensation in both legs. I was. I ordered an EMG.

The EMG revealed a severe peripheral neuropathy.

Because of this, the insurance company approved the use of IVIG, an intravenous blood product consisting of concentrated iG antibodies from a large pool of donors. Without insurance approval for the "right" diagnosis, the cost of this treatment is prohibitive.

After a year of treatment with up and down results. He came into the office recently having now been on IVIG for several months,

"knock on wood," he said.  He felt terrific. The fatigue was dramatically better; the pains were nearly gone, and the cognitive dysfunction had greatly improved. Sensation was returning to his feet.

Like all therapies, IVIG, carries with it serious risks, including the possibility of severe allergic reactions.  Patients with IgA deficiency must recevie a special product.

But these kinds of results have been reproduced in many of my patients.

Super bugs and immune responses

A thirty seven year old female presented for an evaluation at the end of 2010. She had previously been in good health until 18 months before the visit. She had been diagnosed with chronic fatigue syndrome and fibromyalgia by several other doctors. She had been informed that blood tests, including a Lyme test, had all been normal. She had recently moved back to Maryland from North Carolina. She had previous lived in Maryland 2007 to the beginning of 2009.

Her symptoms had included: fatigue, swollen glands, joint pain and swelling, headaches, nausea, vertigo, blurred vision, dizziness, loss of balance, facial twitches, tremor, memory loss, decreased appetite, muscle cramps, abdominal pain, flulike symptoms, night sweats, shortness of breath, numbness and tingling, disorientation, confusion, poor cognitive processing, random lactation, hot flashes and chills.

She is not an outdoor person although she has had many cats. She does recall walking barefoot through tall grasses on several occasions. There is no history of tick bite. There is no history of an EM (bulls eye) rash.

After 6 months of treatment, including 5 months of Rocephin she is feeling reasonably well. She is still weak but has good endurance. The fatigue is all but gone.  Cognitive problems have largely resolved. Muscles pains are gone. Overall, she is about 80% better.

Response to antibiotics is extremely variable amongst patients. Currently the combination of Tindamax and Levaquin have been very effective. The addition of Cortef seems to have been very helpful.
I would like to suggest that I(we) frequently do not know what we are really treating. We do not have a microsopic view of  tissues, the immunological responses, microbiological responses or cellular functions.

For example. From many quarters it would be assumed that I am treating Lyme, Bartonella and adrenal fatigue. Perhaps this is mostly wrong.

Regarding Lyme, we have no data regarding microbial resistance. A patient yesterday asked me if Lyme is a "super bug." Actually a good question. We know Lyme has a complex genome and we know Lyme should have the ability to develop drug resistance. Super bugs like MRSA and VRE have evolved the ability to resist multiple antibiotics. Efflux pumps within the bacteria pump out antibiotics of differing classes rendering these antibiotics to be ineffective.

Perhaps Levaquin works, and/or Tindamax, because the offending germs have not developed resistance to these antibiotics.

And Cortef. Treating adrenal fatigue? Maybe not. Patients with treatment refractory Lyme may have very high levels of cytokines such as IL6 and TNF alpha. These are potent mediators of inflammation. It is well know that one of the ways Lyme makes people so ill is because it causes  excessive inflammatory reactions. Steroids are the best way to tamp down these excessive immunological responses.

I really started writing this blog because of the patients measurable immune responses to the germ. Currently, the standard WB shows no reactivity but the C6 peptide, 1.55, is positive for the first time.  The WB sent to Stony Brook showed only 41 IgM and IgG bands.  One year ago, a Labcorp WB was positive for IgG bands (4/10) 66,58,41 and 28 and IgM band 23.  Six months prior to that, Labcorp found IgG bands (3/10) 66,58 and 41 and a positive IgM (2/3) 39 and 41.  Previous C6 peptides had been 0.4 and 0.7.

It shows that either the tests are completely unreliable or that immune responses are extemely variable over time. Maybe some of both.

Toxoplasmosis and Lyme

The Archives of General Psychiatry has published two studies from Denmark demonstrating the relationship between toxoplasmosis and suicide. Especially violent suicide. Toxoplasma parasities hide within neurons and glial (supporting brain cells) in cystic forms.

Toxoplasma are persistent brain parasites. The immune system is unable to eradicate them. No effective antimicrobial therapy is available. As with Lyme infection, the organisms manipulate the immune system and are associated with alterations in cytokine levels including interleukin 6. Toxoplasma infection and Lyme also impacts metabolic pathways which lead to the production of kynurenic acid and quinolinic acid from tryptophan.

Elevated quinolinic acid levels has been associated with neuroborreliosis in at least one frequently cited study. These neuro-active substances are associated with glutamic acid excito-toxicity.

Toxoplasma infection has been long associated with depression, schizophrenia, autism, congenital disorders and many other brain disorders.

Toxoplasma infection is common, infecting up to 1/3 of the world's population.

As the microbiome projects has shown. Microorganisms inhabit communities within special niches. Many bacteria commonly found in places as prosaic as the skin remain unknowns. It is clear our bodies are loaded with unknown "mystery bugs."

Perhaps the brain also frequently hosts communities of microbes: Toxoplasmosis, Lyme, other spirochetes. Of course, only those in the Lyme community think of Lyme, Babesia, Bartonella and other co-infections as frequent denizens of the human brain.

An unknown, perhaps endogenous, protozoan has been observed within human cells and the nervous system (unpublished) with genetic/morphological features borrowed from both Malaria and Toxoplasma. (We may all be born infected with this unknown parasite). This is all I can say regarding this topic at the present time). 

One investigator has suggested such organisms could even be symbiotic? mutalistic at times. This is certainly the case with many other microbial communities, natural flora. At times usually beneficial organisms, under the right opportunistic conditions can become troublesome.

Most Toxoplasma infected individuals have no symptoms or apparent ill effects. The same is likely true for most individuals harboring brain infection with many of the other microbes listed here.

Why or when infected individuals is unpredictable. Experience has shown that other infection, trauma or stress can provoke illness with Lyme. It does seem clear that mixes of co-infection increase the severity of Lyme syndromes including neuroborreliosis. One could postulate that at times Toxoplasmosis acts a co-infection.

Many patients with extensive, systemic Lyme seem to have immune dysfunction. Many have subtle decreases in varying IgG subclasses. This may turn out to be a key factor.

From a treatment perspective, anti-Babesia drugs are used for chronic forms of the disease. It should be noted that many anti-psychotic medications also have anti-parasitic properties.

The authors note that two other studies have shown the association of toxplasmosis with suicide, one in Maryland, my home state. Great.

Fatigue in a complicated patient

After a long struggle, the patient is doing fairly well. The cognitive improvements have been superb. But the fatigue and lack of endurance have recently been unbearable. The fatigue has improved and worsened in fits and starts. Recently, she has pushed herself just a little too much;  rebound fatigue with no endurance became unbearable. No reserves.

Long term intravenous antibiotics, 7 months and counting, have worked great. For three months, IV Flagyl as mono-therapy has been effective.

Despite normal lab studies, I clinically diagnosed adrenal fatigue. I treated her with Cortef and Florinef with a very positive result. Fatigue and energy much improved.

She has a history of very clear cardiac Lyme and has a permanent pacemaker. Her cardiologist has been carefully adjusting the pacemaker, recently increasing the top heart rate. The increased heart rate allowed with exercise seems to have helped as well.

POTS cannot be easily diagnosed. Her heart rate, recent exam, decreased with standing rather than vice-versa expected with POTS.

Surprising, at our last visit she reported relief in other symptoms. Her face was oily for the first time in more than a year (under autonomic/sympathetic control). A sensation of incomplete bladder emptying resolved (under autonomic/parasympathetic control) control. The sensation of hot/cold temperature dysregulation improved. These are POTS symptoms, not generally considered  adrenal fatigue symptoms.

I prescribed Florinef, a mineralcorticoid analogue of aldosterone made by the adrenals for the treatment of Adrenal fatigue. This hormone is widely prescribed for POTS because it increases salt and water retention helping with postural dizziness. A strictly symptomatic therapy. In this case it was prescribed for adrenal fatigue, not POTS.

Adrenal fatigue patients describe salt cravings. Perhaps this is due to adrenal/aldosterone dysfunction.

My treatment of adrenal dysfunction seemed to improve dysautonomia. An unexpected outcome.

She also started taking Ritalin again which has been very helpful for fatigue. Many clinicians prescribe Provigil/Nuvigil for fatigue. Ritalin usually works the same but is much more affordable.

Stimulants like Ritalin/Adderall, augment the effects of dopamine and norepinephrine. Adrenal insufficiency is associated with decreased norepinephrine excretion - stress hormones.

Taking Ritalin hopefully does not make adrenal fatigue worse. Like cortisol, it may take pressure off a mis-firing adrenal system. Anyway, it helps.

Improvements of symptoms and function hopefully help the overall healing process.

Too much stimulant may have a negative effect causing dependence -  decreased endogenous neuro-transmitter function.

It is all complicated and outside the box, but working for this heretofore desperate and hopeless patient.

Adrenal fatigue

Stress - anxiety - palpable across the room, emanates from her  pores. Everything is going wrong at the same time. Unfortunately, this is not new. There has been no  response to everything I've thrown at her. The tell-tale Babesia symptoms:  night sweats, flu-like feelings, air hunger, have not budged

I prescribe a dose of Cortef/cortisol.

Adrenal fatigue is not a real diagnosis according to the Mayo Clinic. Look for real diagnoses like fibromyalgia or depression the web page suggests. No science.

There are decades of published, peer-reviewed research showing alterations in adrenal function in depression, chronic fatigue syndrome, fibromyalgia and other related conditions. The results are abnormal, but confusing and difficult to make sense of.

Adrenal function is regulated by a system of feedback loops. One structure in the brain, the hypothalmus, sends a message to another part of the brain, the pituitary, which in turn sends a message to the adrenal glands. The system is called the Hypothalmic-Pituitary-Adrenal axis. Abbreviated HPA axis. The brain is able to sense whether enough adrenal hormones are made and take corrective actions.

The same system works for thyroid and reproductive hormones.

Over-worked adrenals, secreting  "stress" hormones such as cortisol and adrenaline, are unable to keep up with the demands placed on them. The whole HPA system becomes sick in variable ways.

Adrenal fatigue is associated with chronic debilitating illness like chronic Lyme disease.

The adrenal gland is complex in anatomy and function, releasing a wide array of hormones which I will not address here.

Organized medicine likes blacks and whites. There is no gluten sensitivity, only Celiac disease or not. Likewise, only extreme adrenal disorders, Cushings and Addison's disease are accepted. Black and white. No shades of gray.

The adrenal fatigue syndrome is associated with a plethora of symptoms :  Total  exhaustion. Lack of endurance. Anxiety, panic attacks and depression. Dizziness. Dizziness with standing. Aches and pains. Brain fog. Inability to cope with trivial stress. Fatigue more prominent in morning - or -evening. Second wind at night. Insomnia.  Salt and/or sugar cravings. Weight gain. And numerous others.

Testing of saliva, urine and blood may give confusing results.

Cortisol levels peak level at around 8 am. There is a slight spike at 4 am. Otherwise, levels  decline and stay low throughout the day and into the night.

For this reason cortisol should usually be given in the morning.

I have found measuring DHEA, another adrenal hormone, which can be supplemented,  to be helpful.

For the most part, the diagnosis is clinical.

The immune system works better with small doses of cortisol called "physiologic", even though it is a "steroid." High doses of steroids suppress the immune system and must be avoided.

A little cortisol hopefully takes pressure off the overworked, dysfunctional, HPA, system. Hopefully the hormone can be gradually withdrawn as the disease abates. Tapering must be done slowly as the sleepy adrenals wake up.

The above patient needs to reduce stress, get more rest and eat a nutritious diet. She is a tough case.

Headache

A generally very happy thirty-four year old female came in for a followup. She feels tired but attributes this to allergy medicines. In fact, Astepro causes drowsiness. She presented for ongoing care for migraine headaches. The headaches seem to originate in her neck and radiate up into her head. These are classic migraines: unilateral,  pounding in nature, associated with nausea and classical visual changes. Migraines run in the family and she has had a longstanding history of migraines. But the headaches have been difficult to control.

By far, the best migraine prevention medicine is Topomax. However, its nick name is "dopomax", because it is frequently associated with brain fog.

She has been off antibiotics for a year and insists her Lyme is "cured."

She presented in 2008 with an illness that went back 12 years.

Previous symptoms have included: memory loss, disorientation, anxiety, depression, nightmares, joint pain, numbness and tingling, night sweats, flu-like symptoms, dyslexia -  problems with writing and reading, brain fog, getting words mixed up and others.

She was previously treated with an aggressive program which included several months of intravenous antibiotics.

When pressed a bit further she admits to some mild muscle and joint pain but all other major symptoms have been  banished.

I would have to agree with her that her Lyme disease is largely in remission.

But headaches frequently persist after Lyme treatment, at times disabling.

Ironically, this patient works in medical research and studies Botox which can be used to treat migraines. (She has given me permission to publish her story).

Some patients are  treated "forever" -  with the thought the headaches are due to Babesia or perhaps another infection. I have found this akin beating a dead horse.

Standard treatments for migraine are usually effective. A new FDA approved treatment which frequently works is Botox which she is reticent to try.

Trouble with ticks

Bumper crop of ticks this year. Our dog came down  with a lame paw and was diagnosed with Lyme disease. Family members have unfortunately had tick bites. (I know).We live in a zero-lot-line community with minimal grass, no deer - but - lots of rabbits. Our dog is always trying to dislocate my shoulders eager to pursue these critters.
The term "deer tick" is misleading. Deer, like us humans are incidental hosts. The animals feed, neck bent, in tick infested brush. Deer heads and necks covered with Ixodes is a testament to just  how dense the population of ticks is. not that deer are a necessary part of the equation. Any warm blooded animal (even us  humans) can severe as the tertiary host for adult female maturation.  In my case, rabbits are generally the final host.

The problem is the primary host: the white footed mouse. Newly hatched larvae take feed on mice having  Borrelia swarming through their bodies (and co-infecting organisms)  then morph into nymph forms which are the primary culprit for human transmission.

The 6 legged larvae become the  8 legged nymphs, well equipped for the job at hand. They can move very quickly and then lie still, perched for action, sniffing out the carbon dioxide and body heat of their next unwitting meal.

When we pull off an adult tick we don't  really know how many others smaller forms may have attacked us unseen. The issue of how long the tick needs to be in place in order to transmit Lyme disease may be a moot point since most tick bites are never seen.

Some have suggested that most of the ticks are not infected and that we need not worry so much. Informal data from Clongen labs indicates the infection rates may range from 30-70 percent depending on the time of year in our area.

Any effective prevention programs must focus on  effective ways to kill the ticks and perhaps the mice if possible. Thinning out deer populations, as some have suggested, will be of no help.

As for my bunnies, their population does thin out - spring to fall - meals for predators like our fox. Unfornuately, the fox become the next host for the stubborn ticks.