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LYME DISEASE






Lyme Disease Often Missed as a Cause of Chronic Fatigue Syndrome.

Lyme disease is caused by a spiral shaped bacteria (spirochete) called Borrelia burgdorferi. They can be transmitted by tics, but also by mosquitoes. The spirochets have been called “the great imitators” because they can mimic virtually any disease, which is why they are often misdiagnosed. Anyone with chronic illness and especially those with chronic fatigue syndrome and fibromyalgia need to consider Lyme disease as the cause.

Patients with chronic Lyme disease most commonly have fatigue, joint and muscle pain, sleep disorders and cognitive problems (brain fog). In addition, infection with Borrelia often results in a low grade encephalopathy (infection of the brain) that can result in depression, bipolar disorder, panic attacks, numbness, tingling, burning, weakness, twitching and is associated with neurological disorders such as multiple sclerosis, dementia such as Alzheimer’s disease and amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease). In addition, this infection often results in hormonal deficiencies, abnormal activation of coagulation and immune dysfunction, which potentiate the symptoms. Patients with chronic Lyme disease often complain of “strange” or “weird” symptoms that that cannot be explained even after going to numerous doctors and often results in the patient being told that it must be psychological. Patients are often told that they are hypochondriacs and are referred to psychiatrists and counselors.

Because the symptoms are so variable, patients are usually not even considered for testing or treatment. Even if testing is done, however, standard testing will miss over 90% of cases of chronic Lyme disease. The standard testing is an immunoassay test of IgG and IgM antibodies and then a Western blot for confirmation. The problem is that these tests were designed to detect acute Lyme disease and are very poor at detecting chronic Lyme disease. In addition, doctors (infectious disease, internists, family practice, etc) most often use the Center for Disease Control (CDC) criteria to define a positive test. This criteria was never meant to be used for diagnosis, but rather for epidemiological surveillance (tracking data). If one uses an expanded Western blot with revised requirement criteria for diagnosis, studies have demonstrated an improved sensitivity of detection and a low false-positive rate.

There are also a number of coinfections that are commonly transmitted along with the Lyme bacterium, including Bartonella, Babesia, Ehrlichia and others. There are also different species in different parts of the country, making testing difficult and insensitive. As with Borrelia, the coinfections have a very high percentage of false-negative results (test negative despite infection being present).

Treatment of chronic Lyme disease can also be very problematic as the Borrelia bacteria can transform from the standard cell wall form to a non-cell wall form (l-form) and also into a treatment resistant cyst. Standard antibiotic treatments are only effective against the cell wall form and are ineffective against the L-forms and cystic forms that are usually present in chronic Lyme disease. Consequently, the usual 2-4 weeks of intravenous or oral antibiotics can be of little benefit. Even the use of longer courses of oral or intravenous antibiotics for months or years can be ineffective as well if used a the sole major therapy. A multi-system integrative approach can, however, dramatically increase the likelihood of successful treatment. This includes using a combination of synergistic antibiotics that are effective against the l-forms and cystic forms, immune modulators, directed anti-Lyme nutriceuticals, anticoagulants, hormonal therapies and prescription lysosomotropics (medications that increase the effectiveness and penetration of antibiotics into the various forms of the Borrelia spirochete). To adequately detect and treat chronic Lyme disease, physicians must understand that standard testing will miss the majority of these patients and standard treatment will fail the majority of time. One must undergo more specialized testing and treatment to achieve success in the majority of these patients.








Lyme Disease Hits Home
by Stacy Troiano, Town Times

Initially discovered 30 years ago in Lyme, Connecticut, Lyme disease has not only continued to affect lives, but it has become a widespread epidemic in the northeast almost without residents knowing. Stories about West Nile virus and encephalitis are taking over front pages everywhere, while Lyme disease flies under the radar. Doctors and citizens alike need to become more aware of this rampant, debilitating illness.

Lyme disease is reported worldwide and throughout the United States, but the states of New York, Massachusetts and Connecticut account for the majority of the cases. It is a bacterial infection caused by a spirochete form of bacteria known as Borrelia burgdorferi, and it is transmitted to animals and man through the bite of infected ticks. The tick usually responsible for transmitting the disease in northeastern United States is the black leg tick, also known as the deer tick, however, there is growing evidence that there may be other vectors of transmission besides this isolated type. A tick bite is painless, so most victims do not know they've been bitten, which allows the tick to remain attached long enough to spread its infection.

In about 50 percent of Lyme disease cases, a characteristic bull's eye rash appears around the site of the tick bite after a few days, but it's very important to understand that even if a rash does not appear, it does not mean there is no Lyme infection; the rash is just one symptom. Other common symptoms of the beginning stages of Lyme disease include flu-like symptoms, headache, sore throat, stiff neck, fever, muscle aches, fatigue and general malaise. If left untreated, later stages of Lyme disease can cause complications such as arthritis, meningitis, facial palsy, heart abnormalities and other neurological symptoms. Heart, eye, respiratory and gastrointestinal problems can also develop.

"There is not a person who I've met in Durham that doesn't either have Lyme disease or know someone closely who has it," said Sandra Ulbrich of Durham, who has been infected with Lyme disease for 16 years. I had a chance to talk to Sandra about her journey through the disease, and I was totally taken by her story. In 1989, Sandra began feeling ill, and her records read like a classic Lyme patient with throbbing headaches, fatigue, swollen glands and problems with her right shoulder and right hip. At that point doctors medicated her, but they didn't know what it was.

Two years later, Sandra was not only uncured, but she was feeling progressively worse with severe fever added to her growing list of symptoms. She was put on different medications, but doctors still could not tell what it was. She began to have pain all over her body which kept getting worse until it became diffuse achiness everywhere. Some doctors ventured that she suffered from depression or chronic fatigue, but Sandra was not buying it. In 1992, she tested positive for Lyme disease, but the "specialist" at Yale told her she was not positive enough and insisted she didn't have it.

As time went on for Sandra, the infection continued to bring out more and more symptoms including intestinal problems and intense dizziness. She began feeling what she described as lightning bolt shockwaves going into her brain, and she saw a neurologist who also was stumped.

The late stages of Lyme disease wreak havoc on the brain. Sandra went in for a brain biopsy about one and a half years ago, which found a demyelinating lesion in her right parietal lobe. Doctors still were avoiding a Lyme disease diagnosis. Some doctors thought it was cancer, others said maybe she had a stroke, and still others thought it could be multiple sclerosis because of bacterial similarities. Sandra had done her reading on the subject, and with help from her sister who is a doctor herself, she was nearly certain that the other diagnoses were incorrect, and the cause was actually Lyme disease that had now manifested itself in the brain.

The hyperfusion and encapsulated lesion in her right parietal lobe would require brain surgery for Sandra, and at the time she entered the hospital she could not raise a finger or a toe on her left side; it was completely dead. "This was devastating to me. I'm a trained classical pianist. Music is a very big part of my life, and now I couldn't use my left hand," she said. Sandra's new doctor wanted to see all of her records, including any tests given for Lyme disease, from years ago when the symptoms began. The doctor who had performed the test and had deemed Sandra "not positive enough" claimed that he no longer had records from that long ago. Sandra was not satisfied. She persisted and called the doctor's secretary who informed Sandra that she did indeed find her records, including the positive Lyme test. After about 12 years, Sandra was finally diagnosed correctly.

"I wanted to talk about Lyme disease not for myself because the damage is done, but I want people, especially in this area, to be aware of what an epidemic it's become and what it can do to a person," Sandra said. Connecticut has one of the highest infection rates for Lyme disease in the country, and misdiagnosis and proper treatment are clearly a problem. "Any kind of fever, any kind of aches and pains, any stiff neck or headaches, do not let doctors tell you its depression or chronic fatigue or anything else. Investigate Lyme. Get on some antibiotics." Sandra also stressed that the most important thing to remember if you are possibly infected with Lyme is that the tests are not always reliable. Clinical symptoms are the only way to truly tell whether or not the disease is there.

"I was very lucky to have such amazing support from my family. I just want to use my experience to make people aware. That's the most important thing. Just be aware that it does happen, and in this area almost everything carries it. There's no such thing as being too cautious," Sandra said.

There's no way to be completely impervious to a tick bite, and not all deer ticks carry Lyme, but there are precautions to take that will greatly lessen your chances of being infected. Always inspect yourself for ticks whenever you have been outside. Wearing lightly colored clothing will make it easy to see any ticks that may have attached themselves. Wash and dry clothes to kill any remaining ticks. Clear brush from any yard area and keep grassy areas mown. And most of all, wear insect repellent, preferably with Deet. If a tick is found on the body, immediately remove it. To safely remove a tick, grasp the mouth of the tick with tweezers as close as possible to the attachment site, being careful not to squeeze or puncture the body of the tick, which may contain infectious fluids. More information on Lyme disease can be found through the International Lyme and Associated Diseases Society (ILADS).

After being able to talk extensively with Sandra Ulbrich, I found myself very engrossed in her story. Here is a woman who had suffered from nearly every single symptom of Lyme disease, and is now doing everything she can to inform other people. I started reading many articles, researching anything I could find about Lyme disease, and telling a number of people about what an amazing person I had met in Sandra; I couldn't stop thinking about her story. When I was leaving her house after we had talked, she told me that if she could affect even one person and make them become more conscious of the widespread problem of Lyme disease around here, then she would be happy. I hope I am the first of many.







Diagnosis and Treatment of Lyme Disease
(A Culmination of the Literature) Kent Holtorf, M.D.

CHARACTERISTICS of BORRELIA BURGDORFERI
1. Over 1500 gene sequences
2. At least 132 functioning genes (in contrast, T. pallidum has 22 functioning genes)
3. 21 plasmids (three times more than any known bacteria)

IMMUNE EVASION (‘STEALTH’ PATHOLOGY)
1. Immune suppression
2. Phase & antigenic variation
3. Physical seclusion
4. Secreted factors

TYPES OF LYME DISEASE
1. Early Lyme disease (“Stage I”)
... A. At or before the onset of symptoms
... B. Can be cured if treated properly
2. Disseminated Lyme (“Stage II”)
... A. Multiple major body systems affected
... B. More difficult to treat
3. Chronic Lyme Disease (“Stage III”)
... A. Ill for one or more years
... B. Serologic tests less reliable (seronegative)
... C. Treatment must be more aggressive and of longer duration

CHRONIC LYME
1. Disease changes character
2. Involves immune suppression
3. Less likely to be sero-positive for Lyme
4. Development of alternate forms of Borrelia
5. More likely to be co-infected
6. Immune suppression and evasion
7. More difficult to treat
8. Protective niches

ALTERNATE MORPHOLOGIC FORMS
1. Spirochete form has a cell wall
2. L-form (spiroplast) has no cell wall
3. Cystic form

lyme_photo01.jpg

Borrelia burgdorferi develops granules & cysts with environmental stress
Antimicrobial Agents & Chemotherapy, 1995;39(5):1127-33.

IMMUNE SUPPRESSION BY Borrelia burgdorferi
1. Bb demonstrated to invade, inhibit and kill cells of the immune system
2. The longer the infection is present, the greater the effect
3. The more spirochetes that are present, the greater the effect

PROTECTIVE NICHES
1. Within cells
2. Within ligaments and tendons
3. Central nervous system
4. Eye

DIAGNOSING LYME

1. It is a clinical diagnosis supported by appropriate testing (likelihood of a false negative must be understood)

2. Look for multi-system involvement
3. 17% recall a bite; 36% recall a rash
4. 55% with chronic Lyme are sero-negative
5. PCRs- 30 % sensitivity at best- requires multiple samples, multiple sources

NATURAL KILLER CELL ACTIVITY AND NUMBER
1. Low counts seen in active Lyme
2. Reflects degree of infection
3. Can be used as a screening test
4. Can be used to track treatment response
5. Can predict relapse

ELISA ANTIBODY TESTING
1. Over 75% of patients with chronic Lyme are negative by ELISA

WESTERN BLOT
1. Reflects antibody response to specific Bb antigens
2. Different sensitivities and specificities of the bands
3. Some bands are potentially seen in different bacteria- “nonspecific bands”
4. Some bands are specific to spirochetes
5. Some bands are specific to Bb
6. Specific: 18, 23-25, 28, 31, 34, 37, 39, 58, 83 & 93
7. Spirochetes in general: 41 (flagellum)
8. First immune response if present is usually 41 and 23 KD bands
9. Response to the 31 KD proteins is not usually seen for a year after initial infection

lyme_photo02.jpg

CDC IGG WB CRITERIA
1. IGG WB 5 of the 10 bands (18,23,28,30,39,41,45,58,66)
2. Criteria based on early Lyme
3. IGENEX adds 3 specific bands (31,83 and 34) and 3 non-specific bands (22,37,73)

CDC IGM WB CRITERIA
1. IGM WB 2 of the 3 bands 23, 39, 41
2. IGENEX adds 3 specific bands (31,34 and 83) and 3 non-specific bands (22,37,73)

REVISED CRITERIA WITH WB

1. IGG WB: 2 specific band criteria has demonstrated improved sensitivity and maintained specificity

2. Can diagnosis Lyme if any one band (IgG or IgM) of 18, 23, 28, 39 or 58 kDa or if any 2 or more of the following bands are present; 30, 45,41 and 93

3. If negative or require further confirmation, can obtain IGENEX WB (adds specific bands of 31, 34 an 83, which are typically seen in chronic disease)

4. Positive if any one band of 18, 23, 28,31,34, 39, 58 or 83

5. If positive for Borrelia on any test, consider testing for neurotoxins

6. Consider testing for co-infections (discussed below)

7. Check for coagulation defect (See Hypercoaguable State in CFS and FM)

LYME DISEASE TREATMENT

1. Use an integrative treatment for optimal results. NEED MULT-SYSTEM TREATMENT (See CSF/FM pages).

2. Treating with just antibiotics has poor likelihood for success with chronic Lyme.
3. Extended duration often needed for chronic Lyme
4. Use clinical endpoints
5. Watch for Herxheimer reactions (may occur in 3-4 week cycles)
... A. Directed nutraceutical can be beneficial
... B. Immune modulatators
... C. Antibiotics
... ... 1. Oral
... ... 2. Intramuscular
... ... 3. Intravenous
... ... 4. Often need antibiotic combinations with lysomotropics in addition to integrative approach to address different forms (spirochete, L-form, cystic)
... D. Intravenous Antimicrobial IV’s (Viral Plus, etc) or IV Immunoglobulin
...
E. Adjunctive medications (Lysosomotropics) to increase antibiotic effectiveness

NUTRACEUTICAL
1. Samento or improved version Keline
2. Cumanda improved version Eklipse
3. Consider combination of Eklipse, artemesinin I and Keline as a basis
4. Fibrinolytic enzymes and heparin if coagulation defect present (present in approximately 80% of cases)
5. Give probiotics and natural antifungals when using prolonged antibiotics

IMMUNMODULATION
1. Essential to improve immune function
... A. Leukostim
... B. Proboost
... B. Maitaki Mushroom
... C. Transfer Factor-Lyme specific
... D. Low Dose Naltrexone 3.5 mg qhs
... E. Delta-Immune
    F. Neupogen (filgrastim) (Enhanced eradication of Bb demonstrated in mice) 5 mcg/kg SQ

    G. Benicar (Marshal Protocol)

ORAL ANTIBIOTICS
1. Tetracyclines-Doxycycline, Minocycline 100 mg II tabs bid or Tetracycline 500 mg II tabs tid-qid
... A. Good Tissue penetration
... B. Covers Borrelia and Ehrlichia
... C. Anti-inflamatory properties
...
D. Photosensitivity, GI upset frequent

2. Penicillins such as Augmentin 875 mg PO bid-tid or Amoxicillin 875 II tabs bid-tid
... A. Monitor LFT’s with Augmentin
... B. Addition of Probenecid 500 mg/qd-tid
...
C. Cannot exceed 3 tabs Augmentin per day due to clavulanate, thus can give with Amoxicillin

3. Macrolides such as Zithromax 500-600 mg, Biaxin 1000-2000 mg/day or Ketek 800 mg/day
... A. Combination therapy often needed (ie plus cephalosporin or Flagyl or tinidazole)
... B. Well tolerated
...
C. Improved tissue penetration with hydroxycholoroquine or amantadine

4. Cephlosporins (3rd generation) Omnicef 300 mg one po tid or (2nd generation) Ceftin 500 mg II tabs bid

5. Flagyl 250-500 qd-tid or tinidizole (better tolerated) 500 mg bid for 2 weeks every 1-3 months
... A. Kills spore forms of Borrelia
... B. May decrease effect of tetracyclines
... C. Antabuse reaction with alcohol
... D. Potentially neurotoxic
...
E. Adults only

6. Rifampin 300 mg bid

IM ANTIBIOTICS
1. Benzathine Pennicillin 1.2-2.4 Million Units 1-2 times per week
... A. Excellent foundation for combination treatment
... B. No GI Side effects
...
C. Efficacy may be close to IV

IV ANTIBIOTICS
1. Consider if illness for greater than year
2. Failure or intolerance of oral therapy
3. Consider starting with IV antibiotics for 1- 3 months (until clearly improved) then oral/IM maintenance
4. May require extended duration with long term disease and immune supression
5. Ceftriaxone (Rocephin) most commonly used (dose 2 grams qd 4 x/week)
... A. Risk of billiary slugging-use Actigall
... B. Monitor LFT’s
6. Cefotaxime (Claforan)
... A. Requires twice daily dosing 2 grams bid. Can give as continuous infusion of up to 8 grams/day
... B. Monitor LFT’s
7. Doxycycline 400 mg qd (slow infusion)
... A. Requires central line
... B. Do not use in pregnancy or children
8. Azithromycin 500 mg qd
... A. Requires central line
... B. Limited experience
9. Unasyn (ampicillin-sulbactum) 3 grams IV tid
10. Timentim (4th generation penicillin and clavulanate) 3.1 grams IV q 6 hours
11. Primaxin 500-1000 mg IV bid-tid

CO-INFECTIONS IN LYME
1. Very common and nearly universal in chronic Lyme
2. Diagnostic tests even less reliable
3. Co-infected patients more ill
4. Co-infected patients more difficult to treat

POSSILBE CO-INFECTIONS
1. Babesia
2. Bartonella
3. Ehrlichia
4. Mycoplasma
5. Viruses such as EBV, CMV, HHV6, HHV7
6. Others

TESTING
1. Antibody testing has a high rate of false-negative
2. Consider treatment if poor response despite negative test results.

BABESIA
1. Is a parasite (one study showed 66% of chronic Lyme have Babesia co-infection)
2. Many different species found in ticks (13+)
3. Not able to test for all varieties
4. Diagnostic tests insensitive
5. Chronic persistent infection documented
6. Infection is immunosuppressive

TREATING BABESIOSIS
1. Can be treated while on Lyme medications
2. Lariam 250 mg (5 caps loading dose) then 1 po week for 5 weeks with Artemisinin
2. Atovaquone (Mepron) 750 mg qd-bid plus azithromycin 500-600 mg for 4 to 6 months
3. Consider Flagyl or tinidiazole
4. Artemesinin demonstrated to be beneficial (2-3 tabs bid)

BARTONELLA
1. More ticks in NE contain Bartonella than contain Lyme
2. Clinically seems to be a different species than “cat scratch disease”
3. Gastritis and rashes, CNS, seizures, tender skin nodules and sore soles
4. Tests are insensitive

TREATING BARTONELLA
1. Levaquin 750 mg qd
2. Cipro 750 bid
3. Doxy 100 mg II po bid
4. Zithromax 500-600 mg qd

EHRLICHIA
1. Flu-like symptoms of severe headaches, very painful muscles, low WBC counts or elevated liver enzymes
2. Testing insensitive

TREATMENT OF EHRLICHIA
1. Doxy 200 mg bid
2. Rifampin 300 mg bid

ADJUNCTIAL MEDICATIONS TO INCREASE ANTIBIOTIC EFFECTIVNESS
1. (Lysosomotropics) Will increase the effectiveness of antibiotic and improve success
 A. Porbenecid 500 mg qd-tid. Decreases B-lactam excretion and used to achieve higher serum levels.
     1. Will also decrease excretion on NSAIDS, benzodiazepines and other medications
 B. Hydoxychloroquine (200 mg qd-bid)-decreases formation of cystic forms and increases penetration of antibiotics into cysts
 C. Amantadine 100 mg qd-tid. Increases penetration into cells and cysts, immune boosting and is antiviral








Lyme Disease the Cause of 1/3 of Psychiatric Disorders?
From What Psychiatrists Should Know about Lyme Disease, ILADS

In a published study (Hajek et al, Am J Psychiatry 2002;159:297-301), one-third of psychiatric inpatients showed signs of an infection with the Lyme spirochete, Borrelia burgdorferi. It has been found that that even severe neuropsychiatric behavioral symptoms in this population can often be reversed or ameliorated when a multi-system treatment program targeting Lyme disease is used.

 

Patients with late-stage Lyme disease may present with a variety of neurological and psychiatric problems, ranging from mild to severe. These include:

 

  • Cognitive losses including:
  • Memory impairment or loss (“brain fog”)
  • Dyslexia and word-finding problems
  • Visual/spatial processing impairment (trouble
  • finding things, getting lost)
  • Slowed processing of information
  • Psychosis
  • Seizures
  • Violent behavior, irritability
  • Rage attacks/impulse dyscontrol
  • Anxiety
  • Depression
  • Panic attacks
  • Rapid mood swings that may mimic bipolarity (mania/depression)
  • Obsessive compulsive disorder (OCD)
  • Sleep Disorders
  • Attention deficit/hyperactivity disorder
  • (ADD/ADHD)-like syndrome
  • Autism-like syndrome

 

At any time, patients infected with Borrelia may also exhibit cognitive symptoms such as memory and concentration impairments and word-finding difficulties, ADD/ADHD-like symptoms, learning disabilities, OCD, crying spells, rages, depression, bipolar disorder, panic and anxiety disorders and psychoses - all may be caused or exacerbated by Lyme disease. Disorders of the nervous system have been found in 15–40% of late-stage (tertiary) Lyme patients (Caliendo et al, Psychosomatics 1995;36:69-74). When Lyme disease affects the brain, it is often referred to as Lyme neuroborreliosis or Lyme encephalopathy. Unfortunately, only a small percentage of these patients will be properly diagnosed as having Lyme disease and most continue to have relatively unsuccessful treatment with psychiatric medications.

 

Neuroborreliosis can mimic virtually any type of encephalopathy or psychiatric disorder and is often compared to neurosyphilis. Both are caused by spirochetes, are multi-systemic, and can affect a patient neurologically, producing cognitive dysfunction and organic psychiatric illness. Such symptoms may be dormant, only surfacing years later.

 

Dr. Brian Fallon, director of the Lyme Disease Research Program at Columbia University and principal investigator of the NIH-funded study of brain imaging and persistent Lyme disease, cites five questions that imply warning signs of possible Lyme encephalopathy:

 

1. Are there markers of non-psychiatric disease such as erythema migrans rash, arthralgias or arthritis, myalgias, severe headaches, sound or light sensitivity, paresthesias, diffuse fasciculations, cardiac conduction defects, word-finding problems, short-term memory loss, tremors, cranial neuropathies, and/or radicular or shooting pain?

 

2. Is this psychiatric disorder atypical or unusual? For example, does a panic attack last longer than the expected 1/2 hour? Or is it a first ever panic attack at age 50?

 

3. Is there poor or paradoxical response or excessive side effect sensitivity to medications that are expected to be helpful for particular psychiatric symptoms?

 

4. Is this new-onset disease without psychological precipitants such as new stressors or secondary gain?

 

5. Is there an absence of a personal history or family history of major psychiatric disturbances?

 

Negative answers to these questions do not rule out the presence of Lyme disease. But a “yes” to most of the questions, especially in a patient with an out-of-doors lifestyle or a pet, demands further clinical assessment. Dr. Fallon recommends Western blot serologic studies (IGENEX), lumbar puncture, neuropsychological testing, brain MRI and SPECT (single photon emission computerized tomography) scans.

 

Because blood tests at the top three general medical laboratories in the nation fail to detect a majority or large percent of Lyme antibodies, ILADS recommends use of laboratories that specialize in Lyme and other tick-borne illnesses. Blood tests should not be used to rule out Lyme disease when there is a strong clinical presentation because of the high incidence of false negative results.

 

What should a psychiatrist or treating physician do?

 

Patients with a psychiatric disorder should be screened for symptoms related to Lyme, especially those with complicated or atypical presentations. Be suspicious of Lyme if a patient mentions cognitive changes, extreme fatigue, weight changes, headaches, fibromyalgia, a history of “mono,” “spider bites,” multiple sclerosis, explosive rages or sudden mood swings. Consider Lyme disease in children with behavioral changes, fatigue, school phobias, academic problems, learning disabilities, headaches, sore throats, GI complaints and/or migrating pains. In teens, Lyme disease may be complicated by drug abuse.

 

The Lyme spirochete is slow growing and can be difficult to treat, so the patient should be treated with multi-system treatments that include appropriate antibiotics for at least two to four weeks beyond symptom resolution. Most individuals with Lyme disease respond to multi-system treatments, but the treatment course is highly patient specific.

 

Some of the common symptoms of late-stage (tertiary) Lyme disease and other tick-borne co-infections:

 

• Profound fatigue

• Chills, sweats and skin flushes

• Night sweats

• Migrating arthralgias

• Muscle pains/twitching

• Sleep disturbances

• Severe headaches

• Shifting neurologic pains

• Tremors, shakiness

• Numbness, tingling sensations and pain often shifting and unusual in type

• Cranial nerve disturbance (Facial numbness, pain, tingling, paralysis, optic neuritis, trouble swallowing,   distortion of smell or taste)

• Losses in fields of attention/executive functions such as inability to maintain divided or sustained attention and memory

• Impaired emory functions (lost items, missed appointments, retold stories)

• Language difficulties (halting speech, disrupted participation in conversation)

• Impaired visual/spatial Processing (Inability to find things, tendency to get lost, disorganization, difficulty reading, especially for enjoyment)

• Impaired abstract reasoning (Poor problem-solving/ decision-making)

• slowed processing speed (Familiar tasks take longer, can’t follow conversations well).

 

Most or all of these impairments, if caused by neuroborreliosis, may improve with proper antibiotics combined with other appropriate multi-system treatments.






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