memory – F.I.G.H.T for your health!

H.R.T. from Longevity Plus

Linda — Sun, 16 May 2010 06:28:55 +0000

Linda’s comment: I began taking the H.R.T. from www.longevityplus.com and happy that I did. This is an awesome product….This H.R.T. isan herbal remedy from Thailand. Please read about it at the above web site.

Dr. Gordon’s Comments: What you must know about HRT, both kinds, the dangerous pharmaceutical version and the documented safe alternative herbal form, PUERARIA MIRIFICA. You can have happy menopausal patients without doubling their breast cancer recurrence rate. Just read this carefully and, if interested, ask Longevity Plus customer support to email you a packet of scientific information.

Anyone realizing that hormone therapy doubles recurrence of breast cancer should take the time to learn about the alternative to standard HRT that is Longevity Plus’s H.R.T. (Herbal Remedy from Thailand). Here we have epidemiological evidence that those consuming Pueraria Mirifica in their diet regularly have the lowest incidence of Breast Cancer according to the World Health Organization statistics.

Now your patients can have the improved quality of life that the ESTRIOL-like MIROESTROL component to H.R.T. provides without the increased risk of breast cancer associated with the pharmacological based HRT (Hormone Replacement Therapy) so widely used today in the US in spite of its known risks of heart disease and cancer.

Try H.R.T. on your next patient who has memory loss, insomnia, hot flashes, vaginal dryness and the other constellation of symptoms associated with menopause and see for yourself. Remember, the added ingredients in H.R.T. include the VITAL METHYLATION FACTORS like all 3 forms of Folic Acid and Methylcobalamin. The published data about the more natural form of folic acid 5’MTHF shows it helps depression, even when antidepressants have not helped, and helps peripheral neuropathy, and improves memory, and helps to deal with endothelial vascular dysfunction ( vascular disease).

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com

Full article: http://www.medpagetoday.com/HematologyOncology/BreastCancer/tb/8893

Excerpt:

HRT Doubles Recurrence Risk in Breast Cancer Survivors

LONDON, March 25 — Breast cancer survivors treated with hormone replacement therapy had a more than two-fold increased risk of recurrence or a contralateral malignancy, according to long-term follow-up data from a randomized clinical trial.

•Note that this is one of the few randomized, controlled studies that have examined the risk of breast cancer recurrence associated with HRT.
Those randomized to HRT had five-year breast cancer rates of 22.2% compared with 8% in women who received best patient care for menopausal symptoms without hormone therapy, Lars Holmberg, M.D., Ph.D., of King’s College London, and colleagues, reported in the April 2 issue of the Journal of the National Cancer Institute.

“The results of the HABITS [Hormonal Replacement after Breast Cancer — Is It Safe?] trial indicate a substantial risk a new breast cancer event among breast cancer survivors using hormone therapy,” the authors concluded.

“Our results further suggest that hormone therapy not only induces and promotes breast cancer but may also stimulate the growth of tumor microdeposits in breast cancer survivors,” they added.

Despite the statistically significant impact of hormone therapy on breast cancer risk, the authors said more data from randomized studies are needed to define the risk and to clear up inconsistencies in prior studies.

However, Kathleen Pritchard, M.D., a breast cancer specialist at Sunnybrook Odette Cancer Center in Toronto, said in an accompanying editorial that the study “suggests quite definitively that there is a statistically significantly increased risk of recurrence in women given HRT following diagnosis of breast cancer.”

Persistent questions about the potential risks and benefits of HRT in breast cancer survivors provided impetus for several observational studies and analyses of case series. More recently, data from the Women’s Health Initiative and the Million Women Study provided additional compelling evidence of an increased risk of breast cancer among HRT users, the King’s College authors said.

Mercury, new shocking findings

Linda — Fri, 22 Jan 2010 15:48:34 +0000

Linda’s comment: This is a GREAT list compiled by Dr Michael…They are finding moe and more things with Mercury. Everyone puts focus on vaccines, however Mercury is everywhere, including our foods…..Corn syrup, fish, the list goes on and on…..check out this web site >>>>>
http://www.healthobservatory.org/library.cfm?refID=105040 <<<>>>
http://www.atsdr.cdc.gov/toxprofiles/phs46.html….. Here are some human exposures that are important….. http://www.epa.gov/hg/exposure.htm…

How many of you buy your children those cute shoes with flashing lights? Or those cute clothes with flashing lights. Every time those lights flash your child is getting a shot of mercury!! I ask myself, WHAT IS THE INDUSTRY THINKING WHEN THEY LOAD OUR CHILDREN’S CLOTHES WITH MERCURY???? Is money that important?? We the consumer need to stand up and SAY NO MORE!!

When you read information like I have supplied you above and below, it should scare you enough to focus on detoxing these toxins from your body. Everyday you walk out your front door you are getting slammed with 500 to 600 environmental toxins. A lifelong daily detox is vital to your health and well being.

I have been on the FIGHT program for 1 1/2 years now and I thank God daily that I have had this experience. Those of us with chronic illness need to detox daily or we will never get well.

Regards,
Linda or Angel

Toxic Effects of Excess Mercury

Mercury is considered to be the most toxic non-radioactive Heavy Metal.

Cardiovascular System
Excessive ingestion of Mercury can cause Angina.

Ears/Hearing
Mercury toxicity can be an underlying cause of Deafness.
Mercury toxicity can be an underlying cause of Tinnitus.

Excretory System
Mercury accumulates in and damages the Kidneys.

Immune System
Mercury toxicity can be an underlying cause of Autoimmune Diseases.
Mercury weakens the Immune System by interfering with the balance of Helper T-Cells subpopulations:
Mercury inhibits the activity of TH1 Helper T-Cells.
Mercury stimulates the overactivity activity of TH2 Helper T-Cells.
Excessive exposure to Mercury causes Hodgkin’s Disease (a form of Lymphatic Cancer).

Metabolism
Exposure to Mercury (or its vapors) can cause Fatigue.
Mercury stimulates the production of Free Radicals.
Mercury accumulates in and damages the Liver.

Musculoskeletal System
Mercury increases the risk of Arthritis.
Exposure to Mercury can cause Muscle Tension.
Exposure to Mercury can cause Muscle Weakness.

Nervous System
Exposure to Mercury causes impairment in Abstract Reasoning ability.
Exposure to Mercury can cause Aggressiveness.
Mercury accumulation in the Brain is one of the primary causes of Alzheimer’s Disease.
Exposure to Mercury can cause Anxiety.
Exposure to Mercury can cause Apathy.
Exposure to Mercury can cause decreased Attention Span.
Mercury concentrates in and damages the Brain:
Mercury damages the Blood-Brain Barrier.
Mercury concentrates in and damages the Cerebral Cortex.
Exposure to Mercury can cause impairment of Concentration.
Exposure to Mercury can cause impaired Coordination ability.
Exposure to Mercury can cause Depression.
Exposure to Mercury can cause Drowsiness.
Mercury can cause Epilepsy.
Exposure to Mercury can cause Hallucinations.
Exposure to Mercury (or its vapors) can cause Headache.
Exposure to Mercury (or its vapors) can cause Insomnia.
Exposure to Mercury can lower Intelligence.
Exposure to Mercury (or its vapors) can cause Irritability.
Exposure to Mercury can cause impairment of Learning ability.
Exposure to Mercury (or its vapors) can cause Memory impairment.
Mental Retardation can occur as a result of excessive exposure to Mercury.
Exposure to Mercury is associated with poor (“bad”) Mood.
Mercury can cause Multiple Sclerosis (MS).
Exposure to Mercury can cause Nervousness.
Mercury can cause Numbness.
Exposure to Mercury can cause Paralysis.
Exposure to Mercury can cause Speech Impairment (in the form of slurred Speech).
Exposure to Mercury can cause Tremor.

Respiratory System
Mercury concentrates in and damages the Lungs.

Sexual System
Exposure to Mercury during Pregnancy increases the risk of Birth Defects.
Long-term exposure to Mercury can cause Female Infertility.
Long-term exposure to Mercury can cause Male Infertility.

Skin
Mercury toxicity can be an underlying cause of Dermatitis.

Sincerely,

Dr. Michael

Lyme Encephalopathy

Linda — Sun, 29 Nov 2009 05:39:37 +0000

Encephalopathy is like fine art: Most people know it when they see it, but there is very little agreement on how to define it. At the 14th International Lyme Disease Conference, Brian A. Fallon, MD,[1] of Columbia University and the New York State Psychiatric Institute, New York, NY, tried to do just that. More importantly, he described the different ways one can define encephalopathy, the strengths and limitations of each approach, and significantly, what other aspects of life can give the impression of encephalopathy where none exists. First, one must evaluate patients with persistent Lyme encephalopathy by asking the following questions:

Is the diagnosis correct?
Are there comorbid psychiatric disorders that could be treated better? Does the patient have a psychogenic medical illness? What was the patient’s response to prior antibiotics?
Was previous treatment adequate? How long was the course, and what was the route of administration? Was there a subsequent relapse

Defining the Problem
The first question can pose a problem for the clinician. There is currently no agreed-upon definition of Lyme encephalopathy, and this has caused a great deal of confusion in the field. Encephalopathy was not included in the CDC’s case definition of Lyme disease, so NIH-funded studies of this condition can be hard to defend without a government- or society-sanctioned definition.
For investigators in this field, there have been numerous and differing definitions of Lyme encephalopathy. One of the earlier attempts at defining the problem was made by Logigian and colleagues in 1990.[2] This group listed the chronic neurologic abnormalities of Lyme encephalopathy as memory loss, depression, sleep disturbance, irritability, and difficulty finding words. However, there is much overlap between these symptoms and those of depression unrelated to Lyme disease.

Some further possibilities for defining the condition include self reporting of cognitive deficits, self reporting plus laboratory signs of CNS involvement, objective evidence of deficits on cognitive testing, or objective deficits plus laboratory signs of central nervous system (CNS) involvement. Signs of CNS involvement have included elevated cerebrospinal fluid (CSF) protein or pleocytosis, abnormal brain scans or tests (single photon emission computed tomography [SPECT], magnetic resonance imaging [MRI], or electroencephalogram [EEG]), intrathecal antibody production, or a positive polymerase chain reaction (PCR) for Borrelia burgdorferi DNA or a positive culture. However, objective tests often do not agree with patients’ perceptions. This is especially true for memory in depression

One Deficit, or Many?
One challenge is determining which and how many cognitive deficits to include in the definition and evaluation. For instance, some investigators have looked at a single, representative deficit (ie, single-domain methods) such as memory.[3] Others have looked at numerous deficits in each patient (ie, multiple-domain methods), such as memory, verbal fluency, and attention.[4] The advantage of the single domain method is that it focuses on one main problem and makes for a more homogeneous study sample. However, such a study may exclude patients who are impaired in other cognitive areas. The multiple domain method is particularly well suited for a disease that affects multiple cognitive domains, as one would expect for a global term such as encephalopathy. However, if patients have deficits primarily in one domain, this method becomes less sensitive (by dilution with less affected cognitive areas).
A further complication is how one defines and measures these deficits. One approach is to compare to age-matched norms. A second approach is to compare to actual or estimated premorbid or general ability levels. Comparison to age-matched norms provides simple, clear criteria for measurement and comparison, a cut-off score. But if the deficit being compared is correlated with a general ability (such as memory and general intelligence), then people with higher intelligence but with memory impairment may not be detected by this method. For example, if a subject has a general intelligence IQ of 130 and a memory score of 100, his full-scale IQ is 2 standard deviations above the age-norm, while his memory score is exactly at the age-norm. Compared to age-norms, this subject would not have memory impairment. Compared to his full-scale IQ, his memory score would be 2 standard deviations below expected — which clearly would suggest impairment. One method identifies this subject as normal, the next identifies him as impaired.

In contrast to the age-norm method, comparison to general levels of ability can allow for a more customized approach to assessing cognitive impairment, thus enhancing sensitivity. However, general abilities can be decreased by illness, regardless of a specific effect on that ability. In addition, this approach assumes that the domain of interest is strongly correlated with general ability.

The ideal screening tool for Lyme encephalopathy should have maximal sensitivity and specificity. Premorbid ability should be taken into account, by using norms adjusted for age, sex, and education level, or with balanced premorbid assessment of ability. It is still not clear whether a single- or multiple-domain definition of neurocognitive impairment should be used.

There are many screening tools for assessing premorbid ability, including verbal IQ, verbal comprehension index, vocabulary subtest score, reading subtest score (WRAT-R [Wide range achievement test-Revised]), demographic composite (Barona demographic equation), and national adult reading test (NART). Of course, different investigators have used different methods of assessing premorbid ability, thus further complicating comparisons between studies.

One of the few studies that actively evaluated patients with Lyme encephalopathy was conducted by Logigian and coworkers in 1997.[5] This study reveals some of these diagnostic problems discussed above. In this study, the investigators screened patients for Lyme encephalopathy and then evaluated the change in SPECT scan perfusion after treatment. Starting with clearly defined criteria for “definite Lyme encephalopathy” — subjective complaints of cognitive deficits, along with either a past or present CSF abnormality (intrathecal antibodies or PCR positivity) or objective cognitive deficits (as measured by 2 standard deviations below normal on verbal or visual memory tests, or 1 SD below normal on both tests) — they examined whether brain perfusion improved after treatment. While the brain imaging results were of interest in that all of the patients with definite Lyme encephalopathy showed improved perfusion after treatment, this study also demonstrated that the definition of Lyme encephalopathy, if restricted to cognitive testing, would have been too restrictive using their criteria. In other words, 5 of the 13 patients with “definite Lyme encephalopathy” did not have cognitive impairment using their criteria for impairment. Yet, these very same patients had abnormal SPECT scans that improved after treatment. Their cognitive criteria, which used age-norms for comparison, failed to identify 38% of patients with CNS abnormalities.

Dr. Fallon described an ongoing study of Lyme encephalopathy he is conducting at the NY State Psychiatric Institute. Because previous studies disagree about which is more accurate, single- or multiple-domain evaluation, they will collect data in 6 domains: motor skills, psychomotor skills, attention, memory, working memory, and verbal fluency. Data are preliminary, but so far the most sensitive method for the detection of impairment appears to be one that incorporates testing from multiple cognitive domains. Memory and working memory seem to be the most affected neurocognitive areas. Even so, about one quarter of the control subjects appeared to have neurocognitive deficits, compared to two thirds of the patients with complaints of memory impairment secondary to Lyme disease. Dr. Fallon suggested that the best method for detecting memory impairment in particular might be one that makes use of ethnicity- and education-adjusted norms. The Psychological Corporation is expected to publish such norms within the next year.

Complicating Factors
When determining the presence of encephalopathy in patients with Lyme disease, one must take into account other causes of cognitive complaints (Table 1), including the use of medications that can impair neurocognitive function (Table 2).

[Hysterical dementia is often over diagnosed in patients with Lyme encephalopathy, but it is rare for this to occur alone as a conversion symptom. The label of “hysterical” is often applied when phenomena are outside the clinician’s experience. For instance, females and male homosexuals more often receive this label. Based on studies over the past 50 years, many patients who are initially given the diagnosis of hysterical dementia go on to develop an organic CNS disorder.

Dr. Fallon is conducting a randomized, placebo-controlled study of brain imaging and treatment of persistent Lyme encephalopathy (Columbia University – National Institute of Neurological Disorders and Stroke [NINDS]). Treatment will involve IV ceftriaxone for 10 weeks, with a 14-week antibiotic-free follow-up period. At the end of the 24-week study, patients who had been randomized to receive placebo will be given 6 weeks of IV ceftriaxone. Evaluations will be conducted at baseline and 12 and 24 weeks. PET and MRI imaging as well as neuropsychiatric tests are being used to evaluate response to treatment. Patients will be recruited for this study over the course of the next 3 years.

An In-depth Study of Neurocognitive and Behavioral Lyme Disease

Patricia K. Coyle, MD,[6] and colleagues from the State University of New York at Stony Brook School of Medicine have conducted a prospective, controlled study to characterize the neurologic and neurobehavioral manifestations of Lyme disease in North America. They examined 3 groups: adults with acute disease, adults with chronic disease, and children with disseminated disease (ie, more than 1 erythema migrans [EM] lesion). They attempted to characterize changes to the CSF and identify pathogenetic mechanisms and predictors of outcome. This work builds on a previous study by Coyle and colleagues.[7]
The clinical syndromes studied included cranial (facial) neuropathy, radiculoneuritis, meningitis, and arthritis. The major symptoms (ie, seen in more than two thirds of patients) in adults with acute disease included fatigue, headache, sleep problems, stiff neck, and myalgia. Those with chronic disease had a different constellation of major symptoms, such as concentration difficulties, fatigue, arthralgias, myalgias, mood disturbance, memory loss, sleep problems, word-finding difficulties, knee pain, confusion, and stiff neck. Children with disseminated Lyme disease experienced major symptoms of headache and fatigue. By symptom score, the major initial defining syndrome for the acute adult group was meningitis, followed by multifocal EM, cranial nerve palsy, radiculoneuritis, and single EM; for the chronic adult group, single EM was the most common presenting symptom, followed by arthritis, cranial nerve palsy, and multifocal EM; and for children with disseminated disease, extraneural symptoms.

These investigators concluded that the children with disseminated disease are less symptomatic than adults, but they have more inflammatory CSF changes. Among the adult patients, those with chronic disease were more symptomatic than those with acute disease. They had more cognitive, mood, and joint disturbances; more severe symptoms; and more current depression, anxiety, and adjustment problems. However, it was the acute disease patients who were more likely to show objective cognitive deficits.

Surprisingly, CSF changes were not marked in either group of adult patients. In adults with acute disease, 45% had reactive or borderline CSF serology, 7% had intrathecal antibody production (a common test for CNS infection), 30% had an elevated white blood cell count (WBC), 23% had elevated protein, only 14% had evidence of oligoclonal bands, and only 7% had an elevated IgG index. Similarly, in the adult chronic disease group, 35% had reactive or borderline CSF serology, 6% had intrathecal antibody production, 15% had elevated WBC, 15% had elevated protein, 6% had evidence of oligoclonal band testing, and 3% had an elevated IgG index. Dr. Coyle plans to follow up with each group of patients to measure long-term (18-month) sequelae of the disease

Lyme Encepalopathy

Linda — Sun, 29 Nov 2009 05:35:42 +0000

Encephalopathy is like fine art: Most people know it when they see it, but there is very little agreement on how to define it. At the 14th International Lyme Disease Conference, Brian A. Fallon, MD,[1] of Columbia University and the New York State Psychiatric Institute, New York, NY, tried to do just that. More importantly, he described the different ways one can define encephalopathy, the strengths and limitations of each approach, and significantly, what other aspects of life can give the impression of encephalopathy where none exists.
First, one must evaluate patients with persistent Lyme encephalopathy by asking the following questions:

An In-depth Study of Neurocognitive and Behavioral Lyme Disease

Neurological manifestations of Lyme disease in children

Linda — Tue, 24 Nov 2009 07:21:57 +0000

Lyme Disease is transmitted by an arthropod, the Ixodes dammini tick. The spirochete causing the disease is the Borrelia burgdorferi.

Over the past nine years, we have treated over three hundred children for Lyme Disease in the hospital because they had significant neurologic manifestations of Lyme Disease or, in the minority of cases, an arthritis necessitating hospitalization for intravenous antibiotics.

It is impossible to know how many children have Lyme Disease in our area. One pediatrician with a very large practice sees at least three ECM rashes a day and places the children on either Amoxicillin or penicillin for twenty-one days. Obviously, the majority of the children who are seen early on who manifest the rash do not go on to have chronic problems, but a small percentage do.

In some of our communities with populations of 20,000-25,000 people, as many as sixty percent of the ticks are carrying the Borrelia spirochete so the chance for an infection is very high.

Since 1982, I have seen a large number of children who have had neurologic symptoms due to Lyme Disease. Many of these children are not diagnosed initially because their complaints are vague and thought to be all functional. I have treated a patient who has been sick for five years. Others were sick three and four years before being diagnosed. Recently, we have become more concerned about children with, what are considered, vague symptoms and are becoming more aggressive in diagnosing and treating.

I have seen children develop neurologic symptoms within a few weeks after a tick bite. Others will not develop the symptoms for one year or more.

Less than fifty percent of the children even remember being bitten by a tick and even a smaller percentage than that remember any ECM rash.

The parents recall the children having a flu-like illness that preceded their developing these rather persistent symptoms and usually that flu-like illness will occur six weeks or more after the tick bite or the exposure to the ticks. Many parents claim that after this “flu-like illness,” the child never was well again. The majority, over ninety percent, of the children that we have treated complain of headache. The headache, in a few cases, has been very acute accompanied by papilledema but in the majority of cases the headache comes on gradually, becomes quite persistent and does not respond to over-the-counter analgesics.

In addition to the headache, the children complain of photophobia, dizziness, a stiff neck, backache, somnolence and, those that are in school, have problems with memory and difficulty concentrating. Some patients have developed progressive weakness.

The parents complain that preschoolers develop mood swings and become very irritable and they see a personality change.

Among the children that are school-age and those who are in adolescence, chest pain is a very frequent complaint. At least seventy percent have complained of chest pain. About fifty percent have complained of abdominal pain. More than half the children have arthralgia usually involving the knee and sometimes the wrist.

Other complaints include palpitations, tingling, numbness, rashes that come and go, usually malar rashes, and sore throats that are excruciatingly painful.

It is easy to see how this long list can be very non-specific and many of these children are thought to have functional problems.

Children present with central or peripheral nervous system manifestations frequently. The central nervous system manifestations include an encephalopathy. These children have difficulty with memory, concentration and learning new material in school. They have an excessive amount of fatigue and have a wake-sleep disturbance, either becoming hypersomniac or insomniac.

Rarely, we have seen children present with an encephalitic picture.

There have been reports of individuals having stroke from Lyme. We have one child who presented with the sudden onset of a hemiplegia and aphasia.

Patients may have involvement of the optic nerve with an optic neuritis or a papillitis, resultant vision loss.

Peripheral neuropathy with distal parasthesias, subtle weakness, diminished deep tendon reflexes have also been seen.

The laboratory work-up is rather unrevealing. CBC’s are almost always normal. Sed Rates of greater than 30 have occurred in only ten percent of the patients and we have had only two patients who have Sed Rates of 100 or more. EEG’s have been abnormal in one-third of the patients showing bilateral sharp waves and some slowing. The CAT Scans have been normal but a number of MRI’s have been abnormal showing evidence of increased signal in the white matter.

The decision to do a spinal tap on a patient with Lyme Disease is based on the physical findings. Obviously, if a patient has papilledema, they will be tapped after a CAT Scan or MRI shows no mass lesion. But in other cases, the decision to do the tap is based primarily on the need for additional diagnostic information or where there is a question as to whether the diagnosis is something other than Lyme. We have tapped about twenty-five [sic] patients so far. The majority have had normal spinal fluid findings. Usually, they have no elevation of their white cells. Protein and sugars are normal. Cultures are negative. Interestingly, however, at least fifty percent of them show increased pressure with opening pressures greater than 200, sometimes as high as 400. Every patient with papilledema has had a pressure of at least 300 or more except for one girl whose opening pressure was 260 but she had obvious papilledema and also loss of vision in her left eye. Eight of the patients had a pleocytosis with cells ranging from 60 to 700, predominantly lymphocytes. Only two patients showed a positive CSF titer.

The diagnosis of Lyme Disease is a clinical one. The serology, if positive, is helpful. We consider a positive serology as a 1:128 IFA; ELISA that is greater than .79. Urine antigens can also be measured. The tests on urine antigens are still considered investigational.

We will treat patients with negative serologies without hesitation if they truly have a number of the symptoms and are incapacitated by them. We have had children who have been out of school for an entire year because they have been too sick to leave the house.

Other children have had to give up all extracurricular activities, sports, etc. because they are too sick and too weak to participate. Every patient we have treated with the diagnosis of Neurologic Lyme Disease has had persistent complaints. These children have a headache and frequently chest pain. Many of them have seen numerous doctors without any specific diagnosis being made and many of them have had antibiotics for various reasons along the way, sore throats, otitis media, rash and, therefore, never developed an antibody response to their spirochetal infection.

The diagnosis of Neurologic Lyme Disease is a clinical one, not a laboratory one. If the patient’s symptoms are compatible with the diagnosis, the patient is ill, the disease is having a significant effect on the person’s ability to function, then they deserve treatment. I believe it is safer to be aggressive and treat someone under those circumstances than to allow them to continue suffering indefinitely.

Treatment consists of intravenous antibiotics, ceftriaxone, cefotaxime, ampicillin given for as long as is necessary, minimum of four-six weeks initially. Many patients are treated for months if they continue to be clinically ill.

Patients can take Benadryl if they develop pruritis. I encourage them to eat yogurt to try to prevent diarrhea while they are on the antibiotics. Aspirin is the best medication to relieve the pain but, because of the reluctance in the past of physicians to prescribe aspirin in children, many of them are given other NSAIDS.

During treatment and even afterward, they need to rest. They cannot resume full activity as soon as they have been treated. About twenty-five percent of the patients we have treated have had to be re-treated and of these re-treated, the vast majority then do well. Usually, if I treat them initially with ceftriaxone, I will re-treat them with either ceftriaxone or cefotaxime or ampicillin.

Many of the children I have seen with these complaints have been given the benefit of antibiotics by mouth to no avail. Once the patients have these neurologic complaints and, in some cases the positive neurologic findings, they truly deserve a course of aggressive intravenous antibiotic treatment, perhaps more than one time.

Clinical trials validate the severity of persistent Lyme disease symptoms

Linda — Mon, 16 Nov 2009 08:08:26 +0000

BACKGROUND: Persistent Lyme Disease Symptoms (PLDS) have included fatigue, headaches, poor concentration and memory, lightheadedness, joint pain, and mood disturbances. Evidence-based guidelines committees disagree over the severity of PLDS. The 2004 International Lyme and Associated Diseases Society (ILADS) concluded that PLDS are severe. The 2006 Infectious Disease Society of America (IDSA) guidelines committee concluded that PLDS are nothing more than the “aches and pains of daily living” and an ad hoc International Lyme group concluded that PLDS are “symptoms common in persons who have never had Lyme disease.” HYPOTHESIS: Clinical trials validate the severity of persistent Lyme disease symptoms. EVALUATION OF THE HYPOTHESIS: There are 22 standardized instruments used to measure the severity of PLDS among the four published National Institutes of Health (NIH) sponsored double-blind randomized placebo-controlled trials (RCTs). VALIDATING THE HYPOTHESIS: All four NIH sponsored RCTs validate the severity of PLDS. PLDS are as severe as symptoms seen in other serious chronic illnesses, and result in a quality of life lower than for the general population as determined by 22 standardized measures of QOL, including fatigue, pain, role function, psychopathology, and cognition. None of the four RCTs support the IDSA hypothesis that PLDS are nothing more than “the aches and pains of daily living” nor the ad hoc International Lyme group conclusion that PLDS are “symptoms common in persons who have never had Lyme disease.” IMPLICATIONS OF THE HYPOTHESIS: If the QOL of life for these patients is as poor as for patients with other serious chronic diseases, their symptoms need to be addressed by their doctors. Studies differ as to the precise cause of PLDS, the most effective treatments, and whether a cure is possible. But the fact that there is disagreement is not a license for physicians to ignore or turn away patients complaining of PLDS, or to dismiss their symptoms as purely psychosomatic. For physicians, the goal or purpose of treating PLDS should be the same as their purpose in treating other chronic illnesses that result in a poor QOL: vigorous pursuit of a cure, and where a cure proves impossible, amelioration of patients’ symptoms and suffering. Even if this hypothesis fails to be apply to more than a fraction of the total Lyme disease population, this still represents a significant number of patients, and these findings could address a neglected aspect of caring for patients with Lyme disease.

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
Clinical trials validate the severity of persistent Lyme disease symptoms.
Med Hypotheses. 2009; 72(2):153-6 (ISSN: 0306-9877)
Cameron DJ
First Medical Associates, Mt. Kisco, New York 10549, USA. Cameron@Lymeproject.com