Tuesday, June 22, 2010

Relief from Fatigue

Buy Corvalen Ribose at best lowest price FREE shipping.

Corvalen is a non-prescription medical food that specifically addresses a nutritional deficiency associated with particular diseases that result in fatigue and pain. Using GRAS-approved Corvalen, with the active ingredient ribose, patients can overcome this fatigue and pain more quickly.

Corvalen aids patients suffering from compromised heart function, Fibromyalgia (FMS) and Chronic Fatigue Syndrome (CFS) by restoring depleted energy reserves at a cellular level. Clinically-proven studies have shown a reduction of fatigue, muscle soreness, stiffness and pain with patients that use Corvalen.

Scientific and clinical studies have repeatedly shown that Corvalen, with the active ingredient ribose, can restore energy and improve function in ischemic, hypoxic, and failing hearts. Oxygen deprivation causes hearts to use energy faster than it can be replaced through normal processes of tissue energy turnover. The result is a depletion of cellular energy reserves translating to loss of heart function.

Millions of Americans suffer the affects of coronary artery disease, and the prevalence of congestive heart failure is reaching epidemic proportions. Recent research has also proven that high-intensity endurance exercise places a considerable strain on the heart, leading to a loss of diastolic heart function that persists for several weeks to months following an event. Other research, conducted at the Mayo Clinic and published in the Journal of the American Medical Association, showed that an average of 26% of the population, male and female, have symptoms of cardiac diastolic dysfunction. More than half of those affected are unaware of their condition, but all are at risk for developing congestive heart failure.

When hearts lose energy, they first suffer a loss of diastolic function. The diastolic phase of the heartbeat is the relaxation phase, during which the heart fills with blood for the next heartbeat. A loss of diastolic capacity means less blood will circulate to the body during each beat, and frequently leads to a thickening and expansion of the heart muscle, known as hypertrophy. The result of chronic diastolic dysfunction can be congestive heart failure. For patients, the progressive consequence of the disease is shortness of breath, loss of exercise capacity, overwhelming fatigue, etc.

Corvalen increases cardiac energy to help fuel the heart. For patients, this can mean more energy and a higher quality of life. For athletes, it can enhance recovery following strenuous exercise.

Corvalen Ribose - How it Works

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Corvalen energy supplement and clinical nutrition products contain D-ribose (or simply ribose). Ribose is vital for your body to make the primary energy compound, adenosine triphosphate (ATP). ATP gives your body the energy it needs to stay healthy, overcome fatigue, and regain the vitality you need to live a normal, active life. That is why ATP is called the "energy currency" of the cell.

D-ribose, or simply ribose, is a five-carbon monosaccharide that is made in every cell in your body. Ribose stimulates the metabolic pathway used by the body to make a class of compounds called purines and pyrimidines. These compounds are essential for the body's production of many vital constituents, including the genetic material DNA and RNA, and the vital energy compound ATP.

The ribose in Corvalen helps energize your heart and muscles by increasing energy on a cellular level. Aging, strenuous exercise or overexertion, and many metabolic or physiological conditions can drain ATP from your tissue and affect how well your body makes and uses energy. Science has proven that ribose is a necessary ingredient for rebuilding energy in our bodies. So, without ribose we cannot make the energy we need to stay healthy.

Unfortunately, hearts, muscles, and other vital tissues in the body cannot make ribose very quickly, and ribose is not stored in our cells and tissues. That's why supplementing with Corvalen as directed will help your cells make energy quickly, safely, and naturally. This means you can feel more energetic, stronger, and healthier every day.

When a Complement is not a Compliment: The Role of C3a and C4a Complement Proteins in Chronic Lyme Disease

When a Complement is not a Compliment:
The Role of C3a and C4a Complement Proteins in Chronic Lyme Disease
by Ginger Savely, DNP

Readers of this publication are well aware of the controversies surrounding the diagnosis and treatment of Lyme disease. When the disease is missed in its early, easier-to-treat stage, it goes on to become a complex, multi-system disease that eludes diagnosis, mimics many other diseases, and requires aggressive, long-term treatment. Because the testing methods for Lyme and other tick-borne diseases are insensitive, many true cases of infection go undetected. Even when the diseases are detected, the unreliability of the testing makes it difficult to track treatment progress and test for cure.

Work by Drs Stricker and Winger identified CD57 positive natural killer cells as immune markers that tend to be low in chronic Lyme patients and increase with clinical improvement. An earlier article that I wrote for this publication explained how the measurement of CD57+NK cells in the blood has helped Lyme-literate health care providers in making the diagnosis of Lyme disease when tests are inconclusive. It has also provided a convenient marker to assist in following treatment progress and determining treatment end.

Although the CD57 marker has been a helpful tool, it has not been without its problems. We don't yet understand what confounding variables can skew the results. Some very sick patients start out with normal or above-normal CD57 levels. Other patients' levels stay low and never increase with treatment, despite the fact that they are symptom-free and otherwise seem completely cured. There may be large day to day variation in the CD57 level as I observed in a study looking at twice daily blood draws over 3 days for both Lyme patients and well patients. The level can increase or decrease as much as 50% within the same day. So the CD57 level can be a useful marker for some patients but it is not always reliable and consistent.

Enter C3a and C4a, the new kids on the block in the world of Lyme diagnosis and treatment. The "C" in C3a and C4a stands for complement. Complement proteins work with antibodies to destroy pathogens. They activate immunity through control of inflammation, phagocytosis (ingestion of pathogens by white blood cells) and cell death by lysis (breaking of the cell membrane). There are about 30 of these complement proteins that circulate in the bloodstream making up complement "cascades", so called because activation of one protein initiates activation of the next, etc.

Dr. Ritchie Shoemaker and his colleagues published a study in 2008 reporting elevated C3a and C4a levels in acute Lyme disease. Many patients who contract Lyme disease do not develop the diagnostic "bull's eye rash", and Lyme tests are frequently negative shortly following a tick bite when prompt diagnosis is crucial for effective treatment. Shoemaker et al. suggested that elevated C3a and C4a levels can serve as early markers in the diagnosis of acute Lyme disease.

Because CD57+ NK cell levels are not always reliable markers for chronic Lyme, there is an ongoing search for new biomarkers to aid in the diagnosis of chronic, disseminated Lyme disease and to follow treatment progress. Dr. Stricker and I recently published a study in the Scandinavian Journal of Immunology comparing C3a and C4a levels of chronic Lyme patients to those of healthy controls, AIDS patients and patients with systemic lupus. The C3a complement protein level was normal in the AIDS patients, the healthy patients and the chronic Lyme patients. So, although C3a was shown to be elevated in a cohort of early, acute Lyme disease patients, it appears to be normal in chronic Lyme patients.
In our study, only the systemic lupus patients had elevated levels of C3a. Other published studies have associated elevated C3a with autoimmunity as well. Therefore, the C3a may prove to be a useful marker in differentiating ongoing symptoms due to an autoimmune process versus an ongoing infectious process.

For purposes of our C3a/C4a study, Dr. Stricker divided the chronic Lyme patients into two groups: 1) those with primarily musculoskeletal symptoms (MSK) and 2) those with neurological symptoms severe enough to warrant treatment with intravenous antibiotics. Interestingly, C4a levels were significantly elevated in the MSK group, but only slightly (and not statistically significantly) elevated in the neurologic group. C4a levels were also elevated in the AIDS and systemic lupus groups, but not in the healthy controls. In Lyme patients with elevated C4a, the levels decreased in those who responded well to antibiotic treatment. Those patients who did not improve on antibiotics (more often than not, the severe neurological group) had no statistically significant reduction in their C4a levels.

Keep in mind that almost all chronic Lyme patients have some degree of neurological involvement. The neurological Lyme patients in the study who did not have elevated levels of C4a were those with severe cognitive dysfunction as evidenced by abnormal blood flow to areas of the brain noted on their SPECT brain scans. Examples of these patients are those who presented with symptoms mimicking Alzheimer's disease, multiple sclerosis, Parkinson's disease, or Autism Spectrum Disorder. Amyotrophic lateral sclerosis (ALS) patients do not have cognitive deficits and, in fact, Lyme patients with this type of severe neurological presentation did have elevated C4a levels.

The normal range for the C4a is zero to 2830. In my chronically ill Lyme patients I have seen C4a levels as high as about 26,000. However, most of my patients start with a pre-treatment level between 6000 and 12,000. In the two years that I have been using the C4a test to track treatment progress, reduction in C4a levels has consistently correlated with clinical improvement.

Patients often ask if there are other medical conditions that may lower or raise the C3a and/or C4a. Both of these complement products may be increased in normal pregnancy and in certain types of vasculitis (an inflammatory condition that destroys blood vessels). C4a levels are elevated in adult insulin dependent diabetes. Those who suspect that chronic fatigue syndrome (CFS) may actually be misdiagnosed Lyme disease may not be surprised to hear that C4a is also elevated in CFS patients. In fact the C4a is probably elevated in all sorts of infections, and therefore is not specific to Lyme.

If you would like your health care provider to order your C3a and C4a levels, it is extremely important that the tests be performed only at the National Jewish Medical and Research Center Laboratory in Denver. LabCorp has a contract with National Jewish and therefore your health care provider can order LabCorp tests # 840702 (C3a) and # 857334 (C4a). LabCorp uses two different send-out labs for the test and it is important to indicate that samples should be routed to National Jewish for most accurate results. Ask your health care provider to write on the requisition slip in large letters: "ACCESSIONING: C3a & C4a MUST BE ROUTED TO NATIONAL JEWISH". To find the LabCorp drawing station nearest you, go to www.labcorp.com and enter your city or zip code in the space provided in the lower left of the home page.

If your health care provider writes the ICD-9 (diagnostic) code of 279.3 (Immune dysregulation) on your LabCorp requisition slip, insurance will more than likely cover the C3a and C4a tests. However, if your insurance does not cover the tests, the prices are not prohibitive. Each of the tests cost $ 75.60 (valid as of 3-25-09).

Because most lab technicians are unfamiliar with the C3a and C4a tests, it is in your best interest to go to the LabCorp drawing station knowing exactly how your blood should be handled. This way you will be assured that your sample will arrive at the lab satisfactory for testing. The blood needs to be drawn into an EDTA tube ("lavender top") and immediately spun and separated. The plasma should be frozen right away and sent frozen to National Jewish.

The C4a is not as specific to chronic Lyme as the CD57+ level because it may be elevated in many types of infection, including other tick-borne diseases. However, in patients with known tick-borne infections, the C4a complement protein test can provide a useful way to determine initial degree of infection, to follow treatment progress and to aid in deciding upon treatment end. For more information about the C3a and C4a, please see the suggested readings below:

Shoemaker RC, Giclas PC, Crowder C, House D, Glovsky MM.Shoemaker, R. C., Giglas, P.C., Crowder, C., House, D. Glovsky, M.M. Complement split products C3a and C4a are early markers of acute lyme disease in tick bite patients in the United States. International Archives of Allergy and Immunology, 146(3), 255-261.

Stricker, R. B., Savely, V.R., Motanya, N.C. & Giglas, B.C. (2009). Complement split products C3a and C4a in chronic Lyme disease. Scandinavian Journal of Immunology, 69(1), 64-69.

Wednesday, June 9, 2010

Reducing the symptoms of fibromyalgia

According to research published over the past few months, several different energy producing and antioxidant supplements might be beneficial for reducing the symptoms of fibromyalgia.

Creatine and Co-EnzymeQ10 (Co-Q10) help provide fuel to your cells. More importantly, Co-Q10 helps power up your energy factories, your mitochondria, to produce more fuel. However, additional research shows that the mitochondria in fibro patients might be under attack from molecules causing oxidative stress, which can damage cells in your cardiovascular system, your brain, or other tissues in the body. Here is where fat-soluble antioxidants such as omega-3 fatty acids and vitamin E might be beneficial.

Friday, June 4, 2010

Soothe & Relaxx™ Soft Tissue & Stress Support

Soothe & Relaxx™ Soft Tissue & Stress Support
Has anybody tried this? My doctor put me on this for Lyme disease and it works great for me. It also works great for the fibromyalgia symptoms and anything to do with soft tissue pain, stress and relaxation. Thought I would share the information with you.

Product Description
Soft tissue, joint & muscle support with Relaxx™ Complex to calm the mind. (180 capsules)

Special Dietary Usefulness:
Under a physician’s direction, Soothe & Relaxx™ may have special dietary usefulness for individuals suffering from fibromyalgia and other chronic illnesses with soft tissue, joint and muscle pain.

Soothe & Relaxx™ was developed to meet the combination of needs that many chronically ill patients experience: pain and anxiety. The product addresses pain as a result of soft tissue or joint injury and the concomitant anxiety often associated with long-term health issues. The Relaxx™ Complex is designed to take the edge off versus being a sedating micro-formula. This is a favorite of patients who feel the benefit fairly quickly.

Each bottle provides a one month supply of the following complexes and health benefits:

Pro Joint Soothers™:
Proprietary blend of glucosamine sulfate, MSM, chrondroitin sulfate, hyaluronic acid which supports connective tissue, lubricates joints, promotes joint resilience, elasticity and overall strength.

ExInflame™ Complex:
Proprietary blend of White Willow Bark, Boswellin, Curcumin Extract, Holy Basil which promotes a healthy inflammation response.

Muscle & Leg Calmer™:
Proprietary blend of magnesium hydroxide and malic acid which calms muscle contractions and relaxes the body's muscles.

Relaxx™ Complex:
Proprietary blend of 5HTP, Valerian, Lemon Balm, Passion Flower, German Chamomile which relaxes & calms the mind, and promotes healthy sleep patterns.

Suggested Use:
As a dietary supplement, take two capsules three times per day or as directed by your health care professional.

Thursday, June 3, 2010

Lyme Disease & Common Co-Infections

Lyme Disease & Common Co-Infections

Short Symptom List
Borrelia, Babesia, Bartonella, and Ehrlichia

The following symptoms were excerpted from Diagnostic Hints And Treatment
Guidelines For Lyme And Other Tick Borne Illnesses, by Joseph J. Burrascano Jr.,M.D. (Fourteenth Edition, November, 2002). Available online at www.ilads.org/burrascano_1102.html

Borrelia
(Borreliosis, neuroborreliosis; also known as Lyme Disease)
Spread primarily though the bite of infected ticks that live on a wide range of mammalian species; secondary human-to-human transmission through semen, breast milk, and possibly in utero.
**Bladder dysfunction
**Burning or stabbing sensations
**Cardiac impairment
**Change in bowel function
**Chest pain
**Confusion
**Depression
**Difficulty thinking
**Difficulty with concentration and reading
**Difficulty with speech, writing
**Difficulty finding words; name blocking
**Disorientation: getting lost, going to wrong places
**Disturbed sleep: too much, too little, fractionated, early awakening
**Ears/Hearing: buzzing, ringing, ear pain, sound sensitivity
**Exaggerated symptoms or worse hangover from alcohol
**Eyes/Vision: double, blurry, increased floaters, light sensitivity
**Facial paralysis (Bell's palsy)
**Fatigue, tiredness, poor stamina
**Forgetfulness
**Headache
**Heart block
**Heart murmur
**Heart palpitations
**Heart valve prolapse
**Increased motion sickness
**Irritability
**Irritable bladder
**Joint pain or swelling
**Lightheadedness
**Mood swings
**Muscle pain or cramps
**Neck creaks & cracks
**Neck stiffness, pain
**Numbness
**Pelvic pain
**Poor attention
**Poor balance
**Poor short-term memory
**Problem absorbing new information
**Pulse skips
**Rib soreness
**Sexual dysfunction or loss of libido
**Shooting pains
**Shortness of breath; cough
**Skin hypersensitivity
**Sore throat
**Stiffness of the joints or back
**Swollen glands
**Testicular pain
**Tingling
**Tremor
**Twitching of the face or other muscles
**Unavoidable need to sit or lay down
**Unexplained breast pain
**Unexplained fevers, sweats, chills or flushing
**Unexplained hair loss
**Unexplained menstrual irregularity'
**Unexplained milk production
**Unexplained weight loss or gain
**Upset Stomach or abdominal pain
**Vertigo
**Wooziness

Babesia Babesiosis)
Babesia is a protozoan spread by ticks, blood transfusion, and in utero. Despite there being 13 known forms to date, current testing only looks for two of them.
**Air hunger
**Cough
**Fatigue
**Fevers
**Headache
**Hemolysis
**Imbalance without true vertigo
**Mild encephalopathy
**Shaking chills
**Sweats

Bartonella (Bartonellosis, also known as cat scratch fever)
Spread by bites from infected ticks and in utero
**abnormal liver enzymes
**encephalopathy
**endocarditis
**flu-like malaise
**headache
**hemolysis with anemia
**hepatomegaly
**high fever
**immune deficiency
**jaundice
**lymphadenopathy
**myalgias
**myocarditis
**papular or angiomatous rash
**somnolence
**sore throat
**splenomegaly
**weakened immune response

Ehrlichia (Ehrlichiosis)
Bites from infected ticks
**elevated liver enzymes
**headaches
**myalgias
**ongoing fatigue
**persistent leukopenia
**thrombocytopenia

Printed from www.anapsid.org/lyme/symptoms/tbi-symptoms.html
More information on Lyme and other tickborne diseases:
www.calda.intranets.com
www.ilads.org
www.lymenet.org

Basic Information about Lyme Disease

If you have been diagnosed with fibromyalgia, chronic fatigue syndrome, MS, early Alzheimers or early dementia, parkinson's disease or Lou Gerhig's disease, it is recommended that you get tested for Lyme disease. Lyme disease is the great pretender and can mimic these other diseases. Lyme disease is hard to diagnose and lab testing is not reliable. Your best bet for lab testing is IgeneX labs (tick speciality lab).

Basic Information about Lyme Disease
by The International Lyme and Associated Diseases Society

1. Lyme disease is transmitted by the bite of a tick, and the disease is prevalent across the United States and throughout the world. Ticks know no borders and respect no boundaries. A patient's county of residence does not accurately reflect his or her Lyme disease risk because people travel, pets travel, and ticks travel. This creates a dynamic situation with many opportunities for exposure to Lyme disease for each individual.

2. Lyme disease is a clinical diagnosis. The disease is caused by a spiral-shaped bacteria (spirochete) called Borrelia burgdorferi. The Lyme spirochete can cause infection of multiple organs and produce a wide range of symptoms. Case reports in the medical literature document the protean manifestations of Lyme disease, and familiarity with its varied presentations is key to recognizing disseminated disease.

3. Fewer than 50% of patients with Lyme disease recall a tick bite. In some studies this number is as low as 15% in culture-proven infection with the Lyme spirochete.

4. Fewer than 50% of patients with Lyme disease recall any rash. Although the erythema migrans (EM) or “bull’s-eye” rash is considered classic, it is not the most common dermatologic manifestation of early-localized Lyme infection. Atypical forms of this rash are seen far more commonly. It is important to know that the EM rash is pathognomonic of Lyme disease and requires no further verification prior to starting an appropriate course of antibiotic therapy.

5. The Centers for Disease Control and Prevention (CDC) surveillance criteria for Lyme disease were devised to track a narrow band of cases for epidemiologic purposes. As stated on the CDC website, the surveillance criteria were never intended to be used as diagnostic criteria, nor were they meant to define the entire scope of Lyme disease.

6. The ELISA screening test is unreliable. The test misses 35% of culture proven Lyme disease (only 65% sensitivity) and is unacceptable as the first step of a two-step screening protocol. By definition, a screening test should have at least 95% sensitivity.

7. Of patients with acute culture-proven Lyme disease, 20–30% remain seronegative on serial Western Blot sampling. Antibody titers also appear to decline over time; thus while the Western Blot may remain positive for months, it may not always be sensitive enough to detect chronic infection with the Lyme spirochete. For “epidemiological purposes” the CDC eliminated from the Western Blot analysis the reading of bands 31 and 34. These bands are so specific to Borrelia burgdorferi that they were chosen for vaccine development. Since a vaccine for Lyme disease is currently unavailable, however, a positive 31 or 34 band is highly indicative of Borrelia burgdorferi exposure. Yet these bands are not reported in commercial Lyme tests.

8. When used as part of a diagnostic evaluation for Lyme disease, the Western Blot should be performed by a laboratory that reads and reports all of the bands related to Borrelia burgdorferi. Laboratories that use FDA approved kits (for instance, the Mardx Marblot®) are restricted from reporting all of the bands, as they must abide by the rules of the manufacturer. These rules are set up in accordance with the CDCs surveillance criteria and increase the risk of false-negative results. The commercial kits may be useful for surveillance purposes, but they offer too little information to be useful in patient management.

9. There are 5 subspecies of Borrelia burgdorferi, over 100 strains in the US, and 300 strains worldwide. This diversity is thought to contribute to the antigenic variability of the spirochete and its ability to evade the immune system and antibiotic therapy, leading to chronic infection.

10. Testing for Babesia, Anaplasma, Ehrlichia and Bartonella (other tick-transmitted organisms) should be performed. The presence of co-infection with these organisms points to probable infection with the Lyme spirochete as well. If these coinfections are left untreated, their continued presence increases morbidity and prevents successful treatment of Lyme disease.

11. A preponderance of evidence indicates that active ongoing spirochetal infection with or without other tick-borne coinfections is the cause of the persistent symptoms in chronic Lyme disease.

12. There has never been a study demonstrating that 30 days of antibiotic treatment cures chronic Lyme disease. However there is a plethora of documentation in the US and European medical literature demonstrating by histology and culture techniques that short courses of antibiotic treatment fail to eradicate the Lyme spirochete. Short treatment courses have resulted in upwards of a 40% relapse rate, especially if treatment is delayed.

13. Most cases of chronic Lyme disease require an extended course of antibiotic therapy to achieve symptomatic relief. The return of symptoms and evidence of the continued presence of Borrelia burgdorferi indicates the need for further treatment. The very real consequences of untreated chronic persistent Lyme infection far outweigh the potential consequences of long-term antibiotic therapy.

14. Many patients with chronic Lyme disease require prolonged treatment until the patient is symptom-free. Relapses occur and retreatment may be required. There are no tests currently available to prove that the organism is eradicated or that the patient with chronic Lyme disease is cured.

15. Like syphilis in the 19th century, Lyme disease has been called the great imitator and should be considered in the differential diagnosis of rheumatologic and neurologic conditions, as well as chronic fatigue syndrome, fibromyalgia, somatization disorder and any difficult-to-diagnose multi-system illness.

Disclaimer: The foregoing information is for educational purposes only. It is not intended to replace or supersede patient care by a healthcare provider. If an individual suspects the presence of a tick-borne illness, that individual should consult a healthcare provider who is familiar with the diagnosis and treatment of tick-borne diseases.

Distinct pattern of cognitive impairment noted in study of Lyme patients

Distinct pattern of cognitive impairment noted in study of Lyme patients
by Marian Rissenberg, Ph.D. & Susan Chambers, M.D.

the Lyme Times, Vol. 20, January-March 1998, pp. 29 -32

1) Cognitive Characteristics of Chronic Lyme Encephalopathy
On the basis of both a formal neuropsychological study of 49 patients (APA 5/96) and on clinical observation and comprehensive neuropsychological examination of well over 100 patients, a distinct pattern of cognitive impairment occurring chronic Lyme disease can be described. These patients consistently demonstrate deficits in directed, sustained and divided attention, planning and organization of responses, temporal ordering, verbal fluency, abstract reasoning, speed of processing, and motor programming. The overall pattern of intellectual impairment is not unlike that seen with diffuse brain injury, and it most often results in some degree of work-related disability.

Although performance is impaired on measures of cognitive functions associated with specific brain regions -- receptive and expressive language, visuospatial problem solving and memory -- the quality of performance is not suggestive of focal lesions in these areas. Rather, deficits are secondary to impairment of higher level integrative functions, likely mediated by complex neuronal systems. Specifically, the receptive language deficit is secondary to impaired auditory tracking and slowing of mental processing. The expressive language deficit is secondary to impaired word retrieval and response planning, The visuospatial problem solving deficit is secondary to impairment of mental flexibility, conceptualization and the ability to compare and contrast necessary in decision making. Finally, deficits on test of memory function are most often secondary to impairment of the encoding or initial processing of information, which depends on attention, and the retrieval of stored information. The storage of new information, or memory per se, is rarely impaired.

This pattern suggests that cognitive dysfunction in chronic Lyme, while expressed variably across individual patients, results from a common factor -- the breakdown of diffusely represented processes involving both integration and activation, and impacting primarily on attention and reasoning. The fluctuation of impairment over short periods of time suggest that a physiologic rather than a structural mechanism is responsible.

2) Neuropsychological deficits in chronic Lyme disease (A study presented at the annual meeting of The American Psychiatric Association , May 1996)

The neuro-psychological characteristics of 49 patients with Lyme disease were examined. The study set out to answer three questions:
1) Do all patients with subjectively perceived cognitive dysfunction have measurable intellectual impairment on objective testing?

2) In those without measurable impairment, does depression account for the perception of cognitive dysfunction?

3) What is the nature of the cognitive impairment in Lyme disease when it does occur?

Subjects were patients seen consecutively between 1990 and 1994 in a private neuropsycological practice with complaints of cognitive dysfunction and a symptom complex consistent with Lyme disease. Diagnosis was based on former CDC criteria. Mean duration of illness, defined as the time from the onset of general symptoms to the neuro-psychological exam, was 4.7 years (range: 3.3 to 14 years). Mean age was 39.9 years (range: 21 to 58 years) from 18 to 60 years. Mean level of education was 15.3 years (range 12 to 20 years).

Subjects were interviewed and administered a comprehensive battery of tests, including the complete WAIS-R and WMS-R, and additional test of language, attention, reasoning, visuospatial processing and complex motor function. They also completed the Beck Depression Inventory and a symptom checklist. Tests were divided into seven groups based on the cognitive functions they are presumed to measure: Attention, Memory, Language, Visuospatial Processing, Reasoning, Verbal Fluency and Motor programming.

Subjects were grouped into three levels of impairment based on their neuropsychological performance: Intact (N=11; 22%), with no functions impaired, Moderate (N=31; 63%) with two functions impaired, and Severe (N=7; 14%) with three or more functions impaired. Subjects in the Severe group met diagnostic criteria for dementia. The correlation between depression and cognitive impairment was nonsignificant, but the trend was positive, rather that negative. Anxiety by self report was significantly greater in the impaired groups that the Intact group. Duration of illness was greater in the Severe group (nonsignificant).

Of the 38 subjects with cognitive impairment, deficits of attention were most common, occurring in 26 subjects (68%) Deficits of memory storage were least common, occurring in 8 subjects (21%), Motor, Verbal Fluency, Visuospatial, Language and Reasoning deficits occurred in 24, 26, 29, 36 and 36% of the subjects respectively.

3) Possible Pathophysiologic Mechanisms of Cognitive Impairment in Lyme Disease

Based on these findings and on patients' reports, two characteristics of Lyme Encephalopathy arise which provide insight as to possible neurophysiologic mechanisms:
One, the nonfocal nature of the cognitive functions affected, and

Two, the subtle fluctuations and reportedly abrupt and global shifts in cognitive function from one day to another in a given patient.

Four broad categories of possible neurophysiologic mechanisms might be compatible with this pattern:
1) Diffuse cerebral diffusion abnormalities -- Single photon emission computerized tomography (SPECT) scans of the brain in Lyme disease often display a diffuse pattern consistent with heterogeneous areas of hyperfusion and/or diminished neuronal metabolism. While vasodilators are often capable of reversing these abnormal patterns on SPECT scan, this reversal does not consistently correlate with a symptomatic improvement in cognitive function.

2) Alterations in cellular metabolism at the cortical level -- Evidence of alterations in neurotransmitter function is suggested by clinical evidence of cognitive improvement following treatment with selective serotonin reuptake inhibitors (SSRI's) which appears to be independent of their antidepressant effect. Systematic studies of the impact of SSRI's on cognitive function, as well as the role of other transmitters, are required.

3) Neuro transmitter abnormalities (imbalances of synthesis and/or receptor activity) -- Neurotoxic substances may well play a role in Lyme Encephalopathy. given the neurotropic nature to Treponema pallidim , and the close parallel between syphilis and Lyme disease, it is possible that Borrelia burgdorferi could produce intracellular or extracellular neurotoxins which we have yet to identify.

4) Neurotoxic substances produced endogenously or possibly exogenously -- Endogenous neurotoxins have been identified as by-products of the humoral immune response. Among these is quinolinic acid, a product of the interleukin cascade system, which accumulates as a result of the humoral response to acute infectious agents and functions as a neuronal excitotoxin. As there are many similarities between Lyme Encephalopathy and the nonspecific mental dysfunction of acute systemic infections, such as influenza, it is quite possible that continue stimulation of production of quinolinic acid and other cytokines plays a role in the pathophysiology of Lyme encephalopathy.

4) Clinical Impressions and Implications for Diagnosis and Treatment in Chronic Lyme Disease

This study demonstrates that for the majority of chronic Lyme patients with cognitive complaints, there is in fact a measurable and significant decline in intellectual acuity. The nature and severity of the cognitive impairment is such that it interferes with all aspects of normal functioning: employment, home, marriage, social interactions, and general emotional well-being. Rather than the cognitive complaints being secondary to anxiety or depression, as is sometimes suspected, depression and anxiety increase with, and are apparently secondary to, cognitive impairment and the emotional and practical impact of a loss of competence. Thus, while patients with chronic Lyme disease can present a confusing and "psychiatric" picture to the clinician, it is important that their concerns be properly investigated and addressed.

Patients with Lyme encephalopathy complain of problems with memory and concentration, word retrieval, confusion, problems with thinking, "mental fogginess", a decline in job performance, difficulty with calculations, directions, and judgment. Decreased initiative, manifest as difficulty getting started with or following through with projects is often noted. Mood disturbance is common with complaints of irritability, explosiveness or "a short fuse," sadness, hopelessness or guilt, increased anxiety or mood swings. Sleep disturbance is also common, and can present as initial, middle or terminal insomnia or some combination of these. Fatigue is universal. Headache is common, and of course joint and muscle pain. Increased sensitivity to light and noise, visual disturbance, and tingling in the extremities are also common.

On interview patients with Lyme encephalopathy tend to be vague and disorganized in the presentation of the history of their illness. This is despite their close attention to their symptoms and having recounted them many times before. Although in most cases memory of discreet events - tests, dates, diagnoses, responses to medications -- is intact, the patient is unable to recall them spontaneously or organize them in temporal order. They may be unclear as to their chief complaint. They may completely lose track of what they were saying, sometimes repeatedly, or of what the question was. They may get off on a tangent and have trouble re-orienting themselves. Frequent prompting and refocusing will be necessary. beginning the interview with an open-ended question like "Tell me what the problem is" will allow these qualities to become clear.

Often patients with chronic Lyme disease will seem overly focused on their illness, or overly concerned with convincing the clinician that they are ill. The clinician may be tempted to interpret this as evidence of a primary psychiatric disorder. It is important to understand that the frustration many of these patients experience is real, and results from the general attitude of doubt toward Lyme disease as a serious and chronic illness, the invisibility of their symptoms, the difficulty in getting a definitive diagnosis and getting approval for extended treatment from insurance carries. Many have been accused of hypochondriasis or malingering. As with head injury, the patient may "look fin" though they are having difficulty with very basic work, social and day to day functioning.

The cognitive deficits in chronic Lyme disease involve primarily attention and arousal mechanisms. Patients have difficulty keeping track of external and internal events, retrieval of information from memory and with planning and sequencing, as occurs in attention deficit disorder. However their experience is different from that of ADD, in that rather than having the experience that there are many thoughts competing for attention, the Lyme patient has difficulty bringing any thought into clear focus. They experience difficulty thinking. One patient described it as the universe ending six inches from his face. He can't process information that is not immediately apparent, immediately experienced. Another said that when he tries to think about something, or figure something out, all he can do is repeat the question -- he can't get to the meaning. This is like the idea of "surface" versus "deep" processing in cognitive psychology. Reading a passage for typing errors would be surface processing, while reading for meaning is deep processing. One patient, a physician, described it as a "mental intention tremor" -- the more she tries to focus on something the more out of focus it becomes.

The clinician should proceed with empathy and reason. Specific cognitive complaints in previously high functioning individuals are unusual and indicative of serious illness, either psychiatric or neurologic. Comprehensive neuropsychological evaluation will most often differentiate the two.

Where the neuropsychological exam is normal or there is a significant psychiatric component, a psychiatric evaluation is advised. Psychiatric symptomatology is not uncommon in Lyme and the presence of depression, anxiety, obsessive compulsive symptoms, flat affect and so on may cloud the issue of significant cognitive decline. Both the cognitive and psychiatric symptoms would be expected to improve with antibiotic treatment in Lyme encephalopathy. However sometimes concurrent treatment with psychotropic medication is necessary.

Unfortunately for some patients significant cognitive impairment persists even after years of antibiotic treatment. These patients may never be able to return to their premorbid level of employment, or be gainfully employed at all. Cognitive remediation can help them learn strategies for improving memory and concentration and relieving stress. Support and advice in regard to living with a chronic condition is equally important. Strategies include reducing work hours when possible, taking regular rest periods during the day, limiting the number of outings in a week, and using a calendar to stay organized and structure their time.

5) Cognitive impairment in Lyme disease: specific functions and the impact or deficits
1. Attention and mental tracking: includes directed and sustained attention: the ability to direct and maintain one's focus on a particular event or idea, whether in the environment or internally; and divided attention: the ability to simultaneously attend to two events, or dot two or more things at a time, or to retain awareness of one thing while doing another.
Impact: difficulty functioning effectively in many situations, remembering what one was doing before a distraction, keeping track of conversation, taking notes while someone is speaking, remembering that someone is on hold or what you were about to say.

2. Memory: Retaining new information.
Impact: secondary to impaired attention, slowing of processing and the retrieval of stored information, but not storage per se, a tendency to lose or forget things, miss appointments, repeat oneself.

3. Receptive language: understanding spoken or written language
Impact: secondary to impaired attention and speed of processing, difficulty participating in meetings or social conversation, difficulty with reading comprehension.

4. Expressive language: Using spoken or written language to express ideas
Impact: difficulty finding the right word, using the wrong word and not noticing, not being able to express oneself or communicate

5. Visuospatial Processing: Efficient scanning of the visual field, making sense of how things are related in space, visuospatial conceptualization and problem solving.
Impact: a tendency to get lost, difficulty with reading comprehension.

6. Abstract reasoning: The ability to generalize from the particular, to identify the common factor between related concepts, to compare and contrast two things or ideas, to see the "big picture", to identify the critical factor in a situation, to anticipate consequences and make inferences regarding cause and effect.
Impact: difficulty with decision making, planning, and problem solving.

7. Speed of mental and motor processing: the ability to think and respond quickly, critical to understanding speech which occurs at a fairly constant rate.
Impact: difficulty understanding or keeping up a conversation, functioning in a timely manner in day to day situations, meeting deadlines.