In a CBS News Report John Halperin (IDSA & Nervous System Lyme Disease Guideline author- see below) stated:
"FICTION. Some Lyme patients do develop fatigue and have trouble thinking straight. But in most cases this is the result of "toxic-metabolic encephalopathy," a transient condition that occurs with many infectious illnesses."
Looking up "toxic-metabolic encephalopathy" (TME), the quotes are...
NIH states- "Encephalopathy is a term for any diffuse disease of the brain that alters brain function or structure. Encephalopathy may be caused by infectious agent (bacteria, virus, or prion), metabolic or mitochondrial dysfunction, brain tumor or increased pressure in the skull, prolonged exposure to toxic elements (including solvents, drugs, radiation, paints, industrial chemicals, and certain metals), chronic progressive trauma, poor nutrition, or lack of oxygen or blood flow to the brain. The hallmark of encephalopathy is an altered mental state.
Depending on the type and severity of encephalopathy, common neurological symptoms are progressive loss of memory and cognitive ability, subtle personality changes, inability to concentrate, lethargy, and progressive loss of consciousness. Other neurological symptoms may include myoclonus (involuntary twitching of a muscle or group of muscles), nystagmus (rapid, involuntary eye movement), tremor, muscle atrophy and weakness, dementia, seizures, and loss of ability to swallow or speak. Blood tests, spinal fluid examination, imaging studies, electroencephalograms, and similar diagnostic studies may be used to differentiate the various causes of encephalopathy.
Treating the underlying cause of the disorder may improve symptoms. However, the encephalopathy may cause permanent structural changes and irreversible damage to the brain. Some encephalopathies can be fatal."
What is Encephalopathy?
Encephalopathy is a term for any diffuse disease of the brain that alters brain function or structure. Encephalopathy may be caused by infectious agent (bacteria, virus, or prion), metabolic or mitochondrial dysfunction, brain tumor or increased pressure in the skull, prolonged exposure to toxic elements (including solvents, drugs, radiation, paints, industrial chemicals, and certain metals), chronic progressive trauma, poor nutrition, or lack of oxygen or blood flow to the brain. The hallmark of encephalopathy is an altered mental state. Depending on the type and severity of encephalopathy, common neurological symptoms are progressive loss of memory and cognitive ability, subtle personality changes, inability to concentrate, lethargy, and progressive loss of consciousness. Other neurological symptoms may include myoclonus (involuntary twitching of a muscle or group of muscles), nystagmus (rapid, involuntary eye movement), tremor, muscle atrophy and weakness, dementia, seizures, and loss of ability to swallow or speak. Blood tests, spinal fluid examination, imaging studies, electroencephalograms, and similar diagnostic studies may be used to differentiate the various causes of encephalopathy.
Is there any treatment?
Treatment is symptomatic and varies, according to the type and severity of the encephalopathy. Your physician can provide specific instructions for proper care and treatment. Anticonvulsants may be prescribed to reduce or halt any seizures. Changes to diet and nutritional supplements may help some patients. In severe cases, dialysis or organ replacement surgery may be needed.
What is the prognosis?
Treating the underlying cause of the disorder may improve symptoms. However, the encephalopathy may cause permanent structural changes and irreversible damage to the brain. Some encephalopathies can be fatal.
What research is being done?
The NINDS supports and conducts research on brain diseases. Much of this research is aimed at characterizing the agents that cause these disorders, clarifying the mechanisms underlying them, and, ultimately, finding ways to prevent, treat, and cure them.
NIH Patient Recruitment for Encephalopathy Clinical Trials
NIH information located here:
This article indicates support for an MRI of brain if TME is suspected (insurer reimbursement). http://www.ncbi.nlm.nih.gov/pubmed/12148375
Toxic encephalopathy, also known as toxic-metabolic encephalopathy, is a degenerative neurologic disorder caused by exposure to toxic substances.  It can be an acute or a chronic disorder. Exposure to toxic substances can lead to a variety of symptoms, characterized by an altered mental status. Toxic encephalopathy can be caused by various chemicals, some of which are commonly used in everyday life. Toxic encephalopathy can permanently damage the brain and currently, treatment is mainly just for the symptoms.
Toxic encephalopathy has a wide variety of symptoms,  which can include memory loss, small personality changes/increased irritability, insidious onset of concentration difficulties, involuntary movements, fatigue, seizures, arm strength problems, and depression.  . The condition may also be referred to as substance-induced persistent dementia. Acute intoxication symptoms include lightheadedness, dizziness, headache and nausea, and regular cumulative exposure to these toxic solvents over a number of years puts the individual at high risk for developing toxic encephalopathy. 
However, in chronic situations, these effects may not become severe enough to be noticed until much later. Increased exposure time and increased concentration of the chemical solvents will worsen the effects of toxic encephalopathy, due to the associated structural CNS damage and direct functional impairment consequences. 
Treatment is mainly for the symptoms that toxic encephalopathy brings upon victims, varying depending on how severe the case is. Diet changes and nutritional supplements may help some patients. (Alternative measures which they currently deny us)
Toxic encephalopathy is often irreversible. If the source of the problem is treated by removing the toxic chemical from the system, further damage can be prevented, but prolonged exposure to toxic chemicals can quickly destroy the brain.. Long term studies have demonstrated residual cognitive impairment (primarily attention and information-processing impairment resulting in dysfunction in working memory) up to 10 years following cessation of exposure. . Severe cases of toxic encephalopathy can be life threatening.
Acute toxic-metabolic encephalopathy (TME), which encompasses delirium and the acute confusional state, is an acute condition of global cerebral dysfunction in the absence of primary structural brain disease
TME is common among critically ill patients. Furthermore, TME is probably under recognized and undertreated, especially when it occurs in patients who require mechanical ventilation [2-4]. TME is usually a consequence of systemic illness, and the causes of TME are diverse. Most TME is reversible, making prompt recognition and treatment important. Certain metabolic encephalopathies, including those caused by sustained hypoglycemia and thiamine deficiency (Wernicke's encephalopathy), may result in permanent structural brain damage if untreated. Alcohol withdrawal syndromes must be excluded in patients with suspected TME. (See "Management of moderate and severe alcohol withdrawal syndromes".)
"With respect to other systemic diseases—sepsis is a good example—the patient often presents with lethargy and confusion due to the toxic effects of the infection. In most cases, the EEG reveals poor organization and diffuse slowing along with bifrontal delta activity. However, in others, epileptiform discharges may be recorded, suggesting the possibility of clinical epileptic seizures. The risk of epileptic seizures is likely to be increased if the patient has a pre-existing cerebral lesion, such as an infarct. Although the patient may develop obvious clinical seizures characterized by generalized or focal motor activity, the confusional or lethargic state may be a manifestation of CPS."
- Toxic encephalitis
- Toxic metabolic encephalopathy
- Between 1999-2007 there were 570 deaths in the United States where ICD-10 G92 was indicated as the underlying cause of death
ANALYSIS OF THE EVIDENCE- When Lyme borreliosis affects the nervous system, it typically presents with (a) all or part of a triad—meningitis, cranial neuritis, and radiculoneuritis (known in Europe as Garin-Bujadoux-Bannwarth syndrome); (b) parenchymal inflammation of the brain or spinal cord; (c) mild radiculoneuropathy presenting as a more diffuse, predominantly sensory peripheral neuropathy3,4; or (d) encephalopathy (alteration of cognitive function of varying severity, with or without evidence of brain infection).
Although most studies have focused on patients with Lyme meningoradiculitis, two have assessed
treatment response in patients with Lyme encephalopathy, defined as objectively demonstrable cognitive abnormalities on formal mental status testing or neuropsychological testing. In the first 23 (Class III), 27 adults with Lyme encephalopathy, polyneuropathy, or both were treated with ceftriaxone, 2 g IV daily for 2 weeks. Response to therapy, as measured by clinical signs and symptoms, CSF analyses, and neuropsychologic testing, was gradual and typically was not apparent until several months following completion of treatment.
Six months following treatment, 17 (63%) had improved, 6 (22%) improved but relapsed, and 4 (15%) were unchanged. Since symptoms had been prolonged and unremitting prior to treatment, this was believed to be due to the effect of treatment, even though no control group was included for direct comparison. A second study, in which CSF abnormalities were present in 89%, demonstrated efficacy of ceftriaxone (2 g daily for 30 days) in 18 adult patients with Lyme encephalopathy (Class III).24 In this study, at 12 to 24 months follow-up, all patients were somewhat improved (2 patients; 11%), greatly improved (9 patients; 50%), or normal (7 patients; 39%).
While most studies demonstrated excellent responses to a wide range of antimicrobial regimens,
several have raised the possibility that a significant number of patients may have residual difficulties. In one 25 (Class IV), 50 patients were identified who had intrathecal production of anti-B burgdorferi antibody. Of the 44 who were studied, 31 had cranial neuropathies, 12 radicular weakness, 12 other forms of weakness, 29 had pain, 11 had headache (multiple findings in most). At post-treatment follow-up, half the patients reported headache and concentration problems, although their neurologic deficits were better. The authors believed this represented an increase in subjective symptoms, despite improvement in objectively demonstrable abnormalities, similar to findings reported earlier.26
However, in the earlier study fewer than 10% had residual cognitive complaints and the remaining individuals had symptoms suggestive of sequelae of disease, rather than ongoing infection. In another study 27 (Class IV) 25% of the patients assessed 5 years following treatment reported persistent “neurologic” difficulties. However, in this study, sequelae appeared to reflect neurologic damage at the time of infection, not ongoing infection or antibiotic treatment failure. Similarly, in a study of 36 patients28 (Class IV) treated for Lyme meningitis, many described continued problems at 1 year follow-up. However, none appeared to develop new neurologic or arthritic signs or symptoms. Rather, symptoms ranged from nonspecific (headaches, myalgias) to residua of prior cranial or peripheral neuropathies.
PEDIATRIC NEUROBORRELIOSIS- A wide range of Lyme disease-associated neurologic disorders has been described in children, including cranial neuropathies, headache, seizures, meningitis, meningoencephalitis, encephalopathy, focal neurologic signs, ataxia, vertigo, chorea, and transverse myelitis.
Table 2- Syndromes and treatment options
Most available data argue against persistent B burgdorferi infection in patients who have received
what are normally curative courses of antimicrobial therapy. First, antibiotic resistance has not been
demonstrated in this genus.60-62 Second, persistent symptoms do not correlate with any objective measure of nervous system disease or with laboratory measures of inflammation.5,63 Third, there is no precedent for such a phenomenon in other spirochetal infections.64 Fourth, anti-B burgdorferi antibody concentrations often decline, even to undetectable levels, despite persistent symptoms.5,63,65 Such a decline in antibody in the face of persistent infection appears to be without precedent in other bacterial infections.
Fifth, Lyme disease lacks characteristics of other infections that justify longer treatment
courses, such as infections in which available antimicrobials have poor in vitro activity against the or-
ganism, infections caused by an intracellular pathogen, or infections involving a biofilm. Finally,
patients with PLS do not respond to a further course of IV antibiotics. Anecdotally, some experience a subjective improvement while on antibiotics, with symptoms recurring rapidly following medication discontinuation, suggesting a placebo effect. Still, based on a transient improvement in symptoms, some physicians have treated patients with PLS with various antibiotic regimens for months to years.
Guidelines can be located here:
John Halperin - lead author of Neurology Lyme Disease Guidelines and co-author of IDSA Lyme Disease Guidelines
Halperin- DOI 10.1212/01.wnl.0000265517.66976.28
; Prepublished online May 23, 2007; Neurology
J. J. Halperin, E. D. Shapiro, E. Logigian, et al.
Subcommittee of the American Academy of Neurology
(an evidence-based review). Report of the Quality Standards
Practice Parameter: Treatment of nervous system Lyme disease
May 26, 2011 This information is current as of May 26, 2011.]
The Clinical Assessment, Treatment, and Prevention of Lyme Disease, Human Granulocytic Anaplasmosis, and Babesiosis: Clinical Practice Guidelines by the Infectious Diseases Society of America
- 1Divisions of Infectious Diseases and New York University School of Medicine, New York,
- New York
- 2Divisions of Allergy, Immunology, and Rheumatology, Department of Medicine, New York
- Medical College, Valhalla, and New York University School of Medicine, New York, New York
- 3Divisions of New York University School of Medicine, New York, New York
- 4Divisions of Atlantic Neuroscience Institute, Summit, New Jersey
- 5Departments of Pediatrics and Department of Pediatrics, University of Connecticut School
- of Medicine and Connecticut Children's Medical Center, Hartford
- 6Departments of Epidemiology and Public Health and Department of Pediatrics, University
- of Connecticut School of Medicine and Connecticut Children's Medical Center, Hartford
- 7Departments of Section of Rheumatology, Department of Medicine, Yale University School
- of Medicine, New Haven, and Department of Pediatrics, University of Connecticut School of
- Medicine and Connecticut Children's Medical Center, Hartford
- 8Department of Pediatrics, University of Connecticut School of Medicine and Connecticut
- Children's Medical Center, Hartford
- 9Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital,
- Harvard Medical School, and Boston University School of Medicine and Boston Medical
- Center, Boston, Massachusetts
- 10Boston University School of Medicine and Boston Medical Center, Boston, Massachusetts
- 11Section of Infectious Diseases, St. Luke's Hospital, Duluth, Minnesota
- 12Division of Medical Microbiology, Department of Pathology, The Johns Hopkins Medical
- Institutions, Baltimore, Maryland
- 13Department of Infectious Diseases, University Medical Center, Ljubljana, Slovenia
- 14Medical University of Vienna, Vienna, Austria
- Reprints or correspondence: Dr. Gary P. Wormser, Rm. 245, Munger Pavilion, New York Medical College, Valhalla, NY 10595 (Gary_Wormser@nymc.edu).
Link to IDSA Lyme Guidelines
Additional info ALS/Lyme:
CBS NEWS- Lyme disease lies- and truths
They say Lyme is caused by the bite of ticks infected with B. burgdorferi bacteria, and that's true. But lots of other commonly known "facts" about the nation's most common bug-borne viral disease are anything but - and that's leading many people to seek costly and inappropriate treatment. Keep clicking as Dr. Orly Avitzur, medical advisor at Consumer Reports, separates Lyme disease fact from fiction...
FACT OR FICTION? You can catch Lyme from pets
FICTION. You can't catch Lyme from a dog or cat or any other animal - except a tick. Of course, pets can increase your risk for Lyme by bringing ticks into your house. What's more, it's possible to contract Lyme while removing a tick from your pet. It's important to wear latex gloves and use tweezers instead of your unprotected fingers.
FACT OR FICTION? The only way to avoid Lyme is to avoid tick bites
FACT. If you're not around ticks, you're not at risk. If you do spend time in tick-infested areas, what can you do to limit you risk? Stay out of high grass and vegetation - and as far as possible from the deer that carry Lyme-infected ticks. If you must venture into iffy places, wearing light-colored clothing will make it easier to find ticks and remove them before they attach. Be sure to wear a long-sleeved shirt and long pants tucked into your socks. Before venturing out, spray your clothes with insect repellent containing DEET. When you return inside, wash your clothes as soon as possible. Check your body for ticks, paying close attention to skin folds and hairy areas.
FACT OR FICTION? Almost all cases involve a "bull's-eye" rash
FACT. Nine out of 10 cases of Lyme involve the telltale rash, which doctors call erythema migrans. It's characterized by a red ring surrounding normal-looking skin. The rash varies in size, shape, and color. Sometimes it itches or burns, but not always. It typically appears at or near the site of the tick bite one or two weeks after the tick bite. Since the rash often arises in out-of-the-way places like the armpits, groin, or behind the knee, it's important to examine all of your skin as closely as possible.
FACT OR FICTION? Lyme disease can cause facial paralysis
FACT. Five to 10 percent of people with untreated Lyme disease develop a one-sided facial paralysis known as Bell's palsy. Anyone who develops Bell's palsy and who lives in an area where Lyme is endemic should be tested for Lyme.
FACT OR FICTION? The blood test for Lyme is unreliable
FICTION. Some people claim to have "chronic" Lyme disease even though the blood test commonly used to test for the disease found no evidence of infection. But the recommended "two-tier" testing regimen "ELISA testing" followed by "Western blot" testing - is extremely reliable. The sole exception involves patients within three to six weeks of infection, before the body has had a chance to produce antibodies to Lyme bacteria. That's the word from Dr. John J. Halperin, a professor of neurology and medicine at Mount Sinai School of Medicine in New York City and the author of the forthcoming "Lyme Disease: An Evidence-based Approach."
FACT OR FICTION? Testing positive while taking an antibiotic means treatment isn't working
FICTION. The blood test for Lyme indicates not whether Lyme bacteria are present in your body but whether your blood contains antibodies to Lyme. So if you're tested during or even after successful treatment for Lyme, you may test positive. What of the claim that testing positive after treatment means treatment has failed? "Not only is there no evidence - or even theoretical rationale - to support this claim, there is no precedent for this with reference to any other infectious disease," Dr. Halperin says.
FACT OR FICTION? Fatigue and mental "slowness" mean Lyme has invaded the brain
FICTION. Some Lyme patients do develop fatigue and have trouble thinking straight. But in most cases this is the result of "toxic-metabolic encephalopathy," a transient condition that occurs with many infectious illnesses. True brain infection with Lyme - a condition called encephalomyelitis - is exceedingly rare and easily treated with antibiotics.
FACT OR FICTION? Lyme disease often proves deadly
FICTION. Though Lyme "advocacy groups" often cite cases in which people with Lyme disease have died, Halperin says there is almost no evidence to suggest that Lyme is the culprit. "One of the curious aspects of B. burgdorferi infection is how relatively benign it actually is," he says. "In contrast to many other bacterial infections, patients rarely require intensive care or even hospitalization." When Lyme seems to lead to death, odds are it's not the disease but inappropriate treatment that is to blame, he says.
FACT OR FICTION? Lyme can be sexually transmitted
FICTION. Catch Lyme from a sex partner? Fugeddaboudit. "There is no epidemiological evidence or biological foundation for this allegation, yet I've seen a number of patients who believe that they have contracted Lyme disease from a sexual encounter," says Dr. Gary P. Wormser, lead author of Lyme guidelines published by the Infectious Diseases Society of America.
FACT OR FICTION? Prolonged treatment for Lyme is best
FICTION. The notion that an extended course of treatment for Lyme works better than a short course of treatment is false. Numerous studies have shown that even in rare cases in which Lyme bacteria have invaded the central nervous system, a short course of conventional antibiotics does the trick. There's no solid evidence that treatment lasting more than four weeks has any benefit, Halperin says. And long-term use of antibiotics - especially when given intravenously rather than by mouth - can lead to deadly serious drug reactions, severe diarrhea, and potentially deadly blood infections.
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