cognitive decline – F.I.G.H.T for your health!

Lyme disease: A Challenging Diagnosis

Garry Gordon, M.D. — Thu, 08 Oct 2009 22:04:47 +0000

[Originally posted to FACT forum on Tue Aug 12, 2008 1:03 pm]

This article in the NY TIMES changes everything for Lyme disease patients.

Finally our doctors may not have to fight to keep their medical licenses when they are brave enough to become LYME LITERATE DOCTORS.

This article will clearly change the terrain, as it states that the diagnosis is complex and that antibiotic treatment is warranted in spite of negative test results since there are so many false negative and false positive results. It quotes the May issue of the Mayo Clinic proceedings that says patients are best diagnosed by SYMPTOMS.

Doctors must be willing to use antibiotics based on CLINICAL ASSESSMENT rather than Lab findings! They accept the fact that oral antibiotics cannot do everything and IV antibiotics may be needed. It recognized that there are many vectors, not just deer or mice, but even your pet dog. Problems may show up years after the bite with memory and concentration problems, personality changes, heart rhythm abnormalities etc.

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

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NY Times
July 15, 2008
PERSONAL HEALTH
A Threat in a Grassy Stroll: Lyme Disease
By JANE E. BRODY

My friend Anne and her husband, Richard, spend summers at a resort in Westchester County that has a swimming lake, tennis courts, gardens and beautiful grounds surrounded by woods. But Anne never sets foot on the grass.
The reason is Lyme disease. Anne says just about everyone she knows who partakes of the greenery and gardens outside the cabins has contracted the disease. So not only is she cautious about venturing out, but she and her husband also check each other daily from head to toe for the much-feared deer tick, which can transmit the disease when it attaches to skin and feeds on blood.
This tick, which is the size of a pinhead when it starts searching for a bloody meal, is responsible for about 20,000 reported cases of Lyme disease each year in the United States (the actual number is believed to be 10 times that) and 60,000 reported cases in Europe. Cases have been reported in every state, with residents of the Northeast, the Great Lakes region, northwestern Washington and parts of California the most frequent victims.
In some areas, as many as half of the deer ticks are infected with Borrelia, the Lyme disease bacteria. The disease got its name in 1975 from the first identified cluster of cases, among children in Lyme, Conn., who had rheumatoid-like symptoms of swollen, painful joints.
The white-tailed deer and white-footed mouse are the tick’s most frequent hosts, but it also feeds on birds, dogs and other rodents, including squirrels. The tiny nymphal form that emerges in spring and early summer presents the greatest hazard to humans. It is also the hardest to spot, especially on body parts covered with hair.
People usually acquire the tick while walking through grassy or wooded areas. Sometimes pet dogs are the source: in Minnesota one summer, our dog got more than 30 deer ticks on his face, apparently from sticking his nose into a fresh carcass. Unlike the common dog tick, which is round and very dark, the deer tick is elongated and brownish.

A Challenging Diagnosis
The disease can be maddeningly difficult to diagnose. Only 50 to 70 percent of patients recall being bitten by a tick. Ordinary laboratory tests are rarely helpful. Tests for antibodies to the bacterium or for its genetic footprints result in many false-negative and false-positive findings.
Rather, according to Dr. Robert L. Bratton and colleagues at the Mayo Clinic in Scottsdale, Ariz., who reviewed the recent literature on Lyme disease in the May issue of Mayo Clinic Proceedings, most cases are best diagnosed and treated based on patients’ symptoms. Thus, doctors everywhere must be alert when dealing with patients who live or travel in areas where Lyme disease is prevalent, and they must be willing to use appropriate antibiotics based on a clinical assessment rather than laboratory findings.
Since signs and symptoms vary and often do not appear until one to four weeks — or even months — after exposure, anyone bitten by a deer tick may be wise to obtain preventive treatment with an antibiotic, according to Lyme disease experts consulted by Constance A. Bean, the author with Dr. Lesley Ann Fein of the new book “Beating Lyme” (Amacom Books).
The most common sign is a reddish rash called erythema migrans that often resembles a spreading bull’s-eye, though up to 20 percent of patients never develop it. Common sites of the rash are the thigh, groin, buttock and underarm. It may be accompanied by flulike symptoms: fever, chills, body aches, headache and fatigue.
If untreated or inadequately treated, the infection can cause severe migrating joint pain and swelling, most often in the knees, weeks or months later. In addition, several weeks, months or even years after an untreated infection, the bacterium can cause meningitis, temporary facial paralysis, numbness or weakness of the arms and legs, memory and concentration difficulties and changes in mood, personality or sleep habits. Some untreated patients develop temporary heart rhythm abnormalities, eye inflammation or hepatitis.

Controversial Guidelines
Antibiotics for early Lyme disease should be taken for at least two to three weeks. The treatments recommended by the Infectious Diseases Society of America include doxycycline for nonpregnant patients and children 9 and older, or amoxicillin for pregnant women and younger children. Other options include cefuroxime axetil (Ceftin) and erythromycin.
But these guidelines are controversial. They have been challenged by a nonprofit medical group, the International Lyme and Associated Diseases Society, which says they are inadequate to combat the infection in a significant number of patients, who go on to develop debilitating chronic symptoms.
In May, the Infectious Diseases Society agreed to review its guidelines as a result of an antitrust lawsuit by the Connecticut attorney general, Richard Blumenthal, who said some of the society’s experts had financial interests that could bias their judgment. (The society denied that accusation.)
Although I cannot state with authority which side is correct, I have encountered enough previously healthy people who have suffered for months or years after initial treatment to suggest that there is often more to this disease than “official” diagnostic and treatment guidelines suggest.
Pamela Weintraub, a senior editor at Discover magazine, has produced a thoroughly researched and well-written account of the disease’s controversial history in her new book “Cure Unknown: Inside the Lyme Epidemic” (St. Martin’s Press).

Treatment and Prevention
The Mayo doctors concluded that patients who developed arthritis related to Lyme disease should be treated for one to two months and that those with late or severe disease, including neurological and cardiac symptoms, required intravenous antibiotics. Although two studies, neither of which was long-term, found that repeated antibiotic treatment did not reverse the pain and altered cognition associated with Lyme disease, the experience of thousands of patients, including Ms. Bean, contradict these findings.
There are no vaccines to prevent Lyme disease; an early attempt was taken off the market in 2002 because of side effects and limited effectiveness. Those who will not or cannot avoid grassy and wooded areas should wear long sleeves and long pants with legs tucked into socks, and spray exposed skin and clothing with tick repellent containing 20 to 30 percent DEET. Repellents should not be used on children under 2.
Since the tick must usually feed for 24 hours to transmit significant amounts of bacteria, daily body checks and showering with a washcloth can help prevent infection. Clothing should be washed and dried in a dryer. Additional preventive actions are described in “Beating Lyme.”
If a tick is attached to skin, it should be removed with tweezers, not fingers. Press into the skin, grasp the front of the tick’s head and pull at right angles to the skin. Place the tick in a sealed plastic bag for later identification. Then wash the area and your hands thoroughly.

Inflammation Linked to Increased Cognitive Decline in Alzheimer’s Disease

Linda — Mon, 21 Sep 2009 05:03:50 +0000

It would have been nice to test these patients for environmental toxins and also to see how high their heavy metals were?? Simple way to regulate and determine if metal toxicity has an effect on the cognitive decline?

Perhaps someday the conventional docs will get on the band wagon with the alternative world and begin searching for the “cause” and stop treating symptoms??!!

Angel Huggzz

Linda

Inflammation Linked to Increased Cognitive Decline in Alzheimer’s Disease
Susan Jeffrey

INFORMATION FROM INDUSTRY
Find out about a head-to-head comparison of MS treatment options
Dr. Daniel Mikol discusses the findings from the multicenter REGARD study.Click here.September 11, 2009 — A new study finds a link between systemic inflammation and increased cognitive decline in patients with established Alzheimer’s disease (AD).

In this study, both acute and chronic inflammation, which were in turn associated with increased serum levels of proinflammatory cytokine tumor necrosis factor α (TNF-α), were associated with an increase in the rate of cognitive decline in patients with mild to severe AD.

“The role of TNF-α within the brain is controversial, with evidence supportive of both deleterious and protective effects,” the authors, led by Clive Holmes, MRCPsych, PhD, from the University of Southampton, United Kingdom, conclude. “However, if systemic inflammation has different [central nervous system] consequences depending on the existing relative activation state of the central innate immune system, dampening down systemic TNF-α may prove to be beneficial in AD.”
Their report is published in the September 8 issue of Neurology.

Inflammation and Cognitive Decline

Previous studies have shown an association between low-grade systemic inflammation and increased cognitive decline, as well as reduced hippocampal volume in people without dementia, the authors note. Some, but not all, studies have suggested that increased inflammation can increase the risk of developing AD, but few studies have looked at the effect of systemic inflammation in people with established AD.

Acute systemic inflammation from infections or tissue injury and more chronic inflammatory conditions such as atherosclerosis, periodontitis, or diabetes involve the systemic production of C-reactive protein and TNF-α, the authors point out. Previous preclinical research has shown that acute systemic inflammation contributes to neurodegeneration by the activation of primed microglial cells.

In this study, the authors hypothesized that acute systemic inflammatory events such as infections and tissue injury that were sufficient to increase systemic TNF-α would be associated with cognitive decline in AD patients.

A total of 300 community-dwelling patients with mild to severe AD were assessed at baseline and then every other month for 6 months. Testing included cognitive assessment and having blood samples taken and analyzed for systemic inflammatory markers including TNF-α, and caregivers were interviewed to determine whether the patient had developed any incident systemic inflammatory events.

During follow-up, 110 patients had acute inflammatory events that were associated with increases in serum TNF-α. Compared with participants without these events, they had a 2-fold increase in the rate of cognitive decline during this period.

Those who had high levels of TNF-α at baseline had a 4-fold increase in the rate of cognitive decline, independent of age, delirium, or concomitant cholinesterase use, the authors write, suggesting a relationship between serum TNF-α and rates of both cognitive decline and long-term cognitive impairment. Patients with low levels of serum TNF-α throughout the study had no cognitive decline during the study period, they add.

The effect of having both an acute and chronic infection was particularly marked, the authors note; those participants with high baseline levels of TNF-α who then experienced an incident infection or injury had a 10-fold increase in the rate of cognitive decline over those who had low baseline TNF-α levels and no inflammatory events during the course of the study.
“One might guess that people with a more rapid rate of cognitive decline are more susceptible to infections or injury, but we found no evidence to suggest that people with more severe dementia were more likely to have infections or injuries at the beginning of the study,” Dr. Holmes said in a statement from the American Academy of Neurology. “More research needs to be done to understand the role of TNF-α in the brain, but it’s possible that finding a way to reduce those levels could be beneficial for people with Alzheimer’s disease.”

TNF-α and Etanercept

In a separate review article published in the September 1 issue of CNS Drugs, Edward Tobinick, MD, from the Institute for Neurological Research in Los Angeles, California, examined the role of TNF-α modulation as a potential treatment for Alzheimer’s disease, and in particular, the use of perispinal administration of etanercept (Enbrel, Amgen), a potent anti-TNF fusion protein.

In a previously published 6-month open-label pilot study including 15 AD patients, Dr. Tobinick and colleagues reported sustained clinical improvement in these patients with this strategy. Since then, several other case studies from his group have documented rapid improvement after perispinal etanercept administration in AD and primary progressive aphasia, Dr. Tobinick writes in the new review article.

“Recent studies documenting rapid and sustained clinical improvement in AD and related forms of dementia following perispinal etanercept suggest the existence of rapidly reversible TNF-mediated pathophysiological mechanisms in AD, hypothesized to be related to the synaptic effects of TNF,” he concludes. “Accumulating and emerging evidence supports the further study of perispinal etanercept for the treatment of AD in randomized clinical trials.”

The study by Holmes et al was supported by the Alzheimer’s Society. Dr. Holmes has disclosed that he has received research support from the Alzheimer’s Society, the UK Department of Health, and the Medical Research Council. Disclosures for coauthors appear in the article. In the CNS Drugs paper, no outside funds were received in connection with the preparation of the manuscript. Dr. Tobinick owns stock in Amgen, the manufacturer of etanercept, and has multiple issued and pending US and international patent applications describing the use of perispinal etanercept for neurological disorders, including but not limited to AD and other forms of dementia.

Neurology. 2009;73:768–774; CNS Drugs. 2009;23:713–725.

Lyme Disease, Psychiatric Symptoms and Aggressiveness

Linda — Mon, 14 Sep 2009 02:05:31 +0000

I have the highest respect for Dr Robert Bransfield, as a top psychiatriststs, and am priviledged to re-print this information. In my own opinion I feel many psychiatric symptoms with Lyme could be reduced if patient’s would focus more on toxins that we all are dealing with. Lead and Mercury are our biggest culprits. We all know that Lead and Mercury can and do affect our brains.

We must find ways to reduce these toxins and that is why I focus on the FIGHT program. It has worked for me. These toxins are in our foods, water and some medications. Learn to read labels.

Lyme Disease, Psychiatric Symptoms and Aggressiveness

By Robert C Bransfield, MD, DLFAPA (revised 4-1-09)

There has been recent media attention focused upon the issue of Lyme disease and psychiatric symptoms and aggressiveness. Questions arise whether microbes and the immune reactions to them can contribute to cognitive decline, degenerative neurological disease, developmental disabilities, mental illness, personality changes and violent and criminal behavior?

There are several thousand peer-reviewed references demonstrating the association between infections and mental symptoms and at least 65 different microbes have been recognized as causing mental symptoms.^¹ Over two hundred peer-reviewed articles describe the causal association between Lyme/tick-borne diseases and mental symptoms, pathophysiology, morbidity and mortality some of which are included in the attached addendum. Lyme disease: a neuropsychiatric illness is a major and classic article summarizing this association.^² A Controlled Study of Cognitive Deficits in Children With Chronic Lyme Disease is a particularly useful resource for describing some of the cognitive symptoms associated with Lyme/tick-borne diseases. Attempted suicide and completed suicide associated with neuropsychiatric manifestations of Lyme disease and other tick-borne disease has been observed and reported by the author and many other clinicians.^³ An article in the American Journal of Psychiatry, Higher Prevalence of Antibodies to Borrelia Burgdorferi in Psychiatric Patients Than in Healthy Subjects compared 499 psychiatric inpatients to matched pair healthy controls and found significantly more psychiatric patients were seropositive for Borrelia burgdorferi (33% vs. 19%), thereby demonstrating an association between Borrelia burgdorferi infections and psychiatric morbidity.

The recent attention on Lyme disease began after a chimpanzee with Lyme/tick-borne disease became violent and assaulted their owner in February 2009. Then a few weeks later a patient with late stage Lyme/tick-borne disease shot and killed a minister in Illinois. Since these two incidents occurred in close time proximity and both drew considerable media attention there has been an increased attention upon the question of whether tick-borne diseases can cause violent behavior. Lyme disease has been associated with causing aggression in dogs and other animals.^⁴

Although most patients with Lyme/tick-borne disease do not become violent, a small percent of patients who become infected develop a type of neurological dysfunction that can increase their risk of aggressiveness. In working with a number of patients with Lyme/tick-borne diseases it is apparent to many clinicians these conditions can cause reduced frustration tolerance, irritability, depression, cognitive impairments and mood swings in many patients, but more significant suicidal and aggressive tendencies are seen in a few patients. An article about Lyme/tick-borne diseases and suicide in 1998 is at http://www.mentalhealthandillness.com/lymeframes.html Articles on Lyme/tick-borne disease and aggressiveness are Aggression and Lyme Disease (1998). http://www.mentalhealthandillness.com/lymeframes.html , A Tale of Two Spirochetes (1999) http://www.mentalhealthandillness.com/lymeframes.html and Lyme Neuroborreliosis & Aggression. (2001) http://actionlyme.50megs.com/neuroborreliosis%20aggression.htm

There have been a number of suicide attempts, suicides, aggressive episodes, assaults, homicide attempts, homicides and combined homicide/suicide associated with Lyme/tick/borne diseases. A few such cases are currently in the legal system. In the majority of the cases that enter the legal system it is clear the perpetrator is significantly impaired and treatment occurs in the aftermath. Some, but not all, of the individuals involved in these cases have responded to treatment and now leading productive lives.

Most patients who acquire Lyme/tick/borne diseases do not become aggressive and should not be stigmatized. Many of the patients who do become aggressive can respond to effective treatment. However if the seriousness of Lyme/tick-borne diseases are overlooked there will be further tragedies that could be prevented with greater awareness and earlier and more effective treatment now. We need to change the focus of our system away from a primary focus upon guilt and punishment towards a greater emphasis upon insight and prevention. The unfortunate reality is there will be other tragic incidents in the future. It won’t be a chimpanzee in Connecticut or the shooting of a minister in Illinois, but some who are alive and healthy today will become the victims of future tragedies involving the mental symptoms associated with tick-borne diseases.

Some Peer-Reviewed References for Psychiatric Symptoms
and Lyme/Tick-Borne Diseases

Acute disseminated encephalomyelitis [letter]
AUTHORS: Fallon BA, Nields JA.
SOURCE: J Neuropsychiatry Clin Neurosci 1998 Summer;10(3):366-7

Acute and chronic neuroborreliosis with and without CNS involvement: a clinical, MRI, and HLA study of 27 cases.

AUTHORS: Krüger H, Heim E, Schuknecht B, Scholz S.

SOURCE: J Neurol. 1991 Aug;238(5):271-80.

Altered mental status, an unusual manifestation of early disseminated Lyme disease: A case report.

AUTHORS: Chabria SB, Lawrason J.

SOURCE: J Med Case Reports. 2007 Aug 9;1:62.

Alzheimer’s disease and infection: Do infectious agents contribute to progression of Alzheimer’s disease?

AUTHORS: Honjo K, van Reekum R, Rand Nicolaas, VerhoeffNPLG.

SOURCE: Alzheimer’s and Dementia. Vol 5;4, July 2009, p 348-360

The association between tick-borne infections, Lyme borreliosis and autism spectrum disorders
AUTHORS: Bransfield RC, Wulfman JS, Harvey WT, Usman AI.
SOURCE: Medical Hypotheses. 5 Nov 2007

Alzheimer’s disease Braak Stage progressions: reexamined and redefined as Borrelia infection transmission through neural circuits.

AUTHOR: MacDonald AB.

SOURCE: Med Hypotheses. 2007;68(5):1059-64. Epub 2006 Nov 17.

Alzheimer’s neuroborreliosis with trans-synaptic spread of infection and neurofibrillary tangles derived from intraneuronal spirochetes.

AUTHOR: MacDonald AB.

SOURCE: Med Hypotheses. 2007;68(4):822-5. Epub 2006 Oct 20.

Antibodies against OspA epitopes of Borrelia burgdorferi cross-react with neural tissue.

AUTHORS: Alaedini A, Latov N.

SOURCE: J Neuroimmunol. 2005 Feb;159(1-2):192-5. Epub 2004 Nov 26.

Audiologic manifestations of patients with post-treatment Lyme disease syndrome
AUTHORS: Shotland LI, Mastrioanni MA, Choo DL, Szymko-Bennett YM, Dally LG, Pikus AT, Sledjeski K, Marques A
SOURCE: Ear Hear. 2003 Dec;24(6):508-17

Bartonella sp. Bacteremia in Patients with Neurological and Neurocognitive Dysfunction.

AUTHORS: Journal of Clinical Midrobiology. 46(9):2856–2861

SOURCE: Breitschwerdt EB. Maggi RG, Nicholson WL, Cherry NA, Woods CW.

The basic syndromes of neurological disorders in Lyme borreliosis:

AUTHORS: Dekonenko EP, Umanskii KG, Virich IE, Kupriianova LV, Rudometov, IuP, Bagrov FI:

SOURCE: Ter Arkh 1995; 67 (11) : 52-53

Beta-amyloid deposition and Alzheimer’s type changes induced by Borrelia spirochetes.

AUTHORS: Miklossy J, Kis A, Radenovic A, Miller L, Forro L, Martins R, Reiss K, Darbinian N, Darekar P, Mihaly L, Khalili K.

SOURCE: Neurobiol Aging. 2006 Feb;27(2):228-36.

Bell’s Palsy of the Gut and other Manifestations of Lyme and Associated Diseases

AUTHOR: Sherr VT

SOURCE: Practical Gastroenterology April 2006

Bilateral dorsolateral thalamic lesions disrupts conscious recollection.

AUTHORS: Edelstyn NM, Hunter B, Ellis SJ.

SOURCE: Neuropsychologia. 2006;44(6):931-8. Epub 2005 Oct 25.

Biology and neuropathology of dementia in syphilis and Lyme disease

AUTHOR: MIKLOSSY J

EDITORS: Duyckaerts C, Litvan I

SOURCE: Handbook of Clinical Neurology, Vol. 89 (3rd series) Dementias 2008 Elsevier B.V.

Borrelia burgdorferi in the central nervous system: experimental and clinical evidence for early invasion.

AUTHORS: Garcia-Monco JC, Villar BF, Alen JC, Benach JL.

SOURCE: J Infect Dis. 1990 Jun;161(6):1187-93.

Borrelia burgdorferi central nervous system infection presenting as an organic schizophrenialike disorder.
AUTHORS: Hess A, Buchmann J, Zettl UK, Henschel S, Schlaefke D, Grau G, Benecke R.
SOURCE: Biol Psychiatry 1999 Mar 15;45(6):795

Borrelia burgdorferi persists in the brain in chronic lyme neuroborreliosis and may be associated with Alzheimer disease.

AUTHORS: Miklossy J, Khalili K, Gern L, Ericson RL, Darekar P, Bolle L, Hurlimann J, Paster BJ.

SOURCE: J Alzheimers Dis. 2004 Dec;6(6):639-49; discussion 673-81.

Borrelia burgdorferi-seropositive chronic encephalomyelopathy: Lyme neuroborreliosis? An autopsied report.
AUTHORS: Kobayashi K, Mizukoshi C, Aoki T, Muramori F, Hayashi M, Miyazu K, Koshino Y, Ohta M, Nakanishi I, Yamaguchi N.
SOURCE: Dement Geriatr Cogn Disord. 1997 Nov-Dec;8(6):384-90.

[Borreliosis–simultaneous Lyme carditis and psychiatric disorders–case report]

AUTHORS: Legatowicz-Koprowska M, Gziut AI, Walczak E, Gil RJ, Wagner T.

SOURCE: Pol Merkur Lekarski. 2008 May;24(143):433-5. Polish.

Brain SPECT Imaging in Chronic Lyme Disease.
AUTHORS: Plutchok JJ, Tikofsky RS, Liegner KB, Fallon BA, Van Heertum RL.
SOURCE: Journal of Spirochetal and Tick Borne-Diseases, 1999; 6: 10-16.

Carbamazepine in the treatment of Lyme disease-induced hyperacusis.
AUTHORS: Nields JA, Fallon BA, Jastreboff PJ.
SOURCE: J Neuropsychiatry Clin Neurosci 1999 Winter;11(1):97-9

Case report: Lyme disease and complex partial seizures.

AUTHOR: Bransfield RC.

SOURCE: Journal of Spirochetes and Tick-borne Diseases; Fall/Winter 1999, Vol 6, p123-125

Central nervous system manifestations of human ehrlichiosis.
AUTHORS: Ratnasamy N, Everett ED, Roland WE, McDonald G, Caldwell CW.
SOURCE: Clin Infect Dis 1996 Aug;23(2):314-9

Cerebral metabolic changes associated with Lyme disease
AUTHORS: Newberg A, Hassan A, Alavi A.
SOURCE: Nucl Med Commun 2002 August;23(8):773-777

Chronic Bacterial and Viral Infections in Neurodegenerative and Neurobehavioral Diseases.

AUTHORS: Nicholson GL.

SOURCE: Lab Medicine. 2008;39(5):291-9.

Chronic borrelia encephalomyeloradiculitis with severe mental disturbance: immunosuppressive versus antibiotic therapy.

AUTHORS: Kollikowski HH, Schwendemann G, Schulz M, Wilhelm H, Lehmann HJ.

SOURCE: J Neurol. 1988 Jan;235(3):140-2.

Chronic inflammation and amyloidogenesis in Alzheimer’s disease — role of Spirochetes.

AUTHORS: Miklossy J.

SOURCE: J Alzheimers Dis. 2008 May;13(4):381-91. Review.

Chronic neuroborreliosis in infancy

AUTHORS: Zamponi N, Cardinali C, Tavoni MA, Porfiri L, Rossi R, Manca A

SOURCE: Ital J Neurol Sci (1999) 20:303-307

Chronic neurologic manifestations of erythema migrans borreliosis.
AUTHORS: Ackermann R, Rehse-Kupper B, Gollmer E, Schmidt R.
SOURCE: Ann N Y Acad Sci. 1988;539:16-23.

Chronic neurologic manifestations of Lyme disease.

AUTHORS: Logigian EL, Kaplan RF, Steere AC.

SOURCE: N Engl J Med. 1990 Nov 22;323(21):1438-44.

Clinical and demographic characteristics of psychiatric patients seropositive for Borrelia burgdorferi.

AUTHORS: Hájek T, Libiger J, Janovská D, Hájek P, Alda M, Höschl C.

SOURCE: Eur Psychiatry. 2006 Mar;21(2):118-22.

[Clinical manifestations and epidemiological aspects leading to a diagnosis of Lyme borreliosis: neurological and psychiatric manifestations in the course of Lyme borreliosis]

AUTHORS: Créange A.

SOURCE: Med Mal Infect. 2007 Jul-Aug;37(7-8):532-9. Epub 2007 Mar 26. Review. French.

Co-existance of toxoplasmosis and neuroborreliosis – a case report.
AUTHORS: Gustaw K, Beltowska K, Dlugosz E.
SOURCE: Ann Agric Environ Med. 2005;12(2):305-8.

Cognitive functioning in late Lyme borreliosis.

AUTHORS: Krupp LB, Masur D, Schwartz J, Coyle PK, Langenbach LJ, Fernquist SK, Jandorf L, Halperin JJ.

SOURCE: Arch Neurol. 1991 Nov;48(11):1125-9.

Cognitive Impairments after Tick-borne Encephalitis.

AUTHORS: Gustaw-Rothenberg K.

SOURCE: Dementia and Geriatric Cognitive Disorders. 2008;26:165-168.

Cognitive processing speed in Lyme disease.
AUTHORS: Pollina DA, Sliwinski M, Squires NK, Krupp LB.
SOURCE: Neuropsychiatry Neuropsychol Behav Neurol. 1999 Jan;12(1):72-8.

Complaints attributed to chronic Lyme disease: depression or fibromyalgia?

AUTHORS: Berman DS, Wenglin BD.

SOURCE: Am J Med. 1995 Oct;99(4):440.

Concepts of trust among patients with serious illness.

AUTHORS: Mechanic D, Meyer S.

SOURCE: Soc Sci Med. 2000 Sep;51(5):657-68.

Concurrent infection of the central nervous system by Borrelia burgdorferi and Bartonella henselae: evidence for a novel tick-borne disease complex.

AUTHORS: Eskow E, Rao RV, Mordechai E.

SOURCE: Arch Neurol. 2001 Sep;58(9):1357-63.

Concurrent medical conditions with pediatric bipolar disorder.

AUTHORS: Scheffer RE, Linden S.

SOURCE: Curr Opin Psychiatry. 2007 Jul;20(4):398-401. Review.

Consequences of treatment delay in Lyme disease.

AUTHORS: Cameron DJ

SOURCE: J Eval Clin Pract. 2007 Jun;13(3):470-2.

Constipation Heralding Neuroborreliosis
AUTHORS: Shamim A, Shamim S; Liss G; Nylen E; Pincus J; Yepes M.
SOURCE: Arch Neurol. 2005;62:671-673.

A Controlled Study of Cognitive Deficits in Children With Chronic Lyme Disease
AUTHORS: Tager FA, Fallon BA, Keilp J, Rissenberg M, Jones CR, Liebowitz MR.
SOURCE: J Neuropsychiatry Clin Neurosci 13:500-507, November 2001
FULL TEXT: http://www.lymediseaseassociation.org/Tager.pdf

Behavioral Consequences of Infections of the Central Nervous System: With Emphasis on Viral Infections

AUTHORS: Tselis A, MD, Booss J.

SOURCE: J Am Acad Psychiatry Law 31:289–98, 2003

Catatonic syndrome in acute severe encephalitis due to Borrelia burgdorferi infection.

Pfister HW, Preac-Mursic V, Wilske B, Rieder G, Forderreuther S, Schmidt S, AUTHORS: Kapfhammer HP.

SOURCE: Neurology. 1993 Feb;43(2):433-5.

Chronic neurologic manifestations of Lyme disease.
AUTHORS: Logigian EL; Kaplan RF; Steere AC
SOURCE: N Engl J Med 1990 Nov 22;323(21):1438- 44.

Delirium and Lyme disease.
AUTHORS: Caliendo MV, Kushon DJ, Helz JW.
SOURCE: Psychosomatics. 1995 Jan-Feb;36(1):69-74.

Delusional disorders in the course of tick-born encephalitis and borreliosis in patients with hemophilia A and posttraumatic epilepsy–diagnostic and therapeutic difficulties]

AUTHORS: Grzywa A, Karakuła H, Górecka J, Chuchra M.

SOURCE: Pol Merkur Lekarski. 2004 Jan;16(91):60-3. Polish.

Dementia associated with infectious diseases.

AUTHOR: Almeida OP, Lautenschlager NT.

SOURCE: Int Psychogeriatr. 2005;17 Suppl 1:S65-77. Review.

Demyelinating polyradiculitis in neuro borreliosis:

AUTHORS: Corral I, Sanchis G, Garcia-Ribas G, Quereda C, Escudero R, de Blas G:

SOURCE: Neurologia 1995 Feb; 10 (2) : 110-113

Detection of Bartonella henselae by polymerase chain reaction in brain tissue of an immunocompromised patient with multiple enhancing lesions. Case report and review of the literature.

AUTHORS: George TI, Manley G, Koehler JE, Hung VS, McDermott M, Bollen A.

SOURCE: J Neurosurg. 1998 Oct;89(4):640-4. Review.

The diagnosis of Lyme disease.

AUTHOR: Bransfield RC.

SOURCE: Hosp Pract (Minneap). 1996 Aug 15;31(8):35, 40.

Diagnosis, treatment, and prevention of Lyme disease.

AUTHOR: Bransfield RC.

SOURCE: JAMA. 1998 Sep 23-30;280(12):1049; author reply 1051.

Differential Diagnosis and Treatment of Lyme Disease with Special Reference to Psychiatric Practice.
AUTHORS: Nields JA, Fallon BA.
SOURCE: Directions in Psychiatry, 1998, 18: 209-228.

[Differential diagnostic problems in Lyme disease (Borrelia infection resulting in acute exogenous psychosis)]

AUTHORS: Császár T, Patakfalvi A.

SOURCE: Orv Hetil. 1994 Oct 9;135(41):2269-71.

A disease in disguise. Lyme can masquerade as migraine, or as madness.

AUTHORS: Cowley G, Underwood A.

SOURCE: Newsweek. 2004 Aug 23;144(8):62.

Do bartonella infections cause agitation, panic disorder, and treatment-resistant depression?

AUTHORS: Schaller JL, Burkland GA, Langhoff PJ.

SOURCE: MedGenMed. 2007 Sep 13;9(3):54.

Does process-specific slowing account for cognitive deficits in Lyme disease?

AUTHORS: Pollina DA, Elkins LE, Squires NK, Scheffer SR, Krupp LB.

SOURCE: Appl Neuropsychol. 1999;6(1):27-32.

Early disseminated Lyme disease: Lyme meningitis.

AUTHOR: Pachner AR

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Efficacy of a long-term antibiotic treatment in patients with a chronic Tick Associated Poly-organic Syndrome (TAPOS).

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Spirochetal diseases of the nervous system.

AUTHORS: Cintron R, Pachner AR.

SOURCE: Curr Opin Neurol. 1994 Jun;7(3):217-22. Review.

Study and treatment of post Lyme disease (STOP-LD): a randomized double masked clinical trial.

AUTHORS: Krupp LB, Hyman LG, Grimson R, Coyle PK, Melville P, Ahnn S, Dattwyler R, Chandler B.

SOURCE: Neurology. 2003 Jun 24;60(12):1923-30.

Subarachnoid hemorrhage in a patient with Lyme disease.

AUTHORS: Cheherama M, Zagardo MT, Koski CL

SOURCE: Neurology (1997);48:520-523

Successful treatment of Lyme encephalopathy with intravenous ceftriaxone.

AUTHORS: Logigian EL, Kaplan RF, Steere AC.

SOURCE: J Infect Dis. 1999 Aug;180(2):377-83.

Survival strategies of Borrelia burgdorferi, the etiologic agent of Lyme disease.

AUTHORS: Embers ME, Ramamoorthy R, Philipp MT.

SOURCE: Microbes Infect. 2004 Mar;6(3):312-8. Review.

Transfection “Junk” DNA – a link to the pathogenesis of Alzheimer’s disease?

AUTHORS: MacDonald AB.

SOURCE: Med Hypotheses. 2006;66(6):1140-1. Epub 2006 Feb 14.

Treatment of patients with persistent symptoms and a history of Lyme disease.

AUTHORS: Bransfield R, Brand S, Sherr V.

SOURCE: N Engl J Med. 2001 Nov 8;345(19):1424-5.

Treatment-Resistant Depression: Progress and Limitations

AUTHORS: Amsterdam JD, O’Reardon JP

SOURCE: Psychiatric Annals. 1998;28(11):633

Tullio phenomenon and seronegative Lyme borreliosis [letter]
AUTHORS: Nields JA, Kueton JF.
SOURCE: Lancet 1991 Jul 13;338(8759):128-9

The Underdiagnosis of Neuropsychiatric Lyme Disease in Children and Adults
AUTHORS: Fallon BA, Kochevar JM, Gaito A, Nields JA.
SOURCE: Psychiatric Clinics of North America, 1998; 21: 693-703
COMPLETE TEXT AT:
http://www.lymenet.org

Untreated neuroborreliosis: Bannwarth’s syndrome evolving into acute schizophrenia-like psychosis. A case report.
AUTHORS: Roelcke U, Barnett W, Wilder-Smith E, Sigmund D, Hacke W.
SOURCE: J Neurol 1992 Mar;239(3):129-31

An unusual presentation of cat scratch encephalitis.

AUTHORS: Chan L, Reilly KM, Snyder HS.

SOURCE: J Emerg Med. 1995 Nov-Dec;13(6):769-72.

Update on lyme disease: the hidden epidemic.

AUTHOR: Savely VR.

SOURCE: J Infus Nurs. 2008 Jul-Aug;31(4):236-40.

The use of atypical antipsychotics in the treatment of schizophrenia in North Staffordshire.

AUTHORS: Hodgson R, Belgamwar R, Al-tawarah Y, MacKenzie G.

SOURCE: Hum Psychopharmacol. 2005 Mar;20(2):141-7.

Value of clinical symptoms, intrathecal specific antibody production and PCR in CSF in the diagnosis of childhood Lyme neuroborreliosis:

AUTHORS: Issakainen J, Gnehm HE, Lucchini GM, Zbinden R:

SOURCE: Klin Padiatr 1996 May-Jun; 208 (3) : 106-109

WAIS-III and WMS-III performance in chronic Lyme disease.
AUTHORS: Keilp JG, Corbera K, Slavov I, Taylor MJ, Sackeim HA, Fallon BA.
SOURCE: J Int Neuropsychol Soc. 2006 Jan;12(1):119-29

A 25-year-old woman with hallucinations, hypersexuality, nightmares, and a rash.
AUTHORS: Stein SL, Solvason HB, Biggart E, Spiegel D.
SOURCE: Am J Psychiatry. 1996 Apr;153(4):545-51.

A 58-year-old man with a diagnosis of chronic Lyme disease, 1 year later.

Steere AC.

JAMA. 2002 Aug 28;288(8):1002-10.

A 58-year-old man with a diagnosis of chronic Lyme disease, 1 year later.

Burns RB, Hartman EE.

JAMA. 2003 Dec 24;290(24):3247.

Some of the above references are online at:

Neuropsychiatric Lyme Disease Online Resources:
http://www.lymeinfo.net/neuropsych.html

1 Bransfield RC. Preventable cases of autism: relationship between chronic infectious diseases and neurological outcome. Pediatric Health. (2009) April 3(2).

2 Fallon BA, Nields JA. Lyme disease: a neuropsychiatric illness. Am J Psychiatry. 1994 Nov;151(11):1571-83.

3 Fallon BA, Schwartzberg M, Bransfield R, Zimmerman B, Scotti A, Weber CA, Liebowitz MR. Late-stage neuropsychiatric Lyme borreliosis. Differential diagnosis and treatment. Psychosomatics.1995 May-Jun;36(3):295-300.

4Lyme Disease and Pets. Rhode Island Department of Health. Accessed 3-21-09. http://www.health.state.ri.us/disease/communicable/lyme/pets.php