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Post by bugsy on Jul 7, 2007 16:49:18 GMT -5
P.S. I do know that Spirochetes are cell wall deficient (CWD) and do not respond to antibiotics which attack the cell walls of bacteria. Buut, thats what the Aremisinin is for in conjunction with the antibiotics for safe short stints. (sweet wormwood). Am prolly preaching to the choir with you guys but I knew if I did not post this...someone would have a cow and start calling me "ignorant evil" or some daaham thing. lol
~Bugsy
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Post by toni on Jul 7, 2007 22:21:52 GMT -5
Sort of off the wall here, but iron being depleted in the body too...I just wonder if that's a reason for the "orange" hairs and eye lashes many of us have experienced.
Oxidization will do that, in fact when hair is "bleached out" the hair bleach literally oxidizes the hair, which lifts the color and makes it turn orange before it lifts all the color out. But for our bodies to be "maybe oxidizing" or cells oxidizing, maybe that too is the cause of the "orange hairs".
Antioxidants might be very important now to take too.
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Post by Niels on Jul 8, 2007 1:54:00 GMT -5
spirochetes aren't cell wall deficient. they can transform into other forms, however, some of which are CWD, and some which are even more deficient than just their cell walls... spore form.
antibiotics are pretty safe to take long term, assuming they're doing something useful like killing off borrelia or chlamidya...
i just read about a doctor that takes flagyl continuously for prophylaxis against chlamidya pneumoniae, which is probably the "catchy" part of morgellons (transmitted by coughing) and is probably what ends up making nurses and teachers more susceptible to morgellons -- because of their exposure to lots of people and the general prevalence of CpN across the population. CpN, like Lyme, damages the immune system and does bad things to the blood (including deplete iron) and damages, blood vessels and capillaries... which IMHO makes people susceptible to the morgs... as morgs seems to thrive when the immune system is low, and in skin whose "supply lines" in the form of blood and lymph have been disrupted by chlamidia pneumoniae (which infests vessels especially) and lyme, which seems to feed off blood at the capillary level, also doing damage at that level in the process.
IMHO, flagyl is the key -- for both getting rid of chronic Lyme and chronic Chlamidia Pneumoniae
I think I'm finally settling in to full-dose flagyl after a few months. it was really disconcerting to be sitting there at dinner with my parents and son, teeth chattering from "cold", no fever -- 96-97 degree body temps, and wearing like 3 sweaters otherwise i felt like i was gonna die... even though it was normal room temperature and everybody else was in shorts and short-sleeves.... even more disconcerting because everybody's going "why the hell are you taking antibiotics if they're doing this to you" ...
Also, it kinda sucks because my herx's for the last two years have been far worse than what most people with "just Lyme" experience... and i only found out relatively recently that it was a combination of die-off of chlamidia pneumoniae and die-off of borrelia.
That is probably what made the 2-3 months I did on the strongest antibiotic I ever took -- factive, aka gemifloxacin -- particularly excruciating.
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Post by bugsy on Jul 8, 2007 7:33:46 GMT -5
Sounds like a terrible thing you have been through and are going through Niels. Thanks for the clarification of the above. Ha Just wanted to say thanks for all of your informative posts. People may not always say thanks but they are reading these and they do appreciate them whether or not they post a response. ~Bugsy
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Post by Niels on Jul 10, 2007 19:45:03 GMT -5
Hmmm... Lyme OSP-A vaccine via hepatitis B?? isn't that how AIDS got released into NYC in the late 70's? As the experimental Hepatitis B vaccine promised protection from the AIDS of the day -- hep b -- , many people, precisely the people that shouldn't have been given an experimental vaccine, were given a vaccine.... and they spread that "vaccine" through multiple sex partners as quick as bunny rabbits go bouncy-bouncy on the grass.... www3.interscience.wiley.com/cgi-bin/abstract/109875281/ABSTRACT?CRETRY=1&SRETRY=0
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Post by Niels on Jul 10, 2007 19:59:26 GMT -5
Well now we know what some of those mystery plasmids on the borrelia bacteria do... they contain the genetics of bacteriophages released by borrelia... and different strains... release different bacteriophages... what if our "borrelia" happens to emit bacteriophages that somehow mess up stem-cell related processes in the body, when they infect near those cells, usually through "healing" after damage (the fibers are grown to create that damage, by hijacking the stem-cell process)... i guess we could call that "morgellons", huh? (and there's no reason, apparently, that there couldn't be a new strain of borrelia released, which instead of inducing bacteriophages, emits say, agrobacterium instead... and those are the ones that hijack the healing process by producing tissue that eventually cuts itself upl... Lovely frankenbacteria... comes with it's own stiches... Well this article is just about the plasmids and bacteriophages part of the above... jb.asm.org/cgi/reprint/181/23/7308.pdf
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Post by Niels on Jul 10, 2007 20:07:52 GMT -5
On the funky genetics of borrelia, and why it is able to evade our immune system... because it wears a magic coat that changes a little bit each time... iai.asm.org/cgi/content/full/67/6/3146
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Post by Niels on Jul 26, 2007 23:04:05 GMT -5
1: Curr Microbiol. 2006 Apr;52(4):330-2. Epub 2006 Mar 9.Click here to read Links Lyme disease associated with Alzheimer's disease. Meer-Scherrer L, Chang Loa C, Adelson ME, Mordechai E, Lobrinus JA, Fallon BA, Tilton RC.
Laurence Meer-Scherrer, 37 Flammat, Aumatt, Switzerland.
This case report discusses a patient with co-occurring neuroborreliosis and Alzheimer's disease (AD). Although no claim is made for causality nor is there objective evidence that spirochetes are involved in AD, co-infection may exacerbate the symptoms of either neuroborreliosis or AD. Much is to be learned about the role of spirochetes in degenerative central nervous system disease.
PMID: 16528463 [PubMed - indexed for MEDLINE]
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Post by Niels on Jul 26, 2007 23:04:29 GMT -5
1: Br J Cancer. 2006 Mar 27;94(6):879-83.Click here to read Links Mycosis fungoides: is it a Borrelia burgdorferi-associated disease? Tothova SM, Bonin S, Trevisan G, Stanta G.
ICGEB - International Centre for Genetic Engineering and Biotechnology, 99 Padriciano, Trieste 34012, Italy.
Mycosis fungoides (MF) is the most frequently found cutaneous T-cell lymphoma with an unknown aetiology. Several aetiopathogenetic mechanisms have been postulated, including persistent viral or bacterial infections. We looked for evidence of Borrelia burgdorferi (Bb), the aetiologic agent of Lyme disease (LD), in a case study of MF patients from Northeastern Italy, an area with endemic LD. Polymerase chain reaction for the flagellin gene of Bb was used to study formalin-fixed paraffin-embedded lesional skin biopsies from 83 patients with MF and 83 sex- and age-matched healthy controls with homolocalised cutaneous nevi. Borrelia burgdorferi-specific sequence was detected in 15 out of 83 skin samples of patients with MF (18.1%), but in none out of 83 matched healthy controls (P<0.0001). The Bb positivity rates detected in this study support a possible role for Bb in the aetiopathogenesis of MF in a population endemic for LD.
PMID: 16495924 [PubMed - indexed for MEDLINE]
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Post by Niels on Jul 26, 2007 23:04:54 GMT -5
1: Am J Surg Pathol. 2000 Sep;24(9):1279-85.Click here to read Links Primary cutaneous B-cell lymphoma and Borrelia burgdorferi infection in patients from the Highlands of Scotland. Goodlad JR, Davidson MM, Hollowood K, Ling C, MacKenzie C, Christie I, Batstone PJ, Ho-Yen DO.
Department of Pathology, Raigmore Hospital, Inverness, Scotland, UK. John.Goodlad@raigmore.scot.nhs.uk
Although a link between primary cutaneous B-cell lymphoma (PCBCL) and Borrelia burgdorferi infection has long been suspected, previous studies have not demonstrated a significant association. The authors looked for evidence of B. burgdorferi in 20 cases of PCBCL from the Scottish Highlands, an area with endemic Lyme disease, and compared their findings with those in 40 control patients (20 undergoing wide reexcision at sites of malignant melanoma and 20 biopsies of inflammatory dermatoses). All studies were performed on formalin-fixed, paraffin-embedded tissues. The cases of PCBCL were classified according to criteria described by the European Organization for Research and Treatment of Cancer Cutaneous Lymphoma Project Group using a combination of morphology, immunohistochemistry, and seminested polymerase chain reaction (PCR) for immunoglobulin heavy chain gene rearrangement. A nested PCR was performed on deoxyribonucleic acid (DNA) extracts from the lymphoma and control cases using primers to a unique conserved region of the B. burgdorferi flagellin gene. B. burgdorferi-specific DNA was detected in seven of 20 lymphoma cases (five of 12 marginal zone lymphomas, one of five primary cutaneous follicle center cell lymphomas, one of three diffuse, large B-cell lymphomas of the leg) and in one melanoma reexcision patient of 40 control subjects. The relationship between B. burgdorferi and PCBCL was significant when compared with the control groups separately (p <0.05) or in combination (p <0.01). These results provide strong evidence to support the concept of B. burgdorferi-driven lymphomagenesis in the skin.
PMID: 10976703 [PubMed - indexed for MEDLINE]
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Post by Niels on Jul 26, 2007 23:05:19 GMT -5
1: Mol Pathol. 2002 Dec;55(6):374-8.Click here to read Click here to read Links Morphoea and Borrelia burgdorferi: results from the Scottish Highlands in the context of the world literature. Goodlad JR, Davidson MM, Gordon P, Billington R, Ho-Yen DO.
Department of Pathology, Highland Acute Hospitals NHS Trust, Raigmore Hospital, Inverness IV2 3UJ, UK. John.Goodlad@raigmore.scot.nhs.uk
AIMS: Previous studies investigating the link between infection with Borrelia burgdorferi and morphoea have produced conflicting results. Often, these studies have been undertaken in patients from different regions or countries, and using methods of varying sensitivity for detecting Borrelia burgdorferi infection. This study aimed to establish whether a relation could be demonstrated in the Highlands of Scotland, an area with endemic Lyme disease, with the use of a sensitive method for detecting the organism. METHODS: The study was performed on biopsies of lesional skin taken from 16 patients from the Highlands of Scotland with typical clinical features of morphoea. After histological confirmation of the diagnosis, a nested polymerase chain reaction (PCR) using primers to a unique conserved region of the Borrelia burgdorferi flagellin gene was performed on DNA extracts from each biopsy. A literature search was also performed for comparable studies. RESULTS: None of the 16 patients had documented clinical evidence of previous infection with B burgdorferi. DNA was successfully extracted from 14 of the 16 cases but all of these were negative using PCR for B burgdorferi specific DNA, despite successful amplification of appropriate positive controls in every test. The results were compared with those of other documented studies. CONCLUSIONS: Examination of the literature suggests that there is a strong geographical relation between B burgdorferi and morphoea. These results, in which no such association was found, indicate that morphoea may not be associated with the subspecies of B burgdorferi found in the Highlands of Scotland.
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Post by Niels on Jul 26, 2007 23:06:17 GMT -5
1: Histopathology. 2000 Dec;37(6):501-8.Click here to read Links
Comment in: Histopathology. 2001 Jan;38(1):73-7.
Borrelia burgdorferi-associated cutaneous marginal zone lymphoma: a clinicopathological study of two cases illustrating the temporal progression of B. burgdorferi-associated B-cell proliferation in the skin. Goodlad JR, Davidson MM, Hollowood K, Batstone P, Ho-Yen DO.
Department of Pathology, Raigmore Hospital, Inverness, UK. John.Goodlad@raigmore.scot.nhs.uk
AIMS: A relationship between Borrelia burgdorferi and primary cutaneous B-cell lymphoma (PCBCL) has recently been confirmed following demonstration of the organism in lesional skin of patients with PCBCL. We report herein two cases of B. burgdorferi-associated PCBCL which strengthen this association by demonstrating the organism in cutaneous B-cell infiltrates present at sites in which PCBCL subsequently developed. METHODS AND RESULTS: All studies were performed on formalin-fixed paraffin-embedded tissues. These were examined by routine light microscopy and immunohistochemically by a standard streptavidin-biotin-complex technique. Genotypic studies were also undertaken using semi-nested polymerase chain reaction (PCR) for immunoglobulin heavy chain gene rearrangement, and nested PCR for B. burgdorferi flagellin gene. Both patients presented with erythematous skin lesions, biopsy of which showed dense perivascular infiltrates comprising small T-lymphocytes and collections of B-blasts. Primary cutaneous marginal zone lymphoma (MZL) developed subsequently in both cases at the same site. PCR for B. burgdorferi flagellin gene was positive in the perivascular lymphocytic infiltrates and the succeeding lymphomas in both patients. CONCLUSIONS: These results show that, at least in some instances, PCBCL arises from chronically stimulated lymphoid tissue acquired in the skin in response to B. burgdorferi infection. This may have significant therapeutic implications and warrant further studies on the extent of this association.
PMID: 11122431 [PubMed - indexed for MEDLINE]
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Post by Niels on Jul 26, 2007 23:06:45 GMT -5
1: Int J Dermatol. 2000 Apr;39(4):278-83.Click here to read Links Evidence for Borrelia burgdorferi in morphea and lichen sclerosus. Ozkan S, Atabey N, Fetil E, Erkizan V, Günes AT.
Departments of Dermatology and Medical Biology, Faculty of Medicine, University of Dokuz Eylül, Izmir, Turkey.
BACKGROUND: Borrelia burgdorferi (Bb) infection has been implicated in the development of morphea and lichen sclerosus; however, conflicting results have been reported with different investigational methods from different regions. We looked for evidence of Bb in patients with morphea and lichen sclerosus by polymerase chain reaction (PCR) analysis of of skin biopsy samples. METHODS: Formalin-fixed, paraffin-embedded skin biopsy samples from 10 patients with morphea and 12 patients with lichen sclerosus were investigated by PCR analysis for the presence of Bb. RESULTS: The presence of Bb DNA was demonstrated in three of 10 patients with morphea and six of 12 patients with lichen sclerosus by nested PCR. CONCLUSIONS: The data obtained in this study suggest that Bb may play a role in the etiopathogenesis of both morphea and lichen sclerosus at least in the western parts of Turkey.
PMID: 10809977 [PubMed - indexed for MEDLINE]
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Post by Niels on Jul 26, 2007 23:16:54 GMT -5
1: Med Mal Infect. 2007 Mar 26; [Epub ahead of print]Click here to read Links [Dermatological aspects of Lyme borreliosis.] [Article in French]
Lipsker D.
Faculté de médecine et clinique dermatologique, université Louis-Pasteur, 1, place de l'Hôpital, 67091 Strasbourg cedex, France; GEBLY (Groupe d'étude de la borréliose de Lyme), Strasbourg, France.
Lyme borreliosis is a tick-borne zoonosis due to bacterial infection by Borrelia (B.) burgdorferi sensu lato The disease presents differently in Europe or North America and may be called European borreliosis when acquired in Europe. Lyme borreliosis evolves in 3 stages. The main manifestations include cutaneous, neurological, and joint involvement. Erythema migrans (EM) is the most specific and most frequent finding in patients with Lyme borreliosis. It is the hallmark of early-localized borreliosis. EM is a slowly expanding red macula that occurs in about 60-80% of patients contracting Lyme borreliosis. Central clearing of the red patch can occur. It appears at the site of the tick bite, 7 to 20 days after the bite. Borrelial lymphocytoma (BL) occur rarely in patients with the early-disseminated stage of the disease. BL is a red or brown nodule or plaque located on the nipple, the earlobe, the scrotum, or the face. It should not be confused with cutaneous B-cell lymphoma. Acrodermatitis chronica atrophicans (ACA) is the cutaneous manifestation of late borreliosis. It starts as a violaceous patch, usually located on the extensor surface of a limb. Periarticular nodules and cords can also be present. Without treatment, it will evolve over weeks or months to the typical atrophic stage with extensive dermo-epidermal atrophy and visibility of superficial veins. Only these 3 manifestations are clearly related to an infection with B. burgdorferi. The relationship between infection with B. burgdorferi and other dermatoses, especially morphea, lichen sclerosus, and interstitial granulomatous dermatitis is still debated.
PMID: 17391884 [PubMed - as supplied by publisher]
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Post by Niels on Aug 9, 2007 1:43:25 GMT -5
Uhoh!!! The badbioweapons-boys of lyme are pressuring Ct. Attorney General Blumenthal... wow, the names here read like a who's-who from the lymeholes of the web... Durland Fish, Gary Wormser... gee.. what's with the funky names anyways... the names alone sound SLIMY and PUTRID to begin with, and their actions appear to be the same. Expect similar strongarming from the bioweapons boys if someone from the CDC or Kaiser accidentally links Morgs to Lyme, Chlamydia Pneumonia, or Mycoplasma Incognita Fermentans/Penetrans (aks Gulf War Syndrome). That would be just simply too smoking gun... besides, if anybody ever DNA analyzed OUR strain of Lyme... we could probably find out some REALLY INTERESTING STUFF... like which lab's genetics experiments it evolved from... nope... best pretend it isn't there and prevent people from looking and treat the patients as crazy or malingerers or addicts. It worked for Gulf War Syndrome so why not continue the "success story"... ld-50.blogspot.com/2007/03/lyme-disease-experts-butt-out.html
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Post by Niels on Aug 9, 2007 1:51:27 GMT -5
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Post by Niels on Aug 9, 2007 2:36:29 GMT -5
Gee, I wonder if that unknown new to north america in 2001 relapsing-fever spirochete Dr. Fish talks about is called "morgellons"... anybody hear any more of this "new spirochete" Or maybe that "new spirochete" to North America is this? www.cdc.gov/mmwr/preview/mmwrhtml/00001736.htmor this? findarticles.com/p/articles/mi_qn4196/is_20030602/ai_n10871773All's I know is that with all these spirochete-caused lyme-like diseases coming out in different places around the country, howcome the doctors are defining and testing for Lyme in such a narrow fashion that many patients that could be treated for "Lyme" through antibiotics are being denied that treatment because Lyme-testing doesn't seem to be very good at detecting the actual tick-borne spirochetes that are infecting people. Given all the doubt, howcome doctors and insurance are quick to deny lyme based on test results that appear to be coming out negative for other kinds of ticks and non-east coast US variants of borrelia.
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Post by Niels on Aug 10, 2007 15:34:57 GMT -5
I've found very little information on Fish's "unknown spirochete" coinfection found in ticks. Given that people around 2001 were calling this an "important discovery" it is odd that so little information has been gathered in the last seven years. What's more concerning is that the same people who were once mentioning this "unknown spirochete" as being a potential explanation of why some people suffer from chronic lyme whereas others are "cured" by mainstream medicine's lie that "one month of antibiotics cures lyme." In this article, and also in the previous Steere article I posted, there's significant contradiction between the research statements they make, versus the medical guidelines they've authored which paint a much simpler clinical, diagnostic and treatment picture for Lyme. www.astralgia.com/magazine/menagerie.htmAll I know is there's a whole lot of unexplained "unknowns" in the research literature, and they've been completely ignored and glossed over in making the oversimplified recommendations on Lyme treatment from IDSA (see page 1 of this topic) -- these same recommendations will ensure that Morgellons patients lyme status will be clouded by bad assumptions in testing and diagnostics, that HMO's will continue to leave infected patients undiagnosed and untreated, that Kaiser will use those recommendations to whitewash theLyme status of all the morgellons sufferers it tests... I can't understand why people can't see the importance of this. It is 100% CENTRAL TO MORGELLONS BEING DIAGNOSED AND TREATED CORRECTLY.
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Post by Niels on Aug 10, 2007 16:16:18 GMT -5
Lyme Disease and Cognitive Impairments
by Robert Bransfield, M.D.
Introduction:
The patient is a college graduate with Lyme encephalopathy (LE). While stopped at a traffic light, she described her thought processes as having a "fog-like" sluggishness. When the light changes, she knows the change from red to green has significance, but at that moment cannot recall that green means go and red means stop. This is one of many examples of cognitive impairments associated with Lyme disease. Although some cognitive symptoms are indirectly a result of other neurological or emotional impairments, others are a direct result of dysfunction of the cerebral cortex where cognitive processing occurs. Laboratory tests such as SPECT scans, MRI's, PET scans, and psychological testing have demonstrated physiological and anatomical findings associated with dysfunction of the cerebral cortex in patients with Lyme and tick-borne diseases. The examination of human and animal brains have further supported these findings. The cognitive impairments from Lyme disease are very different than we see in Alzheimer's disease. Lyme disease is predominately a disease of the white matter, while Alzheimer's is predominately a disease of the gray matter. Memory association occurs in the white matter, while memory is stored in the gray matter. White matter dysfunction is a difficulty with slowness of recall, and incorrect associations. In contrast, gray matter dysfunction is a loss of the information which has previously been stored. For example, and Alzheimer's patient may not recall the word "pen", while an LE patient may have a slowness of recall or retrieval of a closely related word. Some of the symptoms I will describe are also found in encephalopathies associated with other illnesses, such as chronic fatigue syndrome, lupus stroke, AIDS, or other diseases which affect the brain. Although no single sign or symptom may be diagnostic of Lyme disease in a mental status exam, we instead look for a cluster and a pattern of signs and symptoms that are commonly associated with Lyme disease. Everyone with LE has their own unique profile of symptoms. The assessment of these signs and symptoms is one facet of the total clinical assessment of Lyme disease. There are many ways of categorizing cognitive functioning. Let's begin with a simple model of perception, encoding these perceptions into memory, processing what we perceive, imagery, and finally organizing and planning a response. Simple mental functions such as flexing the index finger of the right hand, correlates with a relatively simple brain circuitry.. More complex functions such as flying an airplane requires the action of a more integrated neural circuitry. The difference between these two actions is like the difference between playing middle C on a piano vs. a symphony playing an entire concert.
Attention Span:
Many Lyme disease patients have acquired attention impairments which were not present before the onset of the disease. There may be difficulty sustaining attention, increased distractibility when frustrated, and a greater difficulty prioritizing which perceptions are deserving of a higher allocation of attention. If we compare attention span to the lens of a camera, we need the flexibility to constantly shift the allocation of attention dependency upon the current life situation. For example, we shift back and forth between a wide angle and a zoom lens focus to increase or decrease acuity of attention depending on the needs of the current situation. A loss of this flexibility results in some combination of a loss of acuity (hypoacusis), and/or excessive acuity to the wrong environmental perceptions (hyperacusis). Hyperacuity can be auditory (hearing), visual, tactile (touch), and olfactory (smell). Auditory hyperacusis is the most common. Sounds seem louder and more annoying. Sometimes there is selective auditory hyperacusis to specific types of sounds. Visual hyperacusis may be in response to bright lights or certain types of artificial lighting. Tactile hyperacusis may be in response to tight fitting or scratchy clothing, vibrations, temperature and merely being touched may be painful. Some patients prefer to wear loose fitting sweat suits and are frustrated that being touched can be painful. Olfactory hyperacusis may result in an excessive reactivity to certain smells, such as perfumes, soaps, petroleum products, etc.
Memory
Memory is the storage and retrieval of information for later use. There are several different memory deficits associated with LE. Memory is broken down into several functions - working memory, memory encoding, memory storage and memory retrieval. Working memory is a component of executive functioning. An example of working memory is the ability to spell the word "world" backwards. Sometimes there are impairments of working memory as it pertains to a working spatial memory, i.e. forgetting where doors are located or where a car is parked. Encoding is the placement of a memory into storage. We cannot retrieve a memory that was not encoded correctly into memory in the first place. One patient described being upset that someone had eaten yogurt in her kitchen during the night. Her activity during the night was not encoded into memory. Short term (recent) memory is the ability to remember information for relatively brief periods of time. In contrast, long term memory is information from years in the past (or remote). In LE, there is first a loss of short term memory followed by a loss of long term memory very late in the illness. Patients may have slowness of recall with different types of explicit (or factual) information, such as words, numbers, names, faces or geographical/spatial cues. Not as common, there may also be slowness of recall if implicit information, such as tying shoes, or doing other procedural memory tasks. Errors in memory retrieval include errors with letter and/or number sequences. This can include letter reversals, reversing the sequence of letters in words, spelling errors, number reversals, or word substitution errors (inserting the opposite, closely related or wrong words in a sentence.
Processing
Processing is the creation of associations which allow us to interpret complex information and to respond in an adaptive manner. Some LE patients say they feel like they acquired dyslexia or other learning disabilities, which were not present previously. Examples of processing functions that may be impaired in the presence of LE include the following: Reading comprehension: The ability to understand what is being read. * Auditory comprehension: The ability to understand spoken language. * Sound localization: The ability to localize the source of a sound. * Visual spatial perception: Impairments result in spatial perceptual distortions. One example is microscopia, in which things seem smaller than they really are. One patient lost depth perception, and had several accidents when the car in front of her stopped. A problem associated with visual spatial processing is optic ataxia, in which there is difficulty targeting movements through space. For example, there may be a tendency to bump into doorways, difficulty driving and parking a car in tight spaces, and targeting errors when placing and reaching for objects.
One patient with optic ataxia, was stopped by a policeman while driving two miles to my office because he kept swerving across the center line. Before Lyme disease he could consistently shoot 13 to 14 out of 15 free throws from the basketball foul line. Now he averages 3 of 15, and misses some shots be several feet.
* Transposition of latrerality: The ability to rotate something 180 degrees in your mind. For example, the ability to copy, rather than mirror, the movements of an aerobics instructor facing you. * Left-right orientation: The ability to immediately perceive the difference between left and right. Although this is a part of congenital Gertsmann's syndrome or angular gyrus syndrome, acquired left-right confusion is the result of an encephalopathic process. * Calculation ability: The ability to perform mathematical calculations without using fingers or calculators. Many LE patients describe an increased error rate with their checkbook. * Fluency of speech: The ability of speech to flow smoothly. This function is dependent upon adequate speed of word retrieval. * Stuttering: The tendency to stutter when speech is begun with certain sounds. * Slurred speech: A slurring of words, which can give the appearance of intoxication. * Fluency of written language: The ability to express thoughts into writing. * Handwriting: The ability to write words and sentences clearly.
Imagery
Imagery is a uniquely human trait. It is the ability to create what never was within our minds. When functioning properly, it is a component of human creativity, but when impaired, it can result in psychosis. Imagery functions that can be affected by LE include: * Capacity for visual imagery: The ability to picture something, such as a map, in our head. * Intrusive images: Images that suddenly appear which may be aggressive, horrific, sexual or otherwise. * Hypnagogic hallucinations: The continuation of a dream, even after being fully awake. * Vivid nightmares: A tendency towards nightmares of a vivid Technicolor nature. * Illusions: Auditory, visual, tactile and/or olfactory perceptions which are distorted or misperceived. * Hallucinations: Hearing, seeing, feeling and/or smelling something that is not present. In LE, sometimes this takes the form of hearing music or a radio station in the background. Unlike schizophrenic hallucinations, these are accompanied by a clear sensorium, and the patient is aware hallucinations are present. * Depersonalization: A loss of a sense of physical existence. * Derealization: A loss of a sense that the environment is real.
Organizing and Planning
Organizing and planning a response is the most complex mental function, and is dependent upon all the functions already described. These functions, along with attention span and working memory, are referred to as executive functioning. Organizing and planning functions that can be affected by LE include:
* Concentration: The ability to focus thought and maintain mental tracking while performing problem solving tasks. * "Brain fog": Described by many LE patients. Although difficult to describe in objective, scientific terms: it is best described as a slowness, weakness, and inaccuracy of thought processes. Prioritizing, organizing, and implementing multiple tasks with effective time management. * Simultasking: The ability to concentrate and be effective while performing multiple simultaneous tasks. * Initiative: The ability to initiate spontaneous thoughts, ideas and actions rather than being apathetic or merely responding to environmental cues. * Abstract reasoning: The capacity for complex problem solving. * Obsessive thoughts: May interfere with productive thought. * Racing thoughts: May interfere with productive thought.
An assessment of each of these areas of functioning is a critical component in the clinical assessment of LE. The cognitive assessment is only a part of the assessment of LE. Other components include the psychiatric assessment, the neurological assessment, a review of somatic symptoms, epidemiological considerations and laboratory testing when indicated. I have gradually developed a structured cognitive assessment which focuses upon the areas mentioned after examining many patients with late stage neuropsychiatric Lyme disease. I have also incorporated concepts from others that have made major contributions in this area, such as Drs. Rissenberg, Nields, Fallon, Freundlich and Bleiwiss. It is difficult to explain exactly how Lyme disease causes cognitive impairments. The variability of these symptoms suggests an episodic release of a endotoxin or cytokine which may contribute to the cognitive dysfunction. This is an area where considerable research is needed, and is beyond the scope of this article. The symptoms described are often very difficult for patients to describe, and are difficult for many physicians to understand. As a result, patients with these impairments are sometimes erroneously viewed as being hypochondriachal, psychosomatic, depression, or malingering. These symptoms are real and must be explained: that cannot be discounted as being imaginary. There are many treatment strategies. Antibiotics and a number of different psychotropics are helpful to many. I have found Aricept to be helpful in the treatment of "brain fog" and problems with slowness of retrieval. To those of you who have LE, be realistic about your limitations and the validity of these limitations. Use strong areas to compensate for areas of weakness. Avoid excessive stress which compounds the problem. Be aware that certain tasks challenge many higher level attributes. Maintain hope and retain an effective working relationship with your family, support system and treatment team.
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Post by Niels on Aug 10, 2007 16:32:44 GMT -5
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