Lyme Disease Information — President Bush
Bush's Doctors Kept Lyme Disease Secret for a Year
Is the Condition Why His Mind is Degenerating?
Trish Ponder | Aug. 8, 2007
We've all seen the video, and if not, you really can't watch it enough: George Bush when he was governor of Texas, using big words and whole sentences, making sense and not embarrassing anyone. It's a marvel!
"Brain fog" involves episodes of cognitive dysfunction or confused thinking and is associated with forgetfulness, losing one's train of thought, depersonalization, and the inability to remember the correct words when speaking or writing But Bush now is a whole different animal, leading many to wonder if it's Alzheimer's, if he's back on the sauce, or if Dick Cheney is slipping something into his fried quail.
An even better explanation is Lyme disease. Although doctors one year ago treated him for what they now claim was early stage Lyme disease, who knows when he got it? And dementia is one of the main manifestations of undiagnosed Lyme disease.
Bush was treated for what his doctors described as "early, localized Lyme disease" last August after developing the characteristic bulls eye rash. The doctors said he has had no recurrence.
White House spokesman Scott Stanzel said the disease was not disclosed earlier because it happened after he had his last physical, on Aug. 1, 2006.
Right. So why bring it up until now? After all, it's not like we ever hear about any of the other Bush health problems, like hangovers "whoops, I mean stomach flu" at global summits.
The president's main form of exercise and recreational activity is biking. His doctors advised him to wear long pants and long-sleeved shirts and use bug spray when in risk-prone areas, such as Maine, where the president is spending a long weekend starting Thursday at his parents' summer home on the coast.
Bush has had a lifetime of opportunities to contract Lyme disease, if you can get it from mountain biking in Maine. But the curious circumstances of his recent annual exam have really got me wondering what gives.
Last year's presidential physical was conducted as usual on a visit to the National Naval Medical Center in suburban Maryland. This year's took place in a series of exams at the White House starting July 17 and ending Tuesday night. The exams were not revealed until Wednesday...
A total of 11 doctors were involved in the exams, overseen by White House physician Richard Tubb and Dr. Kenneth Cooper, the president of The Cooper Aerobics Center in Dallas. The group included skin, hearing, heart, eye, neurological and sports medicine specialists.
Each signed a statement saying that "within the scope of my specialty" he found Bush "fit for duty" with the expectation that he will remain so for the duration of his presidency.
It's all kind of odd, don't you think? It seems like presidents always have their exams at Bethesda. I wasn't aware the White House kept the equipment on hand that you'd need for 11 different specialists to perform tests.
But listen to what happens when, instead of the early stage Lyme disease the White House claims Bush had, you don't know you have it and it goes untreated too long. Symptom types include:
Neurological (can effect central or peripheral components):
And what, you might ask, is "brain fog?" It looks exactly like Bush "now" on the video.
It involves episodes of cognitive dysfunction or confused thinking. Brain fog is associated with forgetfulness, losing one's train of thought, depersonalization, the inability to remember the correct words when speaking or writing (aphasia).
Brain fog is so named because the sufferer can feel like a cloud literally surrounds him or her that reduces the speed at which things can be recognized or clearly seen. Brain fog causes forgetfulness, and promotes feelings of detachment (depersonalization), discouragement and depression.
I'm glad Bush was treated for his secret episode of Lyme disease last year. But I suspect it was too late to save him from earlier exposures.
Niels August 10, 2007 @ 3:18 pm
Journal of Alzheimer's Disease Vol 6 No. 6 Pages 639-649 Dec. 2004
Judith Miklossy, Kamel Khalili, Lise Gern, Rebecca L. Ericson, Pushpa Darekar, Lorie Bolle, Jean Hurlimann, Bruce J. Paster
Borrelia burgdorferi persists in the brain in chronic Lyme neuroborreliosis and may be associated with Alzheimer's disease
Abstract: The cause, or causes, of the vast majority of Alzheimer's disease cases are unknown. A number of contributing factors have been postulated, including infection. It has long been known that the spirochete Treponema pallidum, which is the infective agent for syphilis, can in its late stages cause dementia, chronic inflammation, cortical atrophy and amyloid deposition. Spirochetes of unidentified types and strains have previously been observed in the blood, CSF and brain of 14 AD patients tested and absent in 13 controls. In three of these AD cases spirochetes were grown in a medium selective for Borrelia burgdorferi. In the present study, the phylogenetic analysis of these spirochetes was made. Positive identification of the agent as Borrelia burgdorferi sensu stricto was based on genetic and molecular analyses. Borrelia antigens and genes were co-localized with beta-amyloid deposits in these AD cases.
The data indicate that Borrelia burgdorferi may persist in the brain and be associated with amyloid plaques in AD. They suggest that these spirochetes, perhaps in an analogous fashion to Treponema pallidum, may contribute to dementia, cortical atrophy and amyloid deposition. Further in vitro and in vivo studies may bring more insight into the potential role of spirochetes in AD.
Curr Microbiol. 2006 Apr;52(4):330-2. Epub 2006 Mar 9.
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]
Lyme Disease and Cognitive Impairments
by Robert Bransfield, M.D.
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.
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 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 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.
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:
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:
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.
Niels August 10, 2007 @ 3:45 pm