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Sunday 27 January 2013

Managing Cognitive Problems






Hello all,

Having suffered from Lyme/spirochete infection which was diagnosed as Multiple Sclerosis at first, for a number of years, I have had to adapt my lifestyle to cope with a brain that behaved as though I had a brain injury.

I did not have a brain injury just cognitive dysfunction.

I wanted to know more about how does one cope with a cognitive dysfunction it's well and good knowing and reading about it but how does one cope?

I needed to know so I could help my children as well as my brother.

There is this  one particular article for exactly this problem and this article may be written for CFS/F.M. I feel it can be applied to any autoimmune disease or Lyme/spirochete Infection.

Up until the 1980s, most physicians believed that cognitive dysfunction rarely occurred in people with MS. But since that time, studies have shown that between 55-65 percent of people with MS have some level of difficulty in this area. The best way of managing cognitive problems is to first understand the problems then practise strategies to overcome or compensate for the inconvenience they cause.
Cognitive process involves attention, memory, learning, organising, comprehending, thinking, and judgement. In MS, cognitive problems result from demyelination or plaques in the cerebral tract of the brain. Not everybody will experience cognitive problems, and those who do will usually have quite mild symptoms. Also, the symptoms may vary from person to person. "Only about 10 to 20 percent of individuals develop symptoms severe enough to limit daily functioning," says Dr. Jill Fischer in her article, "Cognitive Impairment in MS: The Forgotten Problem."
Sometimes recognising cognitive impairment is the hardest first step. Family members may be the first to notice some of the following difficulties:
  • Impaired attention, perception and/or memory
  • Disorganised thinking or acting
  • Inefficient processing of information
  • Difficulty processing new information, rules and procedures
  • Unable to remember old or stored information
  • Ineffective problem solving and judgement
  • Inappropriate social behaviour
  • Impaired goal setting, planning or awareness of strengths and weaknesses
The most common cognitive problems associated with MS are short-term memory loss, word-finding (selecting the right word to express a thought), and attention. 

The following strategies can help you compensate if you have problems in these areas.

Memory
 

Remembering things that happened years ago is often easier than remembering something that just happened. To avoid the frustration of short-term memory loss, try some or all of the following:
  • Keep a calendar.
  • Clocks and watches with beepers or alarms can remind you to do something.
  • Use a tape recorder.
  • Keep lists (shopping lists, questions to ask physician, etc.).
  • Hang post-it stickers on the refrigerator door.
  • Writing things down may facilitate memory.
  • Arrange your environment: for example, combine clothing according to outfits, or keep frequently used kitchen things in a certain place.
Word-finding
Remember that communication is the key. The main goal is to convey the idea, even if the exact words are not used. Ask family and friends to give you adequate time to express yourself. When you can't find a word, try some of the following strategies:

Description:
describe the word or idea you can't get out.
Distraction:
think about something else - the word you want might come to you.
Visual Imagery:
painting a picture in your mind helps elicit words.

Non-verbal:
gesturing and drawing can help communicate your idea.
Categorisation and function:
describe what group or function your word or idea belongs to.

Clarification:
clarify your ideas with your listener, repeat back.
Don't let someone leave with the wrong message.

Association:
connect people's names with other people or ideas.


Attention
Attention is the ability to focus on something over time and retain the information for immediate or later use. To improve attention:

  • Reduce background noise and distractions.
  • Maintain eye contact with conversing with others.
  • Rephrase what someone has said.
  • Ask other people to speak more slowly.

Above all else, keep the following in mind:
Poor memory is often the result of poor concentration or trying to do too many things.
Stress, anxiety, and fatigue affect memory.
No body's mind is perfect. We all forget things.
Encouragement, patience and support from family and friends is crucial.

Melissa Kaplan notes...
Many of the techniques for remembering to do things, learning, dealing with attention deficit problems that are taught to post-traumatic brain injury survivors are also very useful when you have the neurocognitive impairment common in CFS, FM, and Lyme. Contact your local brain injury rehab centres to see if they offer any programs that you can participate in. Many insurance companies (and Medicare and Medicaid) will cover structured programs. 

Source :
©1995 Mary K. Rohrer Durham RN BSN, National CFS and FM Association
http://www.anapsid.org/cnd/coping/managecognitive.html 

Lyme Girl x

 **Always consult a LLMD (Lyme Literate Doctor) or your own health care professional.**

Copyright 2012-2013  LymeGirl all rights reserved.

Nightmares & Lyme

"Nightmares can be confusing"

Hello all,

Nightmares are one of the worst symptoms of Lyme/Spirochete infection.
I say one of the worst because all the symptoms are quite bad as it is.

Not only can one suffer from Insomnia and when one finally does get to sleep the sleep disturbance can start from waking up or night terrors or nightmares.

I would suffer from nightmares that could be quite gory, also nightmares of being chased and attacked, nightmares of awful monsters and demons, how can a child explain that?

As I got older my brain was able to cope better but not much real scary stuff to say the least.


Sleeping Pills



After the horse fly bite age 9 my sleep pattern was so bad the doctor prescribed me sleeping tablets,
yes at the age of 10!

Sleeping tablets and Lyme do not mix, well they didn't for me anyway.

All they did was make me hallucinate during the day my nightmares just got more vivid and even more scary than before.

I was taken off them at age 12 at least somebody used their sense, I was sent to a psychologist as it was thought, my disturbed sleep was a  psychological problem.

As I have already mentioned on this page : http://diaryoflymegirl.blogspot.co.uk/2012/07/insomniasleep-disturbance-lyme.html

Treatment and Nightmares


I have found that when I first started taking MMS before bed,
the sleep disturbance , sleep talking, walking and nightmares did carry on for about 6 months.
Now I have found my sleeping pattern has vastly improved,  I do get a restful sleep.
I do not suffer from insomnia, except when I did contract Norovirus, then the insomnia did come back, while I struggled with that and the flu I had afterwards.
Refer to this page :http://diaryoflymegirl.blogspot.co.uk/2013/01/norovirus-lyme.html

and this page:http://diaryoflymegirl.blogspot.co.uk/2013/01/flu-lyme.html

Maybe the insomnia came back because well both illness's are quite a challenge, when one is trying to cope with treating an illness like Lyme/spirochete infection or even the fragments that have been left behind, it really is not surprising something has to give.

I am still recovering from the affects of the flu and slowly but surely am getting better, thank goodness the insomnia is gone.

Since treating the Lyme/spirochete infection the vivid nightmares have ceased.

I am not going to say yet, once and for all  as I am not 100% sure all the spirochetes are gone yet.
Still  the fragments are there which in themselves can be disabling, painful and the swelling comes and goes and yes I will say my condition does fluctuate but treating is oh so worth all of that.

After talking to those who are on antibiotics for their Lyme, they also suffer from nightmares,  most have been on antibiotics for a year or more.

So it seems no matter how one chooses to treat the spirochete infection, one can still suffer from the nightmares, night terrors, sleep walking/talking, insomnia and any sleep disturbance but this will pass eventually.


Don't give up


I feel the most important issue is treating theLyme/spirochete infection, whether one has been diagnosed with any autoimmune disease, which as Dr Lida Mattman said :
" The root cause of any autoimmune disease  is a bacterial infection"

Even if one has been diagnosed with M.S and as I have Quoted Dr Lida Mattman :
 " M.S should be renamed Multiple Spirochetes"
the main issue is treatment whether it be MMS or antibiotics, just be rest assured one day ones body will be rid of the infection for good,  the nightmares will go.

Just do not give up treating yourself.

Treating Lyme/spirochete infection is not a sprint it's a marathon.

I know how hard it can be and yes even when one is feeling better keep on with the treatment cos those spirochetes are crafty little devils.

There is many a time my children and I have given up hope or got fed up with taking MMS day and night but we gently motivate each other to persevere.



Lyme Girl x

**Always consult a LLMD (Lyme Literate Doctor) or your own health care professional.**

Copyright 2012-2013  LymeGirl all rights reserved.



Lyme & Cognitive Impairment


Hello all,

This is again a very intresting article about cognitive impairment and Lyme.

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.


Lyme Girl x


**Always consult a LLMD (Lyme Literate Doctor) or your own health care professional.**

Copyright 2012-2013  LymeGirl all rights reserved.




Saturday 26 January 2013

Lupus & Lyme


Hello all,

The many who lived in the same vicinity and attended the local school developed autoimmune diseases and cancers and various other ailments which can be put down to Lyme.
My best friend who attended the same Primary school as myself and whom lived right across the road, developed Lupus, when she was 18 years old she also  lived right next door to the  puppy which was brought to the village from the place I was  bitten by the horse fly and infected with the spirochete/s infection.
I saw how my friend suffered with Lupus but at the time no one could tell her what was wrong and the medical profession basically wrote her off or told her it was all in her head.
She and I were both going through the same problems with our Doctors only her symptoms were presenting themselves differently to mine I was seen as "lazy" or "a fantasist" or "hypochondriac.
She was just seen as plain old "strange".
I was diagnosed with Multiple Sclerosis first and she was diagnosed with Lupus about a year after me, but her symptoms started well before that of course just like mine.
At the time it was starting to become the norm hearing about former classmates being struck down with debilitating illness's and becoming all too frequent something was just not right.

It may of taken me a good few years to be able to piece the  jigsaw puzzle together but at least I have managed to get there now and have been able to have the right treatment, all too many still to this day do not know about Lyme or some disbelieve Lyme is the actual cause because the medical profession are also still blind to the truth or rather their ego's get in the way.


What is Lupus?



Lupus is yet another autoimmune disease that has no known cause and no known cure.
Apparently the body's immune system becomes hyperactive and attacks normal healthy tissue.
Lupus makes the immune system unable to differentiate between antigens and healthy tissue.

The immune system then directs antibodies against the healthy tissue not just antigens.
This causes swelling,pain and tissue damage.

Symptoms


Lupus symptoms are wide and varied.
Lupus may strike aggressively as an acute severe illness,or grumble and be undiagnosed for years.

The symptoms of Lupus are :
  • Inflammation
  • Swelling
  • Damage to:
  • Joints
  • Skin
  • Kidneys
  • Heart
  • Blood
  • Lungs

 

Symptoms of the skin:



Almost any type of skin rash may occur. "Allergies" are common and indeed the lupus patient may give a history of allergies to drugs such as penicillin long before lupus has been diagnosed.

A pinkish rash on the cheeks is present in approximately one half of hospital patients - in fact the "classical" butterfly shaped rash is seen in a minority. Inflammation in small blood vessels of the skin may give rise to a variety of rashes - the most common is a pinkish spotty rash on the elbows and around the fingers and toes.
Patients with lupus may develop Raynauds phenomenon - a tendency for the fingers to go dead white then bluish on exposure to cold. This phenomenon, which may precede the diagnosis of lupus by many years, is, of course, not unique to SLE and is also seen in otherwise healthy individuals.

Symptoms on hair


Hair loss is one of the common symptoms of Lupus. While it is normal for hair loss to be noticed on combing the hair, much more significant is the complaint of finding considerable amounts of hair on the pillow in the morning. 
The hair grows back after the attack is brought under control, though it may take several months to do so - long after the patient is otherwise better.

Symptoms on the Joints


The majority of lupus patients suffer from aches and pains. During a severe attack, these may occur all over the body, affecting muscles, ligaments and joints. 
In the teenager, the joint pains may be passed off as "growing pains" - it is common, for example, to see pain limited to both knees. (Some years ago, SLE patients were often wrongly diagnosed as having rheumatic fever - a disease now almost extinct in major western countries). 
In older patients, the patient may be suspected of suffering from rheumatoid arthritis.
The joint disease of SLE differs, however, from rheumatoid arthritis. 
To put it in more emotive terms, for the vast majority of patients worldwide, SLE arthritis is not a crippling disease.

Symptoms on the Tendons



Perhaps the most common rheumatic feature of active lupus is inflammation in tendons. The patient may not, for example, be able to stretch the fingers flat - "saying ones prayers". Occasionally, this abnormal pull by tendons on the joints may lead to deformity. 
An unusual, though almost characteristic change is the "lupus thumb" - a locking back into the "hitchhiking" position.
This tendency of the inflammation of tendons waxes and wanes as do so many of the features of lupus.
It is often the only sign of disease activity in an otherwise symptom-free lupus patient.

Symptoms on the Veins and Arteries


Inflammation of veins - "thrombophlebitis" is an occasional complication of lupus, though of course, it is a common enough medical problem on its own. Inflammation in small arteries is obviously capable of producing symptoms anywhere in the body.

In the skin, there may be red or spotty rashes. 
In the kidney, it may produce a disturbance of kidney blood flow and in the brain, it may produce any number of features, from mild depressive attacks to more gross features such as a seizure.


Symptoms on the Brain


There is still uncertainty as to how frequently the brain is affected in SLE ( Systemic Lupus Erythematosus) . This uncertainty is partly because diagnosis of mild brain involvement is very difficult. It is very difficult to be sure clinically, for example whether an attack of depression in lupus is simply the natural reaction to a bad disease and its treatment, or whether it represents the (albeit mild) effects of inflammation in brain tissues. The brain (as is the case with other organs) has only a limited number of ways of reacting to "insults" such as inflammation - there can be disturbances of the normal thought processes (eg depression, hallucinations, odd behaviour), or there can be more marked abnormalities such as an attack of epilepsy, or the development of severe migraines.

It is evident that mild episodes of brain involvement during active lupus are extremely common. If true, this has important implications for families, nurses and medical attendants of lupus patients - to understand that an attack of mental depression, for example, may be due to the disease.

One of the more positive aspects about managing SLE is that these neurological features get better - they generally leave no damage.

One of the intriguing factors of the link with brain disease in lupus is that a number of patients with lupus, first developing at say, twenty, give a past history of epilepsy as a child. 
It is tempting to think that these symptoms are related - possibly that the lupus had been present all along. The question of fitness to drive is a difficult one in the adult SLE patient who has had a seizure during an acute flare. While such a patient may well never have another attack in her life, at the present time there are no medical tests sufficiently clear-cut to convince the powers of the law that lupus patients can be treated more compassionately. (At the present time, patients who have had a seizure are banned from driving for two years in the UK).


Symptoms on the Kidney



The kidney is one of the body's most delicate organs. It differs from the other organs involved in lupus in that it has limited powers of healing. Having said this, we now know that even those patients with active kidney disease can and do, improve enough to come off all medication.

Lupus nephritis, as it is called, is produced by two main factors - deposition of the proteins discussed earlier in the delicate filtering apparatus of the kidney, and inflammation of the blood vessels supplying the kidney.

The kidney protests in three main ways - it becomes "leaky", and protein is detected in the urine, the blood pressure may rise (only in more severe cases), and chemical impurities normally excreted in the urine accumulate in the blood.

Of all the features of lupus, kidney involvement is the most subtle. While joint pains or a rash may quickly bring the patient to the doctor, a "smouldering" inflammation in the kidney may go undetected until irreversible damage is done.

It is for this reason that lupus nephritis has the bad reputation it does.
Conversely, it is obvious that in a patient who is diagnosed as having lupus and in whom there is no major kidney involvement, severe kidney inflammation can usually be thwarted.

In the patient whose disease has "gone into remission" (i.e gone away) - it is wise to check the urine every few months.

Because of the limited ways in which kidney disease may show itself, it may be necessary to perform a needle biopsy - largely to see just how much protein deposition and inflammation there is. Obviously this will influence the choice of how much treatment is needed.
Traditionally, textbooks have tended to quote a figure of 40-50% for "significant" kidney involvement in lupus.
I
It is almost certain that as milder (and earlier) cases of lupus are diagnosed, this figure will fall. In Graham R V Hughes' practise (and this still probably concentrates on patients with more severe disease) the figure is now nearer 20%.


Is Lupus Lyme?



According to Dr Lida Mattman any autoimmune disease root cause is Parasitic or bacterial infection.
Lupus is very like Lyme in so many ways and as Lida Mattman would recommend all patients who are diagnosed with any autoimmune disease should be tested for an infection.
If you are presenting symptoms of Lupus or have been diagnosed with Lupus it is well worth seeking out a Lyme literate Doctor to be tested and to be absolutely sure.


Lyme Girlx

**Always consult a LLMD (Lyme Literate Doctor) or your own health care professional.**

Copyright 2012-2013  LymeGirl all rights reserved. 







Friday 25 January 2013

Distinct pattern of Cognitive Impairment in Lyme patients


Hello all,

I found this very intresting article about a study done on 100 Lyme patients it shows a distinct pattern of cognitive impairment.


Distinct Pattern of Cognitive Impairment Noted in Study of Lyme Patients Marian Rissenberg PhD & Susan Chambers MD, The Lyme Times, Vol. 20, Jan-Mar 1998, pp. 29-32
From: Melissa Kaplan'sChronic Neuroimmune Diseases
Information on CFS, FM, MCS, Lyme Disease, Thyroid, and more...


Synopsis: This study demonstrates that for the majority of chronic Lyme patients with cognitive complaints, there is in fact a measurable and significant decline in intellectual acuity. The nature and severity of the cognitive impairment is such that it interferes with all aspects of normal functioning: employment, home, marriage, social interactions, and general emotional well-being.


I. Cognitive Characteristics of Chronic Lyme Encephalopathy

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

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

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

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

The neuro-psychological characteristics of 49 patients with Lyme disease were examined. The study set out to answer three

I. Cognitive Characteristics of Chronic Lyme Encephalopathy

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

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

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

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

The neuro-psychological characteristics of 49 patients with Lyme disease were examined. The study set out to answer three questions:

1) Do all patients with subjectively perceived cognitive dysfunction have measurable intellectual impairment on objective testing?

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

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

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

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

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

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

III. Possible Pathophysiologic Mechanisms of Cognitive Impairment in Lyme Disease

Based on these findings and on patients' reports, two characteristics of Lyme Encephalopathy arise which provide insight as to possible neurophysiologic mechanisms:

One, the nonfocal nature of the cognitive functions affected, and

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

Four broad categories of possible neurophysiologic mechanisms might be compatible with this pattern:

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

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

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

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

IV. Clinical Impressions and Implications for Diagnosis and Treatment in Chronic Lyme Disease

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

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

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

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

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

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

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

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

V. Cognitive impairment in Lyme disease: specific functions and the impact of deficits

1. Attention and mental tracking. Includes directed and sustained attention: the ability to direct and maintain one's focus on a particular event or idea, whether in the environment or internally; and divided attention: the ability to simultaneously attend to two events, or do two or more things at a time, or to retain awareness of one thing while doing another.

Impact: difficulty functioning effectively in many situations, remembering what one was doing before a distraction, keeping track of conversation, taking notes while someone is speaking, remembering that someone is on hold, or what you were about to say.

2. Memory: Retaining new information.

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

3. Receptive language: understanding spoken or written language

Impact: secondary to impaired attention and speed of processing; difficulty participating in meetings or social conversation; difficulty with reading comprehension.

4. Expressive language: Using spoken or written language to express ideas

Impact: difficulty finding the right word; using the wrong word and not noticing; not being able to express oneself or communicate.

5. Visuospatial Processing: Efficient scanning of the visual field, making sense of how things are related in space; visuospatial conceptualization and problem solving.

Impact: a tendency to get lost; difficulty with reading comprehension.

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

Impact: difficulty with decision making, planning, and problem solving.

7. Speed of mental and motor processing: The ability to think and respond quickly; critical to understanding speech which occurs at a fairly constant rate.

Impact: difficulty understanding or keeping up a conversation; functioning in a timely manner in day to day situations; meeting deadlines.

________________________________________ A PDF version of this article is available for easier printing.

The Lyme Times is published quarterly by the Lyme Disease Association.

http://www.anapsid.org/cnd/diffdx/rissenberg.html

© 1994-2013 Melissa Kaplan

http://lymeblog.com/modules.php?name=News&file=article&sid=1633 

MMS Update 17 Months and 1 Week


Hello all,

I thought I would do another MMS update.
Having reached 17 Months and  1 week I do report that the improvements I have written about on this blog have continued.
Yes I did have my doubts about MMS and the effectiveness with treating chronic Lyme, I did a lot of research about MMS before I even bought a bottle.
I am glad to say the research paid off.
My improvements have increased ten fold yes ten times even more so.
You may say could it be a sort of Placebo effect? or mind over matter?
I have to say categorically no.
How could it not be like a placebo affect? Well I am sure that you do not get things like the stripy leg I experienced refer to this page http://diaryoflymegirl.blogspot.co.uk/2012/08/stripy-leg-swollen-foot.html
Or I am sure you don't find improvements in  cognitive ability or balance or coordination.

I am sure the MMS has done it's job in getting rid of the parasite or parasites in my body.

My children's progress

My children as I have said before decided to take MMS to treat themselves and as they are Gilleck competent (know their own minds) and do have/had congenital Lyme or spirochete infection have also noticed a difference in themselves.
Their coordination is better by about 80% their cognitive function 80% their rashes 95%  this has been increasing over the time they have been taking MMS.
They have both reported that they no longer have dark thoughts anger has subsided.
They probably have a little more to go to become fully well to perhaps get to 100% we do not know we were banking on the MMS taking maybe 3 to 5  years seeing as antibiotics can take up to 10 years.
We are pleasantly surprised at how long or rather short the MMS has taken so far.
My eldest is due another eye test in February so we shall see if her sight has in anyway deteriorated or improved.

My Brother

My brother was actually lucky enough to have another MRI scan (very expensive in the UK) and he got his results back and there were no signs of spirochetes!
He also had a spinal tap and blood tests.
He just seems to have the fragments floating around and as I have said before he too is treating himself with MMS.

So all in all the MMS is working and we are all at last becoming fit humans after all these years of suffering!
Yes I have to say i was waiting for maybe the Spirochete infection to perhaps go dormant and then find I would have a relapse as the spirochete come out of dormancy but from the results of my brothers MRI and blood tests it looks as though this is not the case and the infection is gone for good we just have to get rid of the fragments from the dead parasites, now how long this will take is anyone guess as unfortunately there is very little research into this.

Do not give up!


Do not give up treating any spirochete infection that has turned chronic is a marathon not a sprint there are no quick fixes and it is worth treating rather than not treating the infection.
We have all been on a very long journey but compared to the fact I was bitten age 9, 17 months and 1 week is surely a breeze.

Lyme Girlx

**Always consult a LLMD (Lyme Literate Doctor) or your own health care professional.**

Copyright 2012-2013  LymeGirl all rights reserved.