We (my family) suffer from psychiatric Lyme symptoms. How do I KNOW the psychiatric symptoms are CAUSED from Lyme, Erlichiosis and Babesiosis? We STOPPED having the psychiatric symptoms when we were finally treated for Lyme.

We were on psychiatric meds, which did help some, until we were diagnosed and treated for our tick borne diseases.

We are now OFF ALL of them. One of my children still has some flares, manageable, but my kids are not finished with  treatment.

I wish there were another treatment for our kids. We  don't want to treat them with long, high doses of antibiotics. 

If there were anything else to cure our kids we would do it over abx. Our kids are fed an organic diet. They do not eat dairy, preservatives or food dyes. They do not have white flour in their diet. I care tremendously what I put into their growing bodies.

They NEED the antibiotics so they are able to regain their health, function and live without pain, confusion, rage and fear.

My daughter missed her full 3rd and 4th grade years.

Both my kids were put on psychiatric meds, which increased their weight dramatically, made them groggy and slowed their thinking.

It is much easier to find a doctor willing to put your child on potentially  harmful psychiatric meds than it is to find a doctor that will treat Lyme with antibiotics.

My daughter spent 3 1/2 weeks in a locked pediatric psychiatric unit in the
summer of 1998. She turned nine years old just weeks before. She was
paranoid, delusional, psychotic, suicidal, homicidal, having visual
hallucinations, severe confusion, pain in major and small joints, partially
lost vision (could no longer read, which she had loved), had severe
cognitive regression (which included being unable to add 1 + 2, literally, and she knew it).

Because she could not attend public school she was placed in a "behavioral program" locally. At this "school" she was physically restrained and put in solitary confinement almost daily for 3 months. There she cried, fought with her very real "ogres", screamed, beat on the matt which was used to contain her, and finally would curl up in a fetal ball on the cold floor in the corner and sob. My husband found her in this "room" one day and removed her from the "school" immediately. She then spent 3 months at home with no schooling available for her.

The list of psychiatric meds she took is extensive. The ones she ended up taking that helped her were: lithium, risperdal, tegretol, topamax, and klonapin. Her psychiatric diagnoses were: bipolar, anxiety disorder NOS, ADHD, psychosis, R/O schizoeffective, R/O schizophrenia.

Some of her test results; her IQ dropped 45 points in 6 months, two abnormal MRIs both with MULTIPLE lesions throughout the brain, predominately in the frontal lobes, two abnormal SPECT scans showing low blood flow, hypoprofusion, to the prefrontal lobes, an abnormal visual evoked potential, indicating abnormalities in either the visual cortex of the brain or equal damage to both optic nerves, repeated tests showing ketoglutarate in urine and finally the blood test results which showed the infections.

This child was a patient of 16 doctors and NONE knew what was wrong with her. We heard repeatedly "Your child's case is the most complicated case I have seen" from doctors and medical professionals with many years of experience.

NONE of them diagnosed my daughter. I diagnosed my daughter. I found Dr. Robert Bransfield's "The Neuropsychiatric Assessment of Lyme Disease".
http://www.mentalhealthandillness.com/lymeframes.html  (click link to go to the ARTICLE) and then Dr. Brian Fallon's "Neuropsychiatric Manifestations of Lyme Borreliosis "
http://columbia-lyme.org/dept/nyspi/lymevid/lyme-fr.html 

It took me FOUR months after I found these papers and knew what was plaguing her to find a doctor to diagnose and treat her. Many doctors would not even run new Lyme tests as she had been tested years before and results were negative. She was bounced around from doctor to doctor. Each one in turn "passing the buck" which just happened to be my suffering child.

My kids are under the care of a living Saint (their LLMD) and are in school, they are both on the honor roll, have friends and are miraculously recovering from these devastating diseases.

On this page is a collection of neuro Lyme "stuff" I have found the past few years.

hope,
kay 

Objectives: Five patients who sought help for major personality changes and who later reported physical symptoms were selected from an adult psychiatry private practice near Philadelphia in PA, USA, evaluated via Western Blot antibody tests and, in two cases, PCR blood tests for possible borrelia DNA.  No patient was previously suspected of having Lyme disease but while in psychotherapy each described symptoms compatible with chronic LD. All had recent onset of cognitive deficits, and new episodic irritability.  Neither joint swelling nor other "typical" Lyme symptoms were prominent at the time of initial work up for Lyme disease (LD) and other tick-borne diseases (TBDs).
Patients were tested to ascertain if TBDs could be causing or complicating their mental/emotional symptoms and, if so, would antibiotic treatment help. No patient was aware of having had a tick
bite or bull's eye rash. Rationale: Ticks infect humans with viruses, smaller parasites and bacteria, some or all of which eventually may exert noxious influences on the victim's neural/cognitive systems. Patients may have resultant personality changes but no awareness of causative underlying infections. When multi-system symptoms appear and if the nature
of their illness is unrecognized, patients may describe themselves to psychiatrists as "hypochondriacs" or "complainers". Careful testing of such patients in endemic areas often reveals clear evidence of neuro-Lyme disease (spirochetal neuroborreliosis). Method: Five outpatients, who originally considered themselves well physically but who had manifested notable personality changes, eventually began to describe symptoms of chronic Lyme disease. Four tested positive by the Center for Disease Control Western Blot IgG antibody criteria of 5 or more positive bands and 1 tested positive by IGeneX Ref. Lab WB criteria.  The latter patient's test had 4 CDC positive IgG LD bands plus a positive band #34.  The two PCR-tested cases were positive for the DNA of the causative spirochete. Results: When these neuro-Lyme patients were treated with appropriate antimicrobial medications for extended periods of time, most physical symptoms were reversed completely in every case. One patient was restored
psychologically without the use of any psychotropic medication; the others retained lesser, residual emotional/mental symptoms, requiring intermittent or regular use of psychotropic drugs. Major cognitive symptoms slowly resolved with antibiotics.
Modafinil or methylphenidate helped by relieving mental fog/excessive sleepiness; zolpidem or mirtazapine ended the insomnia.
Conclusions: Greater understanding of the diverse effects of disseminated spirochetal disease should prove helpful to physicians
in their evaluation of anxious, irritable, depressed patients whose brain function and cognitive abilities may be distorted by microbes.
Achieving such diagnostic skills allows psychiatrists to test, then to arrange for and support appropriate medical referrals for on-going
antimicrobial treatment of these widely epidemic, personality-altering, tick-borne infections. Sophisticated history taking and lab
testing are recommended.  It is important to note that some patients with or without PCR positive tick-borne diseases will test sero-negative on early examinations but usually will convert to positive WB
testing as antimicrobial treatment progresses over time and they're able to make appropriate antibodies.

The Neuropsychiatric Assessment of Lyme Disease
Robert Bransfield, M.D.
http://www.mentalhealthandillness.com/tnaold.html

Dr. Bransfield's Mental Health & Illness site
http://www.mentalhealthandillness.com/

FABULOUS!
Audio Visual Presentation
Neuropsychiatric Manifestations of Lyme Borreliosis - Brian Fallon, M.D.
http://columbia-lyme.org/dept/nyspi/lymevid/lyme-fr.html

Neurological Manifestations of Lyme Disease
Aggression & Lyme Disease
Based on the observations and clinical judgment of Robert C. Bransfield
http://www.lymealliance.org/Medical/MedCategory8/medcategory8.html

Neurological and psychological symptoms after the severe acute neuroborreliosis
Click Here for ABSTRACT

Schizophrenia, rheumatoid arthritis and natural resistance genes.
Click here for Abstract

Geographic correlation of schizophrenia to ticks and tick-borne encephalitis.
Click Here for Abstract

Marked psychiatric symptoms induced by borrelia burgdorferi, whose clinical picture was indistinguishable from an endogenous schizophrenia.
Click Here for Abtract

Psychologic disorders in acute and persistent neuroborreliosis
Click here for Abstract

Long-term cognitive effects of Lyme disease in children. "Therefore, in contrast with studies of adults with LD, the results of long-term follow-up of the pediatric population continue to strongly support the finding that children treated appropriately for LD have an excellent prognosis for normal cognitive functioning."
Click Here for Abstract

www.dailyitem.com
Lyme disease turned 180-pound son into 130-pound little boy
By Joanne Troutman
Staff reporter

The nightmare began in September 1997 for then 13-year-old Matt Peters of Northumber-land. It was, at first, the dizzy spells the presumably healthy football player started experiencing. We thought he was having an allergy problem, recalls his mother, Helen Peters.
When the dizziness subsided, Helen and her husband, Monte, didn't think there was anything to be concerned about.
Then, just before Christmas, the cough started.
Matt's parents took him to their family physician, who placed Matt on a series of different antibiotics for a few weeks to treat what he diagnosed as bronchitis.
When the cough persisted, the family and doctor became worried and decided it was time to take a more aggressive approach.
The next stop was an examination in February 1998 at Hershey Medical Center, where Matt was hospitalized for a few days.
It was not long before doctors there told Matt the cough was all in his head, Helen says. They took him off the antibiotics and prescribed Zoloft, an antidepressant medication.
That's when things really took a turn for the worse. Matt walked into Hershey and we had to wheel him out, Helen says, matter-of-factly.
Within a few days, walking became so laborious that it took Matt 15 minutes to get from his hospital room to the end of the hallway, a distance of only 20 to 30 feet. And it didn't get any better. His knees began to swell tremendously, and he wouldn't open his eyes or eat. He soon began needing a walker when he wasn't in a wheelchair.
The Peters decided to take Matt to a local hospital, Geisinger Medical Center in Danville, hoping physicians there would do something for their son.
The doctors performed several tests on Matt. The teen was bounced from department to department, with doctors trying to determine exactly what was wrong. The only test that came back abnormal was a spinal tap, Helen says, with an increased protein level suggesting a possible infection. One doctor did recognize that the reason Matt wasn't opening his eyes was because they were sensitive to light.
But none of the blood tests showed anything out of the ordinary. After another series of tests, including an MRI, Geisinger doctors concurred with the diagnosis at Hershey Matt was severely depressed.
They said the cough was coming from a chemical imbalance in his brain, Helen says.
It wasn't that they weren't trying, she says about her despair in the diagnosis. But they kept saying this was in his head. I could tell he was in pain.
They just didn't recognize that he was feeling real pain and he needed help.
The doctors increased the antidepressant medication and sent him home.
In March, Matt stopped going to school. He was having panic attacks and was routinely dehydrated from refusing to eat or drink. His father had to carry him up steps because he couldn't walk.
He spent a lot of time in bed sleeping, Helen said.
In the meantime, Matt's behavior had become out of control. His parents started taking him to a counselor in Lewisburg.
It was when we saw the counselor that she thought there was something more to this, Helen said.
The counselor was the first to suggest Lyme disease.
Lyme disease is a tick-borne infection caused by Borrelia burgdorferi bacteria, a spirochete similar to the bacteria that causes syphilis. The Borrelia bacteria is typically carried by ticks that embed themselves in deer.
The disease is passed on to humans when deer ticks embed themselves in human skin to feed, subsequently causing a variety of symptoms.
It was first discovered in the United States in the 1970s when Dr. Willy Burgdorfer began researching a cluster of patients diagnosed with juvenile rheumatoid arthritis in Lyme, Conn.
However, the disease is thought to have been around for more than a century worldwide.
The counselor in Lewisburg told the Peters family that Lyme bacteria could manifest itself in the brain, causing many of the neurological symptoms Matt was experiencing.
The Peterses weren't sure what to think of the suggestion.
I didn't see a tick on him, and he didn't have a bulls-eye rash on him that we knew of, Helen said.
Plus, Matt had previously had all the usual blood tests recommended by the Centers for Disease Control for reporting Lyme disease, and none indicated Lyme under the guidelines.
But the counselor suggested a different test and a different doctor.
They needed to do something.
They thought their son was dying.
We saw him rolling up into a ball, Helen said. Everything was shutting down in his body ... I had this very active football player lying in bed in pain. There was something wrong.
His bowels and kidneys no longer functioned properly. He constantly had a severe headache and rarely opened his eyes because light hurt them too badly.
A healthy 180-pound middle school football player had become a feeble 130-pound little boy in a matter of months.
The family sent a urine specimen to Pittsburgh for analysis through a urine antigen test. The results came back borderline for Lyme disease.
The Peterses then scheduled an April visit to a pediatric doctor in New York who specializes in Lyme.
It was at her office that the Peterses learned that the rash Matt developed after cutting weeds in the family's rural Northumberland backyard a few years before was symptomatic of the disease. It was a rash that looked like poison ivy with a black mark in the center.
We didn't know there could be other rashes, Helen said.
Although the ELISA and Western Blot blood tests, as well as more direct tests such as the urine antigen screening, all came back borderline, the New York doctor clinically diagnosed Matt with advanced Lyme disease.
She placed him on antibiotics immediately. By the end of May, with the help of a local family doctor and Hershey Medical Center, Matt was receiving antibiotics intravenously.
Then we started a life with IV antibiotics that lasted a very long time, Helen says.
Matt's behavior continued to be a problem. He says he can't remember much of what happened while he was very sick. His mother won't elaborate on specifics, but she said he would do anything with food but eat it.
He wouldn't get angry, he would get furious, Helen says.
Throughout the summer, Matt had to wear sunglasses for light sensitivity. And the teen was still using a walker and wheelchair regularly. By this time, the muscle tone in his thighs decreased from inactivity, causing his knee caps to drop. He had to go to physical therapy to regain his strength.
He managed to get through seventh grade by doing his work at home. When eighth grade began, he went to school half-days and gradually increased to full days. He couldn't play football, but his teammates convinced the coach to allow him to wear a jersey and stay on the sidelines.
He was getting better. By March 1999, Matt was well enough to stop the IV antibiotics. He continued taking pills for a few months.
His last test for Lyme in June showed that there was less bacteria than was previously detected. And now, he's feeling better than ever. He has been in school full-time and he even played football last fall.
But there are still the emotional issues to deal with.
Helen says Matt kept a journal throughout his illness and refuses to look at it.
And he got really upset if any of us looked at the journal, she says. There were a lot of things in there I'm sure I wouldn't want to know.
Matt doesn't say much about his illness. But the expression on his face when you ask him about the pain says it all.
There was a lot of stuff I wanted to do, but I couldn't, he says, his eyes welling up with tears.
Matt doesn't want pity. What he does want is to be a normal 15-year-old boy who gets recognition for a disease that could have ruined his life and did so briefly.
(People) just don't understand, Matt says. They think it's no big deal ... but it is.
Neuroimaging in Neuropsychiatric Lyme Disease: Uses, Abuses, and the Future

Neuroimaging in Neuropsychiatric Lyme Disease: Uses, Abuses, and the Future
Brian A. Fallon, MD, Columbia University College of Physicians & Surgeons
Structural Brain Imaging

MRI scans among patients with neurologic Lyme disease may demonstrate
punctate white matter lesions on T2 weighted images, similar to those seen in demyelinating or inflammatory disorders, such as multiple sclerosis, systemic lupus erythematosus or cerebrovascular disease. In early neurologic Lyme disease, hyperintensities may be seen in as many as 50% of patients with evidence of meningitis or encephalitis. Comparable to meningo and cerebrovascular syphilis, European authors suggest that CNS micro- and macrovasculitis may cause both clinical symptoms and MRI changes in patients with CNS Borreliosis.
The usefulness of MRI scans in American chronic Lyme encephalopathy is less clear, with abnormalities seen 15% to 41% of the time. After treatment, roughly half of the patients may show resolution of the signal hyperintensity. In late stage encephalomyelitis, MRI scanning often
demonstrates focal areas of inflammation, most commonly in the white matter and occasionally in the cortical and subcortical gray matter of the brain.
Combined MRI and PET studies can help to examine the pathophysiology of these hyperintense areas (perfusion, reactivity to hypercapnia, metabolism)
and whether they have prognostic significance. Do these hyperintensities represent demyelination or perivascular inflammation? Is the disease
process underlying the hyperintensities primarily neuronal metabolic or vascular? FLAIR sequence and magnetization transfer techniques can be used to maximize the yield on identifying white matter hyperintensities.
Functional Brain Imaging
Single photon emission computerized tomography (SPECT) and positron emission tomography (PET), provide a dynamic picture of the brain's
functioning: metabolism, blood flow, and chemistry. In comparison to SPECT scans, PET scanning is able to provide better spatial resolution images
(4-6 mm vs. 6-9 mm) and can be used to provide an absolute quantitative assessment of regional perfusion or metabolic abnormalities. SPECT studies of patients with Lyme disease reveal multifocal areas of decreased perfusion in both the cortex and the subcortical white matter. Logigian
reported that patients with definite Lyme encephalopathy had significantly more perfusion deficits that patients with possible LE who in turn had significantly more deficits than normal controls. After treatment with one
month of IV ceftriaxone, a partial reversal in brain perfusion deficits was observed, raising the question of whether longer antibiotic therapy may
have resulted in even fewer perfusion deficits.
Hypoperfusion defects visualized on SPECT scans may result from any process that alters the radiotracer distribution, including vascular delivery to neurons, transport of the tracer into the cells, and retention of the radioactive tracer in the cells. Problems may arise secondary to direct
infection of neurons, from cellular dysfunction due to the indirect effects of neurotoxic immunomodulators such as cytokines, or from decreased perfusion through arterioles secondary to vasculitis. In other words, areas of hypoperfusion may result from a cellular-metabolic and/or a vascular problem.
How may clinical SPECT scans be useful? First, a scan with diffuse abnormalities may confirm that an objective abnormality is present in a
patient considered to have a factitious disorder. Second, a normal scan in a patient with prominent neuropsychiatric symptoms may suggest that a
psychiatric disorder is the primary cause of a patient's distress and not Lyme disease. Third, improvement after treatment provides objective
evidence of physiologic change.
How may clinical SPECTs be abused? One cannot conclude from a SPECT scan that a patient has Lyme disease, as similar patterns of abnormality may be seen with other diseases as well. Other disease processes that demonstrate a heterogeneous tracer uptake include vascular dementia, chronic fatigue syndrome, CNS Lupus, HIV encephalopathy and chronic or acute stimulant abuse.
Future Studies
Studies combining MRI and PET technology, MR Spectroscopy and functional MRI will each contribute significantly to our understanding of the
patholophysiology of chronic neurologic Lyme disease.  

Contact me: b10g7@mediaone.net

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