Thank you Susie for keeping us updated.

Paul
editor@...

HI folks! Oprah on Tuesday will be showing the start
of a series on "Medical Mysteries". It reportedly will
include interviews with three of the kids featured on
the HBO show "I have Tourettes but it doesn't have
Me"---Susieptmom

Also...

Less then one week left to the airing of "I Have
Tourette's But Tourette's Doesn't Have Me" which will
air on Saturday, November 12, 2005 on HBO at 7:30pm ET
.  Aside from the actual documentary the following
programs will be having segments related to the
documentary and TS:

Oprah Winfrey, Tuesday,  November 8, 2005.  To check
your local listings click on the following link:
http://www.oprah.com/tows/program/tows_prog_whenwhere.jhtml

Paula Zahn NOW, Friday, November 11, 2005 at 8:00pm ET
(5:00pm PT) on CNN.

CBS Early Show will air Friday, November 11, 2005
between 7:00 and 9:00am

     The Insider filmed at our dinner dance as well as
seven of the kids separately the next morning... The
segment will air this Thursday,
November 10.... Click below to find when and where The
Insider airs by entering your zip code:
        http://insider.tv.yahoo.com/watch/
        Here in NY it airs 7:00 pm on CBS channel 2 and
reairs 9:00 am the following morning.


This is a very exciting time for TSA and we must seize
every opportunity for awareness so please forward this
information to everyone you know.

We will keep you updated on more exciting upcoming TV
and print media for the documentary as it becomes
available.
--

TOURETTE SYNDROME ASSOCIATION, INC.

Thank you Susie for keeping us updated.

Paul
editor@...

The Tourette Syndrome Association and HBO have teamed up to film a
half-hour documentary, "I Have Tourette's, but Tourette's Doesn't
Have Me." It focuses on 7- to 12-year-olds with Tourette. It shows
their idiosyncrasies and it voices their desire for acceptance.

The documentary will be aired on Saturday November 12, 2005 at 7:30
both Pacific Standard time and Eastern standard time. If you have
relatives in the Central time zone it will air at 6:30 there.

We recommend that you record this special to share at a later time
with friends, family, or special functions.

Paul Marshall
Editor@...
http://www.tourettes-disorder.com


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This article is more for fun for all those Chocolate Loving
Touretters out there, as well as for those that may follow and
prescribe to the Feingold Diet as part of their alternative
treatment approch to Tourette's Disorder.

Paul Marshall
Owner/Editor

Eat chocolate, improve your health

Middletown chocolatier is nationally known for sweets that may ease
behavioral disorders New shops add service

STORY BY AL KEMP / PHOTOGRAPH BY GINGER WALL

09/21/2005

Chocolatier Nancy Kemble is not accustomed to someone walking into
her Broad Street shop in Middletown with a crinkly bag of Reese's
Peanut Butter Bites and asking her professional opinion of the
contents.

But Kemble has been in the business of making all-natural chocolate
for 25 years, so she knows her stuff -- essentially, sugar, butter,
cocoa and pure vanilla.

She patiently puzzles over the Reese's bag and its list of 20-plus
ingredients. "It's not food," she says with a sigh.

"What you should do when you read a label is go from the bottom
backwards, because that's where the artificial colors and flavors
usually are," she says.

Just as the sweets in the movie "Chocolat" were reputed to have
restorative powers, Kemble's confections at the Squirrel's Nest are
said to work wonders by her primary customers, followers of the
Feingold diet.

The diet is named for Dr. Benjamin Feingold, a pediatrician and
allergist who in 1973 proposed that certain artificial ingredients
aggravate and even cause learning disorders and behavior problems in
some people.

Many adherents are people seeking a non-drug treatment for attention
deficit disorders. Some are simply taking an all-natural approach to
nutrition.

"Eighty-five percent [of her business] is to people with ADD, ADHD,
Tourette's [syndrome] and autism," she says. "I have hundreds of
families who swear by Feingold."

"I can smell artificial ingredients," she says. She's only half
joking.

Preservative-free chocolate such as Kemble's is a tiny slice of the
American chocolate pie, said Susan Smith, senior vice president of
public affairs with the National Confectioners Association, which
has 450 member companies.

But for Feingold adherents, the Squirrel's Nest is a nationally
known resource. "For us, it's a godsend," said Annette Miller, vice
president of the Feingold Association of the United States, which
has 30,000 members.

Kemble's shop smells sweet and pure, like one perhaps run by a young
Willy Wonka before he went global.

The shelves are laden with butter creams (her top seller), toffees
and pretzels, all enrobed in chocolate that's daringly dark or milky
and mellow.

While the Squirrel's Nest attracts foot traffic from a fair number
of garden-variety chocoholics, the bulk of Kemble's business is mail
order.

At Halloween she ships out hollow jack-o'-lanterns and thousands of
lollipops. The top sellers at Christmas are corporate gift boxes. At
Easter, her peak season, her shelves spill over with chocolate cats,
dogs, pigs, ponies, trucks, tractors and "tons of bunnies."

Kemble started making all-natural sweets when she learned that her
firstborn child, Jason, could not tolerate artificial colors or
flavors.

Jason died from a rare cancer when he was almost 16, and Kemble
carried on with the chocolate business as a way to cope with her
grief.

"Coming to work is what kept me going. Helping other kids is what
kept me going," she says. "This store is not about money at all."

"The best thing is that people are becoming more aware of what they
eat.''

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There is growing evidence which has scientist suspecting that a
common childhood throat infection increases the risk of neurological
disorders such as Tourette's syndrome.

These findings are based on a study conducted at the Group Health
Center for Health Studies (CHS) in Seattle, is published in the July
5, 2005 edition of the journal Pediatrics, accessible online at
http://www.pediatrics.org.

The study focused on patients of Dr Davis's co- operative health
service diagnosed with a neurological disorder between 1992 and
1999. The study group consisted of 200 children aged four to 13 and
compared them with healthy children in the same age group.

Based on their medical histories, the results of the study suggests
that strep throat (streptococcal infection) doubles the risk for a
first diagnosis of Tourette's Disorder (TS/TD), obsessive
compulsive
behaviors (OCD) or tic disorder within three months after infection.
In addition, multiple infections appear to approximately triple the
risk for a first diagnosis of these disorders within 12 months.

This could be an indication that the same antibodies that attack
streptococcal infection may also damage brain cells.


Robert L. Davis, MD, MPH, senior researcher at CHS and the study's
corresponding:


"Strep infections share certain proteins that stimulate a set of
antibodies that cross-react with the brain. Many scientists believe
the body's response to infection, and to the antibiotics prescribed
to fight it, is to produce antibodies that attack not only the
infection but may also damage brain cells that control movement and
behavior."

"Although the presence of these antibodies is more frequent among
children with tics or TS, there's much we still don't know, for
example, why do millions of children get strep throat every year,
but only a tiny fraction develop these disorders? Genetics more than
likely play a major role in these conditions, but strep throat might
be one of the triggers,"

"There are likely a number of different causes for these conditions,
which often show up first in childhood or adolescence. Following a
number of different leads from past research, we've found more
tantalizing clues about possible connections between childhood
infections and certain disorders. However, our findings certainly
don't suggest that there is any immediate need for a change in
medical - or parental - practice."

"We still don't know if treatment with common antibiotics helps
prevent these neurological conditions that might follow strep
throat, or reduce their severity, or shorten their duration if they
do occur."


Strep infections are common, but Davis said it was too early to know
whether choosing one treatment option or none at all would help
stave off tics.
"This is scientific research at this point," Davis said. "One thing
we didn't study was whether treatment (with penicillin) modifies
these conditions."


Davis does not suggest that parents and physicians should be more
worried. Nor did he suggest parents do anything differently if their
child gets strep throat. "Right now, this is all still in the
research stage," said Davis. "We still don't know if treatment with
common antibiotics helps prevent these neurologic conditions that
might follow strep throat, or reduce their severity, or shorten
their duration if they do occur."


Other study authors include Loren K. Mell, MD of the Pritsker School
of Medicine, University of Chicago, and David Owens, MD, of the
University of Washington School of Medicine.

Group Health is a consumer-governed, nonprofit health care system
that coordinates care and coverage. Based in Seattle, Group Health
and Group Health Options, Inc. serve nearly 550,000 members in
Washington and Idaho. Group Health's Center for Health Studies
conducts research related to prevention, diagnosis, and treatment of
major health problems.


The team from the Group Health Center for Health Studies in Seattle
aimed to assess the strength of the link between strep infections
and the incidence of neurological disorders.


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http://news.bbc.co.uk/2/hi/health/4647961.stm

http://asia.news.yahoo.com/050705/3/23fsd.html

http://www.smh.com.au/news/health/tourette-link-to-strep-
throat/2005/07/05/1120329448351.html


http://www.psycport.com/showArticle.cfm?
xmlFile=comtex_2005_07_05_pr_0000-3026-wa-group-health-
study.xml&provider=PR%20Newswire

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CEDAR CITY - The lone family photo taken more than two years ago
when Peter Jensen could pose and smile without convulsing into
horrible fits sits on a table next to his hospital bed.

"I took it with us so that Peter could look at it every day and see
his children," Jensen's wife, Roshana, said during a telephone
interview.

Jensen has been battling Tourette's Syndrome - a neurological
disorder characterized by tics and involuntary rapid, sudden
movements or vocalizations that occur repeatedly in the same way -
since being diagnosed at age 11.

Doctors said Jensen's was the worst case ever diagnosed in the state.

Prior to his surgery, he'd been heavily sedated for six months at
Kolob Regional Care and Rehabilitation Center to keep his body from
deteriorating from the muscle spasms, which would have left him
incapable of being accepted for the new Food and Drug Administration-
approved clinical study.

The study requires candidates to be 18, have severe TS not
controlled by medication, physically fit for surgery and able to
travel to Cleveland repeatedly.

Jensen was one of only five patients chosen.

The preventative care enabled him to fulfill the requirements and
Jensen underwent the second phase of the medical procedure called
deep-brain stimulation Friday at University Hospitals of Cleveland
in Ohio.

Deep-brain stimulation works much like a heart pacemaker by
providing a stream of electrical currents to counteract the part of
the body that is not functioning properly. Instead of the heart, it
sends currents to the area affected by the brain disorder.

During the first of three phases of the surgical process, electrodes
are inserted into specific spots in the brain. Jensen was unable to
comment because he was recovering from surgery, but Roshana said the
initial procedure, which took place June 3, took 12 hours. The
second phase consisted of connecting the inserted electrodes through
wires under the skin - beneath the scalp, neck and upper chest - to
a replaceable a battery implanted beneath the collarbone.

"The surgery today took three hours," Roshana said. "He's doing
really well, and actually has done well through both parts of the
surgery. We're now waiting for the time to turn on the generators,
which will be in about two weeks."

According to a press release, only a handful of people have received
this treatment. Jeff Matovic, a Lyndhurst, Ohio, resident who grew
up in Bay Village, was the first person in North America to undergo
deep-brain stimulation for TS. Since his surgery in April, 2004, he
has not had any of the vocal or motor tics that once ravaged his
body and forced him to drink from a sippy cup at the age of
30. "Jeff and Deborah Matovic came down and talked to us and visited
with us and that was an incredible experience," Roshana said. "All
the people at the University Hospital have been stupendous and taken
good care of Peter and good care of me. It's just like having a big
family out here. It's wonderful."

Deep-brain stimulation has been used for more than a decade to treat
other movement disorders, such as Parkinson's disease, tremors and
dystonia, which distorts posture. About 30,000 people around the
world now have such brain implants, the press release said.

However, doctors at University Hospitals of Cleveland are careful to
point out that not everyone with TS requires treatment. The first
line of treatment is medication, which can be very effective.
Surgical treatment is considered a last resort, the news release
said.

Drs. Brian N. Maddux and Robert Maciunas are Jensen's neurosurgeons.
Neither would divulge information regarding his case. Eric
Sandstrom, acting media relations director of University Hospitals
of Cleveland said the physicians are not trying to be uncooperative,
but are in the midst of research and Jensen is their utmost concern.

"Any information is treated with care because of HIPPA and because
Peter is one of five patients in the clinical trial here, and
although he's the first, four others are to follow him in the next
few months," Sandstrom said. "The doctors who are performing the
deep-brain stimulation do not want publicity or information be
divulged about any of these patients until the completion of the
clinical study."

Meanwhile, Roshana said she does a lot of waiting. While waiting,
she does a lot of thinking and becomes overcome with gratitude, she
said.

"First, I want to say 'thank you' to all the people who helped us
raise $118,000 because that has really been what's got us out here
and paid for the surgery," Roshana said. "Secondly, for everyone who
has expressed concern and support, more information will be coming
as things move along, but Peter is fine and doing well."


Originally published June 11, 2005

Source:
http://www.thespectrum.com/apps/pbcs.dll/article?
AID=/20050611/NEWS01/506110303/1002


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Cedar City Man to Receive Implant To Help Against Tourette's Syndrome
Jun. 1, 2005

Source
KLS-TV 5
http://tv.ksl.com/index.php?nid=39&sid=209174
Visit Page Above to: Watch Clip Video from KSL-TV:
Cedar City Man to Receive Implant To Help Against Tourette's
Syndrome


Print Story:

After more than a year, including six months under sedation...a
Cedar City man with uncontrollable muscle spasms and tics is about
to get what he's been waiting for.

Ed Yeates joins us tonight with some long awaited news about Peter
Jensen.

You may remember Peter Jensen from our report last November. He has
one of the most severe cases of Tourette Syndrome doctors have ever
seen.

But as of this hour, he's finally on his way to Cleveland to try
something that just might cure him.

Several weeks ago, Peter was pulled off medications, to get ready
for an experimental implant he was beginning to think would never
come.

The tics, the spasms from his Tourette Syndrome have only worsened.
In fact, his doctor put him in a nursing home, sedated, simply to
keep his body from wearing out.

But now, it's packing day - and a flight to the University Hospital
in Cleveland, Ohio for a procedure that's only been tried on one
other patient with Tourette's.

PETER: "I THINK THE GREATEST THING ABOUT IT IS (TICS) IT'S SOMETHING
I THOUGHT I WOULD NEVER SEE IN MY LIFETIME."

For that first patient, Jeff Matovic, the brain implant worked,
shutting down 85 to 90 percent of his tics.

From this - to this.

Will it now happen for Peter?

It's a risk worth taking, he says, not only for him, but his wife
and kids.

ROSHANA JENSEN: "I THINK IT'S BEEN TRYING NOT TO HAVE A FATHER
FIGURE AROUND ALL THE TIME TO PLAY WITH AND ROMP WITH AND DO WHAT
THEY NORMALLY DO."

PETER: "I THINK THERE IS JUST GOING TO BE A WONDERFUL FEELING AND
ANSWER TO PRAYERS - AS WELL AS JUST (TICS) A TIME FOR PEACE AND
QUIETNESS, I THINK."

ED YEATES: "PETER WILL HAVE HIS FIRST SURGERY THIS COMING FRIDAY - A
SECOND SURGERY A WEEK LATER. AND THEN IN THE THIRD WEEK, THEY TURN
THE IMPLANT ON."

If pacemakers on each side of his chest send signals to electrodes
implanted in the brain - and they work - and the tics stop.

PETER: "IT WILL BE PARTY ON ITS OWN - SMILES"

Peter will stay in Cleveland until the middle or end of July. It
will take a while to custom adjust the pacemakers to his needs - to
stop most if not ALL of the tics.

Editors Comments:

The medical process is known as - Deep Brain Stimulation or DBS.

Source
KLS-TV 5
http://tv.ksl.com/index.php?nid=39&sid=209174
Visit Page Above to: Watch Clip Video from KSL-TV:
Cedar City Man to Receive Implant To Help Against Tourette's
Syndrome


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Chiropractor works to reconnect signals in the brain
By EMILY CHRISTENSEN, Courier Staff Writer

WATERLOO --- Joe Culbertson once suffered from migraines that kept
him out of school for 29 days.

At his lowest point, doctors had diagnosed him with attention
deficit disorder, attention deficit hyperactivity disorder,
depression and Tourette's syndrome. He was on as many as six
medications to stabilize his medical and mental conditions.

Administrators at Expo High School told his family it would take six
years for him to graduate.

That was three years ago. Culbertson, now 17, will graduate next
month --- a year ahead of his former classmates at East High School.

He credits his success to Dr. Kurt Kuhn, a Waterloo
neurochiropractor who specializes in treating children and young
adults with attention deficit and autism-related disorders. Kuhn
said the symptoms from these diagnoses manifest because of a
condition recently coined functional disconnection syndrome. The
condition results in a functional breakdown in the neurological
pathways, which in turn causes the brain to perform at a level below
what is required for higher cognitive function. The human brain's
efficiency depends on a seamless transition of signals from one area
of the brain to another.

Culbertson said the treatment he received at Kuhn's office has made
him a changed man.

"Now I am not afraid of anything," Culbertson says. "I want to get
the word out so people can know, I pretty much hit the bottom rung
and have climbed back up."

Kuhn has offered the specialized treatment for about two years,
though technology continually changes his methods. He is one of only
three neurochiropractors in the state. There are only about 600 such
chiropractors in the world. In general, neurochiropractors use
standard neurological tests and chiropractic adjustments to increase
the brain's capacity.

After an initial consultation, Kuhn starts a rigorous program using
neurological tests to determine each patient's cognitive capacity.

The first, called a go or no-go test, measures a person's ability to
pay attention. The 22-minute test gives Kuhn an insight into how
fast a person's brain fatigues. On Culbertson's first visit, it took
just five minutes for him to lose interest.

"Too many times we find kids with five-minute attention spans who
are stuck in 55-minute classes," Kuhn says.

Another test, the interactive metronome, works by challenging the
patient to synchronize a range of hand and foot exercises to a
computer-generated tone. Studies have shown that over the course of
care, patients learn to focus for longer periods of time, increase
their physical endurance and filter out internal and external
distractions.

Once the tests are completed, Kuhn begins therapy sessions, which
can continue include both tests and a series of other exercises. One
of Culbertson's favorites to master was drumstick twirling. Kuhn has
an entire book that outlines dozens of spins. The repetitive
activity builds brain capacity slowly, allowing Kuhn's patients to
repair their neurological pathways.

"Every kid, well almost every kid, wants to be a rock 'n' roll
star," Kuhn says. "We know this is something every kid will actually
do."

But as soon as Culbertson learns a new spin, he must move on.

"These activities are only useful as long as it is a challenge,"
Kuhn notes.

Other activities, like the "whack-a-mole" game often found at
carnivals, are also used to build brain capacity.

But Kuhn must start small. In the beginning, he often sees a patient
daily, though for a very short visit.

"They only have a small brain capacity. It would be like going to a
gym --- if you are a 98-pound weakling you will need to spend a lot
more time at the gym than someone who is already fit," Kuhn
says. "We are always trying to build up more brain power, but there
has to be the fuel to support it."

The same types of treatments can also work for children with autism.
Kuhn said results aren't always as profound and may take longer, but
many parents have seen improvement in their children.

"I have seen many autistic children who were locked in when they
came to me," Kuhn says. "Now they are talking."

Contact Emily Christensen at (319) 291-1482 or
emily.christensen@...



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A Potential Explanation of Tourette's Syndrome

---------------------------------------------------------------------
-----------

Copyright ă 1997 James Michael Howard, Fayetteville, Arkansas, U.S.A.


---------------------------------------------------------------------
-----------



(Some Potential New Support: Biological Psychiatry 2005 (March 15);
57: 667-673:  The authors found increased levels of interleukin-12
and tumor necrosis factor alpha in their subjects.  DHEA decreases
TNF alpha (Crit Care Med. 2001 Feb;29(2):380-4) and decreases
interleukin-12 (Aliment Pharmacol Ther. 2003 Feb;17(3):409-14).  I
suggest it is possible that these findings may be explained by low
levels of DHEA, or interference of available DHEA, in Tourette's
syndrome.)

This is designed for consumption by people who have knowledge and/or
experience with Tourette's syndrome. (If this interests someone
without these connections to Tourette's syndrome, I suggest some
prior reading.) With that in mind, I can make this very brief. My
work, copyrighted 1985, suggests that the major hormone of the
adrenal glands, dehydroepiandrosterone (DHEA), is necessary for
proper growth and development of all tissues, and maintenance,
thereof, following development, especially the brain. The other
major hormone of the adrenal glands, cortisol, I suggest works to
antagonize the effects of DHEA. Therefore, I would label cortisol
the primary "anti-DHEA" hormone. Currently, there is much study of
the connection of cortisol and DHEA, but the work is backwards to my
idea. That is, searches of the medical literature will produce much
research on DHEA as the major "anti-cortisol" hormone. (In the
medical literature, the general term, "glucocorticoid" is often used
in the place of "cortisol," so you might find references to DHEA as
an "anti-glucocorticoid," if you pursue this.) While this is
important to me and my copyright, I mention this difference only to
demonstrate that a number of investigators think the connection of
DHEA and cortisol is important. It is important to my explanation of
Tourette's syndrome.

There are a number of reports in the literature that connect
increased cortisol with Tourette's syndrome (TS). No one has studied
the levels of DHEA in this syndrome, so this is my hypothesis
regarding TS and DHEA. Just below is a recent citation that sums up
the connection of cortisol and TS. For those without the knowledge,
you should know that cortisol production, by the adrenal glands, is
stimulated by a cascade of molecules. Corticotropin-releasing factor
(CSF) stimulates the release of adrenocorticotropin hormone (ACTH),
which travels to the adrenals and mainly stimulates cortisol
production. (ACTH does stimulate some production of DHEA, prolactin
is more important than ACTH; more on that below.) The important
statement in this citation is: "The TS patients had significantly
higher levels of CSF CRF than both the normal controls and the OCD
patients."

Biol. Psychiatry 1996 May 1; 39(9): 776-783 "Elevated cerebrospinal
fluid corticotropin-releasing factor in Tourette's syndrome:
comparison to obsessive compulsive disorder and normal controls"

"Stress- and anxiety-related fluctuations in tic severity are
cardinal features of Tourette's syndrome (TS), and there is evidence
for involvement of noradrenergic mechanisms in the pathophysiology
and treatment of the disorder. To examine further the pathobiology
of this enhanced vulnerability to stress and anxiety, we measured
central activity of corticotropin-releasing factor (CRF) in patients
with TS and the related condition, obsessive compulsive disorder
(OCD). Lumbar cerebrospinal fluid (CSF) was obtained in a
standardized fashion for measurement of CRF from 21 medication-free
outpatients with TS, 20 with OCD, and 29 healthy controls. The TS
patients had significantly higher levels of CSF CRF than both the
normal controls and the OCD patients. However, there was no
difference in CSF CRF between the OCD patients and the normal
controls. Group differences in CSF CRF were unrelated to current
clinical ratings of depression, anxiety, tics, and obsessive
compulsive behaviors. Although the functional significance of this
finding remains to be elucidated, these results are consistent with
the hypothesis that stress-related neurobiological mechanisms may
play a role in the pathobiology of TS."

The investigators, above, also stated that "Stress- and anxiety-
related fluctuations in tic severity are cardinal features of
Tourette's' syndrome..." Cortisol is known as the "stress hormone."
Therefore, I deduce that cortisol has negative effects in TS. It is
known that cortisol, especially over lengthy time, is a neurotoxin;
cortisol is bad for the brain.

It has also been found that: "The TS patients secreted significantly
more ACTH than the normal controls in response to the stress of
lumbar puncture." Biol. Psychiatry 1994 Jul; 36(1): 35-43 Remember,
CSF stimulates ACTH, which stimulates cortisol.

Now, my basic principle, that DHEA is the positive hormone and
cortisol is its antagonist, suggests that DHEA should have positive
effects against stress and anxiety. This has recently been studied
and supported. "In conclusion, the results presented here show DHEA
to be effective as an antidespair agent in rats with both high
anxiety and despair." Physiol. Behav. 1997 Nov; 62(5): 1053-1057
DHEA may alleviate the stress in TS by increasing the ratio of DHEA
to cortisol.

A number of drugs have been used in Tourette's syndrome. However,
over time these prove to actually increase tics. I suggest that the
initial success of these drugs, and their subsequent failure, is due
to positive, then negative, effects on DHEA production.

Mov. Disord. 1995 Nov; 10(6): 791-793 "Tardive tourettism after
exposure to neuroleptic therapy"

"A case of neuroleptic-induced adult-onset tardive tourettism is
presented with video documentation. After prolonged neuroleptic
therapy, the patient developed motor and vocal tics at 36 years of
age. The tics were identical to those seen in childhood-onset
Tourette's syndrome. These cases are rare and have been considered
by some to represent tardive akathisia"

DHEA is significantly low in schizophrenia (Biol. Psychiatry 1973;
6: 23). (Please read my explanation of schizophrenia.) Some of the
drugs used to treat schizophrenia have been useful in the treatment
of TS. The drugs used to control schizophrenia, I suggest, actually
exert their effect by stimulating DHEA production. That
is, "...antipsychotic potencies of most neuroleptic drugs closely
correspond to their prolactin-releasing potencies at low doses..."
(Biol. Psychiatry 1990; 27: 1204). Prolactin is highly effective at
stimulating DHEA production, and, in fact, may be specific for
stimulating DHEA (Am. J. Ob. Gyn. 1987; 156: 1275, and Endocrinology
1985; 117: 1968). One of these drugs, haloperidol, is effective in
TS (first quotation, below). However, prolonged use of haloperidol
has the negative side effect of increasing tics (second quotation,
below).

Am. J. Ment. Retard. 1997 Mar; 101(5): 497-504 "Tourette's syndrome
associated with mental retardation: a single-subject treatment study
with haloperidol"

"A Tic Checklist and direct observation tic measurement procedure
were developed for the assessment of Tourette's syndrome in
individuals with mental retardation. Using a single-subject reversal
design, we applied this assessment method to the evaluation of
haloperidol treatment for a subject with Tourette's syndrome and
severe mental retardation. Relative to baseline, haloperidol 10
mg/day produced decreases of 66% in simple motor tics, 46% in
complex motor tics, 45% in simple vocal tics, and 50% in complex
vocal tics. Improvement was also seen in careprovider ratings of tic
severity, hyperactivity, and compulsive behaviors."

Aust. N. Z. J. Psychiatry 1996 Jun; 30(3): 392-396 "Tics status"

"OBJECTIVES: To describe two patients with tics status, propose a
definition of this syndrome and draw attention to its clinical
significance. METHOD: Two patients suffering from Tourette's
Syndrome who had developed episodes of continual motor tics that
lasted from minutes to hours, were non-suppressible and intruded
into normal functioning, were treated with an increase in the dose
of haloperidol, in one case with the addition of clonazepam.
RESULTS: The offset of the episodes was gradual and the tic disorder
was worse after the episodes. One patient had further spontaneous
episodes of tics status. CONCLUSIONS: The recognition of tics status
has implications for the management as well as our understanding of
the pathobiology of tics and Tourette's Syndrome. The definition of
tics status should be standardized."

Nicotine has also been found to be useful, again for a limited time,
in Tourette's syndrome. Smoking, i.e., nicotine, increases the
production of DHEA.

J. Steroid. Biochem. Mol. Biol. 1993 Aug; 46(2): 245-251 "Cigarette
smoking is associated with elevated adrenal androgen response to
adrenocorticotropin"

"Cigarette smoking alters the pattern of endogenous steroid levels.
We examined this phenomenon in two separate male groups. Group A
consisted of 189 dyslipidemic men participating in the Helsinki
Heart Study and group B of 100 men including patients with heart
disease and healthy controls. The subjects in the latter group
underwent ACTH-testing. In group A, smokers had significantly higher
basal androstenedione and dehydroepiandrosterone sulfate (DHEAS)
levels and androstenedione/cortisol ratios than nonsmokers. Mean
concentrations of cortisol, dehydroepiandrosterone (DHEA),
androstanediol glucuronide, testosterone, and sex-hormone binding
globulin (SHBG) did not differ between smokers and nonsmokers. In
group B, smokers had lower high density lipoprotein (HDL)-
cholesterol and apolipoprotein AI and higher triglyceride levels
than nonsmokers. Basal androstenedione and ACTH stimulated
androstenedione and DHEA concentrations were higher in smokers. No
significant differences were found in basal insulin, SHBG, estrone,
estradiol, testosterone, free testosterone, and dihydrotestosterone
concentrations between smokers and nonsmokers. These results suggest
that smoking decreases the activity of either 21- or 11 beta-
hydroxylase in the adrenal cortex, which results in increased
secretion of adrenal androgens."

Psychol. Med. 1997 Mar; 27(2): 483-487 "Differential effects of
transdermal nicotine on microstructured analyses of tics in
Tourette's syndrome an open study"

"BACKGROUND: The treatment of Tourette's syndrome (TS) is often
unsatisfactory. However, there is some evidence that transdermal
nicotine patch (TNP) application may improve tics of nonsmoking TS
patients who are refractory to haloperidol treatment. METHODS: In
this open study we applied two 10 mg TNP for 2 consecutive days to
four TS patients whose symptoms were not controlled by haloperidol
and to a never-medicated TS patient, all of whom are non-smokers.
The Yale Global Tic Severity Scale (YGTSS) and a quantified video-
taped micro-structured analysis of tics (head-shake tics, eye-
blinks, vocal tics, facial grimace and other body tics) were both
carried out to assess the change after the application of TNP.
RESULTS: TNP application significantly reduced the YGTSS by an
average of 50%, with no reported side-effects, for up to 4 weeks but
not 16 weeks, as compared with TNP-free period. Consistent with
these results, the total counts of tics also showed a significant
decrease for up to 4 weeks after the TNP application. CONCLUSION:
TNP application differentially affected individually quantified
tics, which may suggest a differential role of nicotinic receptors
in the generation of different tics."

Haloperidol and nicotine both reduced tic severity. However, both of
these drugs were useful for a limited time. My explanation of
Tourette's syndrome is that these individuals produce more cortisol
than they should, and are limited in their ability to produce DHEA.
If this is true, then the use of these two drugs, that stimulate
DHEA production, may overwhelm the ability of the adrenal glands to
produce DHEA. That is, they stimulate DHEA for some time, then the
ratio of cortisol to DHEA may actually increase. The tics that
haloperidol eventually causes may actually result from reduced
availability of DHEA for certain parts of the brain that cause the
tics, characteristic of prolonged haloperidol use. I have developed
an explanation of epilepsy that suggests that epileptic seizures
occur to increase DHEA. Now, in the case of haloperidol, only
certain parts of the brain may be affected, and the tics may
represent small seizures, the purpose of which is to stimulate DHEA.
It is known that tics are sometimes misdiagnosed as seizure
activity. (You may read my hypothesis of epilepsy.) (My work also
suggests that the addiction of smoking is due to the DHEA stimulated
by nicotine, in individuals who can continue to produce DHEA with
nicotine.)

In my study DHEA, I have found references that show that DHEA is low
in childhood, increases through adolescence to a peak in young
adulthood, around age twenty to twenty-five. Now, this means that
DHEA increases from childhood through young adulthood. This period
of increasing DHEA availability should reduce the symptoms of
Tourette's syndrome in some individuals, assuming that undue stress
is not experienced (increased cortisol). This is supported. J.
Psychol. 1997 Nov; 131(6):615-626 "Psychophysiological aspects of
Tourette's syndrome"

"Tourette's syndrome (TS), once considered a rare disorder, has been
investigated extensively in the last two decades. It is inherited,
usually beginning in childhood, and waxes and wanes, usually
decreasing in frequency and severity in adolescence and early
adulthood. Pharmacotherapy is the usual treatment approach, reducing
frequency and severity of symptoms, but it is not a cure and often
has side effects. Psychological help for people with TS and their
families may be needed for this complex disorder."

It is my hypothesis that Tourette's syndrome results from too much
cortisol and too little DHEA. I suggest that children with TS might
benefit from supplemental DHEA.

Source: http://www.anthropogeny.com/A%20Potential%20Explanation%20of%
20Tourette.htm


Paul Marshall
editor @ tourettes-disorder.com
http://www.tourettes-disorder.com

New Data Reported on Tetrabenazine for the Treatment of Pediatric
Hyperkinetic Movement Disorders
Findings Presented at 57th Annual Meeting of the American Academy of
Neurology

Clinical study investigators concluded that tetrabenazine was an
effective and well-tolerated treatment for severe hyperkinetic
movement disorders among children who are resistant to other
medications, according to new data presented today at the 57th
Annual Meeting of the American Academy of Neurology in Miami Beach.

"This is one of the largest reported studies of children treated
with tetrabenazine," said Steven J. Frucht, MD, Assistant Professor
of Neurology, Neurological Institute of New York, Columbia
University Medical, Center for Parkinson's Disease and Other
Movement Disorders, and lead investigator of the study. "We are
encouraged by the fact that nearly three quarters of children
treated with tetrabenazine experienced a reduction in their
involuntary movements."

Study Design and Results

Over the course of 18 years, 30 children aged 18 years and younger
were treated with tetrabenazine at Columbia University Medical
Center for a variety of hyperkinetic movement disorders, including
chorea, dystonia, and Tourette Syndrome or tics. The study was
approved by the medical center's institutional review board, and
neither the study nor the investigators were supported by Prestwick.

A retrospective chart review was conducted to assess the efficacy
and tolerability of tetrabenazine among these patient populations.
Twenty-eight patients (93%) had tried other medications without
adequate relief prior to being placed on tetrabenazine. On average,
patients were treated with a total dose of 150.9 mg/d (4.9 mg/kg/d)
for 1.3 years.

Twenty-two of the 30 patients (73%) experienced a reduction in
movements (as assessed by the examining physician) after starting
tetrabenazine. Sixteen patients continued tetrabenazine along with
at least one other medication to control movements, while movements
were sufficiently controlled with tetrabenazine alone in six
patients. Side effects, which were ameliorated with a reduction in
dose, were experienced in nineteen patients (63%), including
sedation (30%), behavioral changes (20%), depression (10%),
worsening of movements (6%), nausea (3%) and parkinsonism (3%). Nine
patients (30%) discontinued tetrabenazine due to behavior changes
(3), sedation (3), worsening or lack of improvement in movements (2)
and major depression (1).

"The results of this pediatric study support earlier findings in
adults that suggest tetrabenazine may be an effective and well-
tolerated treatment option for severe pediatric hyperkinetic
movement disorders," said Dr. Frucht. "Similarly, side effects were
typically dose-dependent, and we did not observe tardive dyskinesia
in our patient population."

Tetrabenazine

Tetrabenazine is available in some European markets and Australia as
XENAZINE(R) and in Canada as NITOMAN(R) for the treatment of
hyperkinetic movement disorders. Tetrabenazine is not FDA-approved
for marketing in the United States. Side effects can include
drowsiness, insomnia, akathisia and depression.

Prestwick Pharmaceuticals

Prestwick Pharmaceuticals, Inc. is a product-focused specialty
pharmaceutical company engaged in the development and
commercialization of drugs with high commercial potential and
relatively low development risk that target chronic diseases of the
central nervous system. To date, the company has in-licensed rights
relating to product candidates in clinical development for the
treatment of CNS disorders, including chorea associated with
Huntington's Disease, Parkinson's disease and schizophrenia.

In October 2004, Prestwick announced the results of its Phase III
study of tetrabenazine for chorea associated with Huntington's
Disease. The study was conducted in adults only. The company
anticipates filing a New Drug Application (NDA) for tetrabenazine
with the U.S. Food and Drug Administration (FDA) in the near future.
Prestwick was granted both fast track and orphan designation by the
FDA for tetrabenazine.

Source: http://www.genengnews.com/news/bnitem.aspx?
name=504053XSL_NEWSML_TO_NEWSML_WEB.xml

Paul Marshall
editor @ tourettes-disorder.com
http://www.tourettes-disorder.com

Morphine May Help Obsessive-Compulsive Disorder

-------------------------------
Post notes and editors comments before article.
-------------------------------

I post this for the simple fact that OCD and Tourette's can
generate
a disruption in a similar part of the brain. Sometimes what helps
one will also help the other, i.e. SSRI's used to treat both.

First Note,****** Haloperidol (Haldol) is a controlled substance
used to treat Tourettes which acts as a dopamine receptor blocker
and thus indicates that TS is based upon over-productive dopamine
neurons or oversensitive dopamine receptors. Drugs which stimulate
these neurons or receptors aggravate Tourette Symptoms, including
amphetamines, Ritalin, cocaine and morphine.*******

Key Note however, *******(In small doses morphine was observed to
reduce TS, yet is a dopamine stimulator, providing seeming
contradiction. However, this effect actually supports the evidence
since small doses binds first to the receptors, stimulating them and
comparatively inhibiting the neuron discharge. In higher doses it
binds to and stimulates the neurons, making the" symptoms worse.)
…

"Connections between TS and OCD include: Onset early in life,
lifelong development, waxing and waning, intrusive and ego-attacking
behaviors, bizarre violent and aggressive themes, family history,
aggravated by anxiety and depression, responds to medication, can be
caused by other neurological disruptions such as postencephalic
states and amphetamine overdose. In a study of OCD in 93 twins,
concordance was recorded in 70 percent of identical twins and only
15 percent in fraternal twins. All these twins lived separately and
were not aware of each others' symptoms, yet the OCD started at
their same ages and developed a very similar course. (16) Another
study reported 25 percent of OCD patients had a parent or sibling
with the disorder. (17)"


Paul Marshall
editor@...
Paul Marshall
editor@...
http://www.tourettes-disorder.com

---------------------------------

Morphine May Help Obsessive-Compulsive Disorder

NEW YORK (Reuters Health) - For people with obsessive-compulsive
disorder (OCD) who have not been helped by standard drug treatments,
a weekly dose of oral morphine may ease their symptoms, according to
a small pilot study.


The newer class of antidepressants known as SRIs is approved for
treating OCD, but up to 40 percent of patients fail to respond to
two or more of these drugs, Dr. Lorrin M. Koran and his associates
explain in the Journal of Clinical Psychiatry.


Quite why morphine can be effective is not known, but other small
studies have suggested a role for drugs that interact with opioid
receptors because there is a high concentration of opioid receptors
in an area of the brain thought to be involved in OCD.


For their trial, Koran's group enrolled 23 subjects with OCD who had
tried anywhere from two to six different SRIs. The participants were
assigned to once-weekly oral morphine, the anti-anxiety drug
lorazepam, or an inactive placebo, in random order for two weeks
each.


Average scores on a standard OCD scale declined from 29 to 25 while
the subjects were taking morphine, and to 27 in the lorazepam phase.


Seven of the 23 subjects were deemed to be responders to morphine
based on score decreases of 25 percent or more. There were four
subjects who responded to lorazepam.


Among those responding to morphine, the most noticeable effect began
the day after taking the drug and lasted for two to five days. These
individuals reported decreased frequency and persistence of
obsessions and anxiety, as well as an increased ability to resist
their compulsions.


The researchers saw no euphoric effects from taking the drugs --
although one subject later admitted to having abused hydrocodone for
several years, which he said reduced his OCD symptoms.


"The response seen, its rapidity, and the relative tolerability of
the treatment are encouraging and warrant larger and longer term
studies" of morphine or other opiate drugs for treatment-resistant
OCD, the team concludes.


SOURCE: Journal of Clinical Psychiatry, March 2005.

Study says Tourette drug did not cause death

BY EASHA ANAND
Staff Reporter

The death of a test subject in a Yale study was deemed unlikely to
be related to a trial drug for Tourette Syndrome, according to a
study due to be published this June.

The subject, a 34-year-old Tourette sufferer who died five years ago
from a heart attack, was one of 10 Tourette patients treated with
the antipsychotic ziprasidone, according to the paper.

Following audits by the Food and Drug Administration and Pfizer,
Inc., the makers of ziprasidone, the Yale School of Medicine's Child
Study Center group consisting of Lawrence Scahill NUR '89 EPH '97,
Jennifer Blair '97 MED '04, James Leckman and Andres Martin EPH '02
submitted the case report in early 2004.

"We did a bunch of things to reassure ourselves that we were putting
this together in the right way," Scahill said. "Unless we told the
story, the assumption might be that he passed away because of the
drug. We wanted to be transparent."

Deaths caused by drugs in clinical trials are very rare, Yale School
of Medicine Dean Robert Alpern said, because researchers
experimenting on humans have done everything possible to ensure the
drug's safety.

"Researchers bend over backwards to not put a patient at risk," he
said. "A lot of studies are done on animals before [researchers]
even go near a patient."

Ziprasidone, manufactured under the name of Geodon, was not
initially approved by the FDA because of fears of cardiac
complications, specifically disruption of the electrical signals
regulating heartbeat, Scahill said. But the coroner's report
attributed death to blockages of three of the individual's arteries.

Deanna Kelly, a professor at the Maryland Psychiatric Research
Center, said ziprasidone, like hundreds of other drugs, prolongs the
duration of electrical activity, known as the QT interval, that
causes the heart to contract. Though such prolongation could
hypothetically lead to Torsades de Pointes syndrome, a sometimes
fatal irregular heartbeat, extensive safety trials indicate the
danger is minimal, she said.

"There is a black box warning not to use this drug in combination
with other drugs lengthening the QT interval … but that is just a
cautionary measure," she said. "There have been no cases of this
arrhythmia occurring."

Ziprasidone is approved for treatment of schizophrenia in adults,
and Scahill's group was investigating its use in treating children.
The patient who died was the only adult involved in the study, which
included 24 individuals with Tourette Syndrome, autism or obsessive-
compulsive disorder.

"He had a very bad case of Tourette Syndrome and had been through
all the usual medications, which were only partially beneficial,"
Scahill said. "We helped wean him off the medications he was on, and
the ironic part is that he actually did much better on this drug."

Tourette Syndrome, a neurological disease characterized by sudden,
involuntary and repeated movements or vocalizations known as tics,
affects as many as one in 200 people.

The deceased patient had several risk factors for cardiac
complications, including a family history of cardiac arrest and a
smoking habit, according to the study. Scahill said though the
patient gained weight during the trial period, regular monitoring of
the patient indicated no abnormalities in his heart rate or
increases in fat or cholesterol in the bloodstream.

Ziprasidone is one of the newer, so-called atypical antipsychotics,
which are not associated with the extreme side effects of older
schizophrenia treatments. The drug is popular because it is not
linked to the cholesterol increases and cardiovascular risks of
other drugs, Kelly said, and some studies indicate ziprasidone may
improve a patient's cardiac health.

The School of Medicine is one of a number of research units funded
by the National Institute of Mental Health to develop guidelines for
the use of FDA-approved drugs in children.

"Historically, drug companies have been reluctant to do studies on
kids for a lot of reasons, not the least of which is the standard
criticism of, 'Why are you giving drugs to kids?'" Scahill said.

When the study began, ziprasidone had not been approved by the FDA,
and the Yale group made a special request to both Pfizer and the FDA
to allow it to experiment with the drug.

The Child Study Center is currently testing two other antipsychotic
drugs, risperidone and citalopram, on the same populations, Scahill
said.

---------------------------

Source:
http://www.yaledailynews.com/article.asp?AID=28955

-----------------------

Tourette-Updates
Paul Marshall
editor@...

Note * The company anticipates filing a New Drug Application (NDA)
for tetrabenazine with the U.S. Food and Drug Administration (FDA)
in the near future.


Prestwick Pharmaceuticals Launches NITOMAN -Tetrabenazine- Patient
Support Program in Canada; Drug Reimbursement and Pharmacist Support
Services Provided for Eligible Patients

DUNDAS, Ontario--(BUSINESS WIRE)--March 18, 2005--Prestwick
Pharmaceuticals Inc., a CNS specialty pharmaceutical company,
announced today the planned launch of the NITOMAN(R) Access Hotline
in Canada, a free telephone support service established to help
patients suffering from hyperkinetic movement disorders to explore
reimbursement options and obtain disease and treatment support in
relation to NITOMAN therapy.


NITOMAN, a dopamine depletor that works by selectively blocking
vesicular monoamine transporter 2 (VMAT2), is the only product
approved in Canada for the treatment of a series of hyperkinetic
movement disorders, including chorea associated with Huntington's
Disease, tardive dyskinesia and Tourette's syndrome. Approximately
50,000 Canadians suffer from these disorders, which are
characterized by excessive, involuntary and repetitive movements,
which may involve the face, limbs or the entire body.

Through the program, eligible patients will receive a free supply of
NITOMAN for six weeks. All patients will receive reimbursement
assistance, if required, which will include insurance benefits and
coverage verification, and prior authorization assistance.

Patient support services will include scheduled phone calls from
registered pharmacists to encourage compliance with the prescribed
dosing regimen and to discuss the potential side effects of therapy.
Additionally, to help ensure that patients receive optimal benefit
from treatment, pharmacists will collect information on dosing and
treatment experience for feedback to patients' physicians.

Patients or their physicians who are interested in initiating the
reimbursement assessment process should call the NITOMAN Access
Hotline at 1-888-NITOMAN (1-888-648-6626). NITOMAN therapy will be
provided to qualified Canadian patients who are in the process of
obtaining either public or private coverage, and meet the approved
indication for NITOMAN as well as the coverage criteria from
public/private payors.

Tetrabenazine

In 2004, Prestwick Pharmaceuticals acquired the rights from
Cambridge Laboratories Ltd., UK, to commercialize tetrabenazine in
Canada under the brand name NITOMAN. Tetrabenazine is available in
some European markets and New Zealand as XENAZINE(R). Tetrabenazine
can have a profound effect on chorea, with many patients
demonstrating marked to good improvement. Side effects can include
drowsiness, insomnia, akathisia and depression.

Prestwick Pharmaceuticals

Prestwick Pharmaceuticals, Inc., is an emerging specialty
pharmaceutical company that focuses on treatments for CNS disorders.
The company has multiple product candidates in clinical development
for Huntington's Disease, Parkinson's disease and schizophrenia. The
company anticipates filing a New Drug Application (NDA) for
tetrabenazine with the U.S. Food and Drug Administration (FDA) in
the near future. Prestwick was granted both fast track and orphan
designation by the FDA for tetrabenazine as a therapy for chorea
associated with Huntington's Disease.


---------------------------

Source:

-----------------------

Tourette-Updates
Paul Marshall
editor@...

Aripiprazole in a Patient Vulnerable to Side Effects

TO THE EDITOR: Although the involvement of infection/ inflammation
in the pathogenesis of Tourette's syndrome has been discussed,
antipsychotics are still the first choice in pharmacotherapy (1).
Haloperidol and pimozide are well-established therapies (2), but
increasing literature on this topic points out the advantages of
atypical antipsychotics, at least regarding side effects (3, 4).
Adherence to medication is a problem in Tourette's syndrome, often
because of the side effects that patients experience. In the
following, we describe a patient suffering from Tourette's syndrome
who withdrew treatment from different neuroleptics, thus leading to
severe social consequences for many years.

Ms. A, a 19-year-old patient, had suffered from motor and vocal tics
since the age of 6. Her vocal tics included grunting, snorting,
neighing, palilalia, and motor tics, such as beating and strangling
herself. Additionally, she developed compulsions of washing and
controlling. The course of her illness was chronic, not waxing and
waning. She had experienced no tic-free interval during the last 13
years. Pharmacotherapy over the last years included 300 mg/day of
tiapride, leading to an improvement of her motor tics only.
Additional therapy with 300 mg/day of sulpiride first and 400 mg/
day of amisulpride later each caused galactorrhea, without
substantial therapeutic effect. Ms. A stopped taking both
substances. Ms. A also stopped taking 4 mg/day of pimozide and later
80 mg/day of ziprasidone, each taken over several weeks; both caused
amenorrhea and had only marginal effects on the tics.

Afterward, we started treatment with 10 mg/day of aripiprazole
because of the side effect profile. In the first week, Ms. A's motor
and vocal tics showed a marked improvement; after 2 weeks, Ms. A was
nearly tic free for the first time in 13 years. Amenorrhea or
galactorrhea was not present during the next months; other side
effects, such as sedation or weight gain, did not occur. Ms. A
started working as a waiter for the first time. The compulsions were
much improved. Only a blinking tic, which exacerbated during stress,
persisted.

Aripiprazole is an antipsychotic with partial dopamine antagonism
and agonism, showing effects on serotonin 5-HT^sub 2A^ and 5-HT^sub
1A^ receptors. Its advantageous side effect profile has been
described earlier (5); however, no effects in Tourette's syndrome
have been observed. This case might encourage collecting not only
further experience with aripiprazole in the treatment of Tourette's
syndrome but in performing systematic studies in both short- and
long-term therapy.

References

1. Mller N, Riedel M, Zawta P, Gnther W, Straube A: Comorbidity of
Tourette's syndrome and schizophrenia: biological and physiological
parallels. Progr Neuropsychopharmacol Biol Psychiatry 2002; 26:1245-
1252

2. Sallee FR, Nesbitt L, Jackson C, Sine L, Sethuraman G: Relative
efficacy of haloperidol and pimozide in children and adolescents
with Tourette's disorder. Am J Psychiatry 1997; 154: 1057-1062

3. Robertson MM, Schnieden V, Lees AJ: Management of Gilles de la
Tourelle syndrome using sulpiride. Clin Neuropharmacol 1990; 13:229-
235

4. Sallee FR, Kurlan R, Goetz CH, Singer H, Scahill L, Law G,
Dittman VL, Chappell PB: Ziprasidone treatment of children and
adolescents with Tourette's syndrome: a pilot study. J Am Acad Child
Adolesc Psychiatry 2000; 39:292-299

5. McGavin JK, Goa KL: Aripiprazole. CNS Drugs 2002; 16:779-786

SANDRA DEHNING, M.D.

MICHAEL RIEDEL, M.D.

NORBERT MLLER M.D., PH.D.

Munich, Germany

Copyright American Psychiatric Association Mar 2005



Source: American Journal of Psychiatry, The





---------------------------

Source: http://www.rednova.com/news/display/?
id=137033&source=r_health

-----------------------

Tourette-Updates
Paul Marshall
editor@...

I am posting the following because it is just interesting reading.
It has some information in it regarding different types and reasons
for self-mutilation, which is not that common, though has been seen
in various Tourette Syndrome cases.

The self-abusive behaviors could include, head banging especially as
young children, hitting one's self, licking lips sometimes until
they
are bleeding and infected, washing hands until they are raw, constant
picking at sores, grinding and pulling teeth, biting hands, lips,
cheeks, nails or tongue until they bleed, Carving or serious
scratching of the skin, scraping or dragging toes.

Tourette-Updates
Paul Marshall
editor@...
  -----------------------------

Equine Self Mutilation
by: Sue McDonnell, PhD, Certified AAB
March 2000 Article # 3039


It's a beautiful winter weekend, and finally you have a full morning
to spend at the barn. You're happily grooming your horse when you
notice a cluster of patches of wet hair on his side. Peculiar pattern
to the wet hairs -- all are lying forward as if combed with a wet
brush. Oh well, odd but probably nothing, you think. But wait, some
of the wet spots have hairs missing or chopped off bluntly. You check
the other side, and there you find some more patches, like the wet
ones, but as if they have now dried. What's going on? There are more
of these patches on the left side than on the right side, but they
all are in the same area of the abdomen, from the ribs to the stifle.
Just then the barn manager comes in all excited. She's glad you're
there early today, because when she was feeding this morning, she
found your horse spinning in his stall, tearing at his blanket and
biting at his sides. Her first reaction was to scream at him to stop--
and he did. She figured the blanket was the problem, maybe it was
rubbing or pinching him under the leg. She got some help to
investigate. They couldn't find anything out of order with the straps
or the blanket, but took it off anyway. Then, just as they closed the
stall door, he really went nuts, spinning in a very tight circle,
biting his left flank. With each bite, he squealed and kicked out. As
he was turning and nipping, he sometimes was bucking and squealing.
They were too scared to open the door. He went on for what seemed
like forever, as if he wouldn't stop until he tore up the stall or
killed himself. Then he gradually came out of it.

"When we screamed his name, he turned toward the stall door, looking
at us with a sort of a worried, glassy eye, like he didn't know what
was happening. We threw him his hay, and he's been pretty quiet
since."

You run your fingers over the wet areas on his flanks and feel some
crusty bumps on the underlying skin. Separating the hairs, you can
feel little marks in the skin -- anywhere from one-quarter to one
inch in diameter. Some are fresh nicks, some are scabbed over, some
look healed. The rest of his coat is unblemished. No marks, no wet
spots, no chopped or missing clumps of hair other than on his flanks
and over his ribs.

So what is going on here?

This behavior commonly is called flank biting or flank sucking. The
biting is one aspect of a cluster of behaviors called self-
mutilation, because the horse likely will incur serious self-injury
during these explosive episodes.

In addition to biting the flanks, self-mutilation sequences can
include seemingly uncontrollable violent behavior. From horse to
horse, the sequence and form can vary, but most typically includes
spinning in circles, bucking, and kicking out with one or both back
legs while nipping at the flank, shoulders, or chest. In the photos
at the bottom of page 76, there is an example of a horse biting more
violently at his chest, and a resulting chest avulsion.
In extreme cases, the horse can violently lunge its body or head into
a wall or other solid object. More rarely, a horse might "throw
itself" to the ground (from standing to lateral recumbency). A single
episode can last from a few seconds to several minutes,
uninterrupted. The horse can work up a lather and steam in cool
weather. Episodes usually occur in a series separated by a few
seconds to a few minutes over a period of minutes, to hours. The
total daily time spent self-mutilating can vary from a few seconds to
an hour or more. In addition to bite wounds, the most common injuries
are to the legs and feet from the spinning and kicking.

Self-mutilation behavior of one form or another has been described in
many different species, including humans. Dog and cats lick and chew
on their paws or tails. People do all sorts of things--pull out their
hair, bite their fingernails or lips, scratch themselves, or
deliberately inflict burns, cuts, or other wounds.

People who have seen a horse in the midst of attacking itself often
describe the episodes as the most bizarre animal behavior they ever
have seen. Mental health professionals or others with first-hand
experience with human psychopathology often ask whether this might be
the horse equivalent of severe neurotic or even truly psychotic
behavior seen in people. For example, Dr. Nicholas Dodman, a
veterinary animal behavior specialist at Tufts New England Veterinary
College, said he has wondered whether certain forms of self-
mutilation in horses might be similar to Tourette's Syndrome in
humans. There are some interesting similarities, and some clear
differences.

Since self-mutilation occurs in other animal species and a variety of
human psychopathologic syndromes, it's probably too early to conclude
that any of the self-mutilation seen in horses represents the same
pathology as Tourette's in people. In other species, the trend in
clinical veterinary behavior has been to label self-mutilative
behavior "obsessive-compulsive disorder," or OCD.

This syndrome in humans has two distinct components. One component is
the compulsive, repetitive behavior, such as repeatedly checking to
see if the stove has been left on. The other component is the
accompanying obsessive thoughts or worries, such as concerns about
being caught in a burning building. Often the thoughts or worries are
related to the compulsive behavior and logically appear to drive it.
In the case of animals, we don't know whether they think or worry, so
this label of obsessive-compulsive behavior might be too elaborate.
Some behaviorists now are calling these behaviors in animals simply
compulsive behavior.

There are at least three distinct types of self-mutilative behavior
in horses. One type is simply an "extreme" behavioral response to
physical discomfort. We know that physical pain alone, particularly
in the abdominal area, can evoke behavior similar to that of the
horse in the situation described above. We know it is physical pain
because coincident with finding and correcting an apparently or
potentially painful condition, the self-mutilative behavior stops
without any other treatment. For example, the classic behavior we
associate with colic or early labor in broodmares involves turning
the head back toward the flank, either looking or nipping at the
flank, and sometimes kicking out. Although it is not as common, some
horses' behavioral response to physical pain has more violent
episodes, including spinning, kicking, bucking, and serious self-
biting. Some of the less-common physical root causes for violently
colic-like behavior have been a twisted testicular cord, an abdominal
abscess, urethral tears, or gastric ulcers. These sometimes can be
intermittent and difficult to find. This is in contrast to the other
types of self-mutilation. When there is a physical cause, there often
is an increase in the behavior in association with work. The most
explosive episodes might be during or soon after work. As time goes
on, the horse might anticipate the exacerbation of pain with work, so
can become agitated when being prepared for work.

A second type of self-mutilation is what could be called self-
directed intermale aggression. This type occurs in stallions and
geldings. The sequence follows what two stallions at liberty would do
when meeting, except that the stallion himself is the target of his
own behavior. When stallions meet, they typically stand parallel to
one another, head-to-tail. They investigate each other's flank area,
usually sniffing and nipping at the flank and genitals. The encounter
can be pretty noisy. The stallions usually squeal and kick out with
each nip or bite. They also might spin, buck, stomp, and romp, going
around one another in circles. The sniffing of each other's flank and
genitals, and of each other's feces, is an important trigger for the
nipping and biting.

Sometimes the self-mutilation process begins over a stud pile. In the
stallion which is sniffing and biting himself, each episode begins
with the sniffing of his own feces or feces of other stallions in
shared turn-out facilities. Oily body residues on stall walls,
fences, or doorways can trigger episodes. We have seen several cases
of self-mutilation that appeared to have started when a stallion was
exposed to the smelly residues of another stallion in a trailer.
Unlike the pain-related self-mutilation, this type usually develops
over a period of months. It can start as early as the first year of
life or as late as the teens. It typically continues for the life of
the stallion.

A third type of self-mutilation is a more quiet, rhythmic, repetitive
nipping at various areas of the body. It looks similar to stereotypic
weaving or stall walking in that it appears that the horse has
nothing better to do. By formal definition, stereotypic behavior is
characterized by repetitive, highly stylized, and seemingly
functionless movements and sequences of movements.

Spanning the top of pages 76 and 77 is a series of photos of a
stallion which had a very fixed pattern of biting himself from flank
to shoulder to chest to opposite shoulder to opposite flank and on
and on. He did it at the same place in the pasture at the same time
of day for the same length of time, just as some horses walk their
stall in very complex and fixed patterns day after day.
Stereotypies occur in one form or another in all captive wild and
domestic animal species, and are a common feature of human
psychopathology, as well as developmental and neurologic disorders.
Subadequate environment and nutrition seem to be the major factors
predisposing animals to stereotypies.

In horses, the classic stereotypies are cribbing, weaving, pacing,
stall-circling, and head-shaking. Certainly, in cases in which a
physical root cause is not apparent, self-mutilation fits this
definition of a stereotypy. Of course, the performance of a
stereotypy, no matter what the initial precipitating cause, is self-
rewarding. Endorphins are released, and they can be positive
reinforcement sufficient to sustain the behavior as a habit. We often
wonder if self-mutilation, for which we can find no contemporary
physical cause and that doesn't quite fit the self-directed intermale
aggression type, might have started during a period of physical
discomfort, but now is a lingering habit.

How Common Is Self-Mutilation?

It's very difficult to estimate how many horses suffer from self-
mutilation. My guess would be that the problem occurs in less than
0.005% of all horses. Most equine veterinarians might see only a few
cases in their entire careers. Self-mutilation can occur in
stallions, mares, and geldings. Of course, the self-directed
intermale aggression type is almost always in stallions and geldings.
We don't know whether or not the predisposition for self-mutilation
is highly heritable. We know that the behavior probably is the result
of domestic environmental and nutritional factors, in that it
apparently does not occur in wild or feral horses.

Where Does It Hurt?

For those horses whose self-mutilation episodes looks like a violent
form of colic, it is critical to look for and immediately treat any
possible causes of discomfort. Except for classic colic, this often
is easier said than done. It sometimes can be tough to find (see the
boxed table of examples of possible physical causes of discomfort on
page 74). No matter what the slickest animal psychic would have us
believe, our animals, like human infants, have only their non-verbal
behavior as clues to tell us where they hurt. After years of losing
sleep trying to find causes of self-mutilation in horses, I think our
best hope for figuring out potential physical sources of discomfort
that might be provoking episodes of self-mutilation turns out to be
pretty inexpensive and very low tech. It is simply to critically
observe the horse for hours at a time. This can be done live, but
there are many advantages to video recording the behavior.
Long, continuous observation periods allow the horse to go back to
its ongoing behavior, as opposed to being distracted by human
presence. Long observation periods also will enable you to see how
the self-mutilation episodes start and stop, and what in the
environment might provoke them. When casually watching a self-
mutilating horse, your attention is drawn to the noisy, more violent
episodes. When watching the horse continually for hours, you likely
will see mild and violent episodes. The milder episodes often are
more useful than the explosive episodes in localizing potential sites
of discomfort.

Once you have a clue as to where the pain might be, you can be
aggressive with veterinary diagnostics. This might include classic
radiography, scintigraphy, endoscopy, and ultrasound imaging.
Even if it appears to be a classic stereotypy, or a psychological
behavior problem, we should never stop looking for a possible
physical cause. A great example illustrating this point in horses is
the case of head shaking behavior. For many years, veterinarians have
looked for possible sources of discomfort in cases of head shaking.
Many times a source could be found--things like ear mites, tooth
abcess, guttural pouch problems, or allergies. But many times,
nothing physical could be found and it was assumed that the problem
was psychological. Only a few years ago did scientists in the United
Kingdom and California find that some headshaking in horses appears
to be induced by bright light or loud sound. It is a real physical
problem involving hyperactivation of a nerve tract that is physically
irritating to the horse. (See The Horse of October 1996, page 70.)

What Else Can You Do?

The best outcome of immediate and aggressive veterinary evaluation is
to identify and quickly treat a physical cause. An equine behavior
specialist can be a valuable member of a veterinary team. By
evaluating the behavior, possible sites of discomfort can be
identified, and an opinion can be offered on primary or secondary
psychological components to the episodes. If physical discomfort is
eliminated, the self-mutilation typically stops almost immediately.
We have seen cases in which months or years passed before a root
physical cause was found, in which the self-mutilation stopped
immediately when the discomfort was alleviated.

Unfortunately, often a physical cause is not found and the conclusion
is drawn that this is the self-directed intermale aggression type, or
is simply a stereotypy. Over the years, mostly by trial-and-error, we
have found a number of different treatment approaches, each of which
typically is either helpful, or at least does not exacerbate the self-
mutilation. Most are simple management changes that seem to work by
distracting the animal to another activity; some involve
sophisticated pharmacology.

Physical restraint Traditionally, a large percentage of the effort,
thought, and expense of treatment of self-mutilation has involved
various methods of physically preventing or discouraging the
behavior. This often is the first thing you will want to consider
while further evaluation is organized. Special neck cradles and side
poles, grazing muzzles, bibs, and protective wraps and blankets can
be used to prevent injury. Physical restraint alone rarely "cures"
self-mutilation. All too often when the horse is effectively
restrained from performing one behavior, another problem behavior
develops. If biting is prevented, the horse might start kicking or
lunging into walls. In the short term, while looking for and treating
possible causes, it is wise to creatively work at keeping the animal
from further injury.

For any restraint, care must to taken in devising materials that
don't cause new rub sores or other irritations. My favorite of all
the restraints for self-biting is the grazing basket shown on page
78. The horse effectively can eat hay and grass through the openings.
The basket inhibits a substantial grab of flesh, although the
persistent horse still can work a small nip of hair or skin through
the basket openings.

Social, feeding, and work distractions Typically, the most effective
management changes are those that seem to provide motivation for a
substitute behavior or a strong distraction to focus on something
else. For a stallion, self-mutilation sometimes can be relieved
significantly if the stallion is turned out to live in a large
pasture with one or more mares. In that situation, the stallion
becomes a harem stallion with great responsibility to herd and defend
the mares. Those harem maintenance behaviors seem to occupy the
stallion's time and distract him from the problem behavior. If he is
not supplemented with concentrated feed, his grazing and resting
fully occupy the remainder of his time.

Of course, this often is not a plausible solution for the fancy
breeding or busy performing stallion. There might be some difficulty
and danger in taking such a stallion or his mares in and out of such
a situation. Most stallions will not want to leave their mares. But
to the extent that the stallion can be distracted socially, in some
cases it is worth trying.

Horses appear to find meaningful social companionship from animals of
other species. Donkeys, goats, rabbits, and even chickens are useful
as stall or pasture companions. In my experience with chickens as
stall companions for self-mutilators, it seems that the horse
sometimes is reluctant to move around the stall, lest it cause the
chicken to scurry and flutter. Some stallions also seem distracted by
their effort to avoid stepping on the chicken.

Another effective distraction for many self-mutilators is a vigorous
appetite. A change in diet from one heavy with grain to one of grass
and grass hay only (without any grain or richer forage) often can
lead to a remarkable change in behavior. The horse might spend almost
all of its time eating and resting, with seemingly no time for
anything else, including self-mutilation. A grazing muzzle like the
one described earlier can effectively prolong the eating time.
The all-grass, no-grain diet might have other benefits for behavior.
We know from work in horses and other grazing species that grain
diets predispose an animal to stereotypies and other behavior
problems. The grain diet might alter the brain neurochemistry,
setting the animal up for developing abnormal behavior. We long have
appreciated that grain increases the risk of behavior problems and
high-forage diets reduce the risk of behavior problems.

Work For the self-directed intermale aggression type of self-
mutilation, the behavior seldom is seen during work. Moderate work
also stimulates appetite. A horse which works one to two hours a day
and which is fed ad lib grass and grass hay almost always will spend
60% or more of his time eating and 20% of his time resting. This
approaches the natural time budget of a horse at liberty or in the
wild. Breeding work sometimes reduces and sometimes increases the
frequency and intensity of self-mutilation.

Gelding stallions? For the self-directed intermale aggression type
self-mutilating stallions, some veterinarians recommend castration,
and in some cases it works very well. Unfortunately, it also can get
worse or won't change. When advising clients on this option, I always
am reminded of the dozen or so geldings we have known which seemed
normal as colts, but were first seen to self-mutilate soon after
castration.

Medications Pharmacologic aids, which in some cases have appeared
helpful in relieving self-mutilation, include long-acting
tranquilizers, tricyclic anti-depressants such as imipramine and
clomipramine, progesterone, and the nutritional supplement l-
tryptophan. Some of these have been discovered by accident and some
are based on theories of brain neurochemistry. None of these
medications alone or in combination is likely to eliminate self-
mutilation completely. The particular choice depends on the severity
and nature of the self-mutilation. In combination with management
changes, medications often are judged to be valuable parts of the
plan to eliminate self-mutilation. The tendency is for people to over-
estimate their potential. An important concern for clinicians who
medicate the horse early in the evaluation is that the drugs might
help a horse to cope with physical discomfort, thus could effectively
mask the symptoms and delay diagnosis of a treatable physical
problem.

Other treatment tips For horses whose self-mutilation seems to be
triggered by male odors and feces, any number of creative steps can
be taken to reduce the stimulation. Odor-masking preparations can be
applied to the nostrils, the horse can be bathed frequently, and
feces and oily residues can be removed from stalls and pastures.
Sometimes, the sight or smell of another stallion seems to provoke
episodes. Housing changes can reduce the frequency and severity of
self-mutilation.

In our clinic we find that long-term video surveillance of the horse
can reveal events and situations that provoke the behavior. Often
these "provokers" can be simply and inexpensively eliminated. For
example, occasionally you find a horse which only bites himself when
the feed cart is coming down the aisle, or when other stallions are
on their way to the breeding shed.

Tie-stalls For reasons I'm not sure we ever will understand, simply
housing a horse in a tie-stall can effectively eliminate self-
mutilation. Recent work with tie-stalled horses in the pregnant mare
urine industry has indicated that abnormal behavior in general is
very low in tie-stalled horses compared to box-stalled horses.
No one treatment alone is likely to be effective. The cases for which
the greatest relief has been achieved have involved simultaneously
implementing as many of the treatment steps as possible. We recommend
spending time with your veterinarian to develop a custom plan based
on everything you know about the horse. Once everything is organized,
we recommend implementing all the changes and treatments at once.
This is not good science in that you might never know which of the
changes were most effective, but experience has taught us that major
change often is more effective than a systematic, step-wise approach.
In summary, we really know very little about the causes of self-
mutilation, other than physical discomfort. It is important to
realize that except for those cases for which a physical discomfort
can be identified and eliminated, the self-mutilation likely will
never be cured. The current treatments for the self-directed
intermale aggression and stereotypy types of self-mutilation rarely
effect a cure. At best, diligent attention and care will keep the
levels of injury low.
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Source:   http://www.thehorse.com/viewarticle.aspx?ID=3039

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Tourette-Updates
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HOUSTON – (Dec. 17, 2004) – The cosmetic cure-all Botox may have
found another market: sufferers of Tourette's syndrome.

Researchers at Baylor College of Medicine in Houston are using
botulinum toxin type A (Botox) to treat the neurological disorder,
which can cause involuntary motor and vocal tics. Dr. Joseph
Jankovic, professor of neurology and director of the Parkinson's
Disease Center and Movement Disorders Clinic at BCM, was the lead
author of a recent article in Clinical Neuropharmacology, which
showed that Botox can suppress tics in disorders like Tourette's.

"While we have an enormous amount of data showing that Botox is an
extremely safe and effective treatment for a variety of therapeutic
and cosmetic uses, the important thing for patients is whether this
translates into meaningful improvements in their daily lives,"
Jankovic said. "Our review makes clear that treatment with Botox
accomplishes this across a wide range of chronic and debilitating
disorders and conditions."

Although public awareness about Tourette's has generally improved
since medieval times – when it was thought to be demonic possession –
the disorder remains largely elusive to researchers and greatly
misunderstood by the masses.

"We still don't know exactly what causes Tourette's syndrome, but we
do know that it is a genetic disorder," Jankovic said.

Unlike most genetic disorders, Tourette's is caused by bilineal
transmission, a rare event in which both parents contribute defective
genes to their child. Nevertheless, Tourette's syndrome remains
relatively prevalent: roughly three percent of the population carries
some form of the disorder, according to Jankovic.

"We have made tremendous progress with treatments, and even though we
don't know the cause of the disease, we are able to significantly
improve the quality of life for patients with Tourette's syndrome by
a variety of medications," he said.

A common misperception of Tourette's is that coprolalia, the
involuntary utterance of obscenities, is the predominant symptom,
when actually less than half of all patients exhibit it. Furthermore,
most people with Tourette's develop other behavioral problems such as
attention deficit disorder and obsessive compulsive disorder.

In addition to Botox, medications like fluphenazine, pimozide and
risperidol, which block dopamine receptors, suppress involuntary
movements. Jankovic is also conducting studies with other drugs
including tetrabenazine, an investigational drug that depletes
dopamine, and topiramate, an anti-epileptic drug. Finally, new
surgical procedures developed at BCM and The Methodist Hospital hold
promise for curbing uncontrollable tics and other neurological
problems associated with Tourette's.

"Tourette's clearly deserves more attention than it has been paid by
either the scientific community or the funding agencies," Jankovic
said. "For every patient we diagnose in our clinic, there are
probably dozens who suffer the consequences of Tourette's syndrome
without knowing that they have it."

As part of an initiative to spread public awareness and dispel false
notions about the disorder, a biannual conference organized by
Jankovic and other BCM physicians targets both medical professionals
and lay audiences.

The "Tourette Syndrome and Related Neurobehavioral Disorders
Conference" will be held Jan. 14 at the InterContinental Hotel in
Houston and features internationally recognized speakers. The
conference will focus not only on tics but other problems associated
with Tourette's syndrome, including attention deficit disorder,
obsessive compulsive disorder, loss of impulse control, and other
behavioral co-morbidities. For further information about the
conference, contact Baylor Office of Continuing Medical Education at
713-798-8237.

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Brain region identified that controls collecting behavior

Perhaps the Beanie Baby craze wasn't so weird after all.
Most people have a collection of some kind at some point in their
lives. Indeed, historical studies show that acquiring and retaining
objects, even when they are not necessary for survival, is not only
nearly universal, but also has been part of human behavior since the
earliest human societies. Yet despite the ubiquitous nature of this
trait, very little is known about what drives humans to collect.
By studying patients who developed abnormal hoarding behavior
following brain injury, neurology researchers in the University of
Iowa Roy J. and Lucille A Carver College of Medicine have identified
an area in the prefrontal cortex that appears to control collecting
behavior. The findings suggest that damage to the right mesial
prefrontal cortex causes abnormal hoarding behavior by releasing the
primitive hoarding urge from its normal restraints. The study was
published online in the Nov. 17 Advance Access issue of the journal
Brain.

Hoarding behavior is common among animals; around 70 species hoard
and mostly they hoard food, which makes sense from a survival
standpoint. Studies of hoarding behavior in rodents have shown that
collecting is driven by certain primitive structures deep in the
brain and most mammals, including humans, share these subcortical
regions.

"But human collecting goes beyond items that are solely useful for
survival," said Steven Anderson, Ph.D., UI associate professor of
neurology and lead author of the study. "People often collect art or
stamps or pretty much anything. Clearly there is some higher
structure in humans that modulates the collecting drive and that's
what we think we have tapped into."

The UI team studied 86 people with focal brain lesions - very
specific areas of brain damage – to see if damage to particular
brain regions could account for abnormal collecting behavior. Other
than the lesions, the patients' brains functioned normally and these
patients performed normally on tests of intelligence, reasoning and
memory.

A questionnaire completed by a close family member was used to
identify problematic collecting and the behavior was classified as
abnormal if the collection was extensive; the collected items were
not "useful" or aesthetic; the collecting behavior began only after
the brain injury occurred; and the patient was resistant to
discarding the collected items.

The questionnaire very clearly split the patients into two groups –
13 patients who had abnormal collecting behavior and a majority (73
patients) who did not. Unlike normal collecting behavior such as
stamp collecting, the abnormal collecting behavior of these patients
significantly interfered with their normal daily life. Patients with
abnormal collecting behavior filled their homes with vast quantities
of useless items including junk mail and broken appliances. Despite
showing no further interest in the collected items, patients resist
attempts to discard the collection.

To determine if certain areas of damage were common to patients who
had abnormal collecting behavior, the UI researchers used high-
resolution, three-dimensional magnetic resonance imaging to map the
lesions in each patient's brain and overlapped all the lesions onto
a common reference brain.

"A pretty clear finding jumped out at us: damage to a part of the
frontal lobes of the cortex, particularly on the right side, was
shared by the individuals with abnormal behavior," Anderson
said. "Our study shows that when this particular part of the
prefrontal cortex is injured, the very primitive collecting urge
loses its guidance.

"This finding sheds some light on a ubiquitous, nearly universal
human behavior that we really don't know much about, and we can use
this as springboard to think about normal collecting behavior."

Anderson added that the findings also may have implications for
understanding certain neurological conditions such as obsessive-
compulsive disorder (OCD) where abnormal collecting behavior occurs
but the patient has no readily detectable brain defect.

"Patients with OCD and some other disorders such as schizophrenia,
Tourette's syndrome and certain dementias, can have similar
pathological collecting behavior but we don't have a pointer to
locate where in the brain the problem is occurring," Anderson
said. "Our hope is that our findings with these brain lesion studies
will lead to insights in these conditions as well."

Anderson's co-authors on the study were Antonio Damasio, M.D.,
Ph.D., the Maurice Van Allen Professor of Neurology and head of the
department, and Hanna Damasio, M.D., UI Foundation Distinguished
Professor in the Department of Neurology. The study was funded in
part by a grant from the National Institute of Neurological
Disorders and Stroke.

University of Iowa Health Care describes the partnership between the
UI Roy J. and Lucille A. Carver College of Medicine and UI Hospitals
and Clinics and the patient care, medical education and research
programs and services they provide.

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Iowa City, Iowa 52242-1178
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Habit Learning Impaired in Tourette Syndrome

Children and adults afflicted with the tic-causing disease known as
Tourette syndrome have a harder time with tasks requiring habit
learning, report investigators publishing in this month's Archives
of General Psychiatry.

The finding could lead to an animal model of the disease that
researchers could use to study the areas of the brain affected by TS
and to come up with new medications aimed at treating its symptoms.

The study was carried out among 56 children and adults with TS and
67 healthy children and adults who served as the study controls. All
were given a standard test designed to measure people's ability to
learning through habit. Participants also took tests to see how well
they learned through declarative memory functioning, which includes
memorization of facts, words and experiences.

Results show people with TS had a significantly harder time learning
with the habit test than the healthy controls, and learning ability
decreased with the severity of TS symptoms. Conversely, TS
participants scored about the same as healthy controls on tests that
measure the ability to learn via declarative memory functioning.

The researchers believe further study of habit learning in animal
models of TS offers "the exciting promise not only of improving our
knowledge of the neurobiological origins of TS but also of
developing novel therapeutics through bona fide translational
research programs and methods that are not available to human
clinical studies alone."

----------------------------------------------------------------
SOURCE:(Ivanhoe Newswire)Reported December 9, 2004
http://www.ivanhoe.com/channels/p_channelstory.cfm?storyid=10122
----------------------------------------------------------------

2nd Source Content

Habit Learning in Tourette Syndrome
A Translational Neuroscience Approach to a Developmental
Psychopathology

Rachel Marsh, PhD; Gerianne M. Alexander, PhD; Mark G. Packard, PhD;
Hongtu Zhu, PhD; Jeffrey C. Wingard, MPhil; Georgette Quackenbush,
BA; Bradley S. Peterson, MD


Arch Gen Psychiatry. 2004;61:1259-1268.

Background  The etiology of Tourette syndrome (TS) involves
disturbances in the structure and function of the basal ganglia. The
basal ganglia mediate habit learning.

Objective  To study habit learning in persons with TS.

Design  Patients with TS were compared with normal controls in
performance on a probabilistic classification, or habit-learning
task (weather prediction).

Setting  University research institute.

Participants  One hundred twenty-three children and adults, 56 with
a diagnosis of TS and 67 healthy control subjects.

Main Outcome Measures  Habit learning was assessed by the extent of
improvement in accuracy of predictions and reaction times over trial
blocks during performance of the weather prediction task.
Declarative learning was assessed by performance on 3 tasks that
required intact declarative memory functioning.

Results  Children with TS were impaired at habit learning relative
to normal controls (P = .01). This finding was replicated in the
independent sample of adults with TS (P = .01). The rate of learning
correlated inversely with the severity of tic symptoms across both
samples (r = –0.34; P = .01). Thus, impaired learning accompanied
more severe symptoms. Measures of declarative memory functioning, in
contrast, were normal in the TS groups.

Conclusions  Striatal learning systems are uniquely dysfunctional in
both children and adults with TS. The correlation of habit learning
with symptom severity suggests that the number and severity of tics
are a function of the degree to which the system for habit learning
is dysfunctional. Thus, both the deficits in habit learning and the
tic symptoms of TS are likely to be consequences of the previously
reported anatomical and functional disturbances of the striatum in
children and adults who have TS. The existence of a well-developed
animal model for this learning system, which permits study of the
neural and molecular bases of habit learning, has important
implications for the neurobiological study of TS and for the
development of new or improved therapeutics for this condition.


Author Affiliations: Division of Child and Adolescent Psychiatry in
the Department of Psychiatry, New York State Psychiatric Institute
and College of Physicians and Surgeons, Columbia University, New
York (Drs Marsh, Zhu, and Peterson and Ms Quackenbush); Department
of Psychology, Texas A&M University, College Station (Drs Alexander
and Packard); and Department of Psychology, Yale University, New
Haven, Conn (Mr Wingard).



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Solving a medical mystery

Winter 2004/05

For the vast majority of people, a sore throat is no more than an
irritation that lasts a few days. But in a minority of cases — and
more frequently in children — a throat infection caused by
streptococcus bacteria can lead to devastating brain damage…

Paediatric neurologist Dr Russell Dale was working at Great Ormond
Street Hospital when he was struck by the terrifying and dramatic
nature of the symptoms he was seeing in some of his patients.
Previously healthy children would suddenly develop movement and
psychiatric disorders, to the extent that their parents described
them as having `changed personality overnight'.

Often these children required hospitalisation. Dr Dale started to
research the area in his spare time, but what began almost as a
hobby became more and more important to him, eventually leading to
an application for an Action Medical Research grant. "Having seen
the terrible effects on children, and their parents, I wanted to
understand what causes these brain disorders and do my best to
help," says Dr Dale.

Three years on, Dr Dale's research at the Neuroimmunology Unit in
London's Institute of Neurology has formed part of a great leap
forward in the medical world's understanding of this phenomenon. His
work may lead to treatments for a wide range of physical and
psychiatric disorders, from tics and obsessive behaviour to
Tourette's syndrome, Parkinson's disease and encephalitis lethargica
or `sleepy sickness'. And it is all due to a grant of Ł141,000 from
Action Medical Research.

What's the connection?
It seems incredible that something as banal as a sore throat might
cause brain damage. Dr Dale explained to Touching Lives how this can
happen: "When you get an infection of any sort, the body produces
antibodies to try to fight it off. The antibody usually recognises
which cell to attack by the kind of protein found on the cell's
surface.

"What we found in the laboratory stage of our research is that the
proteins on the surface of streptococcus bacteria are very similar
to those on the surface of brain cells. This means that antibodies
produced when you get a streptococcal throat infection can `cross-
react' — the antibodies produced to fight the sore throat attack the
brain as well. It's basically the body making a mistake and
overreacting. It thinks the brain cells are foreign, whereas in fact
they're not."

A wide range of symptoms
The particular range of symptoms is the result of damage to a part
of the mid brain called the basal ganglia, which seems particularly
vulnerable to the antibodies produced. "This part of the brain co-
ordinates and sends out information," says Dr Dale. "It acts as a
modulator, regulating the quality of movements and emotions."

So when this balancing system is damaged, both movements and
emotions are unregulated and can become extreme or unpredictable.
That's why the physical symptoms of the disease include the body
either making extra movements or moving too quickly, resulting in
tics or similar repeated movements, or moving too slowly, resulting
in the stiffness associated with, for example, Parkinson's disease.

Alongside these physical changes are arguably more important
psychiatric symptoms. Sufferers experience emotional changes,
including extreme anxiety, obsessive behaviour and depression. And
what makes these changes even more traumatic is the speed with which
they come on. "There's usually a lag of about two weeks between the
infection and the onset of the symptoms. But when they arise, the
onset is explosive — previously healthy children can suddenly become
very ill. Some even have to be hospitalised. It's extremely
distressing both for children and parents. And that's in part what
motivated me to do this research."

Developing a test, minimising suffering
What's so important about this new discovery is that bacterial
infections, and the antibodies they produce, are relatively easy to
treat. "The general aim of treatment is to remove the antibodies,
which can be done in two ways," says Dr Dale. "Steroids can be used
to suppress the immune system generally, so that fewer antibodies
are produced. But these are quite toxic drugs, with unpleasant side-
effects.

"Alternatively, more specific treatments can be used to remove just
the antibodies — that's a `cleaner' treatment with fewer side-
effects. There is now a test which looks for these antibodies so
that we can treat them directly, but it's very complicated and
expensive to administer, so we're looking for one we could use on
lots of patients. Ultimately an antibiotic could be developed to
reduce the brain damage and improve the patients' condition."

Not everyone who suffers from these disorders will end up with
permanent damage. The earlier they are treated, the less likely it
is that permanent damage will occur — which is why a test of the
kind Dr Dale is looking for is so important. And children are in
fact more receptive to treatment than adults. This is because, up to
the age of about 11, children's brains are more `plastic' than
adults' brains, which means that the brain is more able to take on
different roles and so respond quickly to treatment.

An historic discovery
Dr Dale's work forms part of a distinguished strand in the history
of medical research. "The idea of infection leading to a brain
disorder is very old," explains Dr Dale. "It's been known for over a
hundred years that one particular brain disorder, called Sydenham's
Chorea, is linked to streptococcus. What wasn't known before was how
many other types of brain disorder might be triggered by this sort
of infection."

After clinical work with 60 children with a variety of brain
disorders, together with his laboratory-based research, Dr Dale has
established a connection between the antibodies produced after
streptococcal infection and brain cell death in a much wider range
of conditions than was previously recognised. "This wider
recognition is very important for accurate diagnosis," says Dr
Dale. "Now, a child with any type of movement or psychiatric
disorder after a streptococcal throat infection will be examined for
these antibodies. And given how widespread some of these disorders
are, this could be relevant for up to one per cent of the
population."

What next?
This is only the beginning of the story for Dr Dale. There are still
a number of questions to be asked — why, for example, is it only the
streptococcal infection which causes sore throats that trigger this
brain damage, and not the other common streptococcal infections? "We
still don't understand the brain very well," says Dr Dale, "which is
one of the reasons I chose to specialise in neurology — it's a
fascinating area, with lots of scope for work in the future. And I
wanted to work in paediatrics in particular because working with
children and their parents is so much fun! I've had very positive
experiences as a paediatrician, and you feel you're doing good."

The importance of the Action Medical Research grant to Dr Dale's
work can't be overestimated. "I'm overwhelmingly grateful to the
Charity for supporting this project. Having seen the effects of this
disorder on sufferers, I know how important it is to try to find a
treatment. We simply wouldn't have been able to do this without
Action Medical Research."

Medical Mysteries
Dr Dale's work was featured on the BBC documentary `Medical
Mysteries' earlier this year. The documentary explored a particular
condition called encephalitis lethargica, or `sleepy sickness',
which causes a range of extreme symptoms, including paralysis,
uncontrollable movements, and speech disorders.

Sleepy sickness was brought to popular attention by the Hollywood
film `Awakenings' starring Robert de Niro. It had been thought that
the disease died out after the last major outbreak in the 1920s. But
the BBC programme picked up on a number of cases which have suddenly
appeared over the last few years, and explored the work being done
to try to explain the condition.

The programme featured Dr Dale explaining his alarm at coming across
patients with encephalitis lethargica — a disease he thought he
would never see. And when he let the medical community know that he
was interested in studying the disease, many more cases came to
light. It had long been thought that, as with Sydenham's Chorea,
there was a link between encephalitis lethargica and some kind of
infection — influenza was at one point the prime suspect.

But when he looked for a common factor, Dr Dale found that half the
patients with encephalitis lethargica had reported a sore throat
before they developed the disease. It was this that triggered Dr
Dale to consider streptococcus, the commonest cause of sore throats,
as a possible cause. And sure enough, blood tests showed that every
patient had been infected by a particular strain of streptococcus —
an invaluable insight into the cause of this devastating disease.

The eminent neurologist Dr Oliver Sachs (author of `The Man Who
Mistook His Wife for a Hat') was featured talking about his life-
long work with sufferers of encephalitis lethargica, and hailed Dr
Dale's work as "brilliant, and original, and maybe revolutionary."

Thanks go to the Barnwood House Trust for their support of this
grant.

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Tourette's Patient Hopes Surgery Holds Cure
Nov. 11, 2004
Ed Yeates Reporting

Imagine muscle spasms so bad it's like doing uncontrollable,
exhausting high impact aerobics 24 hours a day. That's what a Utah
man is going through right now - and why a Cleveland hospital wants
to try an experimental procedure that just might cure him.

If I was in Peter Jensen's shoes right now, I might suddenly, and
without warning, break into violent muscle movements. The spasms
coming through my voice would also make it so I could no longer talk
to you.

Peter Jensen's physical and vocal tics are so bad, so continuous, he
sweats profusely. He wears loose clothes and no shoes, trying to
keep his body from overheating -- even going out on the patio in the
winter to cool down.

Peter Jensen: "I'm gone by the end of the day. I mean I have a
headache. It's just so overwhelming."

Peter has Tourette Syndrome, one of the worst cases Dr. Jason North
has ever seen. Though this young 29-year old father of four is
trying to finish school, he can't hold onto a job to support his
family.

Peter Jensen: "Constant effort to get each word out, to just talk."

Tourette Syndrome produces a chemical overload of signals in the
brain. The body can't handle them and goes into spasm. One minute
you're talking and functioning normally, the next you're not.

Peter weighs only 118 pounds right now because in between trying to
control the tics and eat, by the time he's finished he's lost his
appetite.

Earlier this year, surgeons at University Hospital in Cleveland,
Ohio, performed an experimental surgery on Tourette victim Jeff
Matovic. They implanted electrodes deep inside his brain, connecting
them under the skin to pacemaker devices on each side of the upper
chest.

After the surgery Jeff was 85 to 90 percent tic free. For the first
time he could walk and sit in a chair. When Peter saw what
happened..

Peter Jensen: "Honestly, I wept. I was so overcome that I wept."

Now, pending FDA approval, Peter could become only a handful of
Tourette patients in the United States to undergo the same
experimental surgery.

Peter Jensen: "I think that would be a wonderful thing."

Roshana Jensen, Peter's Wife: "It's going to be a pretty incredible
change when it does happen."

Dr. North says it's only a matter of time now until Peter's body
wears out. His options are running out.

Dr. North: "This is pretty much the last straw."

Peter's friends are trying to raise $100,000 to help him get the
Cleveland experiment. So far, they've raised about $30,000.


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Anti-seizure drug inhibits the glutamate system

By David Hodges

MONTREAL – The anticonvulsant topiramate (Topamax) may be an
effective second-line strategy for patients with obsessive-
compulsive disorder (OCD) who do not respond to serotonin reuptake
inhibitors (SRIs), concludes a preliminary study presented at the
Canadian Psychiatric Association meeting here.

Scientists at McMaster University found that topiramate works by
reducing levels of glutamate, a common brain chemical that has been
found in abnormally high concentrations in children with OCD.
Previous research has shown that a decrease in OCD symptom severity
was associated with a decrease in concentrations of glutamate
following SRI treatment.

"We looked at the drug topiramate, which is on the market for
seizures and convulsions. And so we gave it to these (OCD) patients
in the hope that this drug would work on the glutamate system and
improve the patient's symptoms. And low and behold in our
preliminary work . . . we did find that effect in almost two-thirds
of the people," said researcher Dr. Michael Van Ameringen, an
assistant professor in the department of psychiatry and behavioural
neurosciences, and co-director of the anxiety disorders clinic at
the Hamilton Health Sciences Corp.

"Topiramate inhibits the glutamate system," Dr. Van Ameringen
said. "We think there is a group of patients with OCD who get a very
robust effect from this. It clearly does not work in all OCD
patients, but there is a group who go from having very significant
symptoms to virtually nothing on this treatment. That's why were
excited about it."

For the study, Dr. Van Ameringen and colleagues investigated the
adjunctive use of topiramate in 16 consecutive OCD outpatients
referred to their institution's anxiety disorders clinic who were
partial or nonresponders to SRI monotherapy or to SRI combination
therapy with antipsychotics, antidepressants or benzodiazepines.
These patients had topiramate added over 14 to 26 weeks, and were
seen approximately every four weeks for the first 16 weeks or until
a treatment response was achieved. The sample included five men and
11 women who had a mean of age of 41 years, a mean age of onset of
14.9 years and a mean duration of illness of 26.2 years.

Patient responses were measured using the Clinical Global Impression
Scale for Severity (CGI-S), which rates patients' severity of
symptoms from one ("normal/not at all") to seven ("among the most
extremely ill patients"), and the Clinical Global Impressive Scale
for Improvement (CGI-I), which rates patient improvement from one
("very much improved") to seven ("very much worse").

Following a mean response time of 9.2 weeks, the researchers found
11 of the 16 patients (60%) responded to adjunctive topiramate, with
a CGI-I score of two ("much") or one ("very much improved"). The 60%
response rate was considered a good response, said researchers.

CGI-S scores also improved significantly, to an endpoint score of
4.6 ("moderately ill" to "markedly ill") from a mean baseline score
of 6.1 ("severely ill").

During the course of the study, adverse events were experienced by
13 of 16 patients, but no individual withdrew from the study because
of them. The most commonly reported adverse events included weight
loss, sedation and fatigue, memory and word-finding difficulties and
paresthesia (see table).

Some of Dr. Van Ameringen's previous research has also looked at the
adjunctive use of topiramate in women with OCD who were on the drug
and then had to stop taking it when they became pregnant. Within
four weeks of discontinuation, these women were getting all their
OCD symptoms back. But after resuming the drug following the
completion of pregnancy, their symptoms were again alleviated.

Right now, Dr. Van Ameringen and colleagues are working on a placebo-
controlled study of topiramate in obsessive-compulsion disorder
patients.

Pointing to other research initiatives, Dr. Van Ameringen said there
are also some new agents being studied in SRI-refractory OCD
patients that purely work on the glutamate system.

"These drugs may have some really big applications in this area," he
said.

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Tourette Syndrome research at WMU explores tic suppression

By JP Gaylord
News Writer
November 04, 2004


The psychology department at Western Michigan University begun a
study that will extend through mid-2005 on Tourette Syndrome and the
suppression of its related tics.

Jim Carr, associate professor of psychology at WMU, will be the
principal investigator in a study focusing on children with the
syndrome. WMU will be working as a data collection site along with
North Dakota State University and the University of Wisconsin at
Milwaukee.

"What we're looking to do is find out how children can voluntarily
stop their own tics," he said.

Tics are involuntary motor movements. Tourette Syndrome can involve
vocal and motor movements simultaneously.

"They're more complex than a simple tic," said Wayne Fuqua, chairman
of the department of psychology at WMU.

The study will use children as its subjects in order to deepen
knowledge on their ability to suppress their own tics.

Suppression is also known as habit reversal and involves a fairly
simple, self-administered intervention, Fuqua said.

Suppression techniques, Carr said, will be tested in both adults and
children.

"We're relatively confident about adults, but we're really
unconfident about younger children," he said.

There are a number of treatments that involve suppression, he said,
but researchers don't know what happens to children after they stop
suppressing.

The study will find out if tics come back after suppression is
stopped and if they come back more intensely, which is known as a
rebound effect, Fuqua said.

The study is not meant to be a treatment study, but researchers hope
that the knowledge they come away with will be able to influence the
development of future treatment methods.

Researchers will be doing a number of assessments and interviews
with the participants of the study about their tics and history,
Carr said.

The study qualified as a greater than minimal risk study, and needed
to be approved by the Human Subjects Institutional Review Board
(HSIRB) because of the vulnerable population that is being targeted
and the use of a new therapy that has not yet been tested.

The protocol for the study was approved by both the University of
Wisconsin at Milwaukee HSIRB and the WMU HSIRB, said Vicki Janson,
research compliance coordinator at the WMU HSIRB.

"Anything with more than a minimal risk needed to be approved by the
12-member board," she said.

After some suggested revisions, the study's protocol was modified
and then it was approved, she said. A study with minimal risk
involves no risk beyond what a normal person would face in daily
activities if he lives prudently.

The cause of Tourette Syndrome is not fully known to researchers.

"It clearly has some familial and genetic influences," Fuqua
said. "Genetics probably reflect a propensity or a risk for it."

The syndrome tends to emerge in adolescence and early childhood, he
said, beginning with simple motor tics that become more complicated
as a person ages.

"It's very common for people with Tourette Syndrome to have a large
set of tics," Fuqua said.

The severity of the tics can have a major impact on daily life.

"Sometimes they are so severe that they attract attention," Fuqua
said. "They end up with social ostracism."

Tourette Syndrome can also affect the ability to do a job depending
on the frequency, severity and controllability of the tics, he said.

Treatment options involve either behavioral or pharmacological
treatments.

"There's pretty good evidence that behavioral treatments work,"
Fuqua said.

All of the data collection at WMU will take place in Wood Hall.

"We have a history of researching Tourette Syndrome at WMU," Carr
said. "More researchers in psychology have been interested in
Tourette Syndrome."

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News Releases

ADVANCES IN UNDERSTANDING BRAIN CIRCUITS RESPONSIBLE FOR TICS IN
TOURETTE'S SHED LIGHT ON DISORDER

Recent advances are producing a much greater understanding of the
brain circuits responsible for the tics and problem behaviors seen
in Tourette's syndrome.

In one groundbreaking study, investigators have for the first time
measured the number of neurons in a particular area of the basal
ganglia-the brain area involved in Tourette's-in patients with the
disorder. Other studies suggest an imbalance in the basal ganglia's
inhibitory function could interfere with its ability to suppress
unwanted movements and vocalizations and thus lead to Tourette's
syndrome.

One of the least understood brain disorders, Tourette's syndrome
affects about one in 200 children. Symptoms usually appear between
the ages of four and eight and include repetitive involuntary
movements and utterances, or "tics." Tics vary according to where,
how often, and how strongly they are expressed. They are often
preceded by a sensory cue or "urge to tic" that can besiege the
individual's consciousness. Tics wax and wane in severity and are
typically worse during periods of emotional stress or fatigue.

Although many children experience their worst symptoms around the
age of 10 or 11 and then improve, some patients show their worst
symptoms as adults. In its most extreme form, the tics can be
virtually nonstop and include "purposive"-appearing repetitive
behaviors including obscene or socially inappropriate speech and
more rarely self-injurious behaviors. In addition to tics,
individuals with Tourette's also often have obsessions, compulsions,
and attentional deficits.

Scientists now know that symptoms of Tourette's syndrome likely
arise from dysfunction in a region deep within the brain called the
basal ganglia. Neurons in the basal ganglia inhibit or initiate
action plans by processing the information they receive from
the "executive centers" in the brain's prefrontal cortex and sending
it back to motor and sensory areas of the cortex through the
thalamus, new studies suggest.

"Recent imaging and postmortem studies now implicate the ventral
striatum and caudate nucleus—two regions of the basal ganglia—as
areas associated with the brain dysfunction seen in Tourette's,"
says Neal Swerdlow, MD, PhD, of the University of California-San
Diego department of psychiatry, co-chair of a symposium at this
meeting titled "Tourette's: The Self Under Seige."

"Although there is general agreement that the basal ganglia are
implicated in Tourette's syndrome, we know relatively few details.
For example, we know that increased activation in the caudate and
prefrontal cortex is associated with better tic control," says James
Leckman, MD, of the Yale University School of Medicine Child Study
Center and co-chair of the symposium. "There is also evidence that
the actual size of the caudate nucleus is reduced in many
individuals with Tourette's. But we don't know how these findings
are linked to the clinical features of Tourette's including its
waxing and waning course and why the tic symptoms usually peak in
early adolescence."

Knowing that dopamine antagonist drugs reduce the tics associated
with Tourette's and that selective serotonin reuptake inhibitors
reduce the symptoms of obsession and compulsions, Roger Albin, MD,
and colleagues at the University of Michigan department of neurology
investigated the idea that the ventral striatum—a brain region where
both dopamine and serotonin have important functions—could be
involved in Tourette's syndrome.

Noninvasive imaging studies show that the ventral striatum of
Tourette's patients has an excessive amount of dopamine-containing
nerve terminals. Other studies suggest that in normal brain
development, dopamine-containing nerve terminals are overproduced in
the years leading up to adolescence, and that these nerve terminals
are pruned back during adolescence.

"This raises the possibility that Tourette's syndrome is due partly
to abnormal persistence of excessive dopamine terminals in the
ventral striatum due to subtle changes in the timing of brain
development," Albin says.

The ventral striatum is known to be involved in the formation of
habits and is also involved in repetitive, stereotyped movements of
the face and limbs, some of which may be socially significant, Albin
says. "The tics of Tourette's syndrome may disrupt the unconscious
social communication normally mediated by these facial movements,
head position, and other stereotyped movements," he says. "This
could be the basis for the perception of tics as disruptive."
In other work, Flora Vaccarino, MD, also of the Yale University
School of Medicine Child Study Center, shows that patients with
Tourette's have an increased number of neurons that normally silence
brain activity in the internal segment of the globules pallidus and
a decrease in neurons in the caudate nucleus.

Using postmortem brain tissue, Vaccarino and her colleagues found
that Tourette's syndrome patients had about twice as many inhibitory
neurons in the globus pallidus, a part of the basal ganglia that
connects to the thalamus and inhibits its function. Inhibitory
neurons were decreased in other areas of the basal ganglia,
including the caudate nucleus, says Vaccarino.

Vaccarino suggests that the imbalance in inhibitory neurons could
change the timing of activity in the basal ganglia and thus lead to
the tics and other compulsive symptoms of Tourette's syndrome.
"The next step is to increase the number of brains studied, which
may allow us to relate severity of symptoms and anatomical
findings," Vaccarino says.

Leckman and his colleagues at Yale and Columbia University studied
patients who had had brain images taken during childhood to
determine if the size of any basal ganglia structures measured
before the age of 14 predicted their outcome years later as they
entered adulthood. Based on the earlier studies, they predicted that
caudate volumes would influence the course of the disorder.

"We found that the volume of the caudate nucleus and adjacent
structures in the subgenual region, which includes areas of the
ventral striatum and the limbic cortex, could account for nearly a
third of the variance of tic severity at follow-up," says Leckman.
These striatal and limbic regions are involved in the processing of
motivational and affective cues, which in turn may contribute to the
well-known sensitivity of Tourette's patients to emotionally laden
stimuli.

One of the challenges facing a complex nervous system with the
capability for many different behaviors is the need to prevent
potentially competing behaviors from interfering with desired
behaviors, says Jonathan Mink, MD, PhD, of the University of
Rochester Medical School department of child neurology. Mink
hypothesizes that a central role of the basal ganglia is to
facilitate desired behaviors and inhibit those that might compete
with the desired behavior. In Tourette's syndrome, clusters of
neurons in the ventral striatum of the basal ganglia may become
abnormally active, leading to inhibition of neurons in the globus
pallidus and substantia nigra (the basal ganglia's output centers).

"Neurons in these areas normally act to suppress unwanted
movements," says Mink. "But when the neurons themselves are
inhibited, they can no longer act to suppress unwanted movements,
leading to tics."

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Behavior Therapy Best for Kids With OCD
Tuesday, October 26, 2004
By Salynn Boyles


Children and teens with obsessive-compulsive disorder respond better
to talk therapy than to antidepressants alone, but a combination of
the two approaches to treat OCD may work wonders, a government-
funded study group finds.

The findings are being reported less than two weeks after federal
health officials ordered makers of the most widely used
antidepressants to include warnings on their packaging about an
increased risk of suicidal thoughts and behaviors in children and
adolescents who take the drugs.

Medications that were originally approved for treatment of
depression are effective for anxiety disorders. Some of the newer
types of selective serotonin uptake inhibitors (search), such as
Fluoxetine, sertraline, fluvoxamine, paroxetine, and citalopram, are
among the SSRIs commonly prescribed for OCD.

Just more than half of the children and adolescents in the 12-week
study treated with a combination of behavioral therapy (talk
therapy) and the drug Zoloft (search) for three months had no
evidence of OCD four months later. Nearly two in five children
responded to talk therapy. While one in five participants taking
Zoloft alone had similar responses as did just under one in 20
treated with placebo.

The response rate for cognitive-behavior therapy alone was slightly
lower than for behavior therapy with the antidepressant, but
researchers concluded that either approach is an appropriate initial
treatment. The findings are reported in the Oct. 27 issue of the
Journal of the American Medical Association.


"The message is that we now have a clearly effective treatment for
obsessive-compulsive disorder in children and it is cognitive
behavior therapy (search)," researcher John March, MD, tells
WebMD. "In a relatively short period of time we have gone from
having no effective treatment to being able to bring half of the
kids with this disorder into the normal range within three months."

No Evidence of Suicidal Thoughts in OCD Patients

It is estimated that as many as one in 200 children have OCD,
characterized by intrusive thoughts, images, or impulses that lead
to repetitive or compulsive behaviors, such as frequent hand washing
or checking. Between a third and half of adults with OCD develop the
disorder during childhood.

In this study, 97 kids and teens with OCD completed 12 weeks of
treatment with either behavior therapy alone, treatment with Zoloft
alone, a combination of the two, or placebo. Four months later, just
nearly 54 percent of the kids treated with behavior and drug therapy
were considered to be in remission, meaning they were not engaging
in frequent repetitive behaviors. Remission rates, defined as an
obsessive-compulsive behavioral score of less than 10, were 39
percent, 21 percent, and nearly 4 percent for those treated with
behavior therapy alone, Zoloft alone, and placebo, respectively.

There was no evidence of an increase in suicidal thoughts among the
children taking the antidepressant drug Zoloft.

"It is reassuring in this study, as in others, that [antidepressant]
treatment was well tolerated, with no evidence of treatment-emergent
harm to self or others," the researchers wrote.

Drugs Relied on Too Much With OCD

The clear superiority of behavior therapy over drugs alone in this
study, along with the FDA warning, should have a major impact on how
OCD in children is treated in the U.S., child and adolescent
psychiatrist Rachel Ritvo, MD, tells WebMD.

"The sad fact is that economic considerations drive child mental
health care today, and treating a child with drugs is much, much
cheaper than psychotherapy," she says. "We have learned that kids
are very responsive to psychotherapy and psychosocial interventions,
probably even more so than adults."

Ritvo says a parent seeking treatment for a child with OCD should
push for psychotherapy, but she acknowledged that finding a
qualified therapist could be a challenge.

"There are fewer than 100 behavioral pediatricians in this country
and only about 7,000 child psychiatrists. That's it," she says. "I
turn away four or five people a week from my practice."

March counters that the behavioral therapy techniques used in the
treatment of children with OCD are easily learned and can be
administered by any good psychiatrist, psychologist, or mental
health social worker.

"Cognitive behavior therapy is a lot like physical therapy, but
instead of, say, rehabing a damaged knee you are retraining the
brain," he says. "This is a neurobehavioral illness (search) and
there are skillful and unskillful ways to treat it. The wrong
approach is relying on drugs alone or traditional psychotherapy. The
best treatment is clearly evidence-based cognitive behavior therapy."

By  Salynn Boyles, reviewed by  Brunilda Nazario, MD

SOURCES: Pediatric OCD Treatment Study, Journal of the American
Medical Association, Oct. 27, 2004, vol 292: pp 1969-1976. John S.
March, MD, MPH, department of psychiatry, Duke University Medical
Center, Durham, N.C. Rachel Ritvo, MD, general child and adolescent
psychiatrist; clinical associate professor of medicine, George
Washington University, Washington; and spokeswoman, American Academy
of Child and Adolescent Psychiatry




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  CPA: Therapy-resistant Obsessive-Compulsive Patients Respond to
Topiramate
By Louise Gagnon

MONTREAL, QUEBEC -- October 19, 2004 -- Topiramate is effective add-
on therapy for some patients with obsessive-compulsive disorder
(OCD) who have proved resistant to traditional treatment, according
to results of an open-series study presented here at the 54th
Canadian Psychiatric Association Annual Meeting.

"A sub-group of patients…responded to the addition of topiramate in
their therapy," said Michael Van Ameringen, MD, Principal
Investigator and Associate Professor of Psychiatry, Department of
Psychiatry and Behavioural Neurosciences, McMaster University,
Hamilton, Ontario, Canada. "We have taken [patients'] OCD from very
severe to very minimal by adding topiramate to their therapy. It
appears promising."

In 5 men and 11 women with a mean duration of illness of 26.2 years –
the researchers added topiramate at a mean dose of 253.1 mg/day to
selective serotonin reuptake inhibitor (SSRI) monotherapy or SSRI
combination therapy over 14 to 26 weeks. At baseline, the mean
Clinical Global Improvement (CGI) score was 6.1, indicating patients
were regarded as "severely ill".

By the end of the treatment period, 68.8% had a significant drop in
their CGI score. Specifically, 43.8% of subjects had a score of 2,
which indicates they were "much improved," and 25% had a score of 1,
which indicates they were "very much improved."

Dr. Van Ameringen, who is also Co-director of the Anxiety Disorders
Clinic at McMaster University Medical Centre, said that patients
with OCD are typically on SSRIs, which produce response rates of 42%
to 53%.

Dr. Van Ameringen said his team decided to investigate the role of
topiramate therapy in OCD as a result of previous basic science
research showing promise in this area.

"Neuroimaging studies found a deficit in the glutamate system in a
group of children who had [OCD]," he explained. "That may say
something about the neurobiology of the disorder. It made us explore
what agents had an effect on glutamate, such as topiramate."


[Presentation title: "Adding Topiramate to an SRI in Treatment-
Resistant Obsessive-Compulsive Disorder." Abstract 37]
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Food and Drug Administration (FDA) asks manufacturers of all
antidepressant drugs to include in their labeling a boxed warning
and expanded warning statements that alert health care providers to
an increased risk of suicidality (suicidal thinking and behavior) in
children and adolescents being treated with these agents, and
additional information about the results of pediatric studies.


Text of the "black box" warning that the Food and Drug
Administration ordered included on all antidepressants:

Antidepressants increase the risk of suicidal thinking and behavior
(suicidality) in children and adolescents with major depressive
disorder (MDD) and other psychiatric disorders. Anyone considering
the use of (drug name) or any other antidepressant in a child or
adolescent must balance this risk with the clinical need. Patients
who are started on therapy should be observed closely for clinical
worsening, suicidality, or unusual changes in behavior. Families and
caregivers should be advised of the need for close observation and
communication with the prescriber. (Drug name) is not approved for
use in pediatric patients except for patients with (approved
pediatric claim).

Pooled analyses of short-term (four to 16 weeks) placebo-controlled
trials of nine antidepressant drugs (SSRIs and others) in children
and adolescents with MDD, obsessive compulsive disorder (OCD), or
other psychiatric disorders (a total of 24 trials involving over
4,400 patients) have revealed a greater risk of adverse events
representing suicidal thinking or behavior (suicidality) during the
first few months of treatment in those receiving antidepressants.
The average risk of such events on drug was 4 percent, twice the
placebo risk of 2 percent. No suicides occurred in these trials.

http://www.fda.gov/cder/drug/antidepressants/default.htm

---------------
Paul Marshall
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I know what made Mozart tic
(Filed: 13/10/2004)

Mozart was obsessed with filthy verse and breaking wind - evidence,
says the composer James McConnel, that his hero was a fellow
Tourette's sufferer. He tells Robert Gore-Langton why music is his
medicine, too.

You could go quite a while without spotting anything untoward about
him. But sooner or later you become aware that James McConnel has a
bizarre affliction.

At one point, we are sitting in the composer's study in his
magnificent Norfolk rectory, rabbiting on about Mozart. Out of the
blue he does a strange facial twitch - a little one.

By midday lunch is ready. As I pass him the peas, he has a full-
blown twitch, jabs the air repeatedly with his finger, brushes his
face with his other hand, and lets out a brief snort. None of his
family - least of all his wife, the Country Life cartoonist Annie
Tempest - seems to notice this.

McConnel is what you might call Bohemian posh, and looks and sounds
like a hyperactive version of Hugh Grant. He has a background in
musicals but also composes for television and film.

His face, too, is about to become familiar as the presenter of a
documentary for Channel 4 called What Made Mozart Tic?, in which he
suggests that Mozart had Tourette's Syndrome. It's not a new theory.
But it is one which McConnel is in a unique position to argue
because he himself is a sufferer.

"It's horrible; of course, if you've got the swearing and spitting
kind of Tourette's [this affects about 20 per cent of sufferers].
But I haven't. I've got the more charming version, touch wood."

The only time McConnel doesn't twitch (put a gun to his head and you
could make him stop, he says, but only for so long) is when he's at
his piano, composing. In the program he argues that Mozart,
too, "self-medicated" by writing music.

"The self-medicating theory is that music is a replacement for the
twitching. With me it was subconscious. It wasn't until I was about
25 that someone pointed out that I wasn't twitching when I was at
the piano.

"I suspect Mozart didn't have physical jerks as much as me. But
there is definite evidence of his grimacing and feet-tapping.
"We also know a lot about his inability to rein in impulses, the
sudden boredom, his sense of mischief and his scatological
obsession, which all point to Tourette's. He even had a morbid fear
of the trumpet until he was nine. Seriously! He would lie down and
scream if he heard one."

The filthy, excrement-obsessed letters Mozart wrote provide a useful
starting point for McConnel.

"There's a very rare condition in Tourette's called coprographia -
the need to write down filth. We Touretters have filthy minds!
"When you write a song, as Mozart did, called Lick Out My Arsehole,
that in itself is not so shocking judged by the standards of his
day. But what is very odd and Touretty about it is that he set it to
the most gorgeous, sublime tune. It's Tourettishly inappropriate.
"My sense of humor is the same. I never know when to stop."

McConnel - like Mozart - passes wind a lot, staging elaborate wind-
breaking competitions with his daughter. "I love farting," he beams.
Because he suffers from obsessive compulsive disorder (OCD) McConnel
takes half an hour to go through all his bedtime rituals - checking
lights, looking behind doors and so forth.

"When I am doing them I know it is completely barking," he
says. "But I can't not do it and feel comfortable. If I don't, the
house will burn down, the children will fry, there will be some
terrible calamity as a consequence. That's how it feels."

The same was apparently true for the young Mozart. "When he was a
child he had to do his bedtime rituals with his father, Leopold, and
if they weren't right he would do them all over again."

Although Tourette's wasn't recognized in Mozart's day, much has been
made of his constant childhood illnesses. These, apparently, could
have triggered Pandas (pediatric auto-immune neuro-psychiatric
disorder), which can lead to Tourette's. McConnel himself wasn't
diagnosed with Tourette's until 12 years ago - he's now 46. He can,
however, pinpoint the onset.

"I can remember the very instant I started twitching. It was during
the third verse of Hark the Herald Angels Sing at my school carol
service when I was six. It was a sniff and I didn't have a cold. I
started sniffing, which became permanent.

"Later, I heard a man and a woman having a row. She stormed off with
a loud 'huh' and the seeds of my OCD started then, because I started
copying that 'huh' obsessively. Huh, huh, huh, huh. I had to get it
just right."

McConnel believes the root of Mozart's Tourette's is to be found in
the music itself - something McConnel knows from his own experience
of composing.

"Tourette's is a constant battle between having a compulsion and
trying to control it, and that can translate into music. Mozart let
his music run off in chaotic directions but then always brought it
back under control.

"His interest in counterpoint and fugue - its unfashionable
complexity - appealed to his Touretty side. The music for me has
just so much happiness, for want of a better word. There's no
residual misery. You always come away from Mozart feeling better."
Scientific tests have proved the efficacy of Mozart in music
therapy: it is indeed deeply calming. Not that this stops his
greatest fan going about the house trilling, farting and twitching
like a dervish.

The family, however, clearly regard the condition with a sense of
humor; McConnel's e-mail name is McTwitch and there is a plate in
the kitchen inscribed: "Warning: mad twitcher on the loose."
I ask McConnel's wife, Annie, what it's like living with a one-man
tic-ing bomb. "It's his OCD that is the worst of it," she says. His
constant switching off the fax machine in the study drives her mad.
Or as she puts it, rather wittily: "James has Tourette's, whereas I
suffer from it."

It runs in the family. Their son Freddie, 12, is also classed as
having Tourette's. A member of Mensa, he was recently on Mastermind.
His specialist subject? Mozart.

•  What Made Mozart Tic?, October 18, Channel 4, 8pm


Source:
http://www.telegraph.co.uk/arts/main.jhtml?
xml=/arts/2004/10/13/bmoz12.xml&sSheet=/arts/2004/10/13/ixartleft.htm
l

-----------------------------

Tourette-Updates

Paul Marshall
http://www.tourettes-disorder.com

Surgery helps short-circuit Tourette's syndrome

An implant that flips the off-switch on misfiring brain cells could
eventually help treat everything from addictions to depression, PAUL
TAYLOR writes

PAUL TAYLOR

From Tuesday's Globe and Mail


POSTED AT 7:49 AM Tuesday, October 12

Jeff Matovic used to eat with a plastic spoon to prevent himself
from accidentally gouging out one of his eyes.The 31-year-old has
Tourette's syndrome, a neurological disorder characterized by
involuntary muscle movements. Mr. Matovic, who developed symptoms at
age 3, could not sit, walk or even sleep without his body exploding
in an endless series of jerking motions and verbal outbursts. He has
broken glasses in his bare hands and dented walls with his head
because of sudden muscle contractions.
Things got so bad, Mr. Matovic sought out doctors who would implant
electrodes in his brain to quiet his restless body, after hearing
about another patient who had the treatment. The operation took
place six months ago at the University Hospitals of Cleveland, and
his body has been calm ever since.

"It's just amazing. It is truly phenomenal," Mr. Matovic said in a
telephone interview from his home in a Cleveland suburb. Before the
operation, he could barely talk on a phone because of an
irrepressible urge to clear his throat, grunt and hiss -- not to
mention the difficulty of holding the receiver.

Mr. Matovic underwent a treatment known as deep-brain stimulation,
increasingly used to treat a wide range of brain disorders. Much
like a heart pacemaker, the treatment provides a stream of
electrical current to counteract a part of the brain that is
misbehaving.

During surgery, electrodes are inserted into specific spots in the
brain. They are then connected through wires under the skin (beneath
the scalp, neck and upper chest) to a replaceable battery unit
implanted beneath the collarbone.

Only a handful of people (none in Canada) has received the treatment
for Tourette's. But deep-brain stimulation has been used for more
than a decade to treat other movement disorders, such as Parkinson's
disease, tremors and dystonia, which distorts posture. About 30,000
people around the world now have such brain implants.

As neurosurgeons refine their skills, medical experts speculate that
deep-brain stimulation could be used to treat everything from drug
addictions to depression. Studies are under way at various medical
institutions to expand its use. The technique is proving effective
partly because the brain itself operates like an electrical circuit.
When even just a few brain cells are misfiring, they can cause
widespread problems resulting in either a physical or mental
disorder.

A little electrical current, applied in the right place, seems to
restore harmony to the discordant symphony of the disordered brain,
said Dr. Robert Maciunas, the neurosurgeon who operated on Mr.
Matovic.

Years ago, Dr. Maciunas noted, surgeons performed lobotomies in
which connections between dysfunctional parts of the brain were
permanently severed.

"Remember, this was an era when there was no medication for these
horrible psychiatric disorders. So somebody who could demonstrate a
significant benefit in some of these hopeless patients was a
godsend," he said. The problem with lobotomies was that they were
overused -- and irreversible, he added. Surgeons also attempted to
destroy small areas of the brain, which appeared to be the source of
specific disorders. It finally occurred to them that they could
achieve the results though electric probes, and the current could be
fine-tuned to fit the ailment.

Most of the initial deep-brain stimulation operations were performed
on people with Parkinson's disease (which results from the death of
brain cells that produce the neurotransmitter dopamine, which is
involved in body movements). Parkinson's sufferers have difficulty
moving with ease. They develop a stony stare, a shuffling walk and,
at times, their body trembles like leaves in the wind.

"The treatment turns back the clock five to 10 years on the illness,
to a point when the patient had less severe symptoms," said Dr.
Andres Lozano, a neurosurgeon at Toronto Western Hospital, who has
performed the operation on almost 200 Parkinson's patients. But he
cautioned that it is not a cure: It merely controls symptoms for a
time. Parkinson's is a degenerative neurological disorder in which
brain cells continue to die. Eventually, patients develop dementia
and their bodies shut down.

It is uncertain how long deep-brain stimulation can control the
symptoms of Tourette's. But there's a good chance it could be long-
lasting. Unlike Parkinson's disease, Tourette's does not involve the
progressive death of increasing numbers of brain cells.

"If it [Tourette's] is a disorder of brain function only, and if we
improve that function, then the disease should not continue
progressing," said Dr. Lozano.

Mr. Matovic, however, wasn't made any promises when he went under
the knife. As one of the first Tourette's patients to receive deep-
brain stimulation, his doctors were unsure of his outcome.

Yet Mr. Matovic was willing to take a risk because the usual
treatment of drugs and various therapies had failed. What's more, he
was fed up with strangers laughing at his incessant muscle tics. And
even though he has a college education, he had to take menial
jobs. "I'm so grateful they did the operation," Mr. Matovic said,
adding that he is 99-per-cent symptom-free. He now has an office
job, is planning to write a book and his wife is expecting a
baby. "We are certainly very excited about it."

Source:
http://cfcn.theglobeandmail.com/servlet/RTGAMArticleHTMLTemplate/B/20
041012/gthtourettes12?
brand=generic&hub=&tf=CFCNPlus/generic/hubs/frontpage.html&cf=CFCNPlu
s/generic/hubs/frontpage.cfg&slug=gthtourettes12&date=20041012&archiv
e=RTGAM&ad_page_name=&nav=&subnav=fullstory&site=Technology&vg=BigAdV
ariableGenerator&id=RTGAM.20041012.gthtourettes12


Paul Marshall
Editor

Fluphenazine effective for Tourette syndrome
Fluphenazine is an effective treatment for abnormal movements in
Tourette syndrome, according to a study published in the April 13,
2004, issue of Neurology. From 1349 patients diagnosed with Tourette
syndrome at 1 center since 1981, 272 were randomly selected for
chart review. Of these, 63 had been treated with fluphenazine for at
least 1 year (mean 3.9 years). Marked or moderate improvement was
seen in 84% of patients, at a mean daily dose of 3.9 mg/day. Adverse
effects included drowsiness, weight gain, dystonic reaction, and
akathisia. No patient developed tardive dyskinesia. The authors
conclude, "Our study provides evidence that fluphenazine is a safe
and effective drug in long-term treatment of tics." (This summary is
courtesy of WeMove (Worldwide Education and Awareness for Movement
Disorders).

Hundreds of health problems have been caused by, misdiagnosed as or
mimicked by Lyme disease, including facial palsy, Alzheimer's
disease, anxiety, ADD, ADHD, Bell's Palsy, bipolar disorder, brain
tumor, Chronic Fatigue Syndrome, depression, epilepsy, respiratory
distress syndrome, fetal death, fever, fibromyalgia, hearing loss,
heart block, hepatitis, lupus, memory impairment, meningeal
lymphoma, meningitis, migraines, mono, Multiple Sclerosis, Non-
Hodgkin's lymphoma, restless legs syndrome, Rheumatic Fever,
rheumatoid arthritis, seizure disorders, stroke, sudden infant death
syndrome, thyroiditis, Tourette's syndrome, urticaria and vertigo.
Nevertheless, even in late disseminated Lyme disease, intravenous
antibiotic therapy has a high success rate.

      - Information provided by Colin Nicholl

Take precautions to prevent Lyme disease



You and your family live in an area with a high incidence of Tick
Borne Diseases, including Lyme disease, a potentially serious
affliction caused by spiral-shaped bacteria transmitted by infected
deer ticks, tiny spider-like creatures that live in woodland and
grassy areas.

      Named for Old Lyme, Conn., the location where it was discovered
in 1975, Lyme can significantly undermine the quality of your life
if left untreated. The highest risk from these ticks is from April
to October when they are smallest and most active, but they are
active whenever the temperature is above 40 degrees.

      One of the early signs of Lyme disease may be a bull's-eye red
rash. Later signs may include fluish symptoms such as muscle aches,
fever, tiredness and joint pain. More serious complications include
a whole host of symptoms, especially involving the joints, nervous
system and heart. Where there is a combination of severe fatigue,
muscle aches/stiffness, and neurological or arthritic
symptomatology, a diagnosis of Lyme disease should be considered.

      Lyme disease, especially in its early stages, can be treated
with antibiotics. If you suspect that you have Lyme disease, do not
delay consulting with your doctor.

      Take precautions

      Take the following precautions, especially when walking in a
wooded area:


Wear light-colored clothing, making ticks easier to spot.


Avoid common tick habitats such as tall grass, bushes, brush and
woods.


Keep to the center of pathways. Do not rest on fallen logs or sit on
the forest floor.


Wear long trousers and long-sleeved shirts; tuck your trousers into
socks.


Use a tick repellent.


Before going indoors, brush off your clothing.


Once indoors, check your whole body carefully for ticks, removing
and crushing unattached ticks, and following the procedure below if
you find ticks attached to you.

      Note: most people do not feel a tick biting, nor do they sense
the drawing of blood by the tick over the next 2 to 4 days of
attachment.

      Know how to remove a tick

      If you find a tick imbedded in your skin, take the following
measures:


Remove the tick promptly. Ticks removed within 24 hours are less
likely to infect you.


Use a tick removal device (tickedoff.com) or tweezers to remove the
tick. Grasp the tick's head, including its mouth parts, and tug
gently and repeatedly until the tick withdraws its barbed mouth from
your skin. Remember that the bacteria are in the tick's saliva, so
do not squeeze its body, suffocate it with Vaseline, or burn its
bottom with a match, which can cause it to spit or spew.


Preserve the tick in a jar of alcohol, noting the date and location
of the bite and where you think you picked up the tick.


Wipe the area of attachment with antiseptic and wash your hands and
tweezers with antibacterial soap.

      Diagnosing Lyme disease

      If you develop a striking red bull's-eye red rash (typically
within 4-6 weeks of a bite) photograph the rash and keep a record of
the date on which it first appeared. Have a doctor examine the rash,
mentioning your concern that it may be an erythema migrans rash. (If
your doctor suspects that you have a Lyme rash, he/she will
typically prescribe a course of oral antibiotics, which, if taken
faithfully, should take care of the infection.)

      If you develop a "summer flu" (whether or not you recall a
rash), consisting of aching muscles and/or joints, swollen glands,
headaches, exhaustion, fever, neck stiffness or cold sweats, consult
with a medical doctor and request a Lyme test, preferably
the "Western Blot," as the frontline blood test (ELISA) has been
widely questioned.

      All Lyme tests are difficult to interpret and far from
foolproof. Consequently, the CDC insists that Lyme disease is a
clinical, rather than a laboratory, diagnosis.

      If you have Lyme disease and it is undetected and left
untreated, you may develop strange arthritic, neurological and/or
cardiological symptoms over the following months and years, which
could prove difficult to diagnose.

      Hundreds of health problems have been caused by, misdiagnosed
as or mimicked by Lyme disease, including facial palsy, Alzheimer's
disease, anxiety, ADD, ADHD, Bell's Palsy, bipolar disorder, brain
tumor, Chronic Fatigue Syndrome, depression, epilepsy, respiratory
distress syndrome, fetal death, fever, fibromyalgia, hearing loss,
heart block, hepatitis, lupus, memory impairment, meningeal
lymphoma, meningitis, migraines, mono, Multiple Sclerosis, Non-
Hodgkin's lymphoma, restless legs syndrome, Rheumatic Fever,
rheumatoid arthritis, seizure disorders, stroke, sudden infant death
syndrome, thyroiditis, Tourette's syndrome, urticaria and vertigo.
Nevertheless, even in late disseminated Lyme disease, intravenous
antibiotic therapy has a high success rate.

      - Information provided by Colin Nicholl



Paul Marshall
http://www.tourettes-disorder.com
editor@...