Essay/Term paper: Tourette's disorder

Essay, term paper, research paper:  Science Reports

Tourette's Disorder


Table of Contents


Tourette Syndrome And Other Tic Disorders
Definitions of Tic Disorders
Differential Diagnosis
Symptomatology
Associated Behaviors and Cognitive Difficulties
Etiology
Stimulant Medications
Epidemiology and Genetics
Non-Genetic Contributions
Clinical Assessment Of Tourette Syndrome
Treatment Of Tourette Syndrome
Monitoring
Reassurance
Pharmacological Treatment of Tourette Syndrome
Psychodynamic Psychotherapy
Family Treatment
Genetic Counseling
Academic and Occupational Interventions
Bibliography


Today the full-blown case of TS is unlikely to be confused with any other
disorder.
However, only a decade ago TS was frequently misdiagnosed as schizophrenia,
obsessive-compulsive disorder, Sydenham's chorea, epilepsy, or nervous habits.
The
differentiation of TS from other tic syndromes may be no more than semantic,
especially
since recent genetic evidence links TS with multiple tics. Transient tics of
childhood are
best defined in retrospect. At times it may be difficult to distinguish
children with
extreme attention deficit hyperactivity disorder (ADHD) from TS. Many ADHD
children, on
close examination, have a few phonic or motor tics, grimace, or produce noises
similar to
those of TS. Since at least half of the TS patients also have attention
deficits and
hyperactivity as children, a physician may well be confused. However, the
treating doctor
should be aware of the potential dangers of treating a possible case of TS with
stimulant
medication. On rare occasions the differentiation between TS and a seizure
disorder may be
problematic. The symptoms of TS sometimes occur in a rather sharply separated
paroxysmal
manner and may resemble automatisms. TS patients, however, retain a clear
consciousness
during such paroxysms. If the diagnosis is in doubt, an EEG may be useful. We
have seen TS
in association with a number of developmental and other neurological disorders.
It is
possible that central nervous system injury from trauma or disease may cause a
child to be
vulnerable to the expression of the disorder, particularly if there is a
genetic
predisposition. Autistic and retarded children may display the entire gamut of
TS symptoms,
but whether an autistic or retarded individual requires the additional
diagnosis of TS may
remain an open question until there is a biological or other diagnostic test
specifically
for TS. In older patients, conditions such as Wilson's disease, tardive
dyskinesia, Meige's
syndrome, chronic amphetamine abuse, and the stereotypic movements of
schizophrenia must be
considered in the differential diagnosis. The distinction can usually be made
by taking a
good history or by blood tests. Since more physicians are now aware of TS,
there is a
growing danger of overdiagnosis or over-treatment. Prevailing diagnostic
criteria would
require that all children with suppressible multiple motor and phonic tics,
however
minimal, of at least one year, should be diagnosed as having TS. It is up to
the clinician
to consider the effect that the symptoms have on the patient's ability to
function as well
as the severity of associated symptoms before deciding to treat with medication.


TABLE 1. RANGE OF SYMPTOMS OF TS

Motor
Simple motor tics: fast, darting, and meaningless.
Complex motor tics: slower, may appear purposeful

Vocal
Simple vocal tics: meaningless sounds and noises.
Complex vocal tics: linguistically meaningful utterances such as
words and
phrases (including coprolalia, echolalia, and palilalia).

Behavioral and Developmental

Attention deficit hyperactivity disorder, obsessions and compulsions,
emotional problems, irritability, impulsivity, aggressivity, and self-
injurious
behaviors; various learning disabilities



Symptomatology

The varied symptoms of TS can be divided into motor, vocal, and behavioral
manifestations
(Table 2). Complex motor tics can be virtually any type of movement that the
body can
produce including gyrating, hopping, clapping, tensing arm or neck muscles,
touching people
or things, and obscene gesturing. At some point in the continuum of complex
motor tics, the
term "compulsion" seems appropriate for capturing the organized, ritualistic
character of
the actions. The need to do and then redo or undo the same action a certain
number of times
(e.g., to stretch out an arm ten times

Definitions of Tic Disorders

Tics are involuntary, rapid, repetitive, and stereotyped movements of
individual muscle
groups. They are more easily recognized than precisely defined. Disorders
involving tics
generally are divided into categories according to age of onset, duration of
symptoms, and
the presence of vocal or phonic tics in addition to motor tics. Transient tic
disorders
often begin during the early school years and can occur in up to 15% of all
children.
Common tics include eye blinking, nose puckering, grimacing, and squinting.
Transient
vocalizations are less common and include various throat sounds, humming, or
other noises.
Childhood tics may be bizarre, such as licking the palm or poking and pinching
the
genitals. Transient tics last only weeks or a few months and usually are not
associated
with specific behavioral or school problems. They are especially noticeable
with heightened
excitement or fatigue. As with all tic syndromes, boys are three to four times
more often
afflicted than g! irls. While transient tics by definition do not persist for
more than a
year, it is not uncommon for a child to have series of transient tics over the
course of
several years. Chronic tic disorders are differentiated from those that are
transient not
only by their duration over many years, but by their relatively unchanging
character. While
transient tics come and go - with sniffing replaced by forehead furrowing or
finger
snapping, chronic tics - such as contorting one side of the face or blinking -
may persist
unchanged for years. Chronic multiple tics suggest that an individual has
several chronic
motor tics. It is often not an easy task to draw the lines between transient
tics, chronic
tics, and chronic multiple tics. Tourette Syndrome (TS), first described by
Gilles de la
Tourette, can be the most debilitating tic disorder, and is characterized by
multiform,
frequently changing motor and phonic tics. The prevailing diagnostic criteria
include onset
before the age of 21; recurrent, involuntary, rapid, purposeless motor
movements affecting
multiple muscle groups; one or more vocal tics; variations in the intensity of
the symptoms
over weeks to months (waxing and waning); and a duration of more than one year.
While the
criteria appear basically valid, they are not absolute. First, there have been
rare cases
of TS which have emerged later than age 21. Second, the concept of
"involuntary" may be
hard to define operationally, since some patients experience their tics as
having a
volitional component - a capitulation to an internal urge for motor discharge
accompanied
by psychological tension aefore writing, to even up, or to stand up and push a
chair into
"just the right position") is compulsive in duality and accompanied by
considerable
internal discomfort. Complex motor tics may greatly impair school work, e.g.,
when a child
must stab at a workbook with a pencil or must go over the same letter so many
times that
the paper is worn thin. Self-destructive behaviors, such as head banging, eye
poking, and
lip biting, also may occur. Vocal tics extend over a similar spectrum of
complexity and
disruption as motor tics ( The most socially distressing complex vocal symptom
is
coprolalia, the explosive utterance of foul or "dirty" words or more elaborate
sexual and
aggressive statements. While coprolalia occurs in only a minority of TS
patients (from
5-40%, depending on the clinical series), it remains the most well known
symptom of TS. It
should be emphasized that a diagnosis of TS does not require that coprolalia is
present.
Some TS patients may have a tendency to imitate what they have just seen
(echopraxia),
heard (echolalia), or said (palilalia). For example, the patient may feel an
impulse to
imitate another's body movements, to speak with an odd inflection, or to accent
a syllable
just the way it has been pronounced by another person. Such modeling or
repetition may lead
to the onset of new specific symptoms that will wax and wane in the same way as
other TS
symptoms.

TABLE 2. EXAMPLES OF MOTOR SYMPTOMS

Simple motor tics
Eye blinking, grimacing, nose twitching, lip pouting, shoulder shrugging, arm
jerking,
abdominal tensing, kicking, finger movements, jaw snapping, tooth clicking,
frowning,
tensing parts of the body, and rapid jerking of any part of the body.

Complex motor tics
Hopping, clapping, touching objects (or others or self), throwing, arranging,
gyrating,
bending, "dystonic" postures, biting the mouth, the lip, or the arm,
headbanging, arm
thrusting, striking out, picking scabs, writhing movements, rolling eyes
upwards or
side-to-side, making funny expressions, sticking out the tongue, kissing,
pinching,
writing over-and-over the same letter or word, pulling back on a pencil
while writing,
and tearing paper or books.

Copropraxia
"Giving the finger" and other obscene gestures.

Echopraxia
Imitating gestures or movements of other people.

TABLE 3. EXAMPLES OF VOCAL SYMPTOMS

Simple vocal tics
Coughing, spitting, screeching, barking, grunting, gurgling, clacking,
whistling, hissing,
sucking sounds, and syllable sounds such as "uh, uh," "eee," and "bu."

Complex vocal tics
"Oh boy," "you know," "shut up," "you're fat," "all right," and "what's that."

or any other understandable word or phrase Rituals
Repeating a phrase until it sounds "just right" and saying something over 3
times.

Speech atypicalities
Unusual rhythms, tone, accents, loudness, and very rapid speech.

Coprolalia
Obscene, aggressive, or otherwise socially unacceptable words or phrases.

Palilalia
Repeating one's own words or parts of words.

Echolalia
Repeating sounds, words, or parts of words of others.

The symptoms of TS can be characterized as mild, moderate, or severe by their
frequency,
their complexity, and the degree to which they cause impairment or disruption
of the
patient's ongoingctivities and daily life. For example, extremely frequent tics
that occur
20-30 times a minute, such as blinking, nodding, or arm flexion, may be less
disruptive
than an infrequent tic that occurs several times an hour, such as loud barking,
coprolalic
utterances, or touching tics. There may be tremendous variability over short
and long
periods of time in symptomatology, frequency, and severity. Patients may be
able to inhibit
or not feel a great need to emit their symptoms while at school or work. When
they arrive
home, however, the tics may erupt with violence and remain at a distressing
level
throughout the remainder of the day. It is not unusual for patients to "lose"
their tics as
they enter the doctor's office. Parents may plead with a child to "show the
doctor what you
do at home," only to be told that the youngster "just doesn't feel like doing
them" or
"can't do them" on command. Adults will say "I only wish you could see me
outside of your
office," and family members will heartily agree. A patient with minimal
symptoms may
display more usual severe tics when the examination is over. Thus, for example,
the doctor
often sees a nearly symptom-free patient leave the office who begins to hop,
flail, or bark
as soon as the street or even the bathroom is reached. In addition to the
moment-to-moment
or short-term changes in symptom intensity, many patients have oscillations in
severity
over the course of weeks and months. The waxing and waning of severity may be
triggered by
changes in the patient's life; for example, around the time of holidays,
children may
develop exacerbations that take weeks to subside. Other patients report that
their symptoms
show seasonal fluctuation. However, there are no rigorous data on whether life
events,
stresses, or seasons, in fact, do influence the onset or offset of a period of
exacerbation. Once a patient enters a phase of waxing symptomatology, a process
seems to be
triggered that will run its course - usually within 1-3 months. In its most
severe forms,
patients may have uncountable motor and vocal tics during all their waking
hours with
paroxysms of full-body movements, shouting, or self-mutilation. Despite that,
many patients
with severe tics achieve adequate social adjustment in adult life, although
usually with
considerable emotional pain. The factors that appear to be of importance with
regard to
social adaptation include the seriousness of attentional problems, intelligence,
the degree
of family acceptance and support, and ego strength more than the severity of
motor and
vocal tics. In adolescence and early adulthood, TS patients frequently come to
feel that
their social isolation, vocational and academic failure, and painful and
disfiguring
symptoms are more than they can bear. At times, a small number may consider and
attempt
suicide. Conversely, some patients with the most bizarre and disruptive
symptomatology may
achieve excellent social, academic, and vocational adjustments.

Associated Behaviors and Cognitive Difficulties

As well as tics, there are a variety of behavioral and psychological
difficulties that are
experienced by many, though not all, patients with TS. Those behavioral
features have
placed TS on the border between neurology and psychiatry, and require an
understanding of
both disciplines to comprehend the complex problems faced by many TS patients.
The most
frequently reported behavioral problems are attentional deficits, obsessions,
compulsions,
impulsivity, irritability, aggressivity, immaturity, self-injurious behaviors,
and
depression. Some of the behaviors (e.g., obsessive compulsive behavior) may be
an integral
part of TS, while others may be more common in TS patients because of certain
biological
vulnerabilities (e.g., ADHD). Still others may represent responses to the
social stresses
associated with a multiple tic disorder or a combination of biological and
psychological
reactions.

Obsessions and Compulsions

Although TS may present itself purely as a disorder of multiple motor and vocal
tics, many
TS patients also have obsessive-compulsive (OC) symptoms that may be as
disruptive to their
lives as the tics - sometimes even more so. There is recent evidence that
obsessive-compulsive symptomatology may actually be another expression of the
TS gene and,
therefore, an integral part of the disorder. Whether this is true or not, it
has been well
documented that a high percentage of TS patients have OC symptoms, that those
symptoms tend
to appear somewhat later than the tics, and that they may be seriously
impairing. The
nature of OC symptoms in TS patients is quite variable. Conventionally,
obsessions are
defined as thoughts, images, or impulses that intrude on consciousness, are
involuntary and
distressful, and while perceived as silly or excessive, cannot be abolished.
Compulsions
consist of the actual behaviors carried out in response to the obsessions or in
an effort
to ward them off. Typical OC behaviors include rituals of counting, checking
things over
and over, and washing or cleaning excessively. While many TS patients do have
such
behaviors, there are other symptoms typical of TS patients that seem to
straddle the border
between tics and OC symptoms. Examples are the need to "even things up," to
touch things a
certain number of times, to perform tasks over and over until they "feel
right," as well as
self-injurious behaviors.

Attention Deficit Hyperactivity Disorder (ADHD)

Up to 50% of all children with TS who come to the attention of a physician also
have
attention deficit hyperactivity disorder (ADHD), which is manifested by
problems with
attention span, concentration, distractibility, impulsivity, and motoric
hyperactivity.
Attentional problems often precede the onset of TS symptoms and may worsen as
the tics
develop. The increasing difficulty with attention may reflect an underlying
biological
dysfunction involving inhibition and may be exacerbated by the strain of
attending to the
outer world while working hard to remain quiet and still. Attentional problems
and
hyperactivity can profoundly affect school achievement. At least 30-40% of TS
children have
serious school performance handicaps that require special intervention, and
children with
both TS and ADHD are especially vulnerable to serious, long term educational
impairment.
Attention deficits may persist into adulthood and together with compulsions and
obsessions
can seriously impair job performance.

Emotional Lability, Impulsivity, and Aggressivity

Some TS patients (percentages vary greatly in different studies) have
significant problems
with labile emotions, impulsivity, and aggression directed to others. Temper
fits that
include screaming, punching holes in walls, threatening others, hitting, biting,
and
kicking are common in such patients. Often they will be the patients who also
have ADHD,
which makes impulse control a considerable problem. At times the temper
outbursts can be
seen as reactions to the internal and external pressures of TS. A specific
etiology for
such behavioral problems is, however, not well understood. Nevertheless, they
create much
consternation in teachers and great anguish both to TS patients themselves and
to their
families. The treating physician or counselor is often asked whether those
behaviors are
involuntary, as tics are, or whether they can be controlled. Rather than trying
to make
such a distinction, it is perhaps more helpful to think of such patients as
having a "thin
barrier" between aggressive thoughts and the expression of those thoughts
through actions.
Those patients may experience themselves as being out of control, a concept
that is as
frightening to themselves as it is to others. Management of those behaviors is
often
difficult and may involve adjustment of medications, individual therapy, family
therapy, or
behavioral retraining. The intensity of those behaviors often increases as the
tics wax and
decreases as the tics wane.

Etiology

The most intensive research in relation to etiology has focused on neurochemical
alterations in the brain.
Multiple neurochemical systems have been implicated by pharmacologic and
metabolic
evidence. The most convincing evidence for dopaminergic involvement has come
from the
dramatic response to haloperidol and other neuroleptics such as pimozide,
flupenazine, and
penfluridol, as well as exacerbations produced by stimulant medications.
Findings of
reduced levels of dopamine metabolites in cerebrospinal fluid (CSF) have led
investigators
to believe that TS results from a hypersensitivity of postsynaptic dopamine
receptors.
Serotonergic mechanisms have been suggested on the basis of reduced CSF
serotonin
metabolites. Since systems relying on neurotransmitters send projections to the
substantia
nigra and the striatum, they could play an important role in the
pathophysiology of TS.
Medications affecting that system seem somewhat effective for obsessions but
have
inconsistent effects on tics. The role of the cholinergic system is clouded by
contradictory reports. Enhancing cholinergic function by use of physostigmine
has been
associated both with the improvement and the worsening of TS. Elevated levels
of red blood
cell choline have been found in TS patients and their relatives, but the
significance is
unclear. Investigation of the GABAergic system suggests that it may be
implicated. The
proximity and connections between the GABA and dopamine systems support the
possibility of
an interrelationship. Response to clonazepam (a GABAergic agent) has been
positive in some
cases. Yet other GABAergic drugs such as diazepam do not have such positive
effects.
Noradrenergic mechanisms have been most persuasively implicated by observations
that
clonidine, a drug that inhibits noradrenergic functioning by the stimulation of
an
autoreceptor, may improve motor and phonic symptoms. Noradrenergic involvement
has also
been suggested by the exacerbation of the syndrome by stress and anxiety. The
use of
functional neuroimaging techniques such as positron emission tomography may
help clarify
many physiologic relationships and identify important anatomical areas in the
near future.

Stimulant Medications

A particularly important risk factor in tics and TS is the use of stimulant
medication.
Over 25% of all TS patients in some cohorts have had a course of stimulation
medication
early in the emergence of their behavioral or tic symptoms because they have
been diagnosed
as having ADHD. Over the last several years, series of cases have been reported
in which
the use of stimulants (methylphenidate, dextroamphetamine, and pemoline) has
been
correlated with the onset of motor and phonic tics. There is also chemical
evidence to
support the observation that stimulants will increase the severity of tics in
25-50% of TS
patients. In many cases, the tics associated with stimulant medication will
disappear with
the reduction or termination of the medication. It is more controversial
whether stimulants
can actually trigger or produce prolonged chronic multiple tics or TS that will
persist
following their termination. However, cases have been reported in which that
seems to have
occurred. Available information thus indicates that stimulants should be used
cautiously
with ADHD children who have a close relative with tics, should generally be
avoided with
ADHD children with a first-degree relative with TS, and should be terminated
with the onset
of tics in children who previously were tic-free. Children and parents should
be educated
concerning the risks versus benefits in each case prior to being treated with
stimulants.
Alternatives such as behavioral management, environmental manipulation, and/or
other types
of medication should be considered carefully.

Epidemiology and Genetics

While once thought to be rare, TS is now seen as a relatively common disorder
affecting up
to one person in every 2,500 in its complete form and three times that number
in its
partial expressions that include chronic motor tics and some forms of
obsessive-compulsive
disorder. The question of the familial transmission of TS was first raised in
the original
19th century descriptions of the disorder, but a genetic basis for TS was not
considered
seriously until recently. Several genetic studies have now been reported and
other rigorous
studies are now well enough along to draw several important conclusions. Those
studies have
investigated many families in which TS and other tic disorders have been
transmitted over
several generations. Based on available information, it is now clear that TS is
a genetic
disorder. The vulnerability to TS is transmitted from one generation to another.
When we
speak of "vulnerability," we imply that the child receives the genetic or
constitutional
basis for developing a tic disorder; the precise type of disorder or severity
may be
different from one generation to another. That vulnerability is transmitted by
either
mothers or fathers and can be passed on to either sons or daughters. When one
parent is a
carrier or has TS, it appears that there is about a 50-50 chance that a child
will receive
the genetic vulnerability from that parent. That pattern of inheritance is
described as
autosomal dominant. However, not everyone who inherits the genetic
vulnerability will
express any of the symptoms of TS. There is a 70% chance that female gene
carriers will
express any of the symptoms of TS. For a male gene carrier, there is a 99%
chance of
showing some clinical expression of the gene. The degree of expression is
described as
penetrance. In males, the penetrance is higher than in females; thus, males are
more likely
to have some form of expression of the genetic vulnerability. There is a full
30% chance of
female gene carriers showing no symptoms at all. For males, the figure is 1%.
There is a
range of forms in which the vulnerability may be expressed that includes full-
blown TS,
chronic multiple tics, and, as most recently recognized, obsessive-compulsive
disorder.
Some individuals have TS (or chronic tics) and obsessive-compulsive disorder
together;
others may have the conditions singly. There are also differences between the
sexes in the
form of expression of the TS gene. Males are more likely to have TS or tics;
females are
more likely to have obsessive-compulsive disorder; however, both males and
females may have
any combination or severity. The severity of the disorder is also highly
variable. Most
individuals who inherit the TS genetic vulnerability have very mild conditions
for which
they do not seek medical attention. Researchers are actively engaged in
searching for the
chromosomal location of the TS gene of affected individuals. At present, there
is no
genetic or biochemical test to determine if a person with TS or an unaffected
individual
carries the gene. There is no prenatal test for the vulnerability to TS. When
scientists
succeed in locating the gene, such tests may become available.

Non-Genetic Contributions

The individual variations in character, course, and degree of severity by which
TS is
manifested cannot be explained by genetic hypotheses alone. Furthermore, it
appears that
about 10-15% of TS patients do not acquire the disorder genetically. Thus, non-
genetic
factors are also responsible, both as causes and as modifiers of TS. Non-
genetic factors
that have been implicated include such stressful processes or events during the
prenatal,
perinatal, or early life periods as fetal compromise and exposure to drugs or
other toxins.
Findings from one study in which decreased birth weights were observed in the
affected
co-twins of discordant monozygotic pairs lend further support to the influence
of
environmental factors.



Clinical Assessment Of Tourette Syndrome

Assessment of a case of TS involves far more than simple diagnosis. Since
symptoms may
fluctuate in severity and character from hour to hour, a thorough understanding
of the
patient may take a considerable amount of time. As the patient becomes more
comfortable
with the doctor, there will be less likelihood of symptom suppression or
inhibition. Only
when there is confidence in the physician is the patient likely to acknowledge
the most
frightening or bizarre symptoms. The nature, severity, frequency, and degree of
disruption
produced by the motor and vocal tics need to be carefully assessed from the
time of their
emergence until the present. Inquiries should be made about factors that may
have worsened
or ameliorated their severity. A critical question concerns the degree to which
the tics
have interfered with the patient's social, familial, and school or work
experiences. In
those respects interviews with families may be revealing and informative.
During the
evaluation of a patient with TS, the clinician must assess all areas of
functioning to
fully understand both difficulties and strengths. It is important to explore
the presence
of attentional and learning disabilities, a history of school and/or work
performance, and
relationships with family and peers. Before receiving the diagnosis, the
patient and/or
family may have thought he or she "was going crazy." The patient may have
become extremely
distressed by his or her own experiences and by the often negative responses
evoked.
Parents may have scolded, cajoled, ridiculed, threatened, and perhaps beaten
the child to
stop the "weird" and embarrassing behavior, and the emotional sequelae may
affect the
patient far beyond the period of childhood. During the evaluation of a child,
therefore,
family issues including parental guilt need to be addressed. Relevant factors
elicited
through careful diagnostic evaluation can be approached through clarification,
education,
and therapeutic discussion with the youngster and the family. Careful
assessment of
cognitive functioning and school achievement is indicated for children who have
school
problems. TS children with school performance difficulties often do not have
clearly
delineated learning disorders, and the average IQ of TS patients is normal.
Rather, their
problems tend to lie in the areas of attentional deployment, perseverance, and
the ability
to keep themselves and their work organized. Many have difficulties with
penmanship
(graphomotor skills) and compulsions that interfere with writing. Determining
specific
problem areas will help in the recommendation of alternatives (e.g., extended
periods of
time for tests, the use of a typewriter or the emphasis on oral rathe! r than
written
reports). The neurological examination should include documentation of
neuromaturational
difficulties and other neurological findings. About half of TS patients have
non-localizing, so called "soft," neurological findings suggesting disturbances
in the body
scheme and integration of motor control. While such findings have no specific
therapeutic
implications, they are worth noting as "baseline" data since the use of
medications such as
haloperidol may cloud the neurological picture. The EEG is often abnormal in TS,
but the
EEG findings are nonspecific. Computed tomography of the brain produces normal
results in
people with TS. Thus, unless there is some doubt about the diagnosis or some
complicating
neurological factors, an EEG and a computed tomography are not necessary parts
of the
clinical evaluation. Additional studies that may be considered in the
biological work-up
include serum electrolytes, calcium, phosphorous, copper, ceruloplasmin, and
liver function
tests - all related to movement disorders of various types. In practice,
however, they are
rarely needed for the diagnosis. A behavioral pedigree of the extended family,
including
tics, compulsions, attentional problems and the like is useful. Previous
medications must
be reviewed in detail during assessment. If a child has received stimulant
medications, it
is important to determine what the indications for the medications were,
whether there were
any pre-existing tics or compulsions, and the temporal relation between the
stimulants and
the new symptoms. Catecholaminergic agonists are contained in other drugs, such
as in
decongestant combinations used in treating allergies and in medications used
for asthma. If
a patient with TS is on a stimulant or a drug containing an ephedrine like
agent,
discontinuation should be strongly considered. If the physician examines a
previously