Ritalin: Chemistry of the Drug and Route of Access of the Drug
By Emily Gibson
Attention Deficit Disorder (ADD) and Attention Deficit Hyperactivity
Disorder (ADHD) are neurobehavioral conditions with biological causes.
ADD describes difficulties in focusing on and attending to learning,
and in controlling behavior. ADHD refers to the same difficulties as
ADD, with the added component of hyperactivity, or impulsive behavior.
The acronym AD(H)D is used to refer to both disorders. (Booth, 1998)
AD(H)D is a real disability which is not due to lack of motivation or
self control. Based on current theory, AD(H)D is caused by a chemical
imbalance in the brain caused by a flaw in the way the brain manages
neurotransmitter production, storage, or flow. AD(H)D interferes with
learning and behavior control in childhood, and can impact adult
functioning in multiple areas throughout life. (Booth, 1998; Barkley,
1990; Bloomquist and Braswell, 1991)
Many theories have come and gone regarding the cause of AD(H)D,
including brain injury, refined sugar or food additives, and poor
parenting, all of which have been eliminated. New theories include
links to fetal environmental toxins, and genetic links. Some
researchers have found symptoms similar to AD(H)D in people with Fetal
Alcohol Syndrome and other chemically induced birth defects and
disorders. Supporting the genetic link theory, children who have
AD(H)D usually have at least one close relative with the disorder, one
third of fathers with AD(H)D have children with the disorder, and
almost all identical twins share the disorder. The DSM V, 4th ed.,
estimates 3 to 5 percent of school age children have AD(H)D. (What
Causes ADD?, 1999; Booth, 1998)
Psycho stimulants, like amphetamine, cocaine, and methylphenidate,
inhibit the reuptake of dopamine by inhibiting the dopamine
transporters in the presynaptic neuron. This inhibition allows higher
levels of dopamine to exist in synaptic cleft fluid, potentially
increasing the rate of firing of the post synaptic neurons. At least
this is how psycho stimulants effect people without AD(H)D symptoms.
For people with AD(H)D, psycho stimulants have the reverse effect of
calming behavior and increasing attention. (Gainetdinov, 1999)
There is no clear evidence of the mechanism by which Ritalin produces
these mental and behavioral effects. In 1957, Laufer stated that
stimulants activate the mid brain, putting it in a more synchronous
balance with the cerebral cortex (ADHD Medication Information, 1999).
Current researchers theorize Ritalin affects inhibitor sites and an
activator site (Doctor FAQ, 1999), and an effect on dopamine activity
is suspected, with many scientists thinking Ritalin affects all the
catecholamine neurotransmitters, especially dopamine (ADHD Medication
Information, 1999; Bloomquist and Braswell, 1991). People with AD(H)D
symptoms may have a dopamine deficiency. Recent research indicates
about 10 percent of the population has a lowered number of dopamine
receptors. This percentage of the population may have AD(H)D, and are
additionally more prone to drug and alcohol addiction (ADHD Medication
Information, 1999).
In people with AD(H)D, the part of the brain which controls attention
uses less glucose than in people without AD(H)D. This indicates that
the brain is not as active in these areas, since glucose is the fuel
neurons use when they are active. Ninety five percent of people with
AD(H)D benefit from psycho stimulants, which have been used since the
1940's as a treatment option (Booth, 1988; What Causes ADD, 1999). The
psycho stimulant most commonly used in treatment of Attention Deficit
(Hyperactivity) Disorder is Ritalin. The pharmaceutical name of
Ritalin is methylphenidate hydrochloride, and the chemical composition
is methyl alpha phenyl 2 peperidineacetate hydrochloride
(Methylphenidate, 1998). Ritalin is a Central Nervous System stimulant
and is considered a sympathomimetric compound, meaning it is similar in
construction to the brain's own neurotransmitters (Coleman, 1988).
Ritalin is administered in oral tablets or pills. It is water soluble,
and thus easily crosses the blood brain barrier and is rapidly absorbed
from the digestive system, though only 30 percent is available for the
body's use. Ritalin comes in 5mg, 10mg, and 20mg dose pills and is
taken 2 to 5 times per day, depending on the patient's needs and
metabolism. Effects of drug begin 15 to 20 minutes after ingestion,
and continue for 3 to 5 hours, with peak plasma levels 2 hours after
ingestion. Ritalin's water solubility also means it is rapidly
cleared from the body, leaving little to no residue. Average systemic
clearance of all traces of the drug is 10.2 hours, with 78 to 97
percent of the dose excreted in urine within 48 hours after ingestion.
Normal treatment includes over lapping of doses, to sustain a
consistent plasma level of the drug. (Coleman, 1988; CNS Stimulant,
1999; Booth, 1998)
References
ADHD Medication Information (1998 to 1999). Child Development
Institute. Available: www.cdipage.com/ADD_medications.htm
Barkley, R. A., Ph.D. (1990). Attention Deficit Hyperactivity Disorder:
A Handbook for Diagnosis and Treatment. New York, NY: The Guilford
Press.
Bloomquist, M. L., Ph.D., and L. Braswell, Ph.D. (1991). Cognitive
Behavioral Therapy with ADHD Children. New York, NY: The Guilford
Press.
Booth, R. C. (1998). Basic Information About Attention Deficit
Disorder. Attention Deficit Disorder Association. Available:
www.add.org/content/abc/basic.htm
CNS Stimulant (1995 to 1999). Mental Health Network Website. Phillip
W. Long, M.D. Available: www.mentalhealth.com/fr30.html
Coleman, W. S., M.D. (1988). Attention Deficit Disorders,
HyperActivity and Associated Disorders, (5th ed.). Wisconsin: Callipe
Books.
Gainetdinov, R.R., et al. (1999). "Role of Serotonin in the
Paradoxical Calming Effect of Psychostimulants on Hyper Activity."
Science, 283, 394 to 399.
Methylphenidate (1998). Rx List Website. Mosby, Inc. Available:
www.rxlist.com/cgi/generic/methphen.htm
Ritalin ((1996 to 1999). Doctor FAQ. Drug Infonet, Inc. Available:
www.druginfonet.com/faqrital.htm
What Causes ADD? (1999). Attention Deficit Disorder Association.
Available: www.add.org/content/research/causes.htm
Ritalin: Neurotransmitters
By Ray Hammer
Ritalin, generic name Methylphenidate, is the most widely used drug in
the United States to treat Attention Deficit Hyperactivity Disorder
(ADHD). Researchers first believed that Ritalin enhanced catecholamine
activity in the central nervous system, probably by increasing the
availability of dopamine and/or norepinephrine at the synaptic cleft.
The hypothesis is that Ritalin blocks the reuptake of the
neurotransmitter dopamine into presynaptic neuronal stores resulting in
the enhanced activation of dopaminergic neurons (Froimowitz, Patrick,
and Cody, 1995). This hypothesis has been challenged by recent studies,
finding that not only dopamine but also serotonin and norepinephrine
levels are affected in hyperactivity.
Studies of rat brains have discovered how methylphenidate works on
dopamine and norepinephrine. Dopamine uptake in the presynaptic neuron
is affected by the use of methylphenidate. Methylphenidate inhibited
dopamine uptake, therefore increasing the amount of neurotransmitters
allowed across the synaptic cleft. In the rat brains, a correlation was
discovered between the number of compounds inhibiting dopamine uptake
and the compounds that inhibited dopamine methylphenidate in the
striatum area of the brain (Schweri, Skolnick, Rafferty, Rice,
Janowsky, and Paul, 1984). Although methylphenidate binding was
unevenly distributed throughout the brain, highest densities were found
in the striatum. Other research using rat brains investigated the
binding at monoamine transporter sites. Dopamine transporters exhibited
a higher inhibition uptake therefore increasing the binding to release
ratio of the neurotransmitter. The affinities of methylphenidate and
derivatives at dopamine and norepinephrine transporters were very well
correlated, suggesting that both dopamine and norepinephrine reuptake
sites are being inhibited. The serotonin transporters were 2 orders of
magnitude below that of norepinephrine and dopamine (Gatley, Pan, Chen,
Chaturvedi, and Ding, 1996).
The relationship between serotonin and how it effects the brain in
hyperactivity remains uncertain but researchers are closing in on the
relationship. In a study using rats that were injected with
methylphenidate, results showed that both serotonin and dopamine helped
reduce methylphenidate induced behavior. Serotonin receptors directly
modulated dopamine neurotransmission and helped to inhibit
methylphenidate induced behaviors in the rats (Kleven, Prinssen, and
Koek, 1996). Although serotonin receptor agonist properties decreased
some of the methylphedidate behaviors, it didn't control all of them,
suggesting that both serotonin and dopamine receptors need to be
effected in order to balance out the affects of methylphedidate.
Kleven, Prinssen, and Koek's conclusion was that the ability of the
mixed serotonin receptor agonist and dopamine receptor antagonist
buspirone inhibited methylphenidate induced behaviors.
A recent study conducted at Duke University (1999) on hyperactive mice
discovers that both serotonin and dopamine neurotransmitters are
involved in hyperactivity. Duke University made their discovery by
genetically creating "knockout" mice lacking the dopamine transporters
that scavenge the dopamine remaining in the synaptic gap after the
neurotransmitter has triggered a nerve impulse. The mice had five times
the normal amount of dopamine levels and their neurons were firing at
abnormally high rates. Methylphenidate was given to the mice to bring
down the rate in which dopamine was being released across the synaptic
cleft. This brought the level of dopamine release to a normal rate.
Prozac, which inhibit the reuptake of serotonin in the synapse, also
dramatically reduced the hyperactivity in mice. Other drugs that
activated serotonin receptors or increased brain serotonin levels also
reduced hyperactivity in the mice. In the brain of the "knockout" mice
it was concluded that the symptoms associated with ADHD were caused by
too little serotonin and too much dopamine being released into the
synaptic cleft.
In summary methylphenidate effects both dopamine and serotonin
receptors. The connection between the two still is being explored, but
scientists believe that in order to control ADHD both dopamine and
serotonin levels must be balanced.
References
Gatley, S. J., Pan, D., Chen, R., Chaturvedi, G., and Ding, Y. (1996).
Affinities of Methylphenidate Derivates for Dopamine, Norepinephrine
and Serotonin Transporters. Life Science, 58, 231 to 239.
Schweri, M. M., Skolnick, P., Rafferty, M. F., Rice, K. C., Janowsky,
A. J., and Paul, S. M. (1985). (3H)Threo Methylphenidata Binding to 3,
4Dihydroxyphenylethylamine Uptake Sites in Corpus Striatum: Correlation
with the Stimulant Properties of Ritalinic Acid Esters. Journal
Neurochem, 45, 1062 to 70.
Froimowitz, M., Patrick, K. S., and Cody, V. (1995). Conformational
Analysis of Methylphenidate and Its Structural Relationship to Other
Dopamine Reuptake Blockers Such as CFT. Pharmaceutical Research, 12,
1430 to 1434.
Kleven, M., Prinssen E.P., and Koek, W. (1996). Role of Serotonin
receptors in the ability of mixed serotonin receptor agonist / dopamine
receptor antagonists to inhibit methylphenidate induced behaviors in
rats. European Journal Pharmacology, 313, 25 to 34.
New Theory May Explain Ritalin Action in Hyperactivity. (1999).
Http://www.dukenews.duke.edu/Med/CARON.HTM
Ritalin: Inhibitory and Excitatory Potentials
Marlene Gard
Ritalin, or its generic Methylphenidate, is a stimulant drug. In
treatment of ADHD Methylphenidate produces a calming effect in affected
children. It seems contrary to expectation that children would calm
down after taking a stimulant. However, on the same low doses,
children and adults with and without ADHD react in the same way. It
appears that stimulant medications reinforce the brain's ability to
focus attention during problem-solving tasks. This phenomenon was
first reported by Bradley in 1937 and has since been observed in many
other studies (Barlow, 1999).
The way methylphenidate works in the brain and central nervous system
is not completely understood, but it presumable activates the brain
stem arousal system and cortex to produce its stimulant effect. There
is no specific evidence which clearly establishes the mechanism whereby
methylphenidate produces its mental and behavioral effects in ADHD
patients, nor conclusive evidence regarding how these effects relate to
the condition of the CNS.
Methylphenidate is an indirect catecholamine agonist like amphetamine
that is potent as a DA uptake inhibitor; it only weakly blocks
vesicular uptake of DA; and methylphenidate-evoked DA overflow depends
on neuronal activity as well as on the integrity of the vesicular
compartment. From these findings, it has been concluded that
methylphenidate blocks reuptake and to a lesser extent promotes release
of DA from the vesicular (but not the cytoplasmic) pool (Barlow, 1999).
Methylphenidate is rapidly and extensively absorbed from tablets
following administration; however, owing to extensive first-pass
metabolism, bioavailability is low (approx. 30%) and large individual
differences exist (11 to52%9) (Mental Health).
Peak plasma concentration of 10.8 and 7.8 ng/mL were observed, on
average, 2 hours after administration of 0.30 mg/kg in children and
adults. However, peak plasma concentrations showed marked variability
between subjects. Both the area under the plasma concentration curve,
and the peak plasma concentration showed dose proportionality (Mental
Health).
Methylphenidate is eliminated from the plasma with a mean half-life of
2.4 hours in children and 2.1 hours in adults. The apparent mean
systemic clearance is 10.2 and 10.5 L/hr/kg in children and adults, for
a 0.3 mg/kg dose. These indicate that the pharmacokinetic behavior of
methylphenidate in hyperactive children is similar to that in normal
adults. The apparent distribution volume of methylphenidate in
children was approximately 20 L/kg, with substantial variability (11 to
33 L/kg) (Mental Health).
Following oral administration of methylphenidate, 78 to 97 % of the
dose is excreted in the urine and 1 to 3% in the feces in the from of
metabolites within 48 to 96 hours. The main urinary metabolite is
ritalinic acid, unchanged methylphenidate is excreted in the urine in
small quantities (Mental Health).
In blood, methylphenidate and its metabolites are distributed between
plasma (57%) and erythrocytes (43%). Methylphenidate and its
metabolites exhibit low plasma protein binding (approx. 15%) (Mental
Health).
The ability of psychomotor stimulants to alleviate the symptoms of ADHD
implies that the disorder might arise from an underlying pathology of
the catecholaminergic system. Support for this hypothesis comes from
the work of Porrino and Lucignani (1987), who showed that treatment of
rats with a low dose of methylphenidate stimulated glucose utilization
in the nucleus accumbens and olfactory tubercle, two target areas of
the mesolimbic DA pathway. Furthermore, several clinical studies found
abnormally low urinary levels of either the DA metabolite homovanillic
acid or the NE metabolite 3,4-methoxy-phenylglycol in sub-populations
of ADHD children. However, in some cases the already low metabolite
concentrations fell even further following stimulant treatment. It
thus remains unclear whether there are neurochemically distinct
subtypes of ADHD, why some patients show normal catecholaminergic
activity, what differentiates treatment responders from nonresponders,
and what neurochemical processes are responsible for the therapeutic
efficacy of methylphenidate (Barlow, 1999).
Researchers at Duke University have found that methylphenidate raises
the level of Serotonin in the brain, inhibits the reuptake of dopamine,
thus serving as a potent dopamine agonists and causes the release of
both norepinephrine and dopamine from the terminal buttons by causing
the transporters for these neurotransmitters to run in reverse,
propelling DA and NE into the synaptic cleft (Carlson, 1998).
Since the use of stimulant medication with children with ADHD was first
described in 1937, hundreds of studies have documented the
effectiveness of methylphenidate in reducing the core symptoms of the
disorder. Approximately 70% of cases experience reduced hyperactivity
and impulsivity and have improvement in concentration on tasks (ADD,
1999).
References:
Barlow, David H. (1999). Abnormal Psychology. Brooks/Cole Publishing
Company.
Carlson, Neil R. (1998). Physiology of Behavior. Allyn and Bacon
Bob Seay, Attention Deficit Disorder - 1/19/1999 How Does Ritalin Work?
http;//add.about.com/health/disease/add/library/weekly/aao011999.htm
Internet, Mental Health, http://www.mentalhealth.com/drug/p30-r03.html
NEUROTRANSMITTERS AND ION CHANNELS:
Ritalin's Elusive Effects.
Thomas T. Fitzsimon III
Three neurotransmitters in the brain, dopamine, norepinephrine, and
serotonin, are affected by methylpenidate (Ritalin)(Wu X et al., 1999,
p.1). However, it is currently believed that only one of these
neurotransmitters, serotonin, is responsible for the calming effects
associated with Ritalin. (Gainetdinov et al., 1999, p.2)
Ritalin works by blocking the reabsorption of neurotransmitters from
the synapse between neurons.(Volkow et al., 1993, p.1) The result is a
substantial increase in the extracellular levels of those
neurotransmitters.
What has puzzled scientists for years is how the elevated
concentrations of these chemicals exert a therapeutic effect on the
patient. To understand this better we will take a brief look into the
function of each one individually.
Dopamine (DA) is a catecholamine and is synthesized in the cytoplasm of
the terminal buttons. The biosynthetic pathway involves several steps
that convert tyrosine to DA. Once produced, DA is stored in synaptic
vesicles contained within the terminus of the presynaptic
neuron.(Carlson, 1998, p. 103)
Dopamine can elicit both excitatory and inhibitory potentials. Which
one occurs, though, is dependant on the post synaptic receptor.(Dorit
at el., 1991, p.397) D1 receptors, through a pathway involving cAMP,
depolarize the post synaptic neuron, allowing them to fire more easily.
D2,D3, and D4, however cause the opposite effect, resulting in
hyperpolarization.(Alberts et al., 1994, p.741) (Carlson, 1998, pg.103)
High extracellular concentrations of DA cause aggressive behavior and
other symptoms that are associated with hyperactive disorders.
Ritalin, the drug commonly prescribed for these disorders actually
increases the concentrations of DA in the neuronal synapses by
disallowing its reabsorption.(Berl, 1997, p.71-8) This occurrence was
generally accepted as the basis of Ritalin's therapeutic effect.
However, it is rapidly appearing to be a side effect in the scientific
community.
Norepinephrine (NE) begins as dopamine which is synthesized in the
cytoplasm of the terminal buttons.(Carlson, 1998, p.107) Some of this
dopamine is collected into synaptic vesicles where an enzyme, dopamine
B-hydroxylase, converts the dopamine to NE.(Carlson, 1998, p.104) NE,
a catecholamine, is released from axonal varicosities and causes
excitatory behavioral effects when it comes in contact alpha-1, or beta
receptors. These receptors cause a gradual depolarization of the
postsynaptic neurons by slowing the actions of the sodium potassium
pump, allowing them to fire more easily. Alpha-2 receptors, also
affected by NE, produce the opposite effect through slow
hyperpolarization of the postsynaptic neuron. This hyperpolarization
is achieved by the opening of chloride channels which increases the
charge difference across the membrane.(Carlson, 1998,p.104)(Droit et
al., 1991, p. 397, 450)
Extracellular levels of NE are controlled by monoamine oxidase-A, an
enzyme which degrades the neuropeptide.(Carlson, 1998, p.108) Ritalin
affects the levels of NE by blocking the actions of monoamine oxidase-
A, therefore contributing to a rise in NE levels in the synapse. These
increased levels can cause hyperactivity, overconfidence and sometimes
delusions. (Dorit et al., 1991, p397) This rise in NE is also a side
effect associated with Ritalin.
The final neuropeptide that we will be exploring is Serotonin (5-HT).
The pathway for the synthesis of 5-HT begins with the amino acid
tryptophan. Enzymes, tryptophan hydroxylase and 5-HTP decarboxylase
convert tryptophan to 5-HT. The 5-HT produced is stored in
varicosities at the terminus of the axon.(Carlson, 1998, p.110)
Serotonin is the chemical signal responsible for the regulation of
eating, sleep, pain, and arousal. The highest use of serotonin lies in
the pons, medulla, and raphe nuclei of the midbrain.(Carlson, 1998,
p.110) In addition there have been nine different types of serotonin
receptors identified. All 5-HT receptors, except 5-HT3, are
metabotropic receptors. This simply means that once serotonin binds,
an enzyme begins a chain of events that opens an ion channel. 5-HT3
receptor is ionotropic and produces inhibitory post synaptic
potentials.(Carlson, 1998, p.110)(Alberts et al., 1994, p.536)
Individuals lacking a certain amount of 5-HT are prone to depression
and other unpleasant symptoms. Ritalin, which works on hyperactivity,
actually boosts the amount of 5-HT in the brain by blocking
reabsorption. This elevation in the levels of serotonin seems to be
what causes the reduction in aggression and elevation of attention
levels in hyperactive disorders.
Wu X, Gu HH (1999). Molecular Cloning of the Mouse Dopamine
Transporter and Pharmacological Comparison with the Human Homologue.
Gene (FOP), 233, 163-70.
Caron, M., Gainetdinov R, (1999). New Theory May Explain Ritalin
Action In Hyperactivity. ScienceDaily Magazine.
wysiwyg://14http://www.csiencedaily.com/releases/1999/01/990118075443.h
tm
Volkow ND., Wang GJ., Fowler JS, Gatley SJ, Ding YS, Logan J., Dewy SL,
Hitzemann R, Lieberman J. (1996). Relationship Between
Psychostimulant-induced "High" and Dopamine Transporter Occupancy.
Proc Natl Acad Sci USA 1996 Sep 17;93 (19); 10388-92.
Berl, R. (1997). Psychopharmacology, (1st ed.) NY, Udton
Carlson, Neil R. (1998). Physiology of Behavior; (6th ed.) MA,
Viacom.
Dorit, R., Walker, W., Barnes, R. (1991). Zoology (1st ed.) FL,
Saunders College Publishing
Alberts, B., Bray, D., Lewis, J., Raff, M., Roberts, K., Watson, J.
(1994). Molecular Biology of The Cell (3rd ed.) NY, Garland
Publishing.
Whole Body Physiological Effects of Ritalin
Written By: Meggan Blanks
Ritalin, like all stimulants, has the ability to produce varying
physiological effects on different users. Some reactions are grossly
complex and severe, constituting permanent abnormalities in brain and
body structures and functioning. Unsurprisingly, these physiological
effects are surrounded by medical controversy debating the severity,
occurrence, and even the existence of some of these aliments.
Important to remember are the ever changing advancements in medical
science and pharmaceutical technology, offering new insight and
dispelling old theories on the physiological consequences from Ritalin
use. In fact most physiological effects of Ritalin are considered
manageable bi-products and accompany many pharmaceutical treatments.
These bi-products are thought to be a compromise in controlling
Attention Deficit/ Hyperactivity Disorder.
The primary physiological effect of Ritalin can be found in its
interaction with the brain's neurotransmitters or chemical messengers:
Serotonin, Dopamine, and Norepinphrine. Stimulants like Ritalin are
referred to as catecholamine agonists, meaning they directly affect and
alter neurotransmitters. In this process, Ritalin increases the
activity of the brain by first increasing the amount of
neurotransmitters dropped into the synapse area and secondly making the
neurotransmitters remain longer in its receptor space. This results in
an overflow of chemicals in the synapse and an overall arousal in the
central nervous system (Garber, 1996, p.89). Effects on this process
can be seen in the increased motor activity, euphoria, appetite
suppression, and general alertness of people taking Ritalin.
It is important to remember that Serotonin, Dopamine, and
Norepinephrine are some of the most important neurotransmitters in the
brain, each performing separate tasks in the body. Serotonin is in
charge of the brain's regulation of mood and pain and in the control of
eating, sleeping, and arousal. Ritalin is thought to induce
hyperactivity in the Serotonin neurotransmitter system. It is important
to note "that this may contribute to the production of more extreme
mental aberrations in select patients, causing psychosis with
hallucinations and delusions" (Breggin, 1998, p.46). Despite this
finding, very few cases have been reported. Of those reported, it was
thought that Ritalin exacerbated or brought out underlying disorders
that were present prior to treatment (Fisher, 1998, p.243). The next
neurotransmitter Dopamine is involved in movement, attention, learning,
and the reinforcing effects for drugs of abuse. Ritalin causes
hyperactivity in Dopamine neurotransmitters, which is thought to be
responsible for the suppression of spontaneous behaviors associated
with Attention Deficit/ Hyperactivity Disorder. There is some
speculation that impairment in Dopamine systems may cause the robotic
or zombie like behaviors sometimes reported by Ritalin users (Breggin,
1998, p.45). Norepinphrine, the last of the neurotransmitters effected
by Ritalin, regulates the control of alertness and wakefulness. This
neurotransmitter when influenced by Ritalin, is closely tied to over
activity in the cardiovascular system (Breggin, 1998, p.46). Although
research is making strides in comprehending Ritalin's relationship with
neurotransmitters, it is important to remember that science still has a
rudimentary understanding of neurotransmitters and their behavioral
contributions.
The effects of Ritalin on the central nervous system are more widely
understood. These physiological reactions are well documented and
commonly associated in Ritalin use. One of the most common reactions is
a notable increase in systolic and diastolic blood pressure,
Hypertension (irregularly high blood pressure), Palpitations (irregular
heart rate), and Tachycardia (abnormally high heart rate). Decreasing
the dosage of Ritalin controls these reactions; sometimes they simply
vanish over time. Less frequently, dermal reactions occur causing
itching, swelling, hives, and in some cases extreme skin rashes. In
addition, there are some significant changes that occur in the brain.
For example, the brain is found to have increased glucose metabolism in
the areas of motor activity and mental functioning (Fisher, 1991,
p.243). Another aspect altered by the use of Ritalin is the brain's
surface or cortex region, which experiences a decrease in blood flow
(Breggin, 1998, p.38). "Researchers attribute the reduction in blood
flow to constriction of the blood vessels, probably related to the
drug's impact on dopamine" (Breggin, 1998, p.39). There is some
clinical evidence that Ritalin may lower the convulsion threshold in
patients with a prior history of seizures, abnormal EEG results, and in
some cases, no history of either criteria. The cause for this seizure
reaction is most likely associated with Ritalin's classification as a
stimulant. Other rare physiological reactions can include: Anemia
(bleeding disorder), Leukopenia (low white cell count), blurred vision,
liver cancer, organic psychosis, and abnormal spasms and tics.
One of the most publicized debates surrounding Ritalin consumption is
the way in which it effects a child's overall growth. As a product of
scientific dispute, this subject is comprised of conflicting findings
from the scientific community. In the widely publicized book, Talking
Back to Ritalin (1998), Breggin states there "is now a mountain of
evidence that stimulants disrupt growth hormone production on a daily
basis and that they also can reduce the child's overall growth,
including height and weight" (p. 25). It is argued that overall growth
inhibition would also affect the bodies' organs, including the brain
(Breggin, 1998, p.25). Another study from as early as 1977 completed
by D. Aarskog, acknowledges the possible long-term adverse effects of
these drugs on the growth of children indicat[ing] the need for caution
in the widespread use of these agents" (Breggin, p. 26). Other studies
are telling a different story about Ritalin's role in growth
inhibition. Research conducted in 1997, "provides further confirming
evidence that the use of Methylphenidate [Ritalin] does not have a
long-lasting impact upon growth rates" (Fisher, p.242). Yet other
research has also suggested that in some cases, Ritalin does mediate
growth issues during early adolescence only to resolve them in late
adolescence (Fisher, 1996, p.242). Given available research, one may
conclude that Ritalin does have some effect on an individuals growth,
yet it is the extent of growth inhibition and the possibility of long-
lasting effects that remains under suspicion.
One can easily see the many contradictions that surround the
physiological effects of Ritalin. Some day, science will be in the
position to fully understand the relationship between medications and
their physiological, behavioral, and psychological effects. Currently,
the process of medicating an individual can almost seem like trial and
error. If the primary behavioral effects are positive during
treatment, then the medication is considered successful. There is much
to learn about why Ritalin is so effective in treating people with
Attention Deficit/ Hyperactivity Disorder; quite possibly future
research will provide some answers.
References:
Breggin, P.R. (1998). Talking Back to Ritalin: What doctors aren't
telling you about stimulants for children. Monroe, ME: Common Courage
Press.
Fisher, B.C. (1998). Attention Deficit Disorder Misdiagnosis:
Approaching ADD from a brain/neuropsychological perspective for
assessment and treatment. Boca Raton, FL: CRC Press.
Garber, S.W. (1996). Beyond Ritalin: Facts about medication and other
strategies for helping children, adolescents, and adults with Attention
Deficit Disorder. New York, NY: Villard Books.
Ritalin: Primary Behavioral Changes After Use
Written by: Desiree Wallan
Attention deficit hyperactivity disorder or ADHD is an increasing
problem in society today. Attention deficit hyperactivity disorder
effects people of all ages, but mainly school age children. Some
scientists speculate that there has been an increase in the number of
reported cases, due to the increase in familiarity with the disorder
(Hinshaw, 1994). They also speculate that kids in school seem to have
a harder time coping with ADHD because they are expected to behave and
sit for long periods of time in an environment that is not necessarily
stimulating enough for them (Hinshaw, 1994). ADHD behaviors can
persist into adulthood and are often associated with increased risk of
mental disorders, irresponsible and impulsive lifestyles, and
sociopathic behaviors (Fisher, 1998).
Main characteristics of ADHD are age inappropriate levels of
inattention, hyperactivity, impulsivity, and activity level modulation.
Children with ADHD frequently exhibit defiance, aggression, and other
anti social behavior (www.rxlist.com). These characteristics often lead
to a child having major difficulties with achievement in school,
regardless of the fact that they might not display formal learning
disabilities (Tan, and Schneider, 1997). These types of anti social
behavior can lead to problems at home, in school, and may inhibit the
child's ability to form relationships with peers as well as caregivers.
Today there are many methods of treatment, but one of the most common
treatments is a prescription of stimulants. Methylphenidate commonly
known as Ritalin is one of the most prescribed stimulants on the market
(www.rxlist.com). Ritalin has a drastic effect on the behavior of
people with ADHD. Ritalin does a great job of eliciting the expected
or desired positive behavior changes. The expected or desired behavior
changes that occur after taking Ritalin are considered the Primary
behavior changes.
The primary behavior changes after taking Ritalin are increased control
of behavior, compliance, less aggression and disruption (Fisher, 1998).
This is helpful to the children, because it can enable them to stay out
of trouble, get along with others, and behave in a way that is socially
acceptable.
There is also evidence that Ritalin has increased attention span,
impulse control, academic performance, and improved peer relationships
(Fisher, 1998). Increased attention span and impulse control will
enable kids to focus on what is being presented long enough to
comprehend and understand. Ritalin has also increased performance on
cognitive measures. Allowing children to listen better to verbal
instructions, and to pay better attention to auditory or visual
stimulants (Tan, and Schneider, 1997).
Let's take a closer look at a few cases where mothers talk about their
sons ADHD problems, and how Ritalin has helped control most of their
primary symptoms. In the Following, Beth Stevens, who I spoke with on
October 7,1999, talks about her son Johnny, his major problems with
ADHD, putting Johnny on Ritalin, and how Ritalin helped Johnny.
Johnny is a seven-teen year old boy. He has been diagnosed with ADHD
since he was four. Johnny's problems with ADHD did not really affect
him until he entered school. His mother Stevens said that he did act
hyper and would always "buzz" around, but she didn't feel that it was
really that big of a problem. She felt it was normal behavior for a
young boy.
Once Johnny got into school his mother started getting several phone
calls about Johnny's "out of control," behavior. Almost everyday the
teacher would tell his mother about Johnny's inability to sit still,
follow directions, and listen to instructions. The teacher told
Stevens that Johnny would literally "bounce off the walls," or "climb,
and hang" on people. It wasn't long before the teacher told Stevens
she did not want to deal with Johnny anymore. The teacher started
sending Johnny down to the office everyday. Johnny struggled with his
teachers for the first two years, and by his third year of school his
behavior became uncontrollable at school. Things seemed to get so bad
that, one-day, during a conference with one of Johnny's teachers, the
teacher lost it. She started "going off" (Stevens, 1999) right in
Johnny's face, she got so mad that she started to choke Johnny.
At this point Johnny's mother realized that something had to be done.
Stevens hadn't wanted to "medicate" Johnny, because she felt that it
would make her son be someone else other than himself; however she
realized that if Johnny was ever going to get through school something
had to be done.
Johnny's parents took him to the doctor and the doctor immediately put
him on Ritalin. Virtually immediately his demeanor started to change.
His teachers as well as his parents noticed the difference.
Suddenly Johnny could behave and sit still in class. For the first
time he could do homework. Stevens was amazed, now they actually had
something to evaluate Johnny by. Stevens said that Johnny started
getting along better with everyone. People weren't so "Put off," by
him. Now that Johnny could talk to people without "climbing" all over
them, he was able to establish relationships with his peers as well as
his caregivers.
Stevens explained that Johnny was able to focus and pay attention when
he took Ritalin. She said it really seemed to help him get through
school. Stevens did start to notice some problems. Typically if
Johnny's Ritalin was administered correctly things would be okay, but
every now and then a teacher might over medicate him. She explained
that the teachers and sitters liked what Ritalin did for Johnny's
behavior so much that sometimes they would give him one pill, and then
another a little while later. They did not want to deal with him if he
was off of Ritalin so sometimes they ended up giving him too much. She
said that you could tell when Johnny had too much Ritalin, because he
would just space out. He walked around like a zombie (Stevens, 1999).
He would actually be disabled further, because he was so "doped" up
that he couldn't inner act with people or his work. Stevens made it
clear this didn't happen very often, but when it did she would become
frustrated in the fact that Johnny really seemed to need Ritalin.
Johnny used Ritalin for over ten years. Now he is in high school and
is trying to get through school without it. He said he just doesn't
like the way it makes him feel. He said he want to be able to be
himself, and not feel like he was putting on a facade. Johnny said it
is tuff, but now he takes classes that are more hands on like Auto
shop, and he only goes to school for half of the day. The rest of the
day he either works or plays football. He said he still has trouble
sitting in class, and usually has to be doing something while he sits
there. It could be tapping a pen, chewing gum, chewing on a pen cap,
or even just pacing back and forth at the back of the classroom.
He said his teachers sometimes get frustrated, but usually allow him to
do these activities to regulate himself.
Johnny said he feels that he needed the Ritalin when he was younger,
but tries now that he is older to get through everyday life without it.
Another lady named Anita Hadley, whom talked to on October 1,1999,
spoke about her seven-year-old boy, Michael. Hadley said her son like
Johnny had trouble paying attention, sitting still and behaving
properly once he got to school. She said that before he got to school
it didn't seem to be as much of a problem. She admitted that some of
his sitters or pre-school teachers had mentioned a few times that they
had trouble with him being hyper or defiant.
Once Michael started formal schooling he started having trouble in
class, and Hadley found it very; very hard to get Michael to do his
homework. They talked with the teachers that seemed to be having the
most trouble with him and decided to take Michael to the doctor. At
age six the doctor recommended Michael be placed on Ritalin. Soon
after he started taking Ritalin he seemed to improve drastically. He
was able to sit still, pay attention, and focus. The use of Ritalin
enabled him to sit down long enough to get through his schoolwork.
Michael also seems to have better control over himself overall. He
doesn't seem quite so distracted. Hadley mentioned that Michael's self
esteem seems to have gone up since Ritalin. She has also noticed that
he is now invited to more functions like birthday parties. She feels
that this is because people aren't afraid of him acting up anymore, and
feel more comfortable that he will be compliant and "civilized"(Hadley,
1999).
Hadley stated that she is still skeptical of Ritalin, because they
don't know very much about the long-term effects, but she can't ignore
what it has done for Michael, both academically, and socially.
Obviously Ritalin is not a miracle cure by any means; however it does
seem to work to change ADHD primary behaviors. It seems that Ritalin
should not be the sole form of therapy. Ritalin should be used in
conjunction with other forms of therapy.
References:
Hinshaw, S. P., (1997). Attention Deficit and
Hyperactivity in Children. Thousand Oaks, California: Sage.
Fisher, B. C., (1998). Attention deficit disorder
misdiagnosis: approaching ADD from a brain behavior/neuropsychological
perspective for assessment and treatment. Boca Raton, Florida: CRC
Press.
Pediatric Series (Vol. 101, No. 5) (1997). New York:
McGraw-Hill.
Methylphenidate (1998).
Http://www.rxlist.com/cgl/generic/methphen.htm
Hadley, A. (October1,1999). Personal communication.
Stevens, B. (October 6,1999). Personal communication.
Ritalin: Behavioral Side Effects and Effects Reported by Users
By: Brienne Bergo
"By taking Ritalin most youngsters sustain attention better in class,
comply more readily with teacher and parent requests, display better
organization, show less impulsivity in behavioral response, and exhibit
less motoric movement" (Hinshaw, 1995, p. 105). Even though Ritalin is
considered one of the safest drugs for children, it still carries with
it the adverse physiological side effects that you read about above.
Ritalin also causes many adverse behavioral side effects that need to
be noted.
The most common side effects of Ritalin are irritability, loss of
appetite and insomnia. These side effects are most commonly reported
when the child first begins to take Ritalin (Hinshaw, 1995, p. 110).
When a doctor prescribes a child with Attention Deficit Disorder or
Attention Deficit Hyperactive Disorder to take Ritalin, he prescribes a
dose compatible with the child's age, weight, height, and the behaviors
described by his/her parents (Barkley, 1990). However, it usually
takes a trial and error process in order to figure out exactly how much
Ritalin a child needs. Once they have established the right dosage
many of these common side effects fade or completely disappear
(Hinshaw, 1995, p. 115).
There are also many rare or isolated side effects which are associated
with Ritalin. However, many of these effects may have to do with
incorrect doses being administered to children. Users have reported
cognitive overfocusing when they first begin to take Ritalin, or if
they are accidentally given too much in one day (Fisher, 1988, p. 152).
When someone is cognitively overfocusing they are easily frustrated or
"spaced out". They're concentrating so intensely that they can't focus
on the whole picture of what they're doing. Another behavioral side
effect of Ritalin is social withdraw (Fisher, 1988, p. 153). Even
though Ritalin is a stimulant, its effect on ADD and ADHD children is a
sort of calming effect. Therefore, if a child is taking too much
Ritalin he can be "spaced out" and this can lead to a social
withdrawal. Brigit Fowler, the coordinator at Valley Elementary
School, says that she's seen children change in thirty minutes because
of Ritalin. Mrs. Fowler recalled one child who sat on the floor by him
self for over an hour twirling around a dinosaur in his hands. All the
other kids were running around laughing and playing with their
dinosaurs and he was just sitting there with a blank look on his face
(Fowler, 1999). I myself have seen a few cases like this and it is
very disturbing. Fortunately though their behavior usually resumes back
to normal as soon as their doctor figures out the right dose of Ritalin
to give the child. Another cause of social withdrawl could also be the
fact that the other kids may know that the child with ADD or ADHD is
taking medicine; when something is happening that they don't
understand, kids can be very cruel. Finally, Ritalin can exacerbate or
precipitate tics (Fisher, 1988, p. 154). Tics are involuntary motor or
vocal behaviors. Tics can be especially embarrassing for the child,
which can lead to further frustration and social withdrawl. This side
effect can also be eliminated when the child is given the right amount
of Ritalin. Unfortunately there have been isolated cases where the
tics caused by the Ritalin turned into Tourettes syndrome. In this
case the child needs to switch to another stimulant.
Overall, these side effects are quite rare and changing the dosage that
the child is receiving can usually eliminate them. Physicians insist
that the greatest concern in giving children Ritalin is emphasizing the
correct dosage (Hinshaw, 1995, p. 72). Pediatricians try varying the
doses of Ritalin, which usually seem to help early in the day, only to
be followed by an intense period of overactivity late in the afternoon
after the Ritalin wears off. This phenomenon is called the "negative
rebound effect" (Fisher, 1988, p. 129). The negative rebound effect
constitutes a return to the baseline behavior. Ritalin has a half life
of only three and a half hours and is usually given in the morning and
at lunch in order to control the child's behavior at school
(rxlist.com). It is not a good idea to give Ritalin to children in the
afternoon because of the insomnia or lack of appetite that can occur.
Unfortunately, when the child is home interacting with his family and
peers, his behavior is accelerated once again.
These are all facts given by physicians and researchers on the side
effects of Ritalin. But how do these convert over to real, live
children that we deal with on a one to one basis everyday? I
interviewed a long-term survivor of Ritalin, a women whose ten year old
son is on Ritalin and a
Father whose eight year old daughter is on Ritalin. I found some
interesting information, which doesn't always coincide with the facts
given by the experts.
Chris is twenty-three years old now. He was diagnosed with ADHD when
he was nine years old. He remained on Ritalin until he was thirteen.
He explained that Ritalin helped him concentrate in school, and he says
it "mellowed him out" (Chris, 1999). However, when he was thirteen his
doctor decided he didn't need Ritalin anymore. Chris reported that he
struggled in school, his aggression rose and he never felt content.
Chris then decided to get into methamphetamines. Chris was addicted to
speed off and on until he was twenty-one years old. He said that the
speed had the same effect as the Ritalin did; speed made him calm,
slowed him down, and took away his anxiety and nervousness. When Chris
turned twenty-two the side effects from the speed were too great and he
decided to get clean. Chris's story seems very unique, but given the
right context and environment it's very plausible.
Jacob is a ten year old boy who was diagnosed with ADHD when he was
eight and a half. Jacob's mother reported that he takes ten milligrams
of Ritalin three times a day (Mother of Jacob, 1999). As you read
earlier most children only receive Ritalin in the morning and at lunch.
However, Jacob's mother says, "he is unbearable when he comes home at
night and that there is no way she could control him if it wasn't for
his pill." Jacob's daycare workers reported that a half an hour after
he receives his pill he becomes lethargic. Oddly, his aggression level
seems to rise and he has a motor tic in the right side of his face.
Jacob has not been diagnosed with Tourettes Syndrome but his mother
said that he has violent rages where he repeats obscene words over and
over until he wears himself out. Because Jacob shows many of the side
effects from Ritalin which normally occur because the child is taking
too much I asked his mother what her doctor says about lowering his
dosage. She replied that she has never asked him. Jacob illustrates
an extreme need for further evaluation and supervision.
Laura on the other hand is a perfect example of how Ritalin is supposed
to work. Laura was diagnosed with ADD when she was seven years old.
Laura takes one pill in the morning before school to help her
concentrate. Laura's father says that he hasn't noticed any other
changes in her behavior and she hasn't suffered any physiological
differences either (Father of Laura, 1999). A point to be made is that
Ritalin works much better on ADD children than ADHD children because
you don't have to deal with the hyperactivity of the child as well at
his/her attention problems.
Ritalin is indicated as an integral part of total treatment program
which typically includes other remedial measures (psychological,
educational, social) for a stabilizing effect in children with ADD and
ADHD (Berkley, 1990). Changing the dose or the times at which the dose
is given can eliminate most of the side effects from Ritalin. A point
to remember about children that have been diagnosed with ADHD or ADD is
that Ritalin is not a cure. It is only a part of the circle that must
be filled with many other measures in order for the child to benefit
from the Ritalin.
Reference List
Barkley, R. A., Ph.D. (1990). Attention Deficit Hyperactivity Disorder:
A Handbook For Diagnosis and Treatment. New York, NY: The Guilford
Press.
Chris (October 2, 1999). Personal Communication.
Hinshaw, S. P. (1997). Attention Deficits and Hyperactivity in
Children. Thousand Oaks, CA: Sage Publications
Father of Lauren (October 3, 1999). Personal Communication.
Fisher, B. C. (1988). Attention Deficit disorder mis diagnosis
approaching ADD from a brain Behavior/ Neuropsychological perspective
for assessment and
Treatment. Boca Raton, FL: CRC Press
Fowler, Brigit., Valley Elementary School ESS Coordinator. (1999).
Personal Communication.
Methylphenidate (1998)
Http://www.rxlist.com/cgl/generic/methphen.htm
Mother of Jacob (October 3, 1999). Personal Communication.
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