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Ritalin’s
origins began many decades ago when research scientists began to experiment
with a drug using natural stimulants including ephedrine and caffeine.
Initially, it was tested on lab rats and the studies revealed that the rats
were more focused and easier to manage. By 1950, Ritalin was introduced as a
treatment for Mohr’s Syndrome, not for Attention Deficit Hyperactivity Disorder
(ADHD) and Attention Deficit Disorder (ADD). Mohr’s Syndrome is characterized
by a cleft palate, an enlarged roof of the mouth and a forked tongue (1).
Eventually methylphenidate’s calming and stabilizing effects were used to treat
ADHD and ADD.
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In
1980, The National Institute of Mental Health, officially acknowledged ADHD as
a childhood syndrome (1). Ritalin sales increased significantly and it became
one of the most commonly prescribed medications for ADHD. Novartis, a medical
laboratory located in the United States, is a significant producer of the drug
Methylphenidate
(trademark name is Ritalin) primarily works by reducing the removal of dopamine
and norepinephrine (and to the lessor extent serotonin), which improves the
levels, and utility of these neurotransmitters in the brain (2). Ritalin is a
stimulant and therefore speeds up mental as well as physical processes. It does
this by stimulating the underactive neurons in the brain so they work harder,
which allows the person to focus and pay attention. Ritalin also stimulates the
release of dopamine, a chemical in the brain. This chemical is one of the
messengers in the brain that helps one side of the brain communicate with the
other. The function and activity of the central nervous system reacts to the
influences of dopamine (2).
Side
effects of Ritalin include decreased appetite, decreased or disturbed sleep,
sometimes headaches and gastrointestinal pains.
At times motor or vocal tics emerge. There can also be problems with
mood instability and with irritability. In overdose you can see psychotic
symptoms or symptoms of delirium (3). While Ritalin's
mode of action isn't clear, the drug is known to affect the brain's most
ancient and basic structures, which control arousal and attention. In my view
it is not wise to tamper with such a crucial and important part of brain,
particularly with a drug that can cause many possible long-term side effects.
1) Loeber, R. (1990). Development and risk factors of juvenile antisocial
behavior and delinquency. Clinical Psychology Review, 10,
1–42.
2) Loney, J. (1983).
Research diagnostic criteria for childhood hyperactivity. In S. B. Guze,
F. J. Earls, & J. E. Barrett (Eds.), Childhood psychopathology and
development (pp. 109–137). New York: Raven.
3) Loney, J.,
Langhorne, J., & Peternite, C. (1978). An empirical basis for
subgrouping the hyperkinetic/minimal brain dysfunction syndrome. Journal
of Abnormal Psychology, 87, 431–444


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