BIOLOGICAL BASIS OF BEHAVIOR
Psychology 321
Spring, 2005 HGH 225
Dr. John M. Morgan MWF, 8am to 9:00
Risperdal (Risperidone)
Eric Wilcox: Chemistry of the drug and route of access of the drug,
Synaptic Transmitter(s) involved, Part of the neuron affected.
Jeff Slocum: Inhibitory or Excitatory potential changes, Ion channels
effected.
Marchele Robbins: Physiological (whole body) changes, Primary
behavior changes.
Kellie Corbisiero: Side effect behavior changes, effects reported by
users and or/ survivors of the use of the drug
Eric Wilcox
Chemistry of the drug and route of access of the drug, Synaptic
Transmitter(s) involved, Part of the neuron affected.
Risperidone is an atypical antipsychotic used to alleviate the
symptoms of schizophrenia. Schizophrenia is defined by its effects
in altering perception, thoughts, or consciousness called
hallucinations or delusions. It affects about 1% of the population,
with about 2 million people affected in the United States. About 50%
of those affected become severely and permanently disabled and
dependent upon public assistance. Schizophrenics make up about 10%
of the totally disabled population and as much as 14% of the
homeless. The United States spends about $70 billion annually.
About 1 out of 4 patients will attempt suicide, and 1 in 10 will
succeed. There is great social stigma associated with the disease
(Sarason & Sarason, 2001, pg. 350).
The dopamine theory behind the cause of schizophrenia states
that in part excess dopamine is a possible factor or there is more
than an average number of dopamine, Type 2 receptors. Risperidone
acts on the dopamine D2 receptor (Sarason, et al, 2001, pg. 368).
Risperidone is a psychotropic drug and is part of the chemical
class of benzisoxazole derivatives used as a treatment for
schizophrenia, with some results for bipolar manic disorder, as well.
The molecular formula is C23H27FN4O2, with a molecular weight of
410.49 (Ereshefsky & Mascarena, 2003).
(molecule picture, needed to download Chime program to view it)
Route of administration is oral. Once the drug passes the
esophagus and stomach, it makes its way into the small intestines.
There are beds of capillaries within the intestine walls. The
capillaries absorb the risperidone into the blood, called passive
transport. Risperidone readily attaches to plasma protein to be
transported to the brain, via the heart, lung, liver, and then to the
brain. It must cross the blood brain barrier to work at the site of
action, which is the synapse and the presynaptic synapse of the
neuron (Inaba & Cohen, 2004, pg. 45)
The blood brain barrier consists of tightly sealed epithelial cells
that make up the cell walls of the arteries which make a semi
permeable barrier that allows only very small, fat soluble particles
through (passive diffusion) to the neurons of the brain, and keeps
unwanted particles from entering the brain. There is an "active
transport" system for particles that are not fat soluble, which need
to "hitch hike" across the barrier on a protein. Once in the brain,
drugs like risperidone have an effect at specific sites or have
specific actions at locations on the neuron.
Risperidone is prescribed to be taken orally with tablets
available in .025 mg, 0.5 mg, 1 mg, 2 mg, 3 mg, and 4 mg strengths.
There is also an oral solution available as 1mg/ml, as well as,
0.5mg, 1mg, and 2 mg orally disintegrating tablets, all produced by
Janssen Pharmaceutica Products, L.P(Janssen, 2003). Studies show
that each oral form of risperidone is bioequal in efficacy. The
bioavailabilty of risperidone is 70% in tablet form, and tablet is
94% available compared to solution form. Oral administered
risperidone is well absorbed and is highly bound to the plasma
proteins albumin and alpha1 acid glycoprotein. Plasma protein
binding of respiridone is 90%, and the binding of the metabolite 9
hydroxyrisperidone is 77% (Janssen, 2003). The metabolic half life
for risperidone is about 3 hours, and the metabolite, 9 hydroxy
risperidone, is about 22 hours. This can vary per individual due to
genetic differences. The metabolite is also an active antipsychotic.
Metabolization occurs mainly in the liver by hydroxylation of
risperidone by the cytochrome P450 (CYP)2D6 enzyme called debrisoquin
hydrolylase to 9 hydroxyrisperidone (Janssen, 2003). There is a
minor metabolic pathway through N dealkylation. Due to genetic
variability in an individual's CYP 2D6 synthesis, some people may
metabolize risperidone more quickly than others. Neither risperidone
nor the metabolite will displace each other at the binding sites.
Studies approved by the U.S. Drug and Food administration was
carried out by Ereshefsky and Mascarena (2003, pg 18-23) for
risperidone to be given as long-lasting antipsychotic biweekly
gluteal injections has proven the best results in efficacy and better
predictable pharmacokinetics. Injections consist of risperidone
encapsulated in polymere microspheres which release the drug slowly
after injection over several weeks with rapid build up of risperidone
over oral administration. Injections reduce the large differences
between peak and minimal plasma concentrations, thus reducing side
effects and non-compliance of taking the medication. Oral
administration offers better symptom control and less liability for
reversible and persistent motor side effects (Ereshefsky and
Mascarena, 2003).
Risperidone crosses the blood brain barrier finding the neurons
of the brain, specifically neuron protein receptors which are located
on the dendrites. Dendrites are branch like structures that emanate
from the cell body of the neuron, called the soma. Dendrites spread
from the cell body like branches of a tree. Each branch allows for
connections to occur from the axons of presynaptic neurons.
Presynaptic means the neuron upstream of the direction of travel of
the action potential from the neuron we are describing. These
branches receive chemical signals from the presynaptic neurons.
These chemicals are called neurotransmitters, and are released from
the presynaptic neuron when an "all or none" signal travels down that
neuron ending at the terminal button. Once the action potential has
reached the terminal button, calcium ions enter the cell through
protein ion channels. These channels are voltage regulated, and
respond to the action potential by changing their shape, allowing
calcium ions to enter the cell. This chemical action causes
vesicles, lipid capsules filled with neurotransmitters, to bind to
the synapse cell wall and erupt, spewing neurotransmitter into the
synaptic gap. The neurotransmitter crosses this gap to bind to
protein receptors embedded in the postsynaptic dendrite cell wall.
Once again, once the neurotransmitter binds, the protein ion channel
changes shape. A couple of things can happen. If the ion channel is
excitatory, it will open and allow sodium ion into the cell making
the cell positive. This is called EPSP. If the protein channel and
neurotransmitter is an IPSP, a chloride ion channel may open, allow
chloride into the cell, making the membrane potential negative,
inhibiting the cell from firing an action potential. Both of these
protein receptors are called ionotropic.
Risperidone acts at metabotropic receptors. The
neurotransmitter system risperidone interacts with is primarily
dopamine, but also to a lesser extent, serotonin. Dopamine and
serotonin are second messengers. They bind to metabotropic protein
receptors that can have several actions. The effect is an inhibitory
postsynaptic potential (IPSP). This potential inhibits the neuron
from starting an action potential. When dopamine binds to a receptor
such as the D2 receptor, it activates a G-protein that produces and
releases cAMP, cyclic monoamine phosphate. cAMP activates protein
kinease which phosphorolates potassium channels, allowing potassium
to flow outwards, or allowing chloride ion channels to open, letting
chloride ions in, repolarizing the cell membrane potential, an IPSP.
5HT2receptors can be found close to the terminal of the neuron
at certain locations in the brain. Presynaptic connections occur
here to regulate action potentials when the presence of
neurotransmitter is too concentrated about the cell. The presynaptic
connection allows the postsynaptic cell to regulate the outcome of an
action potential. 5HT2A receptor activation has reciprocal effects
on dopamine, inhibiting the release of dopamine cell bodies in the
brainstem substantia nigra, and at the axon terminals in the basal
ganglia neostriatum (University of Nottingham, n.d.).
Risperidone's mechanism of action is not completely known in how
it affects schizophrenia symptoms. Risperidone does not affect the
production or release of neurotransmitters. The dopamine theory of
elevated dopamine levels as a possible cause of schizophrenia has
researchers proposing that the therapeutic value of risperidone in
treating schizophrenia is that it acts as an antagonist at the
dopamine Type 2 and serotonin Type 2 receptors. Erxtrapyrmidal side
effects, such as Parkinsonism, akathisia and dystonia are avoided
because of antagonism at the Type 2 serotonin receptor which
increases dopamine levels enough to compete with the risperidone
antagonism of dopamine, allowing some dopamine to bind at the D2
receptor which prevents these side effects. Risperidone binds and
antagonizes at these receptors blocking the actions of serotonin and
dopamine, thus having varying effects on the neuron. Risperidone is
considered atypical. Atypical drugs have a gentler binding to
receptors than typical drugs, such as haloperidol and are referred to
as serotonin-dopamine antagonists (SDAs). Risperidone will release
from the receptor allowing natural transmission of dopamine several
hours after metabolization of risperidone (Friedman, 2003).
Risperidone antagonizes other receptors as well, such as, alpha1 and
alpha2 adrenergic, and H1 histaminergic receptors which may explain
other effects of risperidone. It has lower affinity for 5HT1c, 5HT1b,
and 5HT1a receptors (Janssen, n.d.). Risperidone's focus of action
is at the D2 receptors on the dendrites, and a lesser extent at 5HT2A
presynaptic receptors affecting the second messenger system in the
soma and axon terminals.
References:
Ereshefsky, L., and Mascarenas, C. (2003). Comparison of the Effects
of Different
Routes of Antipsychotic Administration on Pharmacokinetics and
Pharmacodynamics. Journal of Clinical Psychiatry, 64, suppl 16, 18-
23. Retrieved: February 19, 2005
Friedman, J (2003). Letter to the Editor. Re: Atypical
Antipsychotics Mechanism of
Action. The Canadian Journal of Psychiatry, Vol 48, No1. Retrieved:
February 19, 2005.
Inaba, D., & Cohen, W. (2004). Uppers, Downers, All Arounders.
Fifth Edition. Steinbroner.
Resperdal (Risperidone) Tablets/Oral Solution (n.d.). Retrieved:
February 19, 2005, from
http://www.janssen.com/active/janus/en_US/assets/jan/risperdal.pdf
Sarason, I., & Sarason, B.(2001) Abnormal Psychology the Problem of
Maladaptive Behavior. Preston Hall.
University of Nottingham (n.d.). Retrieved: February 19, 2005, from
http://www.chemsoc.org/exemplarchem/entries/2004/nottingham_chong/Bph
armacology.htm
Jeff Slocum
Inhibitory or Excitatory potential changes, Ion channels effected.
Risperidone is a serotonin antagonist which blocks GABA-evoked
currents in pyramidal neurons (Feng et al, 2001). Risperidone
lengthens action potentials and blocks potassium current in rabbit
heart muscle. In human atrial muscle risperidone decreases outward
current but has no effect on inward current. It lengthens the
repolarization of atrial and ventricular action potentials only at
high drug levels. Risperidone reduces the membrane resting potential
and prolongs action potential duration. In human heart preparations
risperidone, at high drug concentrations, lengthens repolarization of
atrial and ventricular myocardium. (Gluais et al, 2004).Risperidone
lengthens the QT action potential of rabbit heart. It lengthens the
action potential and blocks repolarization potassium flow. (Gluais et
al, 2004). To decrease background noise when using a patch electrode
a patch of membrane is isolated with a micropipette. This allows
current measurement in the pico ampere range. The tube is sealed to
the membrane by suction forming a "gigaseal" which refers to the
electrical resistance across the membrane. Such techniques were
instrumental in finding that ion channels are gated and modulated not
only by voltage and external ligands but also by second messengers,
regulatory proteins and by phosphorylation. Patch clamp recording can
be used with any cell culture. Voltage dependant sodium, calcium, and
potassium channels have a huge number of subtypes. Another large
category is transmitter-gated channels regulated by nucleotides,
intra-cellular sodium, and calcium, and GTP-binding proteins. There
are hundreds of channel subtypes regulated by a variety of
mechanisms. Activity of ion channels directly or indirectly affects
second messenger calcium ionic concentration. Voltage-dependant
calcium channels gate the entry of calcium ions and help shape the
action potentials. The entry of calcium ions activates kinases,
contractile proteins and ion channels. There are voltage-independent
calcium channels activated by ligand binding of receptors on the
outside of the cell membranes. Both receptor-linked GTP-binding
protein and second messengers affect ion channel activity. Modulation
of channel activity by applying agonists to the cell culture
indicates a second messenger system. Patch clamp electrodes have been
used on the calcium transporter channels in organelles such as
endoplasmic reticulum and sarcoplasmic reticulum by rupturing the
cell, isolating the organelle, and inducing the membranes to form
vesicles. To study microbe channels techniques are used to merge
several microbes into a giant microbe large enough to attach a patch
electrode to (Rudy,B. & Iverson, L, 1991). Viruses contain coding to
create ion channels in host membranes. The first demonstration of
this was the M2 protein of influenza virus type A. It was then
targeted with the drug Amantadine. The drug prevents dissociation of
the RNA code during uncoating of the virus in the host cell. The RNA
that escapes this block can again be stopped by Amantidine which
prevents transport by the host endoplasmic reticulum leaving the RNA
susceptible to the acidic cell pH. The viral M2 ion-transporter has
been isolated in vesicles and studied by patch clamp electrodes. It
transports hydrogen ions (Conn, 1998). Ion channels are involved in
the regulation of cell excitability. These may be muscle cells, nerve
cells, cells that release hormones, etc. Potassium channels are the
most common and diverse group of channel proteins. Voltage and, or
ligand-binding induces a conformational change in the regulatory
protein. Inhibitors are useful in the study of channel proteins. One
such group of inhibitors is scorpion venom. To obtain sufficient
volume of the venom either solid-phase synthesis by machine or
recombinant-genetics techniques are used. Nuclear magnetic resonance
was used to determine the structure of the venom. The study of how
point-substitutions affect binding of the ion channel protein
disclosed how the venom interacts with the membrane protein.
Mutagenesis of the ion channel pore and how this affects venom
interaction lead to a model of the receptor in the channel (Conn,p
624).Snake venom has been used as a high-affinity probe of voltage-
gated potassium channels. The venom is for sale from chemical
companies but must be kept frozen as it will decompose overnight. It
can be synthesized as fusion-proteins in bacterial expression
systems. Dendrotoxin (snake venom) is not used as much as
pentapeptide scorpion venom (Conn, p649).CNS presynaptic terminals
are on the order of one micron in diameter. Presynaptic modulation is
involved in learning and memory. There are techniques to measure the
quantitative flow of calcium ions through a channel. Cell patch-clamp
techniques measure current while intracellular calcium is monitored
via fluorescent Fura 2. The optical properties of the indicator
changes depending on whether it is complexed with an ion that it is
buffering. The spectroscopic measurement indicates the ionic
concentration. The indicator has a strong negative charge which
prevents it from leaving the cell into which it was injected. Optical
monitoring of calcium avoids disrupting neuronal events (Conn,
p3).For samples too opaque for optical measurement, spin-label
electron-spin resonance spectroscopy or Fourier transform infrared
spectroscopy can be used (Conn, p59).Capillary electrophoresis patch-
clamp detection is used to fractionate and detect receptor agonists
and antagonists in complexes of extremely small sample solutions.
Capillary electrophoresis uses tubes of less than a micron in
diameter to inject 10-15 to 10-18 liters of biopolymers such as DNA
oligomers. These techniques were used to demonstrate the release of
acetylcholine and glutamate from photoreceptors (Conn, p 190).
Conn, P., editor. Methods in Enzymology 294,490. Academic Press, San
Diego.
Rudy, B. & Iverson, L, editors. Methods in Enzymology 207, 3.
Academic Press, San Diego.
Gluais, P, Bastide, M, Grandmougin, D, Fayad, G, & Adamantidis, M.
Risperidone reduces K+ currents in human atrial myocytes and prolongs
repolarization in human myocardium. European Journal of Pharmacology,
497(2) 215-222.
Feng,J, Cai, X, Zhao, J, Yan, Z. Serotonin Serotonin receptors
modulate GABA-sub(A) receptor channels through activation of anchored
protein kinase C in prefrontal cortical neurons. Journal of
Neuroscience, 21(17) 6502-6511.
Rammmes, G, Eisensamer, B, Ferrari, U, Shapa, M, Gimpl, G, Gilling,
K, Parsons, C, Riering, K, Hapfelmeier, G, Bondy, B, Zieglgansberger,
W, Holsboer, F, Rupprecht, R. Antipsychotic drugs antagonize human
serotonin type 3 receptor currents in a noncompetitive manner.
Molecular Psychiatry, September 2004, 9(9)846-858.
Marchele Robbins
Physiological(whole body) changes, Primary behavior changes.
Hallucinations, delusions, paranoia, psychosis and thought disorder
are all symptoms of Schizophrenia and people who suffer from these
symptoms seek the treatment of atypical anti-psychotic medications.
Those medicines include Risperidone (Risperdal), Clozapine (Clozaril)
, Ziprasidone (Geodon) and Quetiapine(Seroquel). The purpose of
these medications is to alleviate symptoms of Schizophrenia and
lessen the chances of a recurrence. The basic function of Atypical
Antipsychotics is to reduce the effects of blockage in the dopamine
receptors and serotonin and allow communication between nerve cells.
Dopamine is thought to be relevant in Schizophrenic symptoms and
Antipsychotic medications act against these symptoms. While there may
the reward of reducing Schizophrenic symptoms there are risks that
come along with taking such drugs as Risperidone (Risperdal) and
Quietiapine (Seroquel). Commons side effects that exist while taking
Risperidone are dizziness, nausea, tiredness and hyperactivity. More
serious conditions may include Orthostatic Hypotension which is an
extreme drop in blood pressure. Patients may also experience Syncope
which is related to Hypotension in that a person may experience a
loss of consciousness or fainting. Quietiapine can also cause
Hypotension, but with the long term use of this drug it can cause
Tardive Dyskinesia which is involuntary movements of the lips, jaw
and tongue. The features of this condition are tongue protrusion,
lip smacking, rapid eye blinking and rapid arm movements. In the most
extreme cases Risperidone has been said to cause galactorrhea which
is breast growth in males and a secretion of breast milk. In the
article A Troubled History by Carol Marbin Miller of the Miami Herald
she reports of case about the common use of Risperidone among
children in state care. Florida Foster children had been given
Risperdal by foster care providers as "a chemical restraint whose
unruly behaviors were a frustration to caretakers." Antoinette R.
Appel, a plantation Neuropsychologist studied the records of 50 South
Florida foster children taking Risperdal and said, " Many of the
children developed severe side-effects, including obesity, lethargy,
lack of concentration, hormonal disorders and the inappropriate
development of secondary sexual characteristics, such as lactating
breasts in boys and girls." A child identified as M.W. won a Florida
Supreme court case after doctors forced him to take Risperdal and he
developed lactating breasts. The judge's ruling was that foster
children can not be locked up in psychiatric hospitals without a
hearing. In a case of Dissociative Catatonia treated with Risperidone
a 22 year old man identified as W.N. had symptoms of immobility,
mutism and waxy flexibility and stuporous five days after entering a
psychiatric hospital. He was given Lorazepam in which he responded
with a return of return of mobility to his body, but within a few
hours he returned to his original state of stupor and Lorazepam was
discontinued. After four weeks of hospitalization he was classified
as having Catatonic Schizophrenia because of his actions in which he
would be sitting in a chair and all of a sudden fall to the floor
rolling across the room. He would be twisting and turning and
shaping his body into bizarre positions and eventually lost control
over his bladder and bowel functions. Eventually the patient was
treated with 10 mg of haloperidol, doses of Risperidone and 1mg of
Lorazepam. Within twenty four hours the patient returned to a stable
condition with no symptoms of mutism waxy flexibility, bizarre
positions and was discharged into the care of his mother. It was
said that "Risperidone was finally chosen as a potent atypical
neuroleptic with a low profile of side-effects, in combination with
Lorazepam which led to a prompt recovery."
Primary behavior changes:
Risperdal is said to improve positive and negative symptoms of
Schizophrenia. Positive symptoms that improve are anxiety and acting
out behaviors and negative symptoms are emotional withdrawal,
avolition, scarcity of speech and negative affect (Clinical
Toxicology Review). 259 patients with Bipolar 1 disorder
participated in a double blind study conducted by Robert Hirschfeld,
MD, professor and chair of the Department of psychiatry at the
University of Texas Branch in Galveston. Bipolar 1 disorder symptoms
may be classified as high mood, racing thoughts, poor concentration,
and unrealistic beliefs of one's own abilities or powers
(PRNewswire.com). According to Dr. Hirschfeld, "Manic symptoms can
lead to devastating consequences such as squandering family savings,
break up of marriages, and even physically dangerous behaviors."
Using random assignment patients received either a placebo for three
weeks or Risperdal in the amount of 1-6 mg daily. At the beginning
of research patients symptoms were measured with the Young Mania
Rating Scale (YMS) and assessment was measured by the change of YMS
scores at the end of the study. The study showed the patients who
took Risperidal improved in their YMS scores than those who took the
placebo. However patients who took Risperdal reported experiencing
nausea, dizziness, weight gain, and upset stomach (Titusville, N.J.,
Dec.10/ PRNewswire).
References
Retrieved: March 1, 2005 from
http://www. Counseling resource.com/medication/drug-
pages/risperidone.html
Retrieved: March 2, 2005 from
http://www. Maripoisoncenter.com/ctr/9611risperidone.html
Clinical Toxicology Review Vol.19, No.2 November 1996
Retrieved: March 2, 2005 from
http://www.priory.com/psych/catatonia.html
Retrieved: March 3, 2005
Common use of Risperidal among Children
http://www.risperdal-help.org/what_causes.php
www.Schizophrenia.com
Kellie Corbisiero: Side Effects, Adverse Effects, Possible drug
interactions and Behavior changes:
Schizophrenia is a metal illness which is characterized by a
disruption in cognition and emotion that affects the most fundamental
human attributes, such as thought, perception, language, and the
sense of self. There are a large number of symptoms of schizophrenia
which can include hearing internal voices, hallucinations, and
delusions. No single symptom can diagnose a person as schizophrenic,
but rather the collection of multiple symptoms which persist for a
prolonged period of time. Symptoms of schizophrenia are divided into
two categories, positive and negative. These categories define how
the symptoms are defined and treated. Positive symptoms include
delusions, hallucinations, disorganized behavior, disorganized speech
and thinking, difficulty to be goal oriented, the schizophrenic is
unpredictable, silly, or exhibits behaviors that are bizarre to
onlookers. Other positive symptoms include catatonic behaviors, which
would be a decrease in reaction to the current environment. Positive
symptoms, which do not occur very often, are unusual motor behavior,
derealization, depersonalization and somatic preoccupations. Negative
symptoms of schizophrenia include affective flattening, which is a
reduction in the range and intensity of emotional expressions, Alogia
categorized by a lessening of speech fluency and productivity, and
Avolition, which is the reduction, or difficulty to initiate and
persist in goal directed behavior. Schizophrenia is a serious
mental illness, and although there is no known cure there are several
drugs that can be administered to those suffering from the illness to
reduce the severity of the symptoms, or to hopefully get rid of all
of the symptoms of schizophrenia (Mental Health: A Report of the
Surgeon General). These drugs are called anti-schizophrenics, one
drug is Risperidone, or as it is commercially know Risperdal.
Risperidone is a prescription medication that was approved by the FDA
to treat bipolar 1 disorder; although it is used to treat
schizophrenia as well. According to the makers of Risperidone it is
designed to control symptoms of bipolar1 disorder, and schizophrenia
(risperdal). Risperidone is used to treat the positive symptoms of
schizophrenia, but has been shown to help the symptoms of negative
schizophrenia as well (NAMI-NYS). Risperidone is offered in 3
different forms, all of which are taken orally. The first form is a
quick dissolving tablet offered in 3 strengths, .5mg, 1mg; 2mg.
Risperidone is also offered in tablet form in strengths ranging from
.25mg to 4mg, and a liquid form (risperdal). Risperidone is well
tolerated and side-effects rarely occur according to the manufacturer
(risperdal). Risperidone like most anti-schizophrenic drugs has side-
effects; some are temporary and will stop after the medication has
been stopped, but others symptoms will never go away. Some of the
possible temporary side-effects can include muscle stiffness,
tremors, and body shakes, and at higher doses of risperidone, this
side effect increases. While the most significant side effects,
affecting some patients but not all include low blood pressure;
dizziness, especially when standing up suddenly; sleepiness,
lethargy, heart palpitations, constipation, weight gain, sexual
dysfunctions, overall fatigue, and dry mouth (NAMI-NYS). In rare
cases risperidone has been known to cause skin rashes, seizures, low
white blood cell count, involuntary facial or tongue movements,
blurred vision, a reduced urinary output, and numbness in the legs.
Patients that experience the rare symptoms are urged to see a doctor
immediately. Any patient, who has current problems with liver or
kidney functions, should receive a lower dosage (psyweb). Also men
that have a prolonged or painful erection are urged to stop taking
the drug (Drug Resource Center- Risperdal). To receive the full
benefits of risperdal the patient needs to consistently take the drug
for one to two weeks. If any does are missed and if it is within one
hour take the medication, if over an hour patients are urged to skip
that dose and continue on their normal schedule, patients should not
double dose. Other warnings and drug interactions associated with
risperdal include antacids containing aluminum or magnesium, which
should not be taken one hour before, and never right after taking
risperdal. Patients should only take this drug with careful
monitoring. This drug affects the central nervous system, and some
depressants, like antihistamines, hay fever medications, sedatives,
narcotics, anesthetics, barbiturates, or muscle relaxants, can
interact with risperdal. Also taking vasodilator, or a drug that
dilates the blood vessels, may interact with risperdal. Patients who
are pregnant, planning to become pregnant, breast feeding should not
take risperdal. Children should not be allowed any dosage of this
drug, and people over sixty should be given small doses that are
gradually increased. Patients who smoke need to have blood levels of
the drug taken, because smoking drops the level of the drug in the
blood. Patients who have a history of neuroleptic malignant syndrome
should also not use risperdal (psyweb).One of the serious side
effects of using risperidone is called tardive dyskinesia. Tardive
dyskinesia is a neurological syndrome that is recognized by
repetitive movements such as rapid eye blinking, rapid movements of
the legs and trunk, tongue protruding, lip smacking, and involuntary
movements of the fingers. There are no standard treatments for
tardive dyskinesia. Treatment for the syndrome differs based on each
person, but generally the first step is to slowly reduce the amount
of the drug that is causing tardive dyskinesia, yet for patients with
a severe condition, this option may not be feasible. The next
possible step would be to replace the current drug that is causing
tardive dyskinesia, and substitute it with another similar drug. Also
drugs such as benzodiazepines, adrenergic antagonists, and dopamine
agonists may also be helpful in treating tardive dyskinesia. Although
some of the symptoms will remain a long time after discontinuation of
the drug, with careful management some symptoms may improve or
disappear with time (National Institute of Neurological disorders and
Stroke).
Kellie Corbisiero:
Effects reported by users and or survivors of the drug Risperdal:
Risperdal is a relatively new drug, which became available for
prescription in 1994. Little research has been done to help
understand the possible side effects from long term usage, and there
is little information about behavioral changes associated with the
drug (NAMI-NYS). The only information available is that it has been
proven to treat the positive symptoms of schizophrenia, and it has
also shown to help lessen the negative symptoms (NAMI-NYS). According
to some patients who took the drug they felt that the recommended
starting dosage was too strong, and the users of the drug professed
generally dislike of the drug (www.braintalk.org (2)). A personal
account from one paitent said "risperdal took some time to get into
my system, but has really helped. The biggest problem is weight gain,
but in comparison to the voices and continuous paranoia it is well
worth it" (www.braintalk.org (1)). While another individual said "I
tried Risperdal but it made me sleepy and drunk like. So I stopped
that.
I was in the hospital not by my will and took medication there but I
cannot work when I take medication, I wake up like a zombie"
(www.braintalk.org (3)).While another paitent who was very happy with
risperdal said, "I had not too many side effects on risperdal. It
works good on me too" (www.braintalk.org (4)). In clinical trials
almost twice as many people who took risperdal and a mood stabilizer
which was either depakote or lithium had an improvement in their
symptoms compared to the placebo group who took a sugar pill, and a
mood stabilizer. Two different scales were used to confirm this
information in clinical trials (risperdal). No cure has been
discovered for the illness schizophrenia, but with medications like
risperdal and help of a doctor, people suffering from this illness
can live somewhat "normal" lives, free of the majority of their
symptoms of schizophrenia.
References:
(2003, May 29). Do you like risperdal? [Risperdal]. Message posted to
http://www.braintalk.org 2
(2005, February 06). Am I Crazy?. 3
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This page last edited 1-3, 2005
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