---------- Biological Basis of Behavior ------ ----
---------- SPRING, 2005 ----------

                            
                            
                       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).	

risperidone molecule

(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 
(2005, February 17). resperadal . Message posted to 
http://www.braintalk.org  4 
(2005, February 28). Delusions, Hallucinations, Beliefs . Message 
posted to http://www.braintalk.org  1 
Drug Resource Center- Risperdal. (2003). Retrieved February 19, 2005, 
from http://www.drugresourcecenter.com/risperdal/risperdal.htm   
Jannsen.com, . Risperdal. (2005, January 12). Retrieved February 17, 
2005, from 
http://www.risperdal.com/html/ris/consumer/pd_risperidone.xml?article
=safety.jspf   
Mental Health: A Report of the Surgeon General. Retrieved February 
19, 2005, from 
http://www.surgeongeneral.gov/library/mentalhealth/chapter4/sec4.html
#table4_7   
NAMI-NYS. Retrieved February 19, 2005, from 
http://www.naminys.org/abmed_ris.htm   
National Institute of Neorlogical disorders and Stroke, . NINDS 
Tardive Dyskinesia Information Page. (2005, February 09). Retrieved 
February 19, 2005, from 
http://www.ninds.nih.gov/disorders/tardive/tardive.htm   PSY web 
Mental Health. Retrieved February 19, 2005, from 
http://www.psyweb.com/Drughtm/risper.html   
 







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