Depakote Withdrawal. Step by
step Depakote withdrawal procedure. Depakote
withdrawal. Withdrawal from Depakote no longer needs
to be grueling and suffering from the Depakote
withdrawal side effects can be a thing of the past.
Depakote Withdrawal
The web site you are on is The Road Back Program. The
Road Back is a member of California Association of
Alcoholism & Drug Abuse Counselors (CAADAC). We
have been assisting people off psychoactive medication since
1999, and have helped well over 50,000 people off their
drugs.
Head symptoms? Anxiety? Insomnia? Of course you do.
You likely would prefer to cut to the chase and find
out what you can do to get relief quickly.
You can use two natural supplements to help with the
Depakote withdrawal and likely the underlying
symptoms you were experiencing before starting
Depakote.
The first supplement is CBD
oil. You likely have heard or read about CBD oil
already. We are taking about THC Free CBD oil only.
The price of CBD oil may have limited you from using
this amazing product. We have assisted the
manufacturer of a CBD oil to help eliminate the cost
problem and have helped formulate a high quality CBD
oil in the process. How does $34.27 (30 servings) a bottle sound and with 26mg
CBD oil in each serving, you will not find a lower
price per mg of CBD oil anywhere. Plus, it's made in
the United States in an F.F.A. registered facility.
Click here for
Harper Drops Supreme
Optimum Solace is the other supplement recommended.
Undoing some of the unwanted harm Depakote can do is
equally as important as getting off the medication.
Click here
There was a time not so long ago the medical
community felt Depakote was not addictive. In 2012,
the Surgeon General for the U.S. Army acknowledged
Depakote was not just addictive but he went further
to remove Depakote from the psychoactive drug list
approved to give our troops. Well intentioned
physicians may still believe Depakote is not
addictive but this does not make them a bad
physician, it does mean they are still uninformed
about Depakote.
The point I wish to make with the above text is;
clinical studies may be accurate or they may even be
completely false, we at The Road Back as well as
physician’s need to listen to each of you. If the
goal is to assist people off Depakote and have the
person feel real well during the Depakote withdrawal
process,
we need to listen to you and not clinical studies
only. This program was developed by taking Depakote
clinical studies and putting that information to
use. Some of the information has worked quite well,
while other information turned out to be worthless.
An example of this regarding Depakote: If Depakote
is used for a prolonged period of time the Depakote
will deplete the B vitamin biotin from the body. A
deficiency of biotin will cause numbness or tingling
of the extremities, a reaction to loud noise or a
reaction to bright light which could also include
seizures. This is a biotin deficiency and not a
medical problem. Put the right amount of biotin back
in the body and these symptoms vanish. It is that
simple.
This program is a culmination of 18-years of work,
18-years of failure and 18-years of success. None of
us are exactly the same; the Depakote side effects
you may be experiencing may not be the same Depakote
side effects experienced by others, how you do while
tapering the Depakote may not be the same for
others, you may be able to taper Depakote a little
faster than average or you may need to take this a
little slower.
There are some basics that apply to all people
though when it comes to being able to withdrawal
from Depakote. We take those basics, the list of
side effects from the Depakote drug approval process
and from these, you have our program. Read through
the Depakote side effect list found below on this
page, you may have quite a few of them or only a
small quantity. Either way, the program is designed
to guide you through the Depakote withdrawal
process.
You start out with what we call the Pre-Taper. The
Pre-Taper are things you start doing before you ever
reduce the Depakote.
Two of the side effects that tend to be common with
each person taking Depakote are daytime anxiety and
insomnia. Unless we can handle these two side
effects, there really would not be a Depakote
withdrawal program. These two side effects are that
debilitating when left out of control. Once the
daytime anxiety and insomnia are under control,
other Depakote side effects you may be experiencing
have a chance of simply going away on their own
because they were anxiety and sleep related.
It would be hard to argue that constant anxiety on
top of no sleep would not cause a person stress. We
have gene in our cells called the JNK gene. This
gene becomes too active when stress is chronic and
this over activation of the JNK gene will lead to
other body problems and some of those problems can
be mentally related in time. So we also want to
reduce the over activation of the JNK gene during
the pre-taper and keep this gene in check throughout
the taper process as well.
Natural supplements can be used to regulate the JNK
gene, anxiety and insomnia. The Depakote creates a
metabolic disorder bringing some enzymes too high
and when the flow of the metabolic system becomes
stuck or flowing too profusely the body can’t handle
it and a cascading effect takes place. You may
become anxious due to the calcium firing erratically
or by the adrenals out of balance or a host of
proteins being too abundant or even too few.
You will start the Pre-Taper by taking a supplement
called JNK Capsules. This supplement contains
botanicals that have been proven to regulate the JNK
gene, reduce stress, and put back in the cells what
the benzodiazepines have stripped out and more. As
stated earlier, long term use of a benzodiazepine
will create an inadequate amount of the B vitamin
biotin. Biotin has been included in the JNK Capsule
formula to address this issue.
A metabolic disorder will take place with Depakote
usage in an area called nitric oxide and nitric
oxide synthase. These are also known as NO/NOS. Too
much NO will overwhelm NOS and then a substance
called NMDA will go out of balance and this will
lead to the misfiring of calcium. Here you have the
rapid start of anxiety and the start of insomnia.
The Road Back does not sell these supplements. They
are available at the U.S. manufacture
Neuro Genetic Solutions.
Many of you are in the middle of Depakote withdrawal
when you find our web site and the thought of
reading hundreds of pages from the book How to Get
Off Psychoactive Drugs safely is overwhelming.
If you
click How to Start which is located
at the top of this page, all pages of the book are
located there.
Divalproex Sodium
Brand name (Epival and Depakote)
Pharmacology
Divalproex
sodium has anticonvulsant properties, and is chemically
related to valproic acid. Although its mechanism of action
has not yet been established, it has been suggested that its
activity is related to increased brain levels of
gamma-aminobutyric acid (GABA). The effect on the neuronal
membrane is unknown. It dissociates into valproic acid in
the gastrointestinal tract.
Peak serum levels of valproic acid occur in 3 to 4 hours.
The serum half-life of valproic acid is typically in the range of 6 to 16
hours. Half-lives in the lower part of the above range are
usually found in patients taking other drugs capable of
enzyme induction. Enzyme induction may result in enhanced
clearance of valproic acid by glucuronidation and microsomal
oxidation. Because of these changes in valproic acid
clearance monitoring of valproate and concomitant drug
concentrations should be intensified whenever enzyme
inducing drugs are introduced or withdrawn.
A slight delay in absorption occurs when the drug is administered with
meals but this does not affect the total absorption.
Valproic acid is rapidly distributed throughout the body and
the drug is strongly bound (90%) to human plasma proteins.
Increases in dose may result in decreases in the extent of
protein binding and variable changes in valproic acid
clearance and elimination. In epilepsy, the therapeutic
plasma concentration range is believed to be from 50 to 100
mcg/mL. Occasional patients may be controlled with serum
levels lower or higher than this range. A good correlation
has not been established between daily dose, serum level and
therapeutic effect.
In placebo controlled clinical studies in acute mania, 79% of patients
were dosed to a plasma concentration between 50 and 125 mcg/mL.
Protein binding of valproate is saturable ranging from 90%
at 50 mcg/mL to 82% at 125 mcg/mL.
Elimination of valproic acid and its metabolites occurs principally in
the urine, with minor amounts in the feces and expired air.
Very little unmetabolized parent drug is excreted in the
urine. The principal metabolite formed in the liver is the
glucuronide conjugate.
Other metabolites in the urine are products of C-3, C-4 and C-5
oxidation. The major oxidative metabolite in the urine is
2-propyl-3-keto-pentanoic acid; minor metabolites are
2-propyl-glutaric acid, 2-propyl-5-hydroxy-pentanoic acid,
2-propyl-3-hydroxy-pentanoic acid and
2-propyl-4-hydroxy-pentanoic acid.
See Warnings regarding statement on fatal hepatic dysfunction.
Indications
Epilepsy:
Divalproex is indicated for use as sole or adjunctive
therapy in the treatment of simple or complex absence
seizures, including petit mal and is useful in primary
generalized seizures with tonic-clonic manifestations.
Divalproex may also be used adjunctively in patients with
multiple seizure types which include either absence or
tonic-clonic seizures.
Acute Mania:
Divalproex is indicated in the treatment of the manic
episodes associated with bipolar disorder (DSM-III-R).
The effectiveness of divalproex in long-term use, that is for more than 3
weeks, has not been systematically evaluated in controlled
trials.
Dilvalproex is not indicated for use as a mood stabilizer in patients
under 18 years of age.
Contraindications
Patients
with hepatic disease or significant dysfunction.
Hypersensitivity to the drug.
Warnings
Hepatic
failure resulting in fatalities has occurred in patients
receiving valproic acid and its derivatives. These
incidences usually occurred during the first 6 months of
treatment with valproic acid. Experience has indicated that
children under the age of 2 years are at a considerably
increased risk of developing fatal hepatotoxicity,
especially those on multiple anticonvulsants, those with
congenital metabolic disorders, those with severe seizure
disorders accompanied by mental retardation, and those with
organic brain disease.
The risk in this age group decreased considerably in patients receiving
valproate as monotherapy. Similarly, patients aged 3 to 10
years were at somewhat greater risk if they received
multiple anticonvulsants than those who received only
valproate. Risk generally declined with increasing age. No
deaths have been reported in patients over 10 years of age
who received valproate alone.
If divalproex is to be used for the control of seizures in children 2
years old or younger, it should be used with extreme caution
and as a sole agent. The benefits of therapy should be
weighed against the risks.
Serious or fatal hepatotoxicity may be preceded by nonspecific symptoms
such as malaise, weakness, lethargy, facial edema, anorexia,
vomiting, and in epileptic patients, loss of seizure
control. Patients and parents should be instructed to report
such symptoms. Because of the nonspecific nature of some of
the early signs, hepatotoxicity should be suspected in
patients who become unwell, other than through obvious
cause, while taking divalproex.
Liver function tests should be performed prior to therapy and at frequent
intervals thereafter especially during the first 6 months.
However, physicians should not rely totally on serum
biochemistry since these tests may not be abnormal in all
instances, but should also consider the results of careful
interim medical history and physical examination. Caution
should be observed when administering Divalproex to patents
with a prior history of hepatic disease. Patients with
various unusual congenital disorders, those with severe
seizure disorders accompanied by mental retardation, and
those with organic brain disease may be at particular risk.
In high-risk patients, it might also be useful to monitor serum
fibrinogen and albumin for decreases in concentrations and
serum ammonia for increases in concentration. If changes
occur, divalproex should be discontinued. Dosage should be
titrated to and maintained at the lowest dose consistent
with optimal seizure control.
The drug should be discontinued immediately in the presence of
significant hepatic dysfunction, suspected or apparent. In
some cases, hepatic dysfunction has progressed in spite of
discontinuation of drug. The frequency of adverse effects
(particularly elevated liver enzymes) may increase with
increasing dose. The benefit of improved symptom control at
higher doses should therefore be weighed against the
possibility of a greater incidence of adverse effects.
Pregnancy:
According to recent reports in the medical literature,
valproic acid may produce teratogenicity in the offspring of
human females receiving the drug during pregnancy. The
incidence of neural tube defects in the fetus may be
increased in mothers receiving valproic acid during the
first trimester of pregnancy. Based upon a single report, it
was estimated that the risk of valproic acid exposed women
having children with spina bifida is approximately 1 to 2%.
This risk is similar to that which applies to nonepileptic
women who have had children with neural tube defects
(anencephaly and spina bifida).
Animal studies have demonstrated valproic acid-induced teratogenicity,
and studies in human females have demonstrated placental
transfer of the drug.
Multiple reports in the clinical literature indicate an association
between the use of antiepileptic drugs and an elevated
incidence of birth defects in children born to epileptic
women taking such medication during pregnancy. The incidence
of congenital malformations in the general population is
regarded to be approximately 2%; in children of treated
epileptic women, this incidence may be increased 2- to
3-fold. The increase is largely due to specific defects,
e.g., congenital malformations of the heart, cleft lip
and/or palate, craniofacial abnormalities and neural tube
defects. Nevertheless, the great majority of mothers
receiving antiepileptic medications deliver normal infants.
Data are more extensive with respect to phenytoin and phenobarbital, but
these drugs are also the most commonly prescribed
antiepileptics. Some reports indicate a possible similar
association with the use of other antiepileptic drugs,
including trimethadione, paramethadione, and valproic acid.
However, the possibility also exists that other factors,
e.g., genetic predisposition or the epileptic condition
itself may contribute to or may be mainly responsible for
the higher incidence of birth defects.
Patients taking valproic acid may develop clotting abnormalities. If
valproic acid is used in pregnancy, the clotting parameters
should be monitored carefully.
Antiepileptic drugs should not be discontinued in patients to whom the
drug is administered to prevent major seizures, because of
the strong possibility of precipitating status epilepticus
with attendant hypoxia and risks to both the mother and the
unborn child. With regard to drugs given for minor seizures,
the risks of discontinuing medication prior to or during
pregnancy should be weighed against the risk of congenital
defects in the particular case and with the particular
family history.
Epileptic women of childbearing age should be encouraged to seek the
counsel of their physician and should report the onset of
pregnancy promptly to him. Where the necessity for continued
use of antiepileptic medication is in doubt, appropriate
consultation is indicated.
Risk-benefit must be carefully considered when treating women of
childbearing age for bipolar disorder.
Tests to detect neural tube and other defects using current accepted
procedures should be considered a part of routine prenatal
care in childbearing women receiving valproate.
Lactation:
Valproic acid is excreted in breast milk. Concentrations in
breast milk have been reported to be 1 to 10% of serum
concentrations. As a general rule, nursing should not be
undertaken while a patient is receiving divaiproex. It is
not known what effect this may have on a nursing infant.
Fertility:
The effect of valproate on testicular development and on
sperm production and fertility in humans is unknown.
Long-term animal toxicity studies indicate that valproic acid is a weak
carcinogen or promoter in rats and mice. The significance of
these findings for man is unknown at present.
Precautions
Hepatic
dysfunction (see Contraindications and Warnings).
General:
Because of reports of thrombocytopenia, inhibition of the
second phase of platelet aggregation, platelet counts and
coagulation tests are recommended before instituting therapy
and at periodic intervals. It is recommended that patients
receiving divalproex be monitored for platelet count and
coagulation parameters prior to planned surgery.
Clinical evidence of hemorrhage, bruising or a disorder of hemostasis/coagulation
is an indication for dosage reduction or withdrawal of
therapy pending investigation.
Hyperammonemia with or without lethargy or coma has been reported and may
be present in the absence of abnormal liver function tests;
if elevation occurs the divalproex sodium should be
discontinued.
Divalproex is partially eliminated in the urine as a ketone-containing
metabolite which may lead to a false interpretation of the
urine ketone test.
There have been reports of altered thyroid function tests associated with
valproic acid: the clinical significance of these is
unknown.
Renal Impairment:
Renal impairment is associated with an increase in the
unbound fraction of valproate. In several studies, the
unbound fraction of valproate in plasma from renally
impaired patients was approximately double that for subjects
with normal renal function.
Hemodialysis in renally impaired patients may remove up to 20% of the
circulating valproate.
Geriatrics:
The safety and efficacy of divalproex in elderly patients
with epilepsy and mania has not been systematically
evaluated in clinical trials. Caution should thus be
exercised in dose selection for an elderly patient,
recognizing the more frequent hepatic and renal
dysfunctions, and limited experience with Divalproex in this
population.
Occupational Hazards:
Divalproex may produce CNS depression, especially when
combined with another CNS depressant, such as alcohol.
Therefore, patients should be advised not to engage in
hazardous occupations, such as driving a car or operating
dangerous machinery, until it is known that they do not
become drowsy from the drug.
Drug Interactions:
Divalproex
may potentiate the CNS depressant action of alcohol.
The concomitant administration of valproic acid with drugs that exhibit
extensive protein binding (e.g., aspirin, carbamazepine and
dicumarol) may result in alteration of serum drug levels.
Aspirin and Warfarin:
Caution is recommended when divalproex is administered with
drugs affecting coagulation, (e.g., aspirin and warfarin)
(see Adverse Effects).
Phenobarbital:
There is evidence that valproic acid may cause an increase
in serum phenobarbital levels, by impairment of nonrenal
clearance. This phenomenon can result in severe CNS
depression. The combination of valproic acid and
phenobarbital has also been reported to produce CNS
depression without significant elevations of barbiturate or
valproic acid serum levels. Patients receiving concomitant
barbiturate therapy should be closely monitored for
neurological toxicity. Serum barbiturate drug levels should
be obtained, if possible, and the barbiturate dosage
decreased, if indicated.
Primidone:
Primidone is metabolized into a barbiturate and, therefore,
may also be involved in a similar or identical interaction.
Phenytoin:
There is conflicting evidence regarding the interaction of
valproic acid with phenytoin. It is not known if there is a
change in unbound (free) phenytoin serum levels. The dosage
of phenytoin should be adjusted as required by the clinical
situation. There have been reports of breakthrough seizures
occurring with the combination of valproic acid and
phenytoin.
Because divalproex may interact with concurrently administered drugs
which are capable of enzyme induction, periodic serum level
determinations of these drugs are recommended during the
early part of therapy.
Clonazepam:
The concomitant use of valproic acid and clonazepam may
produce absence status in patients with a history of absence
type seizures.
Oral contraceptives:
Evidence suggests that there is an association between the
use of certain drugs capable of enzyme induction and failure
of oral contraceptives. One explanation for this interaction
is that enzyme-inducing antiepileptic drugs effectively
lower plasma concentrations of the relevant steroid
hormones, resulting in unimpaired ovulation. However, other
mechanisms, not related to enzyme induction, may contribute
to the failure of oral contraceptives. Valproic acid is not
a significant enzyme inducer and would not be expected to
decrease concentrations of steroid hormones. However,
clinical data about the interaction of valproic acid with
oral contraceptives are minimal.
Seizures:
In addition to enhancing CNS depression when used
concurrently with valproic acid, tricyclic antidepressants,
MAO inhibitors, and antipsychotics, may lower the seizure
threshold. Dosage adjustments may be necessary to control
seizures.
Carbamazepine:
Concomitant use of carbamazepine with valproic acid may
result in decreased serum concentrations and half-life of
valproate due to increased metabolism induced by hepatic
microsomal enzyme activity. Valproate causes an increase in
the active 10, 11-epoxide metabolite of carbamazepine by
inhibition of its breakdown. Monitoring of serum
concentrations is recommended when either medication is
added to or withdrawn from an existing regimen. Changes in
the serum concentration of the 10, 11-epoxide metabolite of
carbamazepine, however, will not be detected by routine
serum carbamazepine assay.
Cimetidine:
Cimetidine may decrease the clearance and increase the
half-life of valproic acid by altering its metabolism. In
patients receiving valproic acid, serum valproic acid levels
should be monitored when treatment with cimetidine is
instituted, increased, decreased, or discontinued. The
valproic acid dose should be adjusted accordingly.
Chlorpromazine:
A single study has shown that the concomitant use of
chlorpromazine with valproic acid may result in a decrease
in valproic acid clearance. Valproic acid serum
concentrations and effects should be monitored when valproic
acid is unadministered chlorpromazine due to possible
inhibition of valproic acid metabolism.
Selective serotonin re-uptake inhibitors (SSRIs):
Some evidence suggests that SSRIs inhibit the metabolism of
valproate, resulting in higher than expected levels of
valproate.
Tricyclic antidepressants:
The metabolism of amitriptyline and nortriptyline after a
single dose of amitriptyline (50 mg) was inhibited by
multiple dosing with valproic acid (500 mg twice daily) in
16 healthy male and female volunteers. For the sum of
amitriptyline and nortriptyline plasma concentrations, in
the presence of valproic acid, the mean Cmax and
AUC were increased by 19 and 42%, respectively.
Lithium:
In a double-blind placebo-controlled multiple dose crossover
study in 16 healthy male volunteers, pharmacokinetic
parameters of lithium were not altered by the presence or
absence of divalproex. The presence of lithium, however,
resulted in an 11 to 12% increase in the AUC and Cmax
of valproate. Tmax was also reduced. Although
these changes were statistically significant, they are not
likely to have clinical importance.
Benzodiazepines:
Valproic acid may decrease oxidative liver metabolism of
some benzodiazepines, resulting in increased serum
concentrations. In two small studies in healthy volunteers,
valproate produced a 17% decrease in the clearance of
lorazepam, and 26% decrease in the clearance of unbound
diazepam. Displacement of diazepam from plasma protein
binding sites may also occur. During valproate
administration the unbound fraction of diazepam in the senum
increased approximately two-fold.
Adverse Effects
Epilepsy:
The most commonly reported adverse reactions are nausea,
vomiting and indigestion. Since valproic acid has usually
been used with other antiepileptics, it is not possible in
most cases to determine whether the adverse reactions
mentioned in this section are due to valproic acid alone or
to the combination of drugs.
Gastrointestinal:
Nausea, vomiting and indigestion are the most commonly
reported side effects at the initiation of therapy. These
effects are usually transient and rarely require
discontinuation of therapy. Diarrhea, abdominal cramps and
constipation have also been reported. Anorexia with some
weight loss and increased appetite with some weight gain
have also been seen.
CNS:
Sedative effects have been noted in patients receiving
valproic acid alone but are found most often in patients on
combination therapy. Sedation usually disappears upon
reduction of other antiepileptic medication. Ataxia,
headache, nystagmus, diplopia, asterixis, "spots before the
eyes", tremor (may be dose-related), dysarthria, dizziness,
and incoordination have rarely been noted. Rare cases of
coma have been reported in patients receiving valproic acid
alone or in conjunction with phenobarbital.
Dermatologic:
Transient increases in hair loss have been observed. Skin
rash, photosensitivity, generalized pruritus, erythema
multiforms, Stevens-Johnson syndrome and petechiae have
rarely been noted.
Endocrine:
There have been reports of irregular menses and secondary
amenorrhea, breast enlargement, galactorrhea and parotid
gland swelling in patients receiving valproic acid. Abnormal
thyroid function tests have been reported (see Precautions).
Psychiatric:
Emotional upset, depression, psychosis, aggression,
hyperactivity and behavioral deterioration have been
reported.
Musculoskeletal:
Weakness has been reported.
Hematopoietic:
Thrombocytopenia has been reported. Valproic acid inhibits
the second phase of platelet aggregation (see Precautions).
This may be reflected in altered bleeding time. Petechiae,
bruising, hematoma formation and frank hemorrhage have been
reported. Relative lymphocytosis macrocytosis and
hypofibrinogenemia have been noted. Leukopenia and
eosinophilia have also been reported. Anemia, including
macrocytic with or without folate deficiency, bone marrow
suppression and acute intermittent porphyria have been
reported.
Hepatic:
Minor elevations of transaminases (e.g., AST and ALT) and
LDH are frequent and appear to be dose related.
Occasionally, laboratory tests also show increases in serum
bilirubin and abnormal changes in other liver function
tests. These results may reflect potentially serious
hepatotoxicity (see Warnings).
Metabolic:
Hyperammonemia (see Precautions), hyponatremia and
inappropriate ADH secretion. Hyperglycinemia has been
reported and associated with a fall outcome in a patient
with pre-existing nonketotic hyperglycinemia.
Genitourinary:
enuresis.
Pancreatic:
There have been reports of acute pancreatitis occurring in
association with therapy with valproic acid.
Special Senses:
Hearing loss, either reversible or irreversible, has been
reported however, a cause and effect relationship has not
been established.
Other:
Edema of extremities has been reported.
Bipolar Disorder:
The incidence of adverse events has been ascertained based
on data from 2 short-term (21 day) placebo-controlled
clinical trials of divalproex in the treatment of acute
mania, and from 2 long-term (up to 3 years) retrospective
open trials.
Most Commonly Observed:
During the short-term placebo-controlled trials, the 6 most
commonly reported adverse events in patients (N=89) exposed
to divalproex were nausea (22%), headache (21%), somnolence
(19%), pain (15%), vomiting (12%), and dizziness (12%).
In the long-term retrospective trials (634 patients exposed to divalproex),
the 6 most commonly reported adverse events were somnolence
(31%), tremor (29%), headache (24%), asthenia (23%),
diarrhea (22%) and nausea (20%).
Associated With Discontinuation of Treatment:
In the placebo-controlled trials, adverse events which
resulted in valproate discontinuation in at least 1% of
patients were nausea (4%) abdominal pain (3%), somnolence
(2%) and rash (2%).
In the long-term retrospective trials, adverse events which resulted in
valproate discontinuation in at least 1% of patients were
alopecia (2.4%), somnolence (1.9%), nausea (1.7%) and tremor
(1.4%). The time to onset of these events was generally
within the first 2 months of initial exposure to valproate.
A notable exception was alopecia, which was first
experienced after 3 to 6 months of exposure by 8 of the 15
patients who discontinued valproate in response to the
event.
Controlled Trials:
Table I summarizes those treatment emergent adverse events
reported for patients in the placebo-controlled trials when
the incidence rate in the divalproex group was at least 5%.
(Maximum treatment duration was 21 days; maximum dose in 83%
of patients was between 1000 to 2500 mg/day).
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