What is Depakote (valproic acid)?
Depakote (valproic acid) is used to treat convulsions (seizures) and bipolar disorder, and to prevent migraines. Scientists do not know the mechanism of action of valproic acid. The most popular theory is that valproic acid exerts its effects by increasing the concentration of gamma-aminobutyric acid (GABA) in the brain. GABA is a neurotransmitter, a chemical that nerves use to communicate with one another.
Common side effects of Depakote include:
- weight loss,
- tremors, and
- skin reactions such as:
Serious side effects of Depakote include:
- liver injury (symptoms include yellowing skin and eyes, general feeling of being unwell, weakness, swelling in the face, loss of appetite and vomiting),
- pancreatitis (symptoms include weight loss, nausea, vomiting and severe abdominal pain), and
- abnormal bleeding.
Antiepileptic medications like Depakote have been associated with an increased risk of suicidal thinking and behavior.
Drug interactions of Depakote include other medications which inhibit the stickiness of platelets or inhibit other steps in the clotting of blood, which when taken with Depakote can lead to abnormal bleeding due to the inability of blood to clot, such as:
- heparin or low-molecular weight heparin,
- ticlopidine, and
- aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs).
Aspirin and felbamate can reduce the elimination of Depakote and result in toxicity due to the Depakote.
Cholestyramine can reduce the effectiveness of Depakote.
Depakote can significantly decrease the elimination of the following, which can lead to toxicity:
Depakote also increases blood levels of warfarin and phenytoin which may lead to an increase in side effects.
The use of Depakote during pregnancy has been associated with fetal abnormalities such as:
The risk of spina bifida in the offspring of mothers taking Depakote during pregnancy is 1%-2%. Depakote also may cause reduced clotting in the mother and baby. Because of the risk of harm to the newborn, Depakote should only be used by pregnant women when its benefits outweigh the risks.
The concentration of Depakote in breast milk of women taking valproic acid is 1-10%. Although the effect on the nursing infant is not certain, breastfeeding should probably be avoided while using Depakote.
What are the important side effects of Depakote (valproic acid)?
The most common side effects with valproic acid therapy are:
Divalproex may have a lower incidence of stomach upset, and taking valproic acid or divalproex with food can reduce the stomach upset.
Valproic acid also causes skin reactions such as:
The most serious side effects due to valproic acid are:
- liver injury,
- pancreatitis and
- abnormal bleeding.
Liver injury is most common in the first 6 months of treatment. It also is more common in children, especially children less than two years old. Persons taking more than one type of anticonvulsant seem to be at higher risk.
Symptoms of liver damage include:
- swelling in the face,
- loss of appetite and
Pancreatitis due to valproic acid can occur early in treatment or after several years of use.
Symptoms of pancreatitis are:
- unexplained weight loss,
- vomiting and
- severe abdominal pain.
Valproic acid inhibits the formation of blood clots by interfering with the clot-promoting effects of platelets. This can cause abnormal bleeding.
Antiepileptic medications have been associated with an increased risk of suicidal thinking and behavior. Anyone considering the use of antiepileptic drugs must balance this risk of suicide with the clinical need for the antiepileptic drug. Patients who begin antiepileptic therapy should be closely observed for clinical worsening, suicidal thoughts or unusual changes in behavior.
Depakote (valproic acid) side effects list for healthcare professionals
The following serious adverse reactions are described below and elsewhere in the labeling:
- Hepatic failure
- Birth defects
- Decreased IQ following in utero exposure
- Hyperammonemic encephalopathy
- Suicidal behavior and ideation
- Bleeding and other hematopoietic disorders
- Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)/Multiorgan hypersensitivity reactions
- Somnolence in the elderly
Because clinical studies are conducted under widely varying conditions, adverse reaction rates observed in the clinical studies of a drug cannot be directly compared to rates in the clinical studies of another drug and may not reflect the rates observed in practice.
The incidence of treatment-emergent events has been ascertained based on combined data from two three week placebo-controlled clinical trials of Depakote in the treatment of manic episodes associated with bipolar disorder. The adverse reactions were usually mild or moderate in intensity, but sometimes were serious enough to interrupt treatment. In clinical trials, the rates of premature termination due to intolerance were not statistically different between placebo, Depakote, and lithium carbonate. A total of 4%, 8% and 11% of patients discontinued therapy due to intolerance in the placebo, Depakote, and lithium carbonate groups, respectively.
Table 2 summarizes those adverse reactions reported for patients in these trials where the incidence rate in the Depakote-treated group was greater than 5% and greater than the placebo incidence, or where the incidence in the Depakote-treated group was statistically significantly greater than the placebo group. Vomiting was the only reaction that was reported by significantly (p ≤ 0.05) more patients receiving Depakote compared to placebo.
Table 2: Adverse Reactions Reported by > 5% of Depakote-Treated Patients During Placebo-Controlled Trials of Acute Mania1
(n = 89)
(n = 97)
|1 The following adverse reactions occurred at an equal or greater incidence for placebo than for Depakote: back pain, headache, constipation, diarrhea, tremor, and pharyngitis.|
The following additional adverse reactions were reported by greater than 1% but not more than 5% of the 89 Depakote-treated patients in controlled clinical trials:
Hemic and Lymphatic System: Ecchymosis.
Metabolic and Nutritional Disorders: Edema, peripheral edema.
Nervous System: Abnormal dreams, abnormal gait, agitation, ataxia, catatonic reaction, confusion, depression, diplopia, dysarthria, hallucinations, hypertonia, hypokinesia, insomnia, paresthesia, reflexes increased, tardive dyskinesia, thinking abnormalities, vertigo.
Respiratory System: Dyspnea, rhinitis.
Based on a placebo-controlled trial of adjunctive therapy for treatment of complex partial seizures, Depakote was generally well tolerated with most adverse reactions rated as mild to moderate in severity. Intolerance was the primary reason for discontinuation in the Depakotetreated patients (6%), compared to 1% of placebo-treated patients.
Table 3 lists treatment-emergent adverse reactions which were reported by ≥ 5% of Depakotetreated patients and for which the incidence was greater than in the placebo group, in the placebo-controlled trial of adjunctive therapy for treatment of complex partial seizures. Since patients were also treated with other antiepilepsy drugs, it is not possible, in most cases, to determine whether the following adverse reactions can be ascribed to Depakote alone, or the combination of Depakote and other antiepilepsy drugs.
Table 3: Adverse Reactions Reported by ≥ 5% of Patients Treated with Depakote During Placebo-Controlled Trial of Adjunctive Therapy for Complex Partial Seizures
|Body System/Reaction||Depakote (%)|
(n = 77)
(n = 70)
|Body as a Whole|
Table 4 lists treatment-emergent adverse reactions which were reported by ≥ 5% of patients in the high dose valproate group, and for which the incidence was greater than in the low dose group, in a controlled trial of Depakote monotherapy treatment of complex partial seizures. Since patients were being titrated off another antiepilepsy drug during the first portion of the trial, it is not possible, in many cases, to determine whether the following adverse reactions can be ascribed to Depakote alone, or the combination of valproate and other antiepilepsy drugs.
Table 4: Adverse Reactions Reported by ≥ 5% of Patients in the High Dose Group in the Controlled Trial of Valproate Monotherapy for Complex Partial Seizures1
|Body System/Reaction||High Dose (%)|
(n = 131)
|Low Dose (%)|
(n = 134)
|Body as a Whole|
|Skin and Appendages|
|1 Headache was the only adverse reaction that occurred in ≥ 5% of patients in the high dose group and at an equal or greater incidence in the low dose group.|
The following additional adverse reactions were reported by greater than 1% but less than 5% of the 358 patients treated with valproate in the controlled trials of complex partial seizures:
Cardiovascular System: Tachycardia, hypertension, palpitation.
Hemic and Lymphatic System: Petechia.
Metabolic and Nutritional Disorders: SGOT increased, SGPT increased.
Nervous System: Anxiety, confusion, abnormal gait, paresthesia, hypertonia, incoordination, abnormal dreams, personality disorder.
Skin and Appendages: Rash, pruritus, dry skin.
Special Senses: Taste perversion, abnormal vision, deafness, otitis media.
Based on two placebo-controlled clinical trials and their long term extension, valproate was generally well tolerated with most adverse reactions rated as mild to moderate in severity. Of the 202 patients exposed to valproate in the placebo-controlled trials, 17% discontinued for intolerance. This is compared to a rate of 5% for the 81 placebo patients.
Including the long term extension study, the adverse reactions reported as the primary reason for discontinuation by ≥ 1% of 248 valproate-treated patients were:
- alopecia (6%),
- nausea and/or vomiting (5%),
- weight gain (2%),
- tremor (2%),
- somnolence (1%),
- elevated SGOT and/or SGPT (1%), and
- depression (1%).
Table 5 includes those adverse reactions reported for patients in the placebo-controlled trials where the incidence rate in the Depakote-treated group was greater than 5% and was greater than that for placebo patients.
Table 5: Adverse Reactions Reported by > 5% of Depakote-Treated Patients During Migraine Placebo-Controlled Trials with a Greater Incidence Than Patients Taking Placebo1
|Body System Reaction||Depakote|
(N = 202)
(N = 81)
|1 The following adverse reactions occurred in at least 5% of Depakote-treated patients and at an equal or greater incidence for placebo than for Depakote: flu syndrome and pharyngitis.|
The following additional adverse reactions were reported by greater than 1% but not more than 5% of the 202 Depakote-treated patients in the controlled clinical trials:
Body as a Whole: Chest pain, chills, face edema, fever and malaise.
Cardiovascular System: Vasodilatation.
Hemic and Lymphatic System: Ecchymosis.
Metabolic and Nutritional Disorders: Peripheral edema, SGOT increase, and SGPT increase.
Musculoskeletal System: Leg cramps and myalgia.
Skin and Appendages: Pruritus and rash.
Urogenital System: Cystitis, metrorrhagia, and vaginal hemorrhage.
The following adverse reactions have been identified during post approval use of Depakote. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure.
Psychiatric: Emotional upset, psychosis, aggression, psychomotor hyperactivity, hostility, disturbance in attention, learning disorder, and behavioral deterioration.
There have been several reports of acute or subacute cognitive decline and behavioral changes (apathy or irritability) with cerebral pseudoatrophy on imaging associated with valproate therapy; both the cognitive/behavioral changes and cerebral pseudoatrophy reversed partially or fully after valproate discontinuation.
There have been reports of acute or subacute encephalopathy in the absence of elevated ammonia levels, elevated valproate levels, or neuroimaging changes. The encephalopathy reversed partially or fully after valproate discontinuation.
Hematologic: Relative lymphocytosis, macrocytosis, leukopenia, anemia including macrocytic with or without folate deficiency, bone marrow suppression, pancytopenia, aplastic anemia, agranulocytosis, and acute intermittent porphyria.
Endocrine: Irregular menses, secondary amenorrhea, hyperandrogenism, hirsutism, elevated testosterone level, breast enlargement, galactorrhea, parotid gland swelling, polycystic ovary disease, decreased carnitine concentrations, hyponatremia, hyperglycinemia, and inappropriate ADH secretion.
There have been rare reports of Fanconi's syndrome occurring chiefly in children.
Metabolism and nutrition: Weight gain.
Reproductive: Aspermia, azoospermia, decreased sperm count, decreased spermatozoa motility, male infertility, and abnormal spermatozoa morphology.
Special Senses: Hearing loss.
What drugs interact with Depakote (valproic acid)?
Effects Of Co-Administered Drugs On Valproate Clearance
Drugs that affect the level of expression of hepatic enzymes, particularly those that elevate levels of glucuronosyltransferases (such as ritonavir), may increase the clearance of valproate. For example, phenytoin, carbamazepine, and phenobarbital (or primidone) can double the clearance of valproate. Thus, patients on monotherapy will generally have longer half-lives and higher concentrations than patients receiving polytherapy with antiepilepsy drugs.
In contrast, drugs that are inhibitors of cytochrome P450 isozymes, e.g., antidepressants, may be expected to have little effect on valproate clearance because cytochrome P450 microsomal mediated oxidation is a relatively minor secondary metabolic pathway compared to glucuronidation and beta-oxidation.
Because of these changes in valproate clearance, monitoring of valproate and concomitant drug concentrations should be increased whenever enzyme inducing drugs are introduced or withdrawn.
The following list provides information about the potential for an influence of several commonly prescribed medications on valproate pharmacokinetics. The list is not exhaustive nor could it be, since new interactions are continuously being reported.
Drugs For Which A Potentially Important Interaction Has Been Observed
A study involving the co-administration of aspirin at antipyretic doses (11 to 16 mg/kg) with valproate to pediatric patients (n=6) revealed a decrease in protein binding and an inhibition of metabolism of valproate. Valproate free fraction was increased 4-fold in the presence of aspirin compared to valproate alone. The β-oxidation pathway consisting of 2-E-valproic acid, 3-OHvalproic acid, and 3-keto valproic acid was decreased from 25% of total metabolites excreted on valproate alone to 8.3% in the presence of aspirin. Caution should be observed if valproate and aspirin are to be co-administered.
A clinically significant reduction in serum valproic acid concentration has been reported in patients receiving carbapenem antibiotics (for example, ertapenem, imipenem, meropenem; this is not a complete list) and may result in loss of seizure control. The mechanism of this interaction is not well understood. Serum valproic acid concentrations should be monitored frequently after initiating carbapenem therapy. Alternative antibacterial or anticonvulsant therapy should be considered if serum valproic acid concentrations drop significantly or seizure control deteriorates.
Estrogen-Containing Hormonal Contraceptives
Estrogen-containing hormonal contraceptives may increase the clearance of valproate, which may result in decreased concentration of valproate and potentially increased seizure frequency. Prescribers should monitor serum valproate concentrations and clinical response when adding or discontinuing estrogen containing products.
A study involving the co-administration of 1,200 mg/day of felbamate with valproate to patients with epilepsy (n=10) revealed an increase in mean valproate peak concentration by 35% (from 86 to 115 mcg/mL) compared to valproate alone. Increasing the felbamate dose to 2,400 mg/day increased the mean valproate peak concentration to 133 mcg/mL (another 16% increase). A decrease in valproate dosage may be necessary when felbamate therapy is initiated.
A study involving the administration of a single dose of valproate (7 mg/kg) 36 hours after 5 nights of daily dosing with rifampin (600 mg) revealed a 40% increase in the oral clearance of valproate. Valproate dosage adjustment may be necessary when it is co-administered with rifampin.
Drugs For Which Either No Interaction Or A Likely Clinically Unimportant Interaction Has Been Observed
A study involving the co-administration of valproate 500 mg with commonly administered antacids (Maalox, Trisogel, and Titralac - 160 mEq doses) did not reveal any effect on the extent of absorption of valproate.
A study involving the administration of 100 to 300 mg/day of chlorpromazine to schizophrenic patients already receiving valproate (200 mg BID) revealed a 15% increase in trough plasma levels of valproate.
A study involving the administration of 6 to 10 mg/day of haloperidol to schizophrenic patients already receiving valproate (200 mg BID) revealed no significant changes in valproate trough plasma levels.
Cimetidine And Ranitidine
Effects Of Valproate On Other Drugs
Valproate has been found to be a weak inhibitor of some P450 isozymes, epoxide hydrase, and glucuronosyltransferases.
The following list provides information about the potential for an influence of valproate co-administration on the pharmacokinetics or pharmacodynamics of several commonly prescribed medications. The list is not exhaustive, since new interactions are continuously being reported.
Drugs For Which A Potentially Important Valproate Interaction Has Been Observed
Administration of a single oral 50 mg dose of amitriptyline to 15 normal volunteers (10 males and 5 females) who received valproate (500 mg BID) resulted in a 21% decrease in plasma clearance of amitriptyline and a 34% decrease in the net clearance of nortriptyline. Rare postmarketing reports of concurrent use of valproate and amitriptyline resulting in an increased amitriptyline level have been received. Concurrent use of valproate and amitriptyline has rarely been associated with toxicity. Monitoring of amitriptyline levels should be considered for patients taking valproate concomitantly with amitriptyline. Consideration should be given to lowering the dose of amitriptyline/nortriptyline in the presence of valproate.
Serum levels of carbamazepine (CBZ) decreased 17% while that of carbamazepine-10,11epoxide (CBZ-E) increased by 45% upon co-administration of valproate and CBZ to epileptic patients.
The concomitant use of valproate and clonazepam may induce absence status in patients with a history of absence type seizures.
Valproate displaces diazepam from its plasma albumin binding sites and inhibits its metabolism. Co-administration of valproate (1,500 mg daily) increased the free fraction of diazepam (10 mg) by 90% in healthy volunteers (n=6). Plasma clearance and volume of distribution for free diazepam were reduced by 25% and 20%, respectively, in the presence of valproate. The elimination half-life of diazepam remained unchanged upon addition of valproate.
Valproate inhibits the metabolism of ethosuximide. Administration of a single ethosuximide dose of 500 mg with valproate (800 to 1,600 mg/day) to healthy volunteers (n=6) was accompanied by a 25% increase in elimination half-life of ethosuximide and a 15% decrease in its total clearance as compared to ethosuximide alone. Patients receiving valproate and ethosuximide, especially along with other anticonvulsants, should be monitored for alterations in serum concentrations of both drugs.
In a steady-state study involving 10 healthy volunteers, the elimination half-life of lamotrigine increased from 26 to 70 hours with valproate co-administration (a 165% increase). The dose of lamotrigine should be reduced when co-administered with valproate. Serious skin reactions (such as Stevens-Johnson syndrome and toxic epidermal necrolysis) have been reported with concomitant lamotrigine and valproate administration. See lamotrigine package insert for details on lamotrigine dosing with concomitant valproate administration.
Valproate was found to inhibit the metabolism of phenobarbital. Co-administration of valproate (250 mg BID for 14 days) with phenobarbital to normal subjects (n=6) resulted in a 50% increase in half-life and a 30% decrease in plasma clearance of phenobarbital (60 mg single-dose). The fraction of phenobarbital dose excreted unchanged increased by 50% in presence of valproate.
There is evidence for severe CNS depression, with or without significant elevations of barbiturate or valproate serum concentrations. All patients receiving concomitant barbiturate therapy should be closely monitored for neurological toxicity. Serum barbiturate concentrations should be obtained, if possible, and the barbiturate dosage decreased, if appropriate.
Primidone, which is metabolized to a barbiturate, may be involved in a similar interaction with valproate.
Valproate displaces phenytoin from its plasma albumin binding sites and inhibits its hepatic metabolism. Co-administration of valproate (400 mg TID) with phenytoin (250 mg) in normal volunteers (n=7) was associated with a 60% increase in the free fraction of phenytoin. Total plasma clearance and apparent volume of distribution of phenytoin increased 30% in the presence of valproate. Both the clearance and apparent volume of distribution of free phenytoin were reduced by 25%.
In patients with epilepsy, there have been reports of breakthrough seizures occurring with the combination of valproate and phenytoin. The dosage of phenytoin should be adjusted as required by the clinical situation.
The concomitant use of valproate and propofol may lead to increased blood levels of propofol. Reduce the dose of propofol when co-administering with valproate. Monitor patients closely for signs of increased sedation or cardiorespiratory depression.
Based on a population pharmacokinetic analysis, rufinamide clearance was decreased by valproate. Rufinamide concentrations were increased by <16% to 70%, dependent on concentration of valproate (with the larger increases being seen in pediatric patients at high doses or concentrations of valproate). Patients stabilized on rufinamide before being prescribed valproate should begin valproate therapy at a low dose, and titrate to a clinically effective dose. Similarly, patients on valproate should begin at a rufinamide dose lower than 10 mg/kg per day (pediatric patients) or 400 mg per day (adults).
From in vitro experiments, the unbound fraction of tolbutamide was increased from 20% to 50% when added to plasma samples taken from patients treated with valproate. The clinical relevance of this displacement is unknown.
In an in vitro study, valproate increased the unbound fraction of warfarin by up to 32.6%. The therapeutic relevance of this is unknown; however, coagulation tests should be monitored if valproate therapy is instituted in patients taking anticoagulants.
In six patients who were seropositive for HIV, the clearance of zidovudine (100 mg q8h) was decreased by 38% after administration of valproate (250 or 500 mg q8h); the half-life of zidovudine was unaffected.
Drugs For Which Either No Interaction Or A Likely Clinically Unimportant Interaction Has Been Observed
Valproate had no effect on any of the pharmacokinetic parameters of acetaminophen when it was concurrently administered to three epileptic patients.
In psychotic patients (n=11), no interaction was observed when valproate was co-administered with clozapine.
Co-administration of valproate (500 mg BID) and lithium carbonate (300 mg TID) to normal male volunteers (n=16) had no effect on the steady-state kinetics of lithium.
Concomitant administration of valproate (500 mg BID) and lorazepam (1 mg BID) in normal male volunteers (n=9) was accompanied by a 17% decrease in the plasma clearance of lorazepam.
No dose adjustment for olanzapine is necessary when olanzapine is administered concomitantly with valproate. Co-administration of valproate (500 mg BID) and olanzapine (5 mg) to healthy adults (n=10) caused 15% reduction in Cmax and 35% reduction in AUC of olanzapine.
Oral Contraceptive Steroids
Administration of a single-dose of ethinyloestradiol (50 mcg)/levonorgestrel (250 mcg) to 6 women on valproate (200 mg BID) therapy for 2 months did not reveal any pharmacokinetic interaction.
Concomitant administration of valproate and topiramate has been associated with hyperammonemia with and without encephalopathy. Concomitant administration of topiramate with valproate has also been associated with hypothermia in patients who have tolerated either drug alone. It may be prudent to examine blood ammonia levels in patients in whom the onset of hypothermia has been reported.
Depakote (valproic acid) is used to treat convulsions (seizures) and bipolar disorder, and to prevent migraines. Common side effects of Depakote include drowsiness, dizziness, nausea, vomiting, indigestion, diarrhea, weight loss, tremors, and skin reactions such as hair loss, rash, itching, and sensitivity to sunlight. Serious side effects of Depakote include liver injury (symptoms include yellowing skin and eyes, general feeling of being unwell, weakness, swelling in the face, loss of appetite and vomiting), pancreatitis (symptoms include weight loss, nausea, vomiting and severe abdominal pain), and abnormal bleeding. Antiepileptic medications like Depakote have been associated with an increased risk of suicidal thinking and behavior. The use of Depakote during pregnancy has been associated with fetal abnormalities such as spina bifida, cardiovascular abnormalities, and neural tube defects. The concentration of Depakote in breast milk of women taking valproic acid is 1-10%.
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Related Disease Conditions
Migraine headache is a type of headache associated with a sensitivity to light, smells, or sounds, eye pain, severe pounding on one side of the head, and sometimes nausea and vomiting. The exact cause of migraine headaches is not known. Triggers for migraine headaches include certain foods, stress, hormonal changes, strong stimuli (loud noises), and oversleeping. Treatment guidelines for migraines include medicine, pain management, diet changes, avoiding foods that trigger migraines, staying hydrated, getting adequate sleep, and exercising regularly. Prevention of migraine triggers include getting regular exercise, drinking water daily, reducing stress, and avoiding trigger foods.
Seizures Symptoms and Types
Seizures are divided into two categories: generalized and partial. Generalized seizures are produced by electrical impulses from throughout the brain, while partial seizures are produced by electrical impulses in a small part of the brain. Seizure symptoms include unconsciousness, convulsions, and muscle rigidity.
Abdominal Migraines in Children and Adults
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Bipolar II Disorder
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Epilepsy is a brain disorder in which the person has seizures. There are two kinds of seizures, focal and generalized. There are many causes of epilepsy. Treatment of epilepsy (seizures) depends upon the cause and type of seizures experienced.
Abdominal Migraines in Children and Adults
Abdominal migraine in adults and children is a variant of migraine headaches. Abdominal migraine in children generally occurs in children who have a family history of migraines. Causes of abdominal migraine is not known. Symptoms of abdominal migraine include acute, severe, midline abdominal pain, nausea, vomiting, paleness, and inability to eat. Abdominal migraine is diagnosed through patient history, family history, and ruling out other medical causes. Treatment of abdominal migraine include tricyclic antidepressants and triptans.
Migraines and Seizures (Symptoms, Auras, Medication)
Migraines are a type of headache and seizures are the main symptom of epilepsy. Migraine headaches and seizures are two different neurological problems that have similar signs, symptoms, and auras, for example, sensitivity to light (photophobia) and sound, irritability, nausea, and vomiting. Symptoms unique to migraine and migraine auras are water retention, problems sleeping, appetite changes, and talkativeness. Symptoms unique to seizure and seizures auras are depression, a feeling of heaviness, a feeling that a seizure is approaching, and depression. Many of the symptoms of migraine and seizures are the same, however, seizures do not cause migraines; however, people who have seizures are twice as likely to have migraines and vice-versa. People who have migraines are twice as likely to have seizures, and people with seizures are twice as likely to have migraines; however, one condition does not cause the other.
Migraine vs. Headache: Differences and Similarities
Headaches are the most common reason why a person goes to the doctor or other healthcare professional for treatment. There are different types of headaches, for example, migraine, tension, and cluster headaches. The most common type of headache is tension headache. Migraine is much less common. There are few similarities between migraine and other headaches, for example, the severity of the pain can be the same, mild, moderate, or severe; and they can occur on one side or both sides of the head. However, there are many differences between migraine and other types of headaches. Migraine headaches also have different names, for example, migraine with aura and menstrual migraine. Symptoms of migraine that usually aren't experienced by a person with another type of headache include nausea, vomiting, worsens with mild exercise, debilitating pain, eye pain, throbbing head pain. Migraine trigger include light, mild exercise, strong smells, certain foods like red wine, aged cheese, smoked meats, artificial sweeteners, chocolate, alcohol, and dairy products, menstrual period, stress, oversleeping, and changes in barometric pressure. Untreated migraine attacks usually last from 4 to 72 hours, but may last for weeks. Most headaches resolve within 24-48 hours. Doctors don't know exactly what causes migraine headaches; however, other headaches like tension headaches have more specific triggers and causes. Additional tests usually are required to diagnose migraine from other types of headaches, diseases, or other medical problems. Most headaches can be treated and cured with home remedies like essential oils, massage, and over-the-counter pain medication like acetaminophen (Tylenol) and NSAIDs (nonsteroidal anti-inflammatory drugs) like naproxen (Aleve, Anaprox, Naprosyn) or ibuprofen (Advil, Midol, Motrin). Most headaches resolve with OTC and home remedy treatment, while your doctor may need to prescribe medication to treat your migraines. If you have the "worst headache of your life," seek medical care immediately.
Bipolar Disorder vs. Schizophrenia
Bipolar disorder and schizophrenia are mental illnesses that share some risk factors and treatments. Symptoms of bipolar disorder include mood changes and manic and depressive episodes. Symptoms of schizophrenia include unusual behavior, delusions, and hallucinations.
Migraine and Stroke (Symptoms, Types, Causes, Treatment)
Migraine headache is a type of headache in which the exact cause is not known; however, they may be inherited, and certain foods and environmental factors can trigger and may contribute them. A stroke (brain attack) happens when a blood vessel in the brain leaks, bursts, or becomes blocked, which can be caused by many other health problems. Both migraines and strokes can can cause severe head pain (migraine pain usually is only on one side of the head). Migraine aura symptoms may mimic or feel like a stroke or mini-stroke (transient ischemic attack, TIA) because they have similar symptoms and signs like severe headache, numbness in the legs, feet, arms, hands, or face, nausea, vomiting, and dizziness. Other migraine aura symptoms include vision problems like flashing lights or blind spots in one eye. The main difference between migraine headache and stroke symptoms and signs is that a migraine headaches usually come on gradually while a stroke symptoms come on suddenly and unexpectedly. A migraine may cause photophobia (sensitivity to light and sound). Migraine triggers include hormonal changes, alcohol, insomnia, caffeine, stress, anxiety, bright lights, loud noises, strong odors, aspartame, MSG, and changes in the weather. Symptoms of a stroke that do not occur with migraines include confusion, speech, vision, and balance problems. You can have a migraine headache and a stroke at the same time, but migraines do not cause strokes. However, in certain individuals with migraines with auras there may be related to a higher risk of stroke. Stroke is a medical emergency. If you have stroke symptoms, call 9-1-1 and get medical attention immediately.
Seizure vs. Seizure Disorders (Differences and Similarities)
The differences between a seizure, epilepsy, and seizure disorders are confusing to many people. What makes it more confusing, is that they are not the same thing. A seizure begins suddenly, and is a symptom of another disease. When a seizure occurs there is uncontrolled activity in the brain that usually only lasts for a short period. While a seizure disorder is a medical condition, in which the person has episodes of uncontrolled activity in the brain producing symptoms that include one or more seizures. Epilepsy is considered a seizure disorder.There are two types of major seizures, generalized and partial seizure type and the symptoms depend upon the part of the brain affected, and may include: Loss of consciousness Thought disturbances Convulsions Eye rolling Stiff limbs Twitching on only one side or a portion of the body like an arm or leg. Involuntary urination or bowel movement Repetitive shaking or jerking of the body Staring into space, sometimes with eye blinking No loss of consciousness, but the person becomes confused for a few minutes A third type of seizure is called unclassified seizure.Seizure disorders are classified under two types of major seizures (generalized and partial), and a third type called unclassified seizures. There are about 40 types of named seizure disorders. The symptoms and signs are different depending on the part of the brain affected by the seizure. Examples of seizure disorders are: Febrile seizures Benign Rolandic epilepsy Catamenial epilepsy Absence seizures Frontal lobe epilepsy Epilepsy Sometimes there is a known cause for a seizure like alcohol, cocaine or other illegal drug abuse, drug reactions, a severe chemical imbalance in the blood, or medical problems like low blood pressure. Treatment, management, and prevention of seizures include medication and avoiding any known causes or common triggers. REFERENCES: CDC. "Types of Seizures." Updated: Apr 10, 2017.Harvard Health Publications; Harvard Medical School. "Generalized Seizures (Grand Mal Seizures)."
Bipolar disorder (or manic depression) is a mental illness characterized by depression, mania, and severe mood swings. Treatment may incorporate mood-stabilizer medications, antidepressants, and psychotherapy.
Febrile seizures, or convulsions caused by fever, can be frightening in small children or infants. However, in general, febrile seizures are harmless. Febrile seizure is not epilepsy. It is estimated that one in every 25 children will have at least one febrile seizure. It is important to know what to do to help your child if he/she has a febrile seizure. Some of the features of a febrile seizure include: losing consciousness, shaking, moving limbs on both sides of the body, lasts 1-2 minutes. Less commonly, a febrile seizure may only affect one side of the body.
Bipolar Disorder in Children and Teens
Bipolar disorder, or manic-depressive illness, is a disorder that causes unusual and extreme mood changes. Symptoms of bipolar disorder in children and teens include having trouble concentrating, behaving in risky ways, and losing interest in activities they once enjoyed. Treatment for bipolar disorder in children and teenagers incorporates psychotherapy and medications.
Treatment & Diagnosis
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Medications & Supplements
Report Problems to the Food and Drug Administration
You are encouraged to report negative side effects of prescription drugs to the FDA. Visit the FDA MedWatch website or call 1-800-FDA-1088.
FDA Prescribing Information
Meador KJ, Baker GA, Browning N, et al. Fetal antiepileptic drug exposure and cognitive outcomes at age 6 years (NEAD study): a prospective observational study. Lancet Neurology 2013; 12 (3):244-252.