Venlafaxine reviews for anxiety

Effexor XR


The following adverse reactions are discussed in greater detail in other sections of the label:

  • Hypersensitivity
  • Suicidal Thoughts and Behaviors in Children, Adolescents, and Adults
  • Serotonin Syndrome
  • Elevations in Blood Pressure
  • Abnormal Bleeding
  • Angle Closure Glaucoma
  • Activation of Mania/Hypomania
  • Discontinuation Syndrome
  • Seizure
  • Hyponatremia
  • Weight and Height changes in Pediatric Patients
  • Appetite Changes in Pediatric Patients
  • Interstitial Lung Disease and Eosinophilic Pneumonia

Clinical Studies Experience

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.

Most Common Adverse Reactions
Adverse Reactions Reported As Reasons For Discontinuation Of Treatment

Combined across short-term, placebo-controlled premarketing studies for all indications, 12% of the 3,558 patients who received Effexor XR (37.5-225 mg) discontinued treatment due to an adverse experience, compared with 4% of the 2,197 placebo-treated patients in those studies.

The most common adverse reactions leading to discontinuation in ≥ 1% of the Effexor XR treated patients in the short-term studies (up to 12 weeks) across indications are shown in Table 7.

Table 7: Incidence (%) of Patients Reporting Adverse Reactions Leading to Discontinuation in Placebo-controlled Clinical Studies (up to 12 Weeks Duration)

Body System
Adverse Reaction
Effexor XR
n = 3,558
n = 2,197
Body as a whole
Asthenia 1.7 0.5
Headache 1.5 0.8
Digestive system
Nausea 4.3 0.4
Nervous system
Dizziness 2.2 0.8
Insomnia 2.1 0.6
Somnolence 1.7 0.3
Skin and appendages 1.5 0.6
Sweating 1.0 0.2

Common Adverse Reactions In Placebo-Controlled Studies

The number of patients receiving multiple doses of Effexor XR during the premarketing assessment for each approved indication is shown in Table 8. The conditions and duration of exposure to venlafaxine in all development programs varied greatly, and included (in overlapping categories) open and double-blind studies, uncontrolled and controlled studies, inpatient (Effexor only) and outpatient studies, fixed-dose, and titration studies.

Table 8: Patients Receiving Effexor XR in Premarketing Clinical Studies

Indication Effexor XR
MDD 705a
GAD 1,381
SAD 819
PD 1,314
a In addition, in the premarketing assessment of Effexor, multiple doses were administered to 2,897 patients in studies for

The incidences of common adverse reactions (those that occurred in ≥ 2% of Effexor XR treated patients and more frequently than placebo) in Effexor XR treated patients in short-term, placebo-controlled, fixed-and flexible-dose clinical studies (doses 37.5 to 225 mg per day) are shown in Table 9.

The adverse reaction profile did not differ substantially between the different patient populations.

Table 9: Common Adverse Reactions: Percentage of Patients Reporting Adverse Reactions (≥ 2% and > placebo) in Placebo-controlled Studies (up to 12 Weeks Duration) across All Indications

Other Adverse Reactions Observed In Clinical Studies

Body as a whole – Photosensitivity reaction, chills

Cardiovascular system – Postural hypotension, syncope, hypotension, tachycardia

Digestive system – Gastrointestinal hemorrhage , bruxism

Hemic/Lymphatic system – Ecchymosis

Metabolic/Nutritional – Hypercholesterolemia, weight gain , weight loss

Nervous system – Seizures , manic reaction , agitation, confusion, akathisia, hallucinations, hypertonia, myoclonus, depersonalization, apathy

Skin and appendages – Urticaria, pruritus, rash, alopecia

Special senses – Mydriasis, abnormality of accommodation, tinnitus, taste perversion

Urogenital system – Urinary retention, urination impaired, urinary incontinence, urinary frequency increased, menstrual disorders associated with increased bleeding or increased irregular bleeding (e.g., menorrhagia, metrorrhagia)

Vital Sign Changes

In placebo-controlled premarketing studies, there were increases in mean blood pressure (see Table 10). Across most indications, a dose-related increase in mean supine systolic and diastolic blood pressure was evident in patients treated with Effexor XRs. Across all clinical studies in MDD, GAD, SAD and PD, 1.4% of patients in the Effexor XR groups experienced an increase in SDBP of ≥15 mm Hg along with a blood pressure ≥ 105 mm Hg, compared to 0.9% of patients in the placebo groups. Similarly, 1% of patients in the Effexor XR groups experienced an increase in SSBP of ≥ 20 mm Hg with a blood pressure ≥ 180 mm Hg, compared to 0.3% of patients in the placebo groups.

Table 10: Final On-therapy Mean Changes From Baseline in Supine Systolic (SSBP) and Diastolic (SDBP) Blood Pressure (mm Hg) in Placebo-controlled Studies

Effexor XR treatment was associated with sustained hypertension (defined as treatment-emergent Supine Diastolic Blood Pressure ≥ 90 mm Hg and ≥ 10 mm Hg above baseline for three consecutive on-therapy visits (see Table 11). An insufficient number of patients received mean doses of Effexor XR over 300 mg per day in clinical studies to fully evaluate the incidence of sustained increases in blood pressure at these higher doses.

Table 11: Sustained Elevations in SDBP in Effexor XR Premarketing Studies

Indication Dose Range (mg per day) Incidence (%)
MDD 75-375 19/705 (3)
GAD 37.5-225 5/1011 (0.5)
SAD 75-225 5/771 (0.6)
PD 75-225 9/973 (0.9)

Effexor XR was associated with mean increases in pulse rate compared with placebo in premarketing placebo-controlled studies (see Table 12) .

Table 12: Approximate Mean Final On-therapy Increase in Pulse Rate (beats/min) in Effexor XR Premarketing Placebo-controlled Studies (up to 12 Weeks Duration)

Indication (Duration) Effexor XR Placebo
(12 weeks) 2 1
(8 weeks) 2 < 1
(12 weeks) 3 1
(12 weeks) 1 < 1

Laboratory Changes

Serum Cholesterol

Effexor XR was associated with mean final increases in serum cholesterol concentrations compared with mean final decreases for placebo in premarketing MDD, GAD, SAD and PD clinical studies (Table 13).

Table 13: Mean Final On-therapy Changes in Cholesterol Concentrations (mg/dL) in Effexor XR Premarketing Studies

Effexor XR (venlafaxine hydrochloride) extended-release capsules treatment for up to 12 weeks in premarketing placebo-controlled trials for major depressive disorder was associated with a mean final on-therapy increase in serum cholesterol concentration of approximately 1.5 mg/dL compared with a mean final decrease of 7.4 mg/dL for placebo. Effexor XR treatment for up to 8 weeks and up to 6 months in premarketing placebo-controlled GAD trials was associated with mean final on-therapy increases in serum cholesterol concentration of approximately 1.0 mg/dL and 2.3 mg/dL, respectively while placebo subjects experienced mean final decreases of 4.9 mg/dL and 7.7 mg/dL, respectively. Effexor XR treatment for up to 12 weeks and up to 6 months in premarketing placebo-controlled Social Anxiety Disorder trials was associated with mean final on-therapy increases in serum cholesterol concentration of approximately 7.9 mg/dL and 5.6 mg/dL, respectively, compared with mean final decreases of 2.9 and 4.2 mg/dL, respectively, for placebo. Effexor XR treatment for up to 12 weeks in premarketing placebo-controlled panic disorder trials was associated with mean final on-therapy increases in serum cholesterol concentration of approximately 5.8 mg/dL compared with a mean final decrease of 3.7 mg/dL for placebo.

Patients treated with Effexor (immediate release) for at least 3 months in placebo-controlled 12-month extension trials had a mean final on-therapy increase in total cholesterol of 9.1 mg/dL compared with a decrease of 7.1 mg/dL among placebo-treated patients. This increase was duration dependent over the study period and tended to be greater with higher doses. Clinically relevant increases in serum cholesterol, defined as 1) a final on-therapy increase in serum cholesterol ≥50 mg/dL from baseline and to a value ≥261 mg/dL, or 2) an average on-therapy increase in serum cholesterol ≥50 mg/dL from baseline and to a value ≥261 mg/dL, were recorded in 5.3% of venlafaxine-treated patients and 0.0% of placebo-treated patients.

Serum Triglycerides

Effexor XR was associated with mean final on-therapy increases in fasting serum triglycerides compared with placebo in premarketing clinical studies of SAD and PD up to 12 weeks (pooled data) and 6 months duration (Table 14).

Table 14: Mean Final On-therapy Increases in Triglyceride Concentrations (mg/dL) in Effexor XR Premarketing Studies

Pediatric Patients

In general, the adverse reaction profile of venlafaxine (in placebo-controlled clinical studies) in children and adolescents (ages 6 to 17) was similar to that seen for adults. As with adults, decreased appetite, weight loss, increased blood pressure, and increased serum cholesterol were observed .

In pediatric clinical studies, the adverse reaction, suicidal ideation, was observed.

Particularly, the following adverse reactions were observed in pediatric patients: abdominal pain, agitation, dyspepsia, ecchymosis, epistaxis, and myalgia.

Adverse Reactions Identified During Postapproval Use

The following adverse reactions have been identified during postapproval use of Effexor XR. 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:

Body as a whole – Anaphylaxis, angioedema

Cardiovascular system – QT prolongation, ventricular fibrillation, ventricular tachycardia (including torsade de pointes)

Digestive system – Pancreatitis

Hemic/Lymphatic system – Mucous membrane bleeding , blood dyscrasias (including agranulocytosis, aplastic anemia, neutropenia and pancytopenia), prolonged bleeding time, thrombocytopenia

Metabolic/Nutritional – Hyponatremia , Syndrome of Inappropriate Antidiuretic Hormone (SIADH) secretion , abnormal liver function tests, hepatitis, prolactin increased

Musculoskeletal – Rhabdomyolysis

Nervous system – Neuroleptic Malignant Syndrome (NMS) , serotonergic syndrome , delirium, extrapyramidal reactions (including dystonia and dyskinesia), impaired coordination and balance, tardive dyskinesia

Respiratory system – Dyspnea, interstitial lung disease, pulmonary eosinophilia

Skin and appendages – Stevens-Johnson syndrome, toxic epidermal necrolysis, erythema multiforme

Special senses – Angle-closure glaucoma

Read the entire FDA prescribing information for Effexor XR (Venlafaxine Hydrochloride Extended-Release)

Effexor XR Side Effects

Tell your doctor if your symptoms do not get better or if they get worse. Visit your doctor or health care professional for regular checks on your progress. Because it may take several weeks to see the full effects of this medicine, it is important to continue your treatment as prescribed by your doctor.

Patients and their families should watch out for new or worsening thoughts of suicide or depression. Also watch out for sudden changes in feelings such as feeling anxious, agitated, panicky, irritable, hostile, aggressive, impulsive, severely restless, overly excited and hyperactive, or not being able to sleep. If this happens, especially at the beginning of treatment or after a change in dose, call your health care professional.

This medicine can cause an increase in blood pressure. Check with your doctor for instructions on monitoring your blood pressure while taking this medicine.

You may get drowsy or dizzy. Do not drive, use machinery, or do anything that needs mental alertness until you know how this medicine affects you. Do not stand or sit up quickly, especially if you are an older patient. This reduces the risk of dizzy or fainting spells. Alcohol may interfere with the effect of this medicine. Avoid alcoholic drinks.

Your mouth may get dry. Chewing sugarless gum, sucking hard candy and drinking plenty of water will help. Contact your doctor if the problem does not go away or is severe.

User Reviews for Venlafaxine to treat Migraine

Nick Name · Taken for 1 to 6 months June 18, 2017

“Two and a half months ago I was prescribed Venlafaxine to help prevent chronic migraines. It did help the migraines (reduced them by almost half), but with it came a host of side effects that were far worse than the problem I was trying to get rid of. Having now come off of the stuff, I would not recommend anyone ever use Venlafaxine unless they suffer from extreme / suicidal depression. I mean extreme in the most emphatic sense of the word. Before trying Venlafaxine, I was a writer. While on Venlafaxine, I could barely write or speak or communicate at all. More than that, I just didn’t want to. Not normal for a usually outgoing extrovert. Now, I’m beginning to write again – but my ability to speak and converse with others has deteriorated by about 95%. Writing these words is taking forever; keeping up in conversation with even one person is impossible, and I barely see the point of trying either. On Venlafaxine, words pretty much left me – my conversational vocabulary was whittled down to the following: “Mmm” for yes; a sharp and clipped “Mm” for “No” “Okay.” “Really?” “Oh right.” “Cool.” “That sucks” At the moment, I’m a week into withdrawal, and I have to try extremely hard just to make the most mundane small talk. Last night I went to a party with some close friends, cheesy ’90s music, and a barbecue. About half of them are academics, and I couldn’t keep up with conversations I normally would be able to; the other half like to dance and party, but I felt glued to my seat (as well as practically mute) and eventually walked off and found a quiet sofa to lie down on. I have never felt so isolated and lonely in my life. Thanks Venlafaxine. If you consider yourself a social, creative, and curious person, DO NOT TAKE EVEN ONE DOSE OF VENLAFAXINE. Unless of course you are extremely extremely depressed. I’ve suffered from depression in the past, but only mildly. Venlafaxine has shown me what true depression feels like. As for the other side effects: – About two days’ worth of total joyful euphoria during the first 48 hours of taking Venlafaxine. Anxiety of all kinds evaporated. This felt amazing – although I can’t remember what it felt like now. At the time, this extremely brief effect was powerful enough to make me feel that pushing on with Venlafaxine would be a Good Idea. – After that, I started feeling very sleepy. All the time. I slept more. No euphoria; more anxiety. – A week later, the night sweats started. My room was pretty cold (it was only spring in the UK), but I sweated more than I ever have on any tropical holiday. This meant that despite being extremely sleepy, I couldn’t sleep. Since the side effects were supposed to wear off after six weeks or so, I stuck with Venlafaxine for six weeks. Over that time I became so sleep deprived that I lived in a state of permanent exhaustion. Enter the writer’s worst enemy: Brain fog. I spent entire days so braindead that the most challenging thing I could manage was staring blankly at a wall – or lifting my phone to read text messages and attempt to learn something from articles about Venlafaxine. I’ve read the same articles countless times, but nothing sank in; every time I read the same article it felt like I was reading it for the first time. I recognised the layout and design of each webpage, and that way I was able to realise I’d read it before, but the actual text went in one eye and out the other. In conversation, I had a brain like a sieve. Words went in one ear and out the other. Normally, I could pump out a lot of writing on a regular basis; on Venlafaxine, I wrote a small and frankly pitiful handful of short and uninspired pieces, and that was it. If you love being productive and creative, do not go near Venlafaxine. The above was my life for six weeks – and that was enough. I did see family and friends while on Venlafaxine, but I constantly forgot what was going on and must have seemed scatterbrained or borderline retarded at times. Although I did explain to people what was going on with my medication, it just seemed to make people uncomfortable – and I’ve now become the butt of a lot of jokes relating to my consistent uselessness at everything from chatting to party games and my inability to work or do anything productive. Someone even compared me to Lenny from Of Mice And Men and asked when my family were going to take me into the back garden and shoot me in the head rather than continue to care for me. All of this contributed to the worst feeling of loneliness and isolation I have ever experienced in my life. Venlafaxine not only trapped me inside my head – it also emptied my head of anything worth remembering, and left me barely able to learn new things. I’d sit around tables with people and realise I couldn’t remember the names of people I’d know for years – or even family members. I’d hear a song playing and say “Hey – what’s the name of this dance?” Any sentence longer than a few words requires a minute or so to compose when written. Spoken out loud? Forget about it. When I try to speak, I sound like the Goon from Popeye. After six weeks of hell, my doctor and I agreed to taper off my 75mg daily dose. This process lasted a month, not following a particular schedule (which might have been a better idea), and was mostly side effect free until I came down to 18.25mg a day – one half of one 37.5mg tablet. After three days of that, it really hit the fan. I got up one day, pottered around a bit, and suddenly decided that I wanted to kill myself. Literally out of nowhere. Fortunately I was of sound enough mind to call the Samaritans, who recommended I call the emergency services, who sent an ambulance to take me to hospital. For suicidal thoughts. To be honest, I’d rather have gone to Disneyland. Once I was in A&E, I got to wait for several hours, just stewing in a room with a sofa and not much else. Then I met the most useless doctor of all time. After I refused his suggestion that I not only go back on Venlafaxine, but *try a higher dose* than the one that got me into this mess in the first place, he said there wasn’t anything else they could do – and handed me a little leaflet for a local mental health charity meetup that happens every so often. By this point I’d decided that suicide would not be the best option – and nor would going on even more Venlafaxine than before. I also binned the leaflet on my way out, determined to keep going and just deal with the withdrawal. Since that time, my intelligence level has plummeted to the point of being humiliating. But that’s not even the worst of it. As I mentioned before, I started taking Venlafaxine for migraines. Now that I’m not taking it, they’re coming back again – but they’ve also changed. A few days ago, days before the party I should probably have stayed home for only I couldn’t stand sitting at home any longer so I went and ended up alone in a darkened room and felt more depressed than I have in my entire life, I was at home when I collapsed. The right side of my body gave way, I hit the wall, and fell on the floor where I lay frozen for God knows how long. Then when I did get up, I realised I couldn’t speak at all, the right side of my body was almost paralysed, and the right side of my head was numb on the outside, and in agony on the inside. After calling the emergency services again, I was taken through the standard questions I guess they ask everyone when they think the person in question is having a stroke. Like the suicidal thoughts, stroke symptoms were a new experience for me. Thanks, Venlafaxine. When the ambulance arrived, they were able to reassure me that I wasn’t having a stroke, as one side of my face wasn’t drooping. This was good news – but since they couldn’t explain what was actually going on, I was taking to hospital for a brain scan and blood tests and a meeting with a doctor who told me I’d had a right-sided hemiplegic migraine. I’d never had one before, and didn’t know they existed until then; my migraines have always felt like my head is both in a vice and exploding at the same time, and I get them across my whole head, not just one side. At this point, I’m determined to continue fighting the withdrawal symptoms. The only thing that’s really helped me in doing this was the discovery of a cognitive distortion called “emotional reasoning”. This involves assuming that because you feel bad, things must actually be bad. Obviously emotional reasoning (which is worth Googling as it’s quite an in depth subject, or at least feels like it given that my brain’s been hopefully temporarily damaged by Venlafaxine) is pretty common in depression. It’s also been my brain’s default way of operating possibly for as long as I can remember, but definitely since I started taking Venlafaxine. The emotional and physical and psychological rollercoaster Venlafaxine puts you through is utterly exhausting – and while it’s throwing you all over the place and especially during withdrawal it’s tough to keep in mind that a lot of the negative thoughts your mind throws up are going to be based on how you feel (i.e. the levels and mix of different chemicals in your brain), NOT on any Real Life Stuff. You’ll most likely unintentionally filter out all the good stuff in your brain and only remember the darkest and worst things you possibly can, and attach all kinds of apparently logical arguments to make a case against yourself / a case that argues that you and your life are awful. Looking back on this experience, my thoughts were similar to one of those films you see advertised as “…based on a true story”. Works of fiction based very loosely on facts. Rather than a film you’d give two stars and never watch again, emotional reasoning’s end product is a lie – not to mention the most toxic thoughts a human being can think. Depression can definitely make people tell these lies to themselves – but Venlafaxine made my brain malfunction so badly that putting together an apparently sensible argument for any depressive thoughts suddenly seemed like the most obvious thing in the world one day. If I hadn’t had those thoughts, I would’ve just made lunch. So that’s about it for now – if I don’t update this story in the future, assume I got better and decided to never revisit this page again, preferring to leave Venlafaxine and its horrific toxicity behind me. Good luck with your own journey :)”


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26 · Report

In her compelling essay, “In Bed,” novelist Joan Didion wrote, “That no one dies of migraine seems, to someone deep into an attack, an ambiguous blessing.”

For many people, migraines are debilitating events. As Harvard Health editor Christine Junge wrote in this space last year about her battle with migraine:

“On the good days, the pain was just a mild throbbing sensation. Other times, there was a general sense of an ever-tightening pressure. On the days when I couldn’t get out of bed, it felt like someone was tightening screws into the sides of my head and pounding a hammer above my left eye. The pain never went away, unless I was asleep.”

Most migraine sufferers long to prevent these painful episodes. As I write in this month’s Harvard Health Letter, about one-third of migraineurs could benefit from taking a preventive pill. But only a minority of them actually take advantage of this option. New treatment guidelines from the American Academy of Neurology and the American Headache Society profile the best preventive medications, and an herbal preparation, for migraine.

“These drugs can reduce the frequency and severity of migraine attacks, and may require different doses over time to achieve these benefits,” says Dr. Lee H. Schwamm, vice chairman of the neurology department at Massachusetts General Hospital and professor of neurology at Harvard Medical School. “They must be taken daily. They are different from pain-relieving medicines—drugs that halt a migraine once it has started.”

Pills for prevention

The guidelines include two categories of preventive medications. Those with proven effectiveness for preventing migraine include

  • the antiseizure drugs divalproex (Depakote), valproate (Depacon), and topiramate (Topamax)
  • the beta blockers metoprolol, propranolol, and timolol
  • the triptan drug, frovatriptan (Frova), for short-term menstruation-associated migraine

Drugs that are probably effective include

  • two antidepressants, amitriptyline (Elavil and others) and venlafaxine (Effexor)
  • two other beta blockers, atenolol and nadolol
  • two other triptans, naratriptan (Amerge) and zolmitriptan (Zomig)

The guidelines also include an herbal remedy made from butterbur, a plant in the daisy family. Butterbur contains chemicals called pyrrolizidine alkaloids (PA) that can damage the liver and cause other problems. If you want to use a butterbur-based treatment, choose a product that is certified as PA free.

Daily use, side effects may limit use

Since it’s impossible to predict when a migraine will happen, these medications must be taken daily. But the more often you have to take a medicine, the less likely you are to take it faithfully. “If you don’t have the symptom right away when you skip a dose, then you are even more likely to skip doses,” says Dr. Schramm.

All medications, and herbal remedies, have the potential to cause side effects, cautions Dr. Schwamm. Antiseizure medicines can reduce concentration and may cause drowsiness. Beta blockers can slow the heart rate and sometime cause depression or sexual dysfunction. “Topiramate can cause weight loss, so some patients are more compliant with this drug,” says Dr. Schramm.

Personalizing prevention

Migraine prevention doesn’t necessarily require medication. Getting enough sleep, reducing stress, and paying attention to diet and exercise can help. So can identifying whether you have any migraine triggers, like chocolate, caffeine, or alcohol. Keeping a migraine diary that includes your stress level, what you’ve eaten and drunk, and the like can help identify triggers.

Tell us your story

Do you live with migraines? If so, let us know what your migraine triggers are. If you’ve tried medications, herbal remedies, or other preventive efforts, please tell us if they worked for you.

Before choosing any preventative treatments, it is important to eliminate frequent headache triggers. The most common triggers include irregular sleep, missed meals, caffeine, and chocolate. Other common triggers, which are not preventable, are menstrual cycles, weather fronts, and stress releases.

Once the most common preventable triggers have been eliminated, the next most important step is to make sure headaches are not rebound headaches. Rebound headaches are usually caused by medications that are taken daily. However, any medication that is being more than twice weekly could potentially be causing rebound headaches. Migraine prevention programs are less likely to be successful if a patient continues to take a rebounding medication.

Preventative Medications

The next step is to choose a migraine prevention treatment. Fortunately there are many choices. Four common medications that doctor agree are well proven and highly effective are Elavil® (amitriptylene), Inderal®, (propranolol) Depakote® (valproic acid), and Topamax® (topiramate). Botox is also used if the patient has chronic migraines. The most important thing to remember is that there are numerous agents that one can try for migraine prevention. It is most likely that at least one of them will work well for you. If the first medication does not reduce the number of headaches you are having then don’t be discouraged, you may just need a higher dose or you can try a different medication. If you are having frequent headaches, please see your neurologist to discuss possible preventative treatments!

Elavil® (amitriptylene)

The primary advantage of Amitriptylene or Elavil® is its affordability, which can be as low as $5 per month. Unfortunately, Elavil can have numerous side effects, including dry mouth, sedation, constipation, and weight gain.

Inderal® (propranolol)

Another well-established preventative medication is propranolol or Inderal®. This medication is fairly well tolerated in most individuals and is relatively inexpensive, with a twice-daily generic form running about $4 per month. It can worsen asthma, cause fatigue, and limit aerobic exercise. It is generally thought of as a “weight-neutral medication” and most patients do not experience weight gain, but all patients should be monitored for possible weight gain.

Topamax® (topiramate)

Topamax was first licensed as an antiepileptic medication. It is the most popular medication currently prescribed for headache prevention. Among the most commonly prescribed medications, it is the only one that is clearly associated with weight loss. The average obese patient can expect to lose about 10% of their body weight over one year. Since obesity is a risk factor for frequent migraines over time, a large number of migraine patients who need preventatives are medically overweight or obese. Unfortunately, topiramate does have side effects. Some side effects are more of a nuisance. Carbonated drinks taste badly while taking this drug and some patients experience tingling around the mouth, finger, or toes. Renal or kidney stones occur about 1% of the time and do not go away without additional therapy when topiramate is discontinued. A small percentage of patients have an altered ability to think on the medication that commonly expressed as a word-finding problem. This returns to normal with reduction or discontinuation of the medication. Finally, there is a very rare condition of acute narrow angle glaucoma that is very painful but again resolves with discontinuation of the medication and specific medical therapy.

Depakote ER® or valproic acid

The last of the most common preventatives is valproic acid. The most convenient form for patients is Depakote ER®, a once daily migraine prevention agent. Depakote ER® can cause birth defects. In addition, valproic acid can cause weight gain and liver enzyme problems. Despite these warnings, the medication is generally well tolerated and can be used quite safely. However, given the issue with birth defects it is most commonly prescribed to males with migraines who are not overweight. Valproic acid is also widely used as an anticonvulsant to prevent seizures.

Botox (onabotulinum)

Botox is FDA approved for the prevention of headaches in patients with chronic migraine. Because it is one of the more expensive therapies for migraine prevention, it is generally used after patients fail other therapies. Because of its cost, a headache diary should be kept to determine whether the treatment is clearly helpful. The headache diary can also serve as an early warning when the medication is wearing off. The data on botulinum toxin type A or Botox® is quite extensive. Despite this, there continues to be a lot of controversy over its use. It does appear to help some patients with frequent migraines but it remains to be seen how best to choose which patients to treat with Botox®. The cost of the medication is also quite substantial.

Other agents used widely for prevention of migraine include:

Effexor XR® (venlafaxine)

Venlafaxine or Effexor XR® is an antidepressant. Doses of 150 mg or more of this medication have been demonstrated to be a rather robust migraine agent. This medication can have side effects of nausea, sexual dysfunction and sometimes will increase blood pressure.

Cymbalta® (duloxetine)

Another selective serotonin and norepinephrine reuptake inhibitor (SSNRI) on the market is duloxetine or Cymbalta®. It is relatively more balanced than Effexor® and therefore is easier to titrate. It does cause the same amount of nausea as Effexor but is associated with less sexual dysfunction and less hypertension. Cymbalta is FDA-approved in depression, anxiety, diabetic neuropathic pain, chronic low back pain, osteoarthritis pain, and fibromyalgia pain. Since a large percentage of chronic migraine sufferers also have depression, the use of Cymbalta® as a first line agent makes sense and is FDA-approved for their depression.

Verapamil, Coenzyme Q10, Botox® and PFO

There are studies demonstrating verapamil to be a good anti-migraine agent although not as robust as the medications previously mentioned. Coenzyme Q10, which is available over the counter, was demonstrated in one small placebo controlled trial to be beneficial.

Patients with migraines have an increased risk patent foramen ovale (PFO), a small channel between the right atria and left atria of the heart. PFOs in migraine patients also tend to be larger. Some data suggest closing this hole or channel lessens the incidence of migraine. The most important thing to remember is that there are numerous agents that one can try for migraine prevention. It is most likely that at least one of them will work well for you. Unfortunately prevention therapies are under utilized, resulting in excessive disability for migraine patients. If you are having frequent headaches, please see your neurologist and ask to be placed on prevention.

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