What are the common side effects of Zoloft. How does sertraline work in treating depression and anxiety. Can Zoloft cause dizziness and other adverse reactions. What should you know about sertraline interactions and warnings.

Understanding Sertraline: A Comprehensive Overview

Sertraline, widely recognized by its brand name Zoloft, is a prominent medication in the realm of mental health treatment. This selective serotonin reuptake inhibitor (SSRI) plays a crucial role in managing various psychological conditions, including depression, anxiety, post-traumatic stress disorder (PTSD), social anxiety disorder, panic disorder, and premenstrual dysphoric disorder (PMDD).

The primary mechanism of action for sertraline involves increasing serotonin levels in the brain. Serotonin, often referred to as the “feel-good” neurotransmitter, is essential for regulating mood, emotions, and various cognitive functions. By enhancing serotonin availability, sertraline aims to alleviate symptoms associated with these mental health conditions.

How does sertraline work to improve mental health?

Sertraline functions by inhibiting the reuptake of serotonin in the brain. This process allows more serotonin to remain available in the synapses between neurons, facilitating improved communication within the brain’s neural networks. As a result, individuals taking sertraline may experience:

• Enhanced mood regulation
• Reduced anxiety symptoms
• Improved sleep patterns
• Increased energy levels
• Greater interest in daily activities

Dr. Raul Perez-Vazquez, a primary care physician at Tenet Florida Physician Services and West Boca Medical Center, explains, “Sertraline, like all other SSRIs, increases circulating serotonin levels in the human body, promoting a sense of well-being and allowing persons with depression and anxiety to cope better with their current situation or condition.”

Common Side Effects of Zoloft (Sertraline)

While sertraline can be highly effective in treating various mental health conditions, it’s important to be aware of potential side effects. These adverse reactions can vary in intensity and duration among individuals. Some common side effects include:

• Nausea
• Diarrhea
• Constipation
• Sleep disturbances (insomnia or excessive sleepiness)
• Dizziness
• Dry mouth
• Headache
• Changes in appetite or weight
• Sexual dysfunction

Is dizziness a common side effect of Zoloft?

Dizziness is indeed a reported side effect of sertraline. While not everyone experiences this symptom, it’s essential to be aware of its potential occurrence. Dizziness may be more pronounced during the initial stages of treatment or when adjusting dosage. If dizziness persists or becomes severe, it’s crucial to consult with a healthcare provider for guidance.

Managing Sertraline Side Effects: Tips and Strategies

Coping with side effects can be challenging, but there are several strategies that can help mitigate their impact:

1. Gradual dosage adjustment: Starting with a lower dose and gradually increasing it can help minimize initial side effects.
2. Timing of medication: Taking sertraline with food may help reduce nausea and gastrointestinal discomfort.
3. Staying hydrated: Adequate water intake can help alleviate dry mouth and constipation.
4. Regular exercise: Physical activity can improve overall well-being and potentially reduce some side effects.
5. Sleep hygiene: Establishing a consistent sleep routine may help address sleep-related side effects.

It’s important to note that most side effects tend to diminish over time as the body adjusts to the medication. However, if side effects persist or worsen, consulting with a healthcare provider is essential.

Sertraline Interactions: What You Need to Know

Understanding potential drug interactions is crucial when taking sertraline. Certain medications, supplements, and even foods can interact with sertraline, potentially altering its effectiveness or increasing the risk of side effects.

Which medications should not be taken with sertraline?

Several medications can interact with sertraline, including:

• Monoamine oxidase inhibitors (MAOIs)
• Other SSRIs or SNRIs
• Pimozide
• Disulfiram (when taking sertraline oral solution)
• Blood thinners (e.g., warfarin)
• NSAIDs (e.g., ibuprofen, naproxen)
• Certain migraine medications (triptans)

This list is not exhaustive, and it’s crucial to inform your healthcare provider about all medications, supplements, and herbal products you’re taking to avoid potential interactions.

Sertraline Warnings: Important Considerations

While sertraline can be highly beneficial for many individuals, there are several important warnings to keep in mind:

What are the black box warnings for sertraline?

Sertraline carries a black box warning, the most serious type of warning issued by the FDA, regarding an increased risk of suicidal thoughts and behaviors in children, adolescents, and young adults. This risk is particularly pronounced during the initial stages of treatment or when adjusting dosages.

Other important warnings include:

• Potential for serotonin syndrome
• Risk of withdrawal symptoms if discontinued abruptly
• Possibility of increased bleeding risk
• Potential for manic episodes in individuals with bipolar disorder
• Risk of seizures
• Potential for hyponatremia (low sodium levels)

It’s crucial to discuss these warnings with your healthcare provider and report any concerning symptoms promptly.

Sertraline Dosage and Administration

Proper dosing of sertraline is essential for achieving optimal therapeutic effects while minimizing side effects. The dosage can vary depending on the condition being treated and individual patient factors.

What is the typical starting dose for sertraline?

The typical starting dose for sertraline in adults is often 50 mg once daily. However, this can vary based on the specific condition being treated:

• Depression and OCD: 50 mg once daily
• Panic disorder, PTSD, and social anxiety disorder: 25 mg once daily, increased to 50 mg after one week
• PMDD: 50 mg per day during the luteal phase of the menstrual cycle

Dosages may be adjusted over time based on individual response and tolerance. It’s crucial to follow the prescribed dosage and not alter it without consulting a healthcare provider.

Long-term Effects of Sertraline Use

While sertraline is generally considered safe for long-term use, it’s important to be aware of potential long-term effects and to maintain regular check-ups with a healthcare provider.

Can long-term use of sertraline lead to dependence?

Sertraline is not considered addictive in the traditional sense. However, long-term use can lead to physical dependence, meaning the body becomes accustomed to the medication. This can result in withdrawal symptoms if the medication is stopped abruptly. It’s important to note that dependence is not the same as addiction, and any changes in sertraline use should be done under medical supervision.

Some potential long-term effects to be aware of include:

• Changes in weight or metabolism
• Ongoing sexual side effects
• Potential impact on bone density
• Possible effects on cognitive function in older adults

Regular monitoring and open communication with healthcare providers can help manage these potential long-term effects.

Sertraline in Special Populations

The use of sertraline in certain populations requires special consideration and careful monitoring. These groups include pregnant women, breastfeeding mothers, children and adolescents, and older adults.

Is sertraline safe during pregnancy and breastfeeding?

The use of sertraline during pregnancy and breastfeeding is a complex decision that requires careful consideration of the potential risks and benefits. While some studies suggest a slight increase in certain risks (such as birth defects) with SSRI use during pregnancy, untreated depression also carries significant risks for both mother and child.

For breastfeeding mothers, small amounts of sertraline can pass into breast milk. However, the benefits of breastfeeding and treating maternal depression often outweigh the potential risks. It’s crucial to discuss these factors with a healthcare provider to make an informed decision.

Considerations for other special populations include:

• Children and adolescents: Careful monitoring for suicidal thoughts and behaviors is essential
• Older adults: May be more sensitive to side effects and require lower initial doses
• Individuals with liver or kidney disease: May require dose adjustments

Individualized treatment plans and close medical supervision are crucial for these populations.

Side Effects of Zoloft (Sertraline Hcl), Warnings, Uses

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Sertraline side effects and interactions, and how to avoid them

Sertraline, most commonly known by its brand name, Zoloft, is a popular prescription medication used to treat depression, anxiety, post-traumatic stress disorder, social anxiety disorder, panic disorder, and premenstrual dysphoric disorder (PMDD). It belongs to a class of antidepressants called selective serotonin reuptake inhibitors (SSRIs), meaning it works by increasing the amount of serotonin in the brain. As with many antidepressants, people who take sertraline may experience some adverse effects. Continue reading to learn about sertraline side effects, warnings, and possible drug interactions. 

RELATED: Sertraline details | Zoloft details

Common side effects of sertraline

With any medication, there is always a risk of experiencing potential adverse effects. To know when you’re experiencing side effects, it helps to understand how the drug should make you feel when it’s working correctly. In the case of sertraline, patients can expect to feel improvements in mood, appetite, sleep quality, energy level, and interest in daily life. In other words, an easing of symptoms like depression and anxiety. 

“Sertraline, just as all other SSRIs, increases circulating serotonin levels in the human body, promoting a sense of well-being and allowing persons with depression and anxiety to cope better with their current situation or condition,” says to Raul Perez-Vazquez, MD, a primary care physician of Tenet Florida Physician Services and West Boca Medical Center.

These are the most common sertraline side effects:

• Nausea
• Diarrhea
• Constipation
• Difficulty falling asleep or staying asleep
• Dry mouth
• Heartburn or indigestion
• Loss of appetite
• Weight loss or weight gain
• Dizziness
• Excessive tiredness
• Headache
• Nervousness
• Changes in sex drive
• Erectile dysfunction, including delayed ejaculation
• Excessive sweating

When do Zoloft side effects go away?

Many of the common side effects listed below can go away after a few weeks while the body adjusts. 

“Sertraline itself takes about a month to start working, and many of the mild side effects diminish after your body has adjusted to the medication,” says David Nazarian, MD, a primary care physician at My Concierge MD in Beverly Hills. 

It’s a good idea to track side effects that you experience and keep your healthcare professional updated so your physician can effectively monitor reactions and adjust medication as needed. Most importantly, tell a doctor if side effects are severe, worsening, or do not go away.

Serious side effects of sertraline

There are some less common, but severe side effects of sertraline. The following symptoms require immediate medical attention:

• Abnormal bleeding or bruising
• Agitation
• Confusion
• Fever, sweating, shivering
• Hallucinations
• Hives or rash
• Loss of coordination
• Muscle stiffness or twitching
• Nausea, vomiting, or diarrhea
• Rapid heartbeat
• Seizures
• Swelling
• Suicidal thoughts
• Trouble breathing
• Uncontrollable shaking of a part of the body

Zoloft withdrawal

Although most of the side effects are reversible, you should not stop taking sertraline abruptly. Instead, speak with a healthcare provider before discontinuing this medication to avoid withdrawal symptoms. A doctor can devise a plan to slowly taper the medication.   Withdrawal symptoms include: 

• Irritability/mood swings 
• Nausea
• Dizziness
• Vomiting
• Insomnia
• Nightmares
• Headache
• Paresthesias (prickling, tingling sensation on the skin)

Collectively, these symptoms are called antidepressant discontinuation syndrome, which requires immediate medical assistance. 

Sertraline warnings

Other FDA warnings include restrictions for:

• Patients who are allergic to sertraline or any of its inactive ingredients
• Pregnant women or those who may become pregnant, as sertraline may cause problems in newborns following delivery
• Women who are breastfeeding since sertraline may pass through breast milk
• Those with preexisting eye problems that may make them susceptible to develop angle-closure glaucoma, which can cause severe eye pain or even blindness. An eye test may be required before receiving a sertraline prescription. 
• Those with bipolar disorder. If sertraline is taken without a mood stabilizer, a patient may be at risk for shifting into a manic or hypomanic episode.

Suicidal thoughts

Perhaps the most significant warning to be aware of when taking sertraline is the potential for suicidal thoughts or actions, especially in young adults. All antidepressants, in fact, have a boxed warning (the strongest warning required by the FDA) about antidepressants and suicidal thoughts and behaviors. 

According to the drugmaker Pfizer, a patient may become suicidal, especially at the beginning of treatment and any time that the dose is increased or decreased. Pfizer advises patients to call a healthcare provider right away if you notice new or sudden changes in mood, behavior, or thoughts. Patients and their families should be made aware of this rare but possible effect. Otherwise, all patients should regularly follow up with a doctor and call between appointments if experiencing any of the following symptoms:

• Feeling agitated, restless, angry, or irritable
• An increase in activity or talking more than usual
• New or worsening depression
• New or worsening anxiety or panic attacks
• Trouble sleeping
• Acting on dangerous impulses
• Acting aggressive or violent
• Thoughts about suicide or dying
• Attempts to commit suicide
• Other unusual changes in behavior or mood

Drowsiness

A common side effect of sertraline is sleepiness, which could affect your ability to react quickly or make clear decisions. For this reason, there is a strong warning not to drive, operate heavy machinery, or do other dangerous activities until you know how sertraline affects you. 

Serotonin syndrome

Serotonin syndrome is a life-threatening condition that can be caused by taking sertraline with other medications that increase the production of serotonin in the body. These medications include:

• Monoamine oxidase inhibitors (MAOIs—don’t use Zoloft within 14 days of these medications). 
• Other SSRIs (like Prozac, Paxil, Celexa, Lexapro)
• SNRIs (like Effexor, Cymbalta, Pristiq)
• Triptans (Imitrex, Maxalt, etc)
• Tricyclic antidepressants (such as Elavil or Pamelor)
• Fentanyl
• Lithium
• Tramadol
• Tryptophan 
• Buspirone
• St. John’s Wort
• Fanapt (iloperidone)
• Thorazine (chlorpromazine)

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Symptoms of serotonin syndrome include:

• High fever
• Rapid changes in heart rate or blood pressure
• Uncontrolled muscle spasms
• Confusion
• Headache
• Heavy sweating 
• Diarrhea
• Stiff muscles
• Loss of consciousness (passing out)

Sertraline interactions

Before taking a new prescription drug, you should disclose all medications that you’re currently taking. Over-the-counter, prescription drugs, and even natural remedies like supplements have the potential to cause harmful drug-drug interactions.

Certain antipsychotics

Mixing sertraline with antipsychotics increases your risk of heart conditions, including cardiac arrest. One example is Orap (pimozide), an antipsychotic medication often prescribed to people with Tourette syndrome. Geodon (ziprasidone) and droperidol are other antipsychotics that could interact with sertraline.

Blood thinners

Taking sertraline with blood thinners (aspirin, Plavix, heparin, warfarin) can increase your risk of bleeding, including nosebleeds as well as stomach and intestinal bleeding. 

Non-steroidal anti-inflammatory drugs (NSAIDs)

Combining sertraline with NSAIDs, like ibuprofen or naproxen, can also increase the risk of severe stomach issues, including life-threatening bleeding, and low sodium levels.

Alcohol

You should not drink alcohol while taking sertraline as both affect chemicals in the brain. Alcohol may alter the effectiveness of sertraline and lead to side effects, including sleep problems and excessive drowsiness. 

Additionally, Antabuse (disulfiram), which treats alcoholism, cannot be combined with the liquid form of sertraline because of the alcohol content in liquid sertraline.

How to avoid sertraline side effects

The best way to prevent sertraline side effects is to take the medication exactly as prescribed by a doctor and in alignment with the drug manufacturer’s instructions. 

The starting dose of sertraline is 25 to 50 mg per day, which can be slowly tapered up if necessary. Sertraline dosages can be adjusted by the physician through close monitoring of the patient and your response to the medication. “Always begin sertraline at the lowest dose, and increase slowly, reevaluating symptoms periodically, and using the lowest effective dose,” says Dr. Perez-Vazquez.

Sertraline can be taken with or without food, according to Pfizer. However, if the liquid concentrate form of sertraline is prescribed, it must be diluted with water, ginger ale, lemon or lime soda, lemonade, or orange juice.

There are a few other steps you can take to help minimize sertraline side effects while you’re waiting for your body to adjust to the new medication. “Some small lifestyle modifications can assist with sertraline side effects, like taking the medication at night to prevent lethargy or eating small frequent meals to avoid nausea,” says Dr. Nazarian. “By listening to your body, noticing the side effects, and making appropriate interventions early on, discomfort can be minimized.” 

Another sometimes overlooked step in ensuring the medication acts as it should is to follow manufacturer instructions on how to store the prescription carefully. Regarding sertraline, the bottle should be tightly closed, kept out of the reach of children, and stored at room temperature, 68°F to 77°F (20°C to 25°C).

Antidepressant Discontinuation Syndrome – American Family Physician

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Zoloft vs. Lexapro

What are the differences between Zoloft vs. Lexapro?

• Zoloft (sertraline) and Lexapro (escitalopram) are antidepressant drugs in the selective serotonin reuptake inhibitor (SSRI) class used for treating depression, and anxiety disorders.
• Zoloft is also used to treat obsessive-compulsive disorder (OCD), panic disorder, and post-traumatic stress disorder (PTSD), and premenstrual dysphoric disorder (PMDD).
• Lexapro is not approved for treating obsessive-compulsive disorders and panic disorders like other SSRIs.
• Common side effects of Zoloft and Lexapro that are similar include drowsiness, nausea, tremor (shaking), increased or decreased appetite, headache, diarrhea, difficulty sleeping (insomnia), dry mouth, increased sweating, weight changes, sexual difficulties (decreased sexual ability or desire, ejaculatory delay), and upset stomach/indigestion.
• Zoloft can cause different side effects than Lexapro including nervousness, dizziness, skin rash, or constipation. Lexapro can cause different side effects than Zoloft including agitation or restlessness, blurred vision, fever, frequent urination, and taste alterations.
• Some patients experience withdrawal reactions when they stop using SSRIs such as Zoloft or Lexapro. Symptoms may include dizziness, tingling, tiredness, vivid dreams, irritability, or poor mood.

What are Zoloft and Lexapro?

Zoloft (sertraline) is used for treating depression, obsessive-compulsive disorder (OCD), panic disorder, and post-traumatic stress disorder (PTSD), social anxiety disorder, and premenstrual dysphoric disorder (PMDD). It belongs to a class of drugs called selective serotonin reuptake inhibitors (SSRIs). Other drugs in this class are fluoxetine (Prozac, Sarafem), paroxetine (Brisdelle, Paxil, Paxil CR, Pexeva), citalopram (Celexa), and fluvoxamine (Luvox CR).

Lexapro (escitalopram) is a selective serotonin reuptake inhibitor (SSRI) used for treating depression and generalized anxiety disorder.

What are the side effects of Zoloft and Lexapro?

Zoloft

The most common side effects of Zoloft are:

• Sleepiness
• Nervousness
• Insomnia
• Dizziness
• Nausea
• Tremor
• Skin rash
• Constipation
• Upset stomach
• Loss of appetite
• Headache
• Diarrhea
• Abnormal ejaculation
• Decreased interest in sexual activity
• Dry mouth
• Increase in sweating, known as diaphoresis
• Weight loss

Possible serious side effects of Zoloft include:

• Irregular heartbeats
• Serious allergic reactions
• Worsening of depression
• Serotonin syndrome
• Hyponatremia
• Abnormal bleeding
• Priapism (prolonged erection)
• Decreased liver function
• Suicidality
• Activation of mania in patients with bipolar disorder

Important side effects are irregular heartbeats, allergic reactions and activation of mania in patients with bipolar disorder. If Zoloft is discontinued abruptly, some patients experience side effects such as:

• Abdominal cramps
• Fatigue
• Nausea
• Vomiting
• Diarrhea
• Headaches
• Lightheadedness
• Dizziness
• Diminished appetite
• Flu-like symptoms
• Sweating
• Chills
• Sleep disturbances
• Memory impairment

A gradual dose reduction of Zoloft is recommended when therapy is discontinued.

Lexapro

WARNING

Some patients experience withdrawal reactions upon stopping SSRI therapy. Symptoms may include

• dizziness,
• tingling,
• tiredness,
• vivid dreams,
• irritability, or
• poor mood.

In order to avoid these symptoms, the dose of SSRI can be slowly reduced instead of abruptly stopped.

Antidepressants increased the risk of suicidal thinking and behavior (suicidality) in short-term studies in children and adolescents with depression and other psychiatric disorders. Anyone considering the use of Lexapro or any other antidepressant in a child or adolescent must balance this risk with the clinical need. Short-term studies did not show an increase in the risk of suicidality with antidepressants compared with placebo in adults beyond 24 years of age. There was a reduction in risk of suicidality with antidepressants compared with placebo in adults 65 years of age and older. Depression and certain other psychiatric disorders are themselves associated with increases in the risk of suicide. Patients who are started on therapy with antidepressants should be closely observed for clinical worsening, suicidality, or unusual changes in behavior.

Common side effects associated with Lexapro are:

• agitation or restlessness,
• blurred vision,
• diarrhea,
• difficulty sleeping,
• drowsiness,
• dry mouth,
• fever,
• frequent urination,
• headache,
• indigestion,
• nausea,
• increased or decreased appetite,
• increased sweating,
• sexual difficulties (decreased sexual ability or desire, ejaculatory delay),
• taste alterations, tremor (shaking), and
• weight changes.

Other side effects include influenza-like symptoms and pain in neck or shoulders.

Although changes in sexual desire, sexual performance, and sexual satisfaction often occur as a result of depression itself, they also may be a consequence of the drugs used to treat depression. In particular, about one in 11 men given Lexapro report difficulties ejaculating.

Possible serious side effects of Lexapro include:

• Serotonin syndrome
• Suicidal thinking and behavior
• Abnormal bleeding
• Seizures
• Manic episodes
• Low sodium
• Angle closure glaucoma

What is the dosage of Zoloft vs. Lexapro?

Zoloft

• The recommended dose of sertraline is 25-200 mg once daily. Treatment of depression, OCD, panic disorder, PTSD, and social anxiety disorder is initiated at 25-50 mg once daily. Doses are increased at weekly intervals until the desired response is seen.
• The recommended dose for PMDD is 50-150 mg every day of the menstrual cycle or for 14 days before menstruation.
• Sertraline may be taken with or without food.

Lexapro

• The usual starting dose of Lexapro for treating depression in adults or adolescents is 10 mg once daily in the morning or evening. The dose may be increased to 20 mg once daily after 1 week.
• Benefit may not be seen until treatment has been given for up to 4 weeks. A daily dose of 20 mg may not be more effective than 10 mg daily for treatment of depression.
• The dose for treating generalized anxiety disorder is 10 mg once daily.
• Lexapro can be taken with or without food.

What drugs interact with Zoloft and Lexapro?

Zoloft

All SSRIs, including Zoloft, should not be taken with any of the monoamine oxidase inhibitor (MAOI) class of antidepressants, for example

• isocarboxazid (Marplan),
• phenelzine (Nardil),
• tranylcypromine (Parnate),
• selegiline (Eldepryl, Emsam, Elazar), and
• procarbazine (Matulane).

Other drugs that inhibit monoamine oxidase include

• linezolid (Zyvox) and
• intravenous methylene blue.

Such combinations may lead to confusion, high blood pressure, tremor, hyperactivity, coma, and death. (A period of 14 days without treatment should lapse when switching between Zoloft and MAOIs.) Similar reactions occur when Zoloft is combined with other drugs for example, tryptophan, St. John’s wort, meperidine (Demerol, Meperitab), tramadol (ConZip, Synapryn FusePaq, Ultram) that increase serotonin in the brain.

Cimetidine (Cimetidine Acid Reducer, Tagamet HB ) may increase the levels in blood of Zoloft by reducing the elimination of Zoloft by the liver. Increased levels of Zoloft may lead to more side effects.

Zoloft increases the blood level of pimozide (Orap) by 40%. High levels of pimozide can affect electrical conduction in the heart and lead to sudden death. Therefore, patients should not receive treatment with both pimozide and Zoloft.

Through unknown mechanisms, Zoloft may increase the blood thinning action of warfarin (Coumadin, Jantoven). The effect of warfarin should be monitored when Zoloft is started or stopped.

Lexapro

• All SSRIs, including Lexapro, should not be combined with drugs in the monoamine oxidase (MAO) inhibitor class of antidepressants such as isocarboxazid (Marplan), phenelzine (Nardil), tranylcypromine (Parnate), selegiline (Eldepryl) and procarbazine (Matulane) or other drugs that inhibit monoamine oxidase such as linezolid (Zyvox) and intravenous methylene blue. Such combinations may lead to confusion, high blood pressure, high fevers, tremor or muscle rigidity, and increased activity. At least 14 days should elapse after discontinuing Lexapro before starting an MAO inhibitor. Conversely, at least 14 days should elapse after discontinuing an MAO inhibitor before starting Lexapro.
• Similar reactions occur when SSRIs are combined with other drugs that increase serotonin in the brain, for example tryptophan, St. John’s wort, meperidine (Demerol), lithium (Lithobid, Eskalith), triptans (for example, sumatriptan [Imitrex, Alsuma]), and tramadol (Ultram)
• Use of selective serotonin inhibitors may increase the risk of gastrointestinal bleeding in patients taking warfarin (Jantoven, Coumadin), aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and other drugs that cause bleeding.

Are Zoloft and Lexapro safe to use while pregnant or breastfeeding?

Zoloft

• Use of sertraline during the 3rd trimester of pregnancy may lead to adverse effects in the newborn.
• Use of sertraline by nursing mothers has not been adequately evaluated.

Lexapro

• The safety of Lexapro during pregnancy and breastfeeding has not been established. Therefore, Lexapro should not be used during pregnancy unless, in the opinion of the physician, the expected benefits to a patient outweigh unknown hazards to the fetus.
• Lexapro is excreted in human milk. Lexapro should not be given to nursing mothers unless, in the opinion of the physician, the expected benefits to the patient outweigh the possible hazards to the child.

References

FDA Prescribing Information

Vertigo and Psychological Disturbances

Timothy C. Hain,
MD •
Page last modified:

October 24, 2021

Also see: brainfog• psychological causes of dizziness • PPPD

Psychological problems are related to vertigo in a complex way. They may both
be a cause as well as a consequence of dizziness (Staab and Ruckenstein, 2003).

We are not talking about chronic vertigo — As Clark pointed out (2001), “The patient with chronic dizziness should never be labeled with psychogenic dizziness. Chronic does not mean psychogenic. Chronic means that health care has been unsuccessful” .

Psychological abnormalities in dizzy patients — and keeping them in a reasonable perspective

Psychological abnormalities are common in the general population, even more
common in those who are ill, and are certainly also common in individuals with
vertigo. Many studies suggest that about 50% of persons who present to clinics for dizziness have psychological disorder, mainly anxiety. Studies of patients with dizziness also suggests that they mainly have reactive anxiety and depression (Savastano et al, 2007). A review of the prevalence of panic was published by Simon and others (1998). They document prevalance varying from 3 to 41%, in a dizziness specialty clinic. Of this table, our experience matches best the findings of Clark et al (20%).

It should be realized that psychological testing (unlike MRI scans, or even clinical examinations by neurologists) cannot diagnose “organic” disorders of the brain or neurochemistry. Questionnaires are subjective — people can say whatever they please, irregardless of the state of their brain. Accordingly, in our opinion at least, these sorts of tests are not “diagnostic” of a disease, but rather are “descriptive” of a particular mental state, subscribed to at the time that the questionnaire was administered.

In our opinion, shared by Savastino et al (2007), the most likely explanation for these sorts of lists are reactive psychological disturbances, rather than primary psychiatric problems. This differs modestly from the conclusions of Staab et al (2003), a psychiatrist, who in considering a study of 132 undiagnosed or “psychogenic” patients, concluded that there were three groups of roughly equal size — reactive psychiatric disturbances, primary psychiatric disturbances, and a mixture of both. We suspect that the difference in opinion has to do with sampling bias, and a tendency to diagnose what one knows best.

Models for associations between psychiatriac disorders and vestibular dysfunction.

Simon and associates (1998) reviewed three explanatory models (hypotheses) regarding the known association between anxiety (panic) and dizziness.

• Psychosomatic model —

  a primary psychiatric disturbance causes dizziness
  (psychiatric chicken causes dizziness egg)

  • hyperventilation and hyperarrousal increased vestibular sensitivity.
• Somatopsychic model —
  a primary inner ear disturbance causes anxiety.
  (dizziness egg produces psychiatric chicken which produces more dizziness eggs)
  • signals from the inner ear are misinterpreted as signifying immediate danger, which increases anxiety. Increased anxiety increases misinterpretation. Conditioning makes it persistent.
• Network alarm model —
  renamed variant of somatopsychic model
  • Panic is triggered by a “false alarm” via afferents to the locus ceruleus (an area in the brain), which then triggers a “neuronal network”, including limbic, midbrain and prefrontal areas. This explanation seems to us to be the “somatopsychic” model, renamed and attached to a specific brain localization.

I. Non-localized vertigo

At present there is no reliable method of consistently distinguishing among
patients with dizziness caused by a psychiatric condition, nonlocalized dizziness,
and the dizziness accompanied by a psychiatric condition. Thus, discussions
of psychogenic dizziness are characterized by considerable opinion and a paucity
of objective evidence. The biggest problem in evaluation of these patients is
separating psychogenic from nonlocalized vertigo. Accordingly we will first
discuss various types of nonlocalized vertigo, and then proceed to talk about
psychogenic vertigo specifically.

IA. Non-localized vertigo in the acute care setting

We define nonlocalized dizziness vertigo as the situation where there is reasonable
probability that the patient has a structural disorder of the brain or inner
ear, but there no objective evidence to substantiate this hypothesis. Diagnoses
often assigned to patients in acute care settings include: Unknown or nonspecific
(acute) vertigo, Labyrinthitis,
Post traumatic vertigo, “Vasovagal”
syncope, and Hyperventilation syndrome.
The “unknown or nonspecific” vertigo diagnosis is often appropriate in the acute
setting. For example, one might see a patient in the ER (Emergency Room) with
dizziness, note that routine ER labs (CBC, electrolytes, CT scan of head) are
normal, and find no nystagmus, ataxia or otologic disturbance. One might reasonably
in this case simply indicate that the diagnosis is unclear, coding the patient
as “Vertigo”, and either wait for the symptoms to remit spontaneously, or initiate
a more detailed evaluation.

The labyrinthitis diagnosis as
well as vestibular neuritis diagnosis is encountered mainly in emergency room
settings, Strictly speaking, the diagnosis of labyrinthitis cannot be well substantiated
in a non-localized patient as nystagmus and hearing complaints are required
for a well-substantiated diagnosis. Patients typically present with dizziness,
nausea and/or vomiting, and otherwise resemble patients with “unknown/nonspecific
vertigo”. Post traumatic vertigo is a nonlocalized vertigo that follows a significant
head injury. Localizable diagnoses encountered in this setting, roughly in order
of frequency, include benign paroxysmal
positional vertigo, labyrinthine
concussion, post-traumatic migraine,
cervical vertigo, perilymph
fistula, temporal bone fracture, and epileptic vertigo. Frequently these
specific diagnoses are not made in the acute setting.

Vasovagal syncope is a diagnosis
that is ordinarily based entirely on history, and in which there are no physical
findings at the time of examination. Postural hypotension should be ruled out.

Hyperventilation syndrome requires more discussion and can be divided into
three categories: 1) Persons with “normal” lightheadedness from hyperventilation,
2) Persons with structural ear or CNS disorders that are reactive to hyperventilation such as MS, and vestibular nerve injuries 3) Persons with panic/anxiety states
who may hyperventilate inappropriately and are abnormally reactive to hyperventilation.

In a classic study, Drachman and Hart (1972) evaluated 100 patients in a neurotology
setting. Their protocol included two minutes of hyperventilation. In persons
who had no physical findings, and became dizzy after this procedure, a diagnosis
of “hyperventilation syndrome” was assigned. Roughly 30% of their patients were
diagnosed as having hyperventilation syndrome. However, subsequent studies of
large numbers of dizzy patients (e.g. Nedzelski, 1986), have failed to report
such a large proportion of patients with hyperventilation syndrome. So, this
hyperventilation induced dizziness is a controversial diagnosis. In our opinion, there are relatively few patients
with hyperventilation syndrome. The two minute hyperventilation protocol of
Drachman and Hart is overly sensitive, and instead we advocate one minute of
hyperventilation. Hyperventilation sensitivity is nonspecific and a positive
hyperventilation test does not exclude the presence of a vestibular or CNS lesions.
Management consists of a combination of reassurance and small doses of benzodiazepines.

Summary: diagnosis of nonlocalized vertigo in the acute care situation is intrinsically
difficult and often inaccurate.

IB. NONLOCALIZED VERTIGO IN AMBULATORY (NON-ACUTE CARE) SETTINGS

Entities often assigned to patients in ambulatory settings are Unknown or nonspecific
(chronic) vertigo, Disequilibrium of the elderly, Vertebrobasilar insufficiency,
Vestibular Meniere’s disease,
and Unknown or Nonspecific Vertigo: These patients are generally those who have
had intermittent or persistent dizziness or vertigo for several weeks or more,
have a normal physical examination, and normal ENG, audiometry, and MRI. Many
of these patients may have undocumented organic vestibular lesions. At present,
we have no clinical tests that can identify lesions of the vertical semicircular
canals or otolith organs or, for that matter, exclude lesions. For example,
we encountered a case of a woman, presenting with vertigo, who had had a herpes
zoster infection of the seventh and eighth nerve on one side, a year prior to
examination. Caloric testing documented complete loss of lateral canal function
on the side of lesion. Examination demonstrated a classic BPPV type nystagmus on the side of lesion, clearly documenting that posterior canal function remained
in spite of a history and test pattern suggesting complete loss of function.

Disequilibrium of the Elderly: In elderly patients, it is unusual for
the physician to say that he does not know what is causing dizziness. Instead,
dizziness and/or ataxia without localizing signs are often designated as “disequilibrium
of the elderly”, and attributed to the ravages of age. For example, in a series
of 740 patients with dizziness, Belal and Glorig (1986) reported that 79% were
given the diagnosis of “presbyastasis,” a term synonymous with disequilibrium
of aging. According to the authors, this diagnosis was assigned to persons above
the age of 65 in whom no specific cause of dizziness was identified. In a recent
study, 116 elderly patients presenting to a highly subspecialized Neurotology
setting were examined. After a thorough assessment, about 20% of patients were
diagnosed as “Undetermined” and “vestibulopathy, undetermined”; about 10% were
diagnosed as psychophysiologic (Baloh et al, 1989).

Should dizziness in elderly
persons without a localizable lesion be attributed solely to aging? Most elderly
do show some measurable sensory or central nervous system differences from younger
people. However, a potential source of error is to attribute ataxia or dizziness
to lesions that are not causally connected. For example, there are many patients
with small infarction, minor sensory dysfunction, cataracts, etc., which by
themselves would not be enough to cause ataxia, but which, possibly in combination,
may be responsible for ataxia in the elderly. Moreover, how do we know that
an arbitrary combination of sensory, central, and motor deficits is an adequate
explanation for ataxia?

In the elderly, there is a special problem because of
our unwillingness to subject patients to extensive diagnostic evaluations. For
example, Fife and Baloh (1993) recently pointed out the high prevalence of bilateral
vestibulopathy in elderly patients who had disequilibrium or dizziness of
uncertain cause. This diagnosis usually requires rotatory chair testing, a test which
is often difficult to obtain. The approach to the management of dizziness of
nonlocalized cause in the elderly should be cautious and empirical. These patients
usually need to be followed more closely than patients in whom a clear diagnosis
is available. As in the younger population, empirical trials of medication,
psychiatric consultation, and physical therapy may be helpful.

Vertebrobasilar TIA is a diagnosis
that is often assigned to patients with nonlocalized vertigo who have multiple
vascular risk factors (Grad and Baloh, 1989). When there are clear transient
central nervous system symptoms and signs, the diagnosis can be made with confidence.
However, in most instances, this is not the case and one must retain a healthy
skepticism.

Vestibular Meniere’s is a diagnosis
mainly made by Otologists. It usually denotes episodic vertigo without otologic
symptoms, with normal audiometry and MRI. This diagnosis should not be used
to describe all vertigo of unknown cause. It should be used for patients whose
symptoms suggest endolymphatic hydrops without hearing loss.

Overview: Diagnosis of nonlocalized vertigo in the ambulatory setting is ordinarily
tentative and cautious.

II. Psychological Syndromes that can cause dizziness (Psychogenic Vertigo)

Psychogenic dizziness or vertigo consists of a sensation of motion (spinning,
rocking, tilting, levitating etc.) that can be reasonably attributed to a psychiatric
disorder (e.g. anxiety, depression, somatization disorder).

Psychogenic dizziness
is a subcategory of a larger group of patients, including roughly 15% of dizzy patients,
who have a normal examination and laboratory evaluations.

Psychogenic dizziness
is distinct from other members of the group which include dizziness accompanied
by a psychiatric condition (such as benign positional vertigo accompanied by a
reactive phobia or anxiety), and also from nonlocalized dizziness that has no
clear objective correlate (such as dizziness caused by a condition that cannot
be detected by current diagnostic technology).

According to Dietrich and Staab (2016), “functional dizziness” is the “new term” for somatoform or psychogenic dizziness. Why do we need a new term ?

Panic Syndrome

Anxiety and Panic: These are troubling diagnoses to make in dizzy patients, because there is an intrinsic ambiguity in causality — between the chicken and egg — are dizzy patients afraid of getting hurt, or are patients just so “worked up” that they are dizzy.

When someone has a dizzy spell driving down the road, and then becomes anxious when they drive down the road — is the problem the anxiety or is it it the dizziness ?

A situational pattern
(e.g. dizziness that disappears on vacation) is the major factor that helps in
making the diagnosis of anxiety causing dizziness. Other symptoms suggestive of anxiety disorder
such as a lump in the throat (globus) may also be helpful. To us, this seems to be more of a way of saying how strong the anxiety might be, rather than shedding any light on the cause of the distress.

Psychometric testing
may sometimes exclude these diagnoses, as persons without anxiety are unlikely
to have dizziness related to anxiety. However, because many patients with dizziness
are justifiably anxious, psychometric testing rarely makes any causal diagnosis. The
diagnostic criteria for panic unfortunately define a syndrome that may be impossible
to separate from episodic vertigo, accompanied by a reactive anxiety.

Patients
with panic by DSM III criteria often have abnormal vestibular tests (Jacob et
al, 1989) and patients with dizziness often meet criteria for panic (Clark et
al, 1994).

Somatization Syndrome

The criteria for somatization syndrome requires between four and six unexplained
symptoms, excluding dizziness. The problem is that otherwise unexplained nausea,
headache, or fatigue might be caused by a vestibular imbalance, and accordingly
studies reporting high incidence of somatization syndrome in dizzy patients
must be looked upon with considerable suspicion.

I could, for example, define a “syndrome” consisting of a basket of symptoms — but what would that really mean ?

As such, in dizzy patients,
somatization syndrome is usually a “wastebasket” diagnosis. Management is entirely
psychiatric.

Depression

While modest symptoms of depression are more common in dizzy patients(Ketola et al, 2007), patients
will also point out that having an undiagnosed disabling illness can be accompanied
by depression. In our experience, most depression is reactive rather than primary.
The major exception occurs when dizziness symptoms are used by depressed patients
who are attempting to make a contact with the medical system, hoping to obtain
treatment without being labeled as having a socially stigmatizing psychiatric
disorder. Of the antidepressants, tricyclics with a substantial anticholinergic
component (e.g. amitriptyline) are best chosen for those patients in whom there
is a suspicion of mixed organic/psychiatric disturbance or migraine. The SSRI
family (Prozac, Zoloft, etc.), are reasonable choices where one thinks that
depression is primary. Recall that the SSRI family often cause nausea as a side
effect and also that Prozac has an inordinately long half life. Venlafaxine is a good choice when there aspects that resemble migraine.

Malingering.

Dizziness is largely subjective and thus it can be simulated in an attempt
to obtain compensation. The literature suggests that seeking compensation is often a factor in persons with mild head trauma (Binder et al, 1996). Paniak et al (2002), noted that compensation seekers/recievers report symptom incidence and severity as approximately 1 standard deviation higher than persons who were not seeking or receiving financial compensation.

Astute clinicians, armed with sufficient tools to detect nystagmus, can nearly always detect malingering of dizziness. There are also many laboratory methods of detecting malingering of dizziness or malingering of hearing.

In our opinion, patients who have spent perhaps a few hours on the web reading about dizziness, are very arrogant to think that they can successfuly fool a clinician who has several decades of experience with dizzy patients. A discussion concerning how one can detect malingering for the bilateral loss type dizziness can be found here.

III. PSYCHOLOGICAL SYNDROMES THAT MAY BE A CONSEQUENCE OF VERTIGO

Slowed reactions and problems with “multitasking” (see brainfog page for more)

Many individuals with vestibular disorders complain of trouble thinking. Most commonly people say that they can’t “multitask”. Recent work has suggested that this difficult thinking is measurable and significant. Redfern and others recently documented that reaction times are longer in patients with unilateral vestibular loss than normal controls (2003). This effect increases when patients are attempting to balance. Normal subjects also exhibit longer reaction times when responding to postural perturbations. This appears to be due to a diversion of attention to postural demands, leaving less available for cognitive processing of other input (Redfern et al, 2002).

Sometimes stimulants are helpful. Of course, stimulants may make anxiety worse, and may be addictive too, so their use should be judicious.

Anxiety and Depression

It is well recognized that anxiety may accompany vertigo (Pollak et al, 2003).

Formal studies suggest a very high prevalance of anxiety in persons with inner ear disorders (e.g. between 25 and 50%). (Best et al, 2009). Anxiety could be a natural and logical consequence of a medical condition that
is associated with unsteadiness and loss of control of bodily functions. Persons with Menieres’ disease, for example, have reactive anxiety and depression (Savastino et al, 2007). Similarly, persons with migraine or other severe headaches are much more likely to be depressed (3X) than persons without major painful illnesses (Breslau et al, 2000). This is not very surprising.

Having
considerable anxiety provoked by a medical illness does not seem to us to be
a disease, but rather a personality style. Nevertheless, the clinician seeking
to improve the lot of his/her patients needs to be able to recognize reasonable
and appropriate anxiety and separate it from unreasonable, counterproductive
anxiety. All benzodiazepine medications (those in the “valium” family) reduce balance in otherwise normal persons. However, they may improve balance in persons with inner ear or central disturbances.

Similarly, depression is a natural reaction to loss. When depression becomes so severe that it impairs other aspects of ones life, then treatment for depression itself is reasonable. As all antidepressants impair balance to some extent, one should be cautious, and again, seek to take just the “right dose”.

Diagnoses of Exclusion — wastebasket syndromes

• PPV
• CSD
• PPPD
• Functional dizzness.

We presently have four different acronyms for “I don’t know why you are dizzy”. Generally speaking, one would not attribute symptoms of headache to a psychological cause, if one knew that there was a large brain tumor. In other words, many psychiatric disorders are explanations offered for symptoms that lack an “organic explanation”.

This situation causes ambiguity to arise between the “lack of organic diagnosis” label, or the “its all in your head”. In one case, the health care indicates that the problem is intractable. In the other, the health care provider indicates that a cause for symptoms HAS been identified, and it is in the category of mental illness.

Many of us prefer not to say that we can’t figure something out, and one method of doing this, is to make up a word to substitute for the “I can’t figure it out” diagnosis, that sounds as if it is figured out. In our opinion, PPV, CSD, and now PPPD are examples of these.

It seems unlikely that we need all of these terms.

Phobic postural vertigo (PPV)

Brandt (1991) described a symptom complex
that he termed “phobic postural vertigo” characterized by situationally triggered panic attacks, frequently including vertigo with unsteadiness. PPV differs slightly from CSD (below) in that it is triggered rather than constant. The diagnostic criteria for PPV (see below) consist of symptoms without physical signs (Holmberg et al, 2009).

Using Brandt’s words to be sure we identify what he is talking about:

• Patients complain about postural dizziness and subjective postural
  and gait unsteadiness without this being visible to an
  observer.
• Dizziness is described as a numbness with varying degrees of
  unsteadiness of posture and gait, attack-like fear of falling
  without any real falls, in part also unintentional body swaying
  of short duration.
• The attacks often occur in typical situations known to be
  external triggers of other phobic syndromes (e.g., large crowds
  of people in a store or restaurant, bridges, driving a car, empty
  rooms).
• During the course of the illness, the patient begins to generalise
  the complaints and increasingly to avoid the triggering
  stimuli. During or shortly after the attacks (frequently mentioned
  only when asked), patients report anxiety and vegetative
  disturbances; most also report attacks of vertigo without
  anxiety.
• If asked, patients frequently report that the complaints
  improve after imbibing a little alcohol and during sports.
• Frequently at the beginning, there is an organic vestibular
  illness, e.g., resolved vestibular neuritis, benign paroxysmal
  positioning vertigo or psychosocial stress
  situations .
• Patients with phobic postural vertigo often exhibit obsessive– compulsive and perfectionistic personality traits and
  during the course of the disease reactive–depressive symptoms.

Holberg et al suggested that persons with phobic postural vertigo might be more sensitive to proprioceptive disturbances than healthy subjects and also refrain from use of vision (2003). In essence then, they are suggesting that PPV might be a “somatosensory dependence” syndrome. As other authors suggest that phobic vertigo is typified by visual dependence, it seems that there is a conflict in definitions.

PPV is mainly reported in the Eastern European literature (i.e. in Germany). It is not a popular diagnosis in the USA. We suspect that in other parts of the world, the same symptoms are called something else — such as “I don’t know why you are dizzy”. We wish that an acronym that wasn’t so easily confused with BPPV had been chosen.

Chronic Subjective Dizziness (CSD) also known as PPPD (see below).

Staab and Ruckenstein (2007) outlined a new acronym for unexplained dizziness — “CSD” for Chronic Subjective Dizziness. They stated:

“Chronic subjective dizziness is a specific clinical syndrome with the cardinal feature of persistent nonspecific dizziness that cannot
be explained by active medical conditions. It is not a diagnosis
of exclusion”.

To our way of thinking, if it “cannot be explained by active medical conditions”, it is a “diagnosis of exclusion”. Active medical conditions are excluded. In other words, the the definition of this entity is problematic.

Paraphrasing their criteria, from their paper in 2007, CSD is dizziness that has these features:

• Lack of other explanation
• Persistent (>= 3 months) nonvertiginous dizziness or imbalance on most days
• Chronic (> 3 months) motion sensitivity
• Exacerbation with use of vision

These are broad criteria, nearly identical to later criteria proposed for PPPD. In other words, in our opinion, someone diagnosed with “CSD” is being told by their doctor that they don’t know why they are dizzy. It primarily differs from PPV, in that PPV is defined as being episodic and triggered.

Again, we remind the reader of what Clark pointed out (2001),

“The patient with chronic dizziness should never be labeled with psychogenic dizziness. Chronic does not mean psychogenic. Chronic means that health care has been unsuccessful” .

Here Clark is pointing out the logical difference between “lack of proof”, and “proof of lack”.

Persistent postural-perceptual dizziness (PPPD).

PPPD is the replacement acronym for CSD — chronic subjective dizziness (Thompson, Goetting, Staab and Shepard; 2015). Bittar et al (2015) defined PPPD as “dizziness that lasts for over three months with no clinical explanation for its persistence.” The full acronym is “Persistent postural perceptual dizziness”. PPPD, or “triple-P D”. According to Dietrich and Staab’s 2016 review, “Functional dizziness is the new term for somatoform or psychogenic dizziness”. PPPD, by definition, has no objective findings.

More detail about PPPD including treatment is found here.

Post-traumatic stress disorder (PTSD)

Some attacks of vertigo are so psychologically stressing that they may cause psychological
disorders (usually panic or anxiety). These are particularly common in accidental
situations — someone who became dizzy, as a consequence of an injury, may be
reluctant to ever again expose themselves to the same environment.
PTSD, like other psychiatric diagnoses, is a judgement call. There is no MRI, blood test, CT scan, electrical study that can diagnose PTSD. It is defined by a committee.

Agoraphobia and acrophobia

Agoraphobia, dread of being in or crossing open places, is usually considered a “functional” — psychogenic,
cause of dizziness. Height phobia, or acrophobia often accompanies agoraphobia.

Agoraphobia and acrophobia, however, might be a logical reactions to dizziness
rather than a cause, as agoraphobia is a reasonable adaptation to a condition
that affects balance in an unpredictable way. Open places neither have surfaces
that can be used for support nor close visual referents. Certainly, agoraphobia
may also have psychic mechanisms. This determination as well as treatment are
best made by a psychiatric professional, after you have made a reasonable
search for an organic disorder.

These disorders are generally treated by desensitization. Virtual reality is presently being explored as a treatment. (Coelho et al, 2009)

Space and Motion Discomfort (SMD)

This term has been used by the University of Pittsburgh group to describe individuals
with agoraphobia, acrophobia, and visual vertigo (Jacob et al, 2009). The term has not been adopted
by most others who work with dizzy patients, and we see no particular reason to use it instead of the root terms themselves.

Visual vertigo

Some authors claim that exacerbation of dizziness and related symptoms by stimulating
visual environments is typical of psychogenic vertigo (Staab and Ruckenstein,
2003. More can be found on this symptom under the heading of visual dependence. The difficulty of this assertion is that organic vertigo often results in sensitivity to visual environments. Another difficulty is that other authors claim the opposite, and that psychogenic vertigo is typified by increased dependence on somatosensory input (Holmberg et al, 2003).

In the author’s opinion, these patterns reflect a sensory reweighting so that vestibular inputs are downweighted and replaced by greater dependence on anything else — vision, somatosensory input, or internal estimates of bodily orientation and movement. They are not necessarily psychogenic, and in fact, usually are accompanied by an organic vestibular disturbance.

References

• Afzelius L, Henriksson NG, Wahlgren L. Vertigo and dizziness of functional
  origin. Laryngoscope 1980; 90:649 656.
• Baloh RW, Sloane PD and Honrubia V: Quantitative vestibular function testing
  in elderly patients with dizziness. Ear, Nose and Throat 1989; 68:935 939.
• Belal A, Glorig A. Disequilibrium of aging (presbyastasis). J Laryngol
  Otol 1986; 100:1037 41.
• Best, C., A. Eckhardt-Henn, et al. (2009). “Psychiatric morbidity and comorbidity in different vestibular vertigo syndromes. Results of a prospective longitudinal study over one year.” J Neurol 256(1): 58-65.
• Binder, L. M. and M. L. Rohling (1996). “Money matters: a meta-analytic review of the effects of financial incentives on recovery after closed-head injury [see comments].” American Journal of Psychiatry 153(1): 7-10.
• Bittar, R. S. and E. M. Lins (2015). “Clinical characteristics of patients with persistent postural-perceptual dizziness.” Braz J Otorhinolaryngol 81(3): 276-282.
• Brandt T. Vertigo. Its multisensory syndromes. Springer Verlag, New York,
  1991. (As this is a book, it did not undergo peer review).
• Brandt T, Dieterich M, and Strupp M. Chapter 5: Psychogenic forms of vertigo and dizziness in “Vertigo And Dizziness: Common complaints: Springer, 1995
• Breslau, N., L. R. Schultz, et al. (2000). “Headache and major depression: is the association specific to migraine?” Neurology 54(2): 308-313.
• Clark DB, Hirsch BE, Smith MG, Furman JMR, Jacob RG. Panic in otolaryngology
  patients presenting with dizziness or hearing loss. Am J Psychiatry 1994;
  151:1223 1225.
• Clark, M. R. and K. L. Swartz (2001). “A conceptual structure and methodology for the systematic approach to the evaluation and treatment of patients with chronic dizziness.” J Anxiety Disord 15(1-2): 95-106.
• Coelho, C. M., A. M. Waters, et al. (2009). “The use of virtual reality in acrophobia research and treatment.” J Anxiety Disord 23(5): 563-574.
• Dieterich, M. and J. P. Staab (2016). “Functional dizziness: from phobic postural vertigo and chronic subjective dizziness to persistent postural-perceptual dizziness.” Curr Opin Neurol.
• Drachman D, Hart CW. An approach to the dizzy patient. Neurology 1972; 22:323
  334.
• Fife TD, Baloh RW. Disequilibrium of unknown causes in older people. Ann
  Neurol 1993; 34:594 702.
• Garcia FV and others. Psychological manifestations of vertigo: a pilot prospective
  observation study in a portuguese population. ITN 9, 1, 42-47. See remarks about journal quality.
• Grad A, Baloh RW. Vertigo of vascular origin. Clinical and electronystagmographic
  features in 84 cases. Arch Neurol 1989; 46:281 284.
• Holmberg J. Phobic postural vertigo: body sway during vibratory proprioceptive stimulation. NeuroReport 14:1007-1011, 2003
• Holmberg, J., F. Tjernstrom, et al. (2009). “Reduced postural differences between phobic postural vertigo patients and healthy subjects during a postural threat.” J Neurol 256(8): 1258-1262.
• Huppert, D., M. Strupp, et al. (2005). “Phobic postural vertigo–a long-term follow-up (5 to 15 years) of 106 patients.” J Neurol 252(5): 564-569.
• Jacob RG, Lilienfeld SO, Furman JMR, Durrant JD, Turner SM. Panic disorder
  with vestibular dysfunction: further clinical observations and description
  of space and motion phobic stimuli. J Anx Dis, 3, 117 130, 1989.
• Jacob, R. G., et al. (2009). “Space and motion discomfort and abnormal balance control in patients with anxiety disorders.” J Neurol Neurosurg Psychiatry 80(1): 74-78.
• Ketola, S., M. Havia, et al. (2007). “Depressive symptoms underestimated in vertiginous patients.” Otolaryngol Head Neck Surg 137(2): 312-315.
• Kroenke K, Lucas CA, Rosenberg ML, Scherokman B, Herberts JE, Wehrle PA,
  Boggi JO. Causes of Persistent dizziness. Ann Int Med 1992; 117: 898 904.
• Kroenke K, Lucas CA, Rosenberg ML, Scherokman B. Psychiatric disorders and
  functional impairment in patients with persistent dizziness. J Gen Int Med
  1993; 8:530 535.
• Nedzelski JM, Barber HO, McIlmoyl L. Diagnoses in a dizziness unit. J Otolaryngol
  1986; 15:101 104.
• Paniak, C., S. Reynolds, et al. (2002). “A longitudinal study of the relationship between financial compensation and symptoms after treated mild traumatic brain injury.” J Clin Exp Neuropsychol 24(2): 187-193.
• Pollak L, Klein C, Rafael S, Vera K, Rabey JM. Anxiety in the first attack
  of vertigo.. Otolaryngol Head Neck Surg. 2003 Jun;128(6):829-34.
• Redfern MS and others. Attentional dynamics in postural control during perturbations in young and older adults. JAG biological sciences, 2002, 57A, 8, b298-303
• Redfern MS and others. Cognitive influences in postural control of patients with unilateral vestibular loss. Gait and Posture 2003, 1-11
• Savastino M, Marioni G, Aita M. Psychological characteristics of patients with Meniere’s disease compared with patients with vertigo, tinnitus or hearing loss. ENT journal, 148-156, 2007
• Simon NM, Pollack MH, tuby KS, Stern TA. Dizziness and Panic disorder: A review of the association between vestibular dysfunction and anxiety. Annals Clin Psych 10, 2, 75-80, 1998
• Sohsten, E., et al. (2016). “Posturographic profile of patients with persistent postural-perceptual dizziness on the sensory organization test.” J Vestib Res 26(3): 319-326. Although this journal is among the stronger ones according to SNIP score, this paper must have somehow escaped a rigorous review.
• Staab, J. P. and M. J. Ruckenstein (2003). “Which comes first? Psychogenic dizziness versus otogenic anxiety.” Laryngoscope 113(10): 1714-1718.
• Staab, J. P. and M. J. Ruckenstein (2007). “Expanding the differential diagnosis of chronic dizziness.” Arch Otolaryngol Head Neck Surg 133(2): 170-176.
• Staab, J. P. (2012). “Chronic subjective dizziness.” Continuum (Minneap Minn) 18(5 Neuro-otology): 1118-1141. (Continuum is not truly a journal – it is a collection of review articles).
• Thompson, K. J., et al. (2015). “Retrospective review and telephone follow-up to evaluate a physical therapy protocol for treating persistent postural-perceptual dizziness: A pilot study.” J Vestib Res 25(2): 97-104.

Zap Mama: My long, slow, dizzy breakup with my antidepressant

The first time I had a real sobbing, desperate, I-know-the-truth-and-it’s-terrible panic attack was when I submitted my early decision application to college, which coincidentally was at the same time my little sister was getting in a near-fatal car accident. I don’t think it was a moment of psychic connection between siblings — I think I’ve just always been obsessively scared of dying and my college application meant I was one step closer to it.

I continued to have similar panic attacks through my later teens and early 20s, and they came randomly and without warning: while watching “The Girl With the Dragon Tattoo,” in a nail salon, during sex. I was taught to self-medicate with over-the-top television consumption which meant hours spent in a ball next to my glowing laptop, watching “How I Met Your Mother” reruns. These years of an undiagnosed anxiety disorder undoubtedly instilled a powerful attachment to sitcoms as well as a powerful attachment to Neil Patrick Harris, whose voice is still a super-effective sedative.

It wasn’t until I vomited after reading Mona Simpson’s devastating eulogy for her brother, Steve Jobs, that I actually sought psychiatric help, which came in the form of one adorable little blue pill.

Even 50 mg of Zoloft is a fucking revelation. After just two weeks of serious constipation and sharp, Dali-level whack dreams, I basically forgot why I was ever scared in the first place. Zoloft took my shivering, lonely brain and swaddled it in cashmere. I was able to read books by dead authors without manically eating plain slices of bread. Soon, I could fall asleep without Netflix. Zoloft and I easily settled into a standard long-term relationship — meaning I gained 10 pounds and he stayed exactly the same.

Why, then, would I ever want to break up with the thing that had brought me actual mental health? And why hadn’t I known how hard it would be?

To be honest, I hated how I looked and thought Zoloft was to blame, and the idea of being on any medication for my whole life made me feel seriously uneasy. Also, my psychiatrist had suggested that I start the tapering process now that I had been (relatively) panic-free for three years. So I did it. And it sucked.

Long-term antidepressant use is increasingly common in the United States. According to a National Health and Nutrition Examination Survey study, of the estimated 16 million people who have used antidepressants for over 24 months, 70 percent are female. (In fact, Julie Holland’s book “Moody Bitches” outlines just how female emotions are being pharmaceutically regulated.)

“People can get started on [antidepressants] for anxiety, obesity, menopause. You see people prescribe the drugs for anything under the sun. I think they’re among the most difficult drugs to come off — harder to come off than alcohol and opiates,” said Dr. Peter Breggin, an expert in psychiatric withdrawal in an interview with Al Jazeera. “Almost anything emotionally and behaviorally destructive can happen during withdrawal because serotonin is the most widespread neurotransmitter in the brain.”

Pfizer, Zoloft’s manufacturer, recommends that Zoloft users wean off the drug through a “gradual reduction in dose rather than abrupt cessation.” So that’s what I did.

When I reduced my dose to half of what it was (50 mg to 25) I noticed a slight uptick in my evening death thoughts. They came to me in short bursts like I was remembering hazy snippets of my own past burials. I stayed on 25 mg for eight months because every time I went lower, I would have a sinking feeling that someday, I would be in a coffin and very, very lonely.

Breggin told Al Jazeera’s Rebecca White that coming off the drugs can cause a wide range of symptoms including “shocklike feelings in the head, imbalance, odd feelings in different parts of your body, depression, hopelessness, suicidal feelings and actions, disabling anxiety and persisting sexual dysfunction.”

At the end of May, I said fuck it and flat-out stopped taking the pill every night. I had basically been tapering for a year now and thought my big, strong brain could handle a small uptick of worries. I felt literally every feeling that Breggin mentioned. I got brain zaps (when it feels like your brain circuitry is sparking), I was unhinged (I cried at least 14 times writing an article about a dying dog), I was very, very cranky.

So I went back on.

Not all the way, but just enough to calm my brain storms enough to work and not actively drive my friends to hate me.

I am currently down to 12.5 mg, a ridiculously small dose that, at this point, might be just placebo (although I highly doubt it). I continue to be unsure about whether this long, stupid, painful, dizzy process is even worth it. For the past four years, I have been so happy not having to confront eternal loneliness every time I think about where I want to go on vacation — why the hell would I ever willingly go back to those days?

One blogger, who appropriately goes by the moniker “GLOOM,” describes withdrawal as “hell on earth.” But so is, for me and so many other anxious people, life off antidepressants.

Treatment of anxiety and depression-related vertigo and dizziness with SSRIs and SNRIs — Keio University

TY – JOUR

T1 – Treatment of anxiety and depression-related vertigo and dizziness with SSRIs and SNRIs

AU – Goto, Fumiyuki

AU – Araki, Yasutomo

AU – Saito, Akira

AU – Kunihiro, Takanobu

AU – Ogawa, Kaoru

PY – 2006/2

Y1 – 2006/2

N2 – Recently, vertigo or dizziness has been linked to abnormal serotonin regulation in the hippocampus. According to the DSM-VI and ICD-10, vertigo or dizziness is a common symptom of anxiety disorder, somatoform disorder, and depression. In today’s stressful society, we are now observing record increases in the number of patients with depression. Because of this increase, otolaryngologists are now encountering an increasing number of patients with depression-related dizziness or vertigo. We treated 41 patients with depression-related vertigo or dizziness with a selective serotonin reuptake inhibitor (SSRI: paroxetine or fluvoxamine) or a selective norepinephrine reuptake inhibitor (SNRI: milnacipran). We graded the effects of treatment according to three levels: outstanding, effective, or not effective. Besides dizziness, the chief complaints of patients we treated were problems with sleep, headache, heavy headedness, shoulder stiffness, and loss of motivation. Drug effectiveness or the overall recovery rate was defined as the ratio of the number of patients showing outstanding and effective improvements to the total number of patients treated with a particular drug. The overall recovery rate for patients treated with paroxetine was 82% (14/17), for patients treated with fluvoxamine it was 90% (10/11), and for patients treated with milnacipran it was 62% (8/13). Side effects were observed in 22% (9/41) of the patients. Symptoms disappeared in about 2 weeks after drug treatment began. SSRIs and SNRIs are now the drugs-of-choice for treating anxiety- or depression-related vertigo because they are associated with fewer adverse effects than traditional antidepressants. Moreover, when compared to tranquilizers, SSRIs and SNRIs tend to be less habit-forming. As an adjunct to psychological counseling, dizziness associated with psychiatric disorders can also be treated in otolaryngological outpatient clinics with relevant drugs. To effectively treat these dizzy patients, collaboration between the patients’ otolaryngologists and psychiatrists or psychological counselors is also important.

AB – Recently, vertigo or dizziness has been linked to abnormal serotonin regulation in the hippocampus. According to the DSM-VI and ICD-10, vertigo or dizziness is a common symptom of anxiety disorder, somatoform disorder, and depression. In today’s stressful society, we are now observing record increases in the number of patients with depression. Because of this increase, otolaryngologists are now encountering an increasing number of patients with depression-related dizziness or vertigo. We treated 41 patients with depression-related vertigo or dizziness with a selective serotonin reuptake inhibitor (SSRI: paroxetine or fluvoxamine) or a selective norepinephrine reuptake inhibitor (SNRI: milnacipran). We graded the effects of treatment according to three levels: outstanding, effective, or not effective. Besides dizziness, the chief complaints of patients we treated were problems with sleep, headache, heavy headedness, shoulder stiffness, and loss of motivation. Drug effectiveness or the overall recovery rate was defined as the ratio of the number of patients showing outstanding and effective improvements to the total number of patients treated with a particular drug. The overall recovery rate for patients treated with paroxetine was 82% (14/17), for patients treated with fluvoxamine it was 90% (10/11), and for patients treated with milnacipran it was 62% (8/13). Side effects were observed in 22% (9/41) of the patients. Symptoms disappeared in about 2 weeks after drug treatment began. SSRIs and SNRIs are now the drugs-of-choice for treating anxiety- or depression-related vertigo because they are associated with fewer adverse effects than traditional antidepressants. Moreover, when compared to tranquilizers, SSRIs and SNRIs tend to be less habit-forming. As an adjunct to psychological counseling, dizziness associated with psychiatric disorders can also be treated in otolaryngological outpatient clinics with relevant drugs. To effectively treat these dizzy patients, collaboration between the patients’ otolaryngologists and psychiatrists or psychological counselors is also important.

KW – Depression

KW – Dizziness

KW – SNRI

KW – SSRI

KW – Vertigo

UR – http://www.scopus.com/inward/record.url?scp=33745738922&partnerID=8YFLogxK

UR – http://www.scopus.com/inward/citedby.url?scp=33745738922&partnerID=8YFLogxK

U2 – 10.3757/jser.65.17

DO – 10.3757/jser.65.17

M3 – Article

AN – SCOPUS:33745738922

VL – 65

SP – 17

EP – 23

JO – Equilibrium Research

JF – Equilibrium Research

SN – 0385-5716

IS – 1

ER –

Zoloft Withdrawal Syndrome | Center for the treatment and rehabilitation of drug addiction and alcoholism

Zoloft – what is this drug? The active ingredient of the drug is sertraline. It belongs to the pharmacological group of antidepressants and is prescribed for patients with the following symptoms: depression, OCD, panic disorder, PTSD, social phobia. Zoloft is a powerful inhibitor of serotonin reuptake in human brain cells.

More than 1/3 of people are faced with the dangerous consequences of the abrupt cancellation of Zoloft.In narcology, this phenomenon is called withdrawal symptoms or withdrawal symptoms. The time of onset of withdrawal symptoms when consumed is directly proportional to the half-life of the drug from the body. A drug such as Zoloft is addictive with systematic irregular use, therefore there is also a Zoloft withdrawal syndrome, which usually occurs 3-5 days after the last use of the drug. The symptoms of Zoloft’s withdrawal are quite difficult to recognize, so people think the illness has returned and are starting to use the drug again.

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  to persuade
  for treatment

  ?

• We will help you with motivation for treatment. As a rule, close people find it difficult to persuade or force the addict to be treated. World experts have developed EFFECTIVE motivation schemes, using which, you can lead the addict to the decision to seek help.
  
  8 (800) 333-20-07

How to reduce the dose of Zoloft correctly?

The course of treatment with Zoloft usually lasts no more than 8 weeks (about two months).As with the use of other antidepressants, an unreasonable increase in the duration of its administration leads to negative consequences on the part of human health. However, it is not recommended to stop taking the drug even earlier than the term prescribed by the doctor, since the gradual disappearance of symptoms is not a reason to complete the course. How long can you take Zoloft?

How much can you drink Zoloft?

Many patients are wondering how much Zoloft should be drunk? Naturally, the duration of the course is strictly individual.So how long can you take Zoloft? Only the attending physician, depending on the symptoms present, will be able to tell you how much Zoloft should be taken in your case. A specialist can prescribe a medication for 6-12 months, but this happens in exceptional cases.

The risk of developing withdrawal symptoms increases in the following cases:

• abrupt withdrawal of the drug and its withdrawal from the body;
• regular visits for more than two months;
• excessive anxiety;
• combination with drugs for hypertension, allergies, as well as antipsychotic drugs.

Do you want to know about the cost of services?

8 (800) 333-20-07 – call our specialist

How to cancel and stop drinking Zoloft?

Zoloft causes a withdrawal syndrome if it is abruptly discontinued. This drug affects the processes taking place in the human brain, therefore, the medicine should be taken only with a doctor’s prescription. How to stop taking the drug and get off Zoloft? To avoid the withdrawal syndrome, the dosage of the medication according to the medical plan is reduced by 25 mg every 14 days.If after the course of treatment a stable remission is achieved, the doctor will stop taking the drug. However, the specialist will cancel the drug if the patient experiences side effects, often insomnia and headaches from Zoloft.

In which case the doctor can stop taking the medicine:

• the patient has a headache;
• there is causeless sadness, anxiety;
• feeling empty;
• nervousness, irritability;
• weakness;
• suicidal tendencies;
• Sleep and appetite disorders;
• decreased concentration of attention.

If a person has lost appetite from or have regular headaches, the doctor begins a gradual process of reducing the dosage. The therapeutic dose is reduced over several weeks, and sometimes months.

Manifestation of withdrawal syndrome after taking

Is it possible to abruptly stop taking the medication? Abrupt withdrawal of the drug threatens the occurrence of withdrawal symptoms or withdrawal symptoms. The human body, accustomed to a certain dose of the drug, will respond without a period of adaptation.Most often, a deterioration in the patient’s health is noted within 2-4 days after the last use. Depending on the individual characteristics and the state of the central nervous system, withdrawal symptoms can be different.

Symptoms and signs of withdrawal

• nervousness;
• hyperexcitability;
• irritability;
• insomnia;
• nausea, vomiting;
• headaches;
• violation of coordination of movements, balance z.

In some cases, a person will not even feel dangerous signs, and sometimes it may be necessary to call an ambulance for drug treatment of the Center for Healthy Youth.Therefore, if you feel a worsening of your condition, you should consult a doctor who will help reduce the dose and improve your overall well-being.

How long does Zoloft’s withdrawal syndrome last?

Symptoms of drug withdrawal can persist without the provision of drug treatment for a long time, for several weeks. While taking antidepressants, the activity of neurons changes, therefore, after the drug is canceled, the body needs time to rebuild and adapt to new conditions.The longer the course of treatment has been, the longer the rehabilitation period will be. Withdrawal symptoms will not disappear until the active substance of the drug is excreted from the body. If general weakness lasts for a month, it is worth contacting your doctor or specialists from the Center for Healthy Youth.

When does Zoloft start to act and help?

It is important to understand that Zoloft does not begin to act immediately, but after a certain period of time. How long does Zoloft take effect? As a rule, the first positive dynamics begins to be noticeable to the patient only after 2-3 weeks of regular use.The maximum effect is noticeable after 2-3 months of admission.

Peculiarities of cancellation

It is important when choosing antidepressants to know which drugs the patient has previously taken and which drugs he is currently taking. Before prescribing an effective agent that normalizes the work of the central nervous system, the doctor conducts a number of necessary examinations, identifies existing contraindications and prevents side effects. If Zoloft is not recommended for you, the specialist will offer you a wide range of analogues of this drug, including Cipralex, Prozac, Paxil, Tsipramil and other equally effective drugs.The drug Velaxin, Amitriptyline, etc. has a similar effect.

If you have withdrawal symptoms after taking Zoloft, seek help from the Healthy Youth Drug Treatment Center. We have been treating addictions for over 15 years.

Video about the treatment of drug addiction and alcoholism at the CZM

Zoloft withdrawal syndrome, schemes, symptoms, how long

Approximately a third of patients face the consequences of abrupt cessation of Zoloft.In medicine, this is called withdrawal syndrome. The time of onset of symptoms corresponds to the half-life of the drug from the body – on average, symptoms appear no later than 5 days later. They differ in severity and are sometimes mistaken for a relapse of the disease or somatic pathology.

How to properly reduce the dose of “Zoloft”

The course of antidepressant treatment lasts about 8 weeks. Increasing or decreasing it is unreasonable and poses a health hazard.If the patient’s state of health has improved earlier than 2 months later, this is not a reason to discontinue therapy. And therapy for 6-12 months can be recommended by a doctor only as an exceptional case and in the absence of chronic mental illness. Factors that increase the risk of Zoloft withdrawal syndrome include:

• rapid elimination of the drug from the body
• long-term use (more than 8 weeks)
• history of increased anxiety
• simultaneous administration with antipsychotic, antihypertensive and anti-allergic drugs.

“Zoloft” affects the processes of the brain, its reception should not be stopped abruptly. Usually, the dose is reduced by 25 mg every two weeks according to the schedule drawn up by the attending physician. The drug is canceled not only after a stable remission is achieved, but also with strong, long-term side effects, in the absence of positive dynamics. Signs of therapy ineffectiveness include:

• constant and unreasonable sadness
• anxiety, emptiness
• irritability
• loss of interest in work or hobbies
• loss of attention and concentration
• sleep disorders
• changes in general appetite
• weakness
• pain
• suicidal thoughts

The dose reduction process takes from several weeks to months.Its duration is influenced by the volume of the therapeutic dose, the general condition of the patient. It should be borne in mind that with a decrease in the volume of the drug, part of the compound will leave the depot. This slows down the cleansing of the drug metabolites from the body.

Withdrawal syndrome after taking “Zoloft”

Abrupt withdrawal of “Zoloft” is fraught with “breakage”, the body will not have time to adapt to new conditions. Basically, a deterioration in well-being is recorded three days after the drug is discontinued, but this is possible even if a dose is missed.It can manifest itself in different ways, depending on the state of the nervous system. Often a person feels worse during this period than at the beginning of treatment. Zoloft Withdrawal Symptoms:

• Abdominal Problems: Nausea, Vomiting, Diarrhea or Cramps
• Sleep Disorders: Insomnia or Nightmares
• Headache
• Balance Problems: Dizziness, Loss of Coordination
• Sensory and Balance Disorders: On , tingling, trembling and lack of coordination
• irritability, agitation or restlessness

For most people, these manifestations cause a little discomfort without impairing their performance.In severe cases, hospitalization is required for several days. In order to recognize drug withdrawal in time, you need to keep a dose reduction schedule in writing. If you experience severe withdrawal symptoms, your doctor will recommend reducing your intake even more slowly. Even if the doctor’s recommendations are followed, the patient may have complaints. In addition, there is a risk of recurrence of depression or disorder. Therefore, you need to inform the specialist about any changes in well-being.

Duration

Zoloft withdrawal symptoms persist for up to two weeks.The reason for their appearance is due to the fact that the activity of the neurons in the brain changes during the course of treatment. After the cessation of the effect of the active substance on the body, the nervous system takes some time to resume its functions. It is clear that the higher the dose and the longer the treatment, the slower the process of stopping the antidepressant will go. Until the blood is completely cleared of the active substance, the symptoms will not disappear. Cancellation may be accompanied by a deterioration in general well-being (lethargy, loss of strength).In order not to confuse this condition with a relapse of the disease, you need to carefully monitor the dynamics of the condition. If it progresses within 2-4 weeks, we are talking about a repeated episode of pathology. In any case, if complaints persist for more than a month, you need to inform a specialist.

Peculiarities of cancellation of “Zoloft” e

When choosing a drug for the treatment of depression and other mental disorders, the doctor should ask what drugs the patient has previously taken. Before starting the course of treatment, you should familiarize yourself with possible side reactions and contraindications for admission.If Zoloft does not suit you, the doctor may recommend replacing it with another remedy with a similar effect (Prozac, Paxil, Tsipramil, Tsipralex). You can also replace it with other antidepressants:

• selective serotonin-norepinephrine reuptake inhibitor, for example, Velaxin
• tricyclic antidepressants, for example, Amitriptyline
• MOA inhibitors (a break after treatment should be at least five weeks)

Sometimes the symptoms of physical withdrawal are so severe that the person has to resume taking the antidepressant.And after achieving remission, the drug is discontinued on an individual basis.

How to help the body in other ways

To reduce the effect of cancellation after treatment with Zoloft, you need to change your lifestyle, you can also use alternative therapy. In most cases, drug treatment is not fundamental, it is necessary to attend psychotherapy sessions, working out the reasons that provoked the changes.

Recommendations:

• Exercise regularly – small but constant physical activity promotes the production of endorphins and helps to overcome depression.At the same time, it is not necessary to visit the gym, you can choose an activity to your liking.
• Change your diet. It is a proven fact that omega-3 fatty acids help to restore mental health. They are sourced from kale, spinach, soybean oil, walnuts, and sea fish. The pharmacy sells fish oil gelatin capsules.
• Normalization of the daily routine: you need to rest for at least 8 hours. Go to bed, go to bed and get up at the same time. It is advisable not to overexcite the nervous system by watching TV or a gadget before going to bed.Avoid alcohol and caffeine at night. More walks in the fresh air – this reduces the risk of disorientation, complications of depression. According to medical research, sunlight increases serotonin levels, but don’t forget sunscreen.
• Various psychotherapy techniques (cognitive-behavioral, interpersonal, body-oriented, psychodynamic) reduce the risk of recurrence of the disease. With their help, a person learns to manage his stress, anxiety, thoughts.The method of treatment is selected based on the type of disorder, the characteristics of its course, the severity of the disease and other factors.

Conclusion

In addition to the attending physician, close people should support the patient during the treatment period. Communication is a great way to distract yourself from negative thoughts. If mood swings appear while taking an antidepressant, you should immediately inform your doctor to rule out bipolar disorder. Acupuncture and meditation can be recommended as alternative methods of treatment.It is important to recognize the withdrawal symptoms in time after taking Zoloft. Prevention of this condition is a gradual decrease in the therapeutic dose. This process is lengthy and may take several months, but it is impossible to violate the recommendations of specialists. If, after recovery, the patient is prescribed the drug in prophylactic doses, the dosage reduction should also occur in stages.

Question: How to stop taking Zoloft? – Health

Contents of the article:

ANTI-DEPRESSANT ZOLOFT.MY REVIEW

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Lerivon. Stimulaton (Zoloft).

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Cancellation of antidepressants

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ANTIDEPRESSANT ZOLOFT, sertraline, stimuloton, serlift, sertraline

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Sertraline is anti-anxiety and analgesic.

Show Description

Channel Psikhpharm TV and MD M.Yu. Drobizhev continues the story about selective serotonin reuptake inhibitors (SSRIs), which are anti-anxiety drugs. Today we are talking about sertraline. This drug has the main property – to activate serotonin neurons, which block anxiety. But sertraline also has a much weaker – “additional” property. This drug blocks sigma receptors. As a result, sertraline has an analgesic effect.This significantly expands the possibilities of the drug in the treatment of anxiety disorders, which are often accompanied by pain. Unfortunately, the same blockade of sigma receptors leads to the fact that sertraline can hinder the growth and differentiation of a neuron. Despite this, sertraline is currently the most popular SSRI in the United States. Some might think something unflattering about the intelligence of Americans. After all, sertraline is difficult to prescribe to all patients for whom the growth and differentiation of neurons is critically important: children, the elderly, patients with severe brain diseases (for example, strokes).But the fact is that in the United States there are numerous factors that to a large extent smooth out the potential adverse effects of the drug: significant expenses for education, a fairly high welfare in the elderly, and a low incidence of stroke. Unfortunately, our country cannot boast of this. However, Psychpharm TV recommends sertraline in the treatment of anxiety, taking into account its additional analgesic effect. However, it is advisable to take this drug in middle-aged patients who do not have concomitant severe brain diseases….
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Video taken from the channel: Psikhpharm TV

Nearly died from antidepressants. Withdrawal syndrome. Zoloft.

Video taken from the channel: Eva Gray

Antidepressant ZOLOFT / SERTRALINE | depression, anxiety, bulimia | Overdose and the effect of Zoloft

Show Description

Sertraline is an antidepressant, a potent specific inhibitor of serotonin reuptake in neurons.It has very little effect on the reuptake of norepinephrine and dopamine. In therapeutic doses, sertraline blocks the uptake of serotonin in human platelets. It does not have a stimulating, sedative or anticholinergic effect.
In this video you will learn:
0:33 What is sertraline?
0:43 Who is given sertraline?
1:29 Zoloft dosage ..
2:21 How does sertraline or zoloft work?
2:39 The effect of zoloft ..
3:37 Application of zoloft in the practice of a doctor….
4:25 Indications for the use of zoloft: depression, anxiety, apathy ..
5:38 Sertraline overdose ..
8:01 Combining a psychotropic substance with alcohol ..
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Vasily Shurov is a renowned psychiatrist and narcologist in Russia. For more than 13 years, Vasily Shurov has been engaged in the effective rehabilitation of drug addicts and alcoholics, carries out diagnostics and treatment of mental disorders, participates in major international symposia and conferences in the field of drug addiction and psychiatry….
The content available on this information resource is not propaganda of narcotic drugs, psychotropic substances or their precursors, plants containing narcotic drugs or psychotropic substances or their precursors, and their parts containing narcotic drugs or psychotropic substances or their precursors, new potentially dangerous psychoactive substances according to article 6.13 of the Administrative Code of the Russian Federation ..
The content was created for the prevention and treatment of chemical addiction ..
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# zoloft # sertraline # drugs # antidepressant # depression # anxiety # bulimia # psychologist # first_step # Vasiliyshurov

Video taken from the channel: Clinic of Vasily Shurov FIRST STEP

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