How does Cymbalta affect sleep patterns. What strategies can improve sleep quality while taking Cymbalta. When should you consult a doctor about Cymbalta-related sleep issues. How can you establish a healthy sleep routine while on Cymbalta.

Understanding Cymbalta: Mechanism and Uses

Cymbalta, also known by its generic name duloxetine, is a medication classified as a serotonin and norepinephrine reuptake inhibitor (SNRI). This dual-action antidepressant works by influencing the levels of two crucial neurotransmitters in the brain: serotonin and norepinephrine. These chemical messengers play vital roles in regulating mood, stress responses, and pain perception.

Healthcare providers often prescribe Cymbalta for various conditions, including:

• Major Depressive Disorder (MDD)
• Generalized Anxiety Disorder (GAD)
• Chronic pain conditions (e.g., fibromyalgia, arthritis, diabetic neuropathy)

The effectiveness of Cymbalta typically becomes noticeable within 2-8 weeks of consistent use. During this initial period, patients may experience some side effects as their body adjusts to the medication.

Cymbalta’s Impact on Sleep Patterns

While Cymbalta can be highly effective in treating its intended conditions, it may also influence sleep patterns in some individuals. Insomnia is reported as a common side effect, affecting approximately 10% or more of patients taking Cymbalta. This sleep disturbance can manifest in various ways:

• Difficulty falling asleep
• Trouble staying asleep throughout the night
• Waking up earlier than desired
• Feeling unrefreshed upon waking

It’s important to note that these sleep-related issues may be temporary and could resolve as the body adapts to the medication. However, for some individuals, sleep disturbances may persist and require further intervention.

Is Cymbalta-induced insomnia a cause for concern?

While insomnia can be frustrating, it’s essential to weigh the benefits of Cymbalta against its potential side effects. In many cases, the therapeutic benefits outweigh the sleep-related challenges. However, persistent insomnia can negatively impact overall well-being and potentially exacerbate the very conditions Cymbalta is meant to treat. If sleep issues persist or significantly impact daily functioning, it’s crucial to consult with a healthcare provider for guidance.

Strategies for Improving Sleep While Taking Cymbalta

For those experiencing sleep disturbances while taking Cymbalta, several strategies can help improve sleep quality and duration:

1. Gradual dose adjustment
2. Timing of medication
3. Sleep hygiene practices
4. Relaxation techniques
5. Environmental modifications

Gradual Dose Adjustment

Healthcare providers often start patients on a lower dose of Cymbalta and gradually increase it to the therapeutic level. This approach allows the body to adjust more slowly, potentially minimizing side effects like insomnia. If sleep issues arise during dose increases, your provider may recommend slowing the titration process or even reducing the dosage if therapeutic benefits can still be maintained.

Timing of Medication

The timing of Cymbalta intake can influence its impact on sleep. Some patients find that taking the medication in the morning helps mitigate sleep disturbances. However, others may benefit from evening dosing. It’s essential to work with your healthcare provider to determine the optimal timing for your specific situation.

Establishing a Healthy Sleep Routine

Developing and maintaining a consistent sleep routine can significantly improve sleep quality, even when taking medications like Cymbalta. Consider implementing the following practices:

• Set a consistent sleep schedule: Go to bed and wake up at the same time each day, even on weekends.
• Create a relaxing bedtime ritual: Engage in calming activities like reading, gentle stretching, or listening to soothing music before bed.
• Optimize your sleep environment: Ensure your bedroom is dark, quiet, and cool for optimal sleep conditions.
• Limit screen time: Avoid electronic devices for at least an hour before bedtime, as blue light can interfere with melatonin production.
• Mind your diet: Avoid caffeine, large meals, and alcohol close to bedtime.

How can relaxation techniques improve sleep while taking Cymbalta?

Incorporating relaxation techniques into your bedtime routine can help calm the mind and prepare the body for sleep. Some effective methods include:

• Deep breathing exercises
• Progressive muscle relaxation
• Guided imagery
• Meditation or mindfulness practices

These techniques can help reduce anxiety and racing thoughts that may contribute to insomnia, making it easier to fall asleep and stay asleep throughout the night.

Managing Cymbalta-Related Fatigue

While insomnia is a common side effect of Cymbalta, some individuals may experience the opposite effect: excessive daytime sleepiness or fatigue. This paradoxical reaction can be equally challenging to manage. If you’re experiencing daytime drowsiness while taking Cymbalta, consider the following strategies:

• Discuss dosage timing with your healthcare provider
• Engage in regular physical activity to boost energy levels
• Maintain a balanced diet and stay hydrated
• Practice good sleep hygiene to ensure quality nighttime rest
• Consider short power naps (15-20 minutes) if needed, but avoid long daytime sleep sessions

Can exercise help mitigate Cymbalta-related sleep issues?

Regular physical activity can have a positive impact on both sleep quality and overall mood. Exercise can help regulate circadian rhythms, reduce anxiety and depression symptoms, and promote better sleep. However, it’s important to time your workouts appropriately. Engaging in vigorous exercise too close to bedtime may have a stimulating effect and interfere with sleep. Aim to complete intense workouts at least 3-4 hours before your intended bedtime.

Monitoring and Addressing Cymbalta Withdrawal

It’s crucial to note that abruptly stopping Cymbalta can lead to withdrawal symptoms, including sleep disturbances. If you and your healthcare provider decide to discontinue Cymbalta, a gradual tapering process is typically recommended to minimize withdrawal effects. During this period, you may experience temporary changes in sleep patterns. Some individuals report vivid dreams or nightmares as part of the withdrawal process.

What are the signs of Cymbalta withdrawal?

Common symptoms of Cymbalta withdrawal, often referred to as discontinuation syndrome, may include:

• Sleep disturbances (insomnia or excessive sleepiness)
• Dizziness or vertigo
• Nausea or gastrointestinal upset
• Headaches
• Irritability or mood swings
• Electric shock-like sensations (often described as “brain zaps”)
• Flu-like symptoms

If you experience any of these symptoms while tapering off Cymbalta, inform your healthcare provider. They may adjust the tapering schedule or provide additional support to manage these effects.

When to Seek Professional Help

While some sleep-related side effects are common when starting or adjusting Cymbalta, certain situations warrant immediate attention from your healthcare provider:

• Severe or persistent insomnia that significantly impacts daily functioning
• Development of new or worsening symptoms of depression or anxiety
• Thoughts of self-harm or suicide
• Extreme daytime drowsiness that interferes with work, driving, or other essential activities
• Any unusual or severe side effects not previously discussed with your provider

How often should you discuss Cymbalta-related sleep issues with your healthcare provider?

It’s advisable to maintain open communication with your healthcare provider throughout your Cymbalta treatment. During the initial weeks of treatment or after any dose adjustments, consider keeping a sleep diary to track your sleep patterns and any related symptoms. Share this information with your provider during follow-up appointments, typically scheduled every few weeks at the start of treatment. As your condition stabilizes, these check-ins may become less frequent, but don’t hesitate to reach out if new concerns arise between scheduled visits.

Complementary Approaches to Improving Sleep

In addition to medication management and sleep hygiene practices, several complementary approaches may help improve sleep quality for individuals taking Cymbalta:

1. Cognitive Behavioral Therapy for Insomnia (CBT-I): This evidence-based therapeutic approach helps identify and change thoughts and behaviors that may be contributing to sleep problems.
2. Acupuncture: Some studies suggest that acupuncture may help improve sleep quality and reduce insomnia symptoms.
3. Herbal supplements: Certain herbs like valerian root, chamomile, and passionflower have been traditionally used to promote relaxation and sleep. However, always consult with your healthcare provider before combining any supplements with Cymbalta to avoid potential interactions.
4. Light therapy: Exposure to bright light during the day can help regulate circadian rhythms and improve nighttime sleep quality.
5. Yoga or tai chi: These mind-body practices combine gentle physical activity with relaxation techniques, potentially benefiting both mood and sleep.

Can melatonin supplements be used alongside Cymbalta to improve sleep?

Melatonin is a hormone naturally produced by the body that helps regulate sleep-wake cycles. Some individuals find melatonin supplements helpful for managing occasional sleep difficulties. However, it’s crucial to consult with your healthcare provider before combining melatonin with Cymbalta. While there are no known direct interactions between the two, your provider can offer personalized advice based on your specific health profile and treatment goals.

Long-Term Considerations for Sleep and Cymbalta Use

As you continue Cymbalta treatment, it’s important to regularly assess its impact on your sleep and overall well-being. Some individuals find that sleep-related side effects diminish over time, while others may need ongoing management strategies. Consider the following long-term approaches:

• Regular sleep assessments: Periodically evaluate your sleep quality and patterns, discussing any persistent issues with your healthcare provider.
• Lifestyle adjustments: Continue to refine your sleep hygiene practices and daily routines to support optimal rest.
• Stress management: Develop and maintain stress-reduction techniques to minimize anxiety’s impact on sleep.
• Ongoing communication: Keep your healthcare provider informed about any changes in your sleep patterns or overall response to Cymbalta.
• Exploring alternatives: If sleep issues persist despite interventions, discuss with your provider whether alternative treatments or medications might be more suitable for your needs.

How does long-term Cymbalta use affect sleep architecture?

Research on the long-term effects of Cymbalta on sleep architecture (the structure and pattern of sleep stages) is ongoing. Some studies suggest that SNRIs like Cymbalta may alter sleep patterns, potentially reducing rapid eye movement (REM) sleep and increasing lighter stages of sleep. However, these effects can vary significantly between individuals. Your healthcare provider can help monitor any long-term impacts on your sleep quality and adjust your treatment plan as needed.

By implementing these strategies and maintaining open communication with your healthcare provider, you can work towards achieving restful sleep while benefiting from Cymbalta’s therapeutic effects. Remember that finding the right balance may take time and patience, but with persistence and professional guidance, it’s possible to manage sleep-related side effects effectively.

How To Sleep While Taking Cymbalta: What To Know

Cymbalta is a prescription medication that can help alleviate symptoms of depression, anxiety, and chronic pain.

But it can also have side effects, most commonly nausea, fatigue, and dry mouth.

Many people starting Cymbalta also have insomnia, or difficulty sleeping.

Poor sleep can have adverse effects on your physical health, and it can also make it difficult to find joy in daily life activities, a common goal for many people seeking treatment for mental health conditions. 

In this article, I’ll describe how Cymbalta works, how it may affect your sleep, and some strategies that may help to improve your sleep while taking Cymbalta.

I’ll also tell you some signs that you should talk to your doctor.

What is Cymbalta?

Cymbalta is a type of medication called a serotonin and norepinephrine reuptake inhibitor, or SNRI.

SNRIs work by affecting chemicals in the brain known as neurotransmitters.

These neurotransmitters (serotonin and norepinephrine) can help regulate mood, stress, and even pain perception.

Because Cymbalta works by affecting two specific neurotransmitters, it can also be referred to as a dual reuptake inhibitor or dual-acting antidepressant.

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What does it treat?

Cymbalta is often prescribed to treat major depressive disorder, or MDD.

It can also be prescribed to treat:

• Generalized anxiety disorder (GAD)
• Chronic pain, including fibromyalgia, arthritis, and diabetic neuropathy

It can take between 2-8 weeks for Cymbalta to start taking effect.

Some mild side effects can occur during that period, including nausea, dizziness, fatigue, dry mouth, and insomnia.

Many of these side effects will resolve on their own, but not always.

To ensure you’re reducing the risk for side effects as much as possible, take Cymbalta exactly as directed by your provider.

Don’t take Cymbalta more or less frequently than recommended by your provider, and don’t double up on doses.

If you feel that you need to adjust your Cymbalta dose, don’t do so on your own.

Talk to your prescriber before making any changes.

Cymbalta and Insomnia

Unfortunately, insomnia is a common side effect experienced by some people who take Cymbalta.

Roughly 10% or more of patients taking Cymbalta report insomnia.

Insomnia can mean difficulty falling asleep, difficulty staying asleep, waking up earlier than desired, or waking up and still feeling tired.

There are many possible causes of insomnia, but if you’re experiencing signs for the first time after starting medication, it’s possible that you have Cymbalta-induced insomnia.

Insomnia can also be a side effect of Cymbalta withdrawal and discontinuation. 

If you’re experiencing signs of insomnia or any other bothersome side effects while taking Cymbalta, reach out to your provider for guidance and help.

How to Sleep While Taking Cymbalta

During the first few weeks on a new antidepressant like Cymbalta, it’s helpful to let your provider know if new symptoms or side effects emerge, including insomnia.

In some cases, your provider may recommend waiting to see if your insomnia resolves on its own as you continue the medication.

If not, they may recommend one of the following alternatives. 

Slowly increase dosage

When starting a new antidepressant, it’s common for your provider to start you at a lower dose and gradually increase the dosage until you reach the recommended therapeutic amount (usually 60 mg per day).

However, if you start to experience new side effects like insomnia as the dosage increases, your provider may recommend slowing the dose increase to minimize side effects and give your body time to adjust to the medication.

Reduce dosage if needed

Your provider may recommend reducing your dosage or discontinuing the medication altogether.

Higher doses of Cymbalta can exacerbate insomnia and other sleep disturbances, which is why your provider may recommend lowering the dosage if you’re still able to reap the therapeutic benefits of the medication.

Otherwise, stopping the medication may be the best option for you. 

In that case, do not stop taking Cymbalta abruptly or suddenly.

It’s crucial that you work with your provider to gradually taper off of Cymbalta to avoid experiencing withdrawal symptoms.

Establish a routine

One way to support getting adequate, quality sleep is to establish a regular sleeping routine. 

Going to bed at the same time every night (within one hour of variation) and waking up at the same time each day (also within one hour of variation) can help get your circadian rhythms into a reliable pattern.

Avoiding screens for at least an hour before bed can also help, as can sleeping in a cool room.

Relaxation techniques including deep breathing exercises, imagery, and others, can also help your mind and body relax before bed.   

Use sleep aids

Over-the-counter (OTC) sleep aids have become a popular resource in recent years for people hoping to get good, consistent sleep. 

Melatonin, when taken at typical doses of 1-5 mg nightly, is safe to use while taking Cymbalta. 

Evidence suggests that melatonin supplements can help some people to improve total sleep time, sleep quality, and sleep latency (how long it takes to fall asleep).

Melatonin may also be particularly helpful in treating chronic insomnia in people aged 55 and older. 

However, some supplements can cause adverse reactions when taken with Cymbalta and should be avoided, including St. John’s wort. 

Check with your provider or pharmacist before adding any OTC sleep aid or supplement to your routine to be sure it will not have an adverse interaction with Cymbalta.

Avoid caffeine or exercise before bed

Regular exercise can support a healthy sleeping schedule, but exercising right before bedtime may impair the quality of your sleep.

Though there’s little evidence to suggest that you need to avoid exercising in the afternoon or evening (in fact, some research suggests that afternoon workouts can yield the best performance in some athletes), make sure that the end of your workout occurs at least 60-90 minutes before bedtime.

Drinking or consuming caffeine close to bedtime can interfere with circadian melatonin rhythms and block sleep-promoting chemical receptors, making it difficult to sleep.

Though the rate at which you metabolize caffeine can vary depending on the individual, one study found that consuming caffeine even six hours before bedtime can reduce sleep time by one hour.

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When to See a Doctor

For most people, Cymbalta can be a safe and effective treatment option for depression, anxiety, or chronic pain.

But if you’re experiencing insomnia or any other bothersome side effects while taking the medication, reach out to your provider to discuss whether adjusting the dose or switching to another antidepressant may help.  

Reach out to your provider if you experience any of these rare, but serious, symptoms:

• Severe dizziness
• Hives, or a red or purple rash with blistering or peeling
• Itching or swelling, particularly of the mouth, face, or throat
• Trouble breathing
• Seizure

Additional signs that the medication may not be working appropriately can include these serious side effects:

• Panic attacks
• Worsening mood
• Feeling agitated, impulsive, aggressive, restless, or hyperactive
• Confusion
• Thoughts of suicide

If you experience any of the above symptoms, talk to your provider as soon as possible.

If you’re having a mental health emergency, call 911 or go to the nearest emergency room. You can also get free 24/7 support from a suicide and crisis expert by calling or texting 988. If you’d prefer to chat online, you can chat with a suicide and crisis expert by visiting the Lifeline Chat.

How K Health Can Help

Think you might need a prescription for Cymbalta (Duloxetine)?

K Health has clinicians standing by 24/7 to evaluate your symptoms and determine if Cymbalta is right for you.

Get started with our free assessment, which will tell you in minutes if treatment could be a good fit. If yes, we’ll connect you right to a clinician who can prescribe medication and have it shipped right to your door.

Frequently Asked Questions

Can Cymbalta make it hard to sleep?

Yes. Insomnia, or difficulty sleeping, is a common side effect when taking Cymbalta. For some people, insomnia will resolve on its own as your body adjusts to taking the medication.

Can I take a sleep aid with Cymbalta?

Melatonin can be used to help you sleep while taking Cymbalta, but some drugs should be avoided when taking the antidepressant medication, including St. John’s wort. Check with your provider or pharmacist before adding any OTC sleep aid or supplement to your routine to be sure it will not have an adverse interaction with Cymbalta.

Can you take Cymbalta at night before bed?

Though many people prefer to take Cymbalta in the morning, it can cause drowsiness in some people. If you experience drowsiness as a side effect of taking Cymbalta, talk to your provider about taking the medication in the evening.

How common is insomnia with Cymbalta?

Insomnia is very common when taking Cymbalta. Over 10% of patients taking the drug reported insomnia as a side effect.

K Health articles are all written and reviewed by MDs, PhDs, NPs, or PharmDs and are for informational purposes only. This information does not constitute and should not be relied on for professional medical advice. Always talk to your doctor about the risks and benefits of any treatment.

K Health has strict sourcing guidelines and relies on peer-reviewed studies, academic research institutions,
and medical associations. We avoid using tertiary references.

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How to Sleep While Taking Cymbalta

Sleep is essential to keep us healthy, both physically and mentally. However, many things can affect the quality of our sleep.

If you’re struggling with a mood disorder, for example, you may be experiencing a lack of sleep as a side effect. Or if you live with debilitating chronic pain, your sleep may be affected as well.

Around 21 percent of adults in the U.S. experienced a mental illness, including depression and bipolar disorder, in 2020, respectively. Additionally, in 2019, over 20 percent of American adults experienced chronic pain.

If you struggle with major depression or chronic pain, chances are you’ve been prescribed Cymbalta®.

Cymbalta is a drug primarily used to treat the aforementioned conditions, which can include depression, anxiety and certain chronic pain issues.

But Cymbalta, as with many medications, may come with some side effects — some of which can affect your sleep.

In this guide, we’ll talk about how this drug works, its common side effects and how to sleep while taking Cymbalta.

Overview of Cymbalta

One of the more common antidepressants prescribed, Cymbalta is used to treat mental health disorders like major depressive disorder and generalized anxiety disorder.

Cymbalta has also been approved by the FDA for use in helping those with fibromyalgia, nerve pain and damage from diabetes (diabetic peripheral neuropathy) and long-term musculoskeletal pain.

The brand name for duloxetine, Cymbalta is a serotonin-norepinephrine reuptake inhibitor.

Serotonin-norepinephrine reuptake inhibitors (or SNRIs) work primarily on two chemicals in your brain: serotonin and norepinephrine. Cymbalta works to prevent your brain from reabsorbing these two neurotransmitters. This then has a positive effect on your mood and helps relieve pain.

This works differently from selective serotonin reuptake inhibitors, which only prevent the reabsorption of serotonin.

Cymbalta can also help break the vicious cycle between depression and chronic pain. Chronic pain can lead to depression, which can then make the pain worse, or vice versa, according to research.

You may be prescribed an SNRI like Cymbalta if it’s the right treatment for your diagnosis and health at the time, or if selective serotonin reuptake inhibitors (SSRIs) have not worked before.

Cymbalta is sometimes used to treat depression from bipolar disorder. However, as with other SNRIs, it can cause several negative side effects. If you struggle with or have been diagnosed with bipolar disorder, talk to a healthcare professional before taking Cymbalta.

It’s possible to see improvements in energy, sleep or appetite within the first week or two of taking Cymbalta, indicating that the medication is working.

A depressed mood may take longer to see signs of improvement though, taking anywhere from six to eight weeks.

Side Effects of Cymbalta

Many medications often have side effects, and Cymbalta is no exception.

Here are some of Cymbalta’s more common side effects:

Typically, these side effects go away or improve within a week or two.

As with any medication, there is a possibility of more adverse effects. These can include liver failure, severe dizziness, abnormal bleeding, abdominal pain, seizures or serotonin syndrome. Reach out to your healthcare provider if you experience any of these rare, but serious, symptoms.

Going off Cymbalta can also cause withdrawal symptoms, so be sure to speak with your healthcare provider before you stop taking the medication.

Our complete Guide to Duloxetine Side Effects goes over all the common side effects and risks of using Cymbalta for mood disorders.

Does Cymbalta Affect Sleep?

Yes, Cymbalta does affect sleep — but in different ways. Two common side effects of Cymbalta are feeling tired and sleepy or having trouble sleeping.

How is it possible that one medication can produce opposite side effects? Well, different medications can have different side effects on different people.

In most cases, the more common side effects of Cymbalta are temporary.

Fatigue can be described as a constant feeling of tiredness or weakness and can be mental, physical or both. If you’re having trouble starting or maintaining activities, difficulty concentrating or a combination of the two, you may be experiencing fatigue as a side effect of Cymbalta.

However, a large number of people who take Cymbalta experience difficulty sleeping or insomnia. Insomnia, or trouble falling or staying asleep, has been reported in nine percent of those taking Cymbalta.

Some people also reported waking up earlier as a mild side effect.

How Does Cymbalta Affect Sleep?

Cymbalta and other serotonin-norepinephrine reuptake inhibitors work primarily to prevent your brain from reabsorbing serotonin and norepinephrine — chemicals that keep our brains active when we’re awake.

Norepinephrine and serotonin also play a part in suppressing rapid eye movement (REM) sleep, or the sleep that happens about 90 minutes after you fall asleep. This is when your brain has a mix of activity and most of your dreaming occurs.

Since Cymbalta helps keep more serotonin and norepinephrine in your system, you may feel more energized and have trouble falling asleep.

There are many reasons why you may be experiencing insomnia. But if you’re having trouble sleeping after starting medication, you may have Cymbalta-induced insomnia.

Trouble sleeping or insomnia can also be an adverse effect of Cymbalta withdrawal.

Poor sleep can also worsen depression in addition to your physical health, leading to a cycle of deteriorating emotional health and overall wellbeing.

How to Sleep While Taking Cymbalta

If your sleep has been affected while taking Cymbalta, don’t worry. We have tips and strategies to help you manage any sleep-related issues.

Pay Attention to Your Side Effects

Whenever you start a new treatment for depression or generalized anxiety disorder, it’s always good to keep track of side effects. It’s also a good idea to let your healthcare provider know if any new ones emerge.

For the first few weeks on Cymbalta, pay attention to your sleep and if you’re having trouble falling or staying asleep.

Your healthcare provider may recommend waiting to see if the side effect resolves itself on its own. If your insomnia doesn’t go away, they may try a different medication or treatment for your depression.

Increase or Reduce Dosage

When starting a new antidepressant, you’ll typically be prescribed a lower dosage and your healthcare provider may gradually increase it until reaching the recommended amount (up to 60mg a day).

You should take the same dose for at least 14 days before increasing the dosage. If you start experiencing insomnia after increasing your dosage, your provider may wait for the side effects to subside and your body to adjust before increasing the amount of medication again.

Your healthcare provider may also reduce your Cymbalta dosage or have you fully stop taking the medication if insomnia persists. A higher dosage can make insomnia worse, as found in a single patient trial. 

If your healthcare provider believes you’ll still benefit from Cymbalta for a depressive disorder or generalized anxiety disorder, they may reduce your dosage over time.

If stopping the use of Cymbalta is the best option for you, talk to your healthcare provider before you stop taking it. You’ll need to gradually taper off use so you don’t experience withdrawal effects. 

Use Sleep Aids

If you’re having insomnia since starting Cymbalta, certain sleep aids can help.

Melatonin has been shown in some research to ease falling asleep and help establish better-sleeping patterns.

Melatonin is safe to use with the typical dosage of 1mg to 5mg nightly. However, using melatonin while taking Cymbalta can increase side effects of dizziness, drowsiness, confusion and difficulty concentrating. 

You should speak with your healthcare provider if you are currently taking Cymbalta before taking melatonin as well.

Other sleep supplements and medications can have adverse effects when taken with Cymbalta. Some drugs that don’t interact well with Cymbalta include St. John’s wort, other antidepressants like monoamine oxidase inhibitors, non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen, blood thinners, some migraine medications, high blood pressure medications and more.

Make sure to let your healthcare provider know about any other medications you are taking before starting a Cymbalta prescription to treat anxiety or depression.

Change Your Cymbalta Schedule

If you notice that you’re feeling fatigued or more alert and energized after taking your Cymbalta dose, you may want to change up your dosage schedule.

Cymbalta can be taken any time of day so long as it is taken at the same time every day for the most effective results.

If you currently take Cymbalta at night but are having trouble sleeping, switch to taking it first thing in the morning. Be sure to pay attention to your energy levels and talk to your healthcare provider if you’re still struggling with insomnia.

Avoid Caffeine

While many of us turn to coffee to beat the afternoon slump, caffeine comes back with a vengeance when you’re trying to sleep.

Caffeine counteracts sleepiness by blocking the brain chemical adenosine, which signals our body to become drowsy and sleep to rebuild energy levels.

Try to eliminate that post-lunch cup of coffee or switch to a drink with lower levels of caffeine, such as green tea. You can also try some stretching or go for a quick walk around the block for an energy boost that won’t mess with your sleep.

Practice Good Sleep Hygiene

A good way to make sure you get a good night’s rest is to make sure you have good sleep hygiene.

Keep a set bedtime and wake-up time, avoid large meals too close to bedtime, limit or stop screen time at least 30 minutes before bed and take time to unwind from the day. Establishing a routine before your head hits the pillows will help you sleep better at night.

More Information on Treating Depression

Cymbalta is a common treatment option for depression, anxiety, bipolar disorder, nerve pain, fibromyalgia and more. As with many medications, there can be mild side effects or more serious adverse effects.

Having trouble sleeping or insomnia is a common side effect of Cymbalta. There are techniques though to improve your sleep.

Some effective ways to sleep while taking Cymbalta are to ensure you’re taking the correct dosage, using sleep aids and establishing good sleep hygiene to start.

These tips alone may not help your insomnia so talk to your healthcare provider about your side effects.

There isn’t a universal medication or treatment option for depression. You can seek medical advice online from our psychiatry service for an evaluation to learn about all your options and figure out which is the best fit for you.

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Hims & Hers has strict sourcing guidelines to ensure our content is accurate and current. We rely on peer-reviewed studies, academic research institutions, and medical associations. We strive to use primary sources and refrain from using tertiary references.

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9. Brain Basics: Understanding Sleep National Institute of Neurological Disorders and Stroke. (2022, April 1). National Institute of Neurological Disorders and Stroke. Retrieved from https://www.ninds.nih.gov/health-information/patient-caregiver-education/brain-basics-understanding-sleep
10. Sleep Basics: REM & NREM, Sleep Stages, Good Sleep Habits & More. (2020, December 7). Cleveland Clinic. Retrieved from https://my.clevelandclinic.org/health/articles/12148-sleep-basics
11. Label for CYMBALTA (Duloxetine Delayed-Release Capsules). (n.d.). Accessdata.fda.gov. Retrieved from https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/021427s049lbl.pdf
12. DULOXETINE (CYMBALTA). (n.d.). Johns Hopkins Medicine. Retrieved from https://www.hopkinsmedicine.org/neurology_neurosurgery/centers_clinics/peripheral_nerve/patient_info/duloxetine_2007.pdf
13. Magnuson, V., Wang, Y., & Schork, N. (2016). Normalizing sleep quality disturbed by psychiatric polypharmacy: a single patient open trial (SPOT). F1000Research, 5, 132. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5527988/
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15. Xie, Z., Chen, F., Li, W. A., Geng, X., Li, C., Meng, X., Feng, Y., Lu, W., & Yu, F. (2017, May 01). A review of sleep disorders and melatonin. Taylor & Francis. Retrieved from https://www. tandfonline.com/doi/full/10.1080/01616412.2017.1315864
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The use of duloxetine, a dual reuptake inhibitor, in the treatment of painful diabetic neuropathy | Guryeva

Diabetic neuropathy is known to be a common complication of diabetes mellitus and is registered in 30% of patients on the basis of the hospital registry, in 25% of patients during large-scale population studies [1]. The incidence is 2% per year. Symmetrical distal polyneuropathy (DSN) is the most common type of diabetic disorder, accounting for about 80% of all cases of diabetic neuropathy. The main etiological factors associated with DPN are the duration of the disease, poor glycemic control, age, smoking, and dyslipidemia [2, 3]. Pain is the most common disturbing symptom, forcing the patient to seek medical attention [4]. Not only diabetic polyneuropathy, but focal and multifocal diabetic neuropathies, such as isolated cranial nerve palsy or proximal motor neuropathy of the lower extremities, can be accompanied by pain. The incidence of painful diabetic neuropathy according to studies varies from 8 to 26% among diabetic patients, depending on the criteria for assessing pain [5]. Distal symmetric polyneuropathy is combined with autonomic disorders.

The onset of DPN is usually sudden and, in the absence of early intervention, the course is chronic and progressive. A decrease or loss of function of thin nerve fibers leads to a violation of pain perception (pain from hot touch and injection), as well as temperature perception – cold (Aδ) and heat (C-fibers). When thick (Aα and Aβ) nerve fibers are involved, nerve conduction velocity slows down and sensitivity to touch, pressure, and vibration decreases, which in severe cases can lead to sensory ataxia (ataxic gait).

Involvement of sensory fibers in the process causes “positive symptoms”, which include paresthesia, dysesthesia and pain, and may also be accompanied by “negative” symptoms – a decrease in sensitivity.

Persistent or episodic pain is usually localized in the feet, increases at night and decreases during walking. Patients describe the pain as deep aching, but also as a stabbing or burning sensation in the legs. Pain caused by stimuli that are not usually accompanied by pain—allodynia and hyperalgesia —significant pain caused by stimuli that are usually accompanied by mild pain—may also be present. The pain may at the same time be accompanied by a decrease in sensitivity. Neuropathic pain in diabetes mellitus persists for several years in a number of patients, causing both physical and emotional suffering, while in others it disappears completely or partially, despite a progressive decrease in the function of fine nerve fibers. Pain remission is associated with sudden metabolic changes, short duration of pain, prior weight loss, and less severe sensory loss [6].

Chronic pain is a common condition, accompanied by a decrease in quality of life and is associated with disability, however, one third of patients do not receive any treatment, 40% of patients receive inadequate therapy, and only 2% are treated by pain specialists [7].

Although the pathogenesis of pain has not yet been sufficiently elucidated, it is clear that chronic neuropathic pain arises as a result of damage and impaired adaptation mechanisms in both the peripheral and central nervous systems.

Primary pain receptors (nociceptors) are sensory endings of nerves located in various tissues and organs. The transmission and perception of pain is a two-way process and is carried out through ascending and descending neuronal pathways. Following tissue damage, there is a massive release of inflammatory mediators – histamine, prostaglandins and bradykinin, which activate and sensitize nociceptors. Further, the pain impulse through the primary afferent neurons enters the synapses of the posterior horns of the spinal cord, where the impulse passes into second-order neurons, while substance P is released into the intersynaptic gap. Through the second-order neurons of the posterior horns, the pain impulse ascends along the anterolateral spinothalamic tract, affecting the synapses in thalamus, and then goes to the somatosensory cortex for interpretation. In turn, the brain modulates ascending impulses through descending neuronal mechanisms that exercise their control through descending spinothalamic pathways [8]. Among various modulators and neurotransmitters, serotonin (5-hydroxytryptophan, 5-HT) and norepinephrine (NA) are especially important [9]. Experimental animal studies have demonstrated the involvement of the serotonergic and noradrenergic systems in pain modulation [10]. The descending pathways are designed to suppress incoming stimuli from the gastrointestinal tract and the musculoskeletal systems. Dysfunction of these pathways is accompanied by increased sensitivity to pain and even painful responses to normal non-painful stimuli. Thus, an increase in the content of 5-HT and NA is accompanied by an endogenous analgesic effect, acting through a descending inhibitory neuronal pathway at the level of the brain and spinal cord [11].

Painful diabetic neuropathy is the result of both metabolic and microcirculatory disturbances in neurons caused by chronic hyperglycemia, which lead to pathological impulses from peripheral nociceptors recognized by the brain as pain. Over time, “central sensitization” occurs, leading to further intensification and chronicization of pain. Central sensitization leads to neuronal plasticity and changes in pain conduction, which eventually transform into states where a small painful stimulus can be recognized as very strong, or pain can persist even in the absence of any stimuli [12].

Recent studies have shown that diabetes affects all levels of the nervous system, from the peripheral nerve to the brain [13]. Magnetic resonance imaging confirmed a lesion of the type of demyelination at the level of the spinal cord already in the early stages of neuropathy, identical to the consequences observed in spinal cord injury 145]. Magnetic resonance spectroscopy studies show the presence of thalamic dysfunction in diabetic sensorimotor polyneuropathy [15]. Thus, diabetes has a much more generalized effect on the nervous system than previously thought.

Dysfunction of the noradrenergic and/or serotonergic systems of the brain and spinal cord has common psychopharmacological mechanisms involved in the development of both pain and depression. The use of antidepressants has been shown in animal experiments to cause the growth of hippocampal neurons and thus induce neurogenesis. This property of antidepressants promotes neuroplasticity, and thus helps to influence the main symptoms of depression associated with mood and motivation. Studies show that “dual action” drugs that act on both the serotonin and norepinephrine systems have the most significant effect on both depression and chronic pain [11].

Chronic pain associated with diabetic neuropathy ranks second in the structure of neuropathic pain after back pain. Treatment of pain involves the impact on the pathophysiological mechanisms of its formation. The main goal of this approach is to ensure the analgesic activity of the drug or drug combinations while reducing the number of side effects, which improves the patient’s adherence to treatment.

The management of pain associated with diabetic peripheral nervous system disease is a difficult task. The progression of DPN largely depends on the severity of diabetes and the degree to which glycemic control is maintained over time. In the treatment of pain, various non-drug methods of treatment are used (acupuncture, magnetotherapy, transcutaneous electrical nerve stimulation, massage, etc.), the effectiveness of which remains unproven [13]. Currently, drug therapy is the most effective in the treatment of neuropathic pain [14, 15]. It should immediately be emphasized that simple analgesics and non-steroidal anti-inflammatory drugs in the treatment of pain in DPN are not recommended due to their inefficiency and the high frequency of adverse events with long-term use (complications from the gastrointestinal tract, liver and blood).

The main groups of drugs for the treatment of neuropathic pain in DPN are: antidepressants, anticonvulsants, opioid analgesics (Table 1).

Currently, the possibility of pathogenetic treatment of painful neuropathy is being discussed. The results obtained in multicenter placebo-controlled studies on the use of alpha-lipoic (thioctic) acid show the possibility of short-term relief of pain symptoms accompanying mild or moderate neuropathy, which recovers 3-6 months after discontinuation of the drug [16, 17]. Long-term treatment of severe persistent pain generally requires the administration of systemic or topical pharmacological agents with analgesic activity alone or in combination.

Tricyclic antidepressants (TCAs) have long existed as first-line therapy for the treatment of painful diabetic neuropathy. Amitriptyline given in gradually increasing doses of 10 to 150 mg per day. (see Table 1), provides an analgesic effect, regardless of the antidepressant effect in 7-58% of patients, which may not occur immediately, but after 2-3 weeks from the start of treatment.

TCAs inhibit the reuptake of serotonin and norepinephrine, reduce sympathetic activity, and act on receptors in the central nervous system. The use of TCAs is limited by known intolerable side effects such as sedation, blurred vision, dry mouth, orthostatic hypertension, and cardiac arrhythmia.

Currently, there is ample evidence of the effectiveness and validity of antidepressant treatment of neuropathic pain syndrome. Tricyclic antidepressants inhibit the reuptake of 5-HT and NA, but they have additional effects on muscarinic, histamine, and a-adrenergic receptors, thereby exhibiting side effects that limit their use [18]. Selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine and citalopram, have no clear evidence of analgesic effect, although preclinical studies have shown their effect on pain [8].

Recently, interest has been shown in the so-called “dual-acting inhibitors”, which simultaneously reduce the reuptake of both serotonin and norepinephrine, which include duloxetine and milnacipram. The results obtained in numerous animal studies in experimental models of chronic pain have convincingly shown that the effect on the serotonergic and noradrenergic systems is more effective than on the serotonergic system alone. At the same time, the perception of pain is inhibited both at the level of the posterior horns of the spinal cord and at the level of supraspinal mechanisms (transmission of central pain).

A particularly effective and well-studied selective and balanced inhibitor of dual action is duloxetine (Cymbalta), the effect of which, apparently, is mediated by effects on a1-adrenergic receptors and 5-HT2 receptors [31]. The effect of duloxetine on neuropathic pain has been studied in animal models (rat models) [11]. It has been shown to be similar to paroxetine in its effect on 5-HT and to desipramine in its ability to maintain NA levels. Compared to other dual-acting inhibitors (venflaxin and milnacipran), it was superior in efficacy. This effect was dose-dependent, did not cause neurological deficit, and had a positive effect on mechanical allodynia. Thus, the potential use of duloxetine in the treatment of persistent neuropathic pain conditions in humans has been substantiated.

The effectiveness of duloxetine for the treatment of painful diabetic peripheral neuropathy has been proven in three double-blind, placebo-controlled studies [21-24]. These studies included 1139 patients with type 1 and type 2 diabetes mellitus and pain diabetic neuropathy lasting more than 6 months; all had a 12-week duloxetine fixed-dose phase.

In the first study (Goldstein et al 2005) [21], patients received 20 mg, 60 mg once and 60 mg twice daily, and placebo for 12 weeks. The second (Raskin et al. 2006) [22] and the third (Wernicke et al. 2006) studies compared doses of duloxetine 60 and 120 mg daily with placebo, also given for 12 weeks. The second and third studies had an extended open-label phase comparing duloxetine with conventional treatment. The main objective of this phase of the study was to assess the safety and satisfaction of patients with treatment, as well as assess the quality of life (EQ-5D).

The mean age of the patients included in the studies was 60 years, the duration of diabetes was 11.7 years, and the duration of neuropathy was 3.9 years (Table 2). All patients had symptoms of painful diabetic neuropathy of a typical symmetrical nature, which lasted at least 6 months. Pain intensity was ≥4 on the mean pain intensity scale over 24 hours (maximum 10). The level of glycated hemoglobin at inclusion was ≤12%, i.e. patients were mostly in a state of poor glycemic control. In order to avoid an indirect effect of duloxetine by acting on the depressive component of pain, patients with depressive symptoms, as well as other mental and somatic diseases that could affect the outcome of treatment, were excluded from the study. The study assessed the primary criteria for effectiveness – the scale of average pain intensity within 24 hours Likert; Secondary efficacy measures included Most Intensive Pain Scale and Nocturnal Pain Intensity, Brief Description of Pain (BPI), Clinical Global Impression of Severity (CGI), Patient Global Impression of Improvement (PGI-Improvement), McGill Brief Pain Inventory, dynamic allodynia, short health questionnaire (SF-36). In all three studies, patients with symptomatic episodes of depression were excluded from the study.

The result of treatment in studies was a reduction of more than 30% in the average daily pain intensity. If duloxetine at a dose of 60 mg and 120 mg per day was superior to the placebo effect, then at a dose of 20 mg it did not differ from placebo (Fig. 2 and 3). After the analysis, it turned out that the change in the results of some psychological tests may also indicate the influence of depression on the result of pain reduction. However, this indirect component of the effect of duloxetine on pain is small and amounted to no more than 20%.

The results of the studies showed that the analgesic effect of duloxetine develops quickly – after a week of treatment with both 60 mg and 120 mg duloxetine. The reduction in pain was statistically significant and remained significant throughout the 12 weeks of treatment. The magnitude of pain reduction was 65% for 60 mg, 64% for 120 mg in the first study, 63% and 69%, respectively, in the second study and significantly exceeded the placebo response rate (42%). It was found that changes in the Beck Anxiety Scale did not affect the outcome, but analysis of the Beck Depression Scale showed a moderate effect on the pain score. Thus, it was concluded that the direct effect of duloxetine on the daily average pain scale is 88.6%, and the indirect effect reaches 11.4%.

As a result of the studies, both primary: pain intensity (average, strongest and weakest), assessed on a 24-hour intensity scale, and secondary criteria were significantly different compared to placebo. Patients also noted an improvement in health status in certain domains of the SF-36 scale, as well as in quality of life (EQ-5D).

The safety and tolerability of duloxetine was assessed in three studies, as well as in three extended (52 weeks) open-label comparative studies [23, 25, 26]. The study was not completed due to side effects in 20% of patients in the placebo group, 20.9% of patients receiving 60 mg and 25.8% of patients receiving 120 mg of duloxetine. A study of the safety and tolerability of duloxetine (Cymbalty) showed a dose-related dependence of side effects of the drug, the most typical of which is at a dose of 60 mg per day. were nausea (22%), dizziness (13%), drowsiness (18%), constipation (11%) and weakness (7%) [23, 25, 26]. These side effects were observed slightly more often when taking 120 mg of duloxetine per day. However, in most patients, side effects were moderate to mild, regardless of the type of treatment.

When compared with standard therapy in open-label 52-week studies (amitriptyline, carbamazepine, gabapentin and venlaflaxine), duloxetine showed sufficient safety and tolerability. The most common (more than 10%) side effects when taking duloxetine were nausea, and with standard therapy – peripheral edema, pain in the extremities, drowsiness and dizziness [27].

During the studies, insignificant changes in the level of glycated hemoglobin and lipids were noted, but only the change in high density lipoproteins was statistically significant in all three studies [12].

The impact of duloxetine on quality of life was evaluated in an extended 52-week phase of the study. In the domains of bodily pain, physical condition and physical functions, a positive effect of the drug was noted. For other SF-36 domains, the changes were negative, but to a lesser extent compared to the changes in the standard treatment groups [12]. On a quality-of-life scale, duloxetine significantly outperformed standard treatment.

Duloxetine is metabolized in the liver under the influence of the cytochrome P450 enzyme with the appearance of two active metabolites, its half-life is 12 hours [28]. Excretion of the drug occurs mainly through the kidneys (70%). The use of duloxetine in patients with renal insufficiency requires caution. After taking 60 mg of simbalta, the maximum plasma concentration of the drug and the distribution of the drug are approximately 2 times higher in patients with end-stage renal disease on hemodialysis than in patients with normal renal function. However, the elimination half-life is the same in both groups. Population pharmacokinetic analysis has shown that in mild to moderate renal insufficiency (creatinine clearance 30-80 ml/min. ), there is no significant effect on the pharmacokinetics of duloxetine. Cymbalta is not recommended for patients with end-stage renal disease and creatinine clearance less than 30 ml/min.

The effectiveness of duloxetine, as well as the incidence of side effects in the treatment of diabetic neuropathy, does not differ significantly with increasing age of patients. However, when prescribing the drug to elderly patients, caution is required when increasing the dose of the drug [11]. During pregnancy, especially in the third trimester, it is desirable to reduce the dose as much as possible [29].

With a sharp withdrawal of the drug, phenomena such as dizziness, nausea, headache, paresthesia may occur. The frequency of these symptoms is small and is about 2%, and therefore it is recommended to gradually reduce the dose of the drug.

Thus, neuropathic pain in diabetes mellitus is complex and, unlike nociceptive pain, is caused by disorders in both the peripheral and central nervous systems. More and more data are accumulating, indicating a whole range of disorders, including changes in the structure and function of the spinal cord, thalamic neuronal dysfunction, and a decrease in the inhibitory effect of descending neuronal pathways. Progress in the study of the pathogenesis of neuropathy opens up new ways to search for drugs that have a direct effect on the pathophysiological mechanisms of pain. The use of duloxetine (Cymbalty), a balanced selective double serotonin and norepinephrine reuptake inhibitor, in patients with diabetes mellitus occupies an important place in the complex treatment of painful diabetic neuropathy.

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How to understand that the doctor needs to be changed? – Empathy

Everyone can get into a situation that he cannot cope with on his own and will require the help of a mental health specialist. It is assumed that each doctor in his work is guided by modern data on drugs and clinical recommendations. Unfortunately, this does not always happen, so further we will discuss appointments that should alert and make you think about changing a doctor.

Let’s start with the general points. How does the doctor determine where to begin treatment? Prescribes any antipsychotic or antidepressant you like? Of course not. For the treatment of each mental disorder, there are first-line drugs, second-line drugs, and so on. Such a hierarchy was created for a reason. It is based on the proven effectiveness of drugs, the profile of effects on certain symptoms, as well as their tolerability and safety.

1. Typical antipsychotics

Haloperidol, chlorpromazine, triftazine, etc. are NOT first-choice drugs for the treatment of psychotic disorders in the outpatient setting. There is an opinion that they are more powerful and have a better effect on productive symptoms (hallucinations, delirium), but this is not so. This impression is created due to the fact that typical antipsychotics begin to work faster than atypical ones. But in the long run, their effectiveness is the same. Typical antipsychotics very often cause “neurolepsy” – movement disorders in the form of muscle stiffness, trembling of the limbs, slowness of movement, smoothness of facial reactions, or, conversely, restlessness and excessive anxiety. They are also able to increase the emotional-volitional decline and cognitive impairment in a person with schizophrenia, which is interpreted by some doctors as “negative symptoms” and “increased defect”, and the person does not receive proper treatment. In addition, for fear of such side effects, the patient may simply not take the drugs, which will cause the return of psychotic symptoms.

First line of choice – atypical antipsychotics

Olanzapine, quetiapine, ziprasidone, cariprazine, etc. Since, in addition to dopamine, they have an affinity for serotonin receptors, they affect depressive symptoms, and the risk of developing “neurolepsy” when they are used is low. Atypical antipsychotics have a significant disadvantage – the risk of developing metabolic syndrome, especially in people with a predisposition (obesity, diabetes, cardiovascular disease). But now the choice of modern antipsychotics is wide, so it is possible to choose the optimal tolerability.

2. Tricyclic antidepressants

Another class of drugs that is NOT prescribed first-line for the treatment of affective, anxiety and other mental disorders is tricyclic antidepressants (TCAs): amitriptyline, clomipramine, imipramine, etc. Primarily because of their poor tolerability and insecurity.

What are the side effects of TCAs?

1. – cardiological: orthostatic hypotension (a sharp drop in blood pressure and dizziness when getting out of bed), tachycardia, life-threatening arrhythmias;
2. – anticholinergic: dry mouth, constipation, urinary retention, blurred vision;
3. – in the elderly, it can cause confusion and aggravate cognitive impairment;
4. – drowsiness;
5. – weight gain;
6. – the risk of developing seizures.

The danger of outpatient use of TCAs by patients with depression and suicidal thoughts is that there is a high probability of death in case of overdose.

First line of choice – SSRI or SNRI

SSRI: Sertraline, escitalopram, fluoxetine, fluvoxamine, paroxetine or SNRI: venlafaxine, duloxetine, milnacipran. SNRIs are comparable to TCAs in terms of potency, i.e. they treat even severe depressive episodes, especially those accompanied by pain. Since these antidepressants selectively block the uptake of serotonin and noradrenaline and have little to no effect on other receptors, the number and severity of side effects are much less. The most frequent – gastrointestinal (nausea, diarrhea, intestinal cramps) – pass in the first weeks. At the initial stages, anxiety may increase – this is corrected by the appointment of anti-anxiety drugs in a short course. And another possible side effect is sexual dysfunction, which can also be corrected.

Unfortunately, even with an adequate selection of dosage, duration of therapy and the use of a combination of several drugs, persistent depressive symptoms may persist. In such cases, it is necessary to prescribe TCAs, but with caution and a slow increase in doses.

3. Thioridazine (Sonapax)

Thioridazine belongs to the group of typical antipsychotics. The main danger of its use lies in the toxic effect on the heart: prolongation of the QT interval, which leads to the development of severe arrhythmia and the risk of sudden cardiac death. Because of this, Novartis, which produced the original drug, discontinued it back in 2005, and now only analogues of this drug are on sale. Thioridazine continues to be used in several countries, incl. Russia.

Unfortunately, it is very often thoughtlessly prescribed by some physicians as a “behavior corrector” for adults with personality disorders, older adults with dementia, and children and adolescents with intellectual disability and autism spectrum disorders. In this case, a sedative effect develops – the child becomes drowsy, obedient and does not bother anyone, which suits the parents and the doctor quite well, but this does not help the child himself and does not improve his condition, does not have a positive effect on the underlying disorder and can even harm.

The appointment of thioridazine in the elderly, in addition to cardiac disorders, is dangerous by lowering blood pressure, dizziness, falls and fractures, in addition, the drug aggravates cognitive impairment and can cause confusion.

For the relief of psychosis, high doses of thioridazine are required, in which the already high probability of life-threatening arrhythmias increases, plus the development of drug-induced hepatitis and retinitis pigmentosa (damage to the retina and visual impairment up to blindness) is possible. Is it worth the risk with a huge selection of modern drugs?

4. Nootropics

Nootropics are quite popular among doctors in Russia and the CIS countries. They are prescribed for children with mental retardation, ASD, elderly people with dementia and after a stroke, with neurological diseases, and are also recommended to improve memory and attention for schoolchildren and students.

And do they really work? As much as we would like to, but faith in the power of nootropics alone is not enough. The effectiveness of these drugs in randomized controlled trials has not been proven.

Piracetam is the first and most common nootropic. Presumably, it increases the resistance of brain neurons to hypoxia and toxic effects, but the specific mechanism of action and points of application are unclear. According to studies, piracetam does not differ from placebo in its effect on cognitive function in people with dementia and pre-dementia disorders. In addition, it can have an activating effect on the nervous system, which can lead to agitation, anxiety, confusion, especially in older people with dementia.

Vinpocetine (Cavinton) is positioned as a drug “improving cerebral circulation” and is prescribed for vascular diseases of the brain. However, there is no reliable data on its positive effect in stroke and dementia.

In most countries of the world, piracetam, vinpocetine and other nootropics are registered only as biologically active additives (BAA) and are not considered drugs.

Only two groups of drugs have proven efficacy in the symptomatic treatment of dementia

It is worth remembering that many factors are involved in the pathogenesis of neurocognitive disorders, so it is rather difficult to create a drug that would have many points of application and influence all these factors. There are only two groups of drugs with proven efficacy for the symptomatic treatment of dementia – acetylcholinesterase inhibitors (donepezil, rivastigmine, galantamine) and a glutamate receptor antagonist (memantine).

5. Alimemazine (Teraligen)

Alimemazine does not have a sufficient evidence base and is not found in any foreign clinical guidelines for the treatment of mental disorders. In some European countries, it is used as an antiallergic agent and in preparation for surgery. Approved in the USA by the FDA (Food and Drug Administration) for veterinary use only(!) for the treatment of itching and coughing in animals.

In Russia, teraligen is positioned as a “small antipsychotic”, although its antipsychotic activity is extremely low. Some neurologists and psychiatrists like to prescribe it for sleep disorders, anxiety, panic, depressive, obsessive-compulsive, somatophoric disorders and non-existent “vegetative-vascular dystonia”, and for everyone – from small to large. Often it is prescribed in combination with non-working nootropics and phenibut.

Side effects of teraligen are similar to those of tricyclic antidepressants:

1. – orthostatic hypotension (especially dangerous in the elderly, because falls and fractures are possible), tachycardia;
2. – excessive sleepiness;
3. – confusion, deterioration of cognitive functions in the elderly;
4. – urinary retention, constipation;
5. – increased appetite and weight gain.

Teraligen has a pronounced sedative (calming) effect. But this is not enough, because it is important to influence the pathogenesis, and, if possible, the factors that aggravate the course of the disease, and not simply try to “put down” the patient

Treatment of anxiety disorders

In the treatment of anxiety disorders, complex treatment is prescribed, namely psychotherapy and medications: antidepressants from the SSRI groups (sertraline, escitalopram, fluoxetine, fluvoxamine, paroxetine), SNRIs (venlafaxine, duloxetine, milnacipran), pregabalin, and to compensate for the possible increase in anxiety at the beginning of the intake antidepressants add benzodiazepines (clonazepam, phenazepam, alprazolam) or non-benzodiazepine anxiolytics (etifoxine, hydroxyzine)

6.

Azafen and Pyrazidol

In conclusion, let’s consider two antidepressants of the original Russian production – pipofezin (Azafen) and pirlindol (Pyrazidol). There is not much information about these drugs in reliable sources, they are practically unknown abroad and are used only in Russia and the CIS countries.

Azafen is described by some authors as a “small” tricyclic antidepressant, without anticholinergic side effects (difficulty urinating, constipation, dry mouth, blurred vision) and does not cause orthostatic hypotension, i.e. with good tolerance. It has a sedative and anti-anxiety effect. But there are doubts about how effective it is as an antidepressant. Evidence for this is not enough – there are only uncontrolled studies with a very small sample of patients (up to 50 people).

Pyrazidol is a reversible monoamine oxidase inhibitor (MAOI). In Russian sources, it is positioned as an antidepressant with a regulatory effect (depending on the type of depression, it has either a sedative or an activating effect) and even indicates that it has a positive effect on cognitive functions.