The printed version of our new paper “Development and persistence of patient-reported visual problems associated with serotonin reuptake inhibiting antidepressants” has just been published.
We couldn’t afford open access, so it would normally only be available to purchase or for subscribers of the journal. However, we’ve paid a fee of $200 USD which allows us to post the full paper on the RxISK website at the above link. We hope it will be of interest to ophthalmologists and neuro-ophthalmologists as well as any healthcare professionals who are involved with the use of antidepressants.
For years the standard story about vision problems on antidepressants was that they stemmed from the anti-cholinergic effects that were present in older tricyclic antidepressants. Anticholinergic effects got blamed for all the problems of antidepressants such as urinary retention, dry mouth, memory issues, and vision problems. These ideas are wrong.
In addition to the main study, the paper also includes a brief analysis of vision and eye related adverse events from Study 329, a randomized controlled trial involving paroxetine and imipramine. Although imipramine is classed as a tricyclic antidepressant, it’s also a potent serotonin reuptake inhibitor.
Despite a wealth of published literature about vision problems linked to serotonin reuptake inhibiting antidepressants, and despite warnings in the product labels, many doctors still don’t believe that these drugs cause vision problems – because they are free of anticholinergic effects. The data from Study 329 in young, otherwise healthy children on very few other drugs, provides additional evidence that SSRIs can impair vision.
RxISK has been interested in vision problems linked to antidepressants for several years, and we have wanted to investigate and raise the profile of these issues. There has been no shortage of reports to us about changes in vision linked to antidepressants, but unless these effects were particularly serious in their own right, they were often listed alongside other side effects. This made it impossible to investigate the vision problem in isolation, and it therefore took a long time to get enough suitable reports for a study.
Several different vision disorders were reported in the study, such as palinopsia in the image here, but there were a couple that were particularly noteworthy and are mentioned below.
Night blindness, also known as nyctalopia, means having difficulty seeing properly in low light. It was the second most reported side effect in our study. This finding is very interesting as there is almost nothing about night blindness linked to SSRIs and SNRIs in the published literature, and there are no specific warnings for this in most of the drug labels.
Visual snow is when you see flickering dots or static, like the “snow” that used to appear on old analogue televisions when they weren’t tuned into a TV channel. It can be accompanied by other visual and non-visual symptoms thereby resulting in a visual snow syndrome.
There has been increasing interest in visual snow syndrome in recent years. The Visual Snow Initiative website contains a lot of information including videos, patient stories, and a list of healthcare professionals who are familiar with the condition. At the moment, there doesn’t seem to be much that can be done for visual snow sufferers. The focus is predominantly on better understanding the condition and raising awareness.
We became aware of possible links between SSRIs and visual snow several years ago, and we tried to connect with the visual snow community to see if there might be an opportunity for collaboration. However, it became apparent that visual snow isn’t exclusively linked to antidepressants. Many visual snow sufferers have never used them and don’t attribute the onset of their condition to the use of a medication.
When we started writing up our study, there didn’t appear to be anything in the medical literature linking visual snow syndrome to serotonin reuptake inhibiting antidepressants. During the course of writing it, a case report from Eren et al was published: “Visual snow syndrome after start of citalopram—novel insights into underlying pathophysiology”.
The Eren paper together with the data from our study suggest that serotonin reuptake inhibiting antidepressants may be a cause of visual snow in some patients.
There is currently no data on whether vision is affected from pre-natal exposure to antidepressants. If you’ve had visual snow since birth, it might be worth checking whether you could have been exposed to a serotonin reuptake inhibiting medication during pregnancy. This doesn’t necessarily mean an antidepressant – lots of medications have serotonin reuptake inhibiting properties including some antihistamines and tetracycline antibiotics like doxycycline.
Patients who complain of vision problems linked to medications are typically sent for a standard eye examination which may include assessment of visual acuity and eye pressure. When these come back normal, no further action is usually taken.
However, there can be problems with the functioning of the eye that can’t be seen on standard tests. There are a whole range of eletrophysiological tests that can be carried out to assess this – the electroretinogram (ERG), electrooculogram (EOG) and visual evoked potentials (VEPs). Many patients and doctors may not be aware of these.
In a blog post from 2012, we reported a case of vision problems linked to the previous use of an SSRI which showed an unusual abnormality on an ERG, and we wanted to know if other antidepressant users or former users had the same abnormality. See Keeping an Eye on the Ball: Visual Problems on SSRIs.
We hoped that other people with similar issues would arrange the same testing. We also reached out to several people who had reported vision issues via RxISK Reports to ask if they would be willing to speak to their doctor about arranging an ERG. Unfortunately, there was little interest.
In some ways, this is understandable. This type of specialized testing isn’t available at every hospital, and it can sometimes be difficult to persuade doctors to arrange it. However, if the same abnormality could be found in even just a few patients, this could be a game changer not only for vision problems but also for post-antidepressant problems more generally.
An ERG assesses the electrical function of the eye in response to light, so if a patient’s only symptom is blurred vision which is corrected with glasses or contact lenses, it seems unlikely that anything would show up. This test may be more appropriate if there are symptoms that could be linked to the functioning of the retina, even if a retinal photo and all other testing is completely normal.
If you are considering having an ERG, you might want to take note of the ophthalmologist’s comment from the other blog post:
“Retinal electrophysiology is not universally available. Where it is done, not all centres comply with international ISCEV (International Society for Clinical Electrophysiology of Vision) testing standards. This can make results difficult to compare between centres.
A minimum examination should involve an ISCEV standard electroretinogram (ERG) to test generalised rod, cone and inner retinal function, along with pattern or multifocal ERG to test macular function.”
It might be worth speaking to your doctor to check whether your test will meet the appropriate standard.
It was clear from the reports in our study that some of the vision problems that patients had developed were life-changing. It isn’t known how many patients develop changes to their vision from using SSRIs and related antidepressants, or how many are left with persistent problems after stopping. Most of the published literature focuses on specific eye conditions such as cataracts or glaucoma rather than looking at the full range of vision problems that patients experience.
Learning how antidepressants cause these problems might help to explain other adverse effects. For example, the comparison between vision problems and post-SSRI sexual dysfunction (PSSD) is particularly interesting given that both genital anesthesia and vision problems involve sensory impairment. When we also take into account that PSSD patients can have reductions in smell, taste and skin sensation across various parts of the body, this creates an intriguing picture of sensory dysregulation, although it remains unknown whether there is a common mechanism.
We are indebted to all the people who reported to RxISK their visual problems on or after taking antidepressants. Reports have continued to flood in after this paper was submitted with fascinating further details.
Do you have a similar problem to any of those reported in the study, or do you have another type of vision problem that wasn’t mentioned? Please let us know.
We are also interested to hear about your experiences of trying to report antidepressant-related vision problems to a doctor or other healthcare professional. Leave a comment below and tell us what happened.
You can download the article and take to your doctor.
You can continue to report your vision problems to us by completing a RxISK Report, even if you aren’t interested in the causality score or taking the report to your doctor.
I had vertical diplopia and other vision issues confirmed as being the result of taking SSRIs/SNRIs some years ago. The woman who diagnosed it put me through extensive testing – two hours – and was a Birmingham-trained ophthologist based in New Zealand. My visual issues also include issues with night vision – particularly when driving, as oncoming headlights “splinter” into hundreds of coloured rays, rather like we used to draw the sun when children. Consequently, I wear amber-coloured sunglasses when driving at night. The vertical diplopia began when my dose of Effexor-XR was raised and has not resolved 10 years later. However, visual problems overall developed within weeks of beginning SSRI therapy, as did dystonia. Unfortunately, the post-marketing data that would have rung alarm bells wasn’t available. The dystonia also persists to this day. I’d be interested to know whether others have experienced issues with muscles less talked about, including those in the rectal area.
After taking escitalopram I developed some weird sensations behind my eyes. It feels like my muscles are cramping or some sort of spasms, sadly it didnt go away after quitting the ssri. I cant find much information about this.
Also eye pain, sensitivity to light, feeling of high pressure, snow/grain vision, small pupils, motion illness and blurry vision.
You can’t find much information because there is very little or almost none – other than here
OMG, I have been searching for this information, i take palexia(tapentadol)18months, duloxetine 10 years and quetiapine12 years. I get severe headaches after 4 pm EVERY day that is medication/analgesic resistant for the past 6 months that i believe are getting worse and my vision within 18 months has become very very bad, I was told it’s unlikely but I’ve always had great hearing and vision my whole life. For the last 6 months, I keep researching and the closest thing I’ve come to is possibly serotonin syndrome and this article helps in that understanding. Thank you, I really wish more doctors read these forums to understand what patients are going through especially long-term effects, however, I’m now worried my eyesight may not come back. 🙁
Lot of the similar affects after using escitalopram for 9 years. Shadow images, blurry vision, lesser vision quality at night. Did not go away after quitting for 3 months. Rapidly reducing distance vision and early onset of near vision problems.
I also have vision issues after being on Cymbalta for about 18 years. I have problems with night vision, it is so bad my licence has been restricted so I am not allowed to drive after sunset. I asked my GP about it and she said it could not be related to my medications. I now believe different.
I read in your comment you refer to developing Dystonia. I was shocked when I read that. I am 52yo and developed Cervical Dystonia a few years ago. I asked my Neurologist if it could be linked to being on Cymbalta for so long and he said it isn’t known to cause Dystonia. Nobody knows what caused my Dystonia and so far no treatments have helped. I have now lost most of my mobility as a result. I can’t help but feel my Dystonia is directly related to Cymbalta. Have you read anywhere else of a link to Dystonia? I am really desperate for some info/help. I am about to start a slow taper off my Cymbalta.
I’ll posit this as a hypothesis in gestation to see if anyone thinks it has merit or gives anyone ideas that they can develop further:
Fluvoxamine (and I assume all other SSRI’s) is an agonist for the sigma-1 receptors (S1R), through which it controls inflammation. For this reason (plus its antiviral property) it is been found of help in the treatment of Covid-19. 
S1R’s are in most cells including white blood cells. Fluvoxamine via the S1R’s can suppress or regulate the intracellular voltage-gated sodium channel, NaV1.5. The over abundance of NaV1.5 has been implemented in MS. , [2a]
Quote: “Our results demonstrate that Nav1.5 is expressed within macrophages in active MS lesions”
So could the sudden withdrawal from SSRI result in myelin inflammation which becomes a vicious circle from chemical signals released by the inflamed cells and the white blood cells drawn there to fight a mirage? MRI and PET investigations to rule out Cauda Equina Syndrome would not – I think – detect such inflammation.
[Some three years ago a new PET technique was trialed that could image inflammation from the radio-labeled metabolites of inflammation. So this may be a possible diagnostic route available in the future.]
The CoV-2 spike protein therefore appears to also cause inflammation of the myelin sheath.
Drugs like haloperidol and DMT (the love drug) are ligands to S1R’s and a difference in Covid-19 severity was found between patents taking typical and atypical antipsychotics but with P values of 0.03 and 0.06 I didn’t bother to read the whole article. Still, it adds weight I think to the S1R / Nav1.5 involvement. The common occurrence of Bell’s palsy in Covid -19 may be because the 5th cranial nerve has such a small hole in the skull to pass through that even slight inflammation can squeeze the nerve. On a larger scale it may present as transverse myelitis of the spinal cord. So could PSSD be a form of transverse myelitis down in the Sacral 2-4 region? S2 being the rectal area, S3 the bladder and S4 the reproductive organs.
I think that visual disturbances, heightened sense of smell and hearing with skin sensations (such as formication) mentioned by Redit contributors indicates encephalomyelitis. It sounds so similar to me of ME symptoms caused by inflammation of the brain. [I always always ask the presumptive question on meeting someone else with Me for the first time – “So how many weeks after your first flu shot did you get ME?” Easy to dismiss as a coincidence but these jabs seem to be to me a leading cause of such coincidences.]
S1R are also in the mitochondria (in the endoplasmic reticulum) which may be the cause of the exhaustion experienced with viral infections in general, Long Covid, Vaccine Long Covid and ME/CFS. In the later three, the inflammation maybe caught up in this vicious circle of signalling chemicals and autoimmunity. One research team has found that higher levels of IL2 before Covid-19 and Covid mRNA jabs were predictive of long Covid. Could Interleukin levels be used as diagnostic biochemical markers for the susceptibility of harm from SSRI’s (like PSSD), from the point of view that elevated IL2 encourages inflammation to start in the first place?
At the moment I don’t see how this can be immediately useful, other than suggest possible avenues for research. Ironically, we seem to be in a race to find cures for newly emerging cures.
A pertinent bit of trivia, is that the chemical weapon used by St Johns Wort against browsing animals is hypericin — which is a SSRI. Perhaps prescribing doctors should take that as a lesson against prolonged courses of treatment.
What follows is just a generalization to help make sense of why not everybody experiences the same things. Of course, you’ll still your doctor to objectively unpick your signs and symptoms to offer the best options for treatment or no treatment. Yet, I thought I’d mention this aspect of the immune system, for most doctors don’t seem to think of this as an explanation (and thus can’t offer a time line to their patient) as normally Ab2 antibodies don’t cause such noticeable symptoms. My bet is that it is also Ab2’s from a bad bout of influenza that leaves people feeling not quite right, for several weeks after recovery. Things that are considered not important like this, don’t get taught to medical students.
So. Those people that report a bad ‘delayed’ reaction from either Covid 19 when it is not a full blown cytotoxic storm (you know like with a fever), or the 1st or 2nd jab which fades over the next five to six months (as in the Redit post) AND for those that find their bad symptoms go after a jab. This is most likely due to a regulatory feature the immune system has, when it finds it has produced too many antibodies to the antigen. It generates anti-idiotype (or “Ab2”) antibodies. One can think of them as antibodies that attack the surplus antibodies. Normally one would not be aware of them by way of symptoms. However, to lock onto the original type of antibodies they have form a key that fits the original antibody key that the antibodies used to lock onto part of the original spike antigen. That mirror image therefore becomes the same ‘shape’ as part of the original toxic Spike. Because these tailor-made anti-idiotype antibodies are thus themselves toxic, they go onto produce the same bad symptoms the same mechanistic way. Fortunately they have short lives and are gone typically after some 5 to 6 months. A 2nd jab will also clear them by providing more spike generated antibodies for the remaining Ab2 antibodies to pair up with.
The Redit contributor wished to know if she could have sped up recovery. For that she would have to enlighten her doctor with one of the Long Covid treatment protocols such as I-RECOVER 
The consensus appears to be that Ivermectin is best at clearing both the Spike proteins and these anti-idiotype antibodies in its action as an immune modulator. Low Dose Naltrexone which is another immune modulator is also spoken highly of. The question in my mind is “if these problems are left to resolve naturally, does the probability increase for long lasting damage (such as scarring and autoimmune disorders) to manifest themselves?” Honest debates such as this, was once the roll of medical journals.
 Sukhatme Vikas P., Reiersen Angela M., Vayttaden Sharat J., Sukhatme Vidula V. (2021) Fluvoxamine: A Review of Its Mechanism of Action and Its Role in COVID-19.
Frontiers in Pharmacology. DOI 10.3389/fphar.2021.652688
 Black JA, Newcombe J, Waxman SG. Nav1.5 sodium channels in macrophages in multiple sclerosis lesions. Multiple Sclerosis Journal. 2013;19(5):532-542. doi:10.1177/1352458512460417
[2a] Carrithers, Michael D. Human Macrophage Sodium Channels: Novel Targets for Inflammatory Diseases
Wm S. Middleton Memorial Veterans Hosp, Madison, WI, United States
 William J. Murphy, Ph.D.,and Dan L. Longo, M.D. (2022) A Possible Role for Anti-idiotype Antibodies in SARS-CoV-2 Infection and Vaccination. N Engl J Med 2022; 386:394-396
 An overview of the MATH+, I-MASK+ and I-RECOVER Protocols A Guide to the Management of COVID-19 (Updated as of February 22, 2022)
Most doctors working in the field of Ophthalmology are unaware of this syndrome.
In addition, it is still rare for any visual symptoms to be attributed to SSRIs.
Most of the interest in this area has been driven by Neurologists and Neuro-ophthalmologists.
Neuro-ophthalmology is a small sub-specialty with relatively small numbers of clinicians. Often these doctors provide only a tertiary service. In other words, patients need to be referred by a general ophthalmologist. In the absence of physical signs or a specific diagnostic test it is unlikely that many patients will be referred.
By raising the profile of this syndrome among all eye specialists we can begin to comprehend the true frequency of these problems and construct studies to help understand the underlying chemistry.
This information changes things for me! I have visual snow, and some amount of after-images after moving things, also slight double vision, i had those before i was commited to a psychiatric unit 2012(?), i also have brain fog, anhedonia, castration/pssd, and sensations of strange moving structures in my neck/jaw? consisting of muscles/tension/dystonic?cramps? (hard to explain it), i have poor memory of the period, and believe it or not i have not gotten around to check my journals of the time (i trusted healthcare too much for too long, im also very tired) even though i very much, i assumed my visual problems came from my neck/jaw impairment, but now you say its ssri related, well that makes sense, i have often especially severe visual snow in the dark. I should tell you perhaps of one event, in which a large cyan blot, without any form of texture, completely uniform in color appeared, it grew and became large enough to cover my vision of a chair in front of me, at that point i started to become scared and i managed to “make” it decrease by some kind of focusing (during the period i was desperate to get rid of the sensations in my head because they cannot be turned off, they severly disturb my thinking, breathing affects it, as does moving my head and eyes,as does attempting to focus mentally, i had some psychosomatic relations at the time; with my bodily sensations and tensions in my body and resorted to breathing and meditation and stretching to (partly) improve it i was in general used to the idea of attempting to focusing hard to try to change my symptoms which was partly maladaptive i think, partly because i cannot focus in any real sense because of these symptoms )The point about mentioning the cyan blob is that it is a symptom and in some way either stress/anxiety or som other somewhat conciously controllable factor was able to change it, i only remember it happening once.
During withdrawal my eyes were affected in as much that they contributed to dizzy spells and head zaps.
You’ve seen the old cartoons where eyes stretch out of the sockets then pop back in, it was similar to this. When turning my head, it took longer for my eyes to follow my head. This was just split-second timing but, nonetheless, caused dizzy turns.
I became used to this and was able to rectify it by not turning my head so quickly.
For me it was aural problems. I still suffer to this day. Have an intolerance to sudden loud noises. Nothing rhythmic, just unexpected noises. I, before purchasing digital hearing aids, used to suffer in crowds. I could never hear the person directly in front of me talking but could hear everyone behind me. The hearing aids I have (very small) have an app where I can cancel out background noise. However, they don’t help with the sudden loud noise thing. Most people jump if they hear, for example, a glass break on the floor, for me it’s like cymbals clashing next to my head. I rarely go in coffee shops because of the way they bang coffee filters against metal – this has the same cymbal effect, only much worse.
I never had this problem prior to taking Seroxat.
The head noise thing is pretty awful.
Off cold turkey Seroxat, the head zaps were excruciating and I needed my eyes constantly shut. So it was months of lying in bed with the curtains drawn. No TV or Radio could possibly intrude.
The head zapping has never stopped.
It can abate for weeks at a time and then in the night time, a roaring crash in my head will wake me up. This will set off a high pitch frequency sound which is constantly in the background of whatever I am doing.
I had an MRI scan early on which revealed nothing out of the ordinary. I had hearing tests. I was made a thing to fit in my ear giving out white noise, to supposedly take my mind off the noise. I was offered a psychiatrist –
For raging tinnitus they advise not listening to it, not worrying about it. I don’t think this is tinnitus.
Tinnitus does not have explosions in the head. It is also not ringing in the ears. The sound is deep under my skull.
Sudden noises like chair scrapings, car doors slamming, shouting, a sudden dog bark can be extremely distressing. People don’t get it. I was recently in a car with three dogs barking, Pavarotti blaring out and the person was shouting about a book she was reading – I wanted to jump out of the car, but am far too polite. When I explained about my sounds at a later time, the reply was I must be stressed out to be so neurotic about sound. I just avoid situations like that now.
It is 20 years later. I have macular degeneration, cataracts, dry eye, glasses and contact lenses. I have just received a driving licence for three years which took six months of DVLA investigations with my optometrist. It was a long-winded affair to ascertain my opticians’ diagnosis and prescriptions that I could legally drive a car.
I can’t blame Seroxat for my eye deterioration unless the noise in my head problem is somehow related…
Roll up, Roll up, get your prescriptions here.. Only £65 a month…. for an extra £65 you can access a boot’s Therapist… The NHS surely must be collapsing…
https://www.freethink.com/health/Prozac-blindness…. An article linking Prozac as a treatment that potentially can reduce age related blindness??????
How is it taking so long to help people hooked on their prescription medicines? Thousands are addicted to drugs given to them by their doctors. But promises of support still haven’t been met
By JONATHAN GORNALL FOR THE DAILY MAIL
PUBLISHED: 23:00, 14 March 2022 | UPDATED: 09:07, 15 March 2022
The solution is slow tapering — a carefully controlled, monitored reduction in frequency and dosage of a drug,’ Luke, co-founder of the All-Party Parliamentary Group (APPG) for Prescribed Drug Dependence, told Good Health. But the advice and support needed for this is not available for the vast majority of patients trapped on drugs they no longer need or, too often, should not have been prescribed. Instead, they are abandoned by a healthcare system that is quick to prescribe medication but ill-equipped to end reliance on it.
One of PHE’s key recommendations was new guidance for doctors on how to safely prescribe and wean patients off these drugs, to be issued by the National Institute for Health and Care Excellence (NICE). The guidance is due to be published within weeks.
But campaigners, including leading mental health bodies, fear this unique opportunity to change a system that fails to support the thousands of victims of prescription-drug dependency is about to be squandered. And that as a result, many people who put their faith in the doctors who gave them these drugs will be left battling a problem effectively of the medical authorities’ own making.
‘There is no one-size-fits-all approach to safely withdrawing from medicines associated with dependence,’ Dr Chrisp said.
It’s crazy that there hasn’t been more research on antidepressants and the risk of getting visual snow from them, because there’s more than enough anecdotes to call this a fact. My friend got on Zoloft and two days later he got severe visual snow, halos, starbursts, ghosting and tinnitus, he also started seeing a ton of floaters and blue field entopic phenoma. This has completely ruined his life.
But when it’s caused by antidepressants i believe it’s classified as hallucinogen persistent perception disorder, and not visual snow syndrome, because antidepressants, like cannabis and psychedelics that can cause HPPD, act on the 5HT2-a receptors and do possess hallucinogenic properties. About 1% that gets on an antidepressant experience hallucinations.
23 March 2022 a long article criticising antidepressants in The Nation
“…But if you go by the hundreds of Facebook pages, Web forums, and subreddits
dedicated to negative experiences with antidepressants, it becomes
obvious that at least tens of thousands of people feel their lives have
been negatively affected, or in some cases ruined, by the drugs. And
those are just the ones who feel strongly enough to post about their
The field of psychiatry itself may be going through a similar
reckoning. A wave of research suggests that the drugs are less effective
and more dangerous than many previously believed. And some
medical professionals are concluding what until recently felt too
heretical to say out loud: Antidepressants may often cause more harm
Omg palinopsia is what I think I had on SSRIs. Everything looked plastic like the leaves on trees. The fine detail of the moisture and lines in a healthy tree or plant leaf were gone.
So glad there is a name for it. On mirtazapine I didn’t have the same loss of detail things looked more real but I felt everything just looked darker as if I was wearing sunglasses or something but I wasn’t.
Strange how the vision was different on SSRIs from mirtazapine. SSRIs and mirtazapine are giving different affects.
Plus on SSRIs my pupels were either constricted or dialated, dialated more so on Seroxat. Citalopram they were mainly constricted.
Mirtazapine I also had pressure problems that I dont think I had on the SSRIs.
24 March 2022, BNNVARA (from Dutch)
Health insurer CZ starts pilot project to tapering antidepressants
Health insurer CZ is starting a pilot in which the phasing out of antidepressants is reimbursed and supervised under certain conditions. 150 patients can participate every month, for a minimum of two years. Many people who are no longer depressed continue to take antidepressants because the withdrawal of the medication can cause many complaints. The Association for Tapering Medications [Vereniging Afbouwmedicatie] is critical of the conditions of the pilot.
In the Netherlands, more than a million people are prescribed an antidepressant every year. Some of the patients are unable to stop taking the medication later on because they experience withdrawal symptoms when they are tapered off. These can vary from headaches and dizziness, to sometimes severe sleep disorders and fears. These are complaints that are very similar to depression, so that people can have the idea that they are having a relapse, while it concerns side effects of the tapering. It is estimated that between 60,000 and 180,000 patients who try to quit are affected each year. Zembla made the broadcast ‘Stop with the pills’ [link] about this.
Some people therefore need very low doses of medication to be able to taper off the antidepressants in small steps, otherwise they will develop withdrawal symptoms. These patients may benefit from tapering off tablets with a slightly lower dose of the active ingredient each time. But such tablets are not readily available, because pharmaceuticals do not make them. Some pharmacies do make those tablets. A well-known reduction method is the so-called ‘tapering strip’: a strip of plastic bags containing tablets with a slightly lower dose for each day. This method is relatively expensive, because the strips are custom-made. Most health insurers do not reimburse the strips for tapering. Pills with standard doses for normal use are reimbursed.
Guidance from the pharmacy
The Zembla broadcast showed that in 2020 CZ had reimbursed tapering medication according to a personal tapering plan in only 5 cases. Now CZ states that it cannot be the case that someone who is on antidepressants cannot taper off. That is why the health insurer is starting a pilot together with the Transvaal Pharmacy. This is a pharmacy that can also prepare medication itself. For example, the pharmacy makes the antidepressant venlaxafine – a notorious drug when it comes to withdrawal symptoms – tablets of 1 and 5 milligrams. In comparison, a standard dose of venlafaxine is 37.5 mg per tablet.
The pilot follows the phase-out schedules from the so-called Multidisciplinary Document [link], CZ said. This is a document in which psychiatrists, pharmacists, general practitioners and patient organizations have made agreements about how patients should best wean off antidepressants.
In the pilot of CZ, the Transvaal Pharmacy also provides personal guidance to people who are going to phase out. The goal is to get people to stop taking their antidepressant in an average of eight to ten weeks. It is possible to extend this period by a maximum of four weeks. The supervision consists of at least three contact moments with the pharmacologist of the pharmacy. This is in addition to the contact with the attending physician. The treatment is included in the basic insurance for insured persons with CZ and is therefore free of charge after paying the deductible.
Petition for reimbursement of tapering strips
The Association for Tapering Medications, the patient association for people who want to phase out their medication, is skeptical about CZ’s plans. They point out that the period of eight to ten weeks that CZ charges for tapering will be too short for many people. The association also believes that CZ sticks too closely to the breakdown tables of the Multidisciplinary Document. Those schedules were intended as an example, and should not be set as the norm for everyone, the association explains.
On Tuesday, the Association for Tapering Medications presented a petition to the House of Representatives in which they argue for reimbursement of the reduction of antidepressants through tapering strips.
‘Insufficient scientific evidence’
When asked why CZ opted for this pilot and not for the reimbursement of tapering strips, the health insurer stated that it still saw “insufficient scientific evidence” for the tapering strips. Two studies are currently underway in the Netherlands that investigate how patients can stop taking antidepressants. It could be years before the results of these studies are known.
CZ acknowledges that the method they offer in the pilot will not work for everyone. The health insurer hopes that half of the people participating in the pilot will have actually stopped using antidepressants. CZ expects that the pilot will provide new insights, regardless of whether that result is achieved. People who are unable to reduce within these frameworks should see with their doctor what the cause is and adjust the treatment plan if necessary. If the reduction via the pilot is not successful, this does not automatically mean that tailor-made tapering medication is reimbursed, says CZ.
Hello, would MAOI antidepressants also cause the visual abnormalities described above? Thanks.
How would anyone know. We need reports from people on these drugs to have any idea if there can be a problem
MAO-As primary mechanism is to raise Serotonin levels. So yes from experience they cause similar SSRI effects in the head. Vision problems, ringing ears, emotional blunting. They seem to affect peripheral tissues less, so less sexual side effects, digestive, etc.
I have a lot of this symptoms being constantly stressed, so I wanted to use SSRI to stop them, and now I see it can provoce it. It is clear that this drugs interfere with regulations of vision process in many ways, how it happens that it helps somebody to cure migraine, to get rid of some other visual artifacts there where caused by stress? Completely confused about it. Hard to live with alll that blind spots, blinking spots, black dots with circle and so on, they are result of dysautonomia which is often threaded with ssri. And if ssri provoke it.. what the hell we should do?!
Yes, I have experienced visual snow since starting SSRIs and SNRIs 25 years ago. Also decreased night vision, decreased peripheral awareness and dizziness looking quickly from left to right. Also motion sickness. I didn’t attribute these symptoms definitely to antidepressant use until now.