anti-anxiety medication brain damage Archives

The Repercussions of Long Term Anti-Anxiety Medications

Published on April 28, 2022

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I can remember my anxiety issue starting around 1994, I was driving my then girlfriend and her brother to a concert in St. Louis, MO. I was fine on the way there but as we got closer to the event, I started to feel uneasy, palms were drenched with sweat, my heart beating out of my chest and I felt nauseous. I didn’t go to the concert with them I stayed out in my truck. Every so often I would get out and tell myself I was going in, but that never happened. I have always been the kind of person that has a way out. By that I mean, if I was driving I would have all of these different theories going through my head as to what I would do in a certain situation. The same holds true for being in public places. I would wonder where the exits are and how many are there. I never really thought too much about all this until the middle the to late 90s. I was working as a salesman for my parent’s business and my hands would constantly drip sweat. If I answered the phone the receiver would be wet. I had to wipe my hands on my slacks before shaking someone’s hand. On my honeymoon with my first wife, we were to go and watch the Blue Angels fly, but I just couldn’t force myself to go. We ended up staying at the hotel all day. My mom’s side of the family has a history of depression/anxiety she talked me into going and talking to our family doctor.

The Pill Factory

I explained everything to my doc and he asked the normal questions: have I ever thought of killing myself, was I tired or had felt fatigued throughout the day, how was my social life or did I prefer to stay home? He felt my symptoms were more of anxiety and not depression so he first prescribed Lexapro and told me to let him know if I felt it was working or not. I didn’t like Lexapro, my hands still were sweaty and I just didn’t feel “right”. So after a month or two, my prescription was changed to Prozac. The doctor thought that since my mom was taking it and was doing okay on it, that I should do as well as her. The Prozac didn’t last more than a few weeks. It made me feel “fuzzy” and tired all the time and I felt depressed, which I never felt before. They say the third time is a charm, well in this case it was the beginning of my ongoing issue.

For the third prescription, I was given Effexor. Now, mind you that in most cases, there would be a weaning or purging process to allow time for the other meds to leave my system. That never happened. I was given the Effexor and went home and took it as prescribed. The first night I didn’t seem to have an issue with it. The second night I woke up in a sweat and had what can only be described as an “electrical shock” feeling in my head. I called the doctor’s office as soon as I woke up. I was told to stop taking the Effexor immediately and they would get me in to find something different. As a 20-something back then I just did what I was told to do, it never crossed my mind that I had an adverse reaction to this medication. I got to the doctor’s office the next day and told him what was happening. If I remember correctly, I was told it should subside in a few days. Well, that didn’t happen.

After the Effexor, I talked to my doctor and he said we could try Cymbalta. He said it’s primarily an anti-depressant, but at that point, I was willing to try anything to stop the electrical shock feeling. Within a few days of the Cymbalta being in my system, the feeling was dissipating, and within a few weeks, it was gone. Unless I forgot to take a dose. So here I am, some 20 years down the road taking anxiety medication that I felt I would be off of within a couple of years. Due to the reaction, my system had to the Effexor, I feel as if I’m stuck taking Cymbalta for the rest of my life just so I don’t have to have those shock feelings.

There were times that I have gone to the chiropractor and had a good adjustment and it has alleviated some of the feeling. That tells me that Effexor has managed to mess up my nervous system. I am at present, trying to start the weaning process from the Cymbalta and go with a couple of natural supplements that seem to help. I don’t know how it’s going to go, I’m nervous and scared that because of the 20-plus years of being on an anti-anxiety drug my body is going to do some crazy stuff.

What Now?

I have read the longer one is on an anti-anxiety or anti-depressant, the more apt you are to sustain long-term neurological damage. Essentially the exact same medications we take to help us are really going to make us sicker, the older we get and the longer we take them.

I haven’t been to the doctor in three years except to have my yearly med check done. I’m ready to stop having to go just for that also, but because of other problems that have arisen in the last few years, I may have to keep going. I have always had better than perfect eyesight, last year at work I noticed it was hard for me to read numbers that I have been reading for years. I went to the eye doc and was told I have an astigmatism, glasses were given and this year I went in for my check because my eyes seemed to be getting worse. Of course, a new prescription was given and I was told that in the next 3 years I will have bifocals.

I have a hard time remembering words when talking to people or trying to tell my boss something that I have told him time and time again. I don’t believe that it is age playing a part in these issues. I think it is the years of being on these medications. I have also noticed that I get angry a lot faster than I ever have, I’ve always had a temper but I have been able to keep it in check quite nicely. Over the last couple of years, I have noticed that it doesn’t take much to anger or upset me. This too is a huge factor for weaning myself, I am the father of five daughters, aged 15 months to 21 years old. I cannot allow this to continue for their sake, and if for nothing else, I need to stop this before it makes me forget who I am.

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This article was published originally on January 4, 2018.

My Brain after Long Term Lexapro: Chemically Induced TBI

by C F

Published on December 11, 2017

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In December 2015, I was given Lexapro. I had taken Lexapro previously for 12 years, but because of abnormal blood chemistry and building side effects, my doctor suggested that I cease taking the medication. After five months without the drug, I was improving slightly, but because of life events, my doctor and I decided to begin taking Lexapro again. During the reinstatement of the drug, I immediately began to experience serious neurological reactions that I have come to describe as a brain kindling of sorts. It felt like my head was on fire chemically and electrically. Some of the symptoms that developed included: fatigue, confusion, eye pain, leg weakness, headaches, visual processing disturbances, coordination difficulties, lack of concentration, and short-term memory problems.

Within a few weeks of taking the medication, these symptoms were worsening but my physician was not concerned. In fact, he suggested what I was experiencing was normal and that I continue taking the medication. I did, for a while, until the side effects were so bad that I decided to stop. I published my story on Hormones Matter a year ago. You can read it here: A Kindled Brain: Long Term Lexapro Use Reactions. A year and dozens of doctors later, I have become completely disabled. This is a follow up to my story, told with much help from the editor of Hormones Matter.

Two Years Post Lexapro Damage

I no longer take Lexapro or other medications but the damage was done. I still cannot work, watch TV, read, drive or walk more than a few feet. I have had what seems like a two year long headache and severe vision processing issues. It is going to be another great Christmas at my house.

Though I received diagnoses of Chronic Fatigue Syndrome (CFS) and Fibromyalgia they really were just symptoms of something bigger. Shortly after the CFS diagnosis, an MRI revealed white matter lesions and demyelination. The neurologist dismissed a Lexapro connection. Research suggests otherwise. In the summer of 2017, I was finally given a provisional diagnosis of Lexapro induced neurotoxicity. Just recently, the extent of the brain damage was shown on both on a quantitative electroencephalograph (QEEG) and single-photon emission computed tomography (SPECT) brain scans. Both neurotoxicity and brain injuries were identified by both tests and later confirmed again by additional physicians who reviewed the results independently.

QEEG Results

The QEEG is an EEG with a visual mapping component. It measures the electrical activity or signal transduction between electrodes placed in specific locations on the brain. My test results showed that in certain areas of the brain there was very little organized electrical activity and other areas where there was unusual amount of high activity. What that means is that in some areas of my brain, the signals are very low and essentially not sufficiently strong for the activities that need to be performed but in other areas of my brain, there was way too much electrical activity. Specifically, the report said:

“The patient was found to have a significant amount of low frequency (8-9 Hz) in the right posterior temporal (T6) area. There is an extreme amount of low beta (12-15 Hz) predominantly in the prefrontal and frontal areas that may interfere with executive functioning, organizing, decision making and may also account for fatigue. There is a very unusual amount of high activity for all measured frequencies (1-50 Hz) in the right posterior (O2) area, specifically in the right inferior occipital gyrus (Broadman areas 17, 18, and 19). This may result in sub-optimal functioning in visual processing of color, form, movement, visual perception and spatial processing…
…The analysis of amplitude asymmetries were found to be abnormal for low frequencies (1-12 Hz) stemming from right posterior temporal (T6) area. Also, there are abnormalities for high beta (18-30 Hz) stemming from primarily the right posterior area (02). Both findings are substantiated by LORETA analysis and resembles TBI or other brain damage…
…The TBI index indicated that there was an 85% probability that the patient’s brain is functioning as if there is a TBI 0.95 on a scale of 0-10.”

This was the first confirmation of the cognitive dysfunction that I have been living with for the last few years. Doctor after doctor told me that my symptoms were not real and somehow made up (and some still do, as the QEEG is used mainly in research circles and not always accepted in conventional medicine). The QEEG clearly showed the abnormal electrical activity underlying my symptoms. Next up, the SPECT scan, a test I had to fight for, because again, no one seems to believe that a drug like Lexapro could cause such damage.

SPECT Scans

SPECT imaging shows brain activity (blood flow, which represents local brain metabolism and energy use). The technology uses radiolabeled isotopes that are then reconstructed with algorithms to display in color 3-D images of brain activity. The images below are some of my brain scans. Regions displayed in blue represent a state of very low activity called hypoperfusion and those in red represent hyperperfusion – excessive activity.

SPECT scale — Figure 1. SPECT color coding scale.

CF spect scans — Figure 2. Brain activity after long term Lexapro use.

From my images, you can see several areas of both abnormally low and abnormally high activity with very little normal brain function anywhere. From the report:

At rest, the overall cortical activity was reduced in a diffuse, decreased, patchy pattern.
Focal areas of abnormal cortical hypoperfusion were noted in the bilateral anterior frontal (L>R), left posterolateral frontal, left orbitofrontal, right dorsolateral prefrontal, bilateral anterior and medial temporal (L>R), bilateral superior parietal and bilateral occipital areas.
Focal areas of abnormal subcortical hypoperfusion were noted in the anterior aspect of the pontine portion of the brainstem, bilateral caudate and right lentiform areas.
Focal areas of abnormally increased cortical perfusion were not noted.
Focal areas of abnormally increased subcortical perfusion were noted in the bilateral thalamic and left lentiform areas.

The doctors conclude:

“The nature (diffuse, patchy), location (cortical and subcortical), and pattern (involving all lobes of the brain) of these abnormalities is primarily consistent with the scientific [literature] pertaining to a toxic/hypoxic/neuroinflammatory process and the patient’s clinical history, as obtained, of a medication reaction which was received after the blind review. These results agree in large part with outside EEG data showing hypofrontality and NM report showing left frontal abnormality, likely not to be artefactual.”

What This Means

My brain is a mess. According to the Hormones Matter editor, the areas of low activity in the various regions of the prefrontal cortex would explain my difficulties executive function, things like planning, decision-making and lack of concentration, while the reduced activity in the temporal and occipital lobes would explain my memory and vision difficulties, respectively. The reduced brainstem activity would connect to my walking and balance difficulties, but also, poor to autonomic regulation (the autonomic nervous system controls all automatic bodily functions including things like breathing, heart rate, temperature control, digestion, sleep/wake cycles, etc.). The areas of my brain on hyperdrive may reflect compensatory reactions, last ditch efforts to kick start some of the underactive regions. The thalamus (plural thalami), in particular, acts as a relay station between the brainstem and the rest of the brain for motor, sensory signals and ‘emotional’ signals via its connections to the limbic system. Mine seem to be screaming ‘wake up’ to the rest of the brain.

Please be careful using these medications, particularly psych meds and especially when prescribed for minor issues like a fear of flying or work-related stage fright. If I knew then what I know now, I would have never taken Lexapro.

*TBI: traumatic brain injury

Update: Neurocognitive Testing

In October 2017, I had a battery of neurocognitive assessments. The results have only recently become available (March 2018). According to the report, the decrements in cognitive ability were consistent with the QEEG and SPECT results indicating probable neurotoxicity with brain damage. Some of the findings included:

An approximately 9 point drop in IQ from premorbid (pre-medication reaction) levels.
Impairment of perceptual reasoning, working memory, processing speed, and full scale IQ (FSIQ), which is now at the 7th percentile.
Significant declines memory function including auditory memory, visual memory, visual working memory and immediate memory (2nd percentile).
Significant decline in manual dexterity with performance below the 1^stpercentile.
Severe decline in executive functioning.

According to the doctor’s assessment:

“The neuropsychological testing indicates disability from gainful employment for the foreseeable future. The results of this work is a diagnosis of Toxic Encephalopathy (ICD 10 G92); DSM-5 Substance/Medication Induced Major Neurocognitive Disorder (ICD F13.97).”

He also indicates that

“…the abnormal neuropsychological findings consistent with neurotoxicity; personality testing consistent with neurotoxicity; abnormal advanced brain imaging and QEEG findings; and no other reasonable explanation for the claimant’s illness and resulting disability, in my opinion, Lexapro and associated drug interactions caused this neuropsychological decline.”

Again, I cannot stress strongly enough how dangerous these drugs are. Please consider my story before taking these medications.

Postscript: In 2020, I had an evaluation by an independent forensic medical examiner. She concluded:

Within a reasonable degree of medical certainty, it is my opinion that the decline in your health has been caused by the combination of DNA variants for several CYP450 genes, with reduced metabolic capacity together with prescription psychoactive medication which caused drug-gene, drug-drug and drug-drug-gene interactions leading to severe toxicity and consequently brain damage.