Showing posts with label Brain Damage. Show all posts
Showing posts with label Brain Damage. Show all posts

Thursday, January 3, 2019

The Monster In Our House, What Psychiatric Medication Did To Our Father

"Trust us. We're Professionals."

Mad In America
Roberta Connors January 3, 2019


My cell phone rings.

“Is this ‘Robik’?” someone asks.

“That’s my nickname,” I answer, confused. “Who’s this?” It’s a police officer.

“We think we have your father here. He says he’s trying to get into your house.”

“I’m in my house. Where are you?” They’re outside, down the block. My mother and I run out to the street and approach the unforgettable scene: my father, old, grey and stiff, arms bleeding in handcuffs, is sobbing and yelling, surrounded by officers.

“You hurt me!” my father yells. “Why do you hurt me?” My mother and I, mortified and scared (please don’t shoot him, I pray to myself), run up to them.

“Does he have dementia?” an officer asks.

“Yes, I apologize for this.” I’m relieved to have an explanation. They take him out of the handcuffs and allow us to walk him home. My father tells me that he’s sorry, that he decided to take a walk but coming back he couldn’t discern which house was ours. So he started entering neighbors’ houses. We cry as we hold each other.

We had already warned him not to leave our house. We had already taken his car away. We were making plans to take away his cell phone. We were battling with the million little details of dementia. So we thought.

* * *

My father’s transition from being an independent person to one who could no longer care for himself was messy and prolonged. It took years for us to truly recognize his decline. We knew he was on antidepressants and anti-anxiety medications and that they didn’t seem to be successful. We supported his decision to sell his small business and go on disability because of debilitating stress and anxiety. He was nearing retirement age anyway. We agonized over his deteriorating driving skills and his increasing disorientation. We worried that he wasn’t taking his medications properly, or might even be over-medicating himself. But since he lived on his own — an hour away from family — we couldn’t be entirely sure what he was doing. To make matters worse, he was being sued by his downstairs neighbor for making excessive noise while walking in his home. We hired lawyers and acoustics experts and negotiated a settlement, but this is where my father seemed to spiral.
 

No one tells you when it’s time to take over for a parent’s care. You just realize that someone’s at the end of their rope, and they’re about to fall.

My realization came when my father’s housemate called us to let us know he had driven my father to his first electroshock treatment.

“Why is he getting electroshock treatments?”

“He says he’s depressed. He says he wants to die.”

When I called the clinic that was performing the “emergency” electroconvulsive therapy (ECT) on the advice of my father’s newest psychiatrist, it was clear to me that they did not know what medications he was taking, were expecting him to get himself to and from the clinic without driving (he planned to drive himself until we intervened and paid people to drive), believed he would actually follow their instructions (you’re not supposed to drive for at least a week after your last treatment), and believed he was on the brink of committing suicide. But my father was almost 70 and had never attempted suicide. I was alarmed.

Another important note: an MRI later revealed that my father suffered a mini-stroke (transient ischemic attack) some time before his psychiatrist signed him up for ECT.

“Do you know that my father is showing signs of memory loss and confusion?” I asked the clinician. “Are you sure electroconvulsive therapy won’t exacerbate this?”

“Although there can be mild memory loss from the ECT, your father is suffering from treatment-resistant depression, and the ECT can help him.”

He was wrong. It didn’t help.

* * *

You may have already heard that the statistics behind short-term and long-term effectiveness of psychotropic drugs are dubious — that for many people they simply don’t work or are harmful. You may have heard that the shifting emphasis on prescription drugs for mental health has not necessarily improved mental health. You may have heard about the hidden evidence that some antidepressants can increase a person’s risk of suicide. So consider this anecdote as a warning, with one important message: psychotropic drugs do not “balance” a person’s brain chemistry. They alter it, sometimes to an astonishingly harmful degree.

I never believed my father was clinically depressed. To the contrary, my father was gregarious, energetic and hard-working. He was a born performer, playing guitar, singing, performing as Santa Claus, emceeing wedding receptions, or reciting one of thousands of memorized poems and jokes. He had a witty, if caustic, sense of humor and he was always “on” in the company of others. The term “bipolar” or “manic depressive” would more aptly describe him, though his highs well outweighed his lows. I featured some of my father’s antics and talents in a compilation of old home movies — an entertaining glimpse into his typical disposition.




As I grew up, I recognized my father’s personality in people like Robin Williams (I’ll return to this point later). Like him, and like so many creatives with “dangerous gifts,” my father had demons. His marriage to my mother was deeply dysfunctional. He was a serial adulterer. His drinking of alcohol was likely influenced by his Russian genetic and cultural heritage. (Alcohol, I should note, is one of the most potent depressants a human can ingest.) And, as someone who had a family to support after immigrating to America at almost 40 years old, he shouldered immense levels of stress. He worked constantly. And the career he fantasized about, one full of music, singing and poetry, never materialized.

My father’s first foray into psychiatric medications coincided, not surprisingly, with the collapse of his marriage. A therapist prescribed Zoloft for depression. This was twenty years ago, before the term “chemical imbalance” was in vogue.

Following the Zoloft, two strains of a pattern emerged. Either my father would feel better and stop the medication, or he would feel worse and a doctor would increase his dose or introduce new medications. Throughout this pattern, my father continued to drink and never went to any sort of therapy. This lasted for close to two decades. He altered his mental state with pills and alcohol, which resulted not only in no improvement to his mental or emotional well-being, but ended with him abandoning his business and feeling worse than he ever had.

For me, there are a few clues that my father was misdiagnosed and mistreated. Medical professionals were probably rarely, if ever, exposed to the reality of my father’s bipolar personality, because when he was manically “happy” he was not making doctor’s appointments. It’s doubtful he confided in them about his level of drinking, partying and dysfunctional relationships with young women. Additionally, there was a language barrier. It was easier for my father to make simple statements, like “I’m depressed” and “I don’t want to live,” rather than try to find the appropriate English words to delve into his mental state and his manic lifestyle. He also probably became unable to differentiate between what might have been a side effect of one of the multiple prescriptions he was on, and what was his own self-diagnosed mental health issue. Most people, including doctors, don’t really know what the behavior they are seeing indicates. Unhappiness, sadness, boredom, stress, these can all come across to a doctor or patient as “depression.”

When he signed himself up for the ECT because he “wanted to die” and could hardly move his limbs, I’m betting his doctors and nurses didn’t stop to consider that a recent stroke and his self-medicating with alcohol and multiple psychiatric drugs might be contributing to his psychosis, or at least to cognitive impairment that could have led to the emotional devastation and anxiety he felt at the time.

One other thing I’m sure of: my father was a hedonistic pleasure-seeker. With his doctors, he found a high that could dull his senses and lift his mood. Although medical professionals may believe they are treating someone’s illness, my father, by ignoring things like therapy or sobriety, was enjoying the drug effect and sedation, the chemical fix for the unhappiness that came with the collision of his dreams and his reality. Meanwhile, the drugs wreaked continuous havoc to his brain.

Over the course of twenty years, my father was treated by or consulted with at least 16 different medical professionals who prescribed him a total of at least 21 psychotropic medications. He was frequently taking more than one medication at one time. Eventually, the antidepressants and anti-anxiety medications were not strong enough for him. His prescriptions were increasingly for antipsychotics, drugs that are used to treat schizophrenia and other psychoses, as well as anticonvulsants that are typically prescribed for mania.

Additionally, my father was taking medications for other maladies, like blood pressure, cholesterol and blood clots. It wasn’t until this year that someone pointed out to me that a statin can have neurological side effects, including depression, confusion and memory loss. My father had been on statins for years.

And, this is the hardest part for me to accept: It’s well-understood that SSRIs, along with several other drugs, increase the risk of a stroke. This is particularly true if a person has been on blood thinners, which my father had been. I’m still a bit enraged when I think about the fact that doctors didn’t warn my father that he could increase his chances of a stroke by being on blood thinners and antidepressants, especially considering that his blood pressure and cholesterol levels already made him a stroke risk.

* * *

Upon completing a whopping 11 ECT treatments, my father only became more disoriented, more forgetful and less coherent. We could no longer let him drive, so we sold his car and asked his doctor to notify the DMV that his driving was impaired. Having evidence of my father‘s recent mini-stroke and memory loss, the doctor surmised that it looked like he was beginning to suffer the early stages of dementia.

From then on, my father was ping-ponging between my sister, my mother and me as his caregivers. We prepared every meal, eliminated his access to alcohol, supervised nearly everything he did and dutifully took him to his medical appointments. This included an almost monthly visit with a psychiatrist. By 2018, my father was taking lithium for depression/bipolar disorder, lamotrigine for bipolar disorder, clonazepam for anxiety and sleep, donepezil for dementia, plus his statin and other medications.

Meanwhile, I became more and more alarmed by my father’s mental and physical decline. After reading a well-known tome about caring for someone with dementia — “The 36 Hour Day” — and joining a 20,000-member Facebook group for caregivers of people with dementia and Alzheimer’s, I was introduced to many symptoms that I recognized in my dad. He was emotionally volatile, frequently sobbing for no reason. His physical movements were impaired: he had trouble moving his limbs or bending his body in any way, which meant he never wanted to change his clothes, nor shower. His mental decline was staggering. He no longer understood basic facts, or people’s names, ages and relation to him. He had no ability to read, play guitar, or even watch television. All technology became a frustration to him. He had hand tremors. His writing ability regressed to the point that he couldn’t spell basic words and would write painstakingly and slowly, like a child. He asked the same questions over and over, compulsively agonizing about small facts. He had trouble seeing. He did damaging things on accident, like pour liquid soap into a cup and drink it, or leave a faucet on.

Worst of all, he developed extreme combativeness and aggression, even physically lashing out, and yelling angrily at the top of his lungs, often in public. We began to fear him and the increasing frequency of “catastrophic reactions” that are well-known in the world of dementia.

One thing “The 36 Hour Day” and all medical professionals seemed to agree on was the obligation to treat a patient’s depression, even if (and maybe especially if) the patient has dementia. But this did not make sense to me. His treatment for depression had all but failed for 20 years; I couldn’t understand why medical professionals pursued this unicorn of a cure. While they were busy experimenting with his brain, my father was becoming a monster, and it agonized us that he was behaving so wildly and dangerously with everyone who cared for him (and in front of my small children — who hated being around him). The only reprieve we got was when he slept, which was often. After all, the majority of the drugs he was on had major sedating effects. But when he was awake, it was like dealing with an aggressive, 200-pound zombie. We were nearing the end of our ability to manage him. We considered two end-of-the-road options: a memory care facility and/or much heavier medications. We toured some facilities and asked the psychiatrist for Seroquel. Seroquel is a “black box” drug, which means it comes with the FDA’s most serious warning for serious or life-threatening risks. It also increases the mortality rate for dementia patients. Even though it’s specifically not approved for dementia, it’s well known as an off-label treatment. To my shock, after all the hand-wringing we did about the Seroquel, I found out that my father had already had a prescription for it several years earlier, before the dementia diagnosis.

Between all the appointments, medications and terror in our home, a thought continued to nag at me: how could this man suffer such a massive decline? He was barely 70 years old. The people at the memory care facilities were wheelchair-bound and decades older than him. There was no way he could sit alongside them. He never wanted to sit. He stood and paced frantically, he could walk for hours. If he went to a facility, they would only sedate him more, because he would be a combative nuisance.

When we took my father to a neurologist to see if there was anything new to report on his latest MRI, we learned that nothing had changed. There was nothing more going on in his brain than his original scan showed two years earlier.

“Can you at least test him? Find out how bad his dementia is? We don’t understand why he’s behaving this way,” I said. But the neurologist said my father seemed to be past the point of being capable of sitting through testing. He couldn’t sit at the appointment, he was complaining and yelling from the moment we entered the room, to the moment we exited.

“You know, the dose of Seroquel you have him on is not that high. You might consider increasing it,” the neurologist offered. I felt so defeated. Not a single drug was improving his condition.

“Okay, but can we at least take him off some of these other pills? They’re clearly not helping.”

“That’s a conversation you need to have with his psychiatrist.”

We’d already had that conversation. Her response was to replace lamotrigine with Trileptal. She didn’t even know, and then was fairly unconcerned, about his dementia diagnosis. She asked him how he felt, he talked through his mental fog about how depressed he was and how it was the worst day of his life, and she typed on her tablet and tweaked his prescriptions. It was a textbook case of what I later learned is referred to as the “15 minute med check.” After a few of these appointments, it was clear to me that my father’s brain was a problem no one could solve and no pill had ever seemed to solve. Not only that, the fact that he was making life in our home impossible seemed not to register with anyone.

I came to the conclusion that because doctors are always going to aim for “treatment,” it’s very difficult for them to accept the concept that drugs are doing more harm than good and that abandoning them might be warranted. They are not thinking about discontinuation, tapering and the complicated nature of a body’s and brain’s withdrawal symptoms. When the medical professionals had seemingly no interest in my father’s completely “insane” behavior, I looked more closely at his medications. The side effects were staggering: blurred vision, tooth pain, memory loss, muscle stiffness, depression(!), suicidal thoughts, drowsiness, insomnia, aggression. I read about the tragic misuse of sedating medications on people with dementia and small efforts to end the practice. I read about the use of these incredibly strong psychotropic drugs on children in the foster care system, on prisoners, on migrants. I read in the caregiver Facebook group how many caregivers were sedating their loved ones with hardcore drugs, and treating them for depression and anxiety, and yet still experiencing agitation and violence, just like we were. A study even shows that long-term use of benzodiazepines leads to a significantly higher risk of developing Alzheimer’s. “Unwarranted long term use of these drugs should be considered as a public health concern,” the study concludes.

I also read about “polypharmacy,” which is typically defined by a patient taking more than five medications at one time. Polypharmacy is associated with an increase in adverse drug events, reduced functional capacity and several geriatric syndromes.

What are we participating in, I wondered? Why aren’t the doctors who are seeing my father get worse and worse scrutinizing the medications more closely?

I’m going to cut to the chase here:

My father now uses Skype on his own to talk to friends. He has a tablet to watch YouTube. He reads. He plays guitar. He’s memorizing new poems. He recently transcribed, quickly and with perfect spelling, the song he sings in the YouTube video. He plays with my children almost daily and laughs uproariously. We got him a dog and he walks her and loves her. He rarely sobs. He almost never yells. He changes his clothes and can shower by himself. He can walk to the neighborhood pool by himself, swim, and walk himself back without getting lost. His memory has markedly improved. And his severe muscle stiffness is gone. Hand tremors, gone. He can hop, skip, even sprint. He does push-ups and sit-ups in his room every day without prompting.

How did this happen?

Well, three months ago—without any medical professional’s knowledge or assistance — we eliminated his last psychotropic prescription (please note: abrupt discontinuation is not recommended). We have him on a healthy diet and a routine of physical activity. And no alcohol. And a little THC.

It was as if my father, the one I knew, came back from the dead. As the months go by and I watch him emerge from his chemical stupor, I am in disbelief that such a profound change can happen in a person simply by removing the side effects of medications (by removing the medications themselves). It occurs to me that for so long what we thought was his declining mental state could actually have been a state of disinhibition, the way one might feel when they’re high or drunk. His wild and impulsive behaviors, his disorientation, the loud and combative aggression — in hindsight they seem like that of a person who spent his waking hours inebriated. And now, in a matter of months, he’s sober.

Just imagine if we had let my father stay on the medications, as doctors prescribed. We would have assumed, for example, that his inability to write was a symptom of his dementia. If we had told his psychiatrist “he’s no longer able to write,” she would have chalked it up to the recent dementia diagnosis we told her about, and would have continued right on keeping him in the chemical cage that took away his fine motor skills. He would have spent years in the stupor, unable to write his poems and songs. How many other people, I wonder, are stuck in a chemical cage, not realizing that their mental and physical well-being has deteriorated because of side effects? A mere six months ago, we were considering memory care facilities for my father, and would have put him on more sedatives to manage him, which now seems truly absurd.

Now the flip side: He did have a mini-stroke and we do think there is some mental fallout from that. He is, and will always be, a drug-seeker, looking for the magic fix. He tells us often how terrible he feels, how depressed he is. The more coherent he becomes, the more aware he is of his loneliness, his sadness, and his boredom. A pill — I’m convinced — won’t fix that. It never did. As his voluntary caregivers, we do what we can to keep him active and stimulated, as well as safe and healthy. We’re not going to let him drive, and we still supervise him almost everywhere. But — and I’m not exaggerating — all of the monster-like qualities that we thought were severe symptoms of his dementia have practically disappeared. The spectrum of his emotional volatility narrowed substantially. We’ve found ourselves questioning whether he has dementia at all.

* * *

So, a word about Robin Williams:

When Robin Williams committed suicide in August of 2014, within days the world began talking yet again about the need to treat depression. Everyone seemed to gloss over the fact that Williams was misdiagnosed with Parkinson’s disease. His wife wrote about “chemical warfare” in his brain, the symptoms of which went far beyond depression and into confusion, memory loss, paranoia, intense anxiety and insomnia. She was keen to pinpoint the final diagnosis — Lewy Body Dementia — as the culprit responsible for his suicide. Few talked about Williams’ multiple medications as a potential issue. Like the fact that he had taken two medications for Parkinson’s, which not only can lead to psychosis, but are specifically flagged as inappropriate for people with psychiatric disorders because they can lead to psychosis.

On top of the Parkinson’s drugs, Williams was also taking an antidepressant called mirtazapine, a “black box” drug with noted suicide risk. Additionally, Williams had taken out a prescription for Seroquel mere days before his suicide. Williams did indeed have “chemical warfare” in his brain. But we can never truly know how much of the culprit was his dementia, and how much was the number of psychosis-inducing, sedating, debilitating chemicals that the doctor who was “treating” him prescribed.

Susan Schneider, Williams’ wife, made clear that Robin Williams was being treated for depression. He was, after all, a star with the best medical resources and treatments available to him. It’s not like they weren’t going to treatment. Schneider described at least a year of doctor’s appointments, of trial and error with medications, of worsening symptoms, of a “terrorist” inside her husband’s brain. It was as if she was speaking about my father. But my father got better. He may still call himself depressed, but he’s sober, stable and coherent, the value of which he will probably never admit nor appreciate, because he doesn’t remember what the monster in him was like.

Having had this experience, the way I look at psychiatry and psychotropic medications has completely changed. Of course, I understand that they work for some people (though time and life changes also work). I know stories of people who have had specific mental conditions and behaviors that certain medications helped alleviate, usually in combination with self-care, psychotherapy and eventual discontinuation. Antidepressants might be an important tool in certain situations, though the benefits have repeatedly been shown to be small, especially when compared to a placebo.

However, I can say with certainty that doctors and psychiatrists often don’t really know if they’ve got the diagnosis, the treatment, or the symptoms right when it comes to mental health. They often aren’t taking time to understand the brain they are altering. They are often unaware of what other medications the patient might be taking. They don’t know if they’re treating the patient, or the patient’s side effects. And they can’t be sure that the cure isn’t worse than the disease.

If you are being treated with psychiatric medications, please consider my warning:

They are experimenting.

Every time.

On you.

At the end of the day, the psychiatric drugs you or your loved one are on are sedatives and chemicals. Some go so far as to call them neurotoxins. The longer you use them, the weaker your brain gets at being able to regulate itself on its own. The higher your risk of deleterious effects. And the harder it is to get off them. But sometimes that’s exactly what needs to happen.


Thank You Ms Connors and MIA.

Thursday, November 15, 2018

Litigation Update: ECT Device Manufacturer Issues Warning of "Permanent Brain Damage"


madinamerica
Connor M. Karen November 15, 2018 

Hi everyone. As you may have heard from Dr. Breggin’s recent update, after the judge told us that the case wasn’t a class action, our case on behalf of ECT victims Jose Riera and Deborah Chase settled favorably on the eve of trial. In a development that we didn’t expect, Somatics, LLC has now issued a warning of “permanent brain damage” in its new risk disclosures of October 19, 2018. I wanted to talk a little bit about the implications and how this might affect litigation going forward.

First, you might be curious if this warning (the words “brain damage” buried in the middle of a laundry list paragraph of risks) is enough to shield the manufacturer from future liability. The answer to that is maybe. In product liability law, the adequacy of the warning of a particular risk is a “question of fact” for a jury to decide at trial. That means that even if a jury decides that a manufacturer has included warning of a particular risk, the jury could decide that the warning was insufficient in that it wasn’t prominent enough, the text was too small, not enough attention was given to it, etc.

In my opinion, with respect to the unavoidable risk of brain injury that ECT presents, there needs to be a standalone page with huge red font and a hazard symbol that states “ECT, necessarily the application of sufficient electricity to the cranium to induce a major motor seizure, presents an unavoidable risk of injury to the brain, and both the efficacy and safety of the treatment remain intensely controversial to this day.” We will keep bringing cases against ECT device manufacturers until either the manufacturers start providing that warning, or a jury states that their warning of brain damage is adequate.

That being said, their disclosure will still have effects on future litigation. First, my father DK and I think that this makes the case of anyone who underwent ECT within the statute of limitations — two years before 10/19/18, their date of disclosures — MUCH stronger, as they spent the entire litigation vehemently denying that brain injury was even a possible result of ECT. They basically put their foot in their mouth. (You still might have a good case if you underwent the “treatment” outside the statute of limitations — the arguments just take on a different nature, and we have to take a good look at your case to know whether we can help.)

Also, we think this makes individual medical malpractice cases against psychiatrists and hospitals much stronger. Somatics, LLC’s new disclosure would appear to take the legal force away from their claim that brain damage doesn’t occur from ECT, and winning medical malpractice cases over failure to give informed consent seems to me to be much more of a possibility.

One more interesting point to note: on page 4 or 5 of their disclosures, they state that the FDA “Approved” the Thymatron in 1984. This is false, as the Thymatron was grandfathered in as “substantially equivalent” to a pre-1976 ECT device through the “premarket notification” process, NOT given official premarket approval by the FDA. Further, the FDA’s regulations state:

“Any representation that creates an impression of official approval of a device because of complying with the premarket notification regulations is misleading and constitutes misbranding.” 21 C.F.R. sec. 807.97.

In essence, Somatics, LLC is representing to the public that the FDA has approved its device based on premarket notification, which the FDA’s regulations state is misleading, and constitutes misbranding. Misbranding is significant — if your device is misbranded, it can’t be manufactured or distributed. I’m not sure exactly how this will play out, but you can be sure we will be thinking of creative ways to get the Thymatron’s misbranding in front of future judges to see what shakes out.

I’m happy to answer any questions anyone has here in the comments. I’m also considering doing an AMA on Reddit soon.

If you suffer injury from electroconvulsive shock therapy, please fill out the questionnaire on ectjustice.com or send an email to ect@dk4law.com. Justice for ECT victims has been long delayed, and we think we can help bring it to you.

Previous articleFelitti and Burke Harris Inspire 850+ at National ACEs Conference

 
Connor M. Karen
Connor M. Karen, Esq. is a graduate of UC Davis School of Law, California Bar admittee, and winner of the 2017 national law student class action writing competition hosted by American Association for Justice. Connor's entry was a paper on class certification of injuries caused by violations of FDA regulations. Connor and Jim Truxaw, Esq. conceptualized and drafted the linked litigation documents.


Thank You Mr Karen and MIA.

Thursday, July 31, 2014

Antipsychotics Linked To Cognitive and Memory Impairments

Since there's not much going on with the Blind Juggernaut responsible for Feeding this 26.2% of all Americans - under the Glorious Guidelines of the People's National Institutes for Political Health (NIMH) - will suffer an excuse in any given year for Our Cronies to subject them to a raft of violent, prohibited by Law violations of Federal Racketeering and Civil Rights Statutes in order to fatten Our Cronies bottom lines, today:



Some of our fav Links: (courtesy of nachumlist.com)
Free Republic
Lucianne.com
Breitbart
The Daily Caller
Washington Free Beacon
Matt Drudge
World Net Daily
David Codrea
Sipsey Street Irregulars
Arutz 7: Israel National News
Jewish Voice and Opinion

We'll leave you with another of those boring old studies our bought and paid for Congress can't seem to find, in order to Do Their Job and take all of these drugs, at the very least, Off the CMS Buffet Table.

via madinamerica;



July 23, 2014

Finnish reseachers report in Schizophrenia Research that antipsychotic use is associated with cognitive and memory impairments. The University of Oulu team studied forty people diagnosed with schizophrenia and 73 controls at the ages of 34 and 43 years. “Higher antipsychotic dose-years by baseline were significantly associated with poorer baseline performance in several dimensions of verbal learning and memory, and with a larger decrease in short-delay free recall during the follow-up,” they observed.
“The use of high doses of antipsychotics may be associated with a decrease in verbal learning and memory in schizophrenia years after illness onset,” the researchers concluded. “The results do not support the view that antipsychotics in general prevent cognitive decline or promote cognitive recovery in schizophrenia.”
Lifetime use of antipsychotic medication and its relation to change of verbal learning and memory in midlife schizophrenia — An observational 9-year follow-up study (Husa, Anja P. et al. Schizophrenia Research. Published Online: July 15, 2014. DOI: http://dx.doi.org/10.1016/j.schres.2014.06.035)

Thursday, July 24, 2014

More Evidence Antipsychotics Reduce Brain Volume (To those of you Selling the stuff, That's Brain Damage)

via madinamerica;




July 21, 2014

People diagnosed with schizophrenia experience reductions in brain volume that increase over time, and the amount of those reductions increases in proportion to the quantities of antipsychotics taken and not symptom severity, according to research reported in PLOS One. Investigators from the University of Oulu in Finland performed brain scans on 33 participants diagnosed with schizophrenia and 71 control participants over a ten-year period, and found reductions in the antipsychotic users especially pronounced in the temporal lobe and periventricular area.
Even after adjusting for alcohol use and weight gain, the researchers found that “mean annual whole brain volume reduction was 0.69% in schizophrenia, and 0.49% in controls.”
“Symptom severity, functioning level, and decline in cognition were not associated with brain volume reduction in schizophrenia,” stated the researchers. “The amount of antipsychotic medication… over the follow-up period predicted brain volume loss.”




Thursday, June 20, 2013

Antipsychotics And Brain Shrinkage: An Update From Dr Joanna Moncrieff

Mad In America has;
Antipsychotics And Brain Shrinkage: An Update
Dr.  June 19, 2013
Evidence that antipsychotics cause brain shrinkage has been accumulating over the last few years, but the psychiatric research establishment is finding its own results difficult to swallow. A new paper by a group of American researchers once again tries to ‘blame the disease,’ a time-honoured tactic for diverting attention from the nasty and dangerous effects of some psychiatric treatments.




In 2011, these researchers, led by the former editor of the American Journal of Psychiatry, Nancy Andreasen, reported follow-up data for their study of 211 patients diagnosed for the first time with an episode of ‘schizophrenia’. They found a strong correlation between the level of antipsychotic treatment someone had taken over the course of the follow-up period, and the amount of shrinkage of brain matter as measured by repeated MRI scans. The group concluded that “antipsychotics have a subtle but measurable influence on brain tissue loss”(1).
This study confirmed other evidence that antipsychotics shrink the brain. When MRI scans became available in the 1990s, they were able to detect subtle levels of brain volume reduction in people diagnosed with schizophrenia or psychosis. This lead to the idea that psychosis is a toxic brain state, and was used to justify the claim that early treatment with antipsychotics was necessary to prevent brain damage. People even started to refer to these drugs as having “neuroprotective” properties, and schizophrenia was increasingly described in neo-Kraeplinian terms as a neurodegenerative condition(2).
The trouble with this interpretation was that all the people in these studies were taking antipsychotic drugs. Peter Breggin suggested that the smaller brains and larger brain cavities observed in people diagnosed with schizophrenia in these and older studies using the less sensitive CT scans, were a consequence of antipsychotic drugs(3), but no one took him seriously. It was assumed that these findings revealed the brain abnormalities that were thought to constitute schizophrenia, and for a long time no one paid much attention to the effects of treatment. Where the effects of antipsychotics were explored, however, there were some indications that the drugs might have a negative impact on brain volume(4).
In 2005, another American group, led by Jeffrey Lieberman who headed up the CATIE study, published the largest scanning study up to that point of people with a first episode of psychosis or schizophrenia(5). The study was funded by Eli Lilly, and consisted of a randomised comparison of Lilly’s drug olanzapine (Zyprexa) and the older drug haloperidol. Patients were scanned at the start of the study, 12 weeks and one year later and patients’ scans were compared with those of a control group of ‘healthy’ volunteers. 
At 12 weeks haloperidol-treated subjects showed a statistically significant reduction of the brain’s grey matter (the nerve cell bodies) compared with controls, and at one year both olanzapine- and haloperidol-treated subjects had lost more grey matter than controls. The comparative degree of shrinkage in the olanzapine group was smaller than that in the haloperidol group, and the authors declared the olanzapine-related change not to be statistically significant because, although the result reached the conventional level of statistical significance (p=0.03) they said they had done so many tests that the result might have occurred by chance. In both haloperidol and olanzapine treated patients,however, there was a consistent effect that was diffuse and visible in most parts of the brain hemispheres.
The idea that schizophrenia or psychosis represent degenerative brain diseases was so influential at this point, that the authors first explanation for these results was that olanzapine, but not haloperidol, can halt the underlying process of brain shrinkage caused by the mental condition. They did concede, however, that an alternative explanation might be that haloperidol causes brain shrinkage. They never admitted that olanzapine might do this.
It seems as if Eli Lilly and its collaborators were so confident about their preferred explanation, that they set up a study to investigate the effects of olanzapine and haloperidol in macaque monkeys. This study proved beyond reasonable doubt that both antipsychotics cause brain shrinkage. After 18 months of treatment monkeys treated with olanzapine or haloperidol, at doses equivalent to those used in humans, had approximately 10% lighter brains than those treated with a placebo  preparation.(6)
Still psychiatrists went on behaving as if antipsychotics were essentially benign and arguing that they were necessary to prevent an underlying toxic brain disease (Jarskoget al 07 Annual review). Andreasen’s 2011 paper was widely publicised however, and it started to be increasingly acknowledged that antipsychotics can cause brain shrinkage. Almost as soon as the cat was out of the bag, however, attention was diverted back to the idea that the real problem is the mental condition.
Later in 2011 Andreasen’s group published a paper that reasserted the idea that schizophrenia is responsible for brain shrinkage, in which there is barely a mention of the effects of antipsychotics that were revealed in the group’s earlier paper(7). In this second paper, what the authors did was to assume that any brain shrinkage that could not be accounted for by the method of analysis used to explore the effects of antipsychotic treatment must be attributable to the underlying disease. 
The way they had analysed drug treatment in the first paper only looked for a linear association between antipsychotic exposure and changes in brain volume, however. A linear analysis only detects an association that is smooth and consistent- in other words an association in which brain volume shrinks by a consistent amount with each increment in antipsychotic exposure. The total effect of drug treatment may not follow this pattern however. It seems from other evidence that there is a threshold effect whereby being on any amount of an antipsychotic has the greatest relative effect, with a levelling out of the impact as duration of exposure reaches a certain level.(8) In any case, without a comparison group which has not been medicated, a virtual  impossibility in this day and age, it is simply not possible to conclude that the whole effect is not drug-induced.
The latest paper by this research group replicates the findings on antipsychotic-induced brain shrinkage, but also claims that brain volume reduction is related to relapse of the psychotic disorder(9). Relapse was defined retrospectively by the research team for the purposes of this particular analysis, however, and not at the time the study data were collected. Moreover, the definition used does not refer to any significant change in functioning, but only to a deterioration in the severity of symptoms. But the group’s previous analysis of severity of symptoms, using data collected at the time, found that severity had only a weak association with brain volume changes, and moreover that symptom severity was correlated with antipsychotic exposure.(1)
The most recent analysis ignores the probable association between antipsychotic treatment intensity and relapse, but it seems likely that people undergoing periods of ‘relapse,’ or more accurately deterioration of symptoms, would be treated with higher doses of antipsychotics. If this is so, and the two variables ‘relapse’ and ‘treatment intensity’ are correlated with each other, then the analysis is questionable since the statistical methods used assume that the variables are independent of each other.
So Andreasen’s group have found strong evidence of an antipsychotic-induced effect, which they have replicated in two analyses now. The predictive value of the severity of symptoms, on the other hand (which is essentially what relapse appears to define) is weak in the initial analysis, and in neither analysis was it clearly differentiated from drug-induced effects.
These researchers seem determined to prove that ‘schizophrenia’ causes brain shrinkage, although their data simply cannot establish this, as none of their subjects seem to have gone without drug treatment for any significant length of time. So even though their recent analysis once again confirms the damaging effects of antipsychotics, they conclude that the results demonstrate the need to make sure patients take, and do not stop, their antipsychotic medication. The only concession made to the antipsychotic-induced changes revealed is the suggestion that low doses of antipsychotics should be used where possible.
Yet other prominent psychiatric researchers have now abandoned the idea that schizophrenia is a progressive, neurodegenerative condition, and do not consider that Andreasen’s study provides evidence of this.(10) Bizarrely, Nancy Andreasen is a co-author of a recently published meta-analysis which combines results of 30 studies of brain volume over time, which clearly confirms the association between antipsychotic treatment and brain shrinkage (specifically the grey matter) and finds no relationship with severity of symptoms or duration of the underlying condition.(11)
What should antipsychotic users and their families and carers make of this research? Obviously it sounds frightening and worrying, but the first thing to stress is that the reductions in brain volume that are detected in these MRI studies are small, and it is not certain that changes of this sort have any functional implications. We do not yet know whether these changes are reversible or not. Of course the value of antipsychotics has been much debated on this site and elsewhere, and their utility almost certainly depends on the particular circumstances of each individual user, so it is impossible to issue any blanket advice. If people are worried, they need to discuss the pros and cons of continuing to take antipsychotic treatment with their prescriber, bearing in mind the difficulties that are associated with coming off these drugs.(12) People should not stop drug treatment suddenly, especially if they have been taking it for a long time.
People need to know about this research because it indicates that antipsychotics are not the innocuous substances that they have frequently been portrayed as. We still have no conclusive evidence that the disorders labeled as schizophrenia or psychosis are associated with any underlying abnormalities of the brain, but we do have strong evidence that the drugs we use to treat these conditions cause brain changes. This does not mean that taking antipsychotics is not sometimes useful and worthwhile, despite these effects, but it does mean we have to be very cautious indeed about using them.


Reference List

(1) Ho BC, Andreasen NC, Ziebell S, Pierson R, Magnotta V. Long-term Antipsychotic Treatment and Brain Volumes: A Longitudinal Study of First-Episode Schizophrenia. Arch Gen Psychiatry 2011 Feb;68(2):128-37.
(2) Lieberman JA. Is schizophrenia a neurodegenerative disorder? A clinical and neurobiological perspective. Biol Psychiatry 1999 Sep 15;46(6):729-39.
(3) Breggin PR. Toxic Psychiatry. London: Fontana; 1993.
(4) Moncrieff J, Leo J. A systematic review of the effects of antipsychotic drugs on brain volume. Psychol Med 2010 Jan 20;1-14.
(5) Lieberman JA, Tollefson GD, Charles C, Zipursky R, Sharma T, Kahn RS, et al. Antipsychotic drug effects on brain morphology in first-episode psychosis. Arch Gen Psychiatry 2005 Apr;62(4):361-70.
(6) Dorph-Petersen KA, Pierri JN, Perel JM, Sun Z, Sampson AR, Lewis DA. The influence of chronic exposure to antipsychotic medications on brain size before and after tissue fixation: a comparison of haloperidol and olanzapine in macaque monkeys. Neuropsychopharmacology 2005 Sep;30(9):1649-61.
(7) Andreasen NC, Nopoulos P, Magnotta V, Pierson R, Ziebell S, Ho BC. Progressive brain change in schizophrenia: a prospective longitudinal study of first-episode schizophrenia. Biol Psychiatry 2011 Oct 1;70(7):672-9.
(8) Molina V, Sanz J, Benito C, Palomo T. Direct association between orbitofrontal atrophy and the response of psychotic symptoms to olanzapine in schizophrenia. Int Clin Psychopharmacol 2004 Jul;19(4):221-8.
(9) Andreasen NC, Liu D, Ziebell S, Vora A, Ho BC. Relapse duration, treatment intensity, and brain tissue loss in schizophrenia: a prospective longitudinal MRI study. Am J Psychiatry 2013 Jun 1;170(6):609-15.
(10) Zipursky RB, Reilly TJ, Murray RM. The Myth of Schizophrenia as a Progressive Brain Disease. Schizophr Bull 2012 Dec 7.
(11) Fusar-Poli P, Smieskova R, Kempton MJ, Ho BC, Andreasen NC, Borgwardt S. Progressive brain changes in schizophrenia related to antipsychotic treatment? A meta-analysis of longitudinal mri studies. Neurosci Biobehav Rev 2013 Jun 13.
(12) Moncrieff J. Why is it so difficult to stop psychiatric drug treatment? It may be nothing to do with the original problem. Med Hypotheses 2006;67(3):517-23.


Thank You MIA and Dr Moncrieff.


"Obviously it sounds frightening and worrying, but the first thing to stress is that the reductions in brain volume that are detected in these MRI studies are small, and it is not certain that changes of this sort have any functional implications."

So are the Reductions in Brain Volume that can be detected from being hit in the head with a Baseball Bat.

http://psychroaches.blogspot.com/search?q=18C95


Evidence For The Neurotoxicity Of Antipsychotic Drugs, Dr Grace Jackson