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INTRODUCTION TO MY TWO SUBMISSIONS TO THE INTERNET

        I have written 2 summaries of what I found over many years of exploration and discovery on the surprising extensiveness and impact of akathisia -- the first, a long monograph to explain all its various overlooked, yet highly important aspects and consequences. This one is a consolidation of the other -- a talk to give the highlights of what I wrote in my much longer monograph. 

        I hope you find them stimulating and even exciting and the beginning of a whole new understanding of akathisia, which I believe has been unknowingly preventing a much more successful use of the major psychotropics ever since the psychopharmacologic ‘era’ began over 60 years ago with chlorpromazine (Thorazine) and lithium.

 

William Drucker, MD, 9/1/23

(MY SPEECH)

AKATHISIA: SHINING A NEW LIGHT ON AN EXCEPTIONALLY COMMON, MUCH OVERLOOKED, AND HIGHLY CONSEQUENTIAL SIDE-EFFECT SYNDROME (ESPECIALLY ITS PROMINENT CAUSATION OF TREATMENT-REFRACTORY PSYCHIATRIC ILLNESS)

(Note: Because this was originally meant to be just a speech, I have put citations to the claims I make here into my longer and more complete monograph.)

        I know my talk will say something very new and, I think, very important about the akathisia I believe we have all very inadequately recognized since our residencies! I hope you will be excited by the prospects I offer for achieving far better treatment results for psychosis and depression from my new conception of akathisia – what I have come to call ‘expanded akathisia’. 

        Over about 27 years until my retirement 8 years ago, as a line psychiatrist for a mental health clinic located in Los Angeles’ skid row run by the LA County Department of Mental Health, I made a series of discoveries that made it possible for me to significantly resolve what no doubt is the greatest problem facing psychiatry today --  treatment resistance. Quoting Dr. Thomas Insel, former head of NIMH, “The unfortunate reality is that current medications help too few people to get better and very few to get well.” I believe I know how to change much of that reality! Our current treatment success rate runs roughly at 35-45% but goes down to about 25% in some studies and up to 67% as with STAR*D after a great deal of effort with up to 3 augmentations or switches. But I was able to more easily succeed with my treatment at an 80-90% success level in 2 studies I performed using my discoveries, likely without anywhere near as much frustration and aggravation as other clinicians and clinical investigators have to deal with. But due to my quite limited research abilities and great time limitations at work, these results must be taken with skepticism until (and if) they can be more scientifically proven.  

        I know I have made quite a claim which therefore must be validated using much better research methods than I could provide before my results can be accepted. That is why I am presenting my discoveries to the web in the hope there is someone out there who is looking to further examine and hopefully confirm what I have found. What a boon this can be to a myriad of patients if my findings are shown to be true as I certainly believe

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they are! What I propose offers us a way out of our present dilemma noted by Dr. Insel through a whole new way of medicating our patients due to a new understanding of from what they are suffering.

        So what did I come to understand over these 27 years of exploration which gave me such good outcomes? Well, for one, this understanding required a very different treatment pathway than we are presently on -- over and over again I might add -- as we try to improve our poor treatment results. 

        My adventure began in 1988 when I read two brief quite positive case reports from 1984 and 1987 on 6 patients each, one by George Zubenko and the other by Lawrence Adler, using clonidine, an alpha 2A agonist, for akathisia. I suspect many of you are aware of these two papers, but for some reason, maybe because of clonidine’s somnolence and some orthostasis, none, or nearly none,  of the 9 listed authors did any further investigations I could find. However, I was unhappy enough with my akathisia treatment results with propranolol/Inderol -- what was then the first choice as it still is now -- not to mention the even poorer results from benztropine/Cogentin – to encourage me to try it, anyway, and I quickly saw it gave me better outcomes than propranolol and nowhere near the difficulties these investigators experienced from it. 

        So I continued to use clonidine and to find it superior without the same degree of side-effect difficulties they saw, plus -- and it’s a big plus -- I was gradually coming to see what treating akathisia could do for my treatment of depression and psychosis. After a while, I did come to change the clonidine to guanfacine/Tenex, a congener of it and a more selective 2A agonist, because it has less of several side-effects than clonidine -- somnolence, orthostasis, and dry mouth -- while usually, though not always, retaining the same efficacy. 

        Along the way, I also came to try ropinirole/Requip, a dopamine agonist that came on the market for Restless Legs in 2003 or 4. I soon learned that RLS had many of the symptoms I was coming to recognize as being part of akathisia, and so I thought it could have potential as a second treatment option when clonidine or guanfacine were either inadequate or caused their own limiting side-effects. And it did, working just as well as my original two! Ropinirole’s biggest problem is nausea which occurs in about half the patients, but taking it with food cuts that rate by about half, again. A similar dopamine agonist, Pramipexole/Mirapex, is also on the market for RLS and, interestingly, in a number of articles, has been found valuable as an adjunct for treating

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treatment resistant depression and also psychosis. I can only wonder if it is because it is treating unrecognized akathisia.    

        But I never saw any connection in the literature tying these great benefits of the two dopamine agonists to the treatment of akathisia, even though I was constantly seeing this from ropinirole. Regretably, I never tried pramipexole, being a little unwilling to start something new with new uncertainties when ropinirole seemed to be working well. But there is a chance it might work even better than ropinirole due to its possibly causing less nausea, vomiting, and dizziness and also, possibly having greater effectiveness for RLS and therefore, perhaps, for akathisia, too.      

        How interesting it is that what I first saw to be medications for akathisia could be of such help for psychosis and depression, too. And here is a very important part of my discovery journey. Akathisia is very common, especially as my definition of it grew over the years to include a host of new symptoms beyond what I think is our usual limited concept of it of just restlessness and some anxiety and agitation. The rate of what I came to call my ‘expanded’ view of akathisia is around 85% of all the patients I treated, which I figure reaches about 400-450 in total --  usually with either antipsychotics, antidepressants, and/or mood stabilizers. 

        What is the evidence akathisia exacerbates psychosis? There is much support for this in the literature, though virtually none for it doing the same to depression which I would see all the time. Among a fair number of affirmative acknowledgements, psychotic exacerbation has also been noted in the DSM-IV and IV-TR but only in the Appendix -- in Section 333.99 -- and in a very limited way. However, I could not find any mention of this in the DSM-5, but it was then returned to the DSM-5-TR in a back section entitled  “Medication-Induced Acute Akathisia”. All three acknowledgements in the DSMs state it could cause, quote, “[a] worsening of psychotic symptoms or behavioral dyscontrol, [which] may lead to an increase in neuroleptic medication dose, which may exacerbate the problem” -- in my belief, a very important but long ignored statement. To me, this limited awareness is a sign of a significantly diminished appreciation of its impact. But I would see psychotic and depression exacerbations from akathisia all the time from, basically, all the medicines that treat either. (This does not go for the new meds since I retired, nor clozapine, which I never used.) This diminishment or even lack of recognition of the role played by akathisia was occurring while my recognition of its importance to both was

growing! As I see it, what was warned of for psychosis and then forgotten, plus the even more unrecognized exacerbation of depression, is what is behind much of the polypharmacy and poor results we now see from our treatments as we continue to pursue the wrong medication pathway, piling on more and more akathisia-causing meds when our patient is not doing well. 

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        I must say more about akathisia bringing back depression. Though I see this as mainly my discovery, to give credit, there was some hint it could do this given by UCLA’s late Theodore Van Putten along with Stephen Marder, in one paper I found from 1984 in the Archives of General Psychiatry in which they wrote, “Akathisia is often experienced as anxiety and depression”. Brown, may also have had a sense of this, too, writing, “It [akathisia] is frequently mistaken for anxiety, agitated forms of depression …” But aside from these, I could not find any other statements linking akathisia to a return or exacerbation of depression, yet, as with psychosis, I found it can do it very frequently and quickly, sometimes occurring right before my eyes, up or down, during the course of a visit. My patients have described this as if being on a roller coaster of mood and/or psychotic swings. 

        If my observations are correct, these effects of akathisia will very much change our diagnostic inquiries and then treatments, resulting in much better success rates as they did for mine. The roller coaster sign became a valued diagnostic tool, turning the underlying illness on and off as it came and went, bringing with it a whole raft of other unpleasant symptoms I will speak of below, which I’ll guess you were told about by your patients at times and for which you did not have a good answer.

        Now patients could have difficulty relating to my roller coaster inquiries and to recognize what they were going through, but I would even catch them, at times, often without their realizing it, saying they felt as if on a roller coaster, or had, quote, “mood swings”, or would “go up and down”, or “feel good at times and bad at others”. If they did, I knew what was occurring. I also found that directed questions were usually necessary as opposed to only letting them spontaneously tell me these things in order not to overly influence their responses. As we all know, the mentally ill are not good at analyzing themselves, and my questions can require some reflection, but with this and other recognitions, I began to see the real problem was not an inadequacy of our meds, but instead, the expanded akathisia they so frequently brought with them. 

        That SSRIs can cause akathisia was recognized soon after the first, Prozac/fluoxetine, came on the market in 1988, and then the same occurred with Zoloft/Sertraline and others, though these  recognitions seem to have been all but forgotten. I believe the antidepressants, including the Tricyclics, though perhaps less so, cause just as much of my expanded form of akathisia as do the antipsychotics. That makes for a lot of the depression relapses and treatment resistance cases we face -- needlessly, I believe.

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        And as I began treating akathisia, at first seeing only its restlessness with glimpses of psychotic and depressive exacerbations, I began to also note a whole new array of features which also cause great discomforts, physical pain, and confusion as to just what was going on. Initially, I had no idea these were part of the akathisia syndrome, too, but I soon began to see they would also ease or go away as I treated for the usual akathisia, leading to a great multidimensional improvement in what I could achieve. 

        Here is my list of these symptoms, symptoms which give us continuing difficulties in our treatment efforts: 

        I just covered the first two, the exacerbation, persistence, and/or return of psychosis and/or depression -- clearly the most important ones – but there are many others. They are also intermittent, and several have already been linked to akathisia by other investigators.

        3. Restlessness: This is what we first think of with akathisia. It is fairly common, creating much discomfort and distress, but on any number of occasions it doesn’t seem to occur. We see on and off day or night restlessness and antsiness that derives from uncomfortable muscle and other body sensations and can be somewhat relieved by movement. It is seen as tapping or flexing and extending hands, feet, or toes, rocking, abducting, and adducting the extremities, and swinging, crossing, and uncrossing them, twirling the ankle, tossing in bed, marching in place, and feeling a need to take a long walk to work these out, etc. The restlessness of ADHD can be confused with it. 

        4. Anxious or “edgy” feelings as my patients would fairly often call them. They can precipitate panic attacks. I think anxiety is a core symptom of akathisia, but it seems not to be generally considered as such.

        5. Irritability, anger, and/or agitation. I believe these are just secondary to the increased anxiety and restlessness of akathisia or its exacerbation of depression and/or psychosis. But nevertheless, it is a very important symptom of akathisia. 

        6. Headaches, especially when accompanied by sudden sharp stabs, blows, aching, or strange feelings in the head. These symptoms can help differentiate between akathisia and other causes.

        7. Muscle cramps, spasms, stiffness, and tightenings, including in the larynx. I came to see these as part of akathisia unless they were quite severe, painful, and scary to the patient, such as in oculogyric, glossal, and sternocleidomastoid crises. The severity and scariness of these crampings could, perhaps, be the dividing line between anticholinergic or antihistaminic-responsive muscle dystonias and those coming from akathisia, which could be painful, too, but less so. l found akathisial muscle cramps to be a fairly common symptom, especially in the legs and arms. The one or two patients I had with laryngospasms -- which can be scary, too--

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responded much better when I treated them as having akathisia and not an antipsychotic-induced dystonia. My patients would often call these crampings Charley horses, which implies less severity. By and large, those with muscle cramps responded well to my akathisia meds, so I came to see them as part of it. 

        8. Spontaneous tremors of legs or hands typically starting while at rest. Internal tremors and “shaky” feelings can be felt also.

        9. On and off twitches and myoclonic jerks. These could lead to dropping things or the leg suddenly giving out which could be mistaken for a dizziness from clonidine- or guanfacine-induced orthostasis.

        10. Muscle, joint, bone, or other areas of aching that can be felt deep down. These may be more continuous and less intermittent than other symptoms. Again, could be labeled as a Charley horse or from arthritis.                

         11. Bruxism or feeling a need to “click” the teeth.                                                                                                                 

        12. Dizziness or lightheadedness. Can be confounded with orthostasis from clonidine and guanfacine, but akathisial dizziness often occurs when sitting or lying down, thus reducing the chance orthostasis is to blame.

        13. Feeling an urgency to breathe, a restlessness in breathing, or feeling unable to, “breathe in a leisurely relaxed manner”, as per Hirose who explored akathisia in Japan. I saw it once or twice. Akathisia can also cause grunting, gasping, sighing, snorting, or dyspnea.

        14. A tardive dyskinesia-like picture such as tongue protrusions or eyebrow movements. I’ve seen this in 2-3 patients, and it made me wonder if TD is related to, or part of, akathisia, but I can only speculate because they were just too irregular to accurately evaluate my akathisia treatment, but each told me it helped. 

        15. Paresthesias: These are very common and a significant factor in diagnosis. They come and go with the akathisia. Here are the ones I have seen: 

        a. Unusual and hard-to-get-at itching on or deep under the skin or scalp, under the skull, in the brain, or the back of the throat. 

        b. Crawling on or under the skin or feeling as if you’ve run into a spider web.             

        c. Hot or burning feelings on or under the skin or elsewhere.  

        d. Hot and/or cold flashes, longer lasting feelings of same, sweats, or chills. Can be confused with menopause. 

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        e. Numbness or tingling occurring most anywhere but most commonly in the hands and feet. Can be mistaken for a diabetic neuropathy.

        f. Sudden needle sticks, bee stings, or bites on the surface or penetrating deep into the body. I had some patients who mistakenly attributed these to bed bugs.

        g. Touch sensations as if pushed by a thumb or being gripped or suddenly punched. These could be confused with tactile hallucinations due to the underlying illness. But usually, it was just akathisia.

        h. Sudden electric shocks in part of, or throughout the body. 

        i. Shooting pains that could be attributed to disc problems and arthritis. 

        j. Feeling pressure or aching, especially in the head. Can be confused with just a headache or migraine.  

        k. Stabbing pains, especially in head, joints, sides, back, and chest, confusing it with angina, but often occurs at rest, making this much less likely. 

        l. ‘Icky’ feelings on or under skin. Can make one want to shower, dig at, rip off, or crawl out of one’s skin. 

        m. Weird sensations such as water running down the neck, blood flowing in the veins, tingles or tickling in the brain or that the head might explode, pulling or drawing sensations, strange feelings in muscles, viscera, and the joints. One of my patients felt the need to continually crack his knuckles. In his paper, “The Many Faces of Akathisia”, Van Putten cited a patient complaining that, “My stomach feels strange. It’s like I’m churning inside.” And in a scene from the movie a decade or more ago, “Garden State” (a good movie, I believe, about a depressive), the main character has been put on a variety of psychotropics by his psychiatrist father and complains of strange sensations of, quote, “Intense headaches like a lightning storm in my head for a split second”, and “Like a surge of electricity”. His father sends him to a neurologist who can find nothing wrong. I wanted to shout, THAT’S AKATHISIA! My guess is the screenwriter or a friend suffered from it and so put it in his movie, thinking there were people out there -- perhaps a number in Hollywood who were on our meds -- suffering, also, from unrecognized and misunderstood akathisial paresthesias.

        n. And my final one: dysesthesias such as a touch or gentle brushing feeling as if sandpaper were rubbing the skin.

        My guess is many of us have heard any number of these complaints for which we had little answer, so we would ignore them, refer the patient as happened in Garden State, or try treating them in various and usually unhelpful ways.

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I think of the unnecessary troubles patients and their doctors go through, not to mention the cost of unnecessary consultations and treatments. I have seen such referrals to the gynecologist for pelvic pains and hot flashes mistaken for menopause, the rheumatologist or orthopedist for joint and bone pains, the cardiologist for precordial and substernal pains, the neurologist and diabetologist for burning, tingling, and numbness, and the dentist for bruxism. Yet all these symptoms frequently come from akathisia and have usually responded to my akathisia meds. 

        So it seems to me, akathisia is much more than the very limited picture we have of it. And these other symptoms in addition to the exacerbations of psychosis and depression are all quite important, too, for the great discomforts, pain, and confusion they cause, leading to a kind of jumble of combined medications, referrals to other specialists, and much uncertainty as to just what to do next. I believe a great deal of this can be consolidated into one picture of  akathisia. Of course, my discoveries need corroboration by further and better clinical studies than I could perform. 

        If the doctor were not aware of all this, he or she would think the meds weren’t working well and then do the usual -- up the dose, try a new medicine, or a new combination. Then to add to the confusion and uncertainty, such changes just might work -- for a little while -- but soon, a relapse, or perhaps just a worsening of some of the symptoms, especially insomnia, depression, or voices, will almost always occur. Then more changes will be made, frequently leading to an accumulation of meds – a polypharmacy -- with more side-effects, especially akathisia, and a more treatment- resistant condition! My guess is this has occurred to many of you without an understanding of what was really happening. I can remember going through this same experience many times before it hit me one day that I needed to try going in the other direction with less, not more meds, and keep my eye on my growing understanding of akathisia and how to spot and then treat it, and lo and behold, I began to observe a more permanent improvement in my patients! I came to suspect that much of the polypharmacy heaped on patients who had seen other doctors before me was simply the result of unrecognized akathisia, which I found would stop, or at least, ease, as I treated for it with my anti-akathisia meds and, also, a judicious lowering or discontinuation of the offending ones when I felt I had some room to maneuver, which was frequent. 

        I haven’t yet spoken of this action for dealing with akathisia, but it was an important part of my treatment. What is frequently needed is to attack it from both ends to chip away at both its causes -- too much illness-treating but akathisia-causing medicine and not enough of -- or the right -- anti-akathisia meds. These two actions were the core of my treatment successes because I routinely found it was my patients’ akathisia, and

 

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not their illness, that was the reason for their treatment difficulties in the first place! 

        To illustrate the problem of medicines being piled on top of one another due to treatment resistance from akathisia, in my unpublished paper, I listed 26 patients whose average daily doses I successfully brought to less than the smallest tablet available -- often by a lot -- except for two where it was close! I’ll list these 26 -- outpatients all -- so I cannot generalize my experiences to those in hospital, but I suspect they, too, would benefit. 

        With fluoxetine, I had 1 patient on 10 mg 5 days/wk, 4 on 5 mg/day, 1 on 5 mg 5 days/wk, 1 on 5 mg 4 days/wk, 1 on 5 mg 2 days/wk, and 1 on 10 mg one day and 5 the next. With sertraline, I had 1 on 12.5 mg/day, 1 on 12.5 five days/wk, 1 on 12.5 four days/wk, and another on 12.5 mg every fifth day! Continuing, I had 1 schizoaffective on 1 mg aripiprazole twice/wk, another on 12.5 mg quetiapine 5 days/wk, and 2 on 12.5 mg/day (1 was a major depressive). Another schizoaffective was on perphenazine, 1 mg/day on 5 days/wk and 2 mgs on the other 2 days. Two with major depression were on buproprion, 1 on 75mg every other day and another on 37.5 once every 10 days! I had 3 patients on 12.5 mg lamotrigine/day, 1 on mirtazapine at 3.75/day, and 1 on 3.75 every 4 days. Finally, I had 1 patient on 5 mg nortriptyline, also, once every 10 days!    

        These extremely low doses, along with a good deal of my akathisia meds, were what worked for both their illnesses and the akathisia that had plagued them until we had reached these levels. Fortunately, I found that patients who were very sensitive to akathisia were also usually very sensitive to the beneficial effects of the illness medicines which gave me the room to lower them to doses that still worked. So, instead of raising the dose, or trying a new med, or combining meds, I went against the standard treatment procedure and just lowered the doses again and again when it appeared the med would be working for the illness if it were not for the akathisia it brought with it. Of course, I did it slowly, as I knew I could go below what the illness needed, but I found this to be rare. Usually, I needed decent doses of anti-akathisia meds because I found akathisia could, itself, be quite treatment resistant. Seeking to diminish this problem, just before my retirement, I began starting patients on the smallest tablet to decrease their risk of getting akathisia in the first place. And these low doses seemed to work well, but I did not have enough time to fully investigate the validity of this discovery and just how low my initial dose could be. (I cannot guarantee these regimens remained effective for all 26 over  

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a long period of time. I lost track of them upon my retirement, and the nature of many would cause irregularities and breaks in attendance, but I did have the sense I had found the right meds and doses for all of them.)

        I now need to describe the two studies I did on my patients to see if my findings for both the occurrence of akathisia and response to my meds were true or not. Now I know with my limited research abilities, my results can only be used to engage someone who finds my discoveries both interesting and worthy of further investigation. 

        My first study lasted 8 months and the second, a year. I included 100% of my patients except those who were too non-compliant to cooperate enough for me to at least have some idea as to whether, or by how much, they were following my prescriptions or not and how they were doing with them. 

        In the first one, I evaluated all of the 241 patients I saw at least twice in that 8 month period. Nearly 100% were suffering from depression, be it from my most common DSM-IV diagnosis, Major Depressive Disorder with Psychotic Features, then schizoaffective, then major depressive disorder without psychotic features, then bipolar, and finally, the few non-depressed ones with a straight schizophrenia. Of these 241, 217 (90.0%) suffered from akathisia as I define it and 24 had none. Twenty of these 24 without akathisia were compliant and 4 were not. Another group numbering 31 of the 241 were just too irregular to include in my evaluation of their responses to my illness plus akathisia-treating meds. However, I was still able to judge that 27 of these 31 still suffered from akathisia and 4 were free of it, so I was confident enough to be able to put them in my ratios for the percent suffering or not from akathisia -- but I disregarded them as to their response to my treatments. Therefore, I had 190 -- 241, total, minus 20 compliant patients without akathisia and 31 non-compliant ones -- whom I could evaluate for their reaction or lack thereof to my treatment for both their illnesses and their akathisia. I still evaluated the treatment results of those 20 compliant patients without akathisia who did not need akathisia meds like the other 190 who did, and who had a very unexpected, but quite important and telling response, which also occurred during my second study with a new group of patients, and so I will combine these two subgroups with this same telling response when I discuss my second study below. 

        My akathisia medications were guanfacine, clonidine, ropinirole, and an occasional benzodiazepine along with my gradual lowering of the illness-treating meds when needed which was quite often. Because of inadequate responses to my akathisia meds or side-effects limiting tolerance to them, a good number of my patients were on more than one. When I did these studies, I was no longer using propranolol, but since then, I

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tried it a couple times when nothing was working, and it seems there are some patients for whom it is of value.

        Because of my lack of knowledge and time, I was not able to use any of the known scales for psychosis or depression. The same goes for the Barnes Akathisia Scale which limits itself to only, quote, “objective features of motor restlessness, subjective complaints of restlessness, and associated distress,” the standard recognition for akathisia but which is far less than what I see it to be.

        To grade the reactions to my medication protocol, I used the following 4 categories:   

        I gave an ‘Excellent’ score to those who felt essentially completely relieved of their underlying illness plus akathisia with its recurring depressive, psychotic, and other symptoms, though some could still hear an occasional voice, see flitting shadows, or feel a couple hours of mild depression and/or psychotic symptoms here and there when akathisia would still break through. One hundred thirty-six of the 190 (71.6%) were in this Excellent category.

        ‘Pretty Good’. These still had some residual symptoms of akathisia and underlying illness but my patient generally would feel alright day and night with only occasional and mild occurrences of relapse symptoms and akathisia. Thirty-five of the 190 (18.4%) I put in this category. 

        ‘Fair’. These had a modest to moderate improvement, yet still had a good distance to go to reach the next level. Fourteen of the 190 (7.4%) were here. 

        ‘Poor’. These did no better, or almost no better, than when they began. Five of the 190 (2.6%) did poorly. 

        I listed my top 2 groups as therapeutic successes -- 71.6% excellent and 18.4% pretty good, totaling 90%. If true, these results are clearly considerably better than what has usually been found after treatment. For example, there was the 2010 paper by Fournier et al. that made such a stir in the news about the ineffectiveness of antidepressants for mild to moderate depression. And with my schizophrenics, most of whom I diagnosed as schizoaffective, and whom I combined in my studies with my depressives, I think they, too, did considerably better than what Naber and Lambert opined -- that medications gave “only limited improvement of psychopathology and quality of life” -- when they commented on the CUtLASS and CATIE studies regarding schizophrenic medication response. 

        About a year after concluding my first study and wanting to be as certain as I could as to the validity of my findings, I ran another one on all my new patients since I ended my first. It might be of value to note, of the 241 in my first study, 159 (65.4%) were either still seeing me when I began my second count a year later or had

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returned at some point before or during it to restart. Considering the nature of my patient population -- the homeless mentally ill living on or near our Skid Row -- this might say something about the worth of my discoveries, as it seems to me to be a fairly high percentage for such clients. 

        In this second nearly yearlong study, I saw almost the same number as the first, 246 vs. 241, with a diagnostic breakdown like the first, but I counted only the new patients to avoid a positive bias from the continuing ones. These, too, made 1 or more return visits which allowed me a reasonable sense of their responses to my regimens. Therefore, I evaluated just the 87 new ones (246 minus 159 of my continuing patients). Nearly 100% suffered depression. This time, I added intermediate response rankings between the 4 in my first to have 7, as I felt 4 resulted in too broad a categorization of outcomes. Of the 87 new ones, 11 compliant patients and 1 noncompliant did not experience any akathisia, leaving 75 (86.2%) who did -- essentially the same percentage as my first study where 90.0% had it. Nine of these 87 were too irregular or unwilling to follow my recommendations to include them, but as before, I was able to determine that 8 of them suffered akathisia and 1 did not, so these 8 were included in the 86.2% whom I deemed to have had it. Eleven compliant patients did not suffer akathisia, so I evaluated 67 for their responses to my treatments -- 87 minus 11 compliant ones without akathisia minus 9 more who were too noncompliant to include.

        I put 34 of the 67 in the ‘excellent’ response group, 10 in a new ‘pretty good to excellent’ grade, 9 in ‘pretty good’, 6 in my new ‘fair to pretty good’ rank, 7 in ‘fair’, 0 in a new ‘poor to fair’ group, and 1 in ‘poor’. I think it was reasonable this time to classify my top 3 groups as successes for a success rate of 79.1%, lower than the 90% success rate in my first study but still comparable and still much better than what we usually see. 

        I do not claim my 2 studies have been properly scientific, but if they are fairly true, these success rates merit further investigation as they are quite exceptional compared to what we presently have! 

        Now to get to that telling and noteworthy finding I mentioned a few paragraphs back, which occurred to the same extent in both my studies, and which were a big surprise for me as I had not thought of looking for this diamond in the rough when I began either of them. 

        To review, in one segment of each study, I evaluated the response to the illness-treating medications, alone, for those patients without any akathisia and therefore in no need of akathisia meds. In my first, the 20 compliant patients without akathisia had a 100% treatment success rate -- 13 with an ‘excellent’ result and 7

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with a score of ‘pretty good’. In my second study, with 11 compliant patients who had no akathisia, 10 of these 11 did very well (90.9%) with 7 ‘excellent’, 3 ‘pretty good to excellent’, and one who did poorly. 

        So, in these two segments, when there was no akathisia and no need for akathisia meds, the direct illness response was very good, indeed! If these findings are true, it says our illness-treating medicines can work very well, alone, without any additions or augmentations -- even better with decreases in the doses of many! 

        I believe I can acceptably sum up these two segments without akathisia. With a total of 31 patients from the two, 20 in the first and 11 in the second, I had success with 30 out of 31, or 96.8%! This says something quite different than our present perception of medication inadequacies which is essentially blind to the impact of akathisia, and which reinforces my contention that our difficulties come from the unrecognized akathisia our meds so overwhelmingly bring with them! 

        So if you feel the frustration of our mediocre success rates, I ask you to consider trying something new. I am hoping to team up with someone who will help me confirm my discoveries. Of course, I know they can be wrong, but I think the chances are very good they are not. I have had too much confirmation from my patients to think otherwise!  

        A final thought: it has occurred to me that, as best as I could tell, of the thousands of papers written on akathisia, none of them have seen it as I do. Though various authors have spoken of its impact on psychosis, as noted by the DSM-IV, IV-TR, and -5-TR, the only reference I saw regarding its impact on depression was my above-cited statement by Van Putten and Marder that, “Akathisia is often experienced as anxiety and depression.” And of course, there are the other disparate symptoms, many or most of which I delineated above which I have consolidated into what I think is a much more complete and important picture of it.

        If I am proven correct, I think it will force us to reconsider most of our diagnostic and treatment practices for our patients. I know by the time I retired, I was doing things very differently compared to what I was taught and then practiced for years. If my ideas are shown to be valid, I think I can safely say it will mean a revolutionary change for the better for our patients as we break away from the treadmill we have been on for so long of ever-increasing doses and alterations and with it, the disappointments we and our patients so often have had to face! 

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        A final word regarding my discoveries: It was not unusual for my patients to say they were feeling ‘so great’ they thought they no longer needed my meds or regimen anymore, which, of course, they did. So I would caution them about this dangerous notion, but sometimes without success.

        I think I gave you enough to digest and hope one or more of you would like to work with me to see if what I have found is true. 

William Drucker, MD.  9/10/23

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