178 replies to this topic

[OneScrewLoose]

@gamesguru (quoting you is past blockquote limit)
Yes, including comorbidities makes perfect sense when you are trying to treat a population, but not necessarily when you are trying to describe a population, especially when you are being as specific as this.

EEGs been approved as a tool in the diagnostic process of adult ADHD. They have been around since the 1920s are relatively cheap, and there's no excuse that they were not used in a study this specific.

 

You still did not address my first point, why there is no group of BPD-only symptoms.

And I wouldn't completely disregard a link between inattention and BPD. I just wouldn't use this study to make it.

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Anyway, since I been gone, man…Oh My.

Anyway, one thing at a time. It doesn't look like ADHD cause it's not ADHD. Correlation doesn't imply causation. Just because someone consistently can't pay attention, doesn't mean they have ADHD. For instance, they could be consistently sleep deprived. If it were ADHD, we would be praising how well a job Adderall is doing, not Lamictal.

 

As far as Bupropion and Strattera, this isn't the NET inhibiting super combo you think it is. Bupropion is a relatively weak DAT inhibitor, and and even weak NET inhibitor.

Let's imagine the NET transporter as a catcher, and its ligand (in this case Strattera), as bunch of pitchers' balls. The catchers are trying to catch the pitchers' balls, and they are coming in fast and hard, as Strattera is an effective NET inhibitor. Now imagine a different situation, the pitchers' balls are Bupropion, and they're coming in pretty weak, deactivating NET at a much slower pace. So what happens when the catchers try to catch both balls? Well, you get something in between. This is why, overall, Bupropion is a competitive antagonist to the NET inhibiting effect of Strattera, lowering it. I don't even run into psychiatrists who grasp this, they think proscribing Bupropion strengthens Adderall, instead of weakening it. However, this is offset by the fact that Bupropion slows down Strattera metabolism. So it kinda evens out.

 

As far as I know, low COMT activity should not affect Concerta, in fact, it should make her more sensitive to it, and given her mood disorder, may make her mood become triggered when taking a DAT inhibitor like methylphenidate (Concerta, Ritalin) or Amphetamines (Dexedrine, Vyvanse, Adderall). I mean, the COMT polymorphisms can be a major part of the issue, and the excess monoamines the produce. One way to directly test this is something called methyldopa, an old blood pressure medication. It prevents the conversion of L-DOPA to Dopamine, balancing out the COMT problems. There are a list of side effects, but a small dose may be all you need to see if you’re onto something.

This post made me tired…

Edited by OneScrewLoose, 24 October 2016 - 04:28 PM.

[jack black]

 

 

 

Let's imagine the NET transporter as a catcher, and its ligand (in this case Strattera), as bunch of pitchers' balls. The catchers are trying to catch the pitchers' balls, and they are coming in fast and hard, as Strattera is an effective NET inhibitor. Now imagine a different situation, the pitchers' balls are Bupropion, and they're coming in pretty weak, deactivating NET at a much slower pace. So what happens when the catchers try to catch both balls? Well, you get something in between. This is why, overall, Bupropion is a competitive antagonist to the NET inhibiting effect of Strattera, lowering it. I don't even run into psychiatrists who grasp this, they think proscribing Bupropion strengthens Adderall, instead of weakening it. However, this is offset by the fact that Bupropion slows down Strattera metabolism. So it kinda evens out.

 

As far as I know, low COMT activity should not affect Concerta, in fact, it should make her more sensitive to it, and given her mood disorder, may make her mood become triggered when taking a DAT inhibitor like methylphenidate (Concerta, Ritalin) or Amphetamines (Dexedrine, Vyvanse, Adderall). I mean, the COMT polymorphisms can be a major part of the issue, and the excess monoamines the produce. One way to directly test this is something called methyldopa, an old blood pressure medication. It prevents the conversion of L-DOPA to Dopamine, balancing out the COMT problems. There are a list of side effects, but a small dose may be all you need to see if you’re onto something.
 

 

thanks for explaining wellbutrin vs strattera issue in the first part. i had to read it a few times, but i think i understand it now.

 

now, the 2nd part need clarification on my part. concerta sort of worked, but made her very uncomfortable and worn out (too much stimulation?).

but here is the part that i fail to understand. if concerta and strattera are both NET inhibitor, why she had bad reaction to one and good to the other? is wellbutrin now the answer? but if so, why did she feel more tired when she stopped wellbutrin for a week?

 

i'm not going to try methyldopa, as it's known to cause depression. she tried propranolol and clonidine before and it made her suddenly very depressed, very dangerous for her with all those attempts.
 

Edited by jack black, 24 October 2016 - 08:42 PM.

[OneScrewLoose]

Because you are simplifying things. Yes, Concerta is indeed a NET inhibitor, but it's main function is by far a DAT inhibitor, having a much stronger affinity for the DAT transporter. Strattera has a negligible affinity for the DAT transporter.

So what you are essentially comparing are two very different drugs. And then there's Bupropion, which is a whole different animal, having mild effects on DAT and NET transporters, as well as a variety of receptors.

You can't just dissect one aspect of a drug in isolation and compare it to another aspect in isolation, and then wonder why they don't work alike. Even very similar drugs, like Amitriptyline and Nortriptyline, can have very different effects in a person. 

[bobitza]

So, gentlemen, i registered just to answer this thread.

First of all, yes, i have a successful story. It seemed like the whole idea of the thread was forgotten. 

So, i was diagnosed about 10 years ago. I've been an alcoholic since i was 14, had my first "breakdown" at about 17-18, got diagnosed at about 20, have been on all sorts of stuff ever since.

What worked 100%, in my opinion: Ketamine
I was on it for about 6 months. It cured my alcoholism, i got back to university, started going to the gym regularly, lost 10kg, got a girlfriend, got socially integrated. Nice, huh?

Good side: all of the above and more
Bad side: illegal, needles, effects last about 24-48 hours so it has to be administered every day

 
What works now: Gabapentin+Trazodone
Good side: Sleep like a baby, i'm not agitated anymore, have a decent life, i'm not depressed most days, no idiotic outbursts (although i'm still quite ready to get into arguments, but i haven't broken a phone in two years. I used to destroy about 7/year).
Bad side: Does nothing for the emotional part of the thing, which is the actual trouble of BPD ("i hate you, don't leave me"). However, if you are single, you won't notice. Also, kind of hits libido and ability to climax. Discovered by accident that this is easily treatable with Alpha Men vitamin complex from MyProtein. I took it for the gym and it gave me boners, so that was a nice surprise.

What really makes things chaotic: alcohol and more so hangovers, coffee and black tea (even decaffeinated, they still make me jumpy), benzodiazepines (rebound rage, extreme levels), piracetam (do not touch that if you have BPD), any kind of withdrawal

At the end of the month i'm starting Aripiprazole (Abilfy) in an atempt to chill with the paranoid stuff that keeps me from having nice relationships. I'll also try to get some Memantine, as i'm curious.

 
LE: There is something that works for the emotional outbursts. Weed. However, it's not a solution, as it will evidently get you high and literally addicted. The next day will be even more difficult not to rage. Nonetheless, it works in minuscule amounts. I actually get out of the zone before getting high. I'll try CBD oil soon enough and see how that goes. The thing is, when i'm raging in an emotional context, it's more or less a psychotic experience. You simply forget who the person is, what you feel for her, etc. One small doobie and it's like coming out of a dream. Mind you, this type of state (semi-psychotic) is long-lasting and it can last until actually breaking up. I am absolutely certain that people live their whole lives in this dubious state. So yeah, if you have trouble, just smoke a doobie and it's like waking up from a dream. Amazing, isn't it?

Edited by bobitza, 11 November 2016 - 09:23 PM.

[gamesguru]

found out why olanzapine and risperidone might work: dopamine.  ginger doesn't share this afaik, but ginseng, bee pollen and NAC might.  (however curcumin also restores stress-induced 5-ht1a downregulation, prevents stress-induced 5ht7 expression, inhibits release of prefrontal glutamate, reverses corticosterone-induced PC12 toxicity, rescues vasopressin V2 receptor mutants, and downregulates the production of cytokines/interferons)

Could curry banish bad memories? Turmeric prevents fear being stored in the brain, scientists claim

• Scientists found that curcumin, a compound found in the root of the Indian spice, prevented new fear memories being stored in the brain
• It also removed pre-existing fear memories, researchers found
• Scientists hope findings will contribute to the development of treatments for psychological conditions such as post-traumatic stress disorder

By Sophie Freeman For Mailonline

 

A spice commonly used in curry could help erase bad memories, according to a study.

Curcumin, a bright-yellow compound found in the root of the Indian spice turmeric, prevented new fear memories being stored in the brain, and also removed pre-existing fear memories, researchers found.

It is hoped that the findings will help develop treatments for people suffering with psychological disorders.

Psychologists from The City University of New York trained rats to become scared when they heard a particular sound. Scientists assumed the creatures were frightened when they froze.

Hours later, when the same sound was played to the rats, those who had been given ordinary food froze.

Yet the rats fed the curcumin-rich diet didn’t freeze, suggesting their fearful memories had been erased.

Professor Glenn Schafe, who led the study, said: ‘This suggests that people suffering from post-traumatic stress disorder and other psychological disorders that are characterised by fearful memories may benefit substantially from a curcumin-enriched diet.’

Memories are formed in the brain as new connections between neurons.

They are initially fragile, but gradually stabilise in the brain as they are put into long-term storage - a process known as consolidation.

memories are recalled they also temporarily destabilise in the brain, becoming like new memories for a while.

‘If nothing happens, those destabilised fear memories get put back into long-term storage. In other words, they restabilise, or reconsolidate,’ explained Professor Schafe.

‘But we’ve learned that we can go into the brain during that destabilisation window and prevent those fear memories from reconsolidating.

+2

Memories are formed in the brain as new connections between brain cells of neurons (pictured). They are initially fragile, but gradually stabilise in the brain as they are put into long-term storage

‘Effectively, we can erase them. And that appears to be what we’ve done with a curcumin-enriched diet.’

Curcumin is known to have an anti-inflammatory effect on the body, and this may be how it works on fearful memories, said Professor Schafe.

‘Inflammatory processes have been implicated in a wide range of diseases ranging from allergies to cardiovascular disease to Alzheimer’s,’ he said.

‘Inflammation has also been implicated in psychological disorders such as depression, anxiety and post-traumatic stress disorder.

‘Some of these same inflammatory pathways have also been implicated in memory formation, so it all fits.

 

... COULD TURMERIC PREVENT DEMENTIA TOO?

Another recent study found that a compound in turmeric may also hold the key to repairing the brains of people suffering with neurodegenerative diseases such as Alzheimer's.

In laboratory tests, the aromatic turmerone promoted the proliferation of brain stem cells and their development into neurons.

It is hoped that the findings will help scientists develop treatments for conditions in which brain cells are lost, including Alzheimer's and stroke.

The scientists examined the effect of aromatic turmerone on endogenous neutral stem cells (NSCs) found within adult brains.

NSCs go on to develop into neurons, and play an important role in recovery from neurodegenerative diseases. 

Lead researcher Dr Adele Rueger, from the Institute of Neuroscience and Medicine in Julich, Germany, said: 'While several substances have been described to promote stem cell proliferation in the brain, fewer drugs additionally promote the differentiation of stem cells into neurons, which constitutes a major goal in regenerative medicine.

'Our findings on aromatic turmerone take us one step closer to achieving this goal.' 

‘But we need more studies to examine this further.’

 

It is not yet fully understood how curcumin impairs fear memories while sparing other types of memories, Professor Schafe said, but it is known that different types of memory systems encode different types of memories.

So, the memory of the event could still be there, but without the memory of the fear, removing the frightening aspect of it.

Previous studies have found that the spice may also be useful in the treatment of cancer, heart disease and arthritis, as well as having an anti-depressant effect.

 

Neuroreport. 2010 Dec 29; 21(18): 1172–1176.

Dopamine is released in the striatum during human emotional processing

Rajendra D. Badgaiyan

Abstract

Since the role of dopamine in human emotional processing is unclear, we used a dynamic molecular imaging technique to examine whether striatal dopamine is released during processing of negative emotions in healthy volunteers. After volunteers have received an intravenous injection of a dopamine receptor ligand ¹¹C-raclopride, they were asked to perform a task that elicited negative emotions. During task performance the ligand concentration was measured dynamically using a positron emission tomography camera. Analysis of the data indicated that the task performance is associated with dopamine release in the head of caudate and in the dorsal putamen bilaterally.

The emotional task was similar to the one we used to study extrastriatal dopamine in an earlier experiment [1]. It consisted of a Control and a Test condition. In the Control volunteers were shown a list of emotionally neutral words (e.g., PARK, PENCIL) and asked to indicate the intensity of emotion elicited by each word in a scale of 1-3 (1=no emotion; 3=intense emotional arousal). At 25 min after the ligand injection, unbeknownst to volunteers, task was changed from Control to Test condition.

The results of this experiment complement and extend our earlier observation of increased dopamine release in the amygdala, prefrontal cortex and medial temporal lobe during processing of negative emotions in healthy volunteers [1].

 

J Biomed Sci. 2010; 17(1): 43.

Curcumin modulates dopaminergic receptor, CREB and phospholipase c gene expression in the cerebral cortex and cerebellum of streptozotocin induced diabetic rats

T Peeyush Kumar,¹Sherin Antony,¹G Gireesh,¹Naijil George,¹ and CS Paulose1

Abstract

Curcumin, an active principle component in rhizome of Curcuma longa, has proved its merit for diabetes through its anti-oxidative and anti-inflammatory properties. This study aims at evaluating the effect of curcumin in modulating the altered dopaminergic receptors, CREB and phospholipase C in the cerebral cortex and cerebellum of STZ induced diabetic rats. Radioreceptor binding assays and gene expression was done in the cerebral cortex and cerebellum of male Wistar rats using specific ligands and probes. Total dopaminergic receptor binding parameter, B_max showed an increase in cerebral cortex and decrease in the cerebellum of diabetic rats. Gene expression studies using real time PCR showed an increased expression of dopamine D1 and D2 receptor in the cerebral cortex of diabetic rats. In cerebellum dopamine D1 receptor was down regulated and D2 receptor showed an up regulation. Transcription factor CREB and phospholipase C showed a significant down regulation in cerebral cortex and cerebellum of diabetic rats. We report that curcumin supplementation reduces diabetes induced alteration of dopamine D1, D2 receptors, transcription factor CREB and phospholipase C to near control. Our results indicate that curcumin has a potential to regulate diabetes induced malfunctions of dopaminergic signalling, CREB and Phospholipase C expression in cerebral cortex and cerebellum and thereby improving the cognitive and emotional functions associated with these regions. Furthermore, in line with these studies an interaction between curcumin and dopaminergic receptors, CREB and phospholipase C is suggested, which attenuates the cortical and cerebellar dysfunction in diabetes. These results suggest that curcumin holds promise as an agent to prevent or treat CNS complications in diabetes.

 

Neuropsychopharmacology. 2004 Jun;29(6):1029-39.

Dopamine dysfunction in borderline personality disorder: a hypothesis.

Friedel RO¹.

Abstract

Research on the biological basis of borderline personality disorder (BPD) has focused primarily on the serotonin model of impulsive aggression. However, there is evidence that dopamine (DA) dysfunction may also be associated with BPD. Pertinent research and review articles, identified by Medline searches of relevant topics, books, references from bibliographies, and conference proceedings from 1975 to 2003, were reviewed. Evidence of DA dysfunction in BPD derives from the efficacy of traditional and atypical antipsychotic agents in BPD, and from provocative challenges with amphetamine and methylphenidate of subjects with the disorder. In addition, human and animal studies indicate that DA activity plays an important role in emotion information processing, impulse control, and cognition. The results of this review suggest that DA dysfunction is associated with three dimensions of BPD, that is, emotional dysregulation, impulsivity, and cognitive-perceptual impairment. The main limitation of this hypothesis is that the evidence reviewed is circumstantial. There is no study that directly demonstrates DA dysfunction in BPD. In addition, the therapeutic effects of antipsychotic agents observed in BPD may be mediated by non-DA mechanisms of action. If the stated hypothesis is correct, DA dysfunction in BPD may result from genetic, developmental, or environmental factors directly affecting specific DA pathways. Alternatively, DA dysfunction in BPD may be a compensatory response to alterations in the primary neural systems that control emotion, impulse control, and cognition, and that are mediated by the brain's main neurotransmitters, glutamate, and GABA, or in one or more other neuromodulatory pathways such as serotonin, acetylcholine, and norepinephrine.

Edited by gamesguru, 12 November 2016 - 03:23 PM.

[jack black]

So, gentlemen, i registered just to answer this thread.

First of all, yes, i have a successful story. It seemed like the whole idea of the thread was forgotten. 
 

 

Thanks a lot for jumping all the hoops to respond. The reason the thread lost its focus is because I came to the conclusions that the subject in question probably doesn't have BPD in the first place and instead maybe Asperger syndrome (AS), as AS can mimic BPD in women.

 

But your info is very interesting, as in all that discussion, we didn't talk about serotonin much. My understanding is trazodone works mostly by antagonizing 5HT receptors, right?

 

The subject actually took a very low dose of 5HT2aR inhibitor (serzone) and that made her paradoxically extremely sedated. On the other hand, large doses of another 5HT2aR inhibitor (inositol) were reported to do nothing noticeable. I was stumped by those results and didn't pursue them any further.

 

You are right about weed. The subject reported nice relaxation, but this is not locally legal yet.

There was some minimal response to the legal weed alternative: Kanna, but it's not good enough.
 

[bobitza]

Hi, Jack!

So, about the Trazodone, truth be told i've *almost* stopped caring how things do what they do. Theory is one thing, effectiveness is quite another. While the lack of an antidepressant is quite evident, as i would be extremely emotive, but more in an internalized pain way, like susceptibility to the feeling of wanting to cry (?! i'm a grown man), i can't say that it does too much for me except remove that kind of cry baby feeling.

Trazodone is a really tricky thing. It's a tetracyclic, and it's main metabolite is meta-Chlorophenylpiperazine (mCPP). While Trazodone itself has mild sedative properties, mCPP is the chemical of hell, highly stimulant. Basically, i think it's like being permanently on speed. I am now on a low dose, 100mg, as i've recently had a really terrible episode of mania and agitation which felt, like i said, like being on speed for a month. I am almost certain that it was just a fluke and i took something which was metabolized by the same enzyme. However, that kind of scared me, although this happened one year after starting it. I can actually feel sort of a withdrawal, like i haven't smoked all day, which starts around 4 PM each day (i actually take extended-release tablets at bedtime). I've looked at the plasma concentration levels graph for mCPP and i think 4 PM is when the levels drop, hence the symptoms.

I've stopped the Gabapentin about two weeks ago, as i felt it was making me depressed by itself. Outcome: agitation during the day, permanent desire to smoke, lack of pleasure from smoking, permanently nibbling on stuff, going aimlessly around the house, serious deterioration of hand writing quality, restless legs. The Trazodone did it's job for about a week and put me to sleep at night, but after that i struggled, so in the end i restarted it. Boy, what a diffference.

At this point, i tend to give Gabapentin the winning cup. I am on a low dose (300mg) which i take at night. Now that i think about it, my 4 PM agitation could be caused by Gabapentin levels dropping as well, as it has a very short half-life, around 6 hours. I could, of course, take another pill in the morning and be zen all day, but i like my erections. I haven't tried going higher with dosage as i am quite satisfied by 300mg, but that's an experiment which starts tomorrow. 

As you can actually see, this post is much more disorganised than my first post. Well, it's 6 PM and my agitation kicked in. 

At this point, my simplistic theory, without caring too much about, let's say, different binding sites on receptors, is that the Glutamate is overpowering the GABA. By increasing GABA levels, things even out and i can function more or less properly. But, i dare to call this "speedballing". The solution, in my opinion is to lower Glutamate activity, which i hope will be done with Rapastinel (GLYX-13) in a few years. I'm also hunting for the Esketamine trial (which is in phase III now, like Rapastinel; what a time to be alive, eh?)

Please note that Gabapentin, while *perfectly* handling agitation and, to an extent, impulsivity, does nothing for the psycho-paranoid symptoms. Only weed gets me out of that. The good thing about Gabapentin is that being on such a low dosage compared to, let's say, neuropathic pain sufferers, i can always double, triple or even quadruple my dosage in the event that i would need to be all drooly. I've read that people get high on it, but i'm way past that. I never bothered.

Cheers! 

[Mind_Paralysis]

May I suggest an alternative to weed?

 

A Swedish scientist called Predrag Petrovic is studying the disease from a neurological fMRI and PET-scan point of view, and believes that it's a disorder similar to ADHD - aka, mostly genetic and involving specific parts of the brain. (the PFC and Amygdala)

 

He also happens to be a researcher regarding Paracetamol - the metabolite AM404 has a peculiar way of inhibiting pain - both physical and emotional, it turns out.

 

It's an SCRI - Selective Cannabinoid Reuptake Inhibitor.

 

Focusing its effects on the ACC, wherein emotional and physical pain is sorted out into other parts of the brain for interpreting.

 

 

In theory, Paracetamol actually inhibits ALL emotion - which gives it potential for the treatment of a disorder involving nothing but emotion.

 

So, pop Tylenol - but add Milk Thistle and something glutathion-enhancing, so you don't get liver problems.

 

 

Or...

 

Join the AM404 group buy I'm planning.

[bobitza]

May I suggest an alternative to weed?

 

A Swedish scientist called Predrag Petrovic is studying the disease from a neurological fMRI and PET-scan point of view, and believes that it's a disorder similar to ADHD - aka, mostly genetic and involving specific parts of the brain. (the PFC and Amygdala)

 

He also happens to be a researcher regarding Paracetamol - the metabolite AM404 has a peculiar way of inhibiting pain - both physical and emotional, it turns out.

 

It's an SCRI - Selective Cannabinoid Reuptake Inhibitor.

 

Focusing its effects on the ACC, wherein emotional and physical pain is sorted out into other parts of the brain for interpreting.

 

 

In theory, Paracetamol actually inhibits ALL emotion - which gives it potential for the treatment of a disorder involving nothing but emotion.

 

So, pop Tylenol - but add Milk Thistle and something glutathion-enhancing, so you don't get liver problems.

 

 

Or...

 

Join the AM404 group buy I'm planning.

I'm starting Abilify at the end of the month, which i hope to kill the paranoid symtomps. However, i can't say that i've felt anything with paracetamol. I actually had two today for some mild pain. Also, i believe N-acetylcysteine is a good hepatoprotector if handling large doses of paracetamol. I've actually bought some NAC last week as i've read about good results in treating schizophrenia when combined with sarcosine. Bought some of that as well. Sadly, my kidneys are not tolerating the NAC. At all. I'm still taking the sarcosine, but my girlfriend already got fed up so i'm not really having any issues to deal with as she dumped me so i'm all nice and chill now. Weird bloody thing, BPD, you can either be happy by yourself (which is not possible in the long run, because we're social beings) or be a volcano with somebody else. Chasing my own tail, i'd say. I asked her to wait until the end of the month, when i get the Abilify, and she can dump me afterwards, but i don't think i've convinced her 

[bobitza]

UPDATE:

I wrote a really long post and Chrome crashed before i coud post it. I lost desire to re-write it, but here's a short version:

HOLY SHIT I'VE FOUND A "CURE"

 

ABILIFY (Aripiprazole)

[jack black]

UPDATE:

I wrote a really long post and Chrome crashed before i coud post it. I lost desire to re-write it, but here's a short version:

HOLY SHIT I'VE FOUND A "CURE"

ABILIFY (Aripiprazole)

I never researched this class of drugs for this issue, but abilify's stimulation of 5ht1a and 5ht2c and blocking the other 5ht receptors is ideal for targeting depression and anxiety without SSRI's side effects.

Good to know it works in BPD. Thanks for posting and tell us more about side effects.

[bobitza]

Hello, everybody!

I finally got the time to come back with  proper update. I'm not sure this is allowed, but i will link to another forum where i've kept the story updated. i'll copy/paste here my evolution as well, in case MOD decides it's not ok to have the link (sorry if not allowed, just trying to help).

https://www.mentalhe...read148385.html ->My thread

My story, as it went:

07-12-16, 13:17

 Abilify is the best thing i've ever had for my BPD

 

So, i've recently started Abilify 5mg for my BPD. I also have Gabapentin 300mg daily as a mood stabilizer.

Like everybody, i've been on "everything" up until now.

Nothing compares to it. It's incredibly effective and works from the 3rd day. It's really that AMAZING.

High energy, good libido, good mood, good social involment, etc etc etc etc. 

I will, however, ask my doc to up my dose to 10mg, i feel that more can be gained.

Feel free to ask anything.

GO GET SOME FROM YOUR DOC!


17-12-16, 13:28

Follow-up

So, dear people, i'm now a month into the Abilify treatment. 

I still hold my initial opinion, this is the best thing i've ever took for my BPD.

The hypo-mania has subsided and my sleeping is slowly returning to nomal. I still wake up early and refreshed, so hurrah for that, as i am finally able to get to work without being late, which i never could. 

My surroundings are still clean and semi-tidy, but not like in the first week when i was a hyper efficient robot. However, i put this on the caffeine intake i very courageously had. It might seem counter intuitive to treat agitation with coffee, but it switched agitation to elation, so that was way easier to handle as a side effect.

I gained two kilos, but i also take Gabapentin for the restlesness. My legs are still dancing all day but hey, it's a small price to pay. I'm not even sure it's fat or muscle, because i upped my exercising about 5-fold and went on a high protein diet. 

I haven't had a single rage episode. I haven't lost control. I haven't went ballistic or psychotic on anyone. PEACHY!

All in all, i'm still waiting to see how this goes on the long run. I'm on a low dose (5mg) but i did try 10mg to see if it does something more, but other than additional agitation, couldn't say as i'm currently in a semi-protected environment so i'm waiting to go "out there". I did have a very intense meeting with my boss and i absolutely thrashed him (in the most diplomatic manner). I was running on overdrive and felt like i could win a debate championship. Also, anxiety is gone and i didn't get cotton muouth or anything like that. Before, having to phone call was horrendous for my anxiety. No more.

So, i'm good, and i won't quit it. It's been wonderful up until now. I feel alive again.

Also, i'm seeing my psychiatrist in a few days to see what can be done for the restlessness, except Gabapentin, which at high doses kind of gets me high, and that's not what i'm looking for. I also tried NAC (N-Acetycysteine) which seemed to yield good results and valerian tincture, which also seemed to do the job. All of these combined send me to a nice sleep.

I've went through clinical studies and my next discussion with the psychiatrist will be about getting some Mirtazapine (low dose) and switching to Gabapentin Enacarbil (same stuff, but much higher bio-availability which should be easier on my kidneys) or Pregabalin.

20-12-16, 07:41

GRAPHS HERE<-----

 

Absolute low point for weight is 74.9. You'll need this to make sense of it. The line without points is the trend.

 

I have very little time, as i have to catch a plane, but i'll come back with more explanations. However, these are my weight and sleep charts. The weight chart is obvious. The sleep charts, not so much, but they aren't too cryptic either. Basically, it shows what Abilify does to me, in an objective manner.

 

Abilify is highly stimulant. That's why it's important to start low and slow, i'd reccomend 2mg, because for me 5mg was a bit over the top. I've gotten used to it and now it seemes to be the right dose, but boy, was i agitated in the first week. However,please keep in mind that i also take Ketoprofen for pain, which is metabolised by the same enzyme, so probably that made my Abilify serum concentration to spike, so 5mg shoud be a good dose to hover around to for other people. Just start slow. No matter what your doctor says, always start slow. Just break the pill in half and you get half the dose. Break it in quarters, and it's even better. Do this for a week, and you'll be fine. I can't imagine how it would have been if i would have follow my doctor's advice to start with 10mg. I pressume i would have quit treatment on the first day.

 

I'll come back with more details. Please study the graphs!

01-02-17, 11:03
 

UPDATE

So, it's now been about 3 months since i've started Abilify. 

THANK GOD!

1. All negative effects are a sign of overmedication or going too strong to fast. Starting with 10mg will make you VERY agitated and hypomanic. I started with 5mg and my first week was hell. I wouldn't start again with more that 1-2mg. Every time i felt like i was going mad from akathisia, it was just too high of a dose. Lowered it and, voila! All but gone!

2. I keep my statement that Abilify is the best thing i've ever had for my BPD but it does not work alone. You need things to counteract side effects. I take Gabapentin and Trazodone (at night, minute doses, 1/6-1/12 pill of 150mg)

3. I haven't had a single meltdown until now.

4. I haven't had a single "bad" argument. I always keep civil and i managed to say once "that was very rude of you to say". That's a great achievement as i would have never imagined myself saying that. My modus operandi was "WTF DID YOU SAY I'LL ### YOU UP". No more of that.

5. Going from 5mg to 10mg Abilify let me to a state of anhedonia. No pleasure. No interests. No excitement. I lowered the dose and here i am, human again.

6. I've tried Mirtazapine to calm down the akathisia. FAILED. It's a horrible substance which does no good for me. I would reccomend against it.

7. I've restarted Trazodone for sleep. As i said, minute amounts paired with Gabapentin at night and i sleep like a baby. Plus, being the weird substance that it is (a hypnotic before metabolization, a stimulant after), the next day i'm all good.

8. Things are not perfect. I'm having trouble measuring my mini-doses so not every day is the same, but it's good.

9. Marijuana, as useful as it is to me, has fallen in slight disgrace. More than one toke every two days and i fall into lethargy. Again, same pattern as before, less is more.

10. The hypomania faded (bu-hu, i enjoyed it)

11. I still have restless legs

12. Drugs don't do the same thing anymore (from Abilify). Alcohol lost it's buzz. I drink and get sleepy. Leave early from the party kind of man lately.

13. Anxiety is all but gone. I can now talk on the phone! (for all of you who don't have a problem with this, it might be trivial. I've always been terrorised of having to to a phone call, even to order pizza)

14. Fear less, experiment more. Switch doctors, go dancing, o whatever, be free.

[Mind_Paralysis]

Hello, everybody!

I finally got the time to come back with  proper update. I'm not sure this is allowed, but i will link to another forum where i've kept the story updated. i'll copy/paste here my evolution as well, in case MOD decides it's not ok to have the link (sorry if not allowed, just trying to help).

https://www.mentalhe...read148385.html ->My thread

My story, as it went:

07-12-16, 13:17

 Abilify is the best thing i've ever had for my BPD

 

So, i've recently started Abilify 5mg for my BPD. I also have Gabapentin 300mg daily as a mood stabilizer.

Like everybody, i've been on "everything" up until now.

Nothing compares to it. It's incredibly effective and works from the 3rd day. It's really that AMAZING.

High energy, good libido, good mood, good social involment, etc etc etc etc. 

I will, however, ask my doc to up my dose to 10mg, i feel that more can be gained.

Feel free to ask anything.

GO GET SOME FROM YOUR DOC!


17-12-16, 13:28

Follow-up

So, dear people, i'm now a month into the Abilify treatment. 

I still hold my initial opinion, this is the best thing i've ever took for my BPD.

The hypo-mania has subsided and my sleeping is slowly returning to nomal. I still wake up early and refreshed, so hurrah for that, as i am finally able to get to work without being late, which i never could. 

My surroundings are still clean and semi-tidy, but not like in the first week when i was a hyper efficient robot. However, i put this on the caffeine intake i very courageously had. It might seem counter intuitive to treat agitation with coffee, but it switched agitation to elation, so that was way easier to handle as a side effect.

I gained two kilos, but i also take Gabapentin for the restlesness. My legs are still dancing all day but hey, it's a small price to pay. I'm not even sure it's fat or muscle, because i upped my exercising about 5-fold and went on a high protein diet. 

I haven't had a single rage episode. I haven't lost control. I haven't went ballistic or psychotic on anyone. PEACHY!

All in all, i'm still waiting to see how this goes on the long run. I'm on a low dose (5mg) but i did try 10mg to see if it does something more, but other than additional agitation, couldn't say as i'm currently in a semi-protected environment so i'm waiting to go "out there". I did have a very intense meeting with my boss and i absolutely thrashed him (in the most diplomatic manner). I was running on overdrive and felt like i could win a debate championship. Also, anxiety is gone and i didn't get cotton muouth or anything like that. Before, having to phone call was horrendous for my anxiety. No more.

So, i'm good, and i won't quit it. It's been wonderful up until now. I feel alive again.

Also, i'm seeing my psychiatrist in a few days to see what can be done for the restlessness, except Gabapentin, which at high doses kind of gets me high, and that's not what i'm looking for. I also tried NAC (N-Acetycysteine) which seemed to yield good results and valerian tincture, which also seemed to do the job. All of these combined send me to a nice sleep.

I've went through clinical studies and my next discussion with the psychiatrist will be about getting some Mirtazapine (low dose) and switching to Gabapentin Enacarbil (same stuff, but much higher bio-availability which should be easier on my kidneys) or Pregabalin.

20-12-16, 07:41

GRAPHS HERE<-----

 

Absolute low point for weight is 74.9. You'll need this to make sense of it. The line without points is the trend.

 

I have very little time, as i have to catch a plane, but i'll come back with more explanations. However, these are my weight and sleep charts. The weight chart is obvious. The sleep charts, not so much, but they aren't too cryptic either. Basically, it shows what Abilify does to me, in an objective manner.

 

Abilify is highly stimulant. That's why it's important to start low and slow, i'd reccomend 2mg, because for me 5mg was a bit over the top. I've gotten used to it and now it seemes to be the right dose, but boy, was i agitated in the first week. However,please keep in mind that i also take Ketoprofen for pain, which is metabolised by the same enzyme, so probably that made my Abilify serum concentration to spike, so 5mg shoud be a good dose to hover around to for other people. Just start slow. No matter what your doctor says, always start slow. Just break the pill in half and you get half the dose. Break it in quarters, and it's even better. Do this for a week, and you'll be fine. I can't imagine how it would have been if i would have follow my doctor's advice to start with 10mg. I pressume i would have quit treatment on the first day.

 

I'll come back with more details. Please study the graphs!

01-02-17, 11:03
 

UPDATE

So, it's now been about 3 months since i've started Abilify. 

THANK GOD!

1. All negative effects are a sign of overmedication or going too strong to fast. Starting with 10mg will make you VERY agitated and hypomanic. I started with 5mg and my first week was hell. I wouldn't start again with more that 1-2mg. Every time i felt like i was going mad from akathisia, it was just too high of a dose. Lowered it and, voila! All but gone!

2. I keep my statement that Abilify is the best thing i've ever had for my BPD but it does not work alone. You need things to counteract side effects. I take Gabapentin and Trazodone (at night, minute doses, 1/6-1/12 pill of 150mg)

3. I haven't had a single meltdown until now.

4. I haven't had a single "bad" argument. I always keep civil and i managed to say once "that was very rude of you to say". That's a great achievement as i would have never imagined myself saying that. My modus operandi was "WTF DID YOU SAY I'LL ### YOU UP". No more of that.

5. Going from 5mg to 10mg Abilify let me to a state of anhedonia. No pleasure. No interests. No excitement. I lowered the dose and here i am, human again.

6. I've tried Mirtazapine to calm down the akathisia. FAILED. It's a horrible substance which does no good for me. I would reccomend against it.

7. I've restarted Trazodone for sleep. As i said, minute amounts paired with Gabapentin at night and i sleep like a baby. Plus, being the weird substance that it is (a hypnotic before metabolization, a stimulant after), the next day i'm all good.

8. Things are not perfect. I'm having trouble measuring my mini-doses so not every day is the same, but it's good.

9. Marijuana, as useful as it is to me, has fallen in slight disgrace. More than one toke every two days and i fall into lethargy. Again, same pattern as before, less is more.

10. The hypomania faded (bu-hu, i enjoyed it)

11. I still have restless legs

12. Drugs don't do the same thing anymore (from Abilify). Alcohol lost it's buzz. I drink and get sleepy. Leave early from the party kind of man lately.

13. Anxiety is all but gone. I can now talk on the phone! (for all of you who don't have a problem with this, it might be trivial. I've always been terrorised of having to to a phone call, even to order pizza)

14. Fear less, experiment more. Switch doctors, go dancing, o whatever, be free.

 

11.  That's a bit curious actually... seeing as you're on both Abilify and Gabapentin - the D2 and D3 -partial agonism from Aripiprazole (abilify) is, as you have already noticed, actually QUITE strong...! There have been reports of hypersexuality and gambling as a result of it - much like with other D3-agonists.

 

And then there's Gabapentin - which is also, much like dopamine-agonists, is a very effective treatment of restless legs.

 

However, I think I know why you have restless legs anyway - the Histamine-antagonism of Trazodone, as well as the Alpha-antagonism of Abilify is what's messing with your RLS.

 

Both histamine-agonism and Alpha-agonism was recently discovered to be one of the ways which MODAFINIL actually affects seizures, lowering them - and I have something called PLMD - Periodic Limb Movement Disorder - it makes my arms and legs flail while I sleep (that's why I don't get deep sleep, and am hence a wreck).

 

PLMD is related to RLS and seems to have a crossover when it comes to the treatments - except for the mineral-supplementation which sometimes helps RLS - it's completely useless for PLMD, has no effect whatsoever.

 

I get tons better symptoms from Pramipexole, Gabapentin and Modafinil - and going with all of this, I'd say it's the Alpha-antagonism of Abilify which gives you the most trouble here - since at low-dose, Trazodone is mostly a 5HT2a -antagonist, and not a Histamine-antagonist.

 

I'd recommend simply adding a bit of Gabapentin at night as well - maybe a 150 mg? That could be all you need to decrease the RLS.

 

Already being on a D-agonist with Aripiprazole makes it difficult to add any of the regular D-agonists to your regimen, so I'd go with some more Gaba-P for the night instead.

[Lia-chan]

11.  That's a bit curious actually... seeing as you're on both Abilify and Gabapentin - the D2 and D3 -partial agonism from Aripiprazole (abilify) is, as you have already noticed, actually QUITE strong...! There have been reports of hypersexuality and gambling as a result of it - much like with other D3-agonists.

 

And then there's Gabapentin - which is also, much like dopamine-agonists, is a very effective treatment of restless legs.

 

However, I think I know why you have restless legs anyway - the Histamine-antagonism of Trazodone, as well as the Alpha-antagonism of Abilify is what's messing with your RLS.

 

Both histamine-agonism and Alpha-agonism was recently discovered to be one of the ways which MODAFINIL actually affects seizures, lowering them - and I have something called PLMD - Periodic Limb Movement Disorder - it makes my arms and legs flail while I sleep (that's why I don't get deep sleep, and am hence a wreck).

 

PLMD is related to RLS and seems to have a crossover when it comes to the treatments - except for the mineral-supplementation which sometimes helps RLS - it's completely useless for PLMD, has no effect whatsoever.

 

I get tons better symptoms from Pramipexole, Gabapentin and Modafinil - and going with all of this, I'd say it's the Alpha-antagonism of Abilify which gives you the most trouble here - since at low-dose, Trazodone is mostly a 5HT2a -antagonist, and not a Histamine-antagonist.

 

I'd recommend simply adding a bit of Gabapentin at night as well - maybe a 150 mg? That could be all you need to decrease the RLS.

 

Already being on a D-agonist with Aripiprazole makes it difficult to add any of the regular D-agonists to your regimen, so I'd go with some more Gaba-P for the night instead.

 

 

I totally agree with you, it seems that Mirtazapine SEVERLY worsens worsens both of my RLS and PLMD so I have to take eitheir Bromocriptine or Pramipexole occasionally and when I get nervous it worsens both of my tics (Finger skin biting and piercing playing) and RLS. My mom also has the same problem and my dad. I was taking iron supplement for a month and it's really didn't helped my RLS ;(, pramipexole and bromocriptine were the best drugs so far, that helped with my symptoms, at least I don't have to look like an idiot when I talk to someone, but tics are still all there and it's very annoying that I forget every time about that I have troubles with them and I can't just keep off myself from playing with piercing or anything else in my hands, lol.

[dramachiavellian]

I have a feeling that this is going to be an excessively long post, but there is, in my opinion, a number of factors that have been overlooked in this thread thus far.

 

Approximately a year ago, I was diagnosed with Histrionic Personality Disorder. Subsequent psychiatric evaluations have expanded this diagnosis to include Borderline, Avoidant and possible Narcissistic traits. Emotionally, I suffer from outrageously extreme anhedonic boredom interspersed with very occasional outbursts of excitability, paranoia, anxiety, despondence and, more commonly, spiteful rage.

 

Defining any personality disorder as either a purely inherent neurodevelopmental aberration or a purely social phenomenon is categorically erroneous. Underpinning every single thought, emotion and action is a neurochemical impulse. While traits of personality disorders can often be traced back to childhood or even birth, neuroplasticity in response to environmental influences can attenuate or exacerbate these traits - this is why personality disorders are rarely diagnosed before the patient is 18 years old.

 

Because of this, the abnormalities in brain structure associated with personality disorders are not proof that these disorders are neurodevelopmental rather than psychological or even social. Personality Disorders and completely healthy brain function are 100% mutually exclusive. Furthermore, my personal stance on this chicken-and-egg debate is: who cares? If a neurological aberration is present, it's present. If it's not, it's not. The only plausible way of gaining insight as to how Personality Disorders are manifest would be a longitudinal case study. Considering the topic of this thread is about ameliorating the symptoms of an already existing Personality Disorder, any discussion on their formation is superfluous (albeit interesting).

 

The possibility of misinformation exists in the apparently beneficial use of Piracetam as a modulator of acetylcholine transmission. The exact mechanism of action by which Piracetam exerts its effects is still largely unknown. That being said, theorists tend toward the idea that it raises levels of acetylcholine, which would contradict its apparent reduction of emotional lability in Borderline patients (if the acetylcholine model of emotional regulation carries any scientific credibility). The fact that evidence exists for both elevated acetylcholine levels and dopamine dysfunction in Borderline patients suggests that this model is indeed credible, due to the interplay between these two neurotransmitters.

 

It must be noted that Aripiprazole, or Abilify, is FDA-approved for the treatment of Borderline Personality Disorder. I'm glad to see that it brought about such a high degree of remission for bobitza. With other patients, this medication has been less than forgiving. My personal opinion is that it would be wise to keep the discussion going on how this condition can be treated.

 

Before I offer my own contribution to the discussion, I have to express my shock at the unethical way in which StinkorNinjor attempted to coerce his "dashing young lady" into taking a concoction of substances, which even StinkorNinjor himself now believes may have worsened her disorder. Considering the fact that 1 in 10 Borderline patients successfully commit suicide, I was surprised that nobody spoke up about this presumptuous and dangerous malpractice. Your "dashing young lady" may have accused you of attempting to lobotomise her. I, on the other hand, accuse you of using your own girlfriend as a lab-rat for your ill-conceived and flawed hypotheses, then promptly attempting to use her irrationality to cover up your tracks. I'm aware that overt accusations are impolite, but when I take your immoral  behaviour into account, this is about as diplomatic as I can get - considering my feelings on the matter.

 

Now, to my actual contribution on the topic at hand: supplements and compounds that may alleviate distress caused by BPD. This is a list of compounds that I'm going to take myself, so any effects they have will be brought to you in real time

 

Selegiline: I know it's been mentioned before, but Selegiline actually elevates levels of Acetylcholinesterase in addition to its primary action as a MAO-B inhibitor. This presents the possibility of a triple-threat to Borderline Personality Disorder: lowered levels of Acetylcholine, elevated levels of Dopamine, plus a slower return to homeostasis when compared to DRIs and Anticholinergics.

 

Memantine/Amantadine: noncompetitive NMDA antagonism regulates glutamate levels. Also, alpha-7 nicotinic receptor antagonism might be sustained for a longer period of time when combined with Selegeline's effect on Acetylcholinesterase. However, Memantine has a stronger dissociative effect than Amantadine. Dissociative episodes are endemic to Borderline Personality Disorder, so Amantadine will be used as a second-line treatment in the event that Memantine exacerbates pathological dissociation.

 

NSI-189: This one might be wishful thinking, as I'm only willing to invest in it if I'm 100% sure that I'm going to receive the genuine product. The preliminary studies on rapid hippocampus growth - and the anecdotal evidence of long-term shifts in emotional processing - suggest that this compound may not just treat, but could even cure Borderline Personality Disorder. I'm aware of the boldness of this statement, as well as the unlikeliness of its validity, but the profound effects of NSI-189 on the limbic system show a lot of promise for counteracting the excessive negative rumination lying at the centre of all Personality Disorder types.

 

Piracetam or Tianeptine: this would only be used as an adjunct if Memantine causes dissociation and Amantadine yields no benefit. If this occurs, Memantine treatment will be resumed alongside Piracetam to lessen the severity and frequency of dissociative episodes. If Piracetam is ineffective, I'll consider Tianeptine but my gut feeling says the combination of Memantine, Seligiline and Tianeptine would cause emotional flatlining.

 

D R A M A C H I A V E L L I A N

X

Edited by dramachiavellian, 11 February 2017 - 09:16 PM.

[bobitza]

One mention about Abilify: in my case, it's good in the 3-5mg range. Over this and it's vegetable hell and I never think of sex, I've noticed. Again, this is valid for me. Without it I get angry. With this small dose, I never bother, all is fine. I can happily report that it solved relationship problems, you know the weird "I hate you" stuff, so thumbs up for interpersonal stuff. Very effective.

[jack black]

do we actually know how Abilify works in BPD? Is this all about 5HT2a antagonism? If so, LSD should be a bad idea (5HT2a agonist), while I've heard it's actually good.

[dramachiavellian]

Anecdotal reports on mental health forums and medication reviews suggest extremely mixed results. Considering that Borderline Personality Disorder has a >70% chance of co-occurring with another Personality Disorder, it's very difficult to perform clinical trials with much validity. Assuming patients meeting diagnostic criteria for additional Personality Disorders were excluded from trials, even complete success in the laboratory would still mean less than 30% success among the general population. Once you factor in that 15% efficacy over placebo in clinical trials is regarded to be statistically significant, the actual remission rate for Borderline patients on Abilify (for which Abilify is specifically responsible) could be as low as 5%. Still, I'm happy to see that bobitza has found some degree of relief! There's a fair chance that Abilify works for more than 5% of people with Borderline Personality Disorder. As I say, the reviews are extremely mixed - not extremely negative. I believe D2/D3 dopamine receptor agonism may play a role in its efficacy. It's one of the few antipsychotic medications that doesn't directly antagonise these receptors.

D R A M A C H I A V E L L I A N

X

 

Edited by dramachiavellian, 11 February 2017 - 11:07 PM.

[jjnz]

I'm currently trying to help a family and so far this thread comes the closest to anything I've read so far.

The family raised until 7 weeks ago what was a normal loving 12 year old daughter, until rather suddenly developing a "severe" case of oppositional defiance disorder.

There are 2 or 3 historic aggravating factors such as parents divorce (7 years ago), a recent (12 weeks ago) fight at school, poor school performance,

She has low IQ (70's) and ADHD( recent diagnosis).

Out of what seems like the blue she attempted a homicide with a lot of scary detail and planning.

Escaped police custody and struggled with police officers.

Vandalised property, jumped out of a moving car, threatened a parent with murder (in graphic detail)

Was put in a facility and has smashed windows, attempted escape.

It goes on and on and on and has done for 7 weeks now.

She has made weak but regular attempts at suicide.

She has an absolute hatred of rules.

She shows no empathy or remorse.

I haven't been able to get DNA tests and I doubt I can now as she's now under state care and seems unresponsive to ADHD drugs, Quetiapine Fumarate etc.

 

Being such a massive change in the space of days I am inclined to believe something has "switched" and Im wondering after reading this forum if the onset of puberty, ( has developed body but not had a period) a "possible" acetylcholine issue and the aggravating factors haven't forced her amygdala into a constant on state.

 

The day before she committed the homocide attempt she swallowed 12 Nurofen (Ibuprofen) so I'd expect that whacked her microbiome to hell and back. 

Her eyes are constantly dilated

She craves coffee, sugar and found comfort in the one cigarette we know about ( alpha 7 nicotine receptor?)

The psych unit that has looked at her has stated this is a behavioural problem and not a psychiatric issue. I'm not so sure.

I'm not trying to hijack this thread but I am looking for feedback in terms of should we attempt to modulate her acetylcholine.

she has had some balance and dizzyness issues, in fact of late she could tick everyone of these boxes https://vagusnervesu...-acetylcholine/

I know BPD isn't the same as Oppositional Defiance Disorder but I need some clues  

 

 

[Mind_Paralysis]

I'm currently trying to help a family and so far this thread comes the closest to anything I've read so far.

The family raised until 7 weeks ago what was a normal loving 12 year old daughter, until rather suddenly developing a "severe" case of oppositional defiance disorder.

There are 2 or 3 historic aggravating factors such as parents divorce (7 years ago), a recent (12 weeks ago) fight at school, poor school performance,

She has low IQ (70's) and ADHD( recent diagnosis).

Out of what seems like the blue she attempted a homicide with a lot of scary detail and planning.

Escaped police custody and struggled with police officers.

Vandalised property, jumped out of a moving car, threatened a parent with murder (in graphic detail)

Was put in a facility and has smashed windows, attempted escape.

It goes on and on and on and has done for 7 weeks now.

She has made weak but regular attempts at suicide.

She has an absolute hatred of rules.

She shows no empathy or remorse.

I haven't been able to get DNA tests and I doubt I can now as she's now under state care and seems unresponsive to ADHD drugs, Quetiapine Fumarate etc.

 

Being such a massive change in the space of days I am inclined to believe something has "switched" and Im wondering after reading this forum if the onset of puberty, ( has developed body but not had a period) a "possible" acetylcholine issue and the aggravating factors haven't forced her amygdala into a constant on state.

 

The day before she committed the homocide attempt she swallowed 12 Nurofen (Ibuprofen) so I'd expect that whacked her microbiome to hell and back. 

Her eyes are constantly dilated

She craves coffee, sugar and found comfort in the one cigarette we know about ( alpha 7 nicotine receptor?)

The psych unit that has looked at her has stated this is a behavioural problem and not a psychiatric issue. I'm not so sure.

I'm not trying to hijack this thread but I am looking for feedback in terms of should we attempt to modulate her acetylcholine.

she has had some balance and dizzyness issues, in fact of late she could tick everyone of these boxes https://vagusnervesu...-acetylcholine/

I know BPD isn't the same as Oppositional Defiance Disorder but I need some clues  

 

Recent neuroimaging studies have actually come to the conclusion that ODD is in fact a SEPARATE neuro-developmental disorder - they came to this conclusion by studying inmates in prisons, I believe, and found that even though most of the ADHD-ers in prison also have ODD, a large percentage of the NON-adhd inmates actually have corresponding alterations...! As such, since not everyone with ADHD has ODD, they've come to the conclusion that it's actually a separate disorder.

 

The results are fresh though, so we'll see if this turns out to be the pre-dominant theory as we progress in our understanding.

 

I believe studies have found that GUANFACINE - ak a Intuniv, is an effective medication for the treatment of ODD - have they actually tried THAT drug?

 

 

 

References:

-------------------

A Systematic Review and Meta-analysis of Neuroimaging in Oppositional Defiant Disorder (ODD) and Conduct Disorder (CD) Taking Attention-Deficit Hyperactivity Disorder (ADHD) Into Account

https://www.ncbi.nlm...les/PMC4762933/

 

Treating ADHD in Prison: Focus on Alpha-2 Agonists (Clonidine and Guanfacine)

http://jaapl.org/con.../2/151.full.pdf

[jjnz]

Have tried an ADHD drug but not sure if it was Guanfacine,will check. (edit- NO, it was just Ritalin)

The part that amazes me is the onset, so rapid.

Thanks for the references

Edited by jjnz, 26 April 2017 - 10:29 AM.

[jack black]

I guess people snap (I know, it's not scientific). Could it be a full fledged psychosis?

Any substance use that could have triggered it?

BTW, shouldn't this be called a conduct (antisocial) disorder rather than ODD? CD can have early teen onset.

Edited by jack black, 26 April 2017 - 01:06 PM.

[Finn]

I'm currently trying to help a family and so far this thread comes the closest to anything I've read so far.

 

Has there been any brain scans done on her?

 

That story sounds in someways similar to Daniel Amen's nephew, who had brain cyst pressing his left temporal lobe. 

 

 

From Daniel Amen's book Healing ADD. 

 

 

 

Spoiler

 

Then, in April 1995, nine-year-old Andrew came into my clinic. Andrew is a very special child. He is my godson and nephew. When he was young he was a happy, active child, but in the year and a half before he came to my clinic as a patient, his personality had changed. He appeared depressed. He had serious aggressive outbursts and he complained to his mother of serious suicidal and homicidal thoughts (very abnormal for a 9-year-old). He drew pictures of himself hanging from a tree or shooting other children. When he attacked a little girl on the baseball field for no particular reason, his mother called me late at night in tears. I told his mother to bring Andrew to see me the next day. His parents drove to my clinic, which was eight hours from their home in Southern California.

 

As I sat with Andrew’s parents and then with Andrew, I knew something wasn’t right. I had never seen him look so angry or so sad. He had no explanations for his behavior. He did not report any form of abuse. Other children were not bullying him. There was no family history of serious psychiatric illnesses. He had not sustained a recent head injury. And he had a wonderful family. Unlike most clinical situations in which I do not know what really goes on in a family, this family I knew. Andrew’s parents were loving, caring, pleasant people. What was the matter?

 

The vast majority of my psychiatric colleagues would have placed Andrew on some sort of medication and had him see a counselor for psychotherapy. Having performed more than 1,000 SPECT studies by that time, I first wanted a picture of Andrew’s brain. I wanted to know what we were dealing with. But with the hostility from my colleagues fresh in my mind, I told myself, Maybe this is really due to a family problem that I just don’t know about. Maybe this is a psychological problem. (Incidentally, if you have good psychoanalytic training, you can find dirt in anybody’s family.) I thought, Maybe Andrew is acting out because his older brother is a “perfect” child who does well in school and is very athletic. Maybe Andrew has these thoughts and behaviors to ward off feelings of insecurity related to being the second son in a Lebanese family. (I had personal knowledge of this scenario.) Maybe Andrew wants to feel powerful and these behaviors are associated with issues of control. Then logic took over my brain. Nine-year-old children do not normally think about suicide. Nine-year-old children do not normally think about homicide. I needed to scan his brain. If it was normal, then we could look further into the underlying emotional problems that might be present.

 

I went with Andrew to the imaging center and held his hand while he had the study performed. As his brain appeared on the computer screen, I thought a mistake had been done in performing the procedure. Andrew had no left temporal lobe. Upon quick examination of the complete study, I realized the quality of the scan was fine. He was indeed missing the function of his left temporal lobe. Did he have a cyst or a tumor? Had he had a stroke? I was scared for him as I looked at the monitor, but relieved that we had some explanation for his aggressive behavior. My research and the research of others had implicated the left temporal lobe in aggression. The next day Andrew had an MRI (an anatomical brain study), which showed a cyst (a fluid-filled sac) about the size of a golf ball occupying the space where his left temporal lobe should have been. I knew the cyst had to be removed. Getting someone to take this seriously proved frustrating, however.

 

That day I called Andrew’s pediatrician in Orange, California, and told him of both the clinical situation and the brain findings. I told him to find the best person possible to take this thing out of his head. He contacted three pediatric neurologists. All of them said that Andrew’s negative behavior was probably not in any way related to the cyst in his brain and they would not recommend operating on him until he had real symptoms. When the pediatrician told me this information, I became furious. Real symptoms! I had a child with homicidal and suicidal thoughts who loses control over his behavior and attacks people! I contacted a pediatric neurologist in San Francisco, who told me the same thing. I then called a friend of mine at Harvard Medical School, also a pediatric neurologist, who told me yet again the same thing. She even used the words “real symptoms.” I said to her, “‘Real symptoms’! I have a child with homicidal and suicidal thoughts who attacks people: What do you mean by ‘real symptoms’?” “Oh, Dr. Amen,” the neurologist replied, “when I say ‘real symptoms’ I mean problems like seizures or speech problems.” Could the medical profession really not connect the brain to behavior? I was angry and appalled! But I wasn’t going to wait until this child killed himself or someone else. I called the pediatric neurosurgeon Horhay Lazarette, M.D., at UCLA and told him about Andrew. He told me that he had operated on three other children with left temporal lobe cysts who were all aggressive. He wondered if it was related. Thankfully, after evaluating Andrew, he agreed to take it out.

 

Dr. Lazarette called me right after the surgery in April 1995. He said that he was so glad that I had referred Andrew to him. The cyst had put so much pressure on Andrew’s brain that it had actually thinned the bone over his left temporal lobe. If Andrew had been hit near that part of his head with modest force—with a basketball, for example—it would have killed him. He said the pressure from the cyst might have killed Andrew anyway within six months. When Andrew woke up from the surgery, his mother told me, he smiled at her. He had not smiled at her for a year. Immediately after the surgery, his aggressive thoughts were gone and his temperament changed back to the sweet child he always wanted to be. Now, six years later, Andrew remains nonviolent, happy, and well-adjusted

 

 

French civil servant who lost about 90% of his brain volume to a fluid buildup also had IQ of 75, interestingly he had no behavioral or mental health problems, just tingling in his leg that disappeared when shunt was reinstalled. 

 

http://www.nature.co...s070716-15.html

[Mind_Paralysis]

Have tried an ADHD drug but not sure if it was Guanfacine,will check. (edit- NO, it was just Ritalin)

The part that amazes me is the onset, so rapid.

Thanks for the references

 

Then try Guanfacine - it's sedating in a way that doesn't actually impair attention and self-control, unlike for instance, the Antipsychotics.
 

 

 

I'm currently trying to help a family and so far this thread comes the closest to anything I've read so far.

 

Has there been any brain scans done on her?

 

That story sounds in someways similar to Daniel Amen's nephew, who had brain cyst pressing his left temporal lobe. 

 

 

From Daniel Amen's book Healing ADD. 

 

 

 

Spoiler

 

Then, in April 1995, nine-year-old Andrew came into my clinic. Andrew is a very special child. He is my godson and nephew. When he was young he was a happy, active child, but in the year and a half before he came to my clinic as a patient, his personality had changed. He appeared depressed. He had serious aggressive outbursts and he complained to his mother of serious suicidal and homicidal thoughts (very abnormal for a 9-year-old). He drew pictures of himself hanging from a tree or shooting other children. When he attacked a little girl on the baseball field for no particular reason, his mother called me late at night in tears. I told his mother to bring Andrew to see me the next day. His parents drove to my clinic, which was eight hours from their home in Southern California.

 

As I sat with Andrew’s parents and then with Andrew, I knew something wasn’t right. I had never seen him look so angry or so sad. He had no explanations for his behavior. He did not report any form of abuse. Other children were not bullying him. There was no family history of serious psychiatric illnesses. He had not sustained a recent head injury. And he had a wonderful family. Unlike most clinical situations in which I do not know what really goes on in a family, this family I knew. Andrew’s parents were loving, caring, pleasant people. What was the matter?

 

The vast majority of my psychiatric colleagues would have placed Andrew on some sort of medication and had him see a counselor for psychotherapy. Having performed more than 1,000 SPECT studies by that time, I first wanted a picture of Andrew’s brain. I wanted to know what we were dealing with. But with the hostility from my colleagues fresh in my mind, I told myself, Maybe this is really due to a family problem that I just don’t know about. Maybe this is a psychological problem. (Incidentally, if you have good psychoanalytic training, you can find dirt in anybody’s family.) I thought, Maybe Andrew is acting out because his older brother is a “perfect” child who does well in school and is very athletic. Maybe Andrew has these thoughts and behaviors to ward off feelings of insecurity related to being the second son in a Lebanese family. (I had personal knowledge of this scenario.) Maybe Andrew wants to feel powerful and these behaviors are associated with issues of control. Then logic took over my brain. Nine-year-old children do not normally think about suicide. Nine-year-old children do not normally think about homicide. I needed to scan his brain. If it was normal, then we could look further into the underlying emotional problems that might be present.

 

I went with Andrew to the imaging center and held his hand while he had the study performed. As his brain appeared on the computer screen, I thought a mistake had been done in performing the procedure. Andrew had no left temporal lobe. Upon quick examination of the complete study, I realized the quality of the scan was fine. He was indeed missing the function of his left temporal lobe. Did he have a cyst or a tumor? Had he had a stroke? I was scared for him as I looked at the monitor, but relieved that we had some explanation for his aggressive behavior. My research and the research of others had implicated the left temporal lobe in aggression. The next day Andrew had an MRI (an anatomical brain study), which showed a cyst (a fluid-filled sac) about the size of a golf ball occupying the space where his left temporal lobe should have been. I knew the cyst had to be removed. Getting someone to take this seriously proved frustrating, however.

 

That day I called Andrew’s pediatrician in Orange, California, and told him of both the clinical situation and the brain findings. I told him to find the best person possible to take this thing out of his head. He contacted three pediatric neurologists. All of them said that Andrew’s negative behavior was probably not in any way related to the cyst in his brain and they would not recommend operating on him until he had real symptoms. When the pediatrician told me this information, I became furious. Real symptoms! I had a child with homicidal and suicidal thoughts who loses control over his behavior and attacks people! I contacted a pediatric neurologist in San Francisco, who told me the same thing. I then called a friend of mine at Harvard Medical School, also a pediatric neurologist, who told me yet again the same thing. She even used the words “real symptoms.” I said to her, “‘Real symptoms’! I have a child with homicidal and suicidal thoughts who attacks people: What do you mean by ‘real symptoms’?” “Oh, Dr. Amen,” the neurologist replied, “when I say ‘real symptoms’ I mean problems like seizures or speech problems.” Could the medical profession really not connect the brain to behavior? I was angry and appalled! But I wasn’t going to wait until this child killed himself or someone else. I called the pediatric neurosurgeon Horhay Lazarette, M.D., at UCLA and told him about Andrew. He told me that he had operated on three other children with left temporal lobe cysts who were all aggressive. He wondered if it was related. Thankfully, after evaluating Andrew, he agreed to take it out.

 

Dr. Lazarette called me right after the surgery in April 1995. He said that he was so glad that I had referred Andrew to him. The cyst had put so much pressure on Andrew’s brain that it had actually thinned the bone over his left temporal lobe. If Andrew had been hit near that part of his head with modest force—with a basketball, for example—it would have killed him. He said the pressure from the cyst might have killed Andrew anyway within six months. When Andrew woke up from the surgery, his mother told me, he smiled at her. He had not smiled at her for a year. Immediately after the surgery, his aggressive thoughts were gone and his temperament changed back to the sweet child he always wanted to be. Now, six years later, Andrew remains nonviolent, happy, and well-adjusted

 

 

French civil servant who lost about 90% of his brain volume to a fluid buildup also had IQ of 75, interestingly he had no behavioral or mental health problems, just tingling in his leg that disappeared when shunt was reinstalled. 

 

http://www.nature.co...s070716-15.html

 

 

Excellent point - there COULD be something physical altering her behaviour! Paranoia and aggression have been noted as a result of some brain-tumours - perhaps there's something malevolent growing in her head...?

 

That, or perhaps her diagnosis of ADHD was incorrect - perhaps she really has got Paranoid Schizophrenia, but with some negative symptoms as well? Usually, PS's don't have as great of an amount of negative symptoms, hence why they are sometimes involved in crimes which are executed with sometimes complex plans behind them.

 

I believe I have read that there is actually some evidence of pre-dromal symptoms in CHILDREN with Schizophrenia, which manifest as a form of executive function deficit?

 

Here, have a look at this:

 

Association between Attention-Deficit Hyperactivity Disorder in childhood and schizophrenia later in adulthood

http://www.sciencedi...924933813000783

 

Attentional and neurocognitive characteristics of high-risk offspring of parents with schizophrenia compared with DSM-IV attention deficit hyperactivity disorder children

http://www.sciencedi...920996405000447

 

 

On the other hand, Quetiapine didn't work, so that makes it less plausible she's having a "normal" psychosis, with delusional, paranoid thoughts.

 

 

@jjnz: Is there any family history of schizophrenia, or similar disorders? Could her diagnosis of ADHD be incorrect?
 

Edited by Stinkorninjor, 26 April 2017 - 02:35 PM.

[gamesguru]

abilify works via the D2 receptor.  like Corydalis yanhusuo it enhances reward sensitivity and the conditioned placement test.  like ginseng it may cause agitation and distress as a side effect.

 

ADD/ODD is like a mini-antisocial disorder.  so much overlap going on.  as for the pure BPD group, it's because everybody with BPD is a real piece of work, a sick puppy.  borderline is really a link, a small centerpiece connecting shcizophrenia, depression and antisocial behavior... you change one gene and suddenly youre in a new territory.  perhaps it's not so surprising that 96% have something else, whether it's anxiety, depression, or five more PDs to ice the cake.  as a group, it's too damn expensive to segregate and carry out clinical research.  too damn expensive.  not enough inches.  we've run out of inches!  no more skyscrapers.  comprende amigo?  you can barely separate wheat from chaff, dirt from gold, but you expect to pick 4% of the population out and then recruit them to studies?  good luck sir

 

 

//off topic

Dan Amen's case reminds me of Phineas Gage with the whole hole in his head thing.  the brain is really the biggest mystery of the universe

[Finn]

 

Her eyes are constantly dilated

 

 

Dilated pupils are also one of possible symptoms of temporal lobe seizure.

 

 

 

http://www.nytimes.c...e/overview.html

 

 

Temporal lobe epilepsy can have a number of causes such as head injury, stroke, brain infections, structural lesions in the brain, or brain tumors, or it can be idiopathic and have no apparent cause. So even if no cyst, other fluid buildup or tumor or other obvious damage is found, antiepileptics/anticonvulsants could be tried at some point, since based on symptoms it could be temporal lobe issue.

Edited by Finn, 27 April 2017 - 07:03 AM.

[jjnz]

Just spoken again to family.

Fathers Cousin had Low IQ and depression

Mothers Father had Bipolar in late teens and was institutionalised by age 26 (it's not clear why, seems extreme for BP alone) now has dementia possibly as a result of meds and ECT

 

Anger triggers are boredom and rules, any form of control is intolerable.

Takes 3 adults to restrain her and this takes a minimum of 45 minutes.

She thrives on any sense of danger.

 

She has had a CT scan , not an MRI, this came back with no concerns but I'm noting what Finn said re TLS.

Correction on previous statement re Quetiapine: dosage has been increased and she is now responsive for a few hours.

 

 

[Mind_Paralysis]

Just spoken again to family.

Fathers Cousin had Low IQ and depression

Mothers Father had Bipolar in late teens and was institutionalised by age 26 (it's not clear why, seems extreme for BP alone) now has dementia possibly as a result of meds and ECT

 

Anger triggers are boredom and rules, any form of control is intolerable.

Takes 3 adults to restrain her and this takes a minimum of 45 minutes.

She thrives on any sense of danger.

 

She has had a CT scan , not an MRI, this came back with no concerns but I'm noting what Finn said re TLS.

Correction on previous statement re Quetiapine: dosage has been increased and she is now responsive for a few hours.

 

She should have an MRI, to be certain, because abnormalities are much easier spotted with MRI, than with CT.

 

With that said, I'm glad to hear that Quetiapine seems to be having SOME effect now. Sounds like she may need a secondary dosage during the evening though, if it wears off after such a short period of time as 4-5 hours - usually Quetiapine has a much longer period of effect.

 

Have you told them to consider Intuniv? What do you yourself make of any potential effect it could have on her symptoms? (I'm basing my suggestion entirely on the idea of her simply having the worst case of ODD-CD in history)

 

 

References:

----------------------

Temporal Lobe Epilepsy Workup

http://emedicine.med...84509-workup#c9

 

Temporal-lobe epilepsy: comparison of CT and MR imaging.

https://www.ncbi.nlm.../pubmed/3500615

[jjnz]

Thanks yes, I'm pushing for an mri and Intuniv. Anything is worth trying, She been transferred to a more secure lock down now. So sad, 7 weeks ago she was perfectly normal kid.

[Shai Hulud]

She should try Parnate. Not only is it less toxic and more effective than SSRIs and SNRIs, but it also has the potential to help with her different symptoms all in one medication.
After stabilizing, look into her folate/biopterin and methionine pathways. If there are problems there, this can result in a shortage and/or imbalance of Neurotransmitters : serotonin, dopamine and noradrenaline need Tetrahydrobiopterin for synthesis and Dopamine and Noradrenaline, also Histamine need Methylation to work to be degraded.

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