Posted 14 September 2016 - 06:12 PM
^^ That's because not every symptom can be explained by one neurotransmitter. The blunted affect, facial recognition, emotion, memory/cognition, and articulation ARE glutamatergic. The motivation, low mood, concentration, and lack of energy are mostly dopaminergic. Something like ginseng (a fairly selective D2 agonist) or ginkgo (NDRI) is needed there.
Posted 15 September 2016 - 05:39 PM
The motivation, low mood, concentration, and lack of energy are mostly dopaminergic. Something like ginseng (a fairly selective D2 agonist) or ginkgo (NDRI) is needed there.
Normally I would agree with you, but I'm thinking it's not that simple here.
1. She is taking dopaminergic drugs (bupropion and memantine) already and she took concerta in the past. That didn't help her with the core issue of procrastination and avoidance of dealing with real life issues.
2. Dopaminergic receptors will be downregulated after chronic stimulation.
3. In theory, her issue could be so called escapism, where people escape into fantasy world (and/or various addictions) and get their dopaminergic receptors stimulated that way by instant gratification.
4. In practice, it turned out something else altogether. Finally, I had a chance to talk to her in person last night and she improved her emotions and communication enough to explain that she feels paralyzing fear about making major life decisions or actions and instead she escapes into inaction and denial.
It almost feels like some sort of phobia and I'm researching that on http://phobialist.com/. Maybe it's Atychiphobia- Fear of failure or Decidophobia- Fear of making decisions or Hypengyophobia/Hypegiaphobia- Fear of responsibility or Kakorrhaphiophobia- Fear of failure or defeat or Katagelophobia- Fear of ridicule or Metathesiophobia- Fear of changes???
I really don't know. The http://www.fearof.net/ also have this candidate: Achievemephobia – The fear of success.
Either way, the treatment should be simple (flooding and desensitization, maybe with a help of propranolol).
On a side note, I just realized that symptoms of BPD overlap closely with Asperger's syndrome, especially in females. Since the person in question was quiet, liked to play alone, could concentrate deeply in some activities (puzzles) and had huge pain tolerance since early childhood, it's a viable possibility, too.
I'll keep you posted.
Posted 22 September 2016 - 04:53 AM
Those conditioned maladaptions are due to lifestyle choices, not neurotransmitter imbalances. She can overcome it only with a little help from society.
the progress is slow, she's got some real fears alright facing her school stuff.
but, i'm really posting this to update the thread about an interesting find re: Sceletium tortuosum, a herb known as Kanna, that is known as a psychoactive herb.
i got interested in this because i've heard that this is a legal CB1 agonist (albeit weaker than THC of course). i also knew from some online accounts that THC can be (very) helpful in BPD.
now, according to this: http://www.ncbi.nlm....les/PMC3828542/
Amygdala reactivity to fearful faces under low perceptual load conditions was attenuated after a single 25 mg dose of Zembrin. Follow-up connectivity analysis on the emotion-matching task showed that amygdala–hypothalamus coupling was also reduced. These results demonstrate, for the first time, the attenuating effects of S. tortuosum on the threat circuitry of the human brain and provide supporting evidence that the dual 5-HT reuptake inhibition and PDE4 inhibition of this extract might have anxiolytic potential by attenuating subcortical threat responsivity.
the paper didn't mention the CB1 part, but the action sounds exactly whats needed in BPD. based on that info i ordered a sample of Kanna on ebay and tested a small dose on myself tonight. it was not pleasant to chew (bitter and gritty), but slowly gave a pleasant mild anxiolitic sensation and mood lift. suppressed appetite too. looks promising and sounds like it can benefit not just BPD people.
Edited by jack black, 22 September 2016 - 04:57 AM.
Posted 22 September 2016 - 12:17 PM
In the name of trying things with a laughable affinity to the CB1 receptor, might I also recommend (+)echinachea and (-)carrots? The (+)agonists are going to create a rebound or "low" period, hopefully during sleep, where the drug is not administered and receptors are down-regulated.
The prelimbic cortex is even upstream of the amygdala. Downstream targets (that the amygdala pours into) include the basal ganglia (responsible for voluntary movement), thalamus, hypothalamus, septal area and accumbens. Acetylcholine appears to play a major role in these pathways, and that may be one of the reasons why antipsychotics do not lessen the primed-fear response of borderlines.
Posted 22 September 2016 - 08:44 PM
In the name of trying things with a laughable affinity to the CB1 receptor, might I also recommend (+)echinachea and (-)carrots? The (+)agonists are going to create a rebound or "low" period, hopefully during sleep, where the drug is not administered and receptors are down-regulated.
The prelimbic cortex is even upstream of the amygdala. Downstream targets (that the amygdala pours into) include the basal ganglia (responsible for voluntary movement), thalamus, hypothalamus, septal area and accumbens. Acetylcholine appears to play a major role in these pathways, and that may be one of the reasons why antipsychotics do not lessen the primed-fear response of borderlines.
I wouldn't call it laughable: https://www.research...ium_tortuosum_L
but it all depends how you define laughable.
BTW, today i'm more sluggish and have a tension headache after that trip last night. Must be that acetylcholinesterase inhibitory activity. BPD patients are not going to tolerate it well I'm afraid.
Posted 14 October 2016 - 10:29 PM
This thread is dead, but I thought i would update this for the sake of people searching for BPD (i hate myself when threads are left hanging with no closure).
i don't believe anymore my family member has BPD. in retrospect, her psychiatrist was right to disagree with that diagnosis, but was not smart enough it figure it out. i'm almost positive she has high functioning and compensated Asperger syndrome (AS) with a comorbility of generalized/social anxiety and episodes of severe depression triggered by stress and massive failures in her personal life.
i took me a while to figure it out (by myself) and it was quite a personal journey. i discovered that i had similar traits myself, but with a bit more typical presentation of AS, as expected in males. I also differed in regards to suicide attempts, as i never had that inclination, even though there were some depressive episodes, mostly triggered by stress.
this (old) article that i only found recently summarizes well why women with AS don't present with typical symptoms and are misdiagnosed with something else: https://www.theguard...aspergers-girls
"Girls are not being picked up because there is still a stereotyped view of what Asperger's is, which is based entirely on how boys present with the condition," she said. "Professionals are not up to speed in knowing how girls present. We are working with the government to ensure they highlight this concern in their upcoming consultation. We are hoping to convince them to target this much under-investigated but vitally important issue."
[...]
"We need to draw up a female version of Asperger's that identifies girls on the basis of the way they present, and we need to do this as a matter of urgency: undiagnosed Asperger's can create devastatingly low self-esteem in girls. In my experience, up to 20% of female anorexics have undiagnosed Asperger's."
Girls slip through the diagnostic net, said Attwood, because they are so good at camouflaging or masking their symptoms. "Boys tend to externalise their problems, while girls learn that, if they're good, their differences will not be noticed," he said. "Boys go into attack mode when frustrated, while girls suffer in silence and become passive-aggressive. Girls learn to appease and apologise. They learn to observe people from a distance and imitate them. It is only if you look closely and ask the right questions, you see the terror in their eyes and see that their reactions are a learnt script."
Girls also escape diagnosis, said Attwood, because they are more social than boys with the condition. Their symptoms can also be missed because it is the intensity of their interests that is unusual, and not the oddity of what they do.
"The impairments to their social life or interests tend not to stand out in the same way as boys' do," he said. "They might have one friend, while boys with the condition won't have any. Also, boys hyperfocus on facts and certain interests, such as trains or weather. Girls escape into fiction. They have imaginary friends, live in another world with fairies and witches, obsessively watch soap operas or become intensely interested in celebrities."
Professor David Skuse, head of the behavioural and brain sciences unit at the Institute of Child Health, teaches clinicians to diagnose the condition. "Increasingly fewer girls are diagnosed as their IQ reaches 100, the population average," he said. "Some people maintain this is because girls simply don't have Asperger's, but I would argue that brighter girls, especially those who are more verbal, are able to mask and compensate for their condition. I make sure I emphasise the difference in the ways boys and girls present when I train clinicians, because I am certain that girls are being failed by the system, especially those with higher IQs," he added. "My belief is that, if we can prove the ratio of boys to girls is as high as many of us suspect, it would be as significant a milestone in this field as the discovery that the condition is on a spectrum."
i would venture to say, even though it's just a guess on my part, that a lot of girls with those autistic traits are going be get labeled as BPD or something similar, while boys would be more likely correctly diagnosed, even though a lot of them will end up misdiagnosed as ADHD, anxiety, or depression.
But maybe it's just semantics as a lot of drugs that help in BPD help in AS, too.
Posted 17 October 2016 - 10:27 AM
I was invited to this thread by stinkorninjor due to my discussion of BPD in another thread. My sister had BPD and I had to live with it for much of my early life. It turns everyone else’s lives around that person into hell. She’s a lot better now due to a variety of reasons, but not completely cured.
I disagree with her psychiatrist. If her problem were something along the lines of the autism spectrum, she would not be reacting so positively to the meds she is taking, especially the Lamictal. In fact, as I was reading along the thread, which took a while, I was thinking to myself “she should do a retrial of Lamictal, and be very careful this time, as it’s so effective for BPD”. And what do you know, she did it and it was effective. Lamictal, nor Lithium, isn’t going to jack shit for anything along the autism spectrum.
BPD seems to be closely related to bipolar neurochemically (and not ADHD as others here have suggested). In fact, BPD often, and unfortunately gets diagnosed as bipolar, as treating BPD as bipolar often yields to a poor result. Although, a good portion of the meds that are effective for Bipolar are effective for BPD. In fact, Lamictal is also the gold standard for Bipolar II.
Anyway, I have a lot to say here, but I’m not going to waste my time if you’ve already come to a different conclusion. Let me know.
Posted 17 October 2016 - 02:11 PM
I was invited to this thread by stinkorninjor due to my discussion of BPD in another thread. My sister had BPD and I had to live with it for much of my early life. It turns everyone else’s lives around that person into hell. She’s a lot better now due to a variety of reasons, but not completely cured.
I disagree with her psychiatrist. If her problem were something along the lines of the autism spectrum, she would not be reacting so positively to the meds she is taking, especially the Lamictal. In fact, as I was reading along the thread, which took a while, I was thinking to myself “she should do a retrial of Lamictal, and be very careful this time, as it’s so effective for BPD”. And what do you know, she did it and it was effective. Lamictal, nor Lithium, isn’t going to jack shit for anything along the autism spectrum.
BPD seems to be closely related to bipolar neurochemically (and not ADHD as others here have suggested). In fact, BPD often, and unfortunately gets diagnosed as bipolar, as treating BPD as bipolar often yields to a poor result. Although, a good portion of the meds that are effective for Bipolar are effective for BPD. In fact, Lamictal is also the gold standard for Bipolar II.
Anyway, I have a lot to say here, but I’m not going to waste my time if you’ve already come to a different conclusion. Let me know.
Well, disregarding Jack_Black's cousin, which was the initial subject of the thread, perhaps you could give your 5 cents on the similarity to Bipolar? There are several neurological targets and variations of Bipolar it would seem, but would you say BPD is just another variation or do you see it as a similar disease?
Along the lines of how there are similarities between ADHD and CDD, but the efficacy for the ADHD-meds just aren't quite there when it comes to CDD. (they help to a small extent though, just not enough to be a functional treatment)
Would you hazard a guess as to the potential neurobiology behind it, as well?
If it's a variation of Bipolar, I would hazard a guess that calcium-channels would be implicated - but strangely enough, Lamotrigine seems to be more of a glutamate-modulating drug actually, so that would implicate glutamate, instead of calcium-channels.
Posted 17 October 2016 - 02:48 PM
I'm not saying it's a variation, no no. There just seems to be an overlap in some behaviors, and a definite overlap in their treatment (the kinds of drugs). The truth is, we can theorize all we want, but we still really don't know how these disorders function. Lot's of hypotheses, but nothing concrete enough to go 'ah-hah, there's the mechanism!' So, I could come up with my own hypothesis, but I'd be no further than anyone else.
Likewise, with the medications that treat them, we don't really know how they work. They first mood stabilizer was lithium, first discovered in the later 1800s, begun to put into use in the 1950s, and put into mass use in the 80s. The first mood stabilizer, a natural salt from the fucking ground, and we still don't know how it works! Can you believe that? Getting my degree in Cognitive Science, and then doing my own research in pharmacology, I learned we're still in the dark ages when it comes to the brain.
As for the other medications, we don't know how they fix things, but we at least have an idea of their mechanism(s). Until recently, all bipolar and BPD medications were sodium channel blockers or modulators (not glutamate modulators). This includes Lamotrigine, Valproate and Carbamazepine. Note that sodium channel blockers are a subset of anticonvulsants, and are used on epileptics as well. I suppose it was simple enough that this one class treated bipolar, and gave pathway for research. But things have gotten a bit more complicated, as some of the new antipsychotics, like Saphris (asenapine), have been found effective (for some, there is still a lot of debate about this) in the treatment of Bipolar. Why? Hell if I, or anyone, knows.
It seems that all the meds that work for BDP work for Bipolar, but not the other way around. In other words, only a small subset of BP meds work for BPD, and that makes treatment hard. I can only think of Lamotrigine and Topiramate off the top of my head, though I know there's a couple more.
You should find it interesting that my sister, after getting off Lamotrigine (much to the internal screams of all of us), made huge progress without meds. After another year or two of crazy, she one day, for whatever reason brought her there, decided to stop reacting to people, to just stop. She thought needed to display more love. So when people slighted her, she responded with kindness, instead of the usual fistfights she would get into. But overall, she'd forced herself into having no reaction whatsoever. And she was a chef and would also work the front, so she dealt with a lot of people. Eventually she trained herself to lower her emotional reaction towards people, and she's pretty normal today.
I suppose it helps that she seemed to ignore the labels of Bipolar (which she was [mis]diagnosed with) and BPD), which in western society we deem incurable. But thankfully in her case this was not the conclusion.
Posted 17 October 2016 - 03:05 PM
I'm not saying it's a variation, no no. There just seems to be an overlap in some behaviors, and a definite overlap in their treatment (the kinds of drugs). The truth is, we can theorize all we want, but we still really don't know how these disorders function. Lot's of hypotheses, but nothing concrete enough to go 'ah-hah, there's the mechanism!' So, I could come up with my own hypothesis, but I'd be no further than anyone else.
Likewise, with the medications that treat them, we don't really know how they work. They first mood stabilizer was lithium, first discovered in the later 1800s, begun to put into use in the 1950s, and put into mass use in the 80s. The first mood stabilizer, a natural salt from the fucking ground, and we still don't know how it works! Can you believe that? Getting my degree in Cognitive Science, and then doing my own research in pharmacology, I learned we're still in the dark ages when it comes to the brain.
As for the other medications, we don't know how they fix things, but we at least have an idea of their mechanism(s). Until recently, all bipolar and BPD medications were sodium channel blockers or modulators (not glutamate modulators). This includes Lamotrigine, Valproate and Carbamazepine. Note that sodium channel blockers are a subset of anticonvulsants, and are used on epileptics as well. I suppose it was simple enough that this one class treated bipolar, and gave pathway for research. But things have gotten a bit more complicated, as some of the new antipsychotics, like Saphris (asenapine), have been found effective (for some, there is still a lot of debate about this) in the treatment of Bipolar. Why? Hell if I, or anyone, knows.
It seems that all the meds that work for BDP work for Bipolar, but not the other way around. In other words, only a small subset of BP meds work for BPD, and that makes treatment hard. I can only think of Lamotrigine and Topiramate off the top of my head, though I know there's a couple more.
You should find it interesting that my sister, after getting off Lamotrigine (much to the internal screams of all of us), made huge progress without meds. After another year or two of crazy, she one day, for whatever reason brought her there, decided to stop reacting to people, to just stop. She thought needed to display more love. So when people slighted her, she responded with kindness, instead of the usual fistfights she would get into. But overall, she'd forced herself into having no reaction whatsoever. And she was a chef and would also work the front, so she dealt with a lot of people. Eventually she trained herself to lower her emotional reaction towards people, and she's pretty normal today.
I suppose it helps that she seemed to ignore the labels of Bipolar (which she was [mis]diagnosed with) and BPD), which in western society we deem incurable. But thankfully in her case this was not the conclusion.
An interesting note about your sister there - may I ask how old she was at the time of improvement?
Reason I ask is because there seems to be a clear age-factor to the disease - after the age of 40-45, most patients see a drastic drop-off in symptoms.
My own hypothesis regarding that is because I see the disease as connected to the Cholinergic systems, and choline-levels drop off very drastically after 40 - that's why we get worse memory, et c.
Now, not everyone HAS 40 years though... suicide-rate in BPD is quite high when contrasted to other groups - higher than Bipolar even, because of the great effect of the drugs on bipolar! o.o
That's why I feel we need better meds - it could actually save lives in this case.
Posted 17 October 2016 - 04:19 PM
She started getting better around 24-25, when she forced herself to stop reacting to people. She's 27 now. So, that's pretty young.
About your theory, it doesn't take into account a lot of things. First and foremost is that nicotine is an alpha 7 agonist. If your theory were true, nicotine would send people with BPD through the roof. This would have quickly been recognized, and people with BPD would be strongly advised not to smoke.
Second, you are narrowing emotions down to the amygdala. Although it is important, and does a lot of processing, it acts more like a relay switch for the entire limbic system, of which it is a central part. If you're unfamiliar with the limbic system, now's the time to take a look.
I'm not saying you're theory has no merit, but you're not gonna solve this puzzle in a few weeks. I invite you to do some deeper digging and expend and refine it.
Also, one tool I find indispensable is called 'The Paper Link'. It shows you the impact factor of the journal that published the study you're looking at, right their and then as you search pub med. It's a plugin only available for Google Chrome. If you don't know what an IF is, it's basically a reputation system that measurez how often a journal is cited in other journals, and is a pretty good measurement of the quality of a journal. When looking for studies, the personal system I use is:
IF > 3 - Reliable study
IF b/t 2-3 - Usually reliable
IF b/t 1-2 - Dubious. If I read it I'll have to read the methods section to check for bullshit (I usually skip the methods section)
IF < 1 Usually shit. Pass.
If you're really serious about becoming well-versed in this stuff, and even developing theories, don't do what most here do when they start citing white papers, and that's just read the abstract. Read the whole goddamn paper (you can usually skip the methods section because that just details who the experiment was set up, and in a good journal you can rely on the science to be done right). It may take an hour at first, as it did for me. But I can usually get through a paper in 10-15 minutes these days.
Good luck, mon ami.
Edited by OneScrewLoose, 17 October 2016 - 04:20 PM.
Posted 18 October 2016 - 02:44 AM
I was invited to this thread by stinkorninjor due to my discussion of BPD in another thread. My sister had BPD and I had to live with it for much of my early life. It turns everyone else’s lives around that person into hell. She’s a lot better now due to a variety of reasons, but not completely cured.
I disagree with her psychiatrist. If her problem were something along the lines of the autism spectrum, she would not be reacting so positively to the meds she is taking, especially the Lamictal. In fact, as I was reading along the thread, which took a while, I was thinking to myself “she should do a retrial of Lamictal, and be very careful this time, as it’s so effective for BPD”. And what do you know, she did it and it was effective. Lamictal, nor Lithium, isn’t going to jack shit for anything along the autism spectrum.
BPD seems to be closely related to bipolar neurochemically (and not ADHD as others here have suggested). In fact, BPD often, and unfortunately gets diagnosed as bipolar, as treating BPD as bipolar often yields to a poor result. Although, a good portion of the meds that are effective for Bipolar are effective for BPD. In fact, Lamictal is also the gold standard for Bipolar II.
Anyway, I have a lot to say here, but I’m not going to waste my time if you’ve already come to a different conclusion. Let me know.
Thanks for you time and chiming in. those things are not set in stone and even though i strongly suspect AS now, i strongly suspected BPD before. besides, the label is not that important. i expressed my dissatisfaction with current mental disease labeling here: http://www.longecity...rders-is-wrong/
what's more important is the treatment that works. there is no question lamictal benefits my cousin some. mood stabilizers are known to benefit in BPD but also in AS as well, and this is why i think these 2 diseases are connected in females (along with ADHD and bipolar too).
BTW, I met the young lady on sunday. i showed her a video on female autism from here:
she didn't quite identify with those high functioning autistic ladies, so maybe you are right.
Posted 18 October 2016 - 11:49 AM
Posted 18 October 2016 - 08:03 PM
Cheers to OneScrewLoose for the tips on IF's! = ) I've been wondering about that actually - how to weed out bad journals from good - which ones are reliable?
She stopped the slow dose increase at 100mg. im afraid to escalate more becouse she sometimes forgets to take pills.
Furthermore she got started on a new drug by her general doc: strattera and it seems to be working nice together with her bupropion. She went back to school.
Wait...
WHAT? Strattera? Bupropion? I know Bup could have some potential, in my own research (anti-nicotinic), but Strattera?
Those two drugs actually implicate some form of ADHD, at least as a co-morbidity - which I suppose isn't out of the question, since impairments in the Frontal Lobe are implicated as well in BPD, not just the amygdala - comorbidity with ADHD fits rather nicely then.
(the Swedish scientist I mentioned before, even wants to reclassify it as a form of "Emotional ADHD", and thinks stimulants might help - which I suppose one could call a combo of Strattera and Bupropion - helluva' lot of cathecolaminergic activity on such a combo)
Posted 19 October 2016 - 06:40 PM
Cheers to OneScrewLoose for the tips on IF's! = ) I've been wondering about that actually - how to weed out bad journals from good - which ones are reliable?
She stopped the slow dose increase at 100mg. im afraid to escalate more becouse she sometimes forgets to take pills.
Furthermore she got started on a new drug by her general doc: strattera and it seems to be working nice together with her bupropion. She went back to school.
Wait...
WHAT? Strattera? Bupropion? I know Bup could have some potential, in my own research (anti-nicotinic), but Strattera?
Those two drugs actually implicate some form of ADHD, at least as a co-morbidity - which I suppose isn't out of the question, since impairments in the Frontal Lobe are implicated as well in BPD, not just the amygdala - comorbidity with ADHD fits rather nicely then.
(the Swedish scientist I mentioned before, even wants to reclassify it as a form of "Emotional ADHD", and thinks stimulants might help - which I suppose one could call a combo of Strattera and Bupropion - helluva' lot of cathecolaminergic activity on such a combo)
Yeah, journal quality is a big fucking deal, and it's not discussed enough around or. Or rather, it's not discussed at all. People are happy enough to find an abstract that agrees with their opinion. Before I found 'The Paper Link, I would copy the name of the journal into Google and add "impact factor". Very fucking tedious.
You cannot say it implies ADHD just because Strattera and Bupropion helps her. Although a possibility, that's way jumping the gun, and you can't rush to those conclusions, as exciting as they may be. In fact, if you've talked to a lot of people who have ADHD, you'll find that Strattera doesn't help them. It works for a few, but not many.
Jack, is there any way you can give here her pills daily, without making it seem like you're babysitting her or demeaning her? Just say, 'hey, I notice you forget a lot, so I'd like to help and take a load off your shoulders, just like I would want someone to do the same for me with *insert thing I forget here*'. 200mg is the standard dose of Lamictal, and it even goes up to 400mg. You can tell her Lamictal has even been linked to weight loss (it has), but if she wants a dose increase, you have to give it to her because it's not safe for her not to take it every day.
Posted 19 October 2016 - 07:50 PM
Eminem and Pink are pretty successful.. ? Ayn Rand too, at least financially, socially she's a wet match in a dark cave. I've seen more personality from a robot on spongebob.
You guys are setting your own trap. I had a very nice therapist not too long ago, MSU grad. Professional fucking MSU therapist. I went in completely naturally.. Guess what the bloke diagnosed me as? ADHD + depression. That's his medically credible opinion. To ice the cake, he had me see his psychiatrist friend, who pushed ritalin and celexa. Would stimulants and SSRIs help treat borderline personality? Probably[1], [2], [3]. Fluvoxamine is particularly effective against hyperemotionality (which is weird since bacopa makes it worse, but we think bacopa also boosts TPH and SERT)[4], [5], [6]. Would anyone have hung a question mark on my diagnosis after that point. No one but the man himself. I also didnt make my schizotypy obvious to him, to investigate whether he would mistake it for aspergers, but he overlooked it entirely. Sherlock lost the trail. Like having a cat in your car before a K9 sniffs for weed.
Common ground in Attention Deficit Hyperactivity Disorder (ADHD) and Borderline Personality Disorder (BPD)–review of recent findingsSwantje D Matthies and Alexandra Philipsen
AbstractConsiderable overlap in diagnostic criteria and shared psychopathologic symptoms in attention deficit hyperactivity disorder (ADHD) and borderline personality disorder (BPD) have stimulated research activities in this field. Longitudinal studies have shown that BPD is frequently diagnosed in adult patients who had been diagnosed with ADHD in childhood. The question of whether ADHD and BPD randomly co-occur as comorbidities, have similar origins or share common pathological mechanisms remains unresolved. Some authors suggest that ADHD contributes to the development of BPD via various mechanisms, and therefore consider it a risk factor for later BPD development.
In this article the evidence for the co-occurrence of these disorders will be reviewed as well as studies on their common genetic and environmental influences. Temperamental and developmental issues will be reviewed, and shared features such as impulsivity and emotion dysregulation discussed. From a therapeutic perspective, few studies have investigated psychotherapeutic treatment of the comorbid condition, though the issue is highly important to the management of patients suffering from both disorders. Some thought is given to how therapeutic methods and approaches can be modified to benefit patients, and to their possible succession.
Compr Psychiatry. 2012 Jan;53(1):39-47.
Symptomatic overlap between attention-deficit/hyperactivity disorder and borderline personality disorder in women: the role of temperament and character traits.
van Dijk FE1, Lappenschaar M, Kan CC, Verkes RJ, Buitelaar JK.
Abstract
OBJECTIVE:
There is substantial symptomatic overlap between attention-deficit/hyperactivity disorder (ADHD) and borderline personality disorder (BPD) in adults, but the nature of the relationship between these disorders needs further clarification. The role of temperament and character traits in the differentiation of classes of patients with similar ADHD and BPD symptom profiles was examined and possible pathways between early temperament and future ADHD and/or BPD were hypothesized.
METHODS:
Structured diagnostic interviews were conducted in 103 female patients to assess current Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition symptoms of ADHD and BPD, and parent interviews were used to assess ADHD symptoms in childhood. Classes of subjects with homogeneous symptom profiles were identified using latent class analysis. Temperament and character traits were assessed using the Temperament and Character Inventory of Cloninger et al; scores were then compared across the latent classes.
RESULTS:
Latent class analysis revealed 4 mutually exclusive classes of patients: 1 with only ADHD symptoms; 1 with BPD symptoms and ADHD symptoms of hyperactivity; 1 with BPD symptoms and ADHD symptoms of inattention, hyperactivity, and impulsivity; and 1 with BPD symptoms and ADHD symptoms of inattention and hyperactivity. High Novelty Seeking was found in all classes except for the class with symptoms of BPD and only the hyperactivity aspect of ADHD. The highest Novelty Seeking temperament scores were found in that class of patients with both symptoms of BPD and symptoms in all areas of ADHD. High Harm Avoidance, low Cooperativeness, and low Self-directedness were specifically related to classes containing BPD symptoms.
CONCLUSIONS:
Classes of ADHD and BPD symptoms are associated with specific temperament and character configurations. Novelty Seeking was associated with the inattention symptoms of ADHD. An outspoken Novelty Seeking temperament suggests vulnerability for the development of ADHD and co-occurring BPD. Contrary to patients with combined ADHD and BPD symptoms, patients with only symptoms of ADHD showed normal character development and thus an absence of a personality disorder. Assessment of temperament and character traits can improve our understanding of the complex relationship between ADHD and BPD.
Br J Psychiatry. 2008 Feb;192(2):118-23.
Attention-deficit hyperactivity disorder as a potentially aggravating factor in borderline personality disorder.
Philipsen A1, Limberger MF, Lieb K, Feige B, et al.
Abstract
BACKGROUND:
Clinical experience suggests that people with borderline personality disorder often meet criteria for attention-deficit hyperactivity disorder (ADHD). However, empirical data are sparse.
AIMS:
To establish the prevalence of childhood and adult ADHD in a group of women with borderline personality disorder and to investigate the psychopathology and childhood experiences of those with and without ADHD.
METHOD:
We assessed women seeking treatment for borderline personality disorder (n=118) for childhood and adult ADHD, co-occurring Axis I and Axis II disorders, severity of borderline symptomatology and traumatic childhood experiences.
RESULTS:
Childhood (41.5%) and adult (16.1%) ADHD prevalence was high. Childhood ADHD was associated with emotional abuse in childhood and greater severity of adult borderline symptoms. Adult ADHD was associated with greater risk for co-occurring Axis I and II disorders.
CONCLUSIONS:
Adults with severe borderline personality disorder frequently show a history of childhood ADHD symptomatology. Persisting ADHD correlates with frequency of co-occurring Axis I and II disorders. Severity of borderline symptomatology in adulthood is associated with emotional abuse in childhood. Further studies are needed to differentiate any potential causal relationship between ADHD and borderline personality disorder.
Posted 19 October 2016 - 08:08 PM
First, I've attached the PDF of the whole study. All kinds of problems with it.
Latent class analysis revealed 4 mutually exclusive classes of patients: 1 with only ADHD symptoms; 1 with BPD symptoms and ADHD symptoms of hyperactivity; 1 with BPD symptoms and ADHD symptoms of inattention, hyperactivity, and impulsivity; and 1 with BPD symptoms and ADHD symptoms of inattention and hyperactivity
Anyone else see the missing group?
Participants were consecutively recruited female patients referred to the outpatient ADHD program or outpatient BPD program at the Department of Psychiatry, Radboud University Nijmegen Medical Centre, the Netherlands. The patients were recruited during a period of approximately 3 years and had to meet the DSM-IV criteria for ADHD or BPD to be included in the study. Patients with clinically significant chronic medical conditions, mental retardation, organic brain disorders, or schizophrenia were excluded from the study. Patients with other comorbid psychiatric disorders were not excluded to make the sample as representative of the actual clinical population as possible.
Wut?
The presence of ADHD symptoms in childhood and adulthood (ie, current) was assessed using a semistructured interview for ADHD
Hey bruh, let me tell u bout muh ADD! Never mind interviews with people in their lives, or brain scans or anything like that.
Anyway, I could read on, but I've had enough.
10.1016@j.comppsych.2011.02.007.pdf 553.6KB
1 downloads
Posted 19 October 2016 - 08:39 PM
Wait...
WHAT? Strattera? Bupropion? I know Bup could have some potential, in my own research (anti-nicotinic), but Strattera?
Those two drugs actually implicate some form of ADHD, at least as a co-morbidity - which I suppose isn't out of the question, since impairments in the Frontal Lobe are implicated as well in BPD, not just the amygdala - comorbidity with ADHD fits rather nicely then.
(the Swedish scientist I mentioned before, even wants to reclassify it as a form of "Emotional ADHD", and thinks stimulants might help - which I suppose one could call a combo of Strattera and Bupropion - helluva' lot of cathecolaminergic activity on such a combo)
I don't think a lot reasoning went into this. she went to see her family practice doc because she was tired and i suspected hypothyroidism due to low dose lithium she used to be on (that we stopped since). the thyroid function went down, but only slightly. now, the doc used to prescribe concerta for her old diagnosis of ADHD (that i'm pretty sure she was misdiagnosed with) and he offered a free sample pack of the "new and greatest" ADHD medication. i'm not even sure he remembered he had her on bupropion for her depression episodes. i even asked her to stop bupropion, as it inhibits the p450 and can interfere with Strattera metabolism, but she felt even more tired without bupropion since it takes forever for Strattera to kick in.
she is back on both bupropion and Strattera (in addition to lamictal and the usual vitamin/mineral stack), but i didn't have a chance to talk to her since.
You can tell her Lamictal has even been linked to weight loss (it has), but if she wants a dose increase, you have to give it to her because it's not safe for her not to take it every day.
great idea, will consider it when the current combo is not working.
Posted 20 October 2016 - 01:12 AM
i'm not even sure he remembered he had her on bupropion for her depression episodes. i even asked her to stop bupropion, as it inhibits the p450 and can interfere with Strattera metabolism
Very impressive that you caught that. You're right, Strattera is a substrate of CYP2D6 (all of these enzymes are part of the P450 system, so that's a very broad brush), and Bupropion is a strong inhibitor of CYP2D6. This could be a good thing or a bad thing. It will simply make her dose of Strattera stronger. What dose is she on?
And the fact that he called Strattera 'the latest and great ADHD medication' makes me think twice of the aptitude of the doctor. It's been around for over a decade and has been well known to be a pretty shitty medication for ADHD.
Posted 20 October 2016 - 03:56 PM
Im sure it was a drug rep who left all those sleek samples and marketing materials (probably free dinners too).And the fact that he called Strattera 'the latest and great ADHD medication' makes me think twice of the aptitude of the doctor. It's been around for over a decade and has been well known to be a pretty shitty medication for ADHD.
Edited by jack black, 20 October 2016 - 03:58 PM.
Posted 20 October 2016 - 09:35 PM
Including ComorbiditiesPatients with clinically significant chronic medical conditions, mental retardation, organic brain disorders, or schizophrenia were excluded from the study. Patients with other comorbid psychiatric disorders were not excluded to make the sample as representative of the actual clinical population as possible.
Wut?
Excluding the typical patient: Thirty years of pharmacotherapy efficacy trials for obsessive-compulsive disorder
The presence of ADHD symptoms in childhood and adulthood (ie, current) was assessed using a semistructured interview for ADHD
Hey bruh, let me tell u bout muh
And that's the cheapest way to diagnose someone (i.e. doctor-patient dialectic), short of a combination of the aforementioned brain scans and blood/DNA tests.
Posted 21 October 2016 - 11:49 AM
She showed me the starter pack. Very impressive folded bubble pack covering 6 weeks with slowly increasing dose (up to 40mg IIRC) and clear instructions not to expect any effects before 4 weeks.
i called with her last night and my recollection was wrong. while is is taking 40mg now (finishing second week), the target dose is 60mg. she says that since she started taking it together with bupropion (150mg ER) this week, she noticed improvement in energy level and less eating. she is even making some progress in her studies.
Posted 21 October 2016 - 03:36 PM
Hmm.
Strattera has Kappa-agonism, along with the NE, and a combo of Bup and ATX is NOT just a little bit of a bump in NE... it's one helluva' bump!
It should also be noted that Atomoxetine failed it's trials as an antidepressant - it appears to be at least as sh*tty as Reboxetine, if not more, because of the Kappa-agonism.
The fact that she's reacting favorably AT ALL to this combo... it really does hint at some kind of attention or wakefulness-disorder - no WAY would she approve of the effects of this stuff otherwise. Need I remind everyone that the Kappa-agonism is the hypothesised effect of ATX which causes it to have the greatest amount of Suicidal Ideation of every drug currently on the market, as a side-effect?
There's no way there's NOT something to this response...! This ain't sugar-pills, folks.
So, I'm willing to say there's merit to that ADHD-diagnosis of hers - I'd say it's very likely it's not her only issue, but it does seem to be a factor. The fact that all of a sudden she's making progress into her studies, is another sign - classic ADHD-response to medication: doing better in school.
Posted 21 October 2016 - 08:19 PM
Posted 21 October 2016 - 08:38 PM
There is no question she has some form of executive dysfunction. This is why her parents took her to several different psychologists since she started a junior high school and she struggled with organization. Only the last one suggested possibly ADHD, even though his tests were inconclusive. She was in high school by then. They were told to do concerta trial and continue if helpful. There was some improvement in school and she was on that low dose for a few years. She stopped taking it when in university, because she didn't like the wired feeling and it would make her supposedly more tired. That's when her life got totally messed up.
I didn't know her all that well at that time, but based on what I've heard it didn't sound like typical ADHD. Only recently it surfaced she had multiple episodes of significant self harm and I got involved because it initially sounded like a bunch of mystery medical problems and my profession is related to medicine.
This is when I started looking for something beyond ADHD and depression to explain all the mood issues and self harm, especially since the initial depression treatment wasn't working all that well.
I guess she could have ADHD and another mood disorder rather than another disorder giving ADHD-like symptoms like I favored. Either way, it's semantics. I wish there was a biomarker. I recommended doing 23&me and it turned out to be useless.
Too bad with the 23andme, : ( but then disorders which are similar to ADHD are not as studied as ADHD itself - we don't have much of an idea about what the deal is with the genetics behind SCT for instance - and according to Dr. Barkley and the model of attention, there are 6 different dimensions - ADHD and SCT only correspond to TWO... that leaves 4 more disorders to fuck up your organisatorial skills.
Tell you the truth, I THINK Borderline is another one - and there does seem to be a lot of comorbidity - if Dr. Predrag Petrovic is right, then there's a connection between Borderline and ADHD, but not between Borderline and SCT.
(it actually seems like the PFC-part of our disease is very small... it's almost entirely SPL-based. Borderline however, DOES show PFC-abnormalities, consistently - that's why I thought Intuniv would help, for a while.)
But hey, now with the 23andme and services to run her data through, you can catch any undesirable potential interactions from her metabolism on the drugs! =) For instance, I would not have known I was a slow metabolizer of Strattera otherwise - well, I would have found out the HARD way - the really, really hard way...!
(think: suicide, dude.)
Anyways, I'm MOST pleased to hear that she's doing well though! = ) Every time someone attention-disturbed gets help, it wams my heart - gives hope even to a wreck of a man like me.
Never stop fighting! Never give up! If you must yield, then be like the reed in the wind, like water around a rock! Stick and move, stick and move...
Posted 22 October 2016 - 03:36 PM
Edited by jack black, 22 October 2016 - 03:38 PM.
Posted 22 October 2016 - 05:36 PM
Ey, anybody know if there's any ongoing trials of Hydroxynorketamine? I STILL think HNK has tremendous potential as a mood-stabilizer - it's just that it hasn't been trialled for that - all they did was trial it for depression.
I'm all confused about all those treatment affects. For example she is homozygous for 2 different COMT polymorphisms that suggests too much DA and NE. That explains the poor response to concerta. On the other hand she responded favorably to the strattera and welbutrin combo that also has NE effects. Is the serotonin effect in strattera that makes a difference? If so, why she had no response to 5htp or inositol?
Same with you. If you respond well to (high doses) bupropion and other stimulants, why this bad reaction to strattera?
I don't respond well to Methylphenidate though - in fact, I respond terribly! It's got 5ht1a agonism though, and I'm guessing, because of the selectivity to which parts of the brain in which it attaches, it activates the anxious response - as you recall, anxiety has now been connected to serotonergic hyperactivity in certain parts of the brain.
I've got the alterations to my COMT-enzymes as well, but even so, there are malfunctions in my norepinephrinergic circuitry (a lot of my symptoms really do correlate to abnormalities in the SPL, and that's a mostly NE-region), so even though I may have naturally occuring high NE, it might not do much when a certain part of my brain needs quadruple-fold or whatever levels, than normal.
Even if I've got double the levels than others, then I've still got HALF the juice I actually need, yes?
Never tried Strattera btw - the potential bad reaction is all theoretical at this point. Suicidal Ideation isn't caused by the NE itself though, it's the combination with Opioid KAPPA-receptor agonism which causes that - and in general, only if you have upregulated Kappa-receptors, which a lot of adult ADD-ers have. (it's a natural response to constant failure, which leads to learned helplessness)
In theory though... I might actually have been needlessly worried about that - because it's actually the METABOLITE of Atomoxetine which has that property, not ATX itself. And I don't metabolise ATX to any greater extent - it could take months before I start noticing any such effects, and by then, I might actually have down-regulated Kappa-receptors... it's a very real problem for some people though.
Apparently NOT so your cousin though... she doesn't seem to feel the Kappa-effects at all! Intriguing. Wonder if she's a slow metabolizer as well...?
Edited by Stinkorninjor, 22 October 2016 - 05:44 PM.
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