Increasing motivation

[upright]

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Any drug that does that? Say you have a patient that has a desire to accomplish X task, but is unable to summon the vigor. Perhaps due to depression, perhaps due to something else. Aside from therapy, how would medication aid in this?

 

[Sneezing]

Medication can't correct motivation, with the exception of true depression not confounded by chronic pain or personality disorder.

 

[upright]

Medication can't correct motivation, with the exception of true depression not confounded by chronic pain or personality disorder.

Maybe motivation is the wrong word. The patient obviously has the motivation, yet they lack the vigor.

 

[zenman]

Maybe motivation is the wrong word. The patient obviously has the motivation, yet they lack the vigor.

I'd think maybe nucleus accumbens - pleasure and motivation or deep limbic system - triggers of behavior. Dopamine is involved in motivation. By vigor do you mean "no get up and go?"

 

[xlithiumx]

Maybe motivation is the wrong word. The patient obviously has the motivation, yet they lack the vigor.

I like bupropion in conjunction with behavioral activation therapy (a form of CBT) for the patient who wants to accomplish things but is having trouble getting the ball rolling. I think the mild stimulant effect of the buproprion increases energy/motivation and the structure and accountability of behavioral activation therapy helps as well. Eventually patients seem to be able to accomplish more things on their own, take on responsibility more spontaneously.

 

[erg923]

I think discussing with the patient what they think the road block is here, is likely the best (only?) way to address the problem. There is a whole school of psychotherapy built on not wanting to do something, but just doing it anyway. 😀

http://en.wikipedia.org/wiki/Acceptance_and_commitment_therapy

.

 

[nitemagi]

Indeed. Even the behavioral aspect of CBT can involve doing activities Before the motivation is there, for the purpose of kickstarting things.

 

[loveoforganic]

Smoking crack produces a remarkable motivation to smoke more crack.

Tackle the specific barrier to performance

 

[strangeglove]

If we are thinking about a medication to boost motivation or energy in a depressed individual who has had a partial response to an adequate dose of an antidepressant, then a little stimulant augmentation works well for this. Sometimes behavioral activation is just too difficult for some folks, especially the elderly and medically ill.

 

[splik]

I think the psychopharmacology of motivation and drive are very interesting theoretically. Norepinephrine has a key role in motivation, and dopamine increases the motivation to perform activities that are pleasurable via a reward loop. I believe that amineptine, one of the atypical tricyclics was touted for this particular for this indication, as has tianeptine. I dont think either are available in the US however. Reboxtine, a noradrenaline reuptake inhibitor, has also been promoted for anergia and amotivationality. It would be interesting to test whether it did have such an effect, because this would not be through any antidepressant properties (a meta-analysis in the Lancet some years ago showed reboxetine to be the least efficacious antidepressant). However, again this drug is not available in the US.

Methylphenidate has sometimes been used for this setting.

When talking about the psychopharmacology of motivation one relies of proof-of-concept studies, case series, there aren't really RCTs here.

In clinical practice, the problem with treating motivational problems pharmacologically is you become little more than a glorified drug dealer.

 

[whopper]

Agree with all the above.

Lack of motivation, in and of itself is not a pathology. Several disorders such as depression or psychosis could cause one to lose motivation. There is no medication known that simply improves motivation. If motivation is lost due to, say depression, then an antidepressant could improve the depression, and hence improve motivation that was lowered from the depression.

If the person lacks the "vigor" it could be the person has lack of energy, stamina, or focus. A whole multitude of problems could be causing this such as ADHD, the person merely not caring and really not being in a position where they have to care, hypothyroidism, etc.

I have a patient and the guy just mopes around in his dad's home, not getting a job, and the father is sick of it. All the kid does is sit in his room all day, play video games, and talk as if he's a stoner. The dad brought the kid to my office and told me to fix the kid. After several meetings...several, and I'm feeling guilty because the father paid a lot of money for each visit, I found no conventional Axis I pathology. All of his labs I can think of that would display a medical/biological reason for lack of motivation to do anything is lacking. E.g. normal TSH, Vit B, folate levels, UDS is negative, etc. Psychological testing was all invalid because the kid put no effort into the testing. The kid (actually 21 years old) gives minimal answers. E.g. "What do you want out of life?" Kid: "I don't know. (stares at the ground for a few minutes). Um....I don't know."

I'm stumped. Some of the only theories I got is this kid is in the prodrome phase of schizophrenia, or perhaps has a cluster A personality disorder. I told the father what I could come up, and I felt very disappointed in myself for having seen this kid so many times and that was all I could do. Several antidepressants were tried, no effect. I did try a stimulant thinking this my be inattentive ADHD, and oddly it made the kid tired, bur it didn't improve anything.

 

[nitemagi]

I have a colleague/friend with a book coming out soon that has some great exercises for procrastination. I'll try to remember to post once the book is released. Anecdotally I've tried the exercise myself with good success.

 

[zenman]

Agree with all the above.

Lack of motivation, in and of itself is not a pathology. Several disorders such as depression or psychosis could cause one to lose motivation. There is no medication known that simply improves motivation. If motivation is lost due to, say depression, then an antidepressant could improve the depression, and hence improve motivation that was lowered from the depression.

If the person lacks the "vigor" it could be the person has lack of energy, stamina, or focus. A whole multitude of problems could be causing this such as ADHD, the person merely not caring and really not being in a position where they have to care, hypothyroidism, etc.

I have a patient and the guy just mopes around in his dad's home, not getting a job, and the father is sick of it. All the kid does is sit in his room all day, play video games, and talk as if he's a stoner. The dad brought the kid to my office and told me to fix the kid. After several meetings...several, and I'm feeling guilty because the father paid a lot of money for each visit, I found not conventional Axis I pathology. All of his labs I can think of that would display a medical/biological reason for lack of motivation to do anything is lacking. E.g. normal TSH, Vit B, folate levels, UDS is negative, etc. Psychological testing was all invalid because the kid put no effort into the testing. The kid (actually 21 years old) gives minimal answers. E.g. "What do you want out of life?" Kid: "I don't know. (stares at the ground for a few minutes). Um....I don't know."

I'm stumped. Some of the only theories I got is this kid is in the prodrome phase of schizophrenia, or perhaps has a cluster A personality disorder. I told the father what I could come up, and I felt very disappointed in myself for having seen this kid so many times and that was all I could do. Several antidepressants were tried, no effect. I did try a stimulant thinking this my be inattentive ADHD, and oddly it made the kid tired, bur it didn't improve anything.

Ok, here's your intervention. Remember the Michael Douglas movie, "The Game?" Get the dad to set up something like that.

 

[zenman]

I have a colleague/friend with a book coming out soon that has some great exercises for procrastination. I'll try to remember to post once the book is released. Anecdotally I've tried the exercise myself with good success.

How far behind is he in getting it published? 😀

 

[whopper]

Get the dad to set up something like that.

Heheh.

Yeah well another big handicap is the kid is perfectly content living in his parents basement, doing the absolute bare minimum. He doesn't want anything changed. Patients that have an Axis I problem either want help, or in a position where the government mandates it because the patient is involuntary committed or under a 72-hour hold. He told me he is not depressed, though is very odd, e.g. blank stare, minimal speech, and just sits in the chair during interviews giving me hardly anything.

I certainly find it pathological that this guy at age 21 has no intention of finding a job and just playing video games 12 hours a day while smoking cigarettes.

MMPI-nothing because the results are invalid, I gave him a TOVA-the results are invalid because he just sat there and pressed the buttons without really trying to do it (malingering index was through the roof-but it also goes through the roof if someone just presses the button without trying), interviews are fruitless.

I just told the dad that I treat mental illness, and if this kid has one, it's not something that's in the book, and since he has no motivation to seem to want to do anything that too is a huge obstacle. I told the father I didn't want to take more of his money unless I had something reasonable to latch onto in terms of direction for possible treatment.

 

[nitemagi]

How far behind is he in getting it published? 😀

It's due to be published this year. I don't know where he is in manuscript deadlines and release date.

I would agree with Whopper that at least per DSM, lack of motivation is not a psychopathology. Nor is lack of life aspirations.

However, in regards to his case, avoidance d/t fear/anticipatory anxiety (social anxiety<-->avoidant PD) IS, as is dependent PD, which are both possible reasons for someone to appear to have no motivation and thus not want to leave home. I would probe, as others have discussed, as to what gets in the way of doing things, or in this case how he would feel if he were to leave home, or be Forced to leave home.

Whopper's case sounds like someone who hasn't yet had to assume an adult role, possibly through parental enabling, allowing him to stay maturationally stagnant. What if he was given a time limit to get a job or be evicted? Or just a time limit to be evicted so has to fend for himself? Just some thoughts off the top of my head.

 

[PETRAN]

Agree with all the above.

Lack of motivation, in and of itself is not a pathology. Several disorders such as depression or psychosis could cause one to lose motivation. There is no medication known that simply improves motivation. If motivation is lost due to, say depression, then an antidepressant could improve the depression, and hence improve motivation that was lowered from the depression.

If the person lacks the "vigor" it could be the person has lack of energy, stamina, or focus. A whole multitude of problems could be causing this such as ADHD, the person merely not caring and really not being in a position where they have to care, hypothyroidism, etc.

I have a patient and the guy just mopes around in his dad's home, not getting a job, and the father is sick of it. All the kid does is sit in his room all day, play video games, and talk as if he's a stoner. The dad brought the kid to my office and told me to fix the kid. After several meetings...several, and I'm feeling guilty because the father paid a lot of money for each visit, I found no conventional Axis I pathology. All of his labs I can think of that would display a medical/biological reason for lack of motivation to do anything is lacking. E.g. normal TSH, Vit B, folate levels, UDS is negative, etc. Psychological testing was all invalid because the kid put no effort into the testing. The kid (actually 21 years old) gives minimal answers. E.g. "What do you want out of life?" Kid: "I don't know. (stares at the ground for a few minutes). Um....I don't know."

I'm stumped. Some of the only theories I got is this kid is in the prodrome phase of schizophrenia, or perhaps has a cluster A personality disorder. I told the father what I could come up, and I felt very disappointed in myself for having seen this kid so many times and that was all I could do. Several antidepressants were tried, no effect. I did try a stimulant thinking this my be inattentive ADHD, and oddly it made the kid tired, bur it didn't improve anything.

Very interesting case. Maybe negative symptoms of prodromal shcizophrenia? Was the kid always like that? Teenage years? Personality in the recent past?


Good vignette 😛


p.s. i remember reading a very similar case of a patient who had an undiagnosed frontal-lobe tumour for years wat 😱 (but he was supposed to be much older)

 

[F0nzie]

just playing video games 12 hours a day

JUST playing video games 12 hours a day? What if he's immersed in a world of dungeons, cold-steel, and mighty foes? A world where death is lurking around every corner and it's dependent upon him to gain mastery of the elements of fire, wind, and earth for completion of his quest? What if his journey is an epic tale of good vs. evil, right vs. wrong...and only 1 hero can save the world from ultimate destruction?

 

[whopper]

I don't think this is a video game "addiction" (in qoutations because some definitions of the word addiction require the use of a substance.

Why? People with such a problem usually talk about it. The guy just stares at the ground during the entire interview. He seems to lack passion about anything.

Very interesting case. Maybe negative symptoms of prodromal shcizophrenia? Was the kid always like that? Teenage years? Personality in the recent past?

That's what I was thinking. The problem being am I going to start him on an antipsychotic? My personal algorithm in these cases is this....
1) Do everything you can to rule everything else out. I think I exhuasted this step.
2) Present the possibility of prodrome to the patient. Tell them that there is no way to detect this in a clinical setting until after schizophrenia has already occurred. Yes there are ways to possibly detect earlier but PET scans are not the norm to be done on everyone annually. By the way, I currently have 4 patients where I highly suspect prodrome schizophrenia may be going on.
3) After telling the patient that prodrome is a possibilty, tell the them their options. I usually recommend fish oil, avoidance of marijuana among other illicit substances, recommend the patient read up on their own concerning the nature of psychosis and to keep a diary to see if they notice anything out of the ordinary such as hallucinations, paranoia, etc. Also to have close friends or family members they could trust to be an anchor and reference to see if those people notice the patient changing in a possibly pathologic way.

While I tell the patient an antipsychotic is an option, I never tell them I recommend it, but will provide it only if the patient wants it. I tell them if they got prodrome, the medication can help, if I knew for sure they had it, I'd recommend the med, but I don't ever know if someone is in prodrome for sure until the person actually develops diagnosable schizophrenia.

The kid did not want to take an antipsychotic. So be it. I can't do anything more along that theory. Surely if the kid showed dramatic improvement on one it would indicate with a stronger possibility this is a psychotic spectrum problem.

 

[nitemagi]

I don't think this is a video game "addiction" (in qoutations because some definitions of the word addiction require the use of a substance.

Why? People with such a problem usually talk about it. The guy just stares at the ground during the entire interview. He seems to lack passion about anything.



That's what I was thinking. The problem being am I going to start him on an antipsychotic? My personal algorithm in these cases is this....
1) Do everything you can to rule everything else out. I think I exhuasted this step.
2) Present the possibility of prodrome to the patient. Tell them that there is no way to detect this in a clinical setting until after schizophrenia has already occurred. Yes there are ways to possibly detect earlier but PET scans are not the norm to be done on everyone annually. By the way, I currently have 4 patients where I highly suspect prodrome schizophrenia may be going on.
3) After telling the patient that prodrome is a possibilty, tell the them their options. I usually recommend fish oil, avoidance of marijuana among other illicit substances, recommend the patient read up on their own concerning the nature of psychosis and to keep a diary to see if they notice anything out of the ordinary such as hallucinations, paranoia, etc. Also to have close friends or family members they could trust to be an anchor and reference to see if those people notice the patient changing in a possibly pathologic way.

While I tell the patient an antipsychotic is an option, I never tell them I recommend it, but will provide it only if the patient wants it. I tell them if they got prodrome, the medication can help, if I knew for sure they had it, I'd recommend the med, but I don't ever know if someone is in prodrome for sure until the person actually develops diagnosable schizophrenia.

The kid did not want to take an antipsychotic. So be it. I can't do anything more along that theory. Surely if the kid showed dramatic improvement on one it would indicate with a stronger possibility this is a psychotic spectrum problem.

I wouldn't go so far as to say you have evidence for negative sx's of schizophrenia as much as lack of social skills, which is often what pushes people into excessive computer or video game playing (though not the only factor, of course). Sure prodromal should be in the ddx, but is there some reason it's top of the list for you?

Also, think about other interventions -- http://www.ncbi.nlm.nih.gov/pubmed/16122813

 

[whopper]

The guy pretty much looked schizophrenia minus that he had no positive symptoms of psychosis.

No motivation, asocial, poor eye contact, minimal speech, just sat in his chair during the interview.

Forgot to mention, according to the dad he was like this in high school as well. He did mediocre in school, getting mostly Cs and doing well enough to simply graduate. The father told me the only way he can get this kid to do anything other than ADLs, video games, and smoke is to deny the kid cigarettes because that kid has no source of income. Then the kid becomes irritable but he still just stays in his room and plays video games. The father compared getting him to do anything requires that the father deny cigarettes, then the kid going to his room, upset but in a quiet "silent treatment" manner. Eventually the kid will do something miniscule to acquiesce his father just to get the cigarette with a "common dad" complaint said in a slow manner.

Of course this might not be psychosis, but just WTF this is I don't know. I was thinking perhaps this was really bad inattentive ADHD but the kid's TOVA test was invalid, and after trying that stimulant (that made him tired, stims usually don't do that unless the person truly has ADHD), and doing serial EKGs to make sure he was safe for stims, one was abnormal and it turned out he had hypertrophic cardiomyopathy. A cardiologist saw him and recommended no stims or Stattera--ever.

The only other issue that was strange that gave me some direction was his BP is always abnormally low. They're usually around 80/45. I was speculating maybe he wasn't getting enough blood to his head but given that he has no complaints of hypotension (e.g. headache), and just sits there....this was another dead end.

So my DDX:
Prodrome psychosis: dead end. No way to verify if prodrome is going on without meds, and he doesn't want to try them and I can't blame him.
Depression: denies he's depressed, 2 antidepressant trials-no difference (see below)
Cluster A PD: possible
ADHD: dead end. He won't cooperate to do a TOVA test for real. He just presses the buttons in a manner indicating he's not even trying. Results are invalid. Can't do stimulants or strattera due to the heart condition. Can't do guanfacine or Clonidine due to abnormally low BP. Wellbutrin-max dose x 3 months, no significant difference. Effexor-max dose x 3 months, no significant difference.
Other developmental disorders: doesn't meet the criteria of any of them.

MMPI results are invalid. TOVA is invalid. Labs are all normal and I don't find any reason to start ordering the zebra labs. Don't know what else to do.

There was an article in the Carlat Report about a year ago mentioning that there is a psychological test being developed that has been able to significantly identify people truly in the prodrome phase, but that test is not yet available to the public. If it were out, I definitely would've done one on him.

 

[strangeglove]

Sounds like a personality disorder.

 

[whopper]

I told him and his dad if this was schizoid, there's no real treatment for it other than psychotherapy, and the use of meds may provide some benefit but it's not something studied well. I do have schizoid patients and they don't have a problem looking for work and just moping around doing nothing other than video games. He showed no motivation for psychotherapy when I offered it.

The ones I got that I treat, what's going on is they are forced to interact with people, and that causes them to be anxious or depressed, and the come to me for treatment for that, not due to their desire to be solitary.

Of course this just could be schizoid of another variety that I haven't seen before because this is a phenomenon I don't see mentioned much. All disorders present in varying ways and I haven't had dozens of cases like this--just a handful.

What's going on certainly is pathological. It's to the degree where if his father refused to take care of him, I realistically believe this kid would end up homeless because his detachment from reality in the sense that he seems ambivalent to everything is very strong. He's not even passionate about the video games.

 

[nitemagi]

I told him and his dad if this was schizoid, there's no real treatment for it other than psychotherapy, and the use of meds may provide some benefit but it's not something studied well. I do have schizoid patients and they don't have a problem looking for work and just moping around doing nothing other than video games. He showed no motivation for psychotherapy when I offered it.

The ones I got that I treat, what's going on is they are forced to interact with people, and that causes them to be anxious or depressed, and the come to me for treatment for that, not due to their desire to be solitary.

Of course this just could be schizoid of another variety that I haven't seen before because this is a phenomenon I don't see mentioned much. All disorders present in varying ways and I haven't had dozens of cases like this--just a handful.

What's going on certainly is pathological. It's to the degree where if his father refused to take care of him, I realistically believe this kid would end up homeless because his detachment from reality in the sense that he seems ambivalent to everything is very strong. He's not even passionate about the video games.

Interesting possible zebra!

Schizoid definitely seems in the ddx, and I'm throw in that Asperger's didn't make it into the English Medical literature until the 1980's, and that there's a theorized big overlap between asperger's and schizoid, even that they might be different faces of the same condition.

 

[PETRAN]

Yeah, Asperger could be an explanation but then again he said that he was like that from high-school. If it was Asperger's he would always be like that right? (although it could get more unnoticed during childhood).

It seems to be some kind of overlap between autistic spectrum and psychotic spectrum since they both invlove some-kind of theory-of-mind deficit. It is a very interesting relation but still unclear.


Maybe on the schizoid personality spectrum or prodromal negative schiz but maybe recommend a neuro-exam just in case?

 

[whopper]

If it was Asperger's he would always be like that right?

Yes.

That thought crossed my mind as well. I double checked the Asperger criteria, did some lit-reviews, etc...

But I came to this unfortunate conclusion. Even if it were that...in fact maybe it's both, Asperger's and schizoid, what can I do to help him? Seems like I can't do anything. This is one of the few cases where I ended up in a dead end where I felt I couldn't do anything to move the case along further and I was very bothered by it given how much money the father paid for my work.

The only option I could think of was trying more meds but it would literally be educated guesses in the hope that something would do something, while documenting each trial to see what happened. I would've tried an atypical on the possibility this could be schizophrenia prodrome.

And guess what? Everytime he took the meds, it was because his father strongly encouraged it. He just sat there, moped, and took it.

 

[PETRAN]

Yes.

That thought crossed my mind as well. I double checked the Asperger criteria, did some lit-reviews, etc...

But I came to this unfortunate conclusion. Even if it were that...in fact maybe it's both, Asperger's and schizoid, what can I do to help him? Seems like I can't do anything. This is one of the few cases where I ended up in a dead end where I felt I couldn't do anything to move the case along further and I was very bothered by it given how much money the father paid for my work.

The only option I could think of was trying more meds but it would literally be educated guesses in the hope that something would do something, while documenting each trial to see what happened. I would've tried an atypical on the possibility this could be schizophrenia prodrome.

And guess what? Everytime he took the meds, it was because his father strongly encouraged it. He just sat there, moped, and took it.

Yes, it is sad, but hey, at least you've tried hard (the old good advice 😛). Don't worry, its almost always like that in the neuro clinic i am now 😡


Do atypicals improve negative symptoms? The question has crossed my mind and i wanted to start a thread about that. Almost every single patient i've seen always complained about how the "meds (almost always atypical antipsychotics, usually from risperidone but also sometimes from newer-even more "atypical" ones- like aripiprazole) made them slow, without energy/drive and careless about anything". Could it be that the atypicals actually worsen negative symptoms? I mean, if they work by inhibiting D2 receptors, wouldn't that mean that their drive/motivation/pleasure/working memory would also go down? Or is it because the patients can't really distinquish between the possible side-effects of the drugs from the symptoms of the disorder itself? Or is it because the scientists and doctors can't really distinquish between the two (!)?

 

[nitemagi]

Do atypicals improve negative symptoms? The question has crossed my mind and i wanted to start a thread about that. Almost every single patient i've seen always complained about how the "meds (almost always atypical antipsychotics, usually from risperidone but also sometimes from newer-even more "atypical" ones- like aripiprazole) made them slow, without energy/drive and careless about anything". Could it be that the atypicals actually worsen negative symptoms? I mean, if they work by inhibiting D2 receptors, wouldn't that mean that their drive/motivation/pleasure/working memory would also go down? Or is it because the patients can't really distinquish between the possible side-effects of the drugs from the symptoms of the disorder itself? Or is it because the scientists and doctors can't really distinquish between the two (!)?

Atypicals unfortunately don't improve negative sx's, despite the early hope that they would (via 5HT2A antagonism). The data has not shown such a benefit despite the theoretical benefit.

 

[PETRAN]

Atypicals unfortunately don't improve negative sx's, despite the early hope that they would (via 5HT2A antagonism). The data has not shown such a benefit despite the theoretical benefit.

Yes, but could they actually make them worse due to D2 antagonism?

 

[whopper]

Antipsychotics could worsen the patient in a manner that could resemble negative symptoms of psychosis but for the most part (with rare exceptions) not actually worsen the psychosis itself.

E.g. You give Seroquel and it knocks someone out, sure that could look like negative psychosis, but in reality the person is just gorked.

I've seen several patients with negative signs of psychosis improve with antipsychotics, but you have to be mindful that the goal is to actually improve the patient. For example if a belligerent, irritable, and paranoid patient is knocked out on Thorazine, and the psychosis in reality is left untouched, some idiot doctors equate his lack of complaining with improvement because he's not bothering anyone.

A real test to see if the person improved is to see how they do once the sedation effect wears off, and with Thorazine good luck because that might not happen until the meds are stopped.

The rare exceptions? Too many antipsychotics could cause delirium due to the interactions with the cholinergic system. There's also tardive psychosis, a phenomenon that is not certainly to exist, but in theory is supposed to cause hypersensitivity of D2 receptors due to chronic blockade with antipsychotics. In which case the person becomes psychotic and then the use of strong D2 blockers may cause this problem to become worse.

Another problem is antipsychotics could reduce a comorbid manic component, and several patients like being manic.

I also hypothesize that it could be influencing, in a bad way, dopamine's general effects in the brain including wakefullness, alertness, euphoria, and the nucleus accumbens, and indirectly lower testosterone--thus lowering a person's quality of life in general.

I work in a forensic facility where I often times have several several weeks to months to get patients better because even when stabilized, they cannot be discharged until the court approves, and the court takes their time. In several cases, even if an antipsychotic works, I give the patient the option to try other ones to see which one gives them the best quality of life. In this clinical setting, my threshold for taking a patient off a med due to side effects is very low due to me having a lot of time to get it right.

 

[PETRAN]

Antipsychotics could worsen the patient in a manner that could resemble negative symptoms of psychosis but for the most part (with rare exceptions) not actually worsen the psychosis itself.

E.g. You give Seroquel and it knocks someone out, sure that could look like negative psychosis, but in reality the person is just gorked.

I've seen several patients with negative signs of psychosis improve with antipsychotics, but you have to be mindful that the goal is to actually improve the patient. For example if a belligerent, irritable, and paranoid patient is knocked out on Thorazine, and the psychosis in reality is left untouched, some idiot doctors equate his lack of complaining with improvement because he's not bothering anyone.

A real test to see if the person improved is to see how they do once the sedation effect wears off, and with Thorazine good luck because that might not happen until the meds are stopped.

The rare exceptions? Too many antipsychotics could cause delirium due to the interactions with the cholinergic system. There's also tardive psychosis, a phenomenon that is not certainly to exist, but in theory is supposed to cause hypersensitivity of D2 receptors due to chronic blockade with antipsychotics. In which case the person becomes psychotic and then the use of strong D2 blockers may cause this problem to become worse.

Another problem is antipsychotics could reduce a comorbid manic component, and several patients like being manic.

I also hypothesize that it could be influencing, in a bad way, dopamine's general effects in the brain including wakefullness, alertness, euphoria, and the nucleus accumbens, and indirectly lower testosterone--thus lowering a person's quality of life in general.

I work in a forensic facility where I often times have several several weeks to months to get patients better because even when stabilized, they cannot be discharged until the court approves, and the court takes their time. In several cases, even if an antipsychotic works, I give the patient the option to try other ones to see which one gives them the best quality of life. In this clinical setting, my threshold for taking a patient off a med due to side effects is very low due to me having a lot of time to get it right.

Execellent post Whopper, very informative.


What i've seen (many times) is patient coming in floridly psychotic, paranoid, agitated etc. so patient is given some anti-psychotics. After a few days/weeks patient improves but while he/she was in a kinda hyper-aroused state before the treatment , now he/she lies silent, blank stares, flat-affect, kinda like exhausted and burnt-out. Some attending would say "ah its negative symptoms" but why do these "negative symptoms" occur after the aggressive drug-treatement? I could understand the "negative symptoms" argument if patient was presented with negative symptoms right from the start (like presenting with no emotions, no concentration and drive, abulic, with little speech, usually with thought disorder etc.-and in some cases they do), but in many cases patients present over-active, scared, confused, agitated etc.


Patients themseleves complain that the drugs make them "slow", without energy, emotions and without the ability to concentrate but many psychiatrists would not believe them and respond "well, its due to the disorder and not the drugs". But is it?

It seems very logical to me that if you block the "energy-motivation-reward-concentration" dopaminergic system you'll get something that very much resembles the so-called negative symptoms. Maybe there is no other way since the positive symptoms are an "over-activity" mental state (over-flow of perceptions and thoughts, hyper-associations between events, high emotionality etc.) and the only way to decrease it is by inducing the opposite (too little of all that stuff) and in doing so you might causing some-kind of a mild/subtle deficit. But i guess that there is always a cost-benefit analysis going-on.


Maybe a problem with current drugs is that they are not very selective. Maybe finding a drug that blocks only a hypothetical psychosis-specific brain area/circuit (if it exists, although my guess would be that it would overlap with a lot of "normal functions") would be much better for the quality of life of many patients, but maybe i'm talking science-fiction here. Lets hope that research would lead to some more "intelligent" and "specific" compounds.

 

[nitemagi]

Execellent post Whopper, very informative.


What i've seen (many times) is patient coming in floridly psychotic, paranoid, agitated etc. so patient is given some anti-psychotics. After a few days/weeks patient improves but while he/she was in a kinda hyper-aroused state before the treatment , now he/she lies silent, blank stares, flat-affect, kinda like exhausted and burnt-out. Some attending would say "ah its negative symptoms" but why do these "negative symptoms" occur after the aggressive drug-treatement? I could understand the "negative symptoms" argument if patient was presented with negative symptoms right from the start (like presenting with no emotions, no concentration and drive, abulic, with little speech, usually with thought disorder etc.-and in some cases they do), but in many cases patients present over-active, scared, confused, agitated etc.


Patients themseleves complain that the drugs make them "slow", without energy, emotions and without the ability to concentrate but many psychiatrists would not believe them and respond "well, its due to the disorder and not the drugs". But is it?

It seems very logical to me that if you block the "energy-motivation-reward-concentration" dopaminergic system you'll get something that very much resembles the so-called negative symptoms. Maybe there is no other way since the positive symptoms are an "over-activity" mental state (over-flow of perceptions and thoughts, hyper-associations between events, high emotionality etc.) and the only way to decrease it is by inducing the opposite (too little of all that stuff) and in doing so you might causing some-kind of a mild/subtle deficit. But i guess that there is always a cost-benefit analysis going-on.


Maybe a problem with current drugs is that they are not very selective. Maybe finding a drug that blocks only a hypothetical psychosis-specific brain area/circuit (if it exists, although my guess would be that it would overlap with a lot of "normal functions") would be much better for the quality of life of many patients, but maybe i'm talking science-fiction here. Lets hope that research would lead to some more "intelligent" and "specific" compounds.

Petran,

theoretically D2 blockers do very well getting rid of the positive sx's, and what is left once treated is the negative sx's. Of course the sedation from many meds can easily look like negative sx's as well. Whopper already mentioned anticholinergic effects (which can ultimately cause a delirium but at lower doses just a cognitive cloudiness). 5HT2A antagonism is what was theorized to help negative sx's, which was particular to most atypical/2nd gen antipsychotics. There is pretty good research that those with classical schizophrenia (schneiderian) have cognitive deficits, including (but not limited to) inhibition and acclimation to stimuli (such as measured with pre-pulse inhibition). In the area of PPI a lot of the research shows antipsychotics correct PPI, though, and since antipsychotics don't seem to help negative sx's this doesn't seem to be the sole explanation/component for negative sx's.

Selectivity is a huge problem. We're not bad at hitting receptors, but not the specific brain regions. We talk about the mesolimbic area being related to positive psychotic sx's (paranoia, hallucinations), and mesocortical being related to negative sx's. Conceptually why you would consider limbic encephalitis in the ddx of a new onset psychosis case.

Here's an article I found quickly (review) on neurocog deficits in schizophrenia.
http://www.ncbi.nlm.nih.gov/pubmed/21312407

This is being written about a lot more, as the real frontier being focused on is cognitive rehab for schizophrenics, with a lot of possible meds that Could help (as usual, all theoretical), including galantamine (and other cholineesterase inhibitors) and namenda. Glutamate antagonists are talked about as maybe the next big thing too, but it could all be hype.

 

[PETRAN]

Petran,

theoretically D2 blockers do very well getting rid of the positive sx's, and what is left once treated is the negative sx's. Of course the sedation from many meds can easily look like negative sx's as well. Whopper already mentioned anticholinergic effects (which can ultimately cause a delirium but at lower doses just a cognitive cloudiness). 5HT2A antagonism is what was theorized to help negative sx's, which was particular to most atypical/2nd gen antipsychotics. There is pretty good research that those with classical schizophrenia (schneiderian) have cognitive deficits, including (but not limited to) inhibition and acclimation to stimuli (such as measured with pre-pulse inhibition). In the area of PPI a lot of the research shows antipsychotics correct PPI, though, and since antipsychotics don't seem to help negative sx's this doesn't seem to be the sole explanation/component for negative sx's.

Selectivity is a huge problem. We're not bad at hitting receptors, but not the specific brain regions. We talk about the mesolimbic area being related to positive psychotic sx's (paranoia, hallucinations), and mesocortical being related to negative sx's. Conceptually why you would consider limbic encephalitis in the ddx of a new onset psychosis case.

Here's an article I found quickly (review) on neurocog deficits in schizophrenia.
http://www.ncbi.nlm.nih.gov/pubmed/21312407

This is being written about a lot more, as the real frontier being focused on is cognitive rehab for schizophrenics, with a lot of possible meds that Could help (as usual, all theoretical), including galantamine (and other cholineesterase inhibitors) and namenda. Glutamate antagonists are talked about as maybe the next big thing too, but it could all be hype.

Yeah, i've heard about glutamate too (That eli lilly drug? What happened to it is it still in development?) Lets hope that something good will come from this glutamate hype.


Schizophrenia research and theoretical models is/are a bit chaotic. Symptom-clusters are overlapping and loose and you can't know for sure if it is due to the disorder, the drug, previous drug-abuse, the mental-health ward, various co-morbidities...there are neuro-developmental models, neuro-degenerative models, neuro-normal models, a mix of all of them... some say schiz. is one big spectrum others that they are different disorders grouped under schizophrenia...it is "insane" 😛 it is a very complicated area (and this is why it is probably stimulating)


Neuro-cognition in schiz is an area of great interest to me so thanks for the link! I'm currently doing research on the neurocognition of OCD (reduced cognitive/motor inhibition/set-shifting/reversal learning difficulties). Fronto-striatal pathways are implicated in both of these conditions/spectrums but in somehow different ways. Those fronto-striatal pathways hold the key to almost every single major neuropsychiatric and neurodevelopmental disorder (Schiz., OC-spectrum, Autistic spectrum, ADHD/Impulsivity spectrum, Conduct/antisocial pers., etc.), needs to be (even) more researched 😎

 

[whopper]

Speaking of neurotransmitters glutamate/GABA, I got a few patients and their psychosis improved with Namenda. This is despite data showing Namenda didn't improve schizophrenia.

What's going on there I don't know. Like I said, I got the time to get it right. In the few cases where this happened, the patient dramatically improved with Ativan, but never met a criteria for catatonia. When I say they got better, I mean they really got better, not just tranquilized/euphoric sedation on it. Their concentration and memory significantly improved. Being that I don't like giving out Ativan and that Namenda can affect the glutamate/GABA system I decided to try it. The patients got much better.

I'm still trying to figure out what happened because I don't think this is garden-variety schizophrenia, that in studies is not supposed to respond to Namenda. I'm thinking this might be tardive psychosis or some type of organic psychosis despite that labs, even the zebras are fine.

 

[Uviol]

RE: 21 year old. Sounds exactly like Charles Bukowski's poems about his childhood. The clinical picture is missing many liters of cheap port wine though.