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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 8 of 8. This is the beginning of the thread.
Posted by halcyondaze on November 8, 2006, at 10:55:31
Stimulant Misuse in College for "Pseudo-Attention Deficit Disorder" During Schizophrenia Prodrome
OLIVER FREUDENREICH, M.D., CORINNE CATHER, Ph.D. and DAPHNE HOLT, M.D., Ph.D.
Boston, Mass.To the Editor: Stimulant use to treat attention deficit disorder and stimulant misuse to aid studying has dramatically increased in recent years among college students (1). A phenomenon we have observed is the use of stimulants during the schizophrenia prodrome for presumed attention deficit disorder or attentional difficulties in the absence of any childhood attention deficit disorder. The following case typifies this presentation, which we have seen several times over the past 2 years in our First Episode and Early Psychosis Program.
"Mr. A," a 20-year-old man, with normal childhood development and no behavioral or academic problems, graduated high school with honors despite regular marijuana use. During his sophomore year, he suddenly found it difficult to concentrate and demonstrated difficulty keeping up with his course work. These difficulties prompted him to try a friend’s prescription stimulant Adderall, which he found effective and continued to use it intermittently without a prescription for "cramming." Several months after starting Adderall, he became acutely psychotic after smoking phencyclidine-laced cannabis at a party. He required a lengthy hospitalization but was eventually stabilized and treated with aripiprazole 10 mg/daily. His request for stimulants "to concentrate better" was resisted, and after 6 months of treatment with aripiprazole, he made a full symptomatic and functional recovery without any objective or subjective residual psychotic or cognitive symptoms. His provisional diagnosis of schizophrenia was confirmed when he had a psychotic relapse 3 months after discontinuing his maintenance antipsychotic aripiprazole following 1 year of treatment.
The prodrome of schizophrenia is characterized by nonspecific symptoms that include cognitive problems, often characterized by patients as "difficulties concentrating." The construct of "basic symptoms" attempts to capture these nonpsychotic, subjective cognitive problems that begin during the prodrome and might presage the onset of psychosis. Two basic symptoms that would lead to a complaint of "difficulties concentrating" are thought interference (the intrusion of often banal thoughts) and disturbances of receptive language (problems with the meaning of words). Both are of particular interest because of their potential as specific predictors of schizophrenia (2).
College students who present for treatment with self-diagnosed "pseudo-attention deficit disorder" should be asked about misuse of stimulants and followed closely, since a small percentage will be in the early phases of schizophrenia. Although the impact of stimulants on the course of schizophrenia is not known, sensitization has been described with stimulants (3), raising the possibility that stimulant use is a risk factor for some cases of schizophrenia.
Posted by med_empowered on November 8, 2006, at 14:10:29
In reply to Amphetamines and schizophrenia: thoughts?, posted by halcyondaze on November 8, 2006, at 10:55:31
ummm...that's ridiculous.
"Schizophrenia" is a ridiculously vague, non-descriptive term. The patient pool is heterogenous, outcomes are unpredictable...its more a label than a true diagnosis (I know this sounds anti-psychiatryish; I'm just saying that schizophrenia needs to be replaced by better, more descriptive terms).
Anyway....the guy clearly had some drug-induced problems, and saying that a psychotic relapse months after discontinuing an antipsychotic (which could have made him more prone to psychosis through dopamine sensitization) is simply ridiculous. Given all the things that can contribute to psychosis, and how non-specific the term "psychosis" is, the idea that just b/c he had a psychotic episode after treatment with an atypical he must be schizophrenic is overly simplistic, especially if he has a history of substance use (and especially if he's using hallucinogens).
Sigh. Besides, the dopamine hypothesis of schizophrenia is pretty much crap. I mean, think about: if schizophrenics did have an excess of dopamine, and if antipsychotics did correct this, why do antipsychotics cause Parkinson's like problems? If they're "correcting imbalances," someone on an antipsychotic should function just like someone not on an antipsychotic.
Posted by linkadge on November 8, 2006, at 17:42:08
In reply to Re: Amphetamines and schizophrenia: thoughts?, posted by med_empowered on November 8, 2006, at 14:10:29
I agree with med empowered. He smoked PCP laced marajuanna thats what made him psychotic. Rebound psychosis from AP withdrawl is not indicative of anything.
They study also does nothing to establish the proposed connection between stimulant use and psychosis other than tell the story of a guy who did a lot of drugs and became psychotic.
Linkadge
Posted by halcyondaze on November 8, 2006, at 19:12:49
In reply to Re: Amphetamines and schizophrenia: thoughts?, posted by linkadge on November 8, 2006, at 17:42:08
<< http://focus.psychiatryonline.org/cgi/content/citation/1/2/205 >>
<< http://www.annalsnyas.org/cgi/content/abstract/654/1/160 >>
[Many researchers are also naming glutamate as the true culprit for both amphetamine psychosis and schizophrenia - I work in psych. research and the dopamine theory is scoffed by anyone who involved in psych. research.]
Posted by blueberry on November 8, 2006, at 20:18:43
In reply to Amphetamines and schizophrenia: thoughts?, posted by halcyondaze on November 8, 2006, at 10:55:31
I think PCP along with some vulnerable genetics are what caused the short term and longterm problems. The other drugs just acted to influence the damage one way or the other. But the damage was from the PCP.
Posted by clint878 on November 10, 2006, at 20:02:32
In reply to Re: Amphetamines and schizophrenia: thoughts?, posted by blueberry on November 8, 2006, at 20:18:43
But there are people who take drugs for years and then get clean, but are fine afterwards. Thus, saying that the PCP was "responsible" in this case seems oversimplified. Did it have some effect? Sure, perhaps it brought on the schizophrenia a few months sooner than it would have otherwise.
Since we know so little, the PCP or the Adderall could have actually mitigated the problem and delayed the onset of schizophrenia. I agree that this study means absolutely nothing.
Posted by tessellated on November 11, 2006, at 16:49:38
In reply to well, there are a few other studies:, posted by halcyondaze on November 8, 2006, at 19:12:49
> [Many researchers are also naming glutamate as the true culprit for both amphetamine psychosis and schizophrenia - I work in psych. research and the dopamine theory is scoffed by anyone who involved in psych. research.]
uhmmm, so help me out. i know in the UK, there's been a call to replace schizophrenia with the term dopamine dysregulation syndrome.
my BA/research pointed to the altered dopamine receptor sensitivity in the mesocortical DA system via chronic administration of DA agonist like amph. which makes sense in regard to that area's routing of internal and externally generated output to other parts of the brain i.e. metacortical processing.
IMHO, i can see how an enhanced receptor sensitivity in/around the hypothalamus could trigger various sorts of hallucinations etc, by creating false positive nueral activation/input that is misrecognized as coming from the occipital or temporal lobes.parkinsons occurs due to a deficit of DA receptor activity in the basal ganglia, a seperate structure that creates output to the medulla, less so (as far as i understand) to the cerebral cortex in general. so the DA antagonist would inhibit DA receptor sensitivity therefore potentially causing parkinson like symptoms. as well the SSRI's seem to create parkinson like symptoms due to their indirect affect on DA. parkinsonism can be alleviated via the implantation of stem cells around the basal ganglia, pointing to some form of nueral degeneration aside from mere DA receptor down regulation. If you don't use it you loose it-dendritically.
simply put, the particular structures that are involved with dopamine activity are critically important, as dopamine and the catecholamines are used throughout the body. so i would imagine that dopamine does have a role in psychosis, but only in relation to specific neural curcuitry.
however, i wonder with the MAIO's since they can increase catecholaminergic activity throughout the body, wouldn't they increase dopamine activity accross all neural structures? whereas things like buproprion might be more selective?
or am i just treading on older studies?
l8
Posted by clint878 on November 13, 2006, at 8:31:30
In reply to well, there are a few other studies:, posted by halcyondaze on November 8, 2006, at 19:12:49
While these studies do show that brain damage is correlated with drug users, they do not prove causation. It may be that these altered levels of chemicals are what led the people to use meth in the first place, and were unaltered by meth use. The urge to use meth may have been the body's way of compensating for the "damage."
The studies also don't show what the significance of this change is. There were no cognitive tests, for example. For all we know, it may be inconsequential.
This is the end of the thread.
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