Posted by linkadge on January 6, 2007, at 18:13:06
In reply to Re: Patient paid to accept neuroleptic depot injec, posted by fca on January 6, 2007, at 17:03:18
>And this is due primarily to improvements in APs.
I don't think there is conclusive evidence that atypical antipsychotics are any more effective, have fewer side effects, or are better at treating negative symtpoms as compared to conventional AP's.
A number of large studies have found no clear advantage of atypicals over conventional AP's. For instance, this study of 12,640 patients found no evidence of superiority.
http://www.bmj.com/cgi/content/full/321/7273/1371
>I am sorry for the strength of my response but I >am constantly amazed and gratified by the >progress that has been made.I don't know what progress has been made. The atypicals may be slightly more tollerable, but do not have proven superiority. They are also more likely to cause metabolic problems, which might not show up in the short term. Atypicals have not been around long enough to know the true indidence of TD. So, you are really just trading side effects.
A good percentage of patients quit their medications and lie about compliance. When I was in the hospital, for instance, I "cheeked", my seroquel, then spat it down the drain. I lied about improvement, and faked a reduction in symptoms just so I could get out. If I can do it, so can others.
>Meds, while not preventing decompensation, due >mitigate the damage done.
Do you have any references for this? For instance, there was some intial speculation that antidepressants reduced the damamge done by depressive episodes, but new evidence suggests there is no such protective effect. In a number of studies, antidepressants exaserbate the effects of stress on hippocampal morphology.
AP's can induce cumulative exposure damamge, perhaps through an increase in oxidative stress. It is thought that TD is a result of oxidative stress. People with schizophrenia are already known to have decreased antioxidant defenses and may be even more susceptable to such dammage.
Cognitive deficits induced by antipsychotics are not just due to monoamine disrupting effects. They may too be a result of increased oxidative stress.
Pathological changes in the postmortem brain of schizophrenics also have been reported in the medical literature, from exposure to antipsychotics, as compared no nonexposue. Unbiased, healthy animal studies also show brain morphology dependant on exposure duration. Many antipsychotics also downregulate BDNF, a molecule critical for the survival, growth and maintainance of new brain cells.
A quote from:
http://www.hdlighthouse.org/treatment-care/treatment/drugs/related/updates/0061risperidone.php
Dr. Sahebarao P. Mahadik (left) and Dr. Alvin V. Terry Jr. University of Georgia and the Medical College of Georgia.
"You give them a dose of haloperidol, you study receptors in their brain, you see that they block dopamine receptors so they don't have as many psychotic outbursts. Patients are quiet, docile and more easily managed … but their cognition becomes impaired, and it's worse than it would have been without treatment."
Another study:
Costly Schizophrenia Drugs No Better Than Older Generic:
http://health.dailynewscentral.com/content/view/1654/63
Also, taken from:
http://www.bmj.com/cgi/content/full/329/7474/1058
However, recent critiques have shown that recovery and readmission rates in schizophrenia before 1950 were no different7 and that antipsychotic agents might even do more harm than good.8 Thus the marked decline in the numbers of patients in asylums, from the mid-1950s (in the United Kingdom from some 150 000 in 1956 to under 40 000 in 1990) is usually attributed, at least in part, to effects of the medication. But this decline could equally be seen as socially generated via fiscal policies and community care programmes.8 Enhanced biological vulnerability to psychotic relapse might even be a result of the brain being made supersensitive to dopamine,9 medication thus acting as a double edged sword, relieving the symptoms of illness but creating an increased potential for relapse once drugs are discontinued.
Linkadge
poster:linkadge
thread:719688
URL: http://www.dr-bob.org/babble/20070101/msgs/719936.html