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ketamine/psychosis paper abstract

Jabberwocky

Frumious Bandersnatch
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NMDA hypofunction in the posterior cingulate as a model for schizophrenia: an exploratory ketamine administration study in fMRI

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Georg Northoffa, b, , , Andre Richterc, Felix Bermpohla, Simone Grimmc, Ernst Martinc, Valentine Leslie Marcard, Constance Wahlc, Daniel Hellc and Heinz Boekerc

aDepartment of Neurology, Division of Behavioral Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, 02215 Boston, USA
bDepartment of Psychiatry, University of Magdeburg, Leipziger Str. 44, 39120 Magdeburg, Germany
cZurich University Psychiatric Hospital, Lenggstrasse 31, P.O. Box 68, CH-8029 Zürich 8, Switzerland
dDepartment of Neuropsychology, Institute of Psychology, University of Zurich, Treichlerstrasse 10, CH-8032 Zürich, Switzerland

Received 11 September 2003; revised 5 April 2004; accepted 6 April 2004. Available online 14 July 2004.




Abstract
Background
Based on animal data, NMDA receptor hypofunction has been suggested as a model for positive symptoms in schizophrenia. NMDA receptor hypofunction affects several corticolimbic brain regions, of which the posterior cingulate seems to be the most sensitive. However, empirical support for a crucial role of posterior cingulate NMDA hypofunction in the pathophysiology of positive symptoms is still missing in humans. We therefore conducted an fMRI study using the NMDA antagonist ketamine in healthy human subjects during episodic memory retrieval, which is supposed to activate the posterior cingulate.

Methods
We investigated 16 healthy subjects which were assigned to either placebo (n=7; saline) or ketamine (n=9; 0.6 mg/kg/h) group in a double-blind study design. All subjects received their infusion while performing an episodic memory retrieval task in the scanner. Immediately after the fMRI session, psychopathological effects of ketamine were measured using the Altered States of Consciousness Questionnaire.

Results
The placebo group showed BOLD signal increases in the posterior and anterior cingulate during retrieval. Signal increases were significantly lower in the ketamine group. Lower signal increases in the posterior cingulate correlated significantly with positive (i.e. psychosis-like) symptoms induced by ketamine.

Conclusion
The present study for the first time demonstrates a relationship between NMDA receptors, posterior cingulate and positive (i.e. psychosis-like) symptoms in humans. Confirming findings from animal studies, it supports the hypothesis of a pathophysiological role of NMDA receptor hypofunction in the posterior cingulate in schizophrenia.

Keywords: Positive symptoms; Ketamine; Posterior cingulate; Episodic memory; NMDA receptors; fMRI



Corresponding author. Laboratory for Magnetic Brain Stimulation, Department of Neurology, Division of Behavioral Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, 02215 Boston, USA. Tel.: +1 617 667 5229; fax: +1 617 975 5322.
 
a word for the wise

If you are ever trying to treat yourself or someone else for ketamine psychosis, remember the results of another study that I once read on the subject: olanzapine (Zyprexa) was found to be helpful, while risperidone (Risperdal) was not.
 
^
Could you dig it up and post a link? Sounds interesting.

Thanks!
 
Aren't Risperdal and Zyprexa both atypical antipsychotics? I'm positive that Zyprexa is but can't recall offhand whether or not Risperdal is as well. If it is, what was the reason why Zyprexa proved to be helpful while Risperdal was not?
 
I read that abstract years ago, so of course I can't cite the authors or journal, but I have found from my own past ketamine induced psychoses that Zyprexa was the only thing that helped, and they gave me pretty much everything.

Score: Concrete Scientific References--0. Personal Experience--1.

However, I am not making that particular finding up because I did read it, probably on MedLine or something like that years ago.
 
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