Schizophrenic and Suicide

;

If you are schizophenic you will probably start out your recognisable sickness in a state of intense anxiety.

As a patient things started to go wrong when I divided the world into Knights of the Southern Cross and Freemasons. And one group was out to get me, while the other was sometimes my allies.

I would stand on street corners writing down number plates of cars that I knew were following me. I accused a man publicly of being a Knight of the Southern Cross; tasted poison in my food and laughed when two tall men walked into the resturant as I thought they were police coming to arrest the cook.  MOST IMPORTANTLY, IN THE PARANOIA ABOUT THE MASONS AND CATHOLICS AT ONE TIME I ASSUMED THE IDENTITY OF A MASON AND STARTED SHAKING HANDS WITH PEOPLE IN WHAT I THOUGHT WAS THEIR SECRET.

Eventually I went to the police, but they said (fortunately) that it was a religious problem.

Then the radio started to talk to me and I'd answer back in this conversation with the announcer.
I searched for a microphone under my bed.

In exhaustion after following bird footprints stuck to the ground to guide people around campus, I sat down under a tree to rest.  A bird above me would not stop chirping - this was a sign from God to keep going...

 

Pretty soon one of my brothers must have realised the problem and convinced me to go to hospital with him for my depression. Two doctors signed a form and I was admitted involuntarily. And that was the beginning of about ten years of symptoms.

I have no qualifications in schizophrenia and hope this description helps. One thing about schizophrenia is you can't handle it yourself - see a doctor.  I had one moment of insight when it started and I wondered if what I believed could possibly be true.

For years before I had been suicidal and during my exacerbations made a few attempts. I remember one time though - I was very sad and crying, I didn't want to end my life, but thought there was no way out of my disgrace. My symptoms were that, during years of hypersexuality, I thought I was turning into a woman. It was only years later when I spontaneously (and passionately) kissed a homosexual friend (at a point where he was likely to beat me up because I had been rude to him) that my symptoms rapidly diminished  This particular delusion is mentioned frequently in medical literature, but is held to be uncommon by the DSM.  Schizophrenia has been called the 'bearded lady' disease.  This shows a pre-existing condition (high dopamine levels) was matched to a societally conditioned fear.  Conditioned fears are alleviated in similar ways to schizophrenia in rats - by blocking the d2 receptors.   Socialization in this case brought an impromptu, spontaneous recovery.  Dopamine explains this phenomenon as has been observed with methamphetamine use: heterosexual men veering (as at 3-07-10) towards homosexuality while on meth.

(Although some hold 20% of patients have that problem) [1] - the best thing about it is that 0% of controls have the same symptoms, so if you've had it you can almost be certain you have schizophrenia.

Don't commit suicide. As my doctor said, the first five to seven years are the worst, as you don't know what a delusion is. And you never have complete insight into the fact that it is a delusion. He said, one schizophrenic had said to him: "I know there are no Martians putting thoughts in my head, I just wish they'd stop doing it". Delusions seem to progress from one to the next and the memory of the intensity of a past delusion is totally forgotten. Like waking up from sleep after a nightmare - it is not permanent.

Why do I feel so depressed? Again, I'm only qualified by experience, but I have read that when dopamine levels rise in the brain, serotonin levels fall (O Benkert, H. Gluba and N. Matussek (1973)"Dopamine, Noradrenaline and 5-Hydroxythryptamine in relation to motor activity, fighting and mounting behaviour", Neuropharmacology, p179). Dopamine is one of the chemicals in excess traditionally associated with schizophrenia, while serotonin is your mood regulator and low levels lead to depression. Hence you may feel that depressed. Infact one of the fathers of research into schizophrenia Blueler, said 'suicide is the most dangerous symptom of schizophrenia'. If you feel depressed see your doctor.

Some schizophrenics I know of would like an answer to their symptoms - what causes it. Concisely psychiatrists may tell you they don't know, but the dopamine hypothesis is worth researching. One of its' champions, Philip Seeman, of the University of Toronto, who discovered the antipsychotic receptor d2, wrote in the journal Synapse recently of the many pathways leading to psychosis. It is called: "Psychosis paths converge via d2high dopamine receptors" Volume 60, Issue 4, Date: 15 September 2006, Pages: 319-346. (Ask your library for a copy). We may never know what triggered it in us - it could be hypoxia before or about birth, a gene mutation or drugs or many other causes. But they all result in a more highly sensitive dopamine receptor. Delusions are normally about important things. People even get more psychoticism when they think there is something appaulingly wrong with their appearance, like a small port wine stain - even less than 2 cm squared [2] .
You can trust your doctor's diagnosis. Using similar dignostic techniques scientists study schizophrenia on many levels and are getting closer to the solution. For example, if you doubt this, in 1993 in the Journal Nature, Philip Seeman et al, found that schizophrenics had six times the dopamine d4-like receptors in their brains. This study was replicated many times, which is why I quote it.

More accurately, the results are described as a variant of the d2 receptor, but nevertheless, the results of the initial study were replicated and selection of patients was done by looking at their symptoms before death, which is the same way you or I are diagnosed.
As a last resort, ask your doctor for sickness benefits if the situation is too anxiety provoking. Don't be afraid to go to hospital for more intensive care. Or take sick leave, but tell your doctor straight away so he can write a certificate. Removing yourself from the situation is what one good pamphlet advised as a last resort(the pamphlet was published by SANE Australia, consulted Professor John McGrath and had something to do with Bristol Myers Squibb and had a picture of a mountain and forest and a reflection in a stream, copyrighy <2007 I think it was called "The SANE guide to schizophrenia" 2005 Victoria) The only problem with it is that when you believe you are turning into a woman, or being chased by someone, you truely believe it and may not think you deserve the benefits. Trust the advice of the medical community. There will be times like this when you think you are lying because you don't realise you are sick (see case study p49 "Schizophrenia, Symptoms, Causes, Treatment" by Kayla F. Bernheim & Richard R.J. Lewine, WW Norton & Company NY 1979).

One way to tell if a subject is a delusion or not, (and this is my own theory) is to ask - is it totally egocentric? Is it egodystonic - you would normally repress it - because it would not be me in this crowd, either grandiose or persecutory: grandiose delusions can be ego dystonic:"Ego-dystonic" delusions in psychotic patients  European Psychiatry, Volume 22, Supplement 1, March 2007, Page S323J. Zislin, V. Kuperman, R. Durst. Not only that but the situation which would normally be fun; yet embarrasing; would attract the repression that other people might consider shameful.  These are the mechanisms of repression.  If you've thought about the delusion, or even discretely checked, and it seems 'it is most likely there are no Martians' it must be your hyper functioning ego (or striatum - with more d2high) that is creating important meaning in these things for you.  And the dopamine disabelling the supplementary motor area, so you can't repress it.  But what will happen is you will see aspects of your personality and form another view of yourself, so you can't know.  So when you sense something is just not right, hold your breath and swim over the deep end.  If we can't do that routinely, maybe we should reduce our work hours or ask for a pension - anything but give up.

 

 One site mentions schizophrenia is more common in ego centric societies rather than sociocentric: "Schizophrenia is more common in egocentric, as opposed to sociocentric, cultures" (http://webspace.ship.edu/cgboer/genpsyschiz.html 2003, C. George Boeree as at 11-08-08). That is why precise answers to delusional questions are hard to find and you get no relief when a reasonable answer is proposed: because sciences are based on objective fact, not subjective ego anxieties. Even knowing this you may still be compelled to check to reassure yourself on a very detailed level. One way that sometimes works is to ask honestly and precisely - why wouldn't a reasonable person worry about this? and then try to find it somewhere. But this method has often led me to search for a year for something. Scientists have found the brain circuit for spontaneously abolishing a belief is a separate one to the one maintaining the obsession and the spontaneous extinction can be long lasting [3]. (I personally found the delusions don't disappear if you practice not checking). A better way is to have managed your lifestyle so well that driving questions aren't raised in the first place.  But even if you know this, schizophrenia, especially without medicine is anxiety provoking - this could be because the G-proteins are involved in adrenalyn as well.

I say delusions are ego-centric because the striatum, which has the most d2 receptors, or psychotic receptors, is quoted as being the seat of ego-centric learning. Also in "Effects of (S)-ketamine on striatal dopamine: a [11C]raclopride PET study of a dmodel psychosis in humans", F.X Vollenweider, P Vontobel, I Oye, D Hall and K.L Leenders, in Journal of Psychiatric Research 34(2000) p 35: "...decreases the in-vivo binding...to striatal DA D2 receptors ... including ... ego-disorders...", Notpayingthepsychiatrist (talk) 20:08, 12 April 2008 (UTC)

People with damage to the caudate nucleus are incapable of feeling severe guilt or shame. Schizophrenics are capable of feeling this, and delusionally so (the DSM says delusional guilt is excessive or inappropriate), which is the ego part, or superego part; the 'three strange graphs' on the main page indicated to the authors that schizophrenics may have a problem with empathy: they showed frontal lobe problems. RD Liang in 'The Divided Self', Penguine Books 1995, p130 says: "He had in fact, two entirely antithetical and opposed sources of guilt; one urged him to life, the other urged him to death. One was constructive, the other destructive. The feelings they induced were different but both were intensly painful". This is some reassurance against what most web sites say - that schizophenics are incapable of remorse. While the DSM includes lack of remorse as a diagnostic criteria for antisocial people, it does not do so for schizophrenia.
Since d2 receptors are associated with social dominance, the test is - will dwelling on this mean life or death for others. But harking back to the absense of remorse, this edition of Science says that concerning punishment of other people the pleasure of punishment in the striatum is modulated by the empathy of the prefrontal cortex: The Neural Basis of Altruistic Punishment Dominique J.-F. de Quervain, Urs Fischbacher, Valerie Treyer, Melanie Schellhammer, Ulrich Schnyder, Alfred Buck, Ernst Fehr Science 305, 1254 (2004).

 

People overconcerned with something may draw the wrong conclusion from actions in the first place.

After you've had it for a few years, you will kind of get used to it, (but the nature of it is that every episode is new), and anything you have to give up. I think it was Seneca who said 'Time heals all those things reason can't'. Hopefully the medication helps. In a relatively large percentage it doesn't. In checking to see if the situation was the same with classic amphetamine psychosis I was surprised to find no controlled studies had been done on amphetamine psychosis and antipsychotics: http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=11687172&cmd=showdetailview&indexed=google . I am lucky. Even during the worst times my workplace has supported me. But I have learnt that no amount of reason can help if your sickness is at the stage when you are 'declaring' your sickness. My doctor said: "If we can keep it as a nagging doubt, rather than a conviction, we're winning'. Personally I've found coffee rarely crosses that boundary, but regular alcohol does, missing your medication does.
If you find you can be reassured by a smile, you are relatively healthy.
Beware of the seduction of madness [4]. There is a certain rush to a delusion - just like when people try amphetamines, the first feeling is as if they are the centre of attention. The best advice I can give is never give up your medications. I was doing pretty well until I ran out of money one week and medication (Risperdal) at the same time. I was only without it for two or three days, but have never been as good since. Set up an account at a chemist for this.
You can expect one or two delusional themes to be characteristic of your schizophrenia because in autopsies where they have kept a note of the symptoms, it is usually a one word description.

After the experience of gender confusion, I remember being at work and saying to a student, "I think my conscience has just woken up" and since then my delusions made me go to the police numerous times over what my psychiatirist called picadilos, and which the police dismissed.

 

Cholesterol also influences vasoconstriction (9000).

My experience with guilt is that it is related to hostility.  When I was on respidal I became hostie; when I changed to Olanzapne I felt guilty.

 

Please don't expect a high degree of rigor in the main page or here, I only wanted a general impression and this is sumarised in relating hypoxia to schizophrenia; just as smoking is to lung cancer or sunburn to melanoma.

 

- Steve

L. Borras, P. Huguelet and A. Eytan, (2007), Delusional Pseudotransexualism in schizophrenia, Gilford Publications, Psychiatry: Interpersonal and Biological Processes, 70(2) p175
M. Augustin, I. Zschocke, K. Wiek, M. Peschen, W. Vanscheidt (1998) "Psychosocial Stress of Patients with Port Wine Stains and Expectations of Dye Laser Treatment" Dermatology. Basel: 1998. Vol. 197, Iss. 4; p. 353
Quirk, G.J. (2002) "Memory for extinction of conditioned fear is long-lasting and persists following spontaneous recovery", Learning and Memory.
Podvoil, E. (1990) "The Seduction of Madness" HarperCollins, New York.
Learning and Memory Systemic blockade of D2-like dopamine receptors facilitates extinction of conditioned fear in mice  Ravikumar Ponnusamy1, Helen A. Nissim3, and
Mark Barad doi: 10.1101/lm.96605  Learn. Mem. 2005. 12: 399-406 Copyright © 2005, by Cold Spring Harbor Laboratory Press

 ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

 Ismail et al found that 100% schizophrenics had at least one neurological soft sign: "All of the patients, 81% of the siblings, and 45% of the normal comparison subjects had at least one abnormal neurological sign each." (701)

 

 

[The British Journal of Psychiatry (2002) 181: s50-s57 © 2002 The Royal College of Psychiatrists Neurological soft signs in first-episode psychosis: a systematic review* PAOLA DAZZAN, MRCPsych and ROBIN M. MURRAY, FRCPsych says "Patients with first-episode psychosis show an excess of NSS, particularly in the areas of motor coordination and sequencing, sensory integration and in developmental reflexes" and that increases in neurological abnormalities meant a nonremitting course of illness.]

 

 

 

[Relation of neurological soft signs to psychiatric symptoms in schizophrenia
Schizophrenia Research, Volume 94, Issues 1-3, August 2007, Pages 37-44
Vijay A. Mittal, Wendy Hasenkamp, Michael Sanfilipo, Susan Wieland, Burton Angrist, John Rotrosen, Erica J. Duncan

 

According to the circuits mentioned on the previous page, the schizophrenia circuit invoves the thalamus, which contains serotonin receptors.  Low serotonin contributes to depression or hallucinations.

 

Even though all measures decreased with treatment a factor of BPRS; Psychological discomfort, whether treated or base level, showed a negative correlation with NSS: the more symptoms a patient had the less (and the less symptoms the more) psychological discomfort (anxiety, guilt, somatic concern and depression).  If a measure of NSS is to be taken as the profile of recovery; this would seem to indicate on declining NSS with medication, a significant decrease in positive symptoms like delusions and hallucinations and an increase in psychological discomfort.  The phenomenon of inverse correlation between depressive symptoms and positive symptoms could mean the dopamine stimulation is properly controlled, but because of high dopamine levels remaining, serotonin is lower (see citation in Personal Story).  Methamphetamine for example is known to be more potent than amphetamine and affect serotonin more and leave the clean user with residual guilt.  One of the mechanisms of methamphetamine reduces the serotonin transporter (6011). chronic amphetamine use damages dopamine pre-synaptic neurons leaving negative symptoms.  Also global hypoxia directly damages serotonin capabilities (6009); but more pertinently serotonin transporters are reported to be less in suicide victims of schizophrenics (study by Laruelle et al in 6010) and the transporter resides on the axon.   The lack of transporters is what causes the damage by methamphetamine or schizophrenia to the axon.  Hypoxic damage may be permanent- to adulthood.  It is established that serotonin does play a role in schizophrenic suicide.

[post-mortem hypoxia can indicate pre-mortem hypoxia as has been used to invesigate SIDS deaths]

 

It must work similar to this (the numbers on x and y axis are made up):

 

 

 

 

 

Aside from the physical causes of vasoconstriction, psychological factors, including depression, can play a role (1060).  And while I am aware of depressed people becoming psychotic, I don't think there is a modern theory of guilt causing psychosis.  The two types make sense as the thalamus and serotonin are responsible for hallucinations or mood.

 

Psychotic depressed people who commit suicide commonly have a unique deficit in transporters on serotonin axons (1061),For the dopamine agonist, methamphetamine, one report says subjects can experience death of serotonin axons, resulting in: "For the rest of their lives they are going to be lacking the ability to produce adequate amounts of serotonin. Feelings of depression and guilt could be theirs till they die. The meth user is going to be more inclined towards drug and alcohol abuse." ; and "Meth kills dopamine and serotonin neurotransmitter cells. This is an irreversible consequence since these nerve cells do not grow back with time." while saying methamphetamine reproduces symptoms of schizophrenia 1..http://www.montana.edu/wwwai/imsd/rezmeth/transmit.htm as at 07-03-10; and when dopamine levels rise in the brain, serotonin levels fall (O Benkert, H. Gluba and N. Matussek (1973)"Dopamine, Noradrenaline and 5-Hydroxythryptamine in relation to motor activity, fighting and mounting behaviour", Neuropharmacology, p179)..  So there are many ways by which 'psychological discomfort' can come about.  One of the correlates of schizophrenic suicide attempts is high psychological discomfort (2000).  The DSM describes such 'guilt feelings' for major depression as feelings of worthlessness or excessive or inappropriate guilt.  The symptoms of psychological discomfort are much like those of melancholia, which is noted for coordination difficulties.

Just as dopamine is elicited from the striatum under hypoxia, serotonin comes from the thalamus in hypoxia.  And serotonin is a vasoconstrictor - so the absent mechanism of vasomotor escape is responsible for schizophrenia.  The thalamus, like the striatum, is smaller in schizophrenics.  The test if something is from the thalamus is 'is this from my perceptual consciousness' - inherintantly meaninless and able to be recognized as false and dealing with the sensations or a meaninglessness imposed on the person.

Suicidal schizophrenic women have been found to have lower blood serotonin levels than other schizophrenics or healthy people.

On the other hand, high symptom and vasoconstriction and no depression may be due to elevated serotonin, which is part of normal schizophrenia.  (This correlates with reports that only at high amphetamine (dopamine) doses (reducing serotonin) the occasional subject experiences transsexual delusions).  In trying to find neurological evidence for serotonin dysfunction in schizophrenia, one study pointed out that suicide itself has an impact on serotonin axons and therefore excluded evidence from the schizophrenic suicide subgroup.

 

Somatic concern is dramatically seen in Body Dysmorphic Disorder.  BDD can be confused with Gender Identity DIsorder; but BDD responds to serotonin treatment.

 

The NSS of poor motor performance also applies to mood disorders,

Further adaptation of Dr Murray's graph

 

Graph of coordination in controls and schizophrenics (41) - and Graham Murray's supportive diagnosis.

 

Preincubation also negates the need to invoke a lack of vasomotor escape, which even though seemingly possible, has no morphological proof (5000), yet even recently it was held that: "The traditional view is that increases in sympathetic activity appear to have a limited effect on the cerebral vasculature of humans, particularly at rest" (5500)

 

 

 

 

 

The difficulty in matching live and postmortem imaging results could be because vasoconstriction prevents access to ligands (this was taken seriously by 2500? and is called 'ligand delivery') which is relieved on death and the specimin is saturated in a buffer and blood vessels return to relaxed state, the tissue is homogenized and provides access to all receptors. PET measurements are only possible where there is no difficulty with ligand delivery.  (10000 p46)  This would explain why methylspiperone records more binding in postmortem tissue than live sz - other explanations for the discrpancy seem to be failing and perhaps why GLC 756 shows no results in vivo but profound results in vitro.

The problem with saffron combatting hypoxia.

 

An appealing remedy, if schizophrenia is caused by hypoxia, is saffron, which has oxygen diffusability characteristics.  Unfortunately, the very compound which would help this - crocetin - binds with sigma receptors (1020), which can block dopamine reuptake (1021), and as pointed out previously, hypoxia can induce dopamine to 1000%; which explains experiences of delerium.  It is true, as reported on the main page that crocin can be lethal, but that is derived from the possibly high doses used on mice. 
A recent report states that crocin is reported to be nontoxic and there are a number of references to this remark (7000).  The problem is that crocin is 'hydrolized' into another state on digestion and does not reach the blood stream.  The experiments on mice were done by injection.  So if there is any merit in treating schizophrenia this way it has to be done by health care professionals.

Fortunately, another drug, operating to increase blood flow and oxygenation was shown in some cases to help schizophrenics (7050).  One case study shows ataxia as only becomming present after treatment with an antipsychotic, and then upon treatment with acetazolamide (for oxygen); and another antipsychotic the ataxia dissapeared and the psychosis "ameliorated" (7051).  In a recent experiment with acetazolamide where subjects were given acetazolamide and cerebral blood flow measured; the report concluded that no subjective feelings were reported by patients except for some who experienced mild skin tingling sensations two minutes after administration.  Such sensations have been noted in an older case study where amphetamine cured them (7052).

 

 

Another earlier article, although finding less CSF lactate found: "Surprisingly, however, although we identified an increase in lactate in postmortem brain tissue, we observed a significant decrease in CSF lactate levels in patients with first-onset schizophrenia." (6004)

The degree of oxidization in a cell is shown to be increased in schizophrenics as indicated by the lactate:pyruvate ratio.  Plasma from schizophrenics is shown to produce more anaerobic metabolism. (6005)

Chronic hypoxia decreases cellular content of glutamate while increasing glutamine (6006).  Glutamine is also increased in schizophrenics (2007) and results of decreased glutamate are the foundation of the glutamate hypothesis (as at 20-5-10)

 

As further possible evidence of vasoconstriction in schizophrenia, Bmax declines with the application of dopamine agonists.

 

Another consistent symptom of schizophrenia is the lack of gamma waves in the brain, which may be responsible for self-insight and coordination of thought.  Lowering the frequency of stimulation causes permanent vasoconstriction, even in those species known to have vasomotor release.  Gamma waves are known to increase with meditation on compassion.  If a schizophrenic's capacity for empathy is limited, does this mean less gamma waves? Gamma waves are known to exist in proportion to GABA receptors.  Hypoxia can nullify some actions of the GABA receptor (6008).

 

(41)Murray, G (2005) Early Development and Adult Cognitivie Function in Schizophrenia and the General Population - A longitudinal perspective. Tiivistelmä suomeksi. Academic Dissertation to be presented with the assent of the Faculty of Medicine, University of Oulu, for public discussion in the Auditorium F101 of the Faculty of Medicine (Aapistie 7), on November 25th, 2005,at 12 noon O U L U N Y L I O P I S TO, O U L U 2 0 0 5 University of Oulu, 2005. ISBN 951-42-7891-7. ISBN 951-42-7892-5 (PDF). URI http://herkules.oulu.fi/isbn9514278925/.

 

(701) Am J Psychiatry 155:84-89, January 1998 © 1998 American Psychiatric Association  Regular Article
Neurological Abnormalities in Schizophrenic Patients and Their Siblings Baher Ismail, M.D., Elizabeth Cantor-Graae, Ph.D., and Thomas F. McNeil, Ph.D.

 

(900)The temporal evolution of striatal dopamine receptor binding and mRNA expression following hypoxia-ischemia in the neonatal rat
Developmental Brain Research, Volume 94, Issue 1, 14 June 1996, Pages 81-91
Francis M. Filloux, John Adair, Neelam Narang

 

(901) Journal of Cerebral Blood Flow & Metabolism (2000) 20, 423–451; doi:10.1097/00004647-200003000-00001
Imaging Synaptic Neurotransmission With in Vivo Binding Competition Techniques: A Critical Review
Supported by the National Institute of Mental Health (K02 MH01603-01). Marc Laruelle

 

(902) Eur J Pharmacol. 1996 May 6;303(1-2):123-8.
Critical reevaluation of spiperone and benzamide binding to dopamine D2 receptors: evidence for identical binding sites.
Malmberg A, Jerning E, Mohell N.

 

(903) J Neurochem. 1991 Dec;57(6):1951-61.Effect of unilateral perinatal hypoxic-ischemic brain injury in the rat on dopamine D1 and D2 receptors and uptake sites: a quantitative autoradiographic study.Przedborski S, Kostic V, Jackson-Lewis V, Cadet JL, Burke RE.

 

(1020) Planta Med. 2008 Jun;74(7):764-72. Epub 2008 May 21.
Quality and functionality of saffron: quality control, species assortment and affinity of extract and isolated saffron compounds to NMDA and sigma1 (sigma-1) receptors.
Lechtenberg M, Schepmann D, Niehues M, Hellenbrand N, Wünsch B, Hensel A.

 

(1021) Psychopharmacology (Berl). 1997 Feb;129(4):311-21.
Cocaine toxicity: concurrent influence of dopaminergic, muscarinic and sigma receptors in mediating cocaine-induced lethality.
Ritz MC, George FR.  (The relevant material is in the article).

 
(1050) J Psychiatr Res. 2007 Sep;41(6):502-10. Epub 2006 May 15. Assessment of cerebral blood volume in schizophrenia: A magnetic resonance imaging study.
Brambilla P, Cerini R, Fabene PF, Andreone N, Rambaldelli G, Farace P, Versace A, Perlini C, Pelizza L, Gasparini A, Gatti R, Bellani M, Dusi N, Barbui C, Nosè M, Tournikioti K, Sbarbati A, Tansella M.

 

(1060)Circulation. 1999 Apr 27;99(16):2192-217.
Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy.
Rozanski A, Blumenthal JA, Kaplan J.

 

(1061)Localized decrease in serotonin transporter-immunoreactive axons in the prefrontal cortex of depressed subjects committing suicide
Neuroscience, Volume 114, Issue 3, 11 October 2002, Pages 807-815
M. C. Austin, R. E. Whitehead, C. L. Edgar, J. E. Janosky, D. A. Lewis

(2000)Characteristics of schizophrenic patients with a history of suicide attemptCuneyt Evren, Bilge Evren

 
(2001) It seems the halogen atom detects hypoxia.  Although some place hydrogen as a halogen, it is not normally included - even though it has much the same properties.

(2002) http://www.google.com.au/#hl=en&source=hp&q=hypoxia+halogen&meta=&aq=f&aqi=&aql=&oq=&gs_rfai=&fp=9b8951d8409b077 as at 18-03-10

(2500) Positron emission tomography and ex vivo and in vitro autoradiography studies on dopamine D2-like receptor degeneration in the quinolinic acid-lesioned rat striatum: comparison of [11C]raclopride, [11C]nemonapride and [11C]N-methylspiperone
Nuclear Medicine and Biology, Volume 29, Issue 3, April 2002, Pages 307-316
Kiichi Ishiwata, Nobuo Ogi, Nobutaka Hayakawa, Hiroyuki Umegaki, Tsukasa Nagaoka, Keiichi Oda, Hinako Toyama, Kazutoyo Endo, Akira Tanaka, Michio Senda

(2600) ST'ASTNY Frantisek ^{(1 2)} ; TEJKALOVA Hana ⁽¹⁾ ; SKUBA Iryna ⁽¹⁾ ; BALCAR Vladimir J. ⁽³⁾ ; KAISER Mirosiav ⁽¹⁾ ; YONEDA Yukio ^(4),
Quinolinic acid, n-methyl-d- aspartate receptor and schizophrenia : Testing an integrative theory Amino acid signaling 04
2005, pp. 67-83 [Note(s) :  [121 p.]] [Document : 17 p.] (118 ref.) ISBN 81-308-0047-0 ;  Illustration : Figure

 

(3000)Dopamine receptors in the striatum of rats exposed to repeated restraint stress and alprazolam treatment
European Journal of Pharmacology, Volume 344, Issues 2-3, 5 March 1998, Pages 143-147
Luciana Giardino, Massimo Zanni, Monica Pozza, Carla Bettelli, Vito Covelli

(3001)Behav Brain Res. 2000 Jan;107(1-2):171-5.
Transient birth hypoxia increases behavioral responses to repeated stress in the adult rat.
El-Khodor BF, Boksa P.

(3002)Adaptive changes of dopamine-D2 receptors in rat brain following ethanol withdrawal: A quantitative autoradiographic investigation
Alcohol, Volume 9, Issue 5, September-October 1992, Pages 355-362
Hans Rommelspacher, Corinna Raeder, Peter Kaulen, Gerold Brüning

(3003) Int J Dev Neurosci. 2008 Feb;26(1):77-85. Epub 2007 Sep 11.
Prenatal hypoxia down regulates the GABA pathway in newborn mice cerebral cortex; partial protection by MgSO4.
Louzoun-Kaplan V, Zuckerman M, Perez-Polo JR, Golan HM
(3004)Brain Res. 1994 Nov 14;663(2):191-8.
Ketamine increases the striatal N-[11C]methylspiperone binding in vivo: positron emission tomography study using conscious rhesus monkey.
Onoe H, Inoue O, Suzuki K, Tsukada H, Itoh T, Mataga N, Watanabe Y.

 

(5000) Acta Morphol Acad Sci Hung. 1975;23(2):157-64.
A comparative characteristic of effector innervation of cerebral arteries in mammals and humans.
Motavkin PA, Vlasov GS, Palashchenko LD..mparativecharacter(

(6004) PLoS Med. 2006 Aug;3(8):e327.
Metabolic profiling of CSF: evidence that early intervention may impact on disease progression and outcome in schizophrenia.
Holmes E, Tsang TM, Huang JT, Leweke FM, Koethe D, Gerth CW, Nolden BM, Gross S, Schreiber D, Nicholson JK, Bahn S

(6005)

CHARLES FROHMAN, ELLIOT D. LUBY, GARFIELD TOURNEY, PETER G. S. BECKETT, and JACQUES S. GOTTLIEB

STEPS TOWARD THE ISOLATION OF A SERUM FACTOR IN SCHIZOPHRENIA

Am J Psychiatry 1960 117: 401-408

(6006)J Neurochem. 2001 Mar;76(6):1935-48.
Hypoxia regulates glutamate metabolism and membrane transport in rat PC12 cells.
Kobayashi S, Millhorn DE.

 

(6007)BMC Psychiatry. 2005; 5: 6.
Published online 2005 January 31. doi: 10.1186/1471-244X-5-6.
PMCID: PMC548680
Copyright © 2005 Hashimoto et al; licensee BioMed Central Ltd.
Elevated glutamine/glutamate ratio in cerebrospinal fluid of first episode and drug naive schizophrenic patients
Kenji Hashimoto,1 Göran Engberg,2 Eiji Shimizu,1 Conny Nordin,3 Leif H Lindström,4 and Masaomi Iyo1

 

(6008) Exp Brain Res. 1993;97(2):209-24.
Influence of hypoxia on excitation and GABAergic inhibition in mature and developing rat neocortex.
Luhmann HJ, Kral T, Heinemann U.

(6009)Neuroscience Research Communications
Volume 24 Issue 1, Pages 33 - 40 Density of serotonin receptors in rat brain following global cerebral ischemia: An autoradiographic studyL. Torup 1 2 *, E. Mellerup 1, N.H. Diemer 2Published Online: 18 Mar 1999

 

(6010) Neuroscience. 2002;114(3):807-15.
Localized decrease in serotonin transporter-immunoreactive axons in the prefrontal cortex of depressed subjects committing suicide.
Austin MC, Whitehead RE, Edgar CL, Janosky JE, Lewis DA.

 

(6011) J Neurochem. 2000 Oct;75(4):1608-17.
The effects of methamphetamine on serotonin transporter activity: role of dopamine and hyperthermia.
Haughey HM, Fleckenstein AE, Metzger RR, Hanson GR.

(7000) An overview of structural features of DNA and RNA complexes with saffron compounds: Models and antioxidant activity
Journal of Photochemistry and Photobiology B: Biology, Volume 95, Issue 3, 3 June 2009, Pages 204-212
C.D. Kanakis, P.A. Tarantilis, C. Pappas, J. Bariyanga, H.A. Tajmir-Riahi, M.G. Polissiou

 

(7050)
Psychiatry Res. 1989 Jun;28(3):279-88.
Acetazolamide and thiamine: an ancillary therapy for chronic mental illness.
Sacks W, Esser AH, Feitel B, Abbott K

 

(7051) J Neurol Neurosurg Psychiatry 2003;74:688-689 doi:10.1136/jnnp.74.5.688 Schizophrenia and episodic ataxia type 2
S Mechtcheriakov, M A Oehl, A Hausmann, W W Fleischhacker, S Boesch, M Schocke, E Donnemiller.

 

(7052)

J Natl Med Assoc. 1971 September; 63(5): 380–383.