Does anyone know?
May be loss of grey matter during pychosis or psychotic break…
It is thought to be due to a dopamine deficiency in certain areas of the brain. Sz is weird because in some areas dopamine is too high and this is thought to cause positive symptoms. But then in others it is too low and this leads to negative. This makes finding a med for it difficult bc we don’t know how to have a med that raises dopamine in one specific area while lowering it another. As a result current meds pretty much just focus on lowering dopamine, which can make negative symptoms worse.
I thought the medication I took initially, risperdal, caused my negative symptoms. I know I was disorganized at the time. My room was messy and I was really depressed.
Probably not something permanent. My negative symptoms are worse after a longer psychotic break. But now they’re getting milder.
Both negative and positive symptoms were described before the meds. I think I read that somewhere so they’ve been a part of the disorder forever. It’s a decent question!!!
I suffer from avolition from time to time, This was esp. true in the first days of my impending doom as a 20-year-old too! I DO think the medication is at fault.
Schizophrenia causes changes in our thought processes, and is difficult to reverse.
If they find out what causes symptoms, or what is the cause of schizophrenia we will be nearing a cure.
we don’t know for sure. it’s a mystery…
I would say it’s a psychological response to hostile environment. like paranoia.
That is precisely what abilify does !
really? yeyeyeyeyyeyeeye
I think it is because of a gradual loss in brain volume since the onset of the illness. There are fewer connexions in the neural pathways resulting in the same brain areas being used over and over again. The cognitive decline happens soon after the first couple of psychotic episodes. It appears to have a toxic affect on executive functioning and basic thought processes. Dopamine is important for motivation, self care etc. But too much is dangerous.
Well not for me because ability made my negative symptoms worse than any other med did. Where did you hear it targets both?
Vraylar lowers dopamine when needed and raises it when needed so do other atypical some of them but the problem is it does not work on all receptors of dopamine
Some of the newer APs have some regional selectivity.
ITI-007 is not approved yet but its action is very interesting.
"ITI-007 also exhibits mesolimbic/mesocortical selectivity. The regioselectivity of ITI-007 was demonstrated in a series of studies in rodents [27 Snyder GL, Vanover KE, Zhu H, et al. Functional profile of a novel modulator of serotonin, dopamine, and glutamate neurotransmission. Psychopharmacology (Berl). 2015;232:605–621.
[Crossref], [PubMed], [Web of Science ®], [Google Scholar]
]. ITI-007 was shown to increase:
Dopamine release in the medial prefrontal cortex
Phosphorylation of GluN2B N-methyl-d-aspartate (NMDA) receptors in the nucleus accumbens through indirect D1 receptor interactions, anticipated to enhance glutamate neurotransmission
Phosphorylation of the glycogen synthase kinase 3 (GSK3), a signaling molecule in dopamine D2 receptor containing neurons in the prefrontal cortex and nucleus accumbens
Conversely, ITI-007 was shown to not increase the following processes [27 Snyder GL, Vanover KE, Zhu H, et al. Functional profile of a novel modulator of serotonin, dopamine, and glutamate neurotransmission. Psychopharmacology (Berl). 2015;232:605–621.
[Crossref], [PubMed], [Web of Science ®], [Google Scholar]
]:
Dopamine release in striatum
Phosphorylation of NR2B and GSK3 in striatum
Dopamine turnover/metabolism in striatum
Tyrosine hydroxylase activity in striatum
Motor dysfunction (e.g. cause catalepsy)
The importance of the regioselectivity of ITI-007 is based on the concept that the three major forebrain dopamine pathways subserve different functions. The simplified concept (i.e. currently being expanded) suggests that modulation of mesocortical dopamine affects cognition and memory, of mesolimbic dopamine affects mood, reward, and emotional responses, and of nigrostriatal dopamine affects motor function [28 Howes OO, Kapur S. The dopamine hypothesis of schizophrenia: version III—the final common pathway. Schizophr Bull. 2009;35(3):549–562.
[Crossref], [PubMed], [Web of Science ®], [Google Scholar]
]. This is certainly not an absolute functional distinction, but only a useful organizing principal with likely overlap across brain regions. It is suggested that postsynaptic blockade of dopamine activity (at D2-type receptors) in mesolimbic systems is beneficial in the treatment of psychosis, while blockade of postsynaptic dopamine D2 blockade in mesocortical regions may impair cognitive processes and hedonic drive, and that the postsynaptic blockade of dopamine receptors in nigrostriatal systems leads to motor side effects. "
Thank you! Medical jargon to me.
In my case, my medications or AP’s completely block my dopamine receptors (I’m on three different AP’s), and so, this causes my negative symptoms, I’m pretty sure. Right now, I only take one shower a week and I sleep in my clothes. I only brush my teeth about every other day. I floss once a week. But, I do wash my face and brush my hair everyday. I at least do that much. I am pretty good about doing yoga, meditating and practicing keyboard almost everyday. I usually only miss about one day a week.