If I were my own psychiatrist....I would prescribe myself...

[Petros Agapetos]

If I had the right to prescribe myself the drugs I need; I would choose the following.

1. Abilify 300 mg until the CTO is over; in three months or so. Dopamine tonically inhibitis prolactine release, as seen with most antipsychotics. Due to partial agonism, Abilify reduces prolactin release. Prolactin levels being low allows for testosterone levels to be high in men and estrogen levels in women.


Abilify covers 70% - 90% of D2 type dopamine receptor. For the maintenance treatment of schizoaffective disorder bipolar sybtype. Abilify antagonizes D2 by 25%-40% on the presynaptic neurons (the firing neurons) by activating the D2 autoreceptors with 60%-75% intrinsic activity, whose overall effect is the reduction of dopamine release; Abilify has partial agonist affinity on D2 presynaptic neurons. Abilify activates the postynaptic neurons (receiving neurons) with an intrinsic activity range of 30% - 60%. The activation of dopamine D2 autoreceptors on presynaptic neurons causes a reduction of dopaminergic activity; So on presynaptic neurons agonism means the neuron will send less dopamine signals to begin with; and on postsynaptic neurons; Abilify can be said to be a weak to moderate antagonist; but not nearly as intolerable; as most flat / silent antagonists, such as Ziprazidone (good for mood; may induce a hypomanic state); I am taking Abilify to prevent a manic or psychotic episode from developing. I know abruptly withdrawing puts people at a greater risk of relapsing (developing mania or psychosis). Therefore , I must choose a very gradual discontinuation plan. So for the time being; I'll continue by Abilify treatments.

I would prescribe me a low dose stimulant; to increase my affect and cognition and bring them back to way they were functioning before taking Abilify this year .I need to increase dopamine transmission in the mesocoortical pathway.
I have a diagnosis of ADHD and Schizo-affective disorder, bipolar subtype. Therefore I naturally must lack some dopamine activity here on this pathway in my frontal lobes (if my diagnosis is correct; which I highly doubt); Abilify might increase dopamine here; through partial agonism of D2.

Abilify does not reduce mesocortical pathway due to dopamine D2 partial agonism;

But possible reductions of activity in the mesocortical pathway are possible via 5HT2A antagonism,
This blocks dopamine release in the prefrontal cortex; Whereas an agonist of that receptor causes dopamine release in the prefrontal cortex ( my new therepeutic goal). However, Abilify is a partial agonist on 5HT1A receptors with significant intrinsic activity sufficient to increases dopaminergic neurotrasmission (with intrinsic activity between 0 % < ?< 100%).

2. Dexedrine 20 mg / day (ADHD medicine; while the mesolimbic pathway is partially agonized by Abilify; D2 occupancy 70 % - 90% of the D2 type dopamine receptors are covered by Abilify molecules; my mesocortical pathway needs to be functioning at a higher activity level. Abilify has a range of intrinsic activity on D2 receptors is IA = 30 % - 75% (recorded) depending on the type of D2 receptor: autoreceptors get net inhibition by partially activating D2 autoreceptors (60-75%); whereas postsynaptic receptors get up to 60% (according to Wikipedia).

The addition of Dexedrine would globally release dopamine while the mesolimbic is selectively antagonized by the partial agonist; that is, in the presence of a full agonist, Abilify acts as antagonist; and in the absence of a full agonist, Abilify acts as a agonist in regions where dopamine release is usually low in people diagnosed with certain psychotic disorders. So I am very well aware of the side effects and I understand stimulant use can trigger mania in me even though I am actively taking Abilify a powerful anti-manic agent. which reduces positive symptoms of psychosis by primarily lowering the activity of the mesolimbic pathway which happens to be our key reward pathway in our brain connecting the midbrain to the nucleus accumbens. Psychotic states, schizophrenia, and mania are caused by excessive dopaminergic signalling in the mesolimbic pathway, particularly due to D2 dopamine receptor activation by dopamine, according to the dopamine hypothesis of schizophrenia and psychosis. Taking Dexedrine and Abilify at the same time results in activation of the mesocortical pathway; than Abilify would result on its own; Remember there is not evidence that Abilify reduces mesocortical activity; but there is evidence that Abilify increases dopamine here.

3. Welbutrin (dopamine-noradrenaline reuptake inhibitor) 450mg / day
I have been on Welbutrin 300 mg now for a week; and any higher than 450mg / day; is not recommended due to increased seizure risk; and can likely counteract some of the prime effects of antipscyhotic treatment. An increase in Welbutrin dosage, that I would give to myself, is for more dopaminergic neutrotransmission in the four dopaminergic pathways; put my main therapuetic targets remain the modulation of the mesolimbic and the activation of the mesocortical.

This theoretically would result in a tonic increase in dopaminergic activity and could treat negative and cognitive symptoms here through partial agonism; Even under Abilify, long term heavy usage of antipsychotics can be very nasty to take. still I still feel restrained; neurologically inhibited; chemically lobotomized; signs of reduction in dopamine synaptic content and /or firing patterns. This must be due to excessive reduction of mesolimbim pathway activity or excessive antagonism by Abilify there. I do not get as much pleasure out of drugs as I used to. I feel tranquilized and alienated from my real self. The treatment to this state is dopamine increasing drugs; such as Welbutrin and Sertraline; as well as psychostimulants which are dopamine and norepinephrine releasing agents (such as TAAR 1 receptor agonists, etc.).

4. Pramipexole = D2 agonism and a potent D3 receptor (full) agonist; exhibits also agonistic activity on serotonergic neurons; These drugs are used to treat Parkinson's disease. But for me this is medicine for a different reason, they would reverse the main effects of neuroleptics / antipsychotic drugs; I would use Anti-Parkinsonian agents to treat my anhedonia (lack of pleasure), depression (low mood), sexual dysfunction and total loss of libido; I would use them for their potential to reduce the cognitive and negative side effects caused by neuroleptics [/U](antipsychotic drugs), including Abilify.

5. Lisuride (medicine for Parkinson's disease; dopamine and 5HT2A type serotonin receptor agonist); used to treat low dopaminergic states in all four dopaminergic neuron pathways. Abilify reduces the mesolimbic D2 and D3 receptors with affinity similar to dopamine; and with partial agonism.

OR

Bromocriptine: potent D2 agonist; used for Parkinson's disease, used to reduce prolactin levels, increase testosterone; recover from antispsychotic induced hyposexuality (loss of libido) etc. Bromocriptine is a D2 and 5HT2A complete agonist. which can be useful in reversing some of the side effects cause by the antipsychotic which I have to take for anti-mania and anti-psychosis preventative and maintenance treatment. Bromocriptine would treat symptoms such as anhedonia, neuroleptic induced deficit syndrome, feeling lobotomized, feeling Zombified,; feeling in a straightjacket which dampens down my thoughts and quitens my behaiour. alienated from your former self, akathisia, extrapyramidal symptoms, alogia, avolition (lack of motivation). anhedonia (lack of pleasure); depression (low mood) ~ is being treated with Abilify and Welbutrin. Bromocriptine medication causes hypersexuality; and causes an intensification of sexual prowess, ability, and pleasure; Bromocritpine treatment; for long periods of time can potentially cause some patients to switch to hypomania. A sub-therapeutic amount of dopamine agonist added to Abilify treatment; will likely not do any harm.

6. Vilazidone; solely a 5HT1A agonist or Trintellix (SSRI and 5HT1A agonist). Trintellix has a relatively mild side effects profile.
Trintelliz in combination with the Anti-Parkinsonian agents can cause an drug interaction related adverse side effects; If put on an new antidepressant on top of my Welbutrin (300 mg / day). As the serotonin receptor 5HT1A activates it causes dopamine release in the prefrontal cortex; Welbutrin merely increases dopaminergic neurotransmission globally and tonically - that is it increases synaptic content of dopamine here - which causes more communication between dopamine neurons, on the Mesocortical Pathway; when taking Abilify; not reduce; theoretically speaking.

7. Sertraline: Serotonin-Dopamine Reuptake Inhibitor; stop the recycling process of both serotonin and dopamine (at high doses).
Increases both serotonin activity and dopamine activity. Therefore Sertraline is relatively more effective at treating depression than other SSRI's which only increase synaptic serotonin content. Antidepressants (stimulants, uppers) are known to induce hypomania, and develop mania; and even psychosis - - both in schizoaffective disorder and schizophrenia; and manic- depressive illness / Bipolar Disorder - Antidepressants can often switch people to mania. If mania does come back; I would not mind; in fact, I miss my hypomanic mind. I would engineer a gradual increase in dopaminergic activity for me over the course of the duration of my treatment order.

[Petros Agapetos]

I would order Pramipexole; Rotigotine, Ropinirole , these are dopamine receptor agonists. used for the treatment of Parkinson's disease; which can reverse the sexual side effects caused by Abilify and other antipsychotics; by fully activating D2 type dopamine receptors; which can be found on the mesolimbic pathway. These drugs will counteract the effects of the antipsychotics; by reversing their psychopharmacological target ; instead of D2 antagonism of partial agonism; the person then gets complete agonism , as dopamine would cause an add on treatment against anhedonia, lack of motivation; neuroleptic induced deficit syndrome.These drugs could potentially treat antipsychotic-induced deficit syndrome; However, note that these drugs could cause hypersexuality; ...causing too much libido, more powerful orgasms; reversal antipsychotic-induced sexual dysfunction.

Another drug of choice is Pribedil which is a D3 receptor agonist and α2–adrenergic antagonist; for the treatment of anhedonia and lack of motivation, loss of initiative, and loss of drive. Dopamine agonist can modulate dopaminergic transmission in such a way that the patient is comfortable with the side effects, and at the same time is at a therapeutic dose. Dopamine receptors should ideally only be occupied 60% to 75% at most; not 70% to 90% as it is in the case of Abilify treatment, however, have in minds that Abilify is a partial agonist there activates D2 autoreceptors (which shuts down firing cells) and selectively antagonize D2 postynaptic receptors on the receiving neuron. Thereby lowering both the presynaptic dopamine release as well as postynaptic receiver of the dopaminergic signal.

[TheMaestro]

Now in English please.

[Joso]

cool

[Khamzat]

Now in English please.

He needs a lot of medication.

[Joso]

He needs a lot of medication.

lol

[Petros Agapetos]

I would prescribe myself Venlafaxine at 450mg so that it inhibits the the reuptake of serotonin, noradrenaline and dopamine. All three! This would be a fine addition to my Welbutrin 300 mg. Or the addition of 15 mg Dexedrine (dextroamphetamine) for my ADHD. This is a very low dose; it probably would not cause psychosis, even when taken long term, given that Abilify is reducing dopaminergic activity in my mesolimbic pathway due to partial agonism.

[FinalFlash]

Are you alright buddy?

[Kivan]

[Petros Agapetos]

First column - receptor subtype
Second column - Dissociation constant , Ki
Third column - INTRINSIC ACTIVITY, dopamine is defined = 100%

5-HT1A 2.6 Partial agonist
5-HT2A 18.8 Antagonist
5-HT2B 0.58 Antagonist
α1A 155 Antagonist
D2L 0.49 IA = 40% Partial agonist
D2S 0.69 IA = 40% Partial agonist
D3 0.085 IA = 60% Partial agonist
H1 23.2 Antagonist
mACh >1,000 Antagonist


Unlike many antipsychotics that are D2 and 5-HT2A receptor antagonists, cariprazine is a D2 and D3 partial agonist. It also has a higher affinity for D3 receptors. The D2 and D3 receptors are important targets for the treatment of schizophrenia, because the overstimulation of dopamine receptors has been implicated as a possible cause of schizophrenia.

Cariprazine acts to inhibit overstimulated dopamine receptors (acting as an antagonist) and stimulate the same receptors when the endogenous dopamine levels are low. Cariprazine’s high selectivity towards D3 receptors could prove to reduce side effects associated with the other antipsychotic drugs, because D3 receptors are mainly located in the ventral striatum and would not incur the same motor side effects (extrapyramidal symptoms) as drugs that act on dorsal striatum dopamine receptors. Cariprazine also acts on 5-HT1A receptors, though the affinity is considerably lower than the affinity to dopamine receptors (seen in monkey and rat brain studies). In the same studies, cariprazine has been noted to produce pro-cognitive effects, the mechanisms of which are currently under investigation. An example of pro-cognitive effects occurred in pre-clinical trials with rats: rats with cariprazine performed better in a scopolamine-induced learning impairment paradigm in a water labyrinth test. This may be due to the selective antagonist nature of D3 receptors, though further studies need to be conducted. This result could be very useful for schizophrenia, as one of the symptoms includes cognitive deficits.

Cariprazine has partial agonist as well as antagonist properties depending on the endogenous dopamine levels. When endogenous dopamine levels are high (as is hypothesized in schizophrenic patients), cariprazine acts as an antagonist by blocking dopamine receptors. When endogenous dopamine levels are low, cariprazine acts more as an agonist, increasing dopamine receptor activity. In monkey studies, the administration of increasing doses of cariprazine resulted in a dose-dependent and saturable reduction of specific binding. At the highest dose (300 μg/kg), the D2/D3 receptors were 94% occupied, while at the lowest dose (1 μg/kg), receptors were 5% occupied.