So i found myself in a very sad emotional state caused by my traumatic response to a form of abuse imposed upon me.
This was a possible suicidal state that i found myself in.
The (MAMP or Meth) Methamphetamine was an interesting component as it was a textbook Bipolar assesment but only an affective disorder (caused by drugs) so i named it
Bipolar affective Disorder in which the METH gave me a few hours of relief and then i was plunged back into misery again.
The physical manifestation of this were upper body convulsions and massive twitches of the lower limbs - the paramedics diagnosed this a series of
psuedoseizures or multiple Psychogenic non-epileptic seizureWikis.
I knew that i was in a desperate psychological state of distress but maintained the clarity that comes from inner voice support and an interest in drugs and psychiatry.
During my genuine suicide ideation (by means of drinking drain cleaner dissolved in alcohol) phase, I was so helplessly and hopelessly depressed and sad and didn't have any benzos to mitigate my emotional pain and the alcohol wasn't cutting it, i experienced this phenomena.
It was straight to hospital and was offered 2 mg.
ClonazepamWiki (K-pins/Rivotril) and should've been 4 mg. due to my lifeling GABA tolereance, and which worked a treat but then was followed by another 2 weeks in a Psychiatric Hospital. The first 4 weeks were on Valium then
TemazepamWiki,
AmisulprideWiki and then
PaliperidoneWiki BEFORE the psuedoseizures, then the post-trauma shock brought on the psuedosezures and a further 2 weeks back on
OlanzapineWiki at the psychiatric hospital did the trick.
So now i reflect back and ended up reporting this.
Now, happy and happily back on the METH -- where i want to be.
what a fucking debacle that was but now it's all but a technical memory and of interest me as i continue my foray into drugs, behaviour and matters of the mind and body (haha, my holistic take on getting stoned).
I just wanted to share.
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The following is a neurological technical study on mood and voltage gated ion channel (
GabapentinoidsWiki like Gabapentin and Pregablin are Calcium voltage gated ion channel
blockers, for example):
Major channels involved in neuropsychiatric disorders and therapeutic perspectivessource:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3646240/Abstract (take the source link above for the complete research data)
Voltage-gated ion channels are important mediators of physiological functions in the central nervous system. The cyclic activation of these channels influences neurotransmitter release, neuron excitability, gene transcription, and plasticity, providing distinct brain areas with unique physiological and pharmacological response.
A growing body of data has implicated ion channels in the susceptibility or pathogenesis of psychiatric diseases. Indeed, population studies support the association of polymorphisms in calcium and potassium channels with the genetic risk for bipolar disorders (BPDs) or schizophrenia.
Moreover, point mutations in calcium, sodium, and potassium channel genes have been identified in some childhood developmental disorders.
Finally, antibodies against potassium channel complexes occur in a series of autoimmune psychiatric diseases. Here we report recent studies assessing the role of calcium, sodium, and potassium channels in BPD, schizophrenia, and autism spectrum disorders, and briefly summarize promising pharmacological strategies targeted on ion channels for the therapy of mental illness and related genetic tests.
Voltage-gated ion channels and inward rectifier potassium channels are widely and selectively distributed in the brain, both in neurons and astrocytes, often forming macromolecular complexes with associated proteins or auxiliary subunits within distinct subcellular compartments.
The alternating activation of different ionic currents sets the resting membrane potential, generates the action potential, and regulates the neuronal firing frequency and neurotransmitter release, thus providing neuronal cells with specific electrical identity ( Hibino et al., 2010; Catterall, 2012; Jan and Jan, 2012).
Since the early 1990s, ion channel genes have been mapped on human chromosomes and mutations in these genes have been subsequently identified.