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How to heal brain damage from DXM?

dxm brain damage supplements pqq

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#1 Destiny's Equation

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Posted 19 August 2016 - 11:24 PM


(I know I started another thread on this, but DXM wasn't in the title.)

I have been clean for 3 months.

PQQ is the only thing I have found so far that helps.

Current problems (they are gradually improving with time):

My spatial awareness is warped; I can't tell how far away things are from other things. This drives me nuts because when I throw things away I can't tell whether my hands are touching the garbage in the trash can or not (I hate germs).

My concentration is poor and it "hurts" when I try to concentrate.

My motor coordination was impaired to the point that after some of my DXM trips I had to teach myself how to shower, wash my hands, wipe after using the bathroom, and run all over again. It has since improved to the point that I can mostly pass as normal but I no longer move gracefully and I am still having more difficulty with showering than I normally do.

Past problems (now resolved):

My hands sometimes appeared to be melting downwards, it looked like they were dissolving into liquid (which made it even harder to tell whether or not my hands were touching garbage when throwing things away or not).

#2 Doc Psychoillogical

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Posted 20 August 2016 - 02:29 AM

Problems could be due to DXM being a NMDA antagonist, and your long term exposure and DXM's various receptor antagonism/agonisms.

Possible solution could be to first restore NMDA function i.e:

How NMDA is Modulated:

The NMDA receptor is modulated by a number of endogenous and exogenous compounds:

  • Na+K+ and Ca2+ not only pass through the NMDA receptor channel but also modulate the activity of NMDA receptors.
  • Zn2+ and Cu2+ generally block NMDA current activity in a noncompetitive and a voltage-independent manner. However zinc may potentiate or inhibit the current depending on the neural activity.
  • Pb2+ is a potent NMDAR antagonist. Presynaptic deficits resulting from Pb2+ exposure during synaptogenesis are mediated by disruption of NMDAR-dependent BDNF signaling.
  • It has been demonstrated that polyamines do not directly activate NMDA receptors, but instead act to potentiate or inhibit glutamate-mediated responses.
  • Aminoglycosides have been shown to have a similar effect to polyamines, and this may explain their neurotoxic effect.
  • The activity of NMDA receptors is also strikingly sensitive to the changes in H+ concentration, and partially inhibited by the ambient concentration of H+ under physiological conditions.The level of inhibition by H+ is greatly reduced in receptors containing the NR1a subtype, which contains the positively charged insert Exon 5. The effect of this insert may be mimicked by positively charged polyamines and aminoglycosides, explaining their mode of action.
  • NMDA receptor function is also strongly regulated by chemical reduction and oxidation, via the so-called "redox modulatory site." Through this site, reductants dramatically enhance NMDA channel activity, whereas oxidants either reverse the effects of reductants or depress native responses. It is generally believed that NMDA receptors are modulated by endogenous redox agents such as glutathionelipoic acid, and the essential nutrient pyrroloquinoline quinone.
  • Src kinase enhances NMDA receptor currents.
  • Reelin modulates NMDA function through Src family kinases and DAB1 significantly enhancing LTP in the hippocampus.
  • CDK5 regulates the amount of NR2B-containing NMDA receptors on the synaptic membrane, thus affecting synaptic plasticity.
  • Proteins of the major histocompatibility complex class I are endogenous negative regulators of NMDAR-mediated currents in the adult hippocampus, and are required for appropriate NMDAR-induced changes in AMPAR trafficking and NMDAR-dependent synaptic plasticity and learning and memory.
The NMDA receptor is a non-specific cation channel that can allow the passage of Ca2+ and Na+ into the cell and K+ out of the cell. The excitatory postsynaptic potential (EPSP) produced by activation of an NMDA receptor increases the concentration of Ca2+ in the cell. The Ca2+ can in turn function as a second messenger in various signaling pathways. However, the NMDA receptor cation channel is blocked by Mg2+ at resting membrane potential. Magnesium unblock is not instantaneous, to unblock all available channels, the postsynaptic cell must be depolarized for a sufficiently long period of time (in the scale of milliseconds).

Therefore, the NMDA receptor functions as a "molecular coincidence detector". Its ion channel opens only when the following two conditions are met: glutamate is bound to the receptor, and the postsynaptic cell is depolarized (which removes the Mg2+ blocking the channel). This property of the NMDA receptor explains many aspects of long-term potentiation (LTP) and synaptic plasticity.

NMDA receptors are modulated by a number of endogenous and exogenous compounds and play a key role in a wide range of physiological (e.g., memory) and pathological processes (e.g.,excitotoxicity).

Educate yourself, a good place to start!



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#3 gamesguru

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Posted 20 August 2016 - 03:37 AM

It's a problem of spatial memory and sensory-motor coordination[1], which is due to hippocampal[2] and somatosensory[3] degradation.  It's ironic how I thought the somatosensory aspect would be the more challenging problem to solve, but you've managed to address it first!  I believe to treat this, epicatechin, ginkgo[4], and oddly enough, ginger[5].

 

Edit: it appears depth perception has nothing to do with spatial memory.  Sorry.


Edited by gamesguru, 20 August 2016 - 03:42 AM.






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