Adderall and HPPD?

[gloeek]

I have Schizoaffective disorder and it made my voices go away.

 

[any major dude]

this is interesting. I've heard about d-amph salts exacerbating HPPD, but not mitigating it. Strange. Though I do believe HPPD is at least partially due to negative feedback inhibition of GABA. I'm not completely sure of how amphetamine salts effect this pathway.

 

[ShaolinBomber]

this is interesting. I've heard about d-amph salts exacerbating HPPD, but not mitigating it. Strange. Though I do believe HPPD is at least partially due to negative feedback inhibition of GABA. I'm not completely sure of how amphetamine salts effect this pathway.

i've taken adderall quite a bit in the past couple of months and i can honestly say that it doesn't have negative effects that are permanent, atleast for me anyway.

 

[Mantis Style]

Hmm old thread. I think the current research for the cause of HPPD is leaning towards synaptic plasticity. Reinforced excitatory pathways (AMPA-glutamate receptors) and upregulated SILENCED glutamate receptors is what is thought to be causing the excess excitation with someone that has persistent visual distortions.

Significant 5-ht2a agonism releases pretty large quantities of glutamate, and glutamate is one of the main factors that cause excitotoxicity. When presynaptic 5-ht2a's get activated, theres a large amount of glutamate thats released onto neighboring pyramidal neurons.

I think what they're (researchers) are looking at now is PSD (postsynaptic density) protein kinase families. These proteins are released along with other secondary messenger molecules and neurotrophins to guide neurons through plastic changes. In particular, the PSD-95 protein family can increase the amount of excitatory receptors on a postsynaptic membrane, defending the neuron from excitotoxicity from a glutamate overload, but at the same time making the postsynaptic membrane more readily excitable after the experience is done, leaving the neuron significantly changed.

My thought on the matter is that the plastic changes were primarily made on inhibitory pyramidal cells in the visual cortex. Everytime you look at something, glutamate is released which sends an excitatory current through your brain to your visual cortex and in the very short amount of time it takes this process to unfold, you get your visual perception of the outside world. Well if you have inhibitory neurons that are suppose to keep these excitatory currents from overlapping, so to speak, that now have upregulated excitatory glutamate receptors that shouldn't be there, you would get inhibitory pyramidal neurons in your occipital lobe that abnormally respond to light stimulation and the end results are what HPPD patients would describe as hallucinations.

 

[seep]

My thought on the matter is that the plastic changes were primarily made on inhibitory pyramidal cells in the visual cortex. Everytime you look at something, glutamate is released which sends an excitatory current through your brain to your visual cortex

I think it's in The Duchess of Malfi where a painter/apothecary embeds a poison into a painting of the Duke's family. The ROA was visual: anyone who'd stare at a certain pattern in it would fall dead.

and in the very short amount of time it takes this process to unfold, you get your visual perception of the outside world. Well if you have inhibitory neurons that are suppose to keep these excitatory currents from overlapping, so to speak, that now have upregulated excitatory glutamate receptors that shouldn't be there, you would get inhibitory pyramidal neurons in your occipital lobe that abnormally respond to light stimulation and the end results are what HPPD patients would describe as hallucinations.

Not to mention a sudden fascination with kung-fu.

Visual cortex aside, I wonder how close this rescaffolding comes to the actual eye, and if there's any constitutional changes to the actual photoreceptors. The difference would be one of perceptual vs. sensory disturbances.

I wonder also if different wavelengths elicit different responses (especially 450-495 nm) in patients with HPPD.

The value of targeting the sensory (transductive) component of the pathology is, for instance, one could develop a device to filter the artifact (a noise-canceling contact lens, for instance).

The NODID library is back online. It was down for several months.