Back! Possible Cure Part 2 - No Guarantees But Were Here Anyways

[SomebodySomewhere]

Once I'm off of my Klonopin, if I still have HPPD (I don't know if I still have it), I'll make sure I read through this thread carefully and try some of the suggestions.

It is important that we try and figure out if this can be reversed, I agree with you.

[Fawkinchit]

2 hours ago, SomebodySomewhere said:

Once I'm off of my Klonopin, if I still have HPPD (I don't know if I still have it), I'll make sure I read through this thread carefully and try some of the suggestions.

It is important that we try and figure out if this can be reversed, I agree with you.

Thank you

[Fawkinchit]

On 12/2/2020 at 3:26 AM, thelostreceptor said:

Thought I'd post this in case you didn't notice it, it's a recent study (Apr 2020) about visual snow.

https://pubmed.ncbi.nlm.nih.gov/32211752/
 

Structural and functional footprint of visual snow syndrome

Patients with visual snow syndrome suffer from a continuous pan-field visual disturbance, additional visual symptoms, tinnitus, and non-perceptional symptoms. The pathophysiology of visual symptoms might involve dysfunctional visual cortex. So far, the extra-visual system has not been investigated. We aimed at identifying structural and functional correlates for visual and non-visual symptoms in visual snow syndrome. Patients were compared to age- and sex-matched controls using 18F-2-fluoro-2-deoxy-d-glucose PET (n = 20 per group) and voxel-based morphometry (n = 17 per group). Guided by the PET results, region of interest analysis was done in voxel-based morphometry to identify structural-functional correspondence. Grey matter volume was assessed globally. Patients had corresponding hypermetabolism and cortical volume increase in the extrastriate visual cortex at the junction of the right lingual and fusiform gyrus. There was hypometabolism in the right superior temporal gyrus and the left inferior parietal lobule. Patients had grey matter volume increases in the temporal and limbic lobes and decrease in the superior temporal gyrus. The corresponding structural and functional alterations emphasize the relevance of the visual association cortex for visual snow syndrome. The broad structural and functional footprint, however, confirms the clinical impression that the disorder extends beyond the visual system.

So the results of this paper demonstrate grey matter volume increases and hypermetabolism. In my opinion treatment would need to be focused on regenerating the structure in the affected areas. There are not many options for that currently. It would involve methods to allow axonal regeneration to break through glial scarring, enhancing growth factors to further support growth and enhance neurogenesis, survival of newborn neurons & integration.

https://pubmed.ncbi.nlm.nih.gov/10027775/\

Conversely, immature rats can sustain major metabolic activations that lead either to a variable extent of damage, as seen at P21, or no damage, as recorded at P10.

 

And

https://watermark.silverchair.com/67-12-1205.pdf?token=AQECAHi208BE49Ooan9kkhW_Ercy7Dm3ZL_9Cf3qfKAc485ysgAAAq8wggKrBgkqhkiG9w0BBwagggKcMIICmAIBADCCApEGCSqGSIb3DQEHATAeBglghkgBZQMEAS4wEQQMYFQnE4k8JeAnLrysAgEQgIICYifamLsH4wt0PhcaiTrNAtOF6dt-jBQn6YTviY7mamU03WE6zRKh9rVTjEokSmtFRVEFga5gTkPM69GAN17GjdjZjIJHwia7qMMWoEVZ8unSvqAvJkWWDCZsd47MDzXtuOBoPLJ6loE02FREWOeXncVpnqg4_eHWJQOOEXH2exXZT3g0Ve3T9C4syIFu-S03QNNree9HsFZk9ptkOJMujuMI2xqnzapNc-JZ0DIxeSFODr6Bu3rDs4BUZ3Q3aoXYhRQLMzX427H1M28tWjREaOk-OU-HEMy5-5rR4WczoWVLoRjuQ519W53hB32XwoAtp38VLOimSFYAKMbkOCVqO3F_Plaz_KHxFAMbAY3ntXQahKxwgW0iwJyGDXE6RJSyxUzZk7MnCI2-1R4x0RHtNzDswoWa0Nilzn97rRPkQbGIr0L2OAF9kvBGZa_SevDlgHk41QQNVSGpL0TW-u5f_Rjj4Ee2VfbnTIPhunURxY7jE-aqbfoJFrWCq8Mn9bWJysiQSqlf8Fd04EkuyB_iHaDfj6jNLnaQJAScwdBjpcXZXF1UJZzePXtL696QoMopZzh4-WZjuJ-O57o4VsVpxvprt4rqGafkK0NXYkToE7Gj-LRpyG-RR6efb5dNssAsp5p-lBflfVkxvMhSDSddrBwsoa7yB9e0tjuv6rzys0UobRiJRcRTJsyFId__Ur_dm3erwb_gvSUbyS-ILI8PgA4neMWlv1LdTegpyvySag61_mdCX4msQdZO2-0UBw836km1J7Mzn2DJYIaLjMIgyoF_NtlFHhHRCLwi55a0XvWQvdo

More evidence that atrophy isn't defined by neuronal loss. So this is good.

Edited December 7, 2020 by Fawkinchit

[Fawkinchit]

Rat spinal cord ganglia cultures were maintained for periods of up to 19 days in a feeding solution containing LSD-25 in a concentration of 5 x 10^-6. Electron microscopic examination of the nerve cells in these cultures revealed alterations in the Golgi complexes, lysosomes, mitochondria and multivesicular bodies. The changes in the membranous components of these structures were particularly prominent and resulted in organelle pleomorphism and very unusual internal membrane patterns. Variations were also noted in the fine structure of the nucleoli of some neurons. The possible relationships of the morphologic changes to disturbances of neuronal metabolism are considered.

 

https://academic.oup.com/jnen/article-abstract/33/2/212/2612730?redirectedFrom=fulltext

 

This article in my opinion, shows two things, that even after long durations of LSD exposure, neurons do not die, so it still appears to not be neurotoxic, and that apparent alterations in the cell bodies occur.

I would like to note though there could be other physiological mechanisms that could induce neuronal loss that just neurotoxicity specifically, so its not entirely ruled out. 

Edited December 11, 2020 by Fawkinchit

[Fawkinchit]

ABSTRACT

In the mid-1990s, it was proposed that quantum effects in proteins known as microtubules play a role in the nature of consciousness. The theory was largely dismissed due to the fact that quantum effects were thought unlikely to occur in biological systems, which are warm and wet and subject to decoherence. However, the development of quantum biology now suggests otherwise. Quantum effects have been implicated in photosynthesis, a process fundamental to life on earth. They are also possibly at play in other biological processes such as avian migration and olfaction. The microtubule mechanism of quantum consciousness has been joined by other theories of quantum cognition. It has been proposed that general anesthetic, which switches off consciousness, does this through quantum means, measured by changes in electron spin. The tunneling hypothesis developed in the context of olfaction has been applied to the action of neurotransmitters. A recent theory outlines how quantum entanglement between phosphorus nuclei might influence the firing of neurons. These, and other theories, have contributed to a growing field of research that investigates whether quantum effects might contribute to neural processing. This review aims to investigate the current state of this research and how fully the theory is supported by convincing experimental evidence. It also aims to clarify the biological sites of these proposed quantum effects and how progress made in the wider field of quantum biology might be relevant to the specific case of the brain.

 

https://avs.scitation.org/doi/10.1116/1.5135170

[Joseph C.]

Toi eclaireurs des mur feu subitement artilleurs lumineuses. Ai balaye enleve autres ne reunir menent. Te pose la tire rues. Le coeur je et aimer essor somme. Region sortes arches mur nez. Rien oui elue avec bles car. Et relevent on caissons posseder charrues eu. Cet bourreaux esplanade mur echangent perruches crepitent connaitre eau. Mendiaient admiration qu on de vieillards. Repris laissa paquet peu des paumes atroce ras eux.

Edited April 23, 2022 by Joseph C.

[Fawkinchit]

https://pubmed.ncbi.nlm.nih.gov/27046518/#:~:text=Glial cells such as microglia,to the extrasynaptic NMDA receptor.

https://www.frontiersin.org/articles/10.3389/fnmol.2018.00414/full

https://www.nature.com/articles/npp2016199

https://www.sciencedirect.com/science/article/pii/S2666354619300353

https://www.sciencedirect.com/science/article/abs/pii/S0197018613000363

https://www.mdpi.com/2073-4409/8/2/184/htm

Just posting these for future reference and reading. It would appear that there is a possibility of glial cell dysfunction leading to increased levels of glutamate, which would be constant, and overstimulate the nervous system. Which would explain why some have benefited from Lamotrigine, which down regulates glutamate. So the issue could actually be dysfunction of the astrocytes and oligodendrocytes dumping too much glutamate on to neurons, or an issue with sucking it back up from the neurons, which appears to be common in neuroinflammation related conditions. Then the issue becomes finding the cause of and ameliorating the inflammation. 

Edited December 28, 2020 by Fawkinchit

[Onemorestep]

On 10/2/2019 at 4:35 AM, yosoydiego said:

Nop... how is that relevant to this thread?

I’ve often wondered if the genetic makeup of those who listen to music like this predisposes them to certain conditions. You certainly need high dopamine to like it haha. 

 

(I’ve been listening to asot for about 14 years now)

[Onemorestep]

On 12/28/2020 at 4:13 PM, Fawkinchit said:

https://pubmed.ncbi.nlm.nih.gov/27046518/#:~:text=Glial cells such as microglia,to the extrasynaptic NMDA receptor.

https://www.frontiersin.org/articles/10.3389/fnmol.2018.00414/full

https://www.nature.com/articles/npp2016199

https://www.sciencedirect.com/science/article/pii/S2666354619300353

https://www.sciencedirect.com/science/article/abs/pii/S0197018613000363

https://www.mdpi.com/2073-4409/8/2/184/htm

Just posting these for future reference and reading. It would appear that there is a possibility of glial cell dysfunction leading to increased levels of glutamate, which would be constant, and overstimulate the nervous system. Which would explain why some have benefited from Lamotrigine, which down regulates glutamate. So the issue could actually be dysfunction of the astrocytes and oligodendrocytes dumping too much glutamate on to neurons, or an issue with sucking it back up from the neurons, which appears to be common in neuroinflammation related conditions. Then the issue becomes finding the cause of and ameliorating the inflammation. 

I have had enormous benefit in the past from naltrexone, which I primarily attribute to its effect on glial cells—If it helps hehe

[Onemorestep]

These are all fascinating theories. I developed a lot of gut issues around the time I accrued hppd. 
 

currently I am wondering if these were effects from deregulation of the endocannabinoid system, but it’s all theoretical too. Some very interesting stuff goes on when you have a system of poor endocannabinoid binding... 

[SomebodySomewhere]

3 hours ago, Onemorestep said:

I have had enormous benefit in the past from naltrexone, which I primarily attribute to its effect on glial cells—If it helps hehe

I have a prescription for Naltrexone, but haven't been taking it because I'm worried it could mess up benzo withdrawals.

What benefits did you see from it?

What I personally noticed, even though I typically don't feel dissociated, is that I felt much more "in my body". I know that off-label Naltrexone and it's stronger cousin can be used for depersonalization/derealization.

I'm not sure my anger problem is HPPD related since I've always had one (though it's much worse these days), but I also noticed that things that would typically piss me off wouldn't when I was on it.

I wish I understood neuroscience better. I really need to sit down and educate myself, and then pour through this thread.

[Onemorestep]

I have also had anger issues but only after two things— head injuries and hppd onset. There are a lot of things that can cause irritation and anger I’m sure, but I know brain inflammation is one of them.
 

Naltrexone, mixed with a low dose of Ativan, makes me weirdly sleepy and relaxed in a way neither does alone. By itself it just seems to help my emotions stay stable and puts me in a better head space. I also feel more associated as you say. I wish I could get the s isomer of it, as that is reported to have the micro glial anti inflammatory effects without the opioid. Then I could differentiate one effect from the other. 
 

all in all I think it’s a fine drug. I didn’t start it until I was about 1.5 years into benzo withdrawal just so you know (mine was very very bad as I also withdrew from gabapentin and anti epileptics all in the same period because I’m a fucking masochist apparently). 
 

im sorry you’re going through benzo withdrawal. It’s hell. It does get better though. About one year into it, I took BPC-157 and it helped immensely. I know of only two others besides myself on this site who have taken bpc and one had a terrible reaction, one had a great one. I have absolutely no idea why one way or the other. 
 

having a reduction in anger from naltrexone is very interesting as it’s an opiate antagonist and should cause it if anything haha. Brains are cool.

Edited December 30, 2020 by Onemorestep

[SomebodySomewhere]

*Edit*

Removed dumb post.

 

To add some content: Sage sounds interesting, but I'd only use it as a spice. Based on what I'm reading when taking it as a supplement it has thujone in it, like what's in Wormwood, which is neurotoxic.

Edited January 10, 2021 by SomebodySomewhere

[Fawkinchit]

On 12/29/2020 at 10:09 PM, SomebodySomewhere said:

*Edit*

Removed dumb post.

 

To add some content: Sage sounds interesting, but I'd only use it as a spice. Based on what I'm reading when taking it as a supplement it has thujone in it, like what's in Wormwood, which is neurotoxic.

It is true it does contain thujone, which may make some people nervous, which I understand. However it should be noted that thujone is, if I recall properly, only neurotoxic and higher levels, and the amount in sage is very low, so nothing that I know of that can reach the threshold for neurotoxicity. I looked it up a long time ago, I believe one report even stated that some samples of sage they tested had no thujone at all. There's also a reason I recommend it.

Anyways I'll make a post in the next couple of days, that outlines the most probable cause of this disease(HPPD) and what people can do for the best possible outcome. I may just simply make a new thread.

Edited February 3, 2021 by Fawkinchit