James3524

I haven't tried it, but it heard it can help DP/DR.

You need to taper very slowly if you decide to get off. The taper might even take a few years. My flare up from Phenibut is slowly baselining, though. It is a voltage-gated calcium channel blocker but has some GABA-b agonism.

You would need to have your visual cortex removed. Removing eyeballs wouldn’t do much

Has anyone gone through benzodiazepine withdrawal and had their HPPD permanently worse? I had Phenibut withdrawal (VDCC blocker & GABAb agonist) withdrawal and my symptoms have been quite exacerbated. I think what's happening is GABAb receptor desensitization and AMPA/NMDA sensitivity; leading to a net increase in neuronal excitability and making my condition worse.

May I ask what your main visual symptoms were? I was seeing improvement every year since getting this four years ago until a recent setback

That’s a great way to destroy your life! if you have HPPD and consider taking psychedelics again, you are insane. Please don’t risk it as it can literally ruin your life.

I believe that symptoms resembling those observed during acute psychedelic intoxication may have a distinct origin compared to the symptoms shared between HPPD and VSS. I consider "HPPD" an outdated term, as many individuals refer to psychedelic-induced visual snow syndrome as HPPD, a label I find inaccurate. It has been theorized for a few years that a thalamocortical dysrhythmia is involved in the pathophysiology of VSS. I couldn't find anything that explains how that would really work so I made a note dump and then put it through AI to organize it. I tried pasting it here but it messes it up. Let me know what you think! Visual Snow Syndrome.pdf

presented with 25-year history of pharmaco-resistant focal aware visual seizures frequently evolving to focal impaired awareness seizures. The SOZ was in the right occipital lobe (positron emission tomography-computed tomography/video electroencephalography). Magnetic resonance imaging was normal. She underwent ipsilateral lateral geniculate nucleus (LGN) DBS procedure. After a 24-month follow-up, seizure frequency decreased by 97%, improving quality of life and daily functioning without complications. Lessons: This is the first time the LGN has been targeted in humans. The results support the hypothesis that led to this study. This strategy represents a paradigm shift in the way of treating pharmaco-resistant FASs not amenable to resective surgery.

You could probably fake focal point epilepsy and get this treatment since we have HPPD.

Based on some research, it seems there may be a potential connection between HPPD/VSS and Thalamocortical dysrhythmia (TCD) according to some researchers. I posit that HPPD often encompasses Visual Snow Syndrome, and the persistent psychedelic-like perceptual effects may be attributed to a distinct issue like some sort of serotonin 2a hypersensitivity which may be able to be fixed by something like Pimavanserin 5-ht2a inverse agonist. I think it is inappropriate to automatically label Drug-Induced Visual Snow Syndrome as HPPD unless symptoms like Alice in Wonderland experiences, geometric shapes, and psychedelic CEVs are present. A recent study from King's College reveals that patients with Visual Snow Syndrome exhibit reduced connectivity in 5-ht2a enriched networks. Notably, individuals with a history of substance abuse were excluded from the study. Given that almost all psychedelics bind to 5-ht2a, it appears that drug-induced VSS shares similarities with regular VSS. Since VSS is linked to Thalamocortical dysrhythmia (a synchronization issue, particularly the Lingual Geniculate Nucleus (LGN) and the Medial Geniculate Nucleus (MGN)), the outcome of reduced input is cortical hyperactivity/excitability and hypermetabolism. The Dorsal Cochlear Nucleus (DCN), a component of the thalamus, is implicated in causing this issue. While Thalamocortical dysrhythmia is not deemed the primary cause (more likely a consequence), many scientists believe it stems from an inhibition problem involving various neurotransmitters such as GABA, Glutamate, and Sodium Channels. If the issue is the result of dead or dysfunctional neurons leading to Thalamocortical dysrhythmia (TCD), then addressing the dysrhythmia itself, rather than the dead neurons, may be feasible. The concept here is that even though the neurons might be irreversibly damaged, managing the consequences, such as TCD, could potentially be achieved through interventions like Deep Brain Stimulation and lead to remission of symptoms. DBS involves implanting electrodes in specific brain regions, like the thalamus, and delivering controlled electrical pulses to modulate neuronal activity. DBS can target areas affected by the loss of 5-HT2A-expressing GABAergic neurons. The precisely timed electrical pulses can mimic the inhibitory function of these lost neurons, dampening down the excessive neuronal firing and restoring a proper rhythm to the thalamocortical communication. Growing new neurons with stem cells seems like it is possible in the future as well. There is a company working on it for epilepsy and their product is in human trials. I have a ton of brain fog from Benadryl as I wrote this so please forgive any of my errors.

Has anyone thought of DBS for the treatment of HPPD? According to some studies, it seems that visual snow syndrome is caused by some sort of thalamocortical dysrhythmia. I thought this was interesting as it seems many of us, including myself, have developed OCD after getting HPPD/VSS which associated with thalamocortical dysrhythmia as well. The only thing in our way is figuring out what area to target and then convincing a neurosurgeon to do it for you. DBS is usually used in Parkinson's disease which is caused by dopaminergic cell death. DBS offers Parkinson's patients immense relief but their condition is progressive and the relief wont last forever but will for us. I've only heard of two stories about using DBS to treat VSS/HPPD. One of them was a post from ten years ago saying his HPPD was cured after DBS. Another VSS patient claimed his visual distortiions were cured after undergoing DBS for part of a tinnitus study. "It has been proposed that symptoms of HPPD are caused by damage to inhibitory interneurons expressing 5-HT2A serotonin receptors to which most hallucinogens bind. This loss of cortical inhibition (21, 22) may manifest in aberrant occipital delta oscillations (23–25) associated with visual hallucinations." [source] "The available evidence suggests that HPPD symptoms may be a result from a misbalance of inhibitory-excitatory activity in low-level visual processing and GABA-releasing inhibitory interneurons may be involved." [source]

I made a post on here a few weeks ago about Phenibut withdrawal but I wanted to go more in depth: Phenibut is an anxiolytic drug from Russia that you can buy online in the U.S. It it's primary MOA is Voltage Gated Calcium Channel Blocking but it does have affinity for GABAb and at very high does; GABAa. It is basically Baclofen + Gabapentin combined. Anways, I used about 135 grams over the course of almost exactly a year. Usually spread out in breaks. My HPPD would improve while I was on it and I only had mild issues when I took a high dose. I only had anhedonia for about two weeks but nothing intense and the rebound did not affect my HPPD. The last 25 grams of that 135g, however, I binged over the course of a week during a bad DP/DR episode with high amounts of anxiety and depression. My last dose was on Christmas. On December 27th, I woke up in the middle of the night with glutamate surges. I felt high anxiety, tremors, sweating, stimulated , etc. I started taking NAC which helped and I took one 0.5mg klonopin and one 1mg klonopin spread throughout the acute phase of withdrawal. Besides that, I quit CT. My visuals began so intense and they were that bad since the early development of my HPPD in 2020. Now 25 days since my last dose and my visuals have not went down and I'm quite worried. I basically "recovered" from the visual symptoms of HPPD a long time ago. Do you think that 25 gram binge was enough to cause glutamate excitotoxicity and damage GABA neurons in the process? Through VGCC or GABA downregulation? Could it be my GABA receptors or VGCC have not upregulated causing a hyperexcitable state that should subside?

Hi everyone, I have had HPPD for four years now and made an account the other week. However, I forgot which email I used so I made a new account. Anyways, I found this study on reddit that claims remission of HPPD and DPDR using rTMS. https://www.brainstimjrnl.com/article/S1935-861X(23)01980-0/fulltext Here are the main parts: Hereby, we present a case of a 29-year-old male diagnosed with type-2 HPPD successfully treated with TMS. The patient had no noteworthy medical or chirurgical history. Initially, he reported sporadic cannabis use at the age of 17 and occasional use of cocaine, LSD or MDMA intake a couple times a year by age 23 without exhibiting HPPD symptoms. However, after a singular LSD usage at 26, he experienced panic attacks, peculiar dreams, muscular spasms, and asthenia for several months, ultimately recovering spontaneously. A more severe relapse occurred one year later, following the use of cannabis, LSD and ecstasy. Persistent visual disturbances, including visual snow in the external visual field and fluctuating derealization, became a daily struggle. Chronic symptoms emerged five years later, encompassing visual field distorsion, permanent visual snow, photophobia, palinopsia, and persistent derealization and depersonalization after a week of cannabis and MDMA use. Nonspecific symptoms also occurred such as anxiety, panic attacks, insomnia and depressive symptoms. Despite ceasing all drug use, symptoms persisted without attenuation. No psychotic symptoms or neurological/ophthalmologic causes were identified. The patient underwent various treatments including pharmacological intervention (2 mg clonazepam, 100 mg lamotrigine, and escitalopram for comorbid generalized anxiety), and cognitive-behavioral therapy, yielded no improvement in HPPD symptoms. Based on previous research on depersonalization-derealization disorder A low frequency rTMS of the right TPJ was administered using a cool DB-80 coil. The patient received a course of 1Hz stimulation of right TPJ at 110% motor threshold intensity, 20 min per session, twice daily for five days, within a one-week period delivering a total of 12 000 pulses. The patient reported no adverse effects. Efficacy was evaluated using the Cambridge Depersonalization Scale (CDS) (State-Version) consisting of 22 items rated between 0 and 100%. Before initiating rTMS, 17 items were rated at 0% and none surpassed this level throughout the treatment. Of the remaining five items, scores decreased from 195% to 150%. The patient subjectively noted an improvement in his visual disturbances including attenuation of palinopsia, photophobia and visual snow, along with reduced insomnia and anxiety. The stability of outcomes on visual disturbances, depersonalization, derealization, and nonspecific symptoms persisted for four months following the rTMS course. Following the positive outcome from the initial rTMS course, maintenance courses were administered at four to six-month intervals over a two-year period. The patient consistently reported a reduction in visual distortions, derealization and depersonalization after each subsequent rTMS session, ultimately leading to remission. Additional symptoms such as insomnia, anxiety and depressive symptoms gradually resolved, reaching full remission. The patient did not undergo any other pharmacological or non-pharmacological interventions during this period. Furthermore, he reported no side effects associated with the rTMS sessions. As of the current date, the patient remains in remission from both HPPD and general anxiety. To the best of our knowledge, this case constitutes the first use of rTMS targeting the right TPJ in a patient suffering from type-II HPPD. While we acknowledge the possibility that treating the patient’s general anxiety may have contributed to the amelioration of his HPPD symptoms, available evidence does not strongly support this hypothesis. Despite possessing an anxious personality, the patient had not sought consultation nor experienced functional impairment due to anxiety before the onset of HPPD. The diagnosis of general anxiety disorder occurred years after the initiation of HPPD and resolved before the cessation of HPPD symptoms. In the context of prior research on rTMS in depersonalization-derealization disorder and auditory verbal hallucinations, we faced the choice of targeting either the right or left TPJ. We opted for the right TPJ, as the patient did not exhibit schizophrenia nor auditory verbal hallucinations. While the primary anticipated outcome was a reduction in depersonalization and derealization, we observed a concurrent decrease in visual disturbances, encompassing palinopsia, photophobia, visual field distorsions, and visual snow. Although the possibility of spontaneous resolution of HPPD cannot be ruled out, the patient’s symptoms remained stable for months before the initiation of rTMS, and their incremental reduction following each maintenance course suggests potential treatment efficacy. Considering acceptability and tolerance of rTMS, the functional disability associated with HPPD, and the partial effectiveness of pharmacological treatments for this indication, further investigations are warranted to explore the feasibility and efficacy of rTMS in the treatment of HPPD.