the HPPD thread
Since joining this website months ago, i've started to see a trend amongst older members and newer ones asking about HPPD, the symptoms, what it is, the possibilities of getting it etc.
I've laid out my ideas and explanations in numerous other threads regarding the issue but it seems like most of the time i end up getting involved in an argument with another member. I will refrain from acting in an aggressive manner towards people who have contradicting opinions if they choose to post in this thread. I only ask that anyone who chooses to comment here could do the same.
I feel obligated to say one thing before i write this out. I am in no way an actual medical researcher and all the information im about to post here for everyone in this community are simply ideas i've read from other legit researchers or simple neurological processes in the brain that i've come to understand from self education.
HPPD
According to Dr. Abraham, the first legitamate researcher for HPPD, HPPD is a legitamate neurobiological disorder stemming from past use of hallucinogenic or psychoactive drugs. It was first theorized by Abraham that HPPD is a result of a loss of GABAergic inhibitory interneurons due to excitotoxic cell death caused by LSD or similar hallucinogens. This was the initial hypothesis developed to try and explain why a certain amount of people continue to experience hallucinations after all drug use has ceased. However, since then there has been new research and development done on HPPD and this theory no longer holds as much ground back then as it does now. The exact mechanism causing HPPD is still not known.
My understanding of neurology is a simple understanding, but i will attempt to explain the process of a normal inhibitory process in response to excitatory stimulation in a "normal" persons brain. When visual stimuli enters a persons brain, it causes excitatory currents to develop in the synaptic cleft. This is caused by a chain reaction of released neurotransmitters. With the normal process of inhibition in the brain, there are inhibitory interneurons in place set to calm down excitatory currents caused by presynaptic neurons. Inhibitory receptors are for the most part located on postsynaptic neurons. When the presynaptic neurons fire, they release neurotransmitters onto postsynaptic neurons. These transmitters will bind to their selective receptor subtype and the chemical reaction will take place. There are receptor subtypes located upon inhibitory neurons to trigger the inhibitory response to excitation. This inhibitory response essentially stops the excitatory current and the current fades out. This was termed the "negative feedback loop" between the serotonergic and GABAergic neurons.
Hallucinogens and how they effect this inhibitory process:
Hallucinogens share similar chemical makeup properties with the natural neurotransmitter serotonin. Because of this, hallucinogens have high affinitys for serotonin receptors. They are partial agonists to serotonin receptors, meaning they bind to serotonin receptors, as serotonin would, but activate and excite the receptors in different ways. Research has shown that the receptor subtype responsible for producing the hallucinations associated with hallucinogens are the 5-ht2a/5-ht2c receptors. These receptors are located on numerous serotonergic neurons, but are also located upon GABAergic inhibitory interneurons. Now normally when serotonin binds to these receptors on the GABAergic neurons, it causes the release of GABA, the main inhibitory neurotransmitter, and produces inhibtion, calming whatever excitatory current that caused the release of GABA. This is part of the "negative feedback loop" i mentioned earlier. But under the effects of a hallucinogen, there seems to be a constant state of disinhibtion (excitation) with the GABAergic neurons, preventing them from calming the excitatory currents being produced by the agonistic features of hallucinogens. This is because theres a binding of the said hallucinogen on the 5-ht2a receptors located on the GABAergic inhibitory neurons. This is what gives rise to the hallucinations.
Normally, when the drug has run its course, this inhibitory process should stabilize and return to normal. However, in genuine but rare cases, these hallucinations persist, 24/7, everyday. This occurence is what is now termed Hallucinogen Persisting Perception Disorder, or HPPD.
Clinical tests run on HPPD subjects show evidence for neurobiological causes:
Although HPPD seems to be a rare case for anyone, it has occured in enough people to recieve clinical examination. There are a few very reliable articles that have been published regarding clinical tests that measure brain activity when exposed to visual stimuli. One of these articles,
http://www.nodid.net/Articles/hppd/abraham96b.pdf, presented by Dr. Abraham, shows signs of a very weak but constant state of disinhibtion (excitation) in the cortical areas of the brain. This region of the brain contains the visual cortex and is responisble for filtering visual information. This data was found by running qEEG's on HPPD subjects. EEG's are usually used to detect epileptic activity in persons who suffer from a seizure disorder. When a specialized version of this test is performed on someone complaining of persistent visual disturbances, there are signs for abnormal excitation simply caused by opening of ones eyes and looking around. This overexcited state of the brain causes abnormal activity in regions of the brain. This is perhaps evidence to suggest the reason why some people experience disassociation symptoms comorbid with HPPD onset.
Concluson: Theories, ideas, questions regarding duration of the disorder, predisposition for acquiring it, etc. :
There are no theories in this point in time to determine what exactly has happened to someone who experiences persistent visual disturbances after drug use. One idea that i have involves synaptic plasticity. Synaptic plasticity, or a change in the strength between synaptic connections, is a normal process in the brain. This is what researches now believe to be the reason of how and why we form memories and learn new things. The mechanism of synaptic plasticity is virtually neurons that continually fire together and respond to eachother over periods of time, will develop a "wired" state to one another and therefore will respond stronger and more easily to eachother in future activation. But what does this have to do with HPPD? Well, with HPPD, there
COULD of been an artificial way of producing this effect amonst neurons that respond to eachother after being exposed to visual stimulation. These are the same neurons that are responsible for the excitatory and inhibitory "negative feedback loop." If some form of plasticity has occured between these types of neurons, then its reasonable to assume that new kinds of connections and strengths have been developed, hindering the process of inhibition in response to visual stimulation. This would result in lingering visual information that is commonly seen in HPPD subjects. Examples, persistent and intense afterimages, tracers, ghosting, etc.
There is no known cure as of right now for HPPD. Recommended medication treatments include potent benzodiazepines and anticovulsants such as Keppra.
Warning signs for being susceptible to HPPD can include suttle changes in the way you percieve light after hallucinogenic drug use. This could come in the form of many of the different visual symptoms of HPPD. Heres a link for those of you who are not familiar with the visual symptoms.
http://www.drugs-forum.com/forum/showthread.php?t=20456.