Hallucinogen persisting perception disorder, or HPPD, is a disorder characterized by visual
phenomena that appear following drug use.
While "hallucinogen" is in the name and psychedelics are the most frequently encountered, other
drugs have been implicated.
It often occurs in people with no preexisting psychological issues.
Although a personal or family background of psychiatric problems might be a risk factor.
The symptoms can be distressing, which is a key part of the official HPPD diagnosis,
but the disorder is distinct from psychosis.
People normally understand the visual distortions are not reflective of reality.
For this reason, we can treat HPPD as a perceptual issue, albeit one frequently found in people
with comorbid psychiatric problems.
A substantial portion of those affected have a spontaneous disappearance of symptoms within
a year.
The symptoms may eventually dissipate in other cases, but it can be a very persistent issue
for some people.
Multiple definitions have been used over the years.
As it currently stands, a useful one for the sake of diagnosis is what's found in the DSM-5,
which is a diagnostic manual for mental health professionals.
The DSM-5 lays out three criteria:
First, there must be a reexperiencing of one or more perceptual symptoms associated with
hallucinogens after use has ended.
Second, those symptoms must cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
And third, the symptoms can't be from a medical condition (such as epilepsy) or be better
accounted for by another mental disorder, such as delirium, dementia, or schizophrenia.
There are some difficulties that exist in the area of diagnosis.
HPPD-like symptoms can come from a number of other sources, including psychosis, brain
tumors, and seizures.
The disorder also occurs in relatively few people, so there's a lack of good information.
Basically all of the data comes from individual case reports, some case series, and some open-label
treatment trials.
Since there's a bit of variation in the symptoms, triggers, and causal drugs, it's possible
not all cases can actually be grouped in the same exact disorder.
But we're currently stuck with the single HPPD diagnosis due to an incomplete understanding
of the condition.
The onset varies.
For some, it occurs right after an experience.
The drug effect ends, and the visual changes are immediately present.
For others, the problems set in days after the drug experience.
Having the symptoms appear many weeks or months later, like some people report, is harder
to connect to the drug.
Also, some people only report HPPD after extensive drug use.
These individuals have taken psychedelics many previous times without issue.
There's a high rate of other drug use often present in this group, which complicates the
situation.
Whether there are mechanistic differences between HPPD that arises after minimal or
extensive drug use isn't clear.
It's important to understand what HPPD is not.
Visual floaters, which have a basis in the eye and occur in people with no relevant drug
use history, aren't the same as HPPD.
Having the condition could, however, lead to noticing eye floaters more.
Simple visual changes like seeing bright spots in a dark room or having a visual disturbance
after viewing a bright light also aren't HPPD.
"Flashbacks" are more complicated.
It's a difficult term to use since multiple definitions have been applied to it over the
years.
It is sometimes used to describe episodic experiences that are very psychedelic-like
and nearly the same as being on a psychedelic.
These cases seem to be rare and they can also come from traumatic events not connected to
psychedelics.
In the way I use the term, flashbacks are distinct from HPPD because the effects extend
beyond the visual component and may even be positive.
There are a few categories we can place visual effects associated with psychedelics into.
The first would be "flashbacks."
Like I said, these are short-lived periods of hallucinogen-like activity.
Sometimes they're distressing, but often they're neutral or positive.
A lot of people view them as a "free trip" or a moment of nostalgic psychedelia.
The second is HPPD Intermittent.
Individuals with this experience HPPD in the form of episodes.
They either have no or relatively minor constantly present symptoms.
This condition doesn't cause distress or impairment in all cases, but those are necessary factors
for the current diagnosis.
And the third is HPPD Ongoing.
In this case, visual phenomena are always present, although they can still flare up
in response to triggers.
There's a high rate of co-occurring problems in both HPPD cases, such as depersonalization,
derealization, anxiety, panic, and depression.
Some of the common symptoms are visual snow, trailing, halos, positive afterimages, altered
color intensity, perceived movement of objects, micropsia, and macropsia.
The intensity of these effects differs.
Those with diagnosable HPPD tend to have pretty intense distortions, while other people may
only have a mild case that doesn't lead to a diagnosis.
An example of the impact of the disorder can be found in a survey involving 19 people.
All 19 reported visual snow.
Most of them reported anxiety while on the drug, typically a psychedelic, that they believed
was responsible.
For 12 respondents, the effects began within 24 hours of the drug experience.
Everyone reported symptoms that didn't actually match the drug effects.
Some of the common symptoms were head pressure, ghosted afterimages when looking at text,
movement of stationary objects, trails, and concentration difficulties.
They generally reported cannabis made their symptoms worse, while sedatives were helpful.
LSD is clearly the drug most often associated with HPPD in published papers.
There are also some reports involving cannabis, MDMA, psilocin, and other psychedelics.
However, we have some anecdotal evidence suggesting phenethylamines like those from the 2C series
and NBOMe series could lead to HPPD at a greater tate.
But this doesn't come across in the literature due to relatively low use rates and shorter
histories.
Whether or not they actually cause HPPD more often isn't known.
The most we know right now is that it appears all psychedelics come with some potential
to trigger the disorder.
An interesting aspect of the condition is that there may be similarities to tinnitus,
visual snow, and migraine auras.
They could potentially have some sort of related mechanism.
Although they're certainly different in their presentation.
The first cases were reported in the 1950s and 1960s.
Flashbacks were initially the most discussed issue.
It took a little longer for more typical HPPD cases to populate the literature.
A diagnostic criteria was established in the DSM-3 revised edition, published in 1987.
It had the name "Posthallucinogen Perception Disorder."
That would become Hallucinogen Persisting Perception Disorder in the DSM-4.
Much of the work in this area comes from Dr. Henry David Abraham.
He's published papers on the topic and has extensively discussed his professional experience.
Abraham described instances of people reporting something other than typical "flashbacks"
while at Massachusetts General Hospital in the 1970s.
They complained of ongoing visual changes, usually devoid of any emotional content.
Auditory hallucinations were rare and the majority of patients could distinguish their
symptoms from reality.
These were likely cases of what would now be called HPPD.
Abraham came up with a few possible mechanisms in the 1980s and 1990s.
He wondered if some form of LSD or psychedelic toxicity was responsible for damaging or otherwise
disrupting neurons in the visual system.
He helped to hypothesize what is now the leading view of the condition.
Which is that disinhibition in visual processing centers lead to the core symptoms.
Some interesting bits of information from Abraham are that, from his knowledge, up to
65% of patients have comorbid panic attacks and 50% have depression.
He also noted that his average patient has seen 6 prior doctors, who've collectively
shrugged their shoulders at the symptoms and not provided a diagnosis.
Currently, we still have a limited amount of information to work with.
HPPD is essentially an "orphan disease."
It impacts relatively few people and research funding related to it can be hard to come
by.
We don't know how common the disorder is.
Two of the main problems are that its definition has changed over time and other conditions
could present similarly to HPPD.
It's quite possible HPPD is underreported due to people not visiting physicians and
due to physicians not recognizing a person has the condition.
Some evidence suggests using a psychedelic in a controlled setting reduces the chance
of problems, though this still needs to be verified.
Information from 44 LSD and mescaline investigators was collected around 1960.
The investigators had collectively given psychedelics to 5000 people, both psychiatric patients
and healthy volunteers.
Only 4 cases of "fleeting afterimages" were reported in the mescaline users.
It doesn't appear any participants given LSD reported persistent visual changes.
Separate data covering 500 Navajo members of the Native American Church didn't show
any clear instances of HPPD despite significant peyote use.
More recently, a web-based survey from Matthew Baggott and others found HPPD-like symptoms
in 4.1% of 2,679 people, coming out to 107 people.
Those are the ones who reported psychedelic-related visual changes and considered seeking professional
help.
16 had actually sought help and 2 were diagnosed with HPPD.
Other data has suggested up to 40 or 50% of psychedelic users could experience some sort
of visual phenomena at some point.
But usually the effects are short-lived, not distressing, and aren't as severe as in HPPD.
At the end of the day, we don't know the prevalence, but it appears the majority of people never
develop clinically relevant HPPD.
There are no official risk factors for developing HPPD.
Though we have some reason to believe a few might exist.
They include the number of drug exposures, taking drugs without a good set or setting,
and having a personal or family psychiatric history.
An uncontrolled setting may raise the chance of stress during the experience, which could
be correlated with HPPD.
This is primarily just speculation, but the disorder could also be more common among those
who have preexisting visual snow, tinnitus, or visual migraine aura.
There's a hypothetical genetic component, but that has yet to be explored.
A few groups of triggers have been established.
Environmental ones include transitioning from dark to light and light to dark.
Episodes are also sometimes triggered by things associated with a hallucinogen experience,
such as music, the time of day, and locations.
Personal triggers like psychological stress and being tired are common.
People also report the symptoms increase when you're focusing on them or worrying about
the condition.
Drug triggers include psychedelics, cannabis, stimulants, and alcohol.
Both stimulants and alcohol have been reported to worsen or help the symptoms depending on
the person.
And medication triggers include risperidone, SSRIs, and phenothiazine antipsychotics.
Many case reports exist of risperidone exacerbating the visual symptoms as well as panic.
And SSRIs like sertraline have been helpful in some cases and negative in others.
The over-arching hypothesis is that HPPD comes from a disturbance in visual processing.
The disturbance causes visual symptoms that are usually distinct from psychedelic effects.
It's believed the problem occurs at a low-level in the visual system, allowing more "noise"
to make its way to higher visual centers and into perception.
Given the connection to visual processing, a lot of the focus is on the occipital lobe
and the Lateral Geniculate Nucleus, located in the thalamus.
A disruption in these areas could impact the way visual signals pass through the brain.
More activity could then be noticed and interpreted.
The primary visual cortex, V1, is an attractive target since activity in this area could generate
the visual phenomena.
Neuronal activity might continue beyond the stimulus due to an alteration in inhibitorty
and excitatory activity.
However, the presence of non-visual sensory effects, depersonalization, and derealization
suggest the mechanism may be more complex.
A popular hypothesis is that a drug may lead to the dysfunction of cortical serotonergic
neurons with GABA-ergic outputs.
EEG research has shown evidence of greater occipital activity, which is consistent with
the idea of disinhibition.
Other research looking at the impact of HPPD and psychedelic use sheds some light on how
the visual cortex might be affected.
A test for distinguishing between colors showed that non-psychedelic-using controls performed
best, LSD users scored in the middle, and the HPPD group scored worst.
Another test looking at the ability to notice a light flicker was conducted.
A light was strobed on and off.
The test was used to see how well the subjects could notice the strobing instead of just
interpreting the light as constantly on.
The control group performed best, LSD users were in the middle, and the HPPD group was
worst.
This suggests HPPD and even just heavy psychedelic use could lead to visual stimuli triggering
a prolonged response in the brain.
More research needs to be done to back up these results.
Lastly, anxiety and attention appear to modulate sensitivity in low-level visual processing.
These findings could explain the efficacy of benzodiazepines and the beneficial impact
of focusing on other tasks.
No clear guidelines exist for treating HPPD.
We're mainly working with some open-label trials, case reports, and anecdotes.
The non-drug recommendations include stress reduction and engaging in things that'll leave
you less focused on your symptoms.
Psychotherapy has sometimes been helpful, as has the use of tinted glasses.
For medication, there are reports of success with benzodiazepines, clonidine, naltrexone,
lamotrigine, levetiracetam, and SSRIs.
A case series involving clonazepam demonstrated efficacy.
14 patients with HPPD and anxiety who believed their symptoms came from LSD received 2 mg
of clonazepam per day.
It was adminstered for two months and then gradually discontinued.
The result was significant reductions in anxious mood, tension, and insomnia.
There were also significant improvements in the visual disturbances.
The benefits persisted even after treatment ended.
A combination of tolcapone and carbidopa/levodopa was tested in 20 people.
Results from this trial were presented in 2012.
The combination led to a beneficial response in a third of patients, with little response
in the rest.
This was only an open-label trial, so more research is needed.
Overall, there are some trends that have been seen in treatment.
Benzodiazepines appear helpful for many people.
They usually don't eliminate the symptoms, but they can reduce their intensity and make
them manageable.
The benefits may come from reducing anxiety as well as from a direct effect on visual
processing.
More variable responses exist with SSRIs.
Evidence suggests that if people can get through the adjustment period, during which the symptoms
may increase, SSRIs might be helpful.
But there are cases where it just doesn't appear SSRIs are useful.
And antipsychotics, such as risperidone, have generally been found to be ineffective or
to have a negative impact.
If you have symptoms of HPPD, you should stop using any drugs, especially psychedelics and
cannabis.
Visiting a physician is wise if the symptoms cause impairment or distress.
Hopefully you can then move towards ruling out other possibilities and receiving an accurate
diagnosis.
With a diagnosis, you may benefit from medication as well as stress reduction
and psychotherapy.