Hallucinogen Persisting Perception Disorder (HPPD)

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Hallucinogen Persisting Perception Disorder (HPPD) is a disorder characterized by visual phenomena that appear following drug use. Under DSM-5 criteria, an HPPD diagnosis requires the visual changes be distressing or impairing. There are people who have the same or similar symptoms without distress.

While “hallucinogen” is in the name and psychedelics are the most frequently implicated drugs, other drugs (e.g. cannabis and MDMA) have been associated with the condition.

It often occurs in people with no preexisting psychological issues. Though a personal or familial background of psychiatric issues could be a risk factor.

HPPD is distinct from psychosis. The majority of people understand their symptoms aren’t part of reality. We can therefore treat it as a perceptual issue, albeit one frequently found in people with comorbid psychiatric problems.

A large portion of cases spontaneously resolve within a year. In some situations, the symptoms can persist for years and decades.

DSM-5 Criteria

All of the criteria must be met for a diagnosis.

  • The reexperiencing, following cessation of use of a hallucinogen, of one or more of the perceptual symptoms that were experienced while intoxicated with the hallucinogen (e.g., geometric hallucinations, false perceptions of movement in the peripheral visual fields, flashes of color, intensified colors, trails of images of moving objects, positive afterimages, halos around objects, macropsia, and micropsia)
  • The symptoms in Criterion A cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
  • The symptoms are not due to a general medical condition (e.g., anatomical lesions and infections of the brain, and visual epilepsies) and are not better accounted for by another mental disorder (e.g., delirium, dementia, and Schizophrenia) or hypnopompic hallucinations.

There are some difficulties that appear when trying to provide a diagnosis. Similar symptoms can be caused by psychosis, brain tumor, and seizure disorders.

It occurs in relatively few people, so we have a lack of good information to go on. Most of the information is coming from individual case reports, some case series, and some open-label treatment trials.

As the definition of HPPD/flashbacks has changed over time, it’s difficult to use some of the older info to inform our current understanding of HPPD.

Since there’s a lot of variation in the symptoms, triggers, and causal drugs, it’s also possible that not all cases can actually be grouped in the same exact disorder.

Onset

For some, the symptoms appear immediately after a drug experience. In other cases, the symptoms arise days later. There are also cases where people report their symptoms arose many weeks or months after drug use, but it’s harder to point to the drug as the cause.

Some people only encounter HPPD after extensive drug use, frequently with psychedelics and other substances. But it can appear after minimal drug use.


What It’s Not

Eye floaters have a basis in the eye and occur in many people with no relevant drug use history. They’re not the same as HPPD, but the disorder can lead to noticing them more.

Simple visual changes like seeing bright spots in a dark room or having a temporary visual disturbance after viewing a bright light also frequently occur without HPPD.

“Flashbacks” are more complicated. The term has historically been used in so many ways as to become practically meaningless without an accompanying definition whenever it’s mentioned.

It’s sometimes used to discuss experiences that are very psychedelic-like, both in visual effects and psychological changes. These cases seem to be rare.

When I use the term, it’s to refer to transient and intermittent appearances of symptoms that don’t necessarily cause distress and go beyond the visual component.


Common symptoms

Visual snow, trailing, halos, positive afterimages, altered color intensity, perceived movement of objects, micropsia, and macropsia.

The intensity of the effects varies. Those with HPPD generally have pretty intense effects, while others may have relatively mild distortions that don’t lead to a diagnosis.

An example of HPPD’s presentation can be found in a survey involving 19 people:

  • 19/19 reported visual snow, though some only had the symptom during the nighttime.
  • Drugs they had taken
    • LSD (12), psilocybin (4), MDMA (1), cannabis (1), 2C-I (1), combo of amphetamines/opioids/SSRIs (1)
  • They all reported anxiety or panic while on the drug they believed was responsible.
    • Most said it was “marked” or “extreme” anxiety.
  • Onset
    • 12/19 reported symptoms within 24 hours.
    • 7/19 reported symptoms one week to months later.
  • All reported symptoms that didn’t match their drug experience.
  • Common symptoms
    • Head pressure, ghosted afterimage of text, stationary object swaying or moving, trails, halos, auras, floaters, concentration difficulties, daytime visual snow, and nighttime visual snow.
  • What makes it worse?
    • Cannabis was the most common trigger, followed by alcohol.
  • What improves the symptoms?
    • Sedative/hypnotics drugs ranked highest, followed by alcohol.

Here’s another case series from the Netherlands:

  • All involved at least 2 different visual phenomena that had occurred with at least 1 episode per week.
  • Symptoms
    • Visual snow, afterimages, flashes, illusory movement, and increased observation of floaters.
  • Those who were investigated by ophthalmologists and neurologists didn’t show any abnormalities.
  • Many reported other symptoms
    • 45% had sensations in the head of pressure, clicks, dryness, or a “shrinking brain.”
    • 39% had derealization
    • 32% has depersonalization
    • 71% had anxiety or panic before/following the use of drugs
  • Some experienced symptoms after a single use, but others only experienced symptoms after extensive drug use.

Categories

Flashbacks

These are short-lived periods of hallucinogen-like activity that often occur without distress. Flashbacks tend to occur rarely and the frequency fades over time.

Flashbacks may only last seconds or minutes. Some people enjoy flashbacks, viewing them as a “free trip” or a moment of nostalgic psychedelia.

HPPD Intermittent

Individuals with this form experience HPPD in the form of episodes. They may have no or only minor persistent symptoms, such as visual snow.

The condition is characterized by brevity and intermittency.

Distress is a part of the diagnosis and potentially impairment.

HPPD Ongoing

Visual phenomena are always present, though the intensity may vary. An episodic nature can still exist, with the effects increasing in response to triggers.


Most common drugs

LSD is the most common substance in the published papers. Other drugs include cannabis, MDMA, psilocin, and other psychedelics.

Some anecdotal reports suggest phenethylamines like those from the 2C series and NBOMe series might trigger HPPD at a greater rate. This may not come across in the literature due to relatively use rates and shorter use histories.

Whether or not those substances actually cause HPPD more often isn’t known.

The most we know is that all psychedelics appear to come with some potential to trigger the disorder.


Similarities to other conditions

There might be a similar mechanism to what is seen in visual snow, tinnitus, and migraine aura. Although the presentation of those conditions is different from HPPD.


Review of studies

A review of the major case series involving persistent psychedelic-related visual changes from 1950 onward is available. There are some severe limitations with it due to varying definitions of flashbacks and too little information in many cases to determine whether someone had HPPD.

The reports showed a widely variable prevalence of HPPD, ranging from 0% among hundreds of people to 33% or 77% in other groups.

1 – 1955

  • 8 psychiatric patients were treated with weekly doses of LSD
  • They showed temporary auditory and visual changes, sometimes accompanied by mood swings, changes in body image, and regression to childish behavior.
  • Generally the symptoms resolved within a day, but one patient reported symptoms for 3 weeks.

2 – 1965

  • Review of 34 LSD-related psychiatric admissions
  • 11 reported “spontaneous return of perceptual distortions or feelings of depersonalization similar to those experienced under the influence of LSD.”
  • At least 8 of the patients were psychotic prior to LSD use.

3 – 1969

  • 31 subjects from the drug using community of Haight-Ashbury
  • 8 reported flashbacks
    • 1 had never used hallucinogens
    • 6 were diagnosed with other psychiatric disorders

4 – 1970

  • 20 hallucinogen users were recruited via an ad
  • 11 reported having “recurrences of trip phenomena” lasting up to 3 months
  • All were active cannabis users and most were active amphetamine users.

5 – 1971

  • 431 US Air Force recruits who acknowledged illicit drug use
  • 94 reported flashbacks
    • 10 had them from non-hallucinogens
      • 5 from cannabis
      • 5 from amphetamine or barbiturates
  • Some of the answers may have been given in order to avoid entering the Vietnam War.

6 – 1971

  • Follow-up interviews of 247 people who received LSD as part of psychotherapy or research protocols.
  • 5 reported “major perceptual changes” suggestive of possible HPPD.

7 – 1972/1976

  • 2001 soldiers entering or leaving the Vietnam War
  • 95 reported flashbacks
    • 1 had not used any drugs
    • 26 had never used a hallucinogen

8 – 1974

  • 44 college students with a history of hallucinogen use
  • 22 reported episodes of flashbacks
  • Depression, paranoia, and anxiety or tension were reported among some as well.
    • Those symptoms were listed as typical flashback effects.

9 – 1976

  • 91 young drug users admitted to a Norwegian hospital
  • 65 had a history of hallucinogen use
  • 50 reported flashbacks
    • 2 reported them specifically after cannabis use exclusively
  • By 1.5 to 4 year follow-ups
    • 35/50 still reported flashbacks

10 – 1974/1977

  • 235 people who admitted to using LSD
  • 28% reported flashbacks
    • 36% found these experiences were “disruptive to their normal behavior”
    • 16% stated they sought clinical treatment

11 – 1978

  • 63 psychedelic drug users, mainly college students
  • 34 reported flashbacks
  • 20 reported “perceptual illusions” as a feature of their flashbacks
  • Other symptoms
    • Depersonalization, anxiety, tension, panic, disorientation, confusion, union with the world
  • 22/63 said their flashbacks could be triggered by cannabis or alcohol

12 – 1983

  • 280 Army soldiers interviewed prior to administrative discharge
  • 179 admitted to using hallucinogens
  • Of 207 heavy drug users, 146 reported flashbacks
    • 109 reported simple visual experiences
    • 98 reported trails
    • 76 reported “re-trips”
  • 8 reported flashbacks with no hallucinogen history
  • All six deemed to have “severe” flashbacks also displayed symptoms of “severe psychopathology” other than active psychosis.

13 – 1983

  • 55 LSD users recruited via advertisement at an emergency psychiatric service
  • Documented 16 types of visual disturbances
  • Some popular triggers included dark environment (16%) and intention (14%)
  • 1 was eventually found to have temporal lobe epilepsy
  • 8 were found to have concomitant anxiety or panic
  • 3 had major affective disorders
  • 7 had “temporoparietal abnormalities”

History

The first cases appeared in the 1950s and 1960s. “Flashbacks” were initially discussed more than ongoing HPPD symptoms.

A diagnostic criteria was established in the DSM-3 in 1987 under the name, “Post-hallucinogen Perception Disorder.” The condition then became “Hallucinogen Persisting Perception Disorder (Flashbacks)” in the DSM-4.

Much of the work has been tied to a single individual, Dr. Henry David Abraham. He discussed seeing HPPD cases that were distinct from flashbacks during the 1970s while working at Massachusetts General Hospital.

Abraham hypothesized some possible mechanisms in the 1980s and 1990s, including a form of psychedelic toxicity that could damage or otherwise disrupt neurons in the visual system.

Currently, we’re still working with a limited amount of information. HPPD is an “orphan disease,” affecting relatively few people. Research funding may be harder to come by, which has limited the information that’s available.


Prevalence

The prevalence of HPPD is unknown. Figuring out how common the disorder is has been complicated by a lack of uniform definitions over the years.

Some data suggests up to 40-50% of psychedelic users could experience visual symptoms at some point following their use. There’s a much smaller percentage who develop HPPD or have HPPD-level symptoms.

Based on everything we know, it appears the majority of people never develop clinically relevant HPPD.

Some evidence suggests the rate is lower when psychedelics are used in a more controlled manner.

  • 5000 participants in LSD & mescaline trials (pre-1960, info collected from 44 investigators)
    • Investigators were asked to report problems connected to the drugs.
    • 4 cases of “fleeting afterimages” were reported in the mescaline users.
    • No cases of LSD causing HPPD-like problems appeared to exist.
  • 500 Navajo members of the Native American Church
    • None showed signs of HPPD despite many uses of peyote (mescaline)

A web-based survey from Matthew Baggott and others found HPPD-like symptoms in 107 out of 2,679 psychedelic users (4.1%). Those are the people who reported psychedelic-related visual changes and considered seeking professional help. 16/107 had actually sought help and 2/107 were diagnosed with HPPD.


Risk factors

There are no established risk factors, but some may exist. Those include the number of drug exposures, an uncontrolled setting, and a personal or familial history of psychiatric problems.

An uncontrolled setting or set that’s not ideal may raise the chance of stress during an experience, which could be correlated with HPPD.

It’s primarily speculation right now, but it’s possible the disorder may be more common among those who had preexisting visual snow, tinnitus, or visual migraine aura.

There’s a hypothetical genetic component that has yet to be explored.


Triggers

Environmental, personal, and drug triggers have been identified.

Environmental

Transitioning from dark to light or light to dark.

Some people report HPPD episodes are triggered by things associated with a hallucinogen experience, such as music, the time of day, things in your environment, or location.

Personal

Stress in the form of psychological stress or being tired can increase symptoms.

Paying a lot of attention to the symptoms and being concerned by them is also a common trigger. If you’re heavily focused on the symptoms, they may increase, while focusing on a separate activity can temporarily reduce their prominence.

Drugs

Psychedelics, cannabis, stimulants, and alcohol.

Both stimulants and alcohol have been reported to worsen and help the symptoms depending on the person.

Medications

Risperidone, SSRIs (e.g. sertraline), and phenothiazine antipsychotics.

There are multiple reports of risperidone exacerbating the visual symptoms as well as the panic.

SSRIs may help some people, but they can also increase the symptoms in others.


Possible mechanisms

The overarching hypothesis is that HPPD arises from a disturbance in visual processing. Visual symptoms are caused by the disturbance and they typically differ from what psychedelics cause while on them.

It’s believed the disturbance occurs at a low level in the visual system, allowing more “noise” to make its way to higher visual centers and eventually into perception.

Locations

Due to the condition involving visual processing, much of the focus is on the occipital lobe and lateral geniculate nucleus (LGN), located in the thalamus.

A disruption in these areas could impact the way visual signals pass through the brain and allow more activity to be noticed and interpreted than normal.

The primary visual cortex (V1) is of particular interest. Neuronal activity in this region may continue beyond the stimulus, coming from some sort of altered inhibitory and excitatory activity.

A popular hypothesis is that psychedelics lead to the dysfunction of cortical serotonergic neurons with GABAergic outputs. This leads to a state of chronic disinhibition.

However, the presence of non-visual sensory effects, depersonalization, and derealization in some people suggests the mechanism may be more complex.

EEG

EEG research has shown evidence of greater occipital activity, which is consistent with the idea of disinhibition.

Other

Other research from Henry Abraham looking at the impact of HPPD and psychedelic use sheds some light on how visual cortex activity may be altered.

A test for distinguishing between colors found the control group performed best, LSD users scored in the middle, and the HPPD group scored worst.

Another test for noticing a light flicker (a light would be strobed on/off rapidly) found the controls performed best, LSD users were in the middle, and the HPPD group scored worst.

LSD users were also found to have more difficulty adjusting to the dark from the light.

This data was taken as support of the idea that HPPD and even just heavy psychedelic use can lead to visual stimuli causing a prolonged response in the brain. Though the research needs to be further supported.


Anxiety and attention appear to modulate sensitivity in low-level sensory processing. This could partly explain the beneficial effects of benzodiazepines and the beneficial effect of turning your attention to other tasks.


Resolution without treatment

It’s very common to have the symptoms go away without any treatment. Here’s an example:

Case 1

  • 26-year-old male
  • Five year history of cannabis use
  • Also reported LSD use
    • During which there was macropsia, micropsia, pelopsia, and teleopsia.
    • Symptoms reminiscent of Alice in Wonderland Syndrome (AIWS)
  • Single LSD experience led him to stop all drug use
    • The experience lasted longer than usual and included some anxiety
  • Two days post-LSD
    • Noticed the return of visual effects
    • Including the AIWS-like effects
  • He became preoccupied with the symptoms and distressed by them, feeling intimidated and disheartened.
  • One year later
    • The visual disturbances completely disappeared.
  • Case is unique since it lacked typical HPPD symptoms and had AIWS-like symptoms

Treatments

There are no clear guidelines for treatment.

Non-drug options include stress reduction and engaging in things that’ll leave you less focused on the symptoms. Psychotherapy has sometimes been helpful, as has the use of tinted glasses.

Medication

Reports of success exist with benzodiazepines (often clonazepam), clonidine, naltrexone, lamotrigine, levetiracetam, and SSRIs.

Benzodiazepines seem to be helpful for a large portion of people, though they typically just reduce the symptoms and make them more manageable. It’s possible they’re reducing the symptoms due to an impact on anxiety, but they could also be helpful through a direct effect on visual processing.

There’s a more variable response to SSRIs. Evidence suggests that if people can get through the adjustment period, they may often be useful. But they clearly don’t work for everyone and they sometimes increase the symptoms, especially during the adjustment period.

Antipsychotics, although once proposed as a treatment, have generally been found to be ineffective or to have a negative impact. For example, risperidone has had negative effects in many people.

Clonazepam case series

  • 14 patients with HPPD and anxiety
  • All believed LSD was the cause of their symptoms
  • They had complained of HPPD for at least three weeks
  • Clonazepam was proposed at 2 mg/d
    • Based on their comorbid anxiety and prior reports of success
  • Clonazepam was given for two months and then gradually discontinued
  • Results
    • Significant reductions in visual disturbances
    • Significant reductions in anxious mood, tension, and insomnia.
  • The benefits were maintained after clonazepam was stopped.

Combo of tolcapone and carbidopa/levodopa (Sinemet)

  • 20 patients
  • A significant beneficial response was seen in a third of patients, with little response in the rest.
  • This was only an open-label trial and placebo can’t be ruled out.
  • The benefit could potentially come from affecting sensory gating mechanisms.

Naltrexone cases

  • 1
    • 24-year-old male
    • History of LSD use
    • Reported flashes of color, visual distortions, trails of images, and positive afterimages.
    • Episodes lasted a few minutes and caused distress and impairment.
    • Accompanied by dysphoric mood and suicidal thoughts.
    • 2 months of unsuccessful benzodiazepine and antidepressant treatment
    • Treatment
      • Naltrexone at 25 mg/d for two days, followed by 50 mg/d
      • Significant reduction in frequency and duration of flashbacks within two weeks, along with reduced suicidal thoughts.
      • Full remission within 2 months of therapy.
      • Remission remained months later after discontinuation of treatment.
  • 2
    • 22-year-old male
    • History of LSD and ecstasy use
    • Reported geometric hallucinations, false perception of movement, positive afterimages, and body image distortion.
    • Severe enough to cause substantial stress and anxiety.
    • One month of unsuccessful benzodiazepine treatment
    • Treatment
      • 25 mg of naltrexone for 2 days followed by 50 mg/d
      • Significant improvement in flashbacks and anxiety within 2 weeks.
      • Therapy discontinued after 2 months and improvement remained for months after.

Case reports

Case 1

  • 26-year-old male
  • Five year history of cannabis use
    • Daily without any HPPD symptoms
  • Concomitant tobacco use
  • Two years prior to evaluation
    • Was using synthetic cannabinoids instead of cannabis on a near-daily basis.
    • Tobacco use as well
  • Under influence of synthetic cannabinoids
    • Reported visual disturbances
      • Halos, color intensification, visual snow, positive afterimages, illusions of movement, and trailing.
    • Considered benign and comfortable.
    • Occurred sporadically during two years of consumption.
  • One eventual episode
    • Severe panic attack from synthetic cannabinoids, causing him to abruptly discontinue use.
    • Panic attack included visual disturbances, described as a “horrific trip.”
  • 48-hours post-panic attack
    • Reexperienced visual disturbances with anxiety
  • Continued to report visual disturbances and anxiety
  • Psychiatric examination
    • Reported visual disturbances similar to those caused by synthetic cannabinoids
    • Almost daily episodes of symptoms lasting for a second to a few minutes.
    • Severe enough episodes to cause anxiety, distress, and impaired social/occupational functioning.
  • Placed on clonazepam at 0.25 mg BID and then 1 mg BID
  • During two weeks post-examination
    • Two additional but milder panic attacks with visual disturbances
  • Then the panic attacks ended, but visual changes remained
  • Symptoms dramatically started to improve, initially with episodes becoming more benign and less distressing.
  • Clonazepam continued for 5 weeks and then withdrawn.
  • Even after clonazepam ended, continued improvement occurred.
    • Reduced frequency of perceptual issues and anxiety.
  • 6-month evaluation
    • Nearly complete end to symptoms
    • Only thing that persisted was trailing

Case 2

  • 24-year-old male
  • Three year history of daily cannabis use
    • Also daily tobacco use
  • A year prior to evaluation
    • Replaced cannabis with synthetic cannabinoids (SC)
    • Reported visual disturbances during SC use
      • Considered them “amusingly entertaining” and would occur when viewing stationary and moving objects.
    • Stationary objects: Halos, visual snow, positive afterimages, and dimensional distortion.
    • Moving objects: Illusions of movement, black moving spots with eyes open and closed (speckles/dots in peripheral field), and trailing.
  • One eventual use
    • Severe panic attack under the influence, thought it was a heart attack.
    • Ended up in ED, where diazepam was given.
  • Day after panic attack
    • Another panic attack including visual imagery similar to under SC influence.
  • Then continued to report visual phenomena and anxiety.
    • Episodes occurred daily and lasted from a second to a few minutes.
  • Panic attack was distressing enough to lead to immediate cessation of SC use.
  • Visual problems caused significant distress, anxiety, and infringed upon social and occupational functioning.
  • Withdrawal from SC treated with clonazepam
  • Episodes became more benign and less distressing.
  • Dramatically started to improve, even after clonazepam suspension.
  • Reduced frequency eventually
  • By end of six months
    • Almost no visual disturbances
    • Only non-distressing black moving spots in visual field.

Case 3

  • 48-year-old male
  • Presented with distressing visual experiences
    • Variable severity
    • Present for over 20 years
  • Examples of visual effects
    • Red objects have a green shimmer around them like with 3D glasses
    • Altered sense of distance
    • Alteration of his own reflection
    • Any patterns on objects appear to move constantly
    • Words moving while reading text
    • Vehicles have trails/stretching while driving past
    • Difficulty in focusing vision
  • Symptoms not always present, but when they were, they significantly impaired functioning.
    • Had trouble crossing the road and had to dim the lights.
  • Associated the symptoms with LSD use 25 years prior.
    • LSD was taken alongside cannabis and alcohol.
    • Even felt, at times, the drug put him “in a coma” and he was “dreaming all of this.”
  • Tied back to a single use of LSD with cannabis and alcohol
    • Symptoms began immediately the next day
  • He had taken LSD 15 times prior to the trigger experience
  • Consistently reported depersonalization and his visual distortions caused enough stress to make him suicidal.
  • Low mood, decreased concentration, anxiety, and an inability to cope.
  • Over a period of 25 years, received these diagnoses:
    • LSD-induced depersonalization syndrome, depersonalization-derealization syndrome, LSD induced simple schizophrenia, depressive disorders, and anxiety disorders.
  • Treatment
    • 1 mg of clonazepam four times daily
    • Eventually also given escitalopram (switched to reboxetine) for a depressive episode
    • Result
      • These were gone 3 months later: geometric hallucinations, false perception of movement in peripheral fields, flashes of colour, intensified colours, trails of images of moving objects, positive after images, macropsia, micropsia
      • Remained at a lower intensity and frequency: halos around objects

Case 4

  • Took LSD for the first time at 17
    • Had used cannabis and alcohol as well
  • Began taking LSD every other month, 1-2 blotters of unknown dose
  • At the end of his first year of use
    • One specific trip left him suddenly with severe abnormal visual disturbances.
    • Disturbances
      • Small intensely colored, flickering, geometric shapes within entire visual field
      • Intermittent trailing
      • After images from objects he had just seen
    • Reading was impaired
  • Symptoms aggravated by
    • Mental stress, lack of sleep, and use of caffeine.
  • He tried to alleviate symptoms by using more LSD, which was ineffective.
  • LSD use continued for 6 more years, followed by 5 years of abstinence, and then returning to use of LSD once per month.
  • Alcohol, cannabis, and cocaine use were present during adult life.
  • He eventually became strictly abstinent, but visual problems remained.
  • Three months of clonidine was unhelpful.
  • Treatment
    • 7 months of lamotrigine at 200 mg/d
    • Led to steady improvement of perception issues
      • Afterimages totally went away
      • Color-intensive flickering became fainter, less bright, and more transparent.
      • Reading capacity improved greatly, which provided great relief.
    • He described this as having a “dirty screen” in front of his eyes, which was present for 18 years, and was slowly beginning to clear.
    • Also provided general improvement in overall mental well-being.

Case 5

  • 18-year-old male
  • Hospitalized for perceptual impairment and dysphoric mood that was present for 8 months.
  • Family history of psychiatric problems
  • Had regularly used cannabis, at least some each week.
  • Perceptual distortions began after using psilocybin in the form of Psilocybe semilanceata
  • Reexperienced psilocybin-like effects the following day when using cannabis.
  • Also derealization and depersonalization, as well as difficulty distinguishing distortions from reality.
  • These problems became a daily issue, worsening in the dark.
  • Distressful and upleasant
  • Eventually stopped cannabis two months later
  • Symptoms initially improved post-cannabis cessation, but increased again 6 months post-cessation.
  • Treatment
    • Amisulpride at 100 mg
    • Replaced amisulpride (due to sedation) with Olanzapine at 5 mg
      • Olanzapine exacerbated the symptoms
    • Olanzapine replaced with Risperidone with 2 mg
    • Risperidone continued with addition of sertraline at 150 mg
      • To deal with persistent dysphoric mood and recurrence of anxiety-like symptoms
  • Combo of risperidone and sertraline led to decrease of daily episodes of perception difficulties and depressive symptoms.
    • HPPD disappeared after 6 months of treatment.
    • He also became more active in social settings.

Case 6

  • 30-year-old male
  • Presented to ED after surviving two subsequent suicide attempts.
  • History of depression and bipolar disorder
  • History of trauma
    • Witnessed friends and relatives murdered during Kosovo War as a child.
  • No recent alcohol/drug use, but a distant history of cannabis use.
  • HPPD appeared after using cannabis
    • Vivid & saturated color, macro/micropsia, and seeing things in motion as moving faster than reality.
    • Derealization and dissociation
  • Distortions were continuous, but he could sometimes distract himself with concentration on schoolwork.
  • Responses to treatment
    • Good historical response to SSRIs
    • Negative response in the form of worsened visual symptoms with risperidone
    • 6 months of lamotrigine at 200 mg/d followed by 6 months at 100 mg/d
      • Reported total resolution of macropsia and micropsia.
      • Significant improvement in motion and light perception.
  • He ultimately committed suicide.

Case 7

  • 38-year-old female
  • Had panic attacks for 17 years
  • Took LSD, leading to a severely “bad trip,” about 17 years prior
    • She was disoriented, believed the world was collapsing, and thought she was going insane.
  • No further LSD use, but she reported persistent phenomena.
    • Flashbacks on a near-daily basis for 9 months post-experience.
  • For 8 years post-LSD
    • Panic attacks precipitated by flashbacks similar to first LSD trip.
    • Anxiety attacks lasted for 30 seconds to 1 minute.
  • History of cannabis, alcohol, cocaine, and MDMA use.
  • Treatment
    • Risperidone 0.5 mg/d
    • Significant reduction in frequency and intensity of panic attacks and perceptual disturbances within 3-4 weeks.

Case 8

  • 33-year-old female
  • Used LSD up to 30 times around the age of 18
  • Also took cannabis, ecstasy, psilocybin, and ketamine.
  • 2-3 weeks after last LSD session
    • Persistent visual disturbances developed
    • They were “flashback” episodes described as similar to LSD effects.
    • Afterimages, perception of motion in periphery, flickering, halo effects, macropsia, micropsia, and bright spots of light across visual field.
    • No visual changes with eyes closed.
  • Symptoms persisted for 13 years
    • Led to her having trouble focusing properly with her eyes.
    • She became suicidal and depressed as a result.
    • Had some trouble distinguishing between normal and abnormal perceptions.
  • Attempted treatment
    • Sertraline, citalopram, and fluoxetine relieved depression but not HPPD.
    • Risperidone was also ineffective.
  • Treatment
    • Lamotrigine was initiated and given for over 12 months.
    • 6 months of 200 mg, followed by 100 mg
    • Abnormal sense perception of “levitation” was alleviated
    • All macropsia and micropsia disappeared
    • Reduction in afterimages, halos, and the bright spots.
    • SSRI addition didn’t change anything
      • Actually made derealization and depersonalization worse.
    • Stress was connected to worsening of symptoms.

What to do if you have symptoms

You should stop using drugs, especially cannabis and psychedelics, if you have HPPD symptoms.

Visiting a physician is wise if the symptoms cause impairment or distress. It’s good to rule out other potential causes and to receive an accurate diagnosis.

With a diagnosis, you may benefit from medication as well as stress reduction and psychotherapy.


References

(2016) A Review of Hallucinogen Persisting Perception Disorder (HPPD) and an Exploratory Study of Subjects Claiming Symptoms of HPPD.

(2016) Hallucinogen Persisting Perception Disorder and Risk of Suicide.

(2015) 25 years of Hallucinogen Persisting Perception Disorder- A diagnostic challenge

(2015) LSD-associated “Alice in Wonderland Syndrome”(AIWS): A Hallucinogen Persisting Perception Disorder (HPPD) Case Report.

(2015) Schizophrenia and hallucinogen persisting perception disorder: A clinical investigation.

(2014) Hallucinogen persisting perception disorder and the serotonergic system: a comprehensive review including new MDMA-related clinical cases.

(2014) Improvement of hallucinogen persisting perception disorder (HPPD) with oral risperidone: case report

(2014) Synthetic Cannabis Substances (SPS) Use and Hallucinogen Persisting Perception Disorder (HPPD): Two Case Reports.

(2013) Clinical Characteristics of Individuals With Schizophrenia and Hallucinogen Persisting Perception Disorder: A Preliminary Investigation

(2013) Hallucinogen Persisting Perception Disorder (HPPD) and Flashback-are they Identical?

(2012) Hallucinogen-persisting perception disorder

(2012) Hallucinogen persisting perception disorder in neuronal networks with adaptation.

(2011) Abnormal visual experiences in individuals with histories of hallucinogen use: a Web-based questionnaire.

(2005) Hallucinogen persisting perception disorder after psilocybin consumption: a case study.

(2003) Clonazepam treatment of lysergic acid diethylamide-induced hallucinogen persisting perception disorder with anxiety features.

(2003) Hallucinogen persisting perception disorder: what do we know after 50 years?

(2001) EEG coherence in post-LSD visual hallucinations.

(1996) Stable quantitative EEG difference in post-LSD visual disorder by split-half analysis: evidence for disinhibition.

(1982) A chronic impairment of colour vision in users of LSD.

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  • Jobe Westbrook

    I thought I was literally losing my mind for the past year. Definitely have been seeing tracers, walls slowly drifting, and I have been experiencing pressures in my head. I have also been super anxious to bepresent in populated areas and i tend to over think the smallest things. I found this extremely helpful, I will go find help, thank you.