Hallucinogen persisting perception disorder
|This article needs additional citations for verification. (September 2011)|
|Hallucinogen persisting perception disorder|
|Classification and external resources|
|Patient UK||Hallucinogen persisting perception disorder|
Hallucinogen persisting perception disorder (HPPD) is a disorder characterized by a a continual presence of sensory disturbances, most commonly visual, that are reminiscent of those generated by the use of hallucinogenic substances. Previous use of hallucinogens by the person is necessary, but not sufficient, for diagnosis of HPPD. For an individual to be diagnosed with HPPD, the symptoms cannot be due to another medical condition. HPPD is distinct from flashbacks by reason of its relative permanence; while flashbacks are transient, HPPD is persistent. HPPD is a DSM-IV diagnosis with diagnostic code 292.89.
There are a number of perceptual changes that can accompany HPPD. Typical symptoms of the disorder include: halos or auras surrounding objects, trails following objects in motion, difficulty distinguishing between colors, apparent shifts in the hue of a given item, the illusion of movement in a static setting, air assuming a grainy or textured quality (visual snow or static, by popular description, not to be confused with normal "blue field entoptic phenomenon"), distortions in the dimensions of a perceived object, and a heightened awareness of floaters. The visual alterations experienced by those with HPPD are not homogeneous and there appear to be individual differences in both the number and intensity of symptoms.
Visual aberrations can occur periodically in healthy individuals – e.g. afterimages after staring at a light, noticing floaters inside the eye, or seeing specks of light in a darkened room. However, in people with HPPD, symptoms are typically persistent enough that the individual cannot ignore them.
There is some uncertainty about to what degree visual snow constitutes a true HPPD symptom. There are many individuals who have never used a drug which could have caused the onset, but yet experience the same grainy vision reported by HPPD sufferers. There are a few potential reasons for this, the most obvious of which being the theory that the drug usage may exaggerate the intensity of visual snow. Another theory is that instead, there may be no change in the severity or magnitude of the visual snow, but perhaps the drug usage opens sensory pathways that result in the individual becoming more aware of any visual disturbances that may have simply not been noticed before the incidence of drug use. As for root cause of visual snow, some theories suggest that it is the result of thermal noise in the visual cortex or in the 'Optic Pathway' (encompassing photoreceptor cells on the retina, the optic nerve, and the optic chiasm), as eye tests for individuals who experience visual snow often reveal that physically, the eye is perfectly normal, and in many cases the individual still maintains 20/20 vision.
HPPD usually has a visual manifestation. Drugs affecting the auditory sense, like DiPT, may produce auditory disturbances, though there are few known cases. Some psychedelic drugs can produce temporary tinnitus-like symptoms as a side effect.
It also should be noted that the visuals do not constitute true hallucinations in the clinical sense of the word; people with HPPD recognize the visuals to be illusory, or pseudohallucinations, and thus maintain the ability to determine what is real (in contrast to some mental illnesses such as schizophrenia).
The probability of developing HPPD after consuming a hallucinogen is unknown. In their review article, John Halpern and Harrison Pope write that "the data does not permit us to estimate, even crudely, the prevalence of ‘strict’ HPPD." These authors noted that they had not encountered it in their evaluation of 500 Native American Church members who had taken the hallucinogenic cactus peyote on at least 100 occasions. In a presentation of preliminary results from ongoing research, Matthew Baggott and colleagues from University of California Berkeley found that HPPD-like symptoms occurred in 4.1% of participants (107 of 2,679) in a web-based survey of hallucinogen users. These people reported visual problems after drug use that were serious enough that they considered seeking professional help. This number may overestimate the prevalence of HPPD, since people with visual problems may have been more interested in completing the researchers' questionnaire, while most of these drugs are illegal with serious consequences to people admitting their use. The authors reported that 16,192 people viewed the study information but did not complete the questionnaire. If all these people had used hallucinogens without developing visual problems, then the prevalence of serious visual problems in this larger group would be 0.66%. Since these people were not formally diagnosed in person (and may have had visual problems caused by other disorders), this number may provide a reasonable upper limit on the prevalence of HPPD, or they might be statistically meaningless.
It is possible the prevalence of HPPD has been underestimated by authorities because many people with visual problems relating to drug use either do not seek treatment or, when they do seek treatment, do not admit to having used illicit drugs. In the sample of Baggott, only 16 of the 107 people with possible HPPD had sought help and two of these people had been diagnosed with HPPD. Thus, it may be that HPPD occurs more often than is detected by the health care system.
The cause(s) of HPPD are not yet known. It has been theorized that HPPD is an anomaly in executive function brought on by the dis-inhibition of the COMT enzyme in the breakdown of catecholamines in the brain following hallucinogen use, resulting in sensory gating disruption.
In some cases, HPPD appears to have a sudden onset after a single drug experience, strongly suggesting the drug played a direct role in triggering symptoms. But in other cases, people report gradual worsening of symptoms with ongoing drug use. Drugs that have been associated with HPPD include LSD,DMT, 2C-E, 2C-I, 5-MeO-DMT, MDA, MDMA, psilocybin,  diphenhydramine, PCP, synthetic cannabis, and high doses of dextromethorphan. Additionally there are anecdotal reports of the atypical psychedelic Salvia divinorum causing persisting symptoms consistent with HPPD.
While it is difficult, if not impossible, to establish a clear relationship between the visual and mental symptoms, those with HPPD often testify that a connection indeed exists. For example, some claims that anxiety can cause the visuals to become more prominent and vice versa.
One possible cause of increased anxiety and depression is the person reacting negatively to the visual disturbances.
As yet, there is no cure available for HPPD. A study presented by Dr. Henry Abraham, at the Annual Meeting of the Biological Psychiatry Society in 2012, showed that two drugs, Tolcapone and levocarb that are primarily used in the treatment of Parkinsons Disease improved the symptoms of HPPD in one third of the 20 test subjects who had participated in the trial. As Tolcapone, and levocarb, are not approved for use in HPPD, the principal treatments that are available seek to reduce distress without treating the underlying cause. Primarily Benzodiazepines including clonazepam (Klonopin), diazepam (Valium) and alprazolam (Xanax) are prescribed with a fair amount of success. The anticonvulsant drug levetiracetam has been reported to diminish some of the visual symptoms, as well as reduce depersonalization and derealization symptoms, that can occur along with HPPD. The efficacy of Levetiracetam in treating HPPD has been documented in a prospective study. Another anticonvulsant, lamotrigine, has also been used to successfully treat HPPD.
Some medications have been contraindicated on the basis of their effects on HPPD or the concurrent mental issues. The atypical antipsychotic Risperidone is reported to worsen symptoms of HPPD during the drug's duration in some people. Those with HPPD are often advised to discontinue all drug use, many of which are thought to increase visuals in the short-term. There are also less concrete factors that may be generally detrimental to those with HPPD. For example, sleep deprivation and stress are thought to increase HPPD symptoms. However, no published studies have investigated whether any of these recommendations are helpful.
There is no universal time course of HPPD recovery. The adverse psychological effects of HPPD appear to lessen more rapidly than the visuals; quality of life often returns as a person adjusts. Recovery may be facilitated by a psychological habituation to the visuals, which, in effect, reduces the victim’s inclination to attend to and react negatively to them. The deleterious consequences of the visuals can therefore be reduced even if the HPPD does not disappear.
There is currently little reliable information on how often people fully recover from HPPD. There have been reports of HPPD victims having normal perception totally return. The small number of cases of HPPD that have been studied in depth make it difficult to determine how often and under what conditions the visual symptoms of HPPD resolve.
Other disorders with similar symptoms
It must be emphasized that individuals without HPPD will sometimes notice visual abnormalities. These include floaters (material floating in the eye fluid that appears as black/dark objects floating in front of the eyes and are particularly visible when looking at the bright sky or on a white wall) and the white blood cells of the retinal blood vessels (seen as tiny, fast-moving and quickly disappearing white specks). Likewise, bright lights in an otherwise dark environment may generate trails and halos. Most people don't notice these effects, because they are so used to them. A person fearful of having acquired HPPD may be much more conscious about any visual disturbance, including those that are normal. In addition, visual problems can be caused by migraines, brain infections or lesions, epilepsy, and a number of mental disorders (e.g., delirium, dementia, schizophrenia, Parkinson's disease). For an individual to be diagnosed with HPPD, these other potential causes must be ruled out.
- Baylor, D. A.; G. Matthews; K.-W. Yau (1980). "Two components of electrical dark noise in toad retinal rod outer segments". Journal of Physiology 309: 591–621. PMC 1274605. PMID 6788941.
- Shulgin, Alexander; Shulgin, Ann (1997). "#36. 5-MEO-DET". TiHKAL: the continuation. Berkeley, CA, USA: Transform Press. ISBN 9780963009692. OCLC 38503252. Retrieved 27 October 2012.
- "Erowid Experience Vaults: DiPT - More Tripping & Revelations - 26540".
- Moskvitin, Jurij (1974). Essay on the origin of thought. Ohio University Press. ISBN 0-8214-0156-4.
- Halpern JH, Pope HG (March 2003). "Hallucinogen persisting perception disorder: what do we know after 50 years?". Drug Alcohol Depend 69 (2): 109–19. doi:10.1016/S0376-8716(02)00306-X. PMID 12609692. PDF
- Baggott et al. (2006) Prevalence of chronic flashbacks in hallucinogen users: a web-based questionnaire
- Abraham, McCann, Ricaurte Psychedelic Drugs, Neuropsychopharmacology: The Fifth Generation of Progress. 2002 pg. 1548.
- Hermle, L.; Simon, M.; Ruchsow, M.; Geppert, M. (2012). "Hallucinogen-persisting perception disorder". Therapeutic Advances in Psychopharmacology 2 (5): 199–205. doi:10.1177/2045125312451270. PMC 3736944. PMID 23983976.
- Ikeda A, Sekiguchi K, Fujita K, Yamadera H, Koga Y (April 2005). "5-methoxy-N,N-diisopropyltryptamine-induced flashbacks". Am J Psychiatry 162 (4): 815. doi:10.1176/appi.ajp.162.4.815. PMID 15800171.
- Creighton FJ, Black DL, Hyde CE (November 1991). "'Ecstasy' psychosis and flashbacks" (PDF). Br J Psychiatry 159 (5): 713–5. doi:10.1192/bjp.159.5.713. PMID 1684523.
- McGuire PK, Cope H, Fahy TA (September 1994). "Diversity of psychopathology associated with use of 3,4-methylenedioxymethamphetamine ('Ecstasy')" (PDF). Br J Psychiatry 165 (3): 391–5. doi:10.1192/bjp.165.3.391. PMID 7994514.
- Espiard ML, Lecardeur L, Abadie P, Halbecq I, Dollfus S (August 2005). "Hallucinogen persisting perception disorder after psilocybin consumption: a case study". Eur. Psychiatry 20 (5–6): 458–60. doi:10.1016/j.eurpsy.2005.04.008. PMID 15963699.
- Lerner AG, Skladman I, Kodesh A, Sigal M, Shufman E (2001). "LSD-induced Hallucinogen Persisting Perception Disorder treated with clonazepam: two case reports". Isr J Psychiatry Relat Sci 38 (2): 133–6. PMID 11475916.
- Casa B, Bosio A (2005). "1589 Levetiracetam efficacy in hallucinogen persisting perception disorders: a prospective study". J of Neurological Sciences 238 (1): S504. doi:10.1016/s0022-510x(05)81946-x.
- Abraham, H. D.; Mamen, A. (1996). "LSD-Like Panic from Risperidone in Post-LSD Visual Disorder". Journal of Clinical Psychopharmacology 16 (3): 238–241. doi:10.1097/00004714-199606000-00008. PMID 8784656.
- Morehead, D. B. (1997). "Exacerbation of Hallucinogen-Persisting Perception Disorder with Risperidone". Journal of Clinical Psychopharmacology 17 (4): 327–328. doi:10.1097/00004714-199708000-00020. PMID 9241019.
- Faces of HPPD is a project website for HPPD patients to tell their stories about living with HPPD (2013)
- Newsgroup to support individuals with HPPD, some possible medications are indicated (NOT updated since 2002)
- Erowid's FAQ on HPPD
- HPPDonline.com Support website since 2001 for individuals with HPPD.