Do you Have HPPD?

To those of you reading this blog, and also suffer Hallucinogen Persisting Perception Disorder, you can participate in an online survey to helps aid the awareness of HPPD. The researcher of this project, Doreen Lewis, PhD, is currently working on a book titled, "When The Party Is Over", which is being backed b Dr. Henry David Abraham as well.

Click the link below to visit the webpage.

http://www.facesofhppd.com/

Manipulating Consciousness In Rats

Thalamus Linked To HPPD

Scientists showed that they could alter brain activity of rats and either wake them up or put them in an unconscious state by changing the firing rates of neurons in the central thalamus, a region known to regulate arousal. The studyis published in the journal eLIFE.

“Our results suggest the central thalamus works like a radio dial that tunes the brain to different states of activity and arousal,” said Jin Hyung Lee, PhD, assistant professor of neurology, neurosurgery and bioengineering at Stanford University, and a senior author of the study.

Located deep inside the brain the thalamus acts as a relay station sending neural signals from the body to the cortex. Damage to neurons in the central part of the thalamus may lead to problems with sleep, attention, and memory. Previous studies suggested that stimulation of thalamic neurons may awaken patients who have suffered a traumatic brain injury from minimally conscious states.

Lee’s team flashed laser pulses onto light sensitive central thalamic neurons of sleeping rats, which caused the cells to fire. High frequency stimulation of 40 or 100 pulses per second woke the rats. In contrast, low frequency stimulation of 10 pulses per second sent the rats into a state reminiscent of absence seizures that caused them to stiffen and stare before returning to sleep.

“This study takes a big step towards understanding the brain circuitry that controls sleep and arousal,” Yejun (Janet) He, PhD, program director at the U.S. National Institute of Health (NIH)’s National Institute of Neurological Disorders and Stroke (NINDS).

When the scientists used functional magnetic resonance imaging (fMRI) to scan brain activity, they saw that high and low frequency stimulation put the rats in completely different states of activity. Cortical brain areas where activity was elevated during high frequency stimulation became inhibited with low frequency stimulation. Electrical recordings confirmed the results. Neurons in the somatosensory cortex fired more during high frequency stimulation of the central thalamus and less during low frequency stimulation.

“Dr. Lee’s innovative work demonstrates the power of using imaging technologies to study the brain at work,” said Guoying Liu, PhD, a program director at the NIH’s National Institute of Biomedical Imaging and Bioengineering (NIBIB).

How can changing the firing rate of the same neurons in one region lead to different effects on the rest of the brain?

Further experiments suggested the different effects may be due to a unique firing pattern by inhibitory neurons in a neighboring brain region, the zona incerta, during low frequency stimulation. Cells in this brain region have been shown to send inhibitory signals to cells in the sensory cortex.

Electrical recordings showed that during low frequency stimulation of the central thalamus, zona incerta neurons fired in a spindle pattern that often occurs during sleep. In contrast, sleep spindles did not occur during high frequency stimulation. Moreover, when the scientists blocked the firing of the zona incerta neurons during low frequency stimulation of the central thalamus, the average activity of sensory cortex cells increased.

Although deep brain stimulation of the thalamus has shown promise as a treatment for traumatic brain injury, patients who have decreased levels of consciousness show slow progress through these treatments.

“We showed how the circuits of the brain can regulate arousal states,” said Dr. Lee. “We hope to use this knowledge to develop better treatments for brain injuries and other neurological disorders.”

Article Link

Dr.Gerard Alderliefste

Recently I was emailed by Dr. Abraham about a researcher, Dr. Gerard Alderliefste in Amsterdam who has an HPPD Research Clinic currently established. My team and I will be working on a draft email to send to him about our approach into getting more awareness spread about these disorders and perhaps get him on board for a team research project.

Dr. Alderliefste's website has some intriguing information, including a list of other specialists and and he also has a "Visual Snow Simulation" page that correctly portrays what the symptoms of HPPD/VS look like to an individual that suffers from these disorders. 

Link To His Website

Visual Snow Simulation Programs

Plant Compounds Increase Brain Connections

Brazilian researchers have demonstrated in laboratory that apigenin, a substance found in parsley, thyme, chamomile and red pepper, improves neuron formation and strengthens the connections between brain cells.
Previous experiments with animals had already shown that substances from the same chemical group as the apigenin, known as flavonoids, positively affect memory and learning. Many studies highlight the potential of flavonoids to preserve and enhance brain function. While the effectiveness of flavonoids for brain health is not an entirely new concept, this research is the first to show the positive effects of apigegin directly on human cells and the first to unraveling its mechanism.

Read More Here

Thalamus Linked To HPPD

The thalamus (from Greek θάλαμος, "chamber") is a midline symmetrical structure of two halves, within the vertebrate brain, situated between the cerebral cortex and the midbrain. Some of its functions are the relaying of sensory and motor signals to the cerebral cortex, and the regulation of consciousness, sleep, and alertness. The two parts of the thalamus surround the third ventricle. It is the main product of the embryonic diencephalon.

The role of the thalamus in the more anterior pallidal and nigral territories in the basal ganglia system disturbances is recognized but still poorly understood. The contribution of the thalamus to vestibular or to tectal functions is almost ignored. The thalamus has been thought of as a "relay" that simply forwards signals to the cerebral cortex. Newer research suggests that thalamic function is more selective. Many different functions are linked to various regions of the thalamus. This is the case for many of the sensory systems (except for the olfactory system), such as the auditory, somatic, visceral, gustatory and visual systems where localized lesions provoke specific sensory deficits. A major role of the thalamus is support of motor and language systems, and much of the circuitry implicated for these systems is shared. The thalamus is functionally connected to the hippocampus as part of the extended hippocampal system at the thalamic anterior nuclei with respect to spatial memory and spatial sensory datum they are crucial for human episodic memory and rodent event memory. There is support for the hypothesis that thalamic regions connection to particular parts of the mesio-temporal lobe provide differentiation of the functioning of recollective and familiarity memory.

The neuronal information processes necessary for motor control were proposed as a network involving the thalamus as a subcortical motor centre. Through investigations of the anatomy of the brains of primates the nature of the interconnected tissues of the cerebellum to the multiple motor cortices suggested that the thalamus fulfills a key function in providing the specific channels from the basal ganglia and cerebellum to the cortical motor areas. In an investigation of the saccade and antisaccade motor response in three monkeys, the thalamic regions were found to be involved in the generation of antisaccade eye-movement.

Thalamus Wikipedia Link

Brain Mechanisms of Hallucinogens and Entactogens

This review focuses on recent brain imaging and behavioral studies of sensory gating functions, which assess similarities between the effects of classic hallucinogens (eg, psilocybin), dissociative anesthetics (eg, ketamine), and entactogens (eg, 3,4-methylenedioxymethamphetamine [MDMA]) in humans. Serotonergic hallucinogens and psychotomimetic anesthetics produce overlapping psychotic syndromes associated with a marked activation of the prefrontal cortex (hyperfrontality) and other overlapping changes in temporoparietal, striatal, and thalamic regions, suggesting that both classes of drugs act upon a common final pathway. Together with the observation that both hallucinogens and N-methyl-oaspartate (NMDA) antagonists disrupt sensory gating in rats by acting on 5-hydroxytryptamine (serotonin) 5-HT2 receptors located in cortico-striato-thalamic circuitry these findings suggest that disruption of cortico-subcortical processing leading to sensory overload of the cortex is a communality of these psychoses. In contrast to hallucinogens, the entactogen MDMA produces an emotional state of positive mood, concomitant with an activation of prefrontolimbiclparalimbic structures and a deactivation of amygdala and thalamus.

More On This Article

(click image to enlarge)

Arnold Kriegstein, MD, PhD, on HPPD

Dr. Kriegstein received BA from Yale University and his MD and PhD degrees from New York University in 1977 where his thesis advisor was Dr. Eric Kandel. He subsequently completed Residency training in Neurology at the Brigham and Women’s Hospital, Children’s Hospital, and Beth Israel Hospital in Boston. He has held academic appointments at Stanford University, Yale University, and Columbia University. In 2004 he joined the Neurology Department at the University of California, San Francisco. He is currently the John Bowes Distinguished Professor in Stem Cell and Tissue Biology and Founding Director of the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UCSF. Dr. Kriegstein’s own research focuses on the way in which neural stem and progenitor cells in the embryonic brain produce neurons, and ways in which this information can be used for cell based therapies to treat diseases of the nervous system. His lab found that radial glial cells are neuronal stem cells in the developing brain, and also identified a second type of precursor cell produced by radial glial cells that is responsible for generating specific neuronal subtypes. He has recently begun to characterize the progenitor cells within the developing human brain, to determine the genetic profiles of specific progenitor populations, and to explore how these cells contribute to the huge expansion of neuron number that characterizes human cerebral cortex.

His theory on HPPD is as follows:

The thalamic filter and integrator model. The thalamus, within limbic cortico–striato–(pallido)–thalamo–cortical (CSTC) feedback loops, is proposed to function as a filter in the gating of extero- and interoceptive sensory and cognitive information to the cortex and, within cortico–thalamo–cortical (CTC) re-entrant pathways, it is proposed to be crucial in integrating cortically categorized exteroceptive perception with internal stimuli of the memory and value system.

Thalamic gating is under the control of glutamatergic cortico–striatal pathways projecting to the dorsomedial (MD) and reticular nuclei of the thalamus and under the modulatory influence of serotonergic and dopaminergic projections arising from the raphe and ventral tegmentum (VTA) to several components of the CSTC loops. The model predicts that serotonergic hallucinogens disrupt thalamic gating and produce sensory overload of the prefrontal cortex by excessive stimulation of 5-HT2A receptors located in several components of the CSTC loop, including the prefrontal cortex , limbic striatum and thalamus. The blockade of NMDA-mediated glutamatergic (Glu) cortico–striatal neurotransmission (e.g. by ketamine) or the increase of mesolimbic dopaminergic (DA) neurotransmission (e.g. by D-amphetamine) could lead to a similar neurotransmitter imbalance in CSTC loops, which again results in an opening of the thalamic filter, sensory overload of the cortex and psychosis.

In addition, the excessive stimulation of thalamic and/or cortical 5-HT2A receptors located on GABAergic interneurons by hallucinogens could lead to a disruption of CTC or cortico–cortical integration of distributed neuronal activity (‘binding’), which, in turn, might underlie the more anxious and fragmented experience of egodissolution that is often reported after high doses of hallucinogens. Although application of serotonergic hallucinogens into the frontal cortex in rodents has been demonstrated to increase pyramidal-cell activity via stimulation of 5-HT2A receptors located on apical dendrites of pyramidal cells and/or GABAergic neurons, it remains unclear whether such a local activation without a subsequent disruption of thalamic gating or integration of information processing leads to psychosis in humans or simply to excitation and/or increased sensory awareness.

Abbreviations: VTA, ventral tegmental area; AMY, amygdala; HPC, hippocampus; 5-HT, serotonin, DA,dopamine, Glu, glutamate; receptors: 2A, 5-HT2A; 1A, 5-HT1A; mGlu2/3, metabotropic glutamate receptor subtypes 2 and 3; NMDA, N-methyl-D-aspartate; D2, dopamine D2.


Arnold Kriegstein Profile

Visual Snow Published Data

This section steps into the field of "Visual Snow Syndrome", with published articles and research on subjects such as causes and perception, myths, and more.

There are two primary classes of visual snow. The results of a comprehensive study of visual snow are presented. The study is based on about fifty case studies that have arisen in response to this site since its inception and a subsequent close study of the relevant literature.

In the first class, labeled pulse type visual snow, extraneous dots appear scattered about the visual field suggestive of rain drops on a windshield of a car during very light rain. The dots may be darker or lighter than the average content of the scene. They may also tend to flicker individually, or to appear to swirl around in the visual field (like lines of ants).

In the second class, labeled broadband visual snow, the noise appears as a coarse texture (similar to that seen on a TV turned to a blank channel) of low amplitude obscuring the scene in object space. The noise may appear both lighter and darker than the background.

Rarely the extraneous dots appear to vary in color.

Visual snow is characterized by continuous dynamically flickering dots in the visual field. Most patients also have comorbid migraine. Cortical hyperexcitability is a feature of migraine. Recent studies indicate an association between occipital bending with psychiatric disorders such as depression. Here, we demonstrate a patient with visual snow, migraine with aura, left occipital bending, and cortical hyperexcitability. Treatment response to lamotrigine was objectively assessed by repetitive pattern reversal visual evoked potentials (rVEP).

Website Source

Neuro Research Foundation

THE NEUROSENSORY & NEUROREGENERATIVE RESEARCH FOUNDATION

The Neurosensory & Neuroregenerative Research Foundation (NNRF) is a group dedicated to unravel the neurological underpinnings behind two relatively unknown, under recognized yet highly prevalent neurological conditions; Visual Snow  (VS) and Hallucinogen Persistent Perception Disorder (HPPD). The basis behind the desire to conduct research on VS and HPPD is due to their similarities in symptom complex. With the proper resources placed in research, funding and advocacy the NNRF will certainly make an impact in this desperately deserving patient pool in need of help and relief.

A major factor in the lack of quantified cases of VS and HPPD is lack of proper Physician training and awareness.  The fact of the matter is that physicians by and large are completely unaware of and in managing an individual who has contracted VS or HPPD. The result of this unfamiliarity to these conditions typically yield misdiagnosis and with that the prescription of medications which do considerable more harm than good, oftentimes leading to worsening of symptoms if not tragic outcomes.  Below is an excerpt from 60 minutes “Why doctors often write off visual snow patients.”

In an effort to improve expectations at the physicians office for both patient and practitioner, advocacy campaigns would be tailored primarily to emergency room personnel, psychiatrists and psychologists who are typically the first to encounter individuals that suffer from neurosensory dysfunction. Through advocacy and awareness countless lives can be saved. Through proper treatment by physicians who are empowered with the knowledge in identifying the telltale signs of VS and HPPD quality of life can be preserved and through research can a cure be found.


Update As of 11/24/2015

Letters have been sent to the US Dept of Education, the National Educators Association, National School Psychologist Association and the National School Nurse Association with the intent on working on a national campaign to educate faculty, parents and students of the dangers posed by HPPD. We intend to produce a webinar sponsored and endorsed by these agencies which will create awareness of this neurologically acquired disorder to the point where the NIH will see the need and validity to allocate funding for basic research.


Foundation Website

Contacted Dr. Abraham

I have been in contact with Dr. Henry David Abraham over e-mail, and spoke to him over the phone today. He still treats patients and diagnoses, and does treatments to help cope with the symptoms, and prescribe medications.

Contact Dr. Abraham

"I evaluate patients for HPPD in Boston, and I have several colleagues in Europe who do the same. I can include your name in a database for future projects. As you can imagine, I can't diagnose or treat by internet.

I tend to see patients Tuesdays through Thursdays, but at times I travel. Calling me is best.

Sincerely,

Dr Abraham"

How Do Eyes Function?

Light rays enter the eye through the cornea, the clear front “window” of the eye. The cornea's refractive power bends the light rays in such a way that they pass freely through the pupil the opening in the center of the iris through which light enters the eye. The iris works like a shutter in a camera.

The detection of light by pigments in the retina, called rhodopsin or visual purple, leads to our sense of vision. New experiments by scientists from the Max Planck Institute for the Structure and Dynamics of Matter and the University of Toronto have revealed that the primary photochemical event of this process operates at the fundamental molecular speed limit. These results are reported online in the journal Nature Chemistry today.
The retinal chromophore in rhodopsin, also called vitamin A aldehyde, derives its light sensitivity from a repeating chain of single- and double-bonded carbon atoms. The absorption of a photon by retinal causes an extremely short transient weakening of a specific double bond resulting in rotation about that bond. Pinpointing how fast this so-called chemical isomerization reaction occurs has been difficult, however, and has largely tracked the technological advances in pulsed laser sources. With femtosecond lasers it was shown that the isomerization takes place within 200 femtoseconds (that is 200 millionths of a billionth of a second), and is likely a vibrationally-coherent chemical reaction, meaning the vibrational motions of the retinal chromophore itself help directing the isomerization reaction.

Using a highly sensitive technique from the field of ultrafast spectroscopy called heterodyne-detected transient grating spectroscopy, scientists in the laboratories of Professors R. J. Dwayne Miller (University of Toronto and Max Planck Institute for the Structure and Dynamics of Matter) and Oliver P. Ernst (University of Toronto) revisited the isomerization reaction of bovine rhodopsin with unprecedented sensitivity and temporal resolution. Such an approach revealed that the isomerization takes place on a timescale of 30 femtoseconds. "It turns out that the primary step of vision is nearly ten times faster than anyone thought," says Professor Miller, "and the atomic motions are all perfectly choreographed by the protein."
Temporal analysis of the experimental data revealed these choreographed vibrational dynamics, which are comprised of localized stretching, out-of-plane wagging, and torsional motions. "Such a fast timescale sets distinct limitations on the vibrationally-coherent reaction coordinate," says Dr. Philip Johnson, lead author of the study, "and this work indicates that it is local to the specific isomerizing double bond." "Moreover," he adds, "the isomerization reaction proceeds within a single period of the relevant torsional vibrational motion. The notion of fully vibrationally-coherent chemical reactions has been around since at least the 1930s, but really hasn't been explicitly observed until now."

This research was supported by the Max Planck Society, the Natural Sciences and Engineering Research Council of Canada (NSERC), the Canada Excellence Research Chairs program (CERC), and the Canadian Institute for Advanced Research (CIFAR). Professor Miller and Professor Ernst are co-directors of CIFAR's program Molecular Architecture of Life, which is untangling the details of the complex molecular processes that underlie all living systems.

Source Link

Dr. Abraham on HPPD and VS

Dr. Henry David Abraham, whom has over 40 years experience researching Hallucinogen Persisting Perception Disorder and Visual Snow, described perfectly about what these condition are like, in this video below. The video is appx 25 minutes and goes into some great detail.

From his website, Dr. Abraham sheds more light on his HPPD and VS research:

Hallucinogen Persisting Perception Disorder, HPPD, is a long lived problem arising from past use of strong hallucinogenic drugs. The majority of patients with HPPD report a prior use of lysergic acid diethylamide (LSD). Life LSD dose does not appear to increase the risk to developing HPPD. That is, I have seen some patients who have tripped on acid multiple times and then developed HPPD, and others develop the same disorder after one or two trips. I liken tripping on acid to playing Russian roulette, but using chemicals instead of bullets. Developing HPPD without ever tripping on acid can also happen, but in my experience this is quite rare, and suggestive of another disorder in the nervous system that needs medical attention.

The usual HPPD patient knows better than his doctors what is going on. The patients I see in consultation often have seen an average of six other medical specialists before they found their way to my office. This is probably because HPPD is a rare disorder, and not something that neurologists, psychiatrists, psychologists, and ophthalmologists usually encounter in training. Ironically these are the specialists most often consulted by the HPPD patient. Too often the first (and mistaken) clinical impression is that the patient has a psychosis. This can set treatment on a wrong path.

The majority of HPPD patients do not suffer from psychosis, or other signs of psychotic illness, such as auditory hallucinations and delusions. The disorder is for the most part a perceptual disorder in which visual information from the perceived world enters the brain but then cannot shut itself off. The result is lingering visual information, or a disinhibition of visual information processing, in the form of after-images, the trailing of images as they move through the visual field, flashes of light, and the formation of complex imagery on otherwise blank surfaces. 

The first scientific description of the persisting visual phenomena described by LSD users may be found here.

Research in my laboratory later documented quite clearly that in the HPPD patient, when a visual signal from an image enters the brain, the signal stays around in consciousness longer than it does in the control subject who does not suffer HPPD. This finding has been found in three different studies of visual psychophysics. One finding, shown in Figure Five, was that LSD users see a flickering light as fused more often than non-users, because the eyes of the LSD user continues to see the light after it’s gone. 

A similar event occurred if a subject was exposed to bright light, and then tested for the ability to adapt to darkness. In this experiment, Dr. Ernst Wolf and I found that the dark adaptation of LSD users was reduced compared to non-drug controls because the LSD group could not mentally shut off the original light enough to see a tiny light when in the dark. 

This impairment could be important, for example, to persons needing night vision such as airplane pilots.

My colleague, Frank Duffy, and I also found characteristic abnormalities in the brain’s electrical activity in HPPD subjects, documenting that HPPD is a disorder which clearly takes place in the brain, and not simply in the imagination. 

Dr. Abraham's Website

Doctors Avoiding These Disorders

HPPD Foundation

The   Foundation is a non-for-profit organization created to offer grants to researchers interested in understanding   $100,000 will be given annually in one or more grants to qualified researchers with novel ideas on how to study this disorder.

This has been established for a couple years now, and seriously needs more input and awareness to those with a background in psychology, biochemistry, neurobiology, psychopharmacology, genetics or neuroimaging.


HPPD Foundation Website

Eye on Vision Foundation

It's a start!


The Eye on Vision Foundation strives to raise funds and awareness for research into vitreous floaters, macular degeneration, and visual snow.


Hello Everyone! I have really great news! The Munich IRB has just approved our study and the doctors are starting to recruit now.

They are working through the list of emails that we have received in the last year trying to get in touch with as many patients as possible.

For now, they have only approval for a German consent form - so in the beginning, they will focus on German speaking patients, but the projects in London are coming soon and then they will include English-speaking patients. (This does not mean that you need to be from Germany or live in Germany, but you do need to know how to read and write in German for the purpose of the consent forms.)

For an expedited contact, this email-address was generated and should be used by the German speaking patients who wish to apply:


Click Here for Website

Future Treatment?

The neurotransmitter gamma-aminobutyric acid (GABA) is a major inhibitory agent in the human brain. Medications such as the benzodiazepines are agonists at this site, and so would be expected to reduce the symptoms of HPPD if the disinhibition hypothesis were correct. Indeed, this seems to be the case, but unfortunately only partially so. One possible explanation for an incomplete treatment response may be pharmacokinetic, that is, too little drug reaching its destination in the brain. Indeed, when treating six patients with a short-acting benzodiazepine, the volunteer (a psychologist) excitedly said, ‘I can see normally for the first time in years.’ Similar strong responses were observed in the other volunteers. But the excitement was misplaced, since midazolam must be administered intravenously, and has a half-life of two hours. Clinical studies by my colleague Dr Lerner and his group in Israel have shown that clonazepam appears to be the benzodiazepine drug of choice for HPPD (Lerner et al., 2003)

There is an axiom in clinical medicine that the more mysterious the ailment, the more multitudinous the treatments. That is certainly the case with HPPD. In addition to the benzodiazepines, a long list of other agents have been tried, including antipsychotics, antidepressants, antiepileptics, alpha-two adrenergic agonists, and antiparkinsonian drugs. Levetiracetam was reported helpful in one study (Casa & Bosio, 2005). Some patients report that the use of psychostimulants improved the symptoms, leading me to try a study of tolcapone supplemented with carbidopa and l-DOPA in HPPD. The combination of medications reduced symptoms significantly in about a third of the sample (Abraham, 2012). While this may be a biological effect, it is equally consistent with a placebo response, since the study was an open-label one.



..Persistent flashbacks of the HPPD variety may represent permanent neural disruptions due to “disinhibition of visual processing related to a loss of serotonin receptors on inhibitory interneurons,” says Henry Abraham, a lecturer in psychiatry at Tufts University School of Medicine in Boston who has published several papers on HPPD...

..But there are two different benzodiazepines used as anticonvulsants, Clonazepam and Midazolam, that have shown promise for mitigating HPPD symptoms...

..Levetiracetam, a medication used for epilepsy, also performed well. However, anti-psychotic drugs like risperidone can dramatically worsen symptoms...




Source: http://dana.org/News/Details.aspx?id=43275

Contacting Alex Burmester

Dr. Brumester is a research fellow at NYU who has published several articles on the human visual system. It might be a good idea to contact him with the intent of making him aware of the Eye On Vision Foundation and the Neurosensory & Neuroregenerative Research Foundation! The more interest and publications that cover Visual Snow and Hallucinogen Persistent Perception Disorder the better!

I have been in contact with Alex via e-mail a few times, one e-mail of which he suggested he would be interested in researching HPPD. 

One of the e-mail replies is as follows:

Hi Austin,

I've actually been contacted by Pawel Kaluza who has invited me to be on the scientific board of an organisation that deals with these disorders. I had not heard of them before he approached me, but might be able to contribute in some small way. In a general sense, it seems like it would be quite a difficult disorder to understand in terms of the neural changes accompanying the perceptual disturbances. I will have a look at some of the literature before I get back to Pawel, but am seriously considering his offer.

Thanks for reading my article and getting in touch.

Cheers,

Alex

Reply from this morning is as follows:

Hi Austin,

Sorry have been busy running experiments but will get a chance to look at it more thoroughly tonight! Will let you know.

Thanks,

Alex

Alex Burmester Homepage

Alex Burmester Scholar Citations and Research

What It's Like

Hallucinogen Persisting Perception Disorder does not have the same visual qualities for all. For some it is mild, for others it is very strong and can interfere with daily lifestyles and social life. About 59% of people with HPPD see geometric patterns on blank surfaces like walls. Almost as many, see false movements of still objects, usually in the peripheral visual fields. Others reports flashes of light, trailing images behind moving objects, intensified colors, and afterimagery.

About 1 in 50,000 hallucinogen users will develop HPPD.

H.P.P.D. does not generate hallucinations, technically speaking. Sufferers can appreciate that their perceptual aberrations are unreal—that their surroundings only appear blurred by afterimages (palinopsia) and trails (akinetopsia); shimmered by sparkles and flashed by bright bolts of light; interrupted by transparent blobs of color floating around; electrified by visual snow; magnified or shrunk by “Alice-in-Wonderland” symptoms; adorned by halos around objects, around people’s heads. The pseudo-hallucinations are ultimately unconvincing, if deeply unsettling.

The cluster of symptoms first appeared in the Diagnostic and Statistical Manual of Mental Disorders in 1986. Ever since, the official diagnosis has been lumped together with “flashbacks.” Brief fragments of a trip that occasionally bubble up to one’s consciousness, flashbacks may arise from sudden spikes in the cerebral cortex—stirring perceptions, sensations, or emotions mimicking those of the hallucinogen high, in the absence of any chemical. But as the term has been popularized, flashback has been rendered “virtually useless” diagnostically, writes Dr. John Halpern, an assistant professor of psychiatry at Harvard Medical School and lead author of the most recent literature review of H.P.P.D. In the review, published in Drug and Alcohol Dependence, Dr. Halpern reasons that by conflating two distinct diagnoses, a strict definition of H.P.P.D. has remained elusive, leaving its prevalence obscured. Yet, “it seems inescapable,” he concludes, based on twenty related studies dating back to 1966, “that at least some individuals who have used LSD, in particular, experience persistent perceptual abnormalities reminiscent of acute intoxication, not better attributable to another medical or psychiatric condition.”

Peer-reviewed accounts of drug users whose world had been transfigured permanently can be found as early as 1983, prefiguring the initial D.S.M. entry. In a case-control study of a hundred and twenty-three LSD users, Abraham was among the first to catalogue reports from those who flashed psychedelic and never turned off: a struggling shoe salesman whose dark-brown pairs bled into the navy-blues; a confused student whose text jumbled into “alphabet soup”; a distracted office worker whose flower pot slid back and forth along the windowsill. “This isn’t flashbacks,” said Abraham. “We have to call it what it is: a persisting perception disorder.”

READ MORE: http://www.newyorker.com/tech/elements/a-trip-that-doesnt-end

DSM IV On HPPD

APPENDIX A: DSM IV ENTRY FOR HPPD

Hallucinogen Persisting Perception Disorder

Diagnostic Code: 292.89 

The essential feature of Hallucinogen Persisting Perception Disorder (Flashbacks) is the transient recurrence of disturbances in perception that are reminiscent of those experienced during one or more earlier Hallucinogen Intoxications. The person must have had no recent Hallucinogen Intoxication and must show no current drug toxicity (Criterion A). This re-experiencing of perceptual symptoms causes clinically significant distress or impairment in social, occupational, or other important areas of functioning (Criterion B). The symptoms are not due to a general medical condition (e.g., anatomical lesions and infections of the brain or visual epilepsies) and are not better accounted for by another mental disorder (e.g., delirium, dementia, or Schizophrenia) or by hypnopompic hallucinations (Criterion C). The perceptual disturbances may include geometric forms, peripheral field images, flashes of color, intensified colors, trailing images (images left suspended in the path of a moving object as seen in stroboscopic photography), perceptions of entire objects, afterimages (a same-colored or complementary-colored "shadow" of an object remaining after the removal of the object), halos around objects, macropsia, and micropsia. The abnormal perceptions that are associated with Hallucinogen Persisting Perception Disorder occur episodically and may be self-induced (e.g., by thinking about them) or triggered by entry into a dark environment, various drugs, anxiety or fatigue or other stressors. The episodes may abate after several months, but many persons report persisting episodes for 5 years or longer. Reality testing remains intact (i.e., the person realizes that the perception is a drug effect and does not represent external reality). In contrast, if the person has a delusional interpretation concerning the etiology of the perceptual disturbance, the appropriate diagnosis would be Psychotic Disorder Not Otherwise Specified.

Diagnostic criteria for Hallucinogen Persisting Perception Disorder
The re-experiencing, 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 colors, 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, visual epilepsies) and are not better accounted for another mental disorder (e.g., delirium, dementia, Schizophrenia) or hypnopompic hallucinations.

My Story

In January 2014 I took 2 tabs of LSD and several hours later was completely depersonalized and basically went to a dimension full of demons and terror. I wouldn't exactly call it hell, but a hell in my mind. My mind felt completely separated from my body. There were no improved colors or saturation, just a bland experience with very vivid visual anomalies. I had a near death experience and saw the "light at the end of the tunnel". My ego was completely dissolved and the world before me became new. I thought I had died, yet I accepted death. I challenged it and fought for 18 hours before I found myself returning to reality. I did return to reality... But I brought something back with me from the depths of the experience... A completely new visual outlook both physically and mentally.


This quote from the movie, 'Constantine' hit me pretty hard. I knew exactly what it meant.

"But when you cross over, time stops.
Take it from me, two minutes in hell is a lifetime
When I came back I knew, all the things I could see was real
Heaven and hell are right here.
Behind every wall, every window.

The world behind the world, and we're smack in the middle"

After 50 Years

'Flashbacks' following use of hallucinogenic drugs have been reported for decades; they are recognized in DSM-IV as 'Hallucinogen Persisting Perception Disorder (Flashbacks)', or HPPD. We located and analyzed 20 quantitative studies between 1955 and 2001 examining this phenomenon. However, many of these studies were performed before operational criteria for HPPD were published in DSM-III-R, so they are difficult to interpret in the light of current diagnostic criteria. Overall, current knowledge of HPPD remains very limited. In particular the term 'flashbacks' is defined in so many ways that it is essentially valueless; most studies provide too little information to judge how many cases could meet DSM-IV criteria for HPPD; and consequently information about risk factors for HPPD, possible etiologic mechanisms, and potential treatment modalities must be interpreted with great caution. At present, HPPD appears to be a genuine but uncommon disorder, sometimes persisting for months or years after hallucinogen use and causing substantial morbidity. It is reported most commonly after illicit LSD use, but less commonly with LSD administered in research or treatment settings, or with use of other types of hallucinogens. There are case reports, but no randomized controlled trials, of successful treatment with neuroleptics, anticonvulsants, benzodiazepines, and clonidine. Although it may be difficult to collect large samples of HPPD cases, further studies are critically needed to augment the meager data presently available regarding the prevalence, etiology, and treatment of HPPD.

Source: http://www.ncbi.nlm.nih.gov/pubmed/12609692

Clonazepam Treatment for LSD Induced HPPD

An unique and intriguing characteristic of lysergic acid diethylamide (LSD) and LSD-like substances is the recurrence of some of the symptoms which appear during the intoxication, in the absence of recent intake of hallucinogens. Hallucinogen persisting perception disorder (HPPD) is a condition in which the re-experiencing of one or more perceptual symptoms causes significant distress or impairment in social, occupational or other important areas of functioning and may be extremely debilitating. Benzodiazepines are one of the recommended agents for the treatment of HPPD but it is unclear which of them may be more helpful. The goal of our investigation was to assess the efficacy of clonazepam in the treatment of LSD-induced HPPD. Sixteen patients fulfilled entrance criteria. All complained of HPPD with anxiety features for at least 3 months and were drug free at least 3 months. They received clonazepam 2 mg/day for 2 months. Follow-up was continued for 6 months. They were weekly evaluated during the 2 months of clonazepam administration and monthly during the follow-up period using the Clinical Global Impression Scale, a Self-report Scale and Hamilton Anxiety Rating Scale. Patients reported a significant relief and the presence of only mild symptomatology during the clonazepam administration. This improvement was clearly sustained and persisted during a 6-month follow-up period. This study suggests that high potency benzodiazepines like clonazepam, which has serotonergic properties, may be more effective than low-potency benzodiazepines in the treatment of some patients with LSD-induced HPPD.

Introduction

After having suffered from a rare condition known as 'Hallucinogen Persisting Perception Disorder' (HPPD) and 'Depersonalization Disorder' (DPD) for nearly 2 years now, I have come to the conclusion that it is time to conduct more thorough research into this disorder itself. While very little scientific research has been done, and no known cures have been found, we do have some insight into aiding the suffering of these disorders.



HPPD is a condition of after-effects from drug use that produce the following symptoms, but are not limited to:


Visual Snow (vision like static on a television)

Plethora of Eye Floaters

Light Sensitivity

Object Auras
Nighttime Light Intensity from artificial lighting

Walls appear to "breathe"
After-Images



WikiLinks:

Hallucinogen Persisting Perception Disorder
Depersonalization Disorder


This blog is dedicated to current scientific research, medications, and lifestyle changes that can help to further progress the knowledge of the condition and helpful aids. I will be conducting personal experiments and creating very frequent posts on the status of my lifestyle changes to personally help improve my HPPD symptoms.