Рассказать вам о психическом расстройстве под названием hppd ( Длительное расстройство восприятия, вызванное галлюциногенами)
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HistoryThe 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. PrevalenceThe 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.
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 factorsThere 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. TriggersEnvironmental, 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 mechanismsThe 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. |