Inhale schreef:Voor de mensen die geïnteresseerd zijn in de werking van psychedelica in de hersenen raad ik aan deze lezing te kijken : http://vimeo.com/16782003
Long Term Use Resulting in Permanent Personality Changes- Most of us know somebody who has tripped a few too many times. This person isn't usually dangerous, or altered in any way that is easy to put your finger on. They tend to be just a little bit eccentric, or a little out there.
There are a lot of plausible explanations for this. The most likely seems to be that every time we put our mind through an experience, it burns a memory of that experience into its cells. Do it enough times and there will be noticeable changes. It’s the same theory behind how meditation can lead to enlightenment, or how habitual behaviors are developed.
The mechanism of action behind how this works is complex, and I won't attempt to explain it in detail here. What you need to know is that any excitatory experience (in other words any experience that causes stimulation in the brain, or any experience period) releases neurochemicals which kill some brain cells, at the same time new pathways in the brain are being formed (or strengthened after repeated use). These two mechanisms work to cause changes in our personality based on our experiences. But I digress…
The answer? Moderate your usage.
What Are Visual Hallucinations?
Hallucinations, defined as the perception of an object or event (in any of the 5 senses) in the absence of an external stimulus, are experienced by patients with conditions that span several fields (e.g., psychiatry, neurology, and ophthalmology). When noted by nonpsychiatrists, visual hallucinations, one type of sensory misperception, often trigger requests for psychiatric consultation, although visual hallucinations are not pathognomonic of a primary psychiatric illness.
Visual hallucinations have numerous etiologies. Here, we discuss possible mechanisms and offer a differential diagnosis of visual hallucinations, with an emphasis placed on conditions that arise in the context of medical and surgical illness. Treatment typically rests on the underlying etiology, so timely recognition and an understanding of causative mechanisms are crucial.
What Causes Visual Hallucinations?
Numerous hypotheses have been suggested to explain the genesis of visual hallucinations. These have been summarized and categorized by Asaad and Shapiro1: psychophysiologic (i.e., as a disturbance of brain structure), psychobiochemical (as a disturbance of neurotransmitters), and psychodynamic (as an emergence of the unconscious into consciousness). Visual hallucinations can be the result of all 3 processes, given the interplay among disturbances of brain anatomy, brain chemistry, prior experiences, and psychodynamic meaning.
To date, no single neural mechanism has explained all types of visual hallucinations; however, the similarity of visual hallucinations that are associated with seemingly diverse conditions suggests a final common pathway. Manford and Andermann2 summarized 3 pathophysiologic mechanisms thought to account for complex visual hallucinations.
The first mechanism involves irritation (e.g., seizure activity) of cortical centers responsible for visual processing. Irritation of the primary visual cortex (Brodmann's area 17) causes simple elementary visual hallucinations, while irritation of the visual association cortices (Brodmann's areas 18 and 19) causes more complex visual hallucinations.3 These data are supported by both electroencephalographic (EEG) recordings and direct stimulation experiments.2
Lesions that cause deafferentation of the visual system may lead to cortical release phenomenon, including visual hallucinations.4 Normal inputs are thought to be under the control of inhibitory processes that are effectively removed by deafferentation. It has been further suggested that deafferented neurons undergo specific biochemical and molecular changes that lead to an overall increase in excitability (similar to the denervation hypersensitivity seen in phantom limb syndrome experienced by amputees).5
A multitude of lesions can cause this loss of input and inhibit other cognitive functions.6 Of note, visual hallucinations may be induced by prolonged visual deprivation. One study reported visual hallucinations in 10 of 13 healthy subjects blindfolded for a period of 5 days; this finding lends strong support to the idea that the simple loss of normal visual input is sufficient to cause visual hallucinations.7
Finally, due to its role in the maintenance of arousal, the reticular activating system has been implicated in the genesis of visual hallucinations. Lesions of the brainstem have led to visual hallucinations (as in peduncular hallucinosis). Further, visual hallucinations are common in those with certain sleep disorders, and occur more frequently in those who are drowsy. The observation that visual hallucinations occur more frequently in those who are drowsy (even in the absence of frank sleep pathology) suggests that the reticular activating system plays a role in visual hallucinations, although the precise mechanism has not yet been established.
Einstein schreef:Voor zover ik weet worden in nuchtere status zo goed als alle hersendelen al nuttig ingezet, dus het is niet zo dat LSD extra hersengebieden aanspreekt of zo
During orgasm, almost the whole brain becomes highly active
Neurologist and author Oliver Sacks brings our attention to Charles Bonnet syndrome -- when visually impaired people experience lucid hallucinations. He describes the experiences of his patients in heartwarming detail and walks us through the biology of this under-reported phenomenon.
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