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Nuklear
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When we're hallucinating is it the same part of our brain we use normally that hallucinating or another? Is our subconscious mind seeing things also?
I think the answer is yes, the same areas of the brain we normally use are active – at least some of them. There are many types of hallucinations and I am not sure the brain mechanisms behind the different kinds are well understood yet. In 2005, there was a study done with people who suffered from musical hallucinations. When the hallucinations were occurring, PET scans of subjects showed a pattern of brain activity that was similar to normal subjects who were listening to music, but with an important difference:Nuklear said:When we're hallucinating is it the same part of our brain we use normally that hallucinating or another?
http://www.nytimes.com/2005/07/12/h...en=6ad31758c7334d06&ex=1278820800&partner=rssThe main difference is that musical hallucinations don't activate the primary auditory cortex, the first stop for sound in the brain. When Dr. Griffith's subjects hallucinated, they used only the parts of the brain that are responsible for turning simple sounds into complex music.
These music-processing regions may be continually looking for signals in the brain that they can interpret, Dr. Griffiths suggested. When no sound is coming from the ears, the brain may still generate occasional, random impulses that the music-processing regions interpret as sound. They then try to match these impulses to memories of music, turning a few notes into a familiar melody.
I'm not sure what you mean by that.Nuklear said:Is our subconscious mind seeing things also?
sog said:I seen a mirage in the desert. I think a mirage is a hallucination. I don't take psychedellics.
complexPHILOSOPHY said:Is it your perception of reality that is distorted or are your sensations of reality actually distorted as well, while tripping on psychedelics?
Math Is Hard said:Parkinson's Disease patients who sometimes suffer from visual hallucinations are thought to have these occurrences due to visual cortex malfunctions. There are "normal" parts of the brain's vision system working, but in an abnormal way - some portions are overworking, others are underworking.
Among the many theories that have been advanced to explain the mechanism by which auditory verbal hallucinations (AVH) arise, 2 that have received a degree of empirical support are: the hypothesis that AVHs arise from misinterpreted inner speech and the proposal that they arise from aberrant activation of the primary auditory cortex. To test these hypotheses, we were fortunate to be able to study the interesting and rare case of a woman with schizophrenia who experienced continuous AVH which disappeared when she listened to loud external speech. Functional magnetic resonance imaging (fMRI) was used to measure the patient’s brain activity in the temporal and inferior frontal regions during the AVHs and while the she was listening to external speech. The brain activity of a matched control subject was also recorded under the same experimental conditions. AVHs were associated with increased metabolic activity in the left primary auditory cortex and the right middle temporal gyrus. Our results suggest a possible
interaction between these areas during AVHs and also that the hypotheses of defective internal monitoring and aberrant activation are not mutually exclusive. Potential limitations to the generalization of our results are discussed.
The lack of left dorsolateral prefrontal cortex activation, an area associated with an internal monitor role, could explain why these activations are then misinterpreted as alien.
Overall, our data indicate that the propensity to hallucinate in schizophrenia is associated with functional abnormalities in areas implicated in verbal self-monitoring. This is consistent with the notion that auditory hallucinations are derived from defective monitoring of inner speech.
Revenged said:Why would Parkinson's Disease cause hallucination?
It is caused by a lack of dopamine in the brain to the striatum...
Whereas I thought hallucinations are thought to occur due to a release of glutamate or an effect on serotonin (5-HT)
So, I read that and said, "fair enough, but what's the specific relationship to the vision system?" And I thought this would be of interest to you because you had asked about specific neurotransmitters...there was a striking association between the distribution of temporal lobe LB and well-formed visual hallucinations. Cases with well-formed visual hallucinations had high densities of LB in the amygdala and parahippocampus, with early hallucinations relating to higher densities in parahippocampal and inferior temporal cortices. These temporal regions have previously been associated with visual hallucinations in other disorders.
.. patients with Charles Bonnet syndrome, who report similar visual hallucinations to patients with LB, activate the anterior temporal projection of the ventral visual pathway when hallucinating about landscapes, figures, and vehicles with appropriate emotional context (ffytche et al., 1998 ; ffytche and Howard, 1999 ; Santhouse et al., 2000 ). These hallucinations are thought to occur because of a lack of occipital stimulation due to ocular pathology (ffytche et al., 1998 ; ffytche and Howard, 1999 ; Santhouse et al., 2000 ). Downstream ventral association cortices increase their activity as a result of cortical disinhibition with this abnormal activity in visual processing regions activating complex visual hallucinations. It would appear more than coincidental that the same brain regions concentrating LB in our patients with visual hallucinations were those activated by visual hallucinations in patients with the Charles Bonnet syndrome (Santhouse et al., 2000 ), particularly as decreased occipital glucose metabolism also occurs in patients with LB (Imamura et al., 1999 , 2001; Lobotesis et al., 2001 ). The reduction in occipital metabolism occurs without underlying pathological inclusions, with a recent study suggesting that white matter abnormalities contribute to this metabolic deficit (Higuchi et al., 2000 ). In addition, DLB patients have preserved glucose metabolism in ventral temporal lobe regions, particularly those cases with visual hallucinations (Imamura et al., 1999 ; Higuchi et al., 2000 ; Lobotesis et al., 2001 ). These data suggest that activity in ventral visual pathways in association with underactivity of the primary visual cortices contributes to the well-formed visual hallucinations reported in cases with LB.
While it is generally believed that intracytoplasmic inclusions are a sign of neurodegeneration, several studies quantifying cortical neuronal loss in patients with DLB have shown a remarkable neuronal preservation (Gómez-Isla et al., 1999 ; Broe et al., 2001 ), suggesting that cortical LB may not signify neurodegeneration. If these cortical inclusions do not disrupt neuronal metabolism sufficiently to cause degeneration, they may disrupt cell mechanisms sufficiently to cause an increase in metabolic demand for neuronal survival. This may contribute to the association between the concentration of temporal lobe LB and well-formed visual hallucinations found in the present study. In fact, the overall pattern of temporal lobe LB formation appears to be more relevant to the onset of visual hallucinations than to the onset of dementia in cases with cortical LB disease.
ABSTRACT
Using functional magnetic resonance imaging (fMRI), the authors examined visual cortex function in Parkinson's disease patients who did and did not experience visual hallucinations. Patients with visual hallucinations demonstrated increased activation in the visual association cortex and deficits in the primary visual cortex, suggesting that visual hallucinations are associated with an abnormality of visual-cortex function.
Nuklear said:I've had hallucinations. A couple of times I've seen these little lifgts going at diagnal angles on and off a few seconds in my eyes, swarms of the them baracading me at a time.
I've seen it when I've been indoors, as well, often when I am looking at a sunbeam coming through a window.Blue light (optimal wavelength: 430 nm) is well absorbed by the red blood cells that fill the capillaries. The brain "edits out" the dark lines that would result from this absorption. The white blood cells, which are much rarer than the red ones and do not absorb the blue light well, create gaps in the blood column, and these gaps appear as bright dots.
The dots are due to the white blood cells that move in the capillaries in front of the retina of the eye, near the macula.
Math Is Hard said:Anyway, I don't know very much about the role of specific neurotransmitters during hallucinations so maybe I can pick your brain on this - pun intended. I would like to learn more if you have any studies/links you could direct me to.
Math Is Hard said:Were you looking at the daytime sky when this happened? Or some kind of blue background? When I am outdoors on a sunny day and look at the sky, I see something similar. Tiny bright squiggles jiggling and flying around in random directions. This is not a hallucination, but an entoptic (generated by the eye) phenomenon called Scheerer's Phenomenon:
http://en.wikipedia.org/wiki/Blue_field_entoptic_phenomenon
I've seen it when I've been indoors, as well, often when I am looking at a sunbeam coming through a window.
But doesn't chlorpromazine also block serotonin 5-HT2 receptors?Revenged said:Incidentally, the treatment of schizophrenia is simply to block dopamine receptors in the central nervous system - e.g. chlorpromazine blocks D2 receptors...
Math Is Hard said:But doesn't chlorpromazine also block serotonin 5-HT2 receptors?
Nuklear said:Well what are Serotonin and DOpamine's roles?
Math Is Hard said:Even if we're talking about visual and auditory hallucinations in a person who is shut off from all light and sound stimulation, say in a sensory deprivation tank, I'm still certain the experience is a result of the normal visual and auditory neural systems functioning abnormally for whatever reason. There is not some "not normally used" separate brain area dedicated to hallucinations. But if you find any research that makes a different claim, and it's from a credible source, please do share.
Hallucinations are a sensory experience that is not based on external stimuli. They can be visual, auditory, tactile, or olfactory in nature. The science behind hallucinations involves the complex interactions between our brain, our senses, and our perception of reality.
Yes, there is a strong link between hallucinations and our subconscious mind. Our subconscious mind plays a crucial role in processing sensory information and creating our perception of reality. It can influence our perception in such a way that we may experience things that are not really present.
There are various factors that can trigger hallucinations, such as mental illness, sleep deprivation, drug use, sensory deprivation, and neurological disorders. These triggers can disrupt the normal functioning of our brain and cause hallucinations to occur.
In most cases, hallucinations cannot be controlled by our conscious mind. However, with proper treatment and therapy, individuals with certain mental illnesses or neurological disorders may learn to manage and reduce their hallucinations. Additionally, avoiding triggers and maintaining a healthy lifestyle may also help in controlling hallucinations.
Yes, there is a growing body of scientific research that suggests a strong link between hallucinations and the subconscious mind. Studies have shown that individuals who experience frequent hallucinations have altered brain functioning and activity in areas associated with the subconscious mind. Additionally, treatments that target the subconscious mind, such as cognitive-behavioral therapy, have been found to be effective in reducing hallucinations.