Is the Science of Hallucinating Linked to Our Subconscious Mind?

[Nuklear]

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?

 

[Nuklear]

Guess no one does psychedellics.

 

[sog]

You don't have to be on psychedellics.

I seen a mirage in the desert. I think a mirage is a hallucination. I don't take psychedellics.

 

[Math Is Hard]

When we're hallucinating is it the same part of our brain we use normally that hallucinating or another?

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:

The 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.

http://www.nytimes.com/2005/07/12/h...en=6ad31758c7334d06&ex=1278820800&partner=rss

Is our subconscious mind seeing things also?

I'm not sure what you mean by that.

I seen a mirage in the desert. I think a mirage is a hallucination. I don't take psychedellics.

A http://en.wikipedia.org/wiki/Mirage" is an optical phenomenon, not a hallucination.

 

[Nuklear]

SO if a person is have a total hallucination, one where there's no input from their eyes or ears just out of their mind.....are they using the normally active parts of the visual cortex?

 

[Math Is Hard]

I'm not clear on what you mean by a "total" hallucination, but if a person is having a visual hallucination, yes, most likely some part of the visual cortex is active during the experience. 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.

If you've ever hit the back of your head and seen "stars", that's an example of your visual cortex activating independently of the normal sensory input from your eyes. The jolt of mechanical energy to the back of your skull is enough to cause some neurons to begin firing in the brain's vision processing areas and you see "lights" which obviously aren't really there.

 

[complexPHILOSOPHY]

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]

Is it your perception of reality that is distorted or are your sensations of reality actually distorted as well, while tripping on psychedelics?

Both are possibilities. LSD, for example, is known to produce both delusions (false beliefs or incorrect inferences about external reality) and (typically visual) hallucinations.

 

[Nuklear]

When I say total hallucination I mean in a totally different world. Some people have hallucinations where the normals world get's distorted, odd colored, or see objects and people that aren't there.

I'm talking about an entiley mental genreated hallucination. No input from your eyes ears, etc. I mean you're in another reality, dimension, the way dreams are.

 

[Math Is Hard]

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.

 

[Revenged]

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.

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)

 

[RVBuckeye]

Nuklear,

The following links are to some research on auditory verbal hallucinations in schitzophrenic subjects that I came across looking into another thread in this forum. What I do know is that our neurons have a base rate of firing and information is coded and transmitted by the rate of fire, the number of neurons firing, and which particular neurons are firing. So psychedellics could cause the brain to misinterperate this internally-produced information, much like a schitzophrenic subject.

http://www.julianjaynes.org/pdf/bentaleb-beauregard-liddle-stip_hallucinations.pdf

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.

http://www.julianjaynes.org/pdf/lennox-bert-park-jones_spatialtemporalmapping.pdf

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.

http://www.julianjaynes.org/pdf/shergill-bullmore-simmons-murray-mcguire.pdf

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.

 

[Nuklear]

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.

 

[Math Is Hard]

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)

It's an interesting question – not an association I would have immediately made either. Unfortunately, 20-40% of Parkinson's patients develop cognitive disturbances, sometimes including hallucinations. Visual hallucinations apparently occur in about 25% of individuals with Parkinson's (Aarsland et al., 1999, Fénelon et al., 2000). Source of citations: http://brain.oxfordjournals.org/cgi/content/full/125/2/391

As you mentioned there is a degeneration in the dopamine production regions, and patients are treated with drugs like Levodopa to boost dopamine levels and compensate for the loss. Visual and auditory hallucinations occur sometimes as a side effect of this treatment, although I do not know the specific mechanisms behind it.

Other than that, the pathology of the disease itself may be to blame. One of the nasty things that can happen in the course of Parkinson's is a build-up of Lewy bodies in the neurons. http://en.wikipedia.org/wiki/Lewy_body I was just reading a study published in 2002 examining the brains of deceased individuals who had suffered from Parkinsons (no dementia), Dementia with Lewy Bodies (DLB), or Parkinson's Disease with Dementia (PDD). Of particular interest was the concentration and distribution of Lewy bodies (LB) in the brain and the relationship to (reported) hallucinations that the patient had suffered from while alive.
http://brain.oxfordjournals.org/cgi/content/full/125/2/391

..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.

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.

.. 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.

However, I was thinking of a more recent fMRI study when I originally posted the comment about Parkinson's and visual hallucinations:
http://neuro.psychiatryonline.org/cgi/content/abstract/18/3/402

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.

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]

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.

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

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.

I've seen it when I've been indoors, as well, often when I am looking at a sunbeam coming through a window.

 

[Revenged]

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.

lol... no problem...

You reminded me about levodopa - and it explains fairly simply why giving it to people with Parkinson's causes schizophrenia symptoms (like halluccinations)

Parkinson's => Too low levels of dopamine

Therefore to treat Parkinson's you want to increase the levels of dopamine in the body... The reason you don't give dopamine is that it cannot pass through the blood brain barrier (so can't pass into the central nervous system)... and this is why you give the lipid soluble precursor of dopamine, levodopa... and so it can pass through the blood brain barrier into the CNS where it is then metabolised to dopamine... so levodopa is a prodrug...

Schizophrenia => Too high levels of dopamine

And so if you give too much levodopa, you naturally will cause too much dopamine and therefore would cause the symptoms of schizophrenia...

Incidentally, the treatment of schizophrenia is simply to block dopamine receptors in the central nervous system - e.g. chlorpromazine blocks D2 receptors...

I can do a bit more detail about receptors... I've just had a quick glance at lecture notes...

There are basically two theories as to the mechanism behind halluccination causes...

1) Activation of the serotonin 2A receptor (5-HT2A)... LSD causes hallucinations by activation of this receptor...

2) Activation of the dopamine 2 (D2) receptor... This is the cause of schizophrenia...

I do warn that this is a complicated area of pharmacology... There are about 10 different types of dopamine and 10 different types of serotonin receptor... and that drugs such as chlorprozamine seem are very unspecific and block loads of receptors having multiple actions and multiple side effects...

 

[Nuklear]

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.

Yes I was looking at the sky and I was triped out cause I thought they were realy. I was 20 and that kind of thing had never happened to me.

 

[Math Is Hard]

Incidentally, the treatment of schizophrenia is simply to block dopamine receptors in the central nervous system - e.g. chlorpromazine blocks D2 receptors...

But doesn't chlorpromazine also block serotonin 5-HT2 receptors?

 

[Nuklear]

Well what are Serotonin and DOpamine's roles?

 

[Revenged]

But doesn't chlorpromazine also block serotonin 5-HT2 receptors?

Yes, you are correct... This is another way it will prevent hallucinations and it is another way anti-psychotics drugs work...

 

[Revenged]

Well what are Serotonin and DOpamine's roles?

I don't know what exactly you mean...

 

[braindred]

i usualy get the scheerer's phenomenon when having lack of oxygen, or after a brief moment of increast pressure in the head
just wanted to share that with you
oh and i once read a simple explanation to hallucinations(not imagined)
for example LSD, 'swiches' of your brains 'color' filter which makes the colors run around like rampage.
ofcourse this is over simplified but if someone cares to correct me or explain more detailed info on this 'filter', i would be happy to read

 

[Evo]

How Hallucinogens Play Their Mind-Bending Games

Researchers isolate cells affected by LSD and mescaline, potentially leading to more treatments for neurological and psychiatric disorders

"Zeroing in on a group of cells in a high layer of the cortex, a team of researchers from Mount Sinai School of Medicine, Columbia University and the New York State Psychiatric Institute may finally have found the cause of the swirling textures, blurry visions and signal-crossing synesthesia brought on by hallucinogenic drugs like LSD, peyote and "'shrooms." The group, which published its findings in this week's issue of Neuron, may have settled a long-simmering debate over how psychedelic drugs distort human perception."

http://www.sciam.com/article.cfm?articleID=7A553006-E7F2-99DF-3FC7BF289699B407

 

[braindred]

a great read, thanks

 

[Cincinnatus]

Interesting, can anyone find the Neuron article that Scientific American article is talking about?

 

[Pythagorean]

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.

My education is in physics, but I read this book called "The Minds of Men and Machines" that explained the architecture of the brain in terms of a computer. It basically said there's three types of brain function (input, computation, output). Equivalently (sensory, cognitive, muscles) I think.

Anyway, in these terms (If I have the theory right here) is hallucination a malfunction in sensory (input) or cognitive (computation) or both? Or do different types occur in different functions?

You may have answered this, but I don't understand a lot of the biological terms.

 

[denverdoc]

i think we need to clarify retinally produced images from those further downstream. The interesting thing about schizophrenia where people commonly experience auditory hallucinations, a rare event is a visual hallucination, the ilness affects the entire brain, but there is a combination of frontal lobe dysfunction (judgement, planning, etc) and relative overdrive from the temporal cortices, which among other things process auditory input. Whats more remarkable is that evoked cortical potentials--say a click in headphones or flash on a screen, show far less filtering. In other words if you heard two clicks spaced a few hundred millisec apart, the second is like a no-brainer. It registers but at a relatvely small amplitude, The brain is first and foremost a differential engine. But in the mind of a schizpprenis, that function is lost.