Mind and Meaning

psydoctor8:

This would be one sad neuro blog if I didn’t mention researchers from the University of California, Berkeley, “using fMRI and computational models, were able to decipher and reconstruct movies from our minds” by associating brain activity of subjects with the video being viewed, piecing it together and replaying it.

Watch that video. Amazing. And blurry. Here’s what it means:

While watching the first set of trailers, the fMRI measured blood flow through the visual cortex and this information was directed to a computer, which portrayed the brain as tiny three-dimensional cubes called “voxels,” or volumetric pixels. For each voxel, there was a model that detailed how motion and shapes in the movie are translated into brain activity. The computer program learned to relate visual patterns in the trailers with corresponding brain activity.  Via
“…the technology can only reconstruct movie clips people have already viewed. However, the breakthrough paves the way for reproducing the movies inside our heads that no one else sees, such as dreams and memories, according to researchers.” Via

A highly technical and creative experiment showing an interpretation of what our brain “sees” so that one day we may be able to see what is going on in the minds of non verbal patients, e.g. coma, stroke or severe autism.

Source, Journal Article

We have always been told there is no recovery from persistent vegetative state - doctors can only make a sufferer’s last days as painless as possible. But is that really the truth? Across three continents, severely brain-damaged patients are awake and talking after taking … a sleeping pill. And no one is more baffled than the GP who made the breakthrough. Steve Boggan witnesses these ‘strange and wonderful’ rebirths

No one yet knows exactly how a sleeping pill could wake up the seemingly dead brain cells, but Nel and Clauss have a hypothesis. After the brain has suffered severe trauma, a chemical known as Gaba (gamma amino butyric acid) closes down brain functions in order to conserve energy and help cells survive. However, in such a long-term dormant state, the receptors in the brain cells that respond to Gaba become hypersensitive, and as Gaba is a depressant, it causes a persistent vegetative state.

It is thought that during this process the receptors are in some way changed or deformed so that they respond to zolpidem differently from normal receptors, thus breaking the hold of Gaba. This could mean that instead of sending patients to sleep as usual, it makes dormant areas of the brain function again and some comatose patients wake up.

Wow.

fuckyeahneuroscience:

Bradley VoytekPh.D.:

‘This is such a great question. It’s fun when I realize I know something that, when I really think about it makes me go, “huh”.

The “wrinkles” are known as gyri and sulci, with the gyri being the actual brain tissue and the sulci being the fissues between gyri. (By the way, the singular forms of those words are “gyrus” and “sulcus”).

While neuroanatomical textbooks will often show a nice “regular” brain with clearly defined features such as the central sulcus:

In reality these features can be quite difficult to find on a real brain. So much so, that neurosurgeons will perform electrical stimulation mapping of awake people if they have to remove any brain tissue near what they call “eloquent cortex” (which is not a neuroanatomical term, by the way). Eloquent cortex is defined quite well by wikipedia:

Eloquent cortex is a name used by neurologists for areas of cortex that—if removed—will result in loss of sensory processing or linguistic ability, minor paralysis, or paralysis. The most common areas of eloquent cortex are in the left temporal and frontal lobes for speech and language, bilateral occipital lobes for vision, bilateral parietal lobes for sensation, and bilateral motor cortex for movement.

(Or, as I like to define it, the “cut here and the doc’ll be sued” cortex, or, more simply: malpractice cortex.)

The only way even an experienced surgeon can be sure that specific brain area in a specific person is motor, or speech, or sensory, is via this mapping technique.

This is because, although gross neuroanatomical features are generally conserved across people, there can be a huge range of variation. For example, in the frontal lobes, there are usually three longitudinal gyri: inferior, middle, and superior:


I’ve seen people with a whole extra fourth gyrus just stuck right in there. Totally surprising! What is that?!

The “best practice” way of determining boundaries between cortical brain regions is by examining the cellular composition of those regions. This was first done by Korbinian Brodmann wherein he defined separations now known as “Brodmann’s areas”:

(Source: Mark Dow - University of Oregon (http://lcni.uoregon.edu/~mark/))

Thanks for the question!’

A Cradle for Rest – R. Matthew Hutchison The image shows homologous cortical resting-state networks of the  macaque, identified by independent component analysis, inflated and  wrapped onto spheres. The functional networks are arranged to resemble  Newton’s cradle, an apparatus classically used to demonstrate  conservation of momentum.
That’s the original caption from this amazing neuroscience art image from the 2011 NeuroBureau Brain Art Competition.  There are four categories:  Abstract, 3-D, Connectome, and Humorous.  Each category has entries which combine startling creativity, cutting edge imaging, and artistic vision.  Click on the link to see the other entries.  Clicking the photo takes you to the original image.

A Cradle for Rest – R. Matthew Hutchison

The image shows homologous cortical resting-state networks of the macaque, identified by independent component analysis, inflated and wrapped onto spheres. The functional networks are arranged to resemble Newton’s cradle, an apparatus classically used to demonstrate conservation of momentum.

That’s the original caption from this amazing neuroscience art image from the 2011 NeuroBureau Brain Art Competition.  There are four categories:  Abstract, 3-D, Connectome, and Humorous.  Each category has entries which combine startling creativity, cutting edge imaging, and artistic vision.  Click on the link to see the other entries.  Clicking the photo takes you to the original image.

houseofmind:

The Science of Sleep: A Focus on REM Sleep and Dreaming
(Click on the image for a better view)
As anybody who was gone without sleep for a couple of days would know, sleep is essential for mental health and adequate cognitive function. Regulation of the sleep cycle (and consciousness states) is influenced by monoamines (i.e. serotonin, noradrenaline, histamine, dopamine) and their interaction with cholinergic neurons in the brainstem. There are 3 types of transitions in consciousness identifiable in the human brain: waking, rapid eye movement (REM) sleep and non-rapid eye movement (NREM) sleep. Sleep, particularly REM sleep, has been suggested to be important for brain development by contributing to plasticity processes in the brain and is also implicated in memory processing (i.e. state dependent memory consolidation). 
REM sleep is sleep that results in brain activation, as indexed by electroencephalographic evidence, but with inhibition of muscle tone and (involuntary) saccadic eye movements. REM sleep is regulated by two distinct neuronal populations:
REM-off cells: Active during waking and inactive during REM sleep. Located in the locus coeruleus and the dorsal raphe nucleus and usually serotonergic/noradrenergic neurons.
REM-on cells: Inactive during waking and active during REM sleep. Located primarily in the mesopontine tegmentum and usually cholinergic neurons). 
As indicated above, REM sleep is controlled by the brainstem pontine nuclei and is potentiated by cholinergic mechanisms (REM-on)  while being suppressed by aminergic mechanisms (REM-off). Thus, transitions in states of consciousness (i.e. wakefulness, NREM, REM) are the result of these neuromodulatory neurotransmitter interactions in the “sleep centers” of the brain.
REM sleep is also characterized by the minimal levels of inhibition present in the brain during this stage.REM sleep activates phasic signals (PGO waves) in the pontine brainstem (P), the lateral geniculate body of the thalamus (G), and the occipital cortex (O), which are also prominent in the visual system and in sensorimotor systems in the forebrain. PGO waves are thought to help maintenance of sleep by occluding external sensory input in addition to fostering sensorimotor integration that may be important for perception and motor control. 
Evidence from neuroimaging studies have found increased activation (as indexed by blood flow increases) in several brain areas during REM sleep. These include: the pons, the midbrain, the thalamus and hypothalamus, the amygdala and the basal ganglia, shown below in an image taken from Hobson & Schott (2002) that illustrates differential brain activation during wake-sleep states. It is important to also keep in mind that REM sleep (along with dreaming occuring during REM) induces activation in the forebrain through ascending arousal systems and that this activation is aminergically deficient and cholinergically driven, as depicted in the image above.

For a long period of time, REM sleep was thought of as the “sleep substrate” of dreaming, which may have been due to the higher reports of dreaming sequences during REM sleep compared to NREM sleep. A popular model that dominated the field was Hobson’s Activation-Hypothesis Model, which stated that dreams are actively generated by the brainstem and passively synthesized by the forebrain. However, there is growing evidence supporting the notion that REM sleep and dreaming are dissociable states controlled by different neural mechanisms: REM sleep by cholinergic mechanisms in the brain stem and dreaming sequences via dopaminergic mechanisms in the forebrain. In his 2000 review, Solms lists several of the arguments in favor of this REM sleep-dream association. Some of these are:
REM sleep is not controlled by forebrain mechanisms: Classical studies (Jouvet, 1962) have shown that the forebrain is both incapable of and unnecessary for generating REM sleep. 
Not all dreaming is correlated with REM sleep: REM can occur in the absence of dreaming and dreaming can occur in the absence of REM sleep (NREM). 
Dreaming is preserved in subjects with large pontine brain stem lesions: Manifestations of REM sleep, however, are eliminated. Dreaming is only eliminated when components of both REM and NREM sleep are ablated. 
Dreaming is eliminated by forebrain lesions that completely spare the brainstem: These lesions were typically in the parieto-temporo-occipital (PTO) junction, a region that supports several cognitive processes vital for the construction of mental imagery. However, the REM sleep cycle is preserved. 
Dreams are actively generated by forebrain mechanisms unrelated to REM sleep. The dopaminergic innervation in these forebrain networks originates from the VTA, the source of mesocortical/mesolimbic dopamine. Descending components of these loops come from latter brain areas that are heavily influenced by cholinergic circuit activity. Chemical activation of this dopamine circuit through L-dopa has been shown to promote psychotic symptoms and increase dreaming, which suggests a causal relationship between mesolimbic/mesocortical DA and dreaming.
Dreams are generated by a specific network of forebrain structures: It has been postulated that dreaming involves concerted activity in highly specific group of forebrain structures which include: anterior and lateral hypothalamic areas, the amygdaloid complex, septal-ventral striatal areas, as well as infralimbic, prelimbic, orbitofrontal, anterior cingulate, entorhinal, insular and occipitotemporal cortical areas. Considering all the implicated areas, the construction of imagery during dreaming is a complex cognitive process. 
To sum up, dreaming seems to require: 1) brain activation (not necessarily REM sleep) along with the 2) engagement of specific dopamine circuits in the forebrain that initiate dreaming.
Sources: 
Hobson, J.A. 2009. REM sleep and dreaming: Towards a theory of protoconsciousness. Nature Reviews Neuroscience. 10: 803-813. doi:10.1038/nrn271
Hobson, J.A. & Pace-Schott, EF. 2002. The cognitive neuroscience of sleep: neuronal systems, consciousness and learning. Nature Reviews Neuroscience. 3 (9): 679-693. doi:10.1038/nrn915
Solms, Mark. 2000. Dreaming and REM sleep are controlled by 2 different brain mechanisms. Behavioral and Brain Sciences. 23: 843-850. 

Nice article on sleep via HouseOfPain’s Tumblr.

houseofmind:

The Science of Sleep: A Focus on REM Sleep and Dreaming

(Click on the image for a better view)

As anybody who was gone without sleep for a couple of days would know, sleep is essential for mental health and adequate cognitive function. Regulation of the sleep cycle (and consciousness states) is influenced by monoamines (i.e. serotonin, noradrenaline, histamine, dopamine) and their interaction with cholinergic neurons in the brainstem. There are 3 types of transitions in consciousness identifiable in the human brain: waking, rapid eye movement (REM) sleep and non-rapid eye movement (NREM) sleep. Sleep, particularly REM sleep, has been suggested to be important for brain development by contributing to plasticity processes in the brain and is also implicated in memory processing (i.e. state dependent memory consolidation). 

REM sleep is sleep that results in brain activation, as indexed by electroencephalographic evidence, but with inhibition of muscle tone and (involuntary) saccadic eye movements. REM sleep is regulated by two distinct neuronal populations:

  • REM-off cells: Active during waking and inactive during REM sleep. Located in the locus coeruleus and the dorsal raphe nucleus and usually serotonergic/noradrenergic neurons.
  • REM-on cells: Inactive during waking and active during REM sleep. Located primarily in the mesopontine tegmentum and usually cholinergic neurons). 

As indicated above, REM sleep is controlled by the brainstem pontine nuclei and is potentiated by cholinergic mechanisms (REM-on)  while being suppressed by aminergic mechanisms (REM-off). Thus, transitions in states of consciousness (i.e. wakefulness, NREM, REM) are the result of these neuromodulatory neurotransmitter interactions in the “sleep centers” of the brain.

REM sleep is also characterized by the minimal levels of inhibition present in the brain during this stage.REM sleep activates phasic signals (PGO waves) in the pontine brainstem (P), the lateral geniculate body of the thalamus (G), and the occipital cortex (O), which are also prominent in the visual system and in sensorimotor systems in the forebrain. PGO waves are thought to help maintenance of sleep by occluding external sensory input in addition to fostering sensorimotor integration that may be important for perception and motor control. 

Evidence from neuroimaging studies have found increased activation (as indexed by blood flow increases) in several brain areas during REM sleep. These include: the pons, the midbrain, the thalamus and hypothalamus, the amygdala and the basal ganglia, shown below in an image taken from Hobson & Schott (2002) that illustrates differential brain activation during wake-sleep states. It is important to also keep in mind that REM sleep (along with dreaming occuring during REM) induces activation in the forebrain through ascending arousal systems and that this activation is aminergically deficient and cholinergically driven, as depicted in the image above.

nrn915-f4.gif

For a long period of time, REM sleep was thought of as the “sleep substrate” of dreaming, which may have been due to the higher reports of dreaming sequences during REM sleep compared to NREM sleep. A popular model that dominated the field was Hobson’s Activation-Hypothesis Model, which stated that dreams are actively generated by the brainstem and passively synthesized by the forebrain. However, there is growing evidence supporting the notion that REM sleep and dreaming are dissociable states controlled by different neural mechanisms: REM sleep by cholinergic mechanisms in the brain stem and dreaming sequences via dopaminergic mechanisms in the forebrain. In his 2000 review, Solms lists several of the arguments in favor of this REM sleep-dream association. Some of these are:

  1. REM sleep is not controlled by forebrain mechanisms: Classical studies (Jouvet, 1962) have shown that the forebrain is both incapable of and unnecessary for generating REM sleep. 
  2. Not all dreaming is correlated with REM sleep: REM can occur in the absence of dreaming and dreaming can occur in the absence of REM sleep (NREM). 
  3. Dreaming is preserved in subjects with large pontine brain stem lesions: Manifestations of REM sleep, however, are eliminated. Dreaming is only eliminated when components of both REM and NREM sleep are ablated. 
  4. Dreaming is eliminated by forebrain lesions that completely spare the brainstem: These lesions were typically in the parieto-temporo-occipital (PTO) junction, a region that supports several cognitive processes vital for the construction of mental imagery. However, the REM sleep cycle is preserved. 
  5. Dreams are actively generated by forebrain mechanisms unrelated to REM sleep. The dopaminergic innervation in these forebrain networks originates from the VTA, the source of mesocortical/mesolimbic dopamine. Descending components of these loops come from latter brain areas that are heavily influenced by cholinergic circuit activity. Chemical activation of this dopamine circuit through L-dopa has been shown to promote psychotic symptoms and increase dreaming, which suggests a causal relationship between mesolimbic/mesocortical DA and dreaming.
  6. Dreams are generated by a specific network of forebrain structures: It has been postulated that dreaming involves concerted activity in highly specific group of forebrain structures which include: anterior and lateral hypothalamic areas, the amygdaloid complex, septal-ventral striatal areas, as well as infralimbic, prelimbic, orbitofrontal, anterior cingulate, entorhinal, insular and occipitotemporal cortical areas. Considering all the implicated areas, the construction of imagery during dreaming is a complex cognitive process. 

To sum up, dreaming seems to require: 1) brain activation (not necessarily REM sleep) along with the 2) engagement of specific dopamine circuits in the forebrain that initiate dreaming.

Sources: 

Hobson, J.A. 2009. REM sleep and dreaming: Towards a theory of protoconsciousness. Nature Reviews Neuroscience. 10: 803-813. doi:10.1038/nrn271

Hobson, J.A. & Pace-Schott, EF. 2002. The cognitive neuroscience of sleep: neuronal systems, consciousness and learning. Nature Reviews Neuroscience. 3 (9): 679-693. doi:10.1038/nrn915

Solms, Mark. 2000. Dreaming and REM sleep are controlled by 2 different brain mechanisms. Behavioral and Brain Sciences. 23: 843-850. 

Nice article on sleep via HouseOfPain’s Tumblr.

Here’s a pointer to an article on the science behind the concept of the self. Posted on Edge.org, the article, by V. S. Ramachandran, finds the genesis of the self in mirror neurons.

Some of the initial (over?) enthusiasm about mirror neurons has died down. But Ramachandran raises some interesting points in favor of mirror neurons playing a role in the development of a self, even if the self can’t be attributed solely to them.

cognizingconsciousness:

Nervous System Stem Cells Can Replace Themselves, Give Rise to Variety of Cell Types, Even Amplify

A Johns Hopkins team has discovered in young adult mice that a lone brain stem cell is capable not only of replacing itself and giving rise to specialized neurons and glia – important types of brain cells – but also of taking a wholly unexpected path: generating two new brain stem cells.
A report on their study appears June 24 in Cell.
Although it was known that the brain has the capacity to generate both neurons, which send and receive signals, and the glial cells that surround them, it was unclear whether these various cell types came from a single source. In addition to demonstrating that a single radial glia-like (RGL) brain cell is able to generate two very different functional cell types, the Hopkins researchers, by following the fates of single cells over time, found that a single brain stem cell can even produce two stem cells like itself.
“Now we know they don’t just maintain their numbers, or go down in number, but that stem cells can amplify,” says Hongjun Song, Ph.D., professor of neurology and neuroscience and director of the Stem Cell Program in the Institute for Cell Engineering, the Johns Hopkins University School of Medicine. “If we can somehow cash in on this newly discovered property of stem cells in the brain, and find ways to intervene so they divide more, then we might actually increase their numbers instead of losing them over time, which is what normally happens, perhaps due to aging or diseases.”
The researchers’ findings hinged on a decision to single out and follow lone, radial glia-like cells, instead of labeling and monitoring entire stem cell populations in the mouse brain. They took this approach because they suspected radial glia-like cells were essentially stem cells, having been shown in previous studies to give rise to neurons.
Using mice genetically modified with special genes that color-code cells for easy labeling and tracking, the Hopkins team injected a very small amount of a chemical into about 50 mouse brains to induce extremely limited cell labeling.
“It’s a simple idea that forced us to confront a lot of complex technical issues,” Song says. “With so many millions of cells in the relatively large mouse brain, labeling a single stem cell and then chasing its family history was like finding a needle in a haystack.”
The scientists developed computer programs and devised a new imaging technique that allowed them to examine stained slices of the mouse brain and, ultimately, follow single, randomly chosen radial glia-like stem cells over time. The method allowed them to track down all the new cells derived from a single original stem cell.
“We reconstituted single stem cells’ family trees to look at the progeny they gave rise to,” says Guo-li Ming, associate professor of neurology and neuroscience and a member of the Neuroregeneration Program in the Institute for Cell Engineering. “We discovered that single cells in an intact animal nervous system absolutely do exhibit stem-cell properties; they are capable of both replicating themselves and producing different types of differentiated neural progeny.”
The team followed the fates of all the marked radial glia-like stem cells for at least a month or two, and examined some a full year later to discover that even over the long term, the “mother” cell was still generating itself as well as different kinds of progeny.
In addition, the researchers investigated how these RGLs were activated on a molecular level, focusing, in particular, on the regulatory role of an autism-associated gene called PTEN. Conventional wisdom was that deleting this gene led to an increase in stem-cell activation. However, the scientists demonstrated that was a transient effect in the mouse brains, and that, ultimately, PTEN deletion leads to stem-cell depletion.
(Johns-Hopkins)

Interesting finding about neural cells’ ability to clone themselves and even change cell types.  From CognizingConsciousness.

cognizingconsciousness:

Nervous System Stem Cells Can Replace Themselves, Give Rise to Variety of Cell Types, Even Amplify

A Johns Hopkins team has discovered in young adult mice that a lone brain stem cell is capable not only of replacing itself and giving rise to specialized neurons and glia – important types of brain cells – but also of taking a wholly unexpected path: generating two new brain stem cells.

A report on their study appears June 24 in Cell.

Although it was known that the brain has the capacity to generate both neurons, which send and receive signals, and the glial cells that surround them, it was unclear whether these various cell types came from a single source. In addition to demonstrating that a single radial glia-like (RGL) brain cell is able to generate two very different functional cell types, the Hopkins researchers, by following the fates of single cells over time, found that a single brain stem cell can even produce two stem cells like itself.

“Now we know they don’t just maintain their numbers, or go down in number, but that stem cells can amplify,” says Hongjun Song, Ph.D., professor of neurology and neuroscience and director of the Stem Cell Program in the Institute for Cell Engineering, the Johns Hopkins University School of Medicine. “If we can somehow cash in on this newly discovered property of stem cells in the brain, and find ways to intervene so they divide more, then we might actually increase their numbers instead of losing them over time, which is what normally happens, perhaps due to aging or diseases.”

The researchers’ findings hinged on a decision to single out and follow lone, radial glia-like cells, instead of labeling and monitoring entire stem cell populations in the mouse brain. They took this approach because they suspected radial glia-like cells were essentially stem cells, having been shown in previous studies to give rise to neurons.

Using mice genetically modified with special genes that color-code cells for easy labeling and tracking, the Hopkins team injected a very small amount of a chemical into about 50 mouse brains to induce extremely limited cell labeling.

“It’s a simple idea that forced us to confront a lot of complex technical issues,” Song says. “With so many millions of cells in the relatively large mouse brain, labeling a single stem cell and then chasing its family history was like finding a needle in a haystack.”

The scientists developed computer programs and devised a new imaging technique that allowed them to examine stained slices of the mouse brain and, ultimately, follow single, randomly chosen radial glia-like stem cells over time. The method allowed them to track down all the new cells derived from a single original stem cell.

“We reconstituted single stem cells’ family trees to look at the progeny they gave rise to,” says Guo-li Ming, associate professor of neurology and neuroscience and a member of the Neuroregeneration Program in the Institute for Cell Engineering. “We discovered that single cells in an intact animal nervous system absolutely do exhibit stem-cell properties; they are capable of both replicating themselves and producing different types of differentiated neural progeny.”

The team followed the fates of all the marked radial glia-like stem cells for at least a month or two, and examined some a full year later to discover that even over the long term, the “mother” cell was still generating itself as well as different kinds of progeny.

In addition, the researchers investigated how these RGLs were activated on a molecular level, focusing, in particular, on the regulatory role of an autism-associated gene called PTEN. Conventional wisdom was that deleting this gene led to an increase in stem-cell activation. However, the scientists demonstrated that was a transient effect in the mouse brains, and that, ultimately, PTEN deletion leads to stem-cell depletion.

(Johns-Hopkins)

Interesting finding about neural cells’ ability to clone themselves and even change cell types. From CognizingConsciousness.

neurolove:

  This is a neuron labeled blue for tubulin, green for F-actin, and red for presynaptic protein. Basically, these are all structural parts of a neuron that create its location in space and in relation to other neurons. Tubulin makes up microtubules. Microtubules and actin are the main components of the cytoskeleton (cell skeleton- does the same thing for cells as your bones do for you). Presynaptic proteins are located at the synapses with other cells and serve a variety of functions- here, you can see how many synapses this neuron has with other neurons by the clusters or spots of ‘red’.

[Image Source]

neurolove:

This is a neuron labeled blue for tubulin, green for F-actin, and red for presynaptic protein. Basically, these are all structural parts of a neuron that create its location in space and in relation to other neurons. Tubulin makes up microtubules. Microtubules and actin are the main components of the cytoskeleton (cell skeleton- does the same thing for cells as your bones do for you). Presynaptic proteins are located at the synapses with other cells and serve a variety of functions- here, you can see how many synapses this neuron has with other neurons by the clusters or spots of ‘red’.

[Image Source]

As determined by readers of Dana.org, which is associated with Cerebrum.  The list is broken down into 10 categories.  It was tallied at the end of 2010, though, so you won’t find some of the latest books listed.  Damasio’s Self Comes to Mind, isn’t on it, for instance, while his earlier Looking for Spinoza is. 

These aren’t technical neuroscience texts but books written for a broader audience by authors like Eric Kandel, Gerard Edelman, Jonah Lehrer, etc.  The most difficult may be Gyorgi Buzsaki’s Rhythms of the Brain, which I’m finding a bit slow going. 

Anyway, some interesting books to add to the pile of things to read.  Some good finds, a couple of surprises.  To whet your appetite, here are the categories:

  1. General Books About the Brain
  2.  Neuropharmacology and Brain Chemistry
  3. Development and Life Span
  4. Cognition, Learning, and Memory
  5. Consciousness
  6. The Senses
  7. Emotion and Behavior
  8. Diseases and Disorders
  9. Memoirs and Personal Experience
  10. The Brain in Relation to Other Fields.

 Something for everyone—

 

Split brain with one half atheist and one half theist (by wimsweden).

Neurologist VS Ramachandran explains to the ‘06 Beyond Belief Conference the case of a split-brain patient who has one hemisphere that believes in God and the other that doesn’t.

Could this be indicative of the cognitive dissonance of a person of faith who struggles with doubt? Makes you wonder…