Savant Syndrome

Here is a short video of someone with savant syndrome. It is rather mind boggling.

http://video.stumbleupon.com/#p=0k4lsi1dql

Apparently, some normal people get extraordinary abilities when parts of their brains are switched off.

http://www.bbc.co.uk/worldservice/sci_tech/highlights/010312_autism.shtml

(I don't think I would have volunteered for that experiment)!

Here is an article in Discover Magazine--

http://discovermagazine.com/2002/feb/featsavant

Interesting stuff.

about 20 years ago which I think was when a book of his drawings was first published. To me the most remarkable was the interior of St Pauls Cathederal. An architect was quoted as saying the Stephen's freehand vaulted arches were perfect and would've taken an experienced draughtsman some weeks to contruct.

Here's his website : http://www.stephenwiltshire.co.uk/

are these brain structures that prevent savantism selected for? Put another way, does "non-savantism" confer any survival advantages, or does savantism cause survival liabilities? Is non-savantism an accidental by-product of some other brain adaptation?

Cognitive psychologists have known for years that the main way that you process information is from the bottom up. Some cells in your eye and then your brain percieve every little line of an image. Some cells will fire only in the presence of a line at a specific angle say a / . All of these little bits of information are combined into a broader picture in your visual cortex, and then other processing takes place to consult with memory and contextual cues, etc etc, and verbal areas, etc and then you look at it and say "dog" or whatever the hell it is.

Basically savantism according to this article, is the malfunction of a few "centers" in your brain, perhaps located in the left temporal lobe, that prevents that whole part about you understanding that it's a dog, and what are dogs about? is it a dangerous dog? I have a dog, how is it like my dog? I wonder why the dog has white paws, etc etc etc. So basically savants, according to this theory, are missing higher levels of processing, or can simply not use them to the same degree. Think of your computers web camera: it can see every little line and translate that into code and perform calculations on it, etc etc... but it can't fit the pictures into a broader context.

Not a pretty view of savantism but it definately makes sense.

I wonder why those lucky few haven't displayed a selective advantage. Come to think of it, maybe it's a developmental phenomenon, not genetic. In that case, it would not be heritable.

Great way to gain a greater understanding of the brain, but the ethics of this are highly questionable.

If you have epilepsy using magnets to get your brain to tone down neuronal activity could be a good treatment as epilepsy can cause damage and has dramatic detrimental impact on the patient.

However, neurons have been known to kill themselves when their normal functions are disturbed. This neuronal apoptosis is a normal and integral part of keeping you from developing things like epilepsy (which is basically overactivity, and improper connectivity of the brain). The neuron actually comes equipped with specific genes and proteins designed to know when to, and how to kill itself. When we start out in life we have millions more neurons than we "need". By talking with each other and with supportive neurons like astrocytes, the more "advanced" neurons know that they're doing their thing, and that they're not full of craziness (to put it in english). Screw with that and you risk permanent, irreversible, changes to the brain. Magnetic suppression basically works by keeping neurons from firing. Neurons that don't fire action potentials, could to my understanding not be telling their supportive astrocytes to feed them beneficial chemicals and to regulate their environment appropriately. They could also form the wrong connections, and lose the right connections that they do have. And fairly quickly too! You learn because your brain is constantly rewiring itself! When a neuron makes a completely wrong connection it can choose to take itself out of the picture. Think "Error Error Does Not Compute - Self destruct sequence initiated".

I don't like this one bit except in extreme cases. To my thinking this is like giving Chemotherapy to patients who don't have cancer!


Here's on on neuronal apoptosis and an explanation of a couple mechanisms. Not that the chemical pathways are already present in the neuron itself.

http://www.le.ac.uk/mrctox/MRCTox/research/nicotera/research_mech_neuronal_apoptosis.htm

"Astrocytes are the major cell type in the brain. Recent
studies have revealed that they not only receive signals
from neurons but also release neuroactive substances1 and
provide energy substrates to neurons.2 Moreover, glial cells
secrete various neurotrophic factors and cytokines that stimulate
and protect neurons against oxidative stress.3 In the
central nervous system, astrocytes establish a glial syncytium
through intercellular connection via gap junctions.4 Connexin
43 (Cx43) is the primary component protein in astrocytic gap
junctions.5 Gap junctional intercellular communication
(GJIC) mediates electronic coupling and permits rapid propagation
among cell networks.6 GJIC between astrocytes may
regulate the concentration of extracellular K1 and distribute
neurotransmitters.7 According to these contexts, astrocytes
play an important role in neuronal support in both normal and
pathological conditions.
Stroke lesion increases"

http://stroke.ahajournals.org/cgi/reprint/01.STR.0000079814.72027.34v1.pdf

And more:

A massive neuronal loss during early postnatal development has been well documented in the murine cerebral cortex, but the factors that drive cells into apoptosis are largely unknown. The role of neuronal activity in developmental apoptosis was studied in organotypic neocortical slice cultures of newborn mice. Multielectrode array and whole-cell patch-clamp recordings revealed spontaneous network activity characterized by synchronized burst discharges, which could be blocked by tetrodotoxin and ionotropic glutamate receptor antagonists. The identical neuropharmacological manipulations also caused a significant increase in the number of apoptotic neurons as early as 6 h after the start of drug treatment. Moreover, inhibition of the NMDA receptor subunit NR2A or NR2B induced a differential short-term versus delayed increase in the apoptosis rate, respectively. Activation of L-type, voltage-dependent calcium channels was neuroprotective and could prevent activity-dependent apoptosis during NMDA receptor blockade. Furthermore, this effect involved phosphorylation of cAMP response element–binding protein and activation of the tropomyosin-related kinase (Trk) receptors. Inhibition of electrical synapses and blockade of ionotropic -aminobutyric acid receptors induced specific changes in spontaneous electrical activity patterns, which caused an increase in caspase-3–dependent cell death. Our results demonstrate that synchronized spontaneous network bursts activating ionotropic glutamate receptors promote neuronal survival in the neonatal mouse cerebral cortex.

http://cercor.oxfordjournals.org/cgi/content/abstract/18/6/1335