Neuropsychology

A craniotomy was performed to relieve the pressure, and afterwards another scan showed moderate hemorrhage and herpes encephalitis in the left temporal lobe, and another hemorrhage beneath the outer membrane (the dura) lying over the right frontal lobe.

During his 2 month stay there, he developed epileptic seizures which originated in the left temporal lobe, and amnestic aphasia (an inability to name objects or to recognize their written or spoken names). 

After the rehabilitation period, a series of linguistic tests was administered to determine the extent of his speech deficits. M.H. exhibited deficits in both languages, but the most severe deficits were seen only in Hebrew. In this language he had a severe difficulty in recalling words and names, so that his speech was non-fluent and interrupted by frequent pauses. He had difficulty understanding others' spoken Hebrew, and also had great difficulty reading and writing Hebrew. In Arabic, his native language, all of these abilities were affected only mildy.

The results support a neurolinguistic model in which the brain of bilinguals contains a semantic system (which represents word meanings) which is common to both languages and which is connected to independent lexical systems (which encode the vocabulary of each language). The findings further suggest that the second language (in this case, Hebrew) is represented by an independent subsystem which does not represent the first language (Arabic) and is more succeptible to brain damage.

The breakthrough came in 1972, when psychologist Jonathan Winson came up with a simple theory: The rabbit brain exhibited the same pattern of activity when it was scared and when it was dreaming because it was dreaming about being scared. The theta rhythm of sleep was just the sound of the mind processing information, sorting through the day's experiences and looking for any new knowledge that might be important for future survival. They were learning while dreaming, solving problems in their sleep.

Wilson began his experiment by training rats to run through mazes. While a rat was running through one of these labyrinths, Wilson measured clusters of neurons in the hippocampus with multiple electrodes surgically implanted in its brain. As he'd hypothesized, Wilson found that each maze produced its own pattern of neural firing. To figure out how dreams relate to experience, Wilson recorded input from these same electrodes while the rats were sleeping. The results were astonishing. Of the 45 rat dreams recorded by Wilson, 20 contained an exact replica of the maze they had run earlier that day. The REM sleep was recapitulating experience, allowing the animals to consolidate memory and learn new things. Wilson's lab has since extended these results, demonstrating that "temporally structured replay" occurs in both the hippocampus and visual cortex.

Both types of glia are closely integrated with the nervous system, receiving information from action potentials via synapses22 (which, only a few years ago were thought to be limited to neurons), and returning control of neuron activity through release of neurotransmitters and other modulators. Both, then, demonstrate the potential for considerable intelligent activity, contributing to the overall intelligence of the brain.

Astrocytes probably (IMO) are limited, or mostly so, to maintaining the supplies of energy and necessary metabolites. They receive action potentials,3, 6 which allows them to closely and quickly monitor general activity and increase circulation in response, even before the neurons and NG2-glia have reduced their supply of ATP.21 They appear to be linked in a network among themselves,2, 5 allowing them to communicate their needs without interfering with the higher-level calculations of the brain.

NG2-glia appear to have several functions, but one of the most exciting things about them is that they seem to be able to fire action potentials.33 Their cell membranes, like those of the dendrites of neurons, have all the necessary channels and receptors to perform real-time electrical calculations in the same way as neural dendrites. They have also demonstrated the ability to learn through long term potentiation.

Dividing NG2-glia also retain the ability to fire action potentials, as well as receiving synaptic inputs from neurons.23 Presumably, they continue to perform their full function, including retaining any elements of long term potentiation or depression contained in their synapses.

Oligodendrocytes are responsible for the insulation of the axons, wrapping around approximately 1 mm of each of up to 50 axons within their reach, and forming the myelin sheath.

Although the precise type of neuron formed by maturing cells hasn't been determined, the very fact that cells of this type can change into neurons is very important. We actually don't know whether the cells that do this maturation are the same as those that perform neuron-like activities, there appear to be two separate types of NG2-glia, spiking and non-spiking.26 It may very well be that the "spiking" type have actually differentiated, while the "non-spiking" type may be doing the maturing. Of course, very few differentiated cell types remain capable of division, as even the "spiking" type do.

What's important about both dendrites and NG2-glia isn't so much their ability to propagate action potentials, as that their entire cell membranes are capable of "intelligent" manipulation of the voltage across it.

While there are many ion channels involved in controlling the voltage across the cell membrane, the only type we really need to worry about for action potentials is voltage-gated sodium channels. These are channels that sometimes allow sodium ions to pass through the cell membrane, which they will do because the concentration of sodium ions outside the cell is very much higher than inside. When and how much they open depends, among other things, on the voltage across the membrane.

A normal neuron will have a voltage of around -60 to -80mV (millivolts), in a direction that tends to push the sodium ions (which are positive) into the cell (the same direction as the concentration is pushing). When the voltage falls to around -55mV, the primary type of gate will open for a millisecond or so, after which it will close and rest for several milliseconds. It won't be able to open again until the voltage is somewhere between -55 and around -10mV. Meanwhile, the sodium current has caused the voltage to swing past zero to around +20mV.

When one part of the cell membrane is "depolarized" in this fashion, the voltage near it is also depressed. Thus, if the voltage is at zero at one point, it might be at -20mV 10 microns (μm) away, and -40mV 20μm away, and -60mV 30μm, and so on. Notice that somewhere between 20μm and 30μm, it has passed the threshold for the ion channels, which means that they are open, allowing a current that drives the voltage further down. This will produce a wave of voltage drop along the membrane, which is what the action potential is.

After the action potential has passed, and the gates have closed (see above), the voltage is recovered by diffusion of ions towards and away from the membrane, the opening of other gates (primarily potassium), and a set of pumps that push the ions back to their resting state. These pumps are mostly powered by the sodium gradient, except for the sodium/potassium pump that maintains it, which is powered by ATP.

the vast majority of calculation that goes into human intelligence takes place at the level of the network of dendrites and NG2-glia, with the whole system of axons, dendrites, and action potentials only carrying a tiny subset of the total information over long distances. This is especially important considering that the human brain has a much higher proportion of glial matter than our relatives.

This, in turn, suggests that our overall approach to understanding the brain has been far too axon centric, there needs to be a shift to a more membrane-centric approach to understanding how the brain creates intelligence.