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Understanding the Brain in the 21st(3)

时间:2006-03-09 15:48来源:royalsoc.org 作者:bioguider 点击: 1961次

There is another exiting component to the claim that neuroscience is going to dominate research in the 21st Century. it is that a deeper knowledge of the nervous system will lead to the alleviation of neurological diseases whether this occurs through developmental malfunction, through injury, or through for example the invasion of our brains by a particular virus as probably occurs in multiple sclerosis. The inferior temporal lobe which we are emphasising in this essay is involved in the identification of an object. A vascular stroke results in the destruction of certain parts of our brains. Hypertension leads to a breakdown of the vasculature most commonly in certain areas of our brain. One area in which hypertension most commonly leads to stroke is in the temporal lobe where, as we have seen, information is gathered about the identification of objects and our consciousness of them. Figure 7 shows a self portrait of a painter that suffered a stroke. The stroke occurred in the parietal cortex concerned with the location of an object in space. However the parietal cortex is not only concerned with location and movement but it also subserves the process of attention. There is a mechanism in the parietal cortex which determines which sets of neurones will fire off in phase at 40 to 50Hz throughout the rest of the cortex. The stroke had the effect of blocking the attentional mechanisms in the inferior temporal lobe on one side of the brain so that the painter was not able to recognize one side of his face when he looked in the mirror. This did not occur because there had been a direct injury to the temporal lobe. Rather it occurred because the attentional mechanism in the parietal cortex on one side of the brain could not determine that the temporal lobe on that side should contain neurones that fired in phase at 40 to 50Hz. As a consequence when he was asked to paint a portrait of himself the painter ignored that side of his body which was no longer attended to because of the stoke. He then only painted one side of his body (figure 7). But over a period of about 12 months successive self portraits gradually reconstituted the entire image until finally, after a year, he was able to attend to the entire aspect of his face (figure 7), although recovery is not complete even then.

I emphasise the fact that the reason our painter was unable to see, as it were, one side of his face and body when he did a self portrait a few weeks after the stroke was not due to any injury whatever to the visual pathway. what had been injured was the mechanism in parietal cortex which determine the setting up of 40 to 50HZ in phase firing of neurones which then allows consciousness to be expressed. An easy experiment could be carried out to show You that he could see the other side of his body. All that had to be done was to block off that side of the painter's visual field which allowed him to see the side of his body which he could normally paint. When that occurs he wills tart painting the side of his body and face that he normally doesn't attend to at all. In other words it is the attentional mechanism that has been injured. In fact when some experience a lesion of this kind they don't want to know about the side of their body to which they re not attending. When you carry out this experiment with some people who have had a stroke affecting the parietal cortex they get emotionally upset when they are forced to attend to that part of their body that they don't normally recognize as being there. In fact they regard that part of their body as foreign. It is as if they had a Siamese twin attached to them which they did not want to know about.

Strokes which affect the temporal cortex subserving the actual mechanisms by which you recognize yourself and others is usually accompanied by different kinds of psychological disturbances. Injuries to temporal cortex give rise to epileptic seizures (figure 8). This is because temporal cortex is very closely associated with the hippocampus which is the area of your brain concerned with laying down memory. For example injury to temporal cortex may lead to hallucinations that can involve you seeing people or objects that aren't present in the room (figure 8). This is due to epileptic discharges in the neurones of the temporal cortex which, for example, are normally activated by the image of your mother's face but start to fire despite the fact that your mother is not passing through the room at all. So hallucinations are associated with injuries to temporal cortex and of course hallucinations are also associated with schizophrenia (figure 8). In this case subjective phenomena apparently occur in the room that are more real to a person than sets of phenomena which are really occurring in the room. other forms of temporal lobe epileptic activity occurring as a consequence of stroke in the temporal lobe area are seizures which give rise to the sudden enlargement of the face of someone that you are looking at (figure 8). You may be looking at your mother in the room and then suddenly her face will start to increase in size, become distorted, and fill up the entire room (figure 8). So there are not just perceptions of events occurring in the room which ar not occurring at all but real events in the room may trigger hallucinogenic kinds of phenomena in the way 1 have just indicated, that is they will distort phenomena in the room as well.

Common seizure patterns
Clinical Type Localization
1 Somatic Motor:
Jacksonian (local motor) Prerolandic gyrus
Masticatory Amygdaloid nuclei
Simple contraversive Frontal
2 Somatic and special sensory (auras):
Somatosensory Postrolandic
Visual Occipital or Temporal
Auditory Temporal
Vertigenous Temporal
Olfactory Mesial Temporal
Gustatory Insula
3 Visceral: Autonomic Insuloorbital-frontal cortex
4 Complex partial seizures:
Formed hallucinations Temporal
Illusions Temporal
Dyscognitive experiences (déja, dreamy states, depersonalization) Temporal
Affective states (fear, depression or elation) Temporal
Automatism (ictal and postictal) Temporal
5 Absence "Reticulocortical"
Bilateral epileptic myoclonous "Reticulocortical"
SOURCE: Modified from Penfield and Jasper, Epilepsy and Functional Anatomy of the Human Brain. Boston: Little Brown, 1954
Figure 8
Localization of focal epileptic seizures in the brain. The common form of epileptic fit, as the table shows, occurs as a focal seizure originating in a localized region of the temporal lobe, often referred to as the limbic system. These seizures involving the temporal lobe, are accompanied by visual, auditory and olfactory (smell) hallucinations. They also involve their vivid recall of memories because the limbic system includes the hippocampus, required for the laying down of new memories. The temporal lobe itself includes neurones for the identification of objects, such as faces, as shown in figures 4 and 5. Thus the most common human epileptic condition is not tha of generalized seizures, which start out in the entire neocortex of grey matter as in llpetit mall' or "grand mall' epilepsy, as commonly thought, but as focal seizures in the limbic system.

To what extent will we be able in the 21st Century to bring some kind of alleviation of the symptoms resulting from stroke and to diseases of different kinds which afflict the inferior temporal lobe. This really requires us to focus on a number of different technologies and approaches to understanding the diseases of the brain which have been initiated in the last few years. These are concerned with being able to introduce neuronal tissue into the brain that can replace neuronal tissue which has been diseased or destroyed. When this is achieved it is then encessary to get these new neurones that have been introduced into the brain to form functional connections with the rest of the brain. These must be of an appropriate kind to reconstitute the normal circuitry of the brain. In addition there are now known to be growth factors, referred to as neurotrophic growth factors, which are required in normal health. These provide nutrients for the neurones in your brain and may be introduced exogenously into the brain from outside. They can allow for the survival of neurones which would otherwise degenerate and they can also allow for neurones which have been injured or neurones which have been introduced into the brain to form appropriate synaptic connections.

Rita Levi-Montalcini was able to show something extraordinary in a series of experiments, some of them conducted during hiding from the Nazis in Italy during the last world war. She was able to obtain growth factors that allowed neurones which would otherwise degenerate to survive. Levi-Montalcini won the Nobel prize a few years ago for her discoveries of neurotrophic factors. This work was begun as she hid from the Nazis in a house in Turin. Montalcini had a microtome in an attic room which was used for cutting thin sections through the fixed embryos of birds. This, together with a microscope, enabled her to make fundamental discoveries concerning the development of neurones belonging to that part of your nervous system concerned with the control of your internal organs, such as your heart. Montalcini showed that in this part of your nervous system, called the autonomic nervous system, neurones die normally during development so that you have more neurones very early in your life than when you are an adult. She went on te show that neurones could be rescued from death if they were provided with growth factors which can be supplied by the targets with which these neurones normally make junctional connections. Ten years ago my colleague Bogdan Dreher and 1 set out to see if what Levi-Montalcini had discovered for the peripheral nervous system, namely that autonomic neurones could be induced to survive if provided with the material from their normal targets such as cardiac muscle or smooth muscle, might also apply for neurones in the central nervous system. We first showed that retinal ganglion cell neurones that connect the retina to the rest of the brain, and are shown in figure 9, normally die during development. Furthermore these retinal ganglion cells could be induced to survive when provided with a nutrient neurotrophic molecule from their targets in the brain. Those parts of the brain are called the superior colliculus and the lateral geniculate nucleus. The neurones survived and sprouted nerve processes profusely in a tissue culture plate if provided with the neurotrophic factor, just as Montalcini had described for autonomic neurones (figure 10) The difference was that in this case the retinal neurones were supplied with a factor from the brain and not from muscle. This was probably the first indication that neurotrophic growth factors exist in the brain not just in the peripheral nervous system and these growth factors can allow for the survival and profuse axon spouting of a central neurone such as a retinal ganglion neurone.

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