本書は立花氏による１年間におよぶ取材と膨大な資料に基づいて書かれてい る。 雑誌「文芸春秋」に連載された文章をまとめたものであるため、繰り返し があった り、体系的な構成に欠ける点はあるものの、よくこれだけの資料を集 めたものと感 心する。まず、はじめに、テレビのために膨大な資料を集めて も、本番では、その 内のほんの一部しか使用されなかった事情が述べられてお り、あらためてテレビと いうメディアの危険性を感じる。テレビには登場しな かった多くのエピソードが、 本書の中で紹介されている。その多くが立花氏に よる体験者本人からの取材である ことから、なかなか説得力がある。特に、下 巻、第２２章で紹介された、サリバンさんの例は、手術の後、対面していなかった手術担当医の高田医師と患者のサリバ ンさんが立花氏の目の前で再会し、 つぎつぎと事実が確認されている点、さらに、「ガラスのテーブルの上の心 臓」の謎も後から解かれたことを考えると、事実としての信頼性が非常に高い ように思われる。その他の例については直接あるいは間接 の伝聞であるので疑わしいものもあるかもしれない。しかし、これだけのエピソー ドが集まれば、 その中には相当数の事実が含まれているにちがいない。
本書のもう一つの特徴は、単にエピソードをたくさん紹介するだけでなく、そ の 科学的な考察を試みている点である。紹介されたエピソードの多くが実際に あった 体験であったとして、それは、死後の世界をかいま見た証拠になるのだ ろうか？ 私は、もちろん現役の脳研究者として、これらの「体験」のすべて は最終的には脳 内でおこった現象であると考えている。立花氏がかなり詳しく 紹介しているよう に、臨死体験の大部分は側頭葉てんかんに類似した脳内現象 として説明できる。し かし、その一方で私は、現代の科学が宇宙の、あるいは 生物のすべてを知り尽くし ている、あるいは科学的にすべて説明がつかなければならないとも考えていない。 人類が生き続けるかぎり科学の発展は続き、宇 宙や生物についての理解は深まるで あろう。しかし、将来にわたっても科学が すべてを知り尽くすことはないであろう。まして、脳は自然科学の対象として 最も複雑な研究対象である。また、立花氏 の言うように現在の脳科学の研究レ ベルはまだまだ「プリミティブ」である。サリ バンさんの例のように現代の脳 科学で説明困難な「体験」があっても当然である。 こうした例も、たとえば、 テレパシーのような現象を受け入れれば、医師や看護婦 が見たイメージをサリ バンさんが自分自身のイメージとして「体験」したと説明で きるかもしれな い。現代の脳科学の知識でテレパシーの現象を説明できなくても、 それを否定 する証拠もないのだから。そして、こうした説明の方が、死後の世界を 認める より、現実体験説と矛盾する他の事実、たとえば、年齢や文化的背景による 「体験」の違いを無理なく説明できるように思われる。しかし、テレパシーの 問題 もまだ、事実の確認を含めて科学的には未解決の問題である。臨死体験を 科学的に 説明できるには、まだ時間が必要である。
最後に、臨死体験が現実体験であるにせよ、また、脳内現象であるにせよ、本 書 を読むと、死ぬ瞬間がそれほど苦痛に満ちたものではないらしいということ がよく わかる。これは、われわれにとっては朗報であるにちがいない。
Possible neurophysiological basis of visual images seen in shamanism
A. We have a distorted visual system
Our visual system is different from that of a camera or TV camera designed to project a linear image of the world onto film or a CCD (Charge-Coupled Device: a light sensitive device which correspond to a film of a camera). An image of the outer world is projected in higher resolution on the center of the visual field and in lower resolution on the peripheral vision. We have multiple visual areas and the outer world is represented repeatedly in those areas. This being the case, are we really looking at the real world ?
1. We are looking at the world upside-down.
Our eyes are designed similar to a camera. A light source coming through a lens is reversed upside-down and right-side-left. As a result, images are projected completely reversed onto our retina. Visual information coming out from the retina goes through a relay station called the lateral geniculate nucleus (LGN) and then projects to the primary visual cortex (V1). In the cortex, a visual image is also projected upside-down. The upper cortex represents the lower visual field and the lower cortex represents the upper visual field. Figure 1 illustrates such a retinotopical map in the V1.
We have two eyes and two hemispheres which are almost symmetrical. Both of our eyes are looking at both sides of the visual field, but at the optic hiasm, output coming from the right side of the retina (which is receiving light coming from the left visual field) of the left eye crosses the midline and projects to the right side of the LGN. Similarly, output coming from the left side of the retina (which is receiving light coming from the right visual field) of the right eye crosses the midline and projects to the left side of the LGN. As a result, the right side of the brain (the right hemisphere) receiving input from the left visual world and the left hemisphere receives input from the right visual world. Thus our visual field is divided into a right half and a left half and each half of our brain represents the opposite side. Thus, not only our eyes but also our cortex is looking at the world reversed. In spite of this split and reversal, we neither see any midline gap between the right half and the left half of the visual field nor feel that the world is really reversed.
Information coming from the right and the left eyes are separated at the early stage of vision. It is true of course, since two eyes are separated. The LGN has 6 layers and the information coming from the same side (ipsilateral) enters in layer 2, 3 and 5. The information coming from the other side (contralateral) enters in layer 1, 4 and 6. These layer are separated by the intermediate layers and there is no cross-talk between layers. In the V1, the information coming from different eyes enter separately at first and then they are mixed at this level. Images of the right eye and left eye are slightly different. Visual fields of both eyes are not overlapping completely. We are looking at about 60 degs of both sides of visual field using both eyes, but we use either eye to see for about 30 deg of aural side (ear side). Since our two eyes are physically separated we are looking at things from a different angle. Forthermore, when we are looking at something coming out from behind an obstacle, one of our eyes see it first and the other eye see it later. We do not feel any difference between our two eyes in normal conditions.
2. Resolution is different in the central and the peripheral vision.
The retina of each eye has 120,000,000 rods (brightness sensitive but color non-selective cells) and 6,000,000 cones (color selective cells). Density of light sensory receptors is higher at the center of the retina and lower at the periphery of the retina in general. Cones are most dense on the small spot called the “fovea centralis”. At this spot, no other retinal neurons are present and the visual acuity corresponding to this spot is highest. Rods are densest around the edges of the fovea, but are more numerous than cones over the rest of the retina (Aosterberg, 1935).
In the V1, a wider area is serving central vision compared to peripheral vision. This is reasonable since more information is coming from the central retina than the peripheral retina. In the V1, inputs from ipsilateral and a contralateral eyes are distributed systematically making stripes in an alternating fashion. This organization is called the “ocular dominance column”. The width of each ocular dominance column is not very different between the central representation and the peripheral representation, as seen in Figure 3A. If this ocular dominance pattern of stripes are back-transformed onto the visual field as seen in Figure 3B, stripes in the central vision are narrow and dense (Levay et al., 1985). This means that the same size of area is devoted as a small part of the visual field in the central vision and as a large part of the visual field in the peripheral vision.
3. The outer world is represented repeatedly in multiple visual areas
Neurophysiological and neuroanatomical studies over the last 25 years have revealed that there are multiple sensory areas and motor areas in the neocortex of manmals. In the visual system of macaque monkeys, 32 visual areas are described in the occipital, parietal, temporal and frontal cortices (Felleman and Van Essen,1991). Figure 4A illustrates 32 visual areas which were identified by them on a flattened map of the macaque cortex. Those areas are hierarchically organized from lower processing to higher processing as seen Figure 4B. Although we are still far from fully understanding the multiple visual areas, most of the lower visual areas have a complete map of the visual field. Some of them have a unique function or functions.
For example, the forth visual area (V4) is involved in color and form vision (Desimone and Schein, 1987, Schein and Desimone, 1990) and the fifth visual area (V5 or MT; Middle Temporal area) is a critical area for processing visual motion (Zeki, 1973, Newsome, Wurtz, Durstera and Mikami, 1985, Mikami, Newsome and Wurtz, 1986). In the third visual area (V3), the function of the upper visual field is related to color vision and the function of the lower visual field is related to visual motion (Felleman and Van Essen, 1987). Thus, our visual system is not so simple as to be identified as a single visual area to project a visual image.
4. Can we really ‘see’ the real world ?
Thus, our visual system is distorted and far from a linear projection of the outer world. In spite of these distorted visual systems, we can create a correct image of the real world nevertheless. We can perceive a unified image of the outer world. An image of the outer world created in our brain is not an imaginary image but a reflection of the real world, since we usually have no problem moving around, interacting with and manipulating the outer world. To create a real image using a distorted visual system, we move around in the world and correct our own visual image.
B. Our brain is plastic
Our brain is plastic and has the ability to adjust our image to the outer world. In other words, our image is created on the basis of our own experience after birth. If our experience was limited to a certain extent, then our image of the world may be limited to the same extent. A story which I heard from my friend is a good example. Mubuti Pygmies live in the forest and have no experience of life in the wide view. One day, Dr. Turnble invited a Mubuti man to take a drive with him by jeep. Along the way passing through a wide field, the Mubuti man asked Dr. Turnble “What is that insect ?” He was pointing toward a buffalo far off in the distance. Dr. answered “That is a buffalo”. The man could not believe this. However, as the jeep came closer to the buffalo and it became clear that it was really a buffalo, the man was shocked and became silent. In this episode, the Mubuti man was not prepared to interpret what the object might be so far away since he had never had such an experience before. He can create a correct image in his forest, but out of this enviroment his visual system has a problem properly interpreting objects. Similar data have been reported in the case of a three-dimensional Ponzo illusion (Brislin and Keating, 1976). The plasticity of our brain is maximum during several years after birth. Experience during that period of time has a big influence on tuning up our visual system.
The adult brain is also plastic. When we wear glasses with reverse prisms, we can adapt to the new reversed world within a few days (Straqtton, 1897). For 2 or 3 days after reversal of visual input, we will have motion sickness. In normal conditions, when we move our head, our retinal image moves in opposite direction of head movement. Since the outer world is not moving and we move our head, movement of the retinal image is not real but a result of head movement. Therefore, we are canceling the moving image by moving that image toward the same direction of head movement. We do not feel that the world moved when we moved our head. However with a reversed visual input, when we move our head in one direction, a visual image moves in the same direction. Since we are expecting that the image moves in the opposit direction we try to move the image in the same direction to cancel the motion of the opposite direction. As a result our image moves in the same direction at double the speed of head movement (speed of motion of a real retinal image plus speed of motion for canceling expected illusory motion). If visual input is reversed upside-down also, when we looked down to see our own body, we see our body not on our side but in the opposite side. If you are sitting facing a desk, the desk is on your side and you are on the other side. We have problems reading books, writing letters, drinking water, pouring milk into a cup with reversed image. In spite of all sorts of difficulties with reversed image, within one week we can adapt to the new visual world almost completely. At this point, we no longer have the impression of reversal anymore and we are standing on our side when we look down. We can even ride a bicycle without problems.
Thus, our brain has the ability to create a correct visual image of the outer world in normal conditions.
C. A visual image without visual input
We can create a visual image even without visual input. Dreaming is a good example. In our dreams, we can ‘see’ a vivid image which flows over a certain time like a motion picture. During dreams, we are free from visual input, since we are sleeping. Although we do not fully understand the brain mechanism of dreams, dreaming is considered to be related to the neural spikes originating in the brain stem during paradoxical or REM (Rapid Eye Movement) sleep. When these spikes come up to the cortices and enter the brain system to create visual images, we can ‘see’ visual images as a result of the activation of a group of neurons engaged to create visual images. These neurons are probably the same group of neurons active when we are awake and actually seeing a visual image.
During epileptic seizure of the temporal cortex, patients often see images free from visual input. Let me introduce case MM described by Penfield and Perot (1963). A 26-year-old woman had her first seizure at age 5. Attacks at first consisted of a sensation in one arm and leg followed by weakness in the leg, but when she was in college the pattern changed. She had sudden “flashes” which she described as experiencing something that she had experienced before. She gave such examples as: being under the grape arbour at her grandparents’ farm; sitting in the railroad station of a small town ... it was in winter, the wind was blowing outside and she was waiting for a train. ... She had the same flash-back several times. These had to do with her cousin’s house or the trip there -- a trip she has not made for ten to fifteen years but used to make often as a child. She is in a motor car which had stopped before a railway crossing. The details are vivid. She can see swinging light at the crossing. The train is going by -- it is pulled by a locomotive passing from left to right and she sees coal smoke coming out of the engine and it blowing back over the train. On her right there is big chemical plant and she remembers smelling the odor of it. ... She thinks she hears the rumble of the train. ... In another flash-back she smells coffee. ...
Electrical stimulation of the neocortex of the temporal lobe had produced a sequence of images. During the surgery of this woman, they stimulated gray matter of the temporal cortex. Since the brain itself has no sensation of pain, it is possible to keep patients conscious using local anesthesia around the opening of skin and bone. When Penfield stimulated the point illustrated in Figure 5, she said “Oh, I had the same very very familiar memory in an office somewhere. I could see the desks. I was there and someone was calling to me, a man leaning on a desk with a pencil in his hand.” Electrical stimulation is an artificial condition which will activate a mass of neurons non-selectively. It will activate neurons not only orthodromically (normal direction of information flow) but also antidromically (opposite direction to normal information flow). So, it is surprising that, such stimuli produced a sequence of visual images. Our hypothesis of neuronal mechanisms producing a visual image is that the brain has many states which are relatively easy to fall into. In a specific state, a certain group of neurons are activated and the activated neurons change from time to time. One state corresponds to a spatio-temporal pattern of activated neurons. In another state, another group of neurons will be activated in the same way. At this point, some neurons may be used again, but different neurons may be recruited. Even if the same group of neurons are active, the timing of activation is different in different states. Electrical stimulation or an epileptic seizure may shift the state of the brain toward one of those states. By stimulating the group of neurons involved in such a state, the other neurons involved in the same state become active through orthodromic and antidromic pathways and as a result, a certain image may be obtained.
In abnormal conditions such as fatigue or near-death, an image free from visual inputs can be also observed. Many runners report abnormal images after running for over 30-40 minutes. In near-death states, people often see “heaven”. One possible explanation for such abnormal images is that low blood pressure and a low oxygen level produce similar states as temporal seizures.
In most of normal and abnormal cases, people prevent visual input by closing their eyes with or without intention to do so. Visual input coming from the normal visual pathway interferes with the production of abnormal images. Shamans often close their eyes at least at the initial phase of abnormal states. In the case of Japanese “Itako”, they are blind. Interrupting or preventing visual inputs must help to produce an abnormal image in the brain.
Recently, new technologies have made it possible to visualize a functional map of the human brain. Positron Emission Topography (PET) and functional Magnetic Resonance Imaging (fMRI) are two such powerful techniques. Using these techniques, we can now analyze functions of the human brain in various behavioral conditions. We now have evidence that the visual system works without visual input. Roland et al. (1994) showed us that the parietal, temporal and occipital visual systems are active when normal subjects were asked to close their eyes and recall an image. Sadato et al. (1996) showed that the primary visual cortex is active while a blind people is reading by Braille. We also found neurons active with an incomplete image (Nakamura et al. 1995). Even motor areas are active while imaging movement without real movement (Decety et al., 1994). Considering these results, the visual system serving normal conditions must be working in a similar ways without visual input. The occipital visual areas or early visual areas are active to all sort of visual images. The parietal visual areas are active for spatial location and the temporal visual areas are active for object identity (Moscovitch et al., 1995). A similar processes may be working for other sensory modalities, such as the auditory, somatosensory or olfactory systems.
Our brain is not a machine but a biological organ. It is well designed in certain aspects, but it is not perfect. The brain is a distorted and non-linear system, and has a lot of repetitions. Even using such a brain, we can see a correct image of the outer world. This is possible because our brain is plastic. During development and during learning even in adults, we can adjust our brain to make a correct image of the outer world. While looking at such an image, sensory and association cortical areas are working. In other words, when a group of neurons in such structures are active with certain timing, we can see an image. In normal conditions, such activation occurs when visual input flows into our brain. However even without any visual input, we can re-create such an image. We can see such images during memory retrieval or in dreams. In addition to such normal cases, if the same or similar brain system works, we may be able to see such an image during abnormal conditions such as epileptic attacks, fatigue or near-death conditions. Thus, we can ‘see’ images free from the physical properties of visual input.
Although no data are available at this moment concerning the functional mapping of the brain of Shamans, I believe that the same brain structure which I discussed above must be working when Shamans are seeing a specific image. And similarly corresponding sensory areas must be active when other sensory modalities are involved.
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(Modified From: Mikami, A. Possible neurophysiological basis of visual, auditory and somatosensory images seen in the sharmanism. In: Irimoto, Yamada (eds.), Sharmanism in the northern world. Hokkaidou Univ. Press, pp. 287-295, 1997.)