He has granted you from all that you ask Him. Were you to attempt to count God’s blessings, you could not compute them. But for sure, humankind is much prone to wrongdoing (sins and errors of judgment) and to ingratitude. (Ibrahim 14:34)

Today a large part of modern science focuses on understanding the human body. Researchers working on life sciences hope that one day the secrets of every single detail that make us human will be revealed. Every year billions of dollars are spent by scientific institutions on learning more about us. Actually this fact by itself is enough to suggest how little control we have over things happening in our bodies, and we know even less about the mechanisms of moving, touching, speaking, seeing, or hearing, and so on.

As a scientist, I really cannot guess whether life scientists will ever be able to learn enough to solve the puzzles of the human body, but I feel a lack of satisfaction when the knowledge we have gained from scientific discoveries is compared with what is unknown. In my opinion this is why one of the most intelligent physicists in history, the Nobel laureate Richard Feynman, once said, “I was born not knowing, and have only had a little time to change that here and there” [1]. My understanding is that such a conclusion must be inevitable if the primitive knowledge given to us by modern sciences is not interpreted in the light of a far superior logic that is meant to explain the whole creation. In that sense, I believe that we have to consider every single detail in creation as a vital part of the whole in order not to feel lost before the grand picture of this masterpiece.

Last year, in a seminar at Osaka University Graduate School for Frontier BioSciences, I was thrilled to hear Professor Keichi Namba say, “Japan’s fastest supercomputer dissipates more than billion times the power dissipated by a fly’s brain, yet it is not able to simulate the brain of such a tiny animal.” This worked as a wakening call or a reminder for me to think again about the magnificent arts of the Creator. In particular, I wanted to revise my research on a hearing-related protein from a new perspective, rather than using the mechanical attitude that is followed most of the time.

This article is an attempt to explain an amazing mechanism in our ears that enables us to hear the faintest whispers. A mechanism that is switched off at loud cries to protect us from disturbing noises, yet amplified to make the softest sounds audible. Before starting to explain the basic anatomy of the human ear, I should mention that today the ear’s active amplification mechanism is still being investigated in research centers by biologists and physicists together.

How do we hear? What is happening in the inner ear?

Findings from the last century have shown that our ears are not just simple receivers as we had imagined. In 1979, David Kemp of University College, London discovered that mammalian ears can also emit sound vibrations. By placing a very sensitive microphone close to the eardrum he could detect whistles, implying that there is a source of vibration within the ear [2]. However, before trying to explain the cause of vibrations in the ears, we have to go over the mechanism of hearing briefly: The delicate design of the outer ear, the tympanic membrane (eardrum), and the tiny bones (malleus, incus and stapes) enables to collect sound waves traveling in the medium and transfer them to the inner ear (Figure 1a). In the inner ear the sound waves are sorted according to their frequency and amplitudes and then converted into electrical signals which can be transported to the brain via nerves. At the onset of this process the sound waves are transformed into standing waves on the basilar membrane which is laid along the organ resembling a snail, the cochlea (Figure 1b). The frequency of the incoming sound wave determines the positions of the distortions along the cochlea: High pitches create vibrations at the basal end of the cochlea (i.e. adjacent to the middle ear) whereas low frequencies vibrate closer to the apical end (Figure 1c) where the cochlea gets narrower. This geometry helps our ears to act as a frequency analyzer.

The efferent and afferent nerves that connect the ear to the central nervous system are attached to the organ of Corti, which is situated right next to the basilar membrane, extending over the cochlea. In other words, Corti is the sense organ of hearing, converting the motion of the basilar membrane into electrical signals that are conducted to the brain via neuronal cells [3]. The organ of Corti is also lined with multiple rows of sensory hair cells.

The hair cells of the organ of Corti

Corti is decorated with two different sets of sensory cells: single row of inner hair cells (IHCs) accompanied with 3–4 rows of outer hair cells (OHCs), both spanning the whole cochlear tube (Figure 2a). They are called “hair cells” because both IHCs and OHCs have typical bundles of stereocilia that contain mechanosensitive ion channels (Figure 2b).

The major function of IHCs is to detect the sound waves and then convert them into equivalent electrical signals that are to be interpreted by the brain. When the basilar membrane is perturbed by the incoming sound waves, the IHCs found in that region sense this activity by the movement of their hair bundles (bundles of stereocilia). The hair bundles of IHCs deflect and re-align as the basilar membrane moves up and down (Figure 3). We should note that this is an amazingly sensitive process such that deflections of the stereocilia on the order of a few nanometers (one millionth of a millimeter) can be detected and converted into nerve signals by the IHCs [4].

However, this by itself is not sufficient for hearing; no matter how effective IHCs work, the fluid that fills the cochlear tube is a threat to the sound waves traveling in the inner ear. In 1948, a young astrophysicist named Thomas Gold was the first person who has pointed out that the fluidic nature of the cochlea would dampen the sound vibrations and make them too weak to be detected by IHCs. He has concluded that an inherent vibration amplification mechanism is necessary in order to overcome such a problem [5]. Unfortunately, Gold’s statements were overlooked by the physiologists of his time who had performed their hearing related experiments on dead cochleas.

Gold’s predictions were justified around ten years later by William Rhode, a physiologist from University of Wisconsin, who has shown that the vibrations of the basilar membrane in live tissue samples are stronger than anticipated [6]. In the present day the existence of an amplification mechanism within a live cochlea is a well accepted fact. The only disagreement among scientists is about how the mechanism of the amplification works. Several scientific laboratories have reported different experiments performed on the organ of Corti and they have proposed different models. At the center of one of these models is prestin, a membrane protein which is not found in any cell but OHCs in the human body.

Electro-motile outer hair cells and prestin

In 1985, the distinctive properties of OHCs were first discovered by William Brownell, a University of Geneva neuroscientist, who has shown that these cells can convert electrical signals into motion: A phenomenon called electromotility. Electromotile OHCs can elongate or shrink in response to electrical charge density changes in their membranes. About a decade ago Peter Dallos and co-workers from Northwestern University in Chicago discovered a membrane protein, unique to OHCs, that can respond to electrical signals [3]. The Dallos group coined the name “prestin” for this protein in an analogy with the musical term “presto” (quickly) due to its rapid response to electrical signals. Various kinds of mammalian cells genetically engineered to produce prestin at their membranes displayed the electromotile responses that are very similar to OHCs.

According to Peter Dallos prestin protein works as a tiny machine which is a crucial element for cochlear amplification [7]. His theory is verified by recent studies which show that cochlear sensitivity in mice decreases hundredfold when prestin activity is disrupted by genetic means [8]. As the sound waves reach the inner ear, prestin-driven electromotility enables the OHCs to move like pistons. The piston movement in phase with the basilar membrane motion amplifies the vibrations and makes them stronger for IHC detection (Figure 4a,b). The prestin-driven vibrations were what Thomas Gold proposed and David Kemp had detected so many years ago. However, scientists are still searching and learning new things about this nanometer scale machine. One of the discoveries showed that prestin can adjust itself according to the amplitude of the incoming sound waves: Basically, the amplification is stronger when the sound waves are hard to hear but gets weaker as the volume increases.

Up to this point, we have briefly explained how the amplification mechanism of hearing in mammals works. Unfortunately, even though it took decades of research for scientists to discover and define the active nature of the mammalian ear, this explanation highlights only a minuscule part of the whole picture. That is why we are still incapable of curing most hearing problems. For example, hearing loss due to slightly disturbed hair cells with damaged stereocilia turns out to be chronic (Figure 5). The medical treatments we have to hand are too primitive to mend such delicate structures. Moreover, hearing aids made by today’s technology are not nearly as effective and functional as needed.

On the other hand, the delicacy of the hair cells and the limited control scientists have over them are not the only lessons we have learned from research on the inner ear. We cannot overlook the other messages attached to the research on the grounds that the time given to us is just too short to comprehend. It is an undeniable fact that the sense of hearing is designed in the best way to serve human beings. The different characteristics of hearing amplification at different sound levels make life much easier for us: Prestin-driven hearing is most effective when the sound waves are weak and harder to hear. This way the incoming sound waves are amplified enabling us to hear the faintest whispers. However, as the sound strength increases, the prestin-driven amplification gradually gets weaker and finally diminishes after a point to make sure that loud noises are less disturbing and hazardous for us. In my opinion, this amazing quality of a tiny protein found in our ears is one of the pieces of evidence that remind us of the necessity of pondering the favors of our Creator. Qur’anic verses such as Ibrahim 34 at the beginning of this article give us clues about how to interpret scientific findings that reveal the amazing qualities of our bodily organs. May the Creator of our ears allow us to reflect more on His favors and live accordingly.

Hamdi Sener is a biophysicist living in Boston. He can be contacted at hamdisener@gmail.com.

References

1. Gleick, J., Genius: The Life and Science of Richard Feynman. Reprint ed. 1993: Vintage. 560.
2. Kemp, D.T., The evoked cochlear mechanical response and the auditory microstructure- evidence for a new element in cochlear mechanics. Scand Audiol Suppl., 1979. 9: p. 35–47.
3. Zheng, J., et al., Prestin is the motor protein of cochlear outer hair cells. Nature, 2000. 405(6783): p. 149–55.
4. Robles, L. and M.A. Ruggero, Mechanics of the mammalian cochlea. Physiol Rev., 2001. 81(3): p. 1305–52.
5. Gold, T., Hearing II. The physical basis of the action of the cochlea. Proc. Roy. Soc. B., 1948. 135: p. 492–498.
6. Rhode, W.S., Observations of the vibration of the basilar membrane in squirrel monkeys using the Mossbauer technique. J. Acoust. Soc. Am. , 1971. 49: p. 1218–1231.
7. Cho, A., What’s Shakin’ in the ear? Science, 2000. 288: p. 1954-1955.
8. Liberman, M.C., et al., Prestin is required for electromotility of the outer hair cell and for the cochlear amplifier. Nature, 2003. 419: p. 300-304.
9. Fettiplace, R. and C.M. Hackney, The sensory and motor roles of auditory hair cells. Nat Rev Neurosci., 2006. 7(1): p. 19-29.
10. Dallos, P. and B. Fakler, Prestin, a new type of motor protein. Nat Rev Mol Cell Biol, 2002. 3(2): p. 104-11.

The human ear and hearing

The human ear can be divided into several functional sections: the outer ear, the middle ear, the inner ear, and the auditory nerve. Sound goes through a series of changes as it travels through these sections until reaching the brain. The outer ear picks up sound pressure waves, amplifies them and then converts them into mechanical vibrations on the ear drum, which is connected to a series of small bones in the middle ear. These small bones further amplify or diminish the mechanical vibrations in the ear drum and transfer them to the cochlea, a snail-shaped cavity filled with fluid which is located in the inner ear. Change in fluid pressure caused by vibrations within the cochlea lead to changes in the flexible membrane, called the basilar membrane. These changes contain information about the frequency and strength of the sound that has entered the ear. Attached to the basilar membrane are mechanical receptor cells, called hair cells, which are bent according to the deflections of the basilar membrane.The hair cells have hair-like structures. The bending of these hairs assists the release of an electrochemical substance that causes neurons to send electrical signals to the brainstem through the auditory nerve. These signals are in the form of a message (or a code) that the brain understands.

Cochlear Implant (CI) devices

If there is a broken link in any part of the auditory pathway, the brain does not receive any coded signals, and hearing impairment occurs. If a large number of hair cells or auditory neurons in the cochlea have been damaged, then the person is diagnosed as profoundly deaf. The hair cells can be damaged by certain diseases (e.g., meningitis, Meniere’s disease), by congenital disorders, by certain drug treatments, or by other causes. One negative outcome of damaged hair cells is that they can subsequently lead to the degeneration of adjacent auditory neurons. Research has indicated that the most common cause of deafness is the loss of hair cells (>95%) rather than the loss of auditory neurons. This has encouraged scientists to try implanting a device inside the iner ear or cochlea, bypassing the normal hearing mechanism of the ear, to stimulate the remaining auditory neurons directly through electrical signals. These are called Cochlear Implant (CI) devices, which can restore partial hearing in profoundly deaf people . A standard CI system, shown in Figure 1, composes of and performs the following functions: a microphone picks up sound pressure waves and converts these into electrical signals. The signals are sent to the speech processor that is worn by the patient. The speech processor analyzes and encodes these sound signals, sending them back to the external pick-up coil . After passing through a wireless radio link that lies between the external and implanted coils and an implanted electronic devise, coded signals are sent to the implanted array of electrodes in the cochlea to electrically stimulate the remaining auditory neurons , and the brain receives what it interprets to be sound.

Electrical stimulation of the ear, or CI research, can be traced back to the 1800s. The Italian scientist Alessandro Volta used a battery as a research instrument to demonstrate that electric stimulation could result in a number of human sensations . After connecting a 50- volt battery to his ears, he noted that “…at the moment when the circuit was completed, I received a shock in the head, and some moments after I began to hear a sound, or rather noise in the ears, which I cannot well define: it was a kind of crackling with shocks, as if some paste or tenacious matter had been boiling…”. That electric stimulation of the auditory nerve provides hearing sensation in deaf people was reported more than 100 years after Volta . Electric stimulation in two deaf patients resulting in hearing was reported in 1957. These successes resulted in intensive research into helping deaf people hear in the 1960s and 1970s. One of the early successful single-channel CI devices was developed in the early 1970’s (3MCorp/House) and became the first commercially available CI device approved in the United States in 1984. The University of Utah developed a six electrode implant called the Ineraid or the Symbion device in the early 1990s. It was followed by other devices in Europe, the United States, and Australia.

The present status of Cochlear Implants

Today, around 10% of the population in developed countries suffers from hearing impairment. At present, the number of CI users has reached more than 100,000 worldwide, and is still growing rapidly. Functionally, CI has evolved from the single-electrode device that was used as an aid for lip-reading and

sound awareness to a modern, multielectrode device that can allow an average user to talk on the telephone. Even though significant technological progress has been achieved in the last 50 years, there are still many mysteries about the human hearing process and the parts of the ear. Here, we will compare some aspects of the healthy human ear and CI devices, looking to the future. The human ear operates over a range of sound pressures (its dynamic range) which is greater than one million to one (120dB), with as many as 200 discrete steps in the range. In contrast, today’s CI devices typically provide a dynamic range of three to one (10dB) to ten to one (20dB) with 20 discrete steps. This major difference is mainly due to the fact that the human ear is very adaptive in noisy environments, and is able to suppress noisy background, while picking up and processing appropriate sound signals for better perception. CIs do not differentiate between sounds, but amplify all sounds, which results in poor sound perception. Today, a typical multi-channel CI system uses 16 to 24 electrodes implanted in the cochlea with 8 to 22 signal processing channels. A potential shortcoming of having so many electrodes and channels in current CI technology is the electrical interference of electrodes during simultaneous electrode stimulation. These electrical interactions can disrupt the stimulus waveform prior to neural activity and degrade sound perception. The normal ear contains roughly 3,500 inner hair cells in the cochlea that are tuned to different frequencies from 20 to 20,000 Hz. They are connected to about 35,000 auditory nerves. Hair cells work as signal processing channels, yet each of the inner hair cells has also been wired in a sophisticated and little-understood fashion to 10-20 auditory nerve fibers that carry information to the central nervous system. Since they work in the chemical domain, they do not have the gross interference issues of CI electrodes. While good speech understanding has been achieved by users of modern multi-electrode CIs operating in quiet environments with 70–80% sentence recognition, allowing users to talk on the telephone, the CI devices do not discriminate between noise and the meaningful signals, only achieving speech understanding at between 70% and 80%, which falls to 10% or lower in noisy environments. It is a great challenge for CI users to appreciate music. Some CI listeners reported that they can enjoy music and are able to recognize melodies, but most described musicas sounding unpleasant and noisy, and performance could not be increased with current CI technology. CI users have difficulty in identifying differences in frequencies. Typically, they cannot discriminate any frequency difference for frequencies higher than 500 Hz, while the normal ear can hear up to 20,000 Hz with frequency discrimination between 2 to 3Hz at best. This gross difference is related to the issues surrounding signal processing strategies and electrodes of current CI systems. Predicting post-surgical performance based on presurgical conditions and tests of a CI candidate is still a problem for the physician. The cost of surgery is still high; in the United States, for example, a typical cost is between $40,000 and $75,000. Beyond these issues, the moral, cultural and ethical issues related to CIs are very complex. They are still debated, and are an important part of CI development in the world today. The hair cells in the human ear naturally deteriorate and die as we grow older. This process is typically sped up with exposure to loud noise. In common with all mammals, new hair cell generation in human ears stops right after the birth. However, in fish and amphibians, very similar cells are present and reproduce throughout life. Recently, it was found that hair cells of birds are repaired after being damaged by exposure to noise or ototoxic agents. It was also discovered that hair cells in the mammalian vestibular (balance) organ, very similar to those in the hearing system, can regenerate. These findings, along with other advancements in medical fields, lead to long-term research into different aids for hearing- impaired people. Despite the fact that hearing loss is usually permanent, scientists are optimistic that it may eventually be possible to reverse the damage in the ear by repairing or regenerating the sensory hair cells through gene therapy, stem cell transplantation, or ultimately by replacing the human cochlea with an artificial one. Today, Auditory Brainstem Implants are also being tried on humans for direct brainstem stimulation, bypassing the ears and the auditory nerves. Human beings and most animals on earth are born and equipped with a pair of ears for a good reason: having two ears enhances hearing and sound localization. Scientists are examining whether this is also true for deaf children who receive not one, but two CIs.

Conclusion

The sense of hearing is a gift for human beings which they hold dear and are grateful for, as much as for any of the other senses with which they have been equipped. It is important to strive to find cures for all kind of diseases, yet, more important than the cure is prevention of harm to our body and its amazing senses. Here, we have tried to open a small window onto human hearing, to examine how related impairments are being dealt with through cochlear implant (CI) devices, as well as looking at the issues related to these devices and the future directions of research for restoring hearing to deaf people. It is obvious that we have learned much about human hearing and ear in the past century; yet, this may well be just the tip of the iceberg.

References

1. S.U. Ay, F.-G. Zeng, B.J. Sheu, “ Hearing with bionic ear,” IEEE Circuits & Devices Magazine, Vol. 13, No. 3, pp.18-23, May 1997.

2. F.-G. Zeng, “Trends in cochlear implants,” Trends in Amplification, Vol. 8(1), pp.1-34, 2004.

3. A. Volta, “On the electricity excited by mere contact of conducting substances of different kinds,” Royal Soc. Philos.Trans., vol. 90, pp.403 431, 1800.

4. A.M. Andreev, G.V. Gersuni, A.A.Volokhov, “On the electrical excitability of the human ear: On the effect of alternating currents on the affected auditory apparatus,” Journal of Physiology USSR, Vol. 18, pp.250-265, 1935.

The discipline in which medicine and engineering truly meet and face new challenges is the field of “biomedical engineering,” an emerging discipline that is only a few decades old. In each sub-specialty of biomedical engineering, researchers study the human body, develop new materials and structures using engineering sciences, either as a treatment method for disease (e.g. artificial bone implants, artificial blood, vascular stents, cardiac valves, etc.) or to diagnose them (e.g. imaging methods and other diagnostic instruments in hospitals). Biomedical engineers face the incredible challenge of developing materials and devices that are compatible with biological systems and capable of working inside the human body to substitute bodily functions. Needless to say, the extreme complexity of the human body makes it impossible to mimic the original system or function of the organs in any way. However, even a poor replacement part or a functional improvement provides great benefit to the patients.

One of the most complex systems of the human body is the nervous system, which consists of the central area (the brain and the spinal cord) and the peripheral parts. The branch of biomedical engineering that deals with the nervous system is “neural engineering.” In this article, we will touch upon a specific subject in the broader area of neural engineering, that is, “neural prosthetics.”1 As the name implies, neural prosthetics is an area where engineering knowledge is utilized to treat neural disorders.

The building blocks of the nervous system are called “neurons.” Neurons generate electric pulses to communicate with each other. The fact that these electric pulses can be elicited by artificial means, i.e. by applying small electric currents to the neurons externally, forms the very foundation of the field of neural prosthetics. Neural engineers can input information into the nervous system by taking advantage of this phenomenon, called “neural stimulation.” Likewise, the information content of neuronal activity can be deciphered by recording the electrical pulses from the neurons and interpreting them according to neuronal function. This two way traffic, monitoring and controlling the neural activity, allows researchers in this field to develop methods of treatment for some sensory, motor, and psychological disorders.

Some of the most successful neural prosthetic applications have been in deep brain stimulation in Parkinson’s disease,

cochlear prosthesis in hearing impairment, bladder emptying and respiration in spinal cord injury, and vagus nerve (10th cranial nerve) stimulation in epilepsy and psychological depression. These are neural prostheses that are readily available as a treatment method for the given ailments. There is a whole host of others that are in the research and development phase. We will review a couple of examples.

In certain diseases of the inner ear hearing is lost as a result of damage to the hair cells inside the cochlea. In normal cochlea the sound information reaches these hair cells after traveling through the ear drum (tympanic membrane) and the structures of the middle ear, causing them to vibrate. This vibration of the hair cells is mechanically transported to the spiral ganglion cells that form the hearing (auditory) nerve. The hearing nerve carries the sound information to the brain in the form of electric pulses. The ganglion cells are healthy and functional even if the entire population of hair cells has been lost as a result of disease. Neural engineers take advantage of the fact that the spiral ganglion cells (which normally accept input from the hair cells) can be electrically stimulated, thus mimicking the function of the hair cells and producing the sensation of sound.2 During a simple surgical operation, the surgeon inserts an electrode into the ear canal which spirals into the lumen of the cochlea so that the sites where the electric current emits from the electrode are adjacent to the spiral ganglion cells (Figure 1). To summarize the principle of the operation; the audio signals are captured by a microphone, processed, converted into electric pulses (A in Figure 1), and transmitted to the implant over a transmitting antenna (B in Figure 1), or headpiece, held in place by magnets. The implant (C in Figure 1) applies the signals to the ganglion cells in the cochlea through tiny electrodes (D in Figure 1). The hearing nerve (auditory nerve) carries the sound information to the brain, where it is “heard.”

Even though the human spiral ganglion has tens of thousands of nerve cells that provide a rich sense of hearing, the cochlear implant, using only six stimulation contacts, can produce auditory perception with sufficient fidelity to enable a deaf individual to use an ordinary telephone.3 Individuals with cochlear implants can also improve their hearing with practice. Thousands of patients have been implanted with cochlear prostheses to date, including children.

The second neural prosthesis application we will review is the retinal prosthesis, which, unlike the cochlear implants, is still in the research phase. Retinitis pigmentosa and age-related macular degeneration both lead to photoreceptor degeneration in the eye and result in a significant visual deficit or blindness.4 A growing body of research supports the feasibility of replacing the function of the photoreceptors with an electronic device. 5–7 A retinal prosthesis is analogous to the cochlear implant in many ways. In a healthy retina, the photoreceptors initiate a neural signal in response to light. In a retinal prosthesis, electrical pulses are utilized to initiate a neural response in the remaining cells of the retina, the bipolar and ganglion cells. It is hypothesized that the perception of shapes and images will be possible through pattern stimulation of the retina. Initial results are encouraging, but the quality of vision that can be attained with this approach is still a question to be answered. A conceptual retinal prosthesis system is shown in Figure 2. The system consists of an external unit coupled to an implanted stimulator with a wireless link. A video camera in the external unit captures an image and converts it to digital data. The implanted unit receives the signal, recovers power and data from the signal, and generates the stimulating current. The stimulus pattern is applied to the retina via the electrode array, which contains distinct electrodes that interface at many locations on the retinal surface. Recent implants in human subjects suggest the feasibility of this approach where individuals attain perception of bright dots in the visual field called ‘phosphenes.’ Furthermore, blind subjects are able to perceive edges when a few of these bright dots are lined up in their visual field.

Figure 3: A conceptual diagram of a Brain-Computer Interface for high level spinal cord injury or patients with ‘locked-in syndrome’ (adapted from Wolpaw et al., see note 9). The recorded neural activity from the motor cortex is processed and converted into command signals to control, for instance, a wheelchair, or to generate electrical signals to activate hand muscles for grasping an object.

Both cochlear and retinal implants are sensory prostheses, i.e. aids for sensory impairments. Another family of neural prostheses deals with motor impairments. Severe motor disability results from high level spinal cord injuries (quadriplegia) where most of the body is paralyzed, sparing only some face, neck, and shoulder muscles. Quadriplegic individuals are in extreme need of a means to control their environment; they need to be in control of their wheelchairs, bed, the room temperature, lights, TV, etc. Because of the level of paralysis it is impossible for them to generate any control signal, except perhaps by sipping or puffing on the end of a tube, which produces a very poor control signal. In the case of a ‘locked-in syndrome’ the condition of the patient is even more serious, with only some functions remaining in the facial muscles. The term ‘brain-computer interface’ has been coined to refer to attempts whereby the motor output of the brain is recorded and interpreted to generate the control signals needed by these patients (Figure 3,9). The ultimate objective of this research will be accomplished when the patients are able to control anything they need to control in their environment, including a computer. The brain-computer interfaces vary in the invasiveness of the approach. The least invasive methods utilize the electroencephalogram (EEG) signals recorded from the scalp. Unfortunately, the signal quality is poor and only ‘on/off’ type of command signals can be generated using this method. In the most invasive, yet most successful applications, an array of electrodes is implanted directly into the motor cortex of the brain at a depth of a couple of millimeters. The recorded signals contain volitional information as the patient makes intentions to move their arms or legs. These signals can be controlled by the patient, and they can in turn be used to control their environment. The current level of success in this type of BCI allows the user to have three dimensional control of a robot arm. This is of invaluable benefit to a quadriplegic individual.

Concluding Remarks: Reflections on Divine Wisdom

Even the subtlest parts of the nervous system are extremely complex. Just to name a few examples, from the highest centers in the brain down to the skeletal muscles in a descending order; the neural circuits of the short-term memory in the hippocampus, fine motor control circuits of the cerebellum, central pattern generators in the spinal cord, and even the control of skeletal muscles in graceful movements of the limbs are impossible to reproduce by artificial means. The Seal of Divine Design is clearly visible in these neural systems, as they are far more complex, far more compact, and far more functionally efficient than any system engineered by mankind. If anything, the growing experience in neurosciences teaches us that the vertebrate nervous system is full of wonders of engineering design. Therefore, it is a great blessing to be a student of both neurosciences and engineering disciplines. This bestows neural engineers with a unique perspective to understand the beauty embroidered into the human nervous system and contemplate on the Divine Wisdom. In spiritual terms, we may think of the human nervous system as a window opening to the works of Divine Wisdom, with manifestations of His Beautiful Names at the brightest level. It is an overwhelming joy to be able to open this window a crack, once in a while, and take a little peek.

References

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