Why Do Not Nerve Cells Regenerate?

Why Aren’t We More Like Fish and Frogs?

The question of why the mammalian central nervous system does not regenerate after injury is of extra-ordinary interest at many levels. In terms of descriptive biology, it is remarkable how great the discrepancy is between nerve cells that can, and cannot repair their connections after their axons have been lesioned.

In an invertebrate such as the leech, in fishes and in frogs the central nervous system does show effective regeneration and restoration of function after complete transection. Thus, a leech can swim again after it’s nervous system has regenerated after being cut in two, and a frog can catch flies with it’s tongue after it’s optic nerve has grown back to the tectum(the dorsal portion of the midbrain, containing the superior colliculus and inferior colliculus).

In these “simple” animals the wiring is far more complex than in any man-made circuit, yet somehow fibres grow to find their targets and form effective synapses upon them. In this they resemble their counterparts in the mammalian peripheral nervous system.

What makes the mammalian central nervous system so different in this regard?

At the cellular and molecular level, differences between non-regenerating and regenerating neurons and the satellite cells that surround them are the focus of intense research. Detailed information is accumulating about molecules that enhance or inhibit growth, as well their receptors. And at the level of clinical medicine, there is the essential question about whether and when treatments can be devised for patients with central nervous system injuries so that functions can be restored.

Recent experiments at all of these levels have provided unexpected new findings and insights. Yet one of the most striking features of the field of regeneration today is how many key questions remain. For example, while we have clues, the mechanisms that prevent regeneration in mammalian CNS are still not fully known.

Why is the proportion of axons, that actually elongate, so small, even when the application of suitable techniques does give rise to successful growth across a lesion?

What changes in molecular mechanisms of growth occur in immature mammals during development, that later prevent regeneration in the adult?

While it seems reasonable to guess that understanding of growth promoting and inhibiting mechanisms will continue to proceed rapidly, a baffling question remains. It arises from our ignorance about normal development of the nervous system.



At present it is not known how specific synapses form, so that one type of cell is selected as a target while another one sitting just next door is ignored. 

If hope is to be offered to patients with spinal cord lesions, axons must not only grow (obviously a prerequisite for repair) but they must reform useful connections with the appropriate targets. In the best of all possible worlds no errors would be made. One also can imagine a scenario in which incorrect connections are formed and subsequently tuned by use; pain fibres would, one hopes, not re-form connections in patients.

All the neuroscientists who work on these problems have to face inevitable and quite natural questions about prospects for therapy.

A convenient analogy seems to me to be the repair of a watch. A desirable requirement would surely be to have an understanding of how the watch works and what the various components are doing. Without that knowledge one can still hope for some new insight or fluke that will allow the repair to be made. It would, however, be dangerous to promise how soon the watch will work again until the failure has been diagnosed and only one or two parts remain to be replaced. Because we are not even remotely at this stage in our knowledge of the nervous system, predictions about how and when seem unrealistic. (This analogy is of course flawed: the nervous system has to do the job on it’s own once one has provided the appropriate conditions).

In contrast to the plasticity of the brain, in the spinal cord the degree of plasticity is much less, although perhaps currently underestimated. Once the long tracts are severed or compressed to the point of axotomy, they will not recover and there is usually insufficient overlap in function in the spinal cord for the missing functions to be taken over by surviving tracts, should there indeed be any. The spinal cord is such a narrow structure, normally well protected by the bone forming the spinal canal, that any injury sufficient to damage it in part, may well be severe enough to damage it completely.

In the general strategy of devising spinal repair procedures that could eventually be applied in patients, there are at least four problems to be overcome:

  1. Central nervous system neurons show a variable response in their ability to produce neurites in response to injury, in contrast to peripheral nervous system, which show a consistent ability to do this.
  2. Following damage to the CNS, as for example in a spinal cord injury, any neurites that do appear at the site of injury are unable to cross it, which in patients may involve a substantial length of spinal cord.
  3. Once methods for promotion of growth of axons across the site of injury are available in a clinically applicable form, the axons may have to grow considerable distances to reach appropriate targets and may require specific guidance cues to direct them to functionally appropriate targets.
  4. Having reached appropriate targets, effective functional re-innervation of the targets should occur.

It is not entirely clear how separable are these four components of successful repair. There is increasing evidence that they may indeed be substantially separate processes and that achievement of one will not automatically lead to success with the others.

Thus the work described by Beazley & Dunlop on regeneration in the lizard shows clearly that while axotomised fibres can regrow to the appropriate targets in the visual systems in this species, no functionally effective innervation occurs.

Beazley and Dunlop describe different features of a wide range of species from cold-blooded vertebrates to mammals. Particularly with respect to effectiveness of target re-innervation, there appears to be a spectrum of regeneration. This goes from amphibia and lampreys (with particular respect to the underlying subcellular structures that may be responsible for regenerative outgrowth of injured axons) which can regenerate not only new axons but also functional connections with appropriate targets, through lizards that show excellent axonal growth, but inappropriate target innervation, to mammals in which neither regenerative axon growth nor appropriate target innervation normally occur. The evolutionary significance of this progressive loss of regenerative  ability (an ability which is even more marked in invertebrates) through the animal kingdom is unclear.

The central nervous system of adult mammals, including humans, recovers only poorly from injury. Once severed, major axon tracts (such as those in the spinal cord) never regenerate. The devastating consequences of these injuries—e.g., loss of movement and the inability to control basic bodily functions—has led many neuroscientists to seek ways of restoring the connections of severed axons. There is no a priori reason for this biological failure, since “lower” vertebrates—e.g., lampreys, fish, and frogs—can regenerate a severed spinal cord or optic nerve.

Even in mammals, the inability to regenerate axonal tracts is a special failing of the central nervous system; peripheral nerves can and do regenerate in adult animals, including humans.

Why, then, not the central nervous system?

Neuron injury

At least a part of the answer to this puzzle apparently lies in the molecular cues that promote and inhibit axon outgrowth.

In mammalian peripheral nerves, axons are surrounded by a basement membrane (a proteinaceous extracellular layer composed of collagens, glycoproteins, and proteoglycans) secreted in part by Schwann cells, the glial cells associated with peripheral axons. After a peripheral nerve is crushed, the axons within it degenerate; the basement membrane around each axon, however, persists for months.

One of the major components of the basement membrane is laminin, which (along with other growth promoting molecules in the basement membrane) forms a hospitable environment for regenerating growth cones. The surrounding Schwann cells also react by releasing neurotrophic factors, which further promote axon elongation.

This peripheral environment is so favourable to regrowth that even neurons from the central nervous system can be induced to extend into transplanted segments of peripheral nerve.


Albert Aguayo and his colleagues at the Montreal General Hospital found that grafts derived from peripheral nerves can act as “bridges” for central nervous system neurons (in this case, retinal ganglion cells), allowing them to grow for over a centimeter (Figure
A); they even form a few functional synapses in their target tissues (Figure B).

These several observations suggest that the failure of central neurons to regenerate is not due to an intrinsic inability to sprout new axons, but rather to something in the local environment that prevents growth cones from extending.

This impediment could be the absence of growth-promoting factors— such as the neurotrophins—or the presence of molecules that actively prevent axon outgrowth.

Studies by Martin Schwab and his colleagues point to the latter possibility. Schwab found that central nervous system myelin contains an inhibitory component that causes growth cone collapse in vitro and prevents axon growth in vivo. This component, recognized by a monoclonal antibody called IN-1, is found in the myelinated portions of the central nervous system but is absent from peripheral nerves.

IN-1 also recognizes molecules in the optic nerve and spinal cord of mammals, but is missing in the same sites in fish, which do regenerate these central tracts.

Nogo-A, the primary antigen recognized by the IN-1 antibody, is secreted by oligodendrocytes(they are present in central nervous system), but not by Schwann cells in the peripheral nervous system. Most dramatically, the IN-1 antibody increases the extent of spinal cord regeneration when provided at the site of injury in rats with spinal cord damage. All this implies that the human central nervous system differs from that of many “lower” vertebrates in that humans and other mammals present an unfavourable molecular environment for regrowth after injury.

Why this state of affairs occurs is not known.

One speculation is that the extraordinary amount of information stored in mammalian brains puts a premium on a stable pattern of adult connectivity.

At present there is only one modestly helpful treatment for CNS injuries such as spinal cord transection. High doses of a steroid, methylprednisolone, immediately after the injury prevents some of the secondary damage to neurons resulting from the initial trauma.

Although it may never be possible to fully restore function after such injuries, enhancing axon regeneration, blocking inhibitory molecules and providing additional trophic support to surviving neurons could in principle allow sufficient recovery of motor control to give afflicted individuals a better quality of life than they now enjoy. The best “treatment,” however, is to prevent such injuries from occurring, since there is now very little that can be done after the fact.


  1. Degeneration and Regeneration in the Nervous System  edited by Norman Saunders, Katarzyna Dziegielewska; Anatomy and Physiology, The University of Tasmania, Australia©2000, OPA (Overseas Publishers Association)
  2. Neuroscience, 3rd edition. Editors: Dale Purves, George J Augustine, David Fitzpatrick, Lawrence C Katz, Anthony-Samuel LaMantia, James O McNamara, and S Mark Williams. Sunderland (MA): Sinauer Associates; 2004. ISBN 0-87893-725-0

  3. BRAY, G. M., M. P. VILLEGAS-PEREZ, M. VIDALSANZ AND A. J. AGUAYO (1987) The use of peripheral nerve grafts to enhance neuronal survival, promote growth and permit terminal reconnections in the central nervous system of adult rats. J. Exp. Biol. 132: 5–19.
  4. SCHNELL, L. AND M. E. SCHWAB (1990) Axonal regeneration in the rat spinal cord produced by an antibody against myelin-associated neurite growth inhibitors. Nature 343:269–272.
  5. SO, K. F. AND A. J. AGUAYO (1985) Lengthy regrowth of cut axons from ganglion cells after peripheral nerve transplantation into the retina of adult rats. Brain Res. 359: 402–406.
  6. VIDAL-SANZ, M., G. M. BRAY, M. P. VILLEGASPEREZ, S. THANOS AND A. J. AGUAYO (1987) Axonal regeneration and synapse formation in the superior colliculus by retinal ganglion cells in the adult rat. J. Neurosci. 7: 2894–2909.

Neuroplasticity And Epilepsy: The Effect of Pathological Activity on Neural Circuitry

Epilepsy is a brain disorder characterized by periodic and unpredictable seizures
mediated by the rhythmic firing of large groups of neurons. It seems likely that
abnormal activity generates plastic changes in cortical circuitry that are critical
to the pathogenesis of the disease.

Brain Plasticity: What Is It?

What is brain plasticity?

Does it mean that our brains are made of plastic?

Of course not.

Plasticity, or neuroplasticity, describes how experiences reorganize neural pathways in the brain. Long lasting functional changes in the brain occur when we learn new things or memorize new information. These changes in neural connections are what we call neuroplasticity.

To illustrate the concept of plasticity, imagine the film of a camera. Pretend that the film represents your brain. Now imagine using the camera to take a picture of a tree. When a picture is taken, the film is exposed to new information — that of the image of a tree. In order for the image to be retained, the film must react to the light and “change” to record the image of the tree. Similarly, in order for new knowledge to be retained in memory, changes in the brain representing the new knowledge must occur.

To illustrate plasticity in another way, imagine making an impression of a coin in a lump of clay. In order for the impression of the coin to appear in the clay, changes must occur in the clay — the shape of the clay changes as the coin is pressed into the clay. Similarly, the neural circuitry in the brain must reorganize in response to experience or sensory stimulation.

  • Neuroplasticity includes several different processes that take place throughout a lifetime – Neuroplasticity does not consist of a single type of morphological change, but rather includes several different processes that occur throughout an individual’s lifetime. Many types of brain cells are involved in neuroplasticity, including neurons, glia, and vascular cells.
  • Neuroplasticity has a clear age-dependent determinant – Although plasticity occurs over an individual’s lifetime, different types of plasticity dominate during certain periods of one’s life and are less prevalent during other periods.
  • Neuroplasticity occurs in the brain under two primary conditions:1. During normal brain development when the immature brain first begins to process sensory information through adulthood (developmental plasticity and plasticity of learning and memory).2. As an adaptive mechanism to compensate for lost function and/or to maximize remaining functions in the event of brain injury.
  • The environment plays a key role in influencing plasticity – In addition to genetic factors, the brain is shaped by the characteristics of a person’s environment and by the actions of that same person.

Developmental Plasticity: Synaptic Pruning

Electrical Trigger for Neurotransmission



Gopnick et al. (1999)[Gopnic, A., Meltzoff, A., Kuhl, P. (1999). The Scientist in the Crib: What Early Learning Tells Us About the Mind, New York, NY: HarperCollins Publishers.] describe neurons as growing telephone wires that communicate with one another. Following birth, the brain of a newborn is flooded with information from the baby’s sense organs. This sensory information must somehow make it back to the brain where it can be processed. To do so, nerve cells must make connections with one another, transmitting the impulses to the brain. Continuing with the telephone wire analogy, like the basic telephone trunk lines strung between cities, the newborn’s genes instruct the “pathway” to the correct area of the brain from a particular nerve cell. For example, nerve cells in the retina of the eye send impulses to the primary visual area in the occipital lobe of the brain and not to the area of language production (Wernicke’s area) in the left posterior temporal lobe. The basic trunk lines have been established, but the specific connections from one house to another require additional signals.
Over the first few years of life, the brain grows rapidly. As each neuron matures, it sends out multiple branches (axons, which send information out, and dendrites, which take in information), increasing the number of synaptic contacts and laying the specific connections from house to house, or in the case of the brain, from neuron to neuron. At birth, each neuron in the cerebral cortex has approximately 2,500 synapses. By the time an infant is two or three years old, the number of synapses is approximately 15,000 synapses per neuron (Gopnick, et al., 1999). This amount is about twice that of the average adult brain. As we age, old connections are deleted through a process called synaptic pruning.

Synaptic pruning eliminates weaker synaptic contacts while stronger connections are kept and strengthened. Experience determines which connections will be strengthened and which will be pruned; connections that have been activated most frequently are preserved. Neurons must have a purpose to survive. Without a purpose, neurons die through a process called apoptosis in which neurons that do not receive or transmit information become damaged and die. Ineffective or weak connections are “pruned” in much the same way a gardener would prune a tree or bush, giving the plant the desired shape. It is plasticity that enables the process of developing and pruning connections, allowing the brain to adapt itself to its environment.

Wiring of Brain

Plasticity of Learning and Memory

It was once believed that as we aged, the brain’s networks became fixed. In the past two decades, however, an enormous amount of research has revealed that the brain never stops changing and adjusting. 

Learning, as defined by Tortora and Grabowski (1996)[Tortora, G. and Grabowski, S. (1996). Principles of Anatomy and Physiology. (8th ed.), New York: HarperCollins College Publishers.], is the ability to acquire new knowledge or skills through instruction or experience.

Memory is the process by which that knowledge is retained over time.

The capacity of the brain to change with learning is plasticity.

So how does the brain change with learning?

According to Drubach (2000)[Drubach, D. (2000). The Brain Explained, Upper Saddle River, NJ: Prentice-Hall, Inc.], there appear to be at least two types of modifications that occur in the brain with learning:

  1. A change in the internal structure of the neurons, the most notable being in the area of synapses.
  2. An increase in the number of synapses between neurons.

Initially, newly learned data are “stored” in short-term memory, which is a temporary ability to recall a few pieces of information. Some evidence supports the concept that short-term memory depends upon electrical and chemical events in the brain as opposed to structural changes such as the formation of new synapses. One theory of short-term memory states that memories may be caused by “reverberating” neuronal circuits — that is, an incoming nerve impulse stimulates the first neuron which stimulates the second, and so on, with branches from the second neuron synapsing with the first. After a period of time, information may be moved into a more permanent type of memory, long-term memory, which is the result of anatomical or biochemical changes that occur in the brain (Tortora and Grabowski, 1996)[Tortora, G. and Grabowski, S. (1996). Principles of Anatomy and Physiology. (8th ed.), New York: HarperCollins College Publishers.]

Kindly also read Does Glial Cells Have Any Role in Creativity and Genius ? Nearly 90 % of the Brain is Composed of Glia.

Injury-induced Plasticity: Plasticity and Brain Repair

During brain repair following injury, plastic changes are geared towards maximizing function in spite of the damaged brain. In studies involving rats in which one area of the brain was damaged, brain cells surrounding the damaged area underwent changes in their function and shape that allowed them to take on the functions of the damaged cells. Although this phenomenon has not been widely studied in humans, data indicate that similar (though less effective) changes occur in human brains following injury. Kindly read Why Home Education of a Child is Very Important- Even Kindergarten is Late!

[Source: https://faculty.washington.edu/chudler/plast.html]

The importance of neuronal plasticity in epilepsy is indicated most clearly by an animal model of seizure production called kindling. To induce kindling, a stimulating electrode is implanted in the brain, often in the amygdala (a component of the limbic system that makes and receives connections with the cortex, thalamus, and other limbic structures, including the hippocampus; amygdala came from the latin-greek word, meaning almond, which describe the almond-like structure found in the brain ); Shown in research to perform a primary role in the processing of memory, decision-making, and emotional reactions, the amygdalae are considered part of the limbic system.

  • It can be found easily in mammals under the rhinal fissure and closely related to the lateral olfactory tract. This almond like structure, ranging from 1-4cm , average about 1.8cm, has extensive connection with the brain.

At the beginning of such an experiment, weak electrical stimulation, in the form of a low-amplitude train of electrical pulses, has no discernible effect on the animal’s behaviour or on the pattern of electrical activity in the brain (laboratory rats or mice have typically been used for such studies). As this weak stimulation is repeated once a day for several weeks, it begins to produce behavioural and electrical indications of seizures. By the end of the experiment, the same weak stimulus that initially had no effect now causes full-blown seizures. This phenomenon is essentially permanent; even after an interval of a year, the same weak stimulus will again trigger a seizure. Thus, repetitive weak activation produces long-lasting changes in the excitability of the brain that time cannot reverse. The word kindling is therefore quite appropriate: A single match can start a devastating fire.

The changes in the electrical patterns of brain activity detected in kindled animals resemble those in human epilepsy. The behavioural manifestations of epileptic seizures in human patients range from mild twitching of an extremity, to loss of consciousness and uncontrollable convulsions. Although many highly accomplished people have suffered from epilepsy (Alexander the Great, Julius Caesar, Napoleon, Dostoyevsky, and Van Gogh, to name a few), seizures of sufficient intensity and frequency can obviously interfere with many aspects of daily life. Moreover, uncontrolled convulsions can lead to excitotoxicity.

Up to 1% of the population is afflicted, making epilepsy one of the most common neurological problems.

Modern thinking about the causes (and possible cures) of epilepsy has focussed on where seizures originate and the mechanisms that make the affected region hyperexcitable.

Most of the evidence suggests that abnormal activity in small areas of the cerebral cortex (called foci) provide the triggers for a seizure that then spreads to other synaptically connected regions. For example, a seizure originating in the thumb area of the right motor cortex will first be evident as uncontrolled movement of the left thumb that subsequently extends to other more proximal limb muscles, whereas a seizure originating in the visual association cortex of the right hemisphere may be heralded by complex hallucinations in the left visual field. The behavioural manifestations of seizures therefore provide important clues for the neurologist seeking to pinpoint the abnormal region of cerebral cortex. Epileptic seizures can be caused by a variety of acquired or congenital factors, including cortical damage from trauma, stroke, tumors, congenital cortical dysgenesis (failure of the cortex to grow properly), and congenital vascular malformations. One rare form of epilepsy, Rasmussen’s encephalitis, is an autoimmune disease that arises when the immune system attacks the brain, using both humoral (i.e. antibodies) and cellular (lymphocytes and macrophages) agents that can destroy neurons. Some forms of epilepsy are heritable, and more than a dozen distinct genes have been demonstrated to underlie unusual types of epilepsy. However, most forms of familial epilepsy (such as juvenile myoclonic epilepsy and petit mal epilepsy) are caused by the simultaneous inheritance of more than one mutant gene.

No effective prevention or cure exists for epilepsy. Pharmacological therapies that successfully inhibit seizures are based on two general strategies.

One approach is to enhance the function of inhibitory synapses that use the neurotransmitter GABA;[Gamma-Aminobutyric acid(γ-Aminobutyric acid); (also called GABA for short) is the chief inhibitory neurotransmitter in the mammalian central nervous system. It plays the principal role in reducing neuronal excitability throughout the nervous system. In humans, GABA is also directly responsible for the regulation of muscle tone.] the other is to limit action potential firing by acting on voltage-gated Na+ channels. Commonly used antiseizure medications include carbamazepine, phenobarbital, phenytoin (Dilantin®), and valproic acid.

These agents, which must be taken daily, successfully inhibit seizures in 60–70% of patients. In a small fraction of patients, the epileptogenic region can be surgically excised. In extreme cases, physicians resort to cutting the corpus callosum to prevent the spread of seizures (most of the “split-brain” subjects were patients suffering from intractable epilepsy).

One of the major reasons for controlling epileptic activity is to prevent the more permanent plastic changes that would ensue as a consequence of abnormal and excessive neural activity.

Brain-corpus collosum

    The corpus callosum (Latin for “tough body”) is by far the largest bundle of nerve fibers in the entire nervous system. Its population has been estimated at 200 million axons—the true number is probably higher, as this estimate was based on light microscopy rather than on electron microscopy—
    a number to be contrasted to 1.5 million for each optic nerve and 32,000 for the auditory nerve. Its cross-sectional area is about 700 square millimeters, compared with a few square millimeters for the optic nerve. It joins the two cerebral hemispheres, along with a relatively tiny fascicle of fibers called the anterior commissure, as shown. The word commissure signifies a set of fibers connecting two homologous neural structures on opposite sides of the brain or spinal cord; thus the corpus callosum is sometimes called the great cerebral commissure.
    Until about 1950 the function of the corpus callosum was a complete mystery. On rare occasions, the corpus callosum in humans is absent at birth, in a condition called agenesis of the corpus callosum. Occasionally it may be completely or partially cut by the neurosurgeon, either to treat epilepsy (thus preventing epileptic discharges that begin in one hemisphere from spreading to the other) or to make it possible to reach a very deep tumor, such as one in the pituitary gland, from above. In none of these cases had neurologists and psychiatrists found any deficiency; someone had even suggested (perhaps not seriously) that the sole function of the corpus callosum was to hold the two cerebral hemispheres together. Until the 1950s we knew little about the detailed connections of the corpus callosum. It clearly connected the two cerebral hemispheres, and on the basis of rather crude neurophysiology it was thought to join precisely corresponding cortical areas on the two sides. Even cells in the striate cortex were assumed to send axons into the corpus callosum to terminate in the exactly corresponding part of the striate cortex on the opposite side.
    In 1955 Ronald Myers, a graduate student studying under psychologist Roger Sperry (Roger Wolcott Sperry) at the University of Chicago, did the first experiment that revealed a function for this immense bundle of fibers. Myers trained cats in a box containing two side-by-side screens onto which he could project images, for example a circle onto one screen and a square onto the other. He taught a cat to press its nose against the screen with the circle, in preference to the one with the square, by rewarding correct responses with food and punishing mistakes mildly by sounding an unpleasantly loud buzzer and pulling the cat back from the screen gently but firmly. By this method the cat could be brought to a fairly consistent performance in a few thousand trials. (Cats learn slowly; a pigeon will learn a similar task in tens to hundreds of trials, and we humans can learn simply by being told. This seems a bit odd, given that a cat’s brain is many times the size of a pigeon’s. So much for the sizes of brains.)
    Not surprisingly, Myers’ cats could master such a task just as fast if one eye was closed by a mask. Again not surprisingly, if a task such as choosing a triangle or a square was learned with the left eye alone and then tested with the right eye alone, performance was just as good. This seems not particularly impressive, since we too can easily do such a task. The reason it is easy must be related to the anatomy. Each hemisphere receives input from both eyes, a large proportion of cells in area 17 receive input from both eyes. Myers now made things more interesting by surgically cutting the optic chiasm in half, by a fore-and-aft cut in the midline, thus severing the crossing fibers but leaving the uncrossed ones intact—a procedure that takes some surgical skill. Thus the left eye was attached only to the left hemisphere and the right eye to the right hemisphere. The idea now was to teach the cat through the left eye and test it with the right eye: if it performed correctly, the information necessarily would have crossed from the left hemisphere to the right through the only route known, the corpus callosum. Myers did the experiment: he cut the chiasm longitudinally, trained the cat through one eye, and tested it through the other—and the cat still succeeded. Finally, he repeated the experiment in an animal whose chiasm and corpus callosum had both been surgically divided. The cat now failed. Thus he established, at long last, that the callosum actually could do something—although we would hardly suppose that its sole purpose was to allow the few people or animals with divided optic chiasms to perform with one eye after learning a task with the other.[Source: David Hubel’s-Eye, Brain And Vision]

The corpus callosum is a thick, bent plate of axons near the center of this brain section, made by cutting apart the human cerebral hemispheres and looking at the cut surface. Image source

Here the brain is seen from above. On the right side an inch or so of the top has been lopped off. We can see the band of the corpus callosum fanning out after crossing, and joining every part of the two hemispheres. (The front of the brain is at the top of the picture.) Image source

The Corpus Callosum Defined

Imagine for a moment two people who think and behave in very similar ways yet perceive the world a bit differently from one another.

What if they could share their thoughts, then modify them into a single world view based on both perceptions?

This may seem weird, but our brain works this way thanks to the corpus callosum.

Located near the center of the brain, this structure is the largest bundle of nerve fibers that connects the left and right cerebral hemispheres, much like a bridge. Traffic flows in both directions, but instead of vehicles travelling over the gap, it is information.

Corpus callosum

The corpus callosum is near the center of the brain and is covered by the cerebral hemispheres. Image source

Split Brain Patients

Until the early 1950s, the function of the corpus callosum had alluded scientists. No one knew what it did, except to connect the two cerebral hemispheres. By the 1960s, scientists at least knew that nerve fibers within the callosum connected corresponding areas in the two hemispheres but did not yet understand the complexity involved. However, this limited knowledge was used in an attempt to help patients who suffered from severe and constant seizures.

Normally, electrical activity in the brain flows down specific pathways. This is not so during seizures. The electrical charges could end up anywhere in the brain and stimulate the uncoordinated muscular activity that many people associate with a seizure. Roger Sperry was the scientist who developed a surgical procedure to cut the corpus callosum and stop the spread of this activity from one hemisphere to the other. This procedure was a last ditch effort to normalize the lives of seizure patients, and it was very effective. However, there were a few unexpected results.

After surgery, some patients exhibited contrary behaviours, such as pulling their pants on with one arm while simultaneously pulling them off with the other. Another patient began to shake his wife aggressively with his left hand as his right hand intervened to stop the attack. These results began a plethora of investigations which eventually lead to the understanding that each hemisphere tends to specialize in certain activities, i.e., speech (left side) or emotional reactivity (right side).

After the patient’s callosum was cut, the attack on his wife was instigated by the right hemisphere (via his left hand) because the left hemisphere (right hand) didn’t realize what was happening soon enough to prevent it. Such a conflict ordinarily would have been resolved in the patient’s brain before the external behaviour was produced.

To a greater or lesser degree, both hemispheres contribute to the initiation of a particular behaviour. It is the corpus callosum that provides the communication pathway to coordinate these activities and helps to incorporate them into daily life. Without this brain structure, we literally have two separate personalities in your head, each with its own agenda. [Source: Jay Mallonee – Jay is a wildlife biologist, college professor and writer. His master’s degree is in neurobiology and he has studied animal behaviour since 1976.]


  1. SCHEFFER, I. E. AND S. F. BERKOVIC (2003) The genetics of human epilepsy. Trends Pharm. Sci. 24: 428–433.
  2. ENGEL, J. JR. AND T. A. PEDLEY (1997) Epilepsy: A Comprehensive Textbook. Philadelphia: Lippincott-Raven Publishers.
  3. McNamara, J. O. (1999) Emerging insights into the genesis of epilepsy. Nature 399:

Neuroscience, 3rd edition

Editors: Dale Purves, George J Augustine, David Fitzpatrick, Lawrence C Katz, Anthony-Samuel LaMantia, James O McNamara, and S Mark Williams.

Sunderland (MA): Sinauer Associates; 2004.
ISBN 0-87893-725-0

Epilepsy: Still an Enigma For Common People

“It starts with the sensation of a light switch being pulled violently behind my eyes. I lose cognitive control quickly. I can’t focus on even a simple task, and I forget what I’m doing while I’m in the middle of doing it. I could pick up a pen, then forget why I’m holding it. As the weight behind my eyes intensifies, my eyes roll into my head and start to flutter so rapidly it feels like they are going to pop out. This can last for a split second, a few hours, a few days, or a week.

I have epilepsy, a neurological disorder characterised by recurring, unprovoked seizures. The episodes I described are seizures — they are simply misfiring neurones. Sometimes, these seizures are affected by the season. Other times, they are more easily triggered by stress.

I had my first Tonic-Clonic Seizure in December 1996, my Grade Six year. I fell unconscious into a snow bank in the parking lot of my elementary school. Many people are more familiar with this seizure’s older name, Grand Mal.

I was diagnosed with Generalized Seizures that same year. This news left my family and teachers confused. I had never shown any signs of what they thought of as epilepsy, the violent shaking on the ground portrayed in movies and on TV. No one realised I had been having seizures for many years. Instead, they misread my childhood behaviour as misbehaving.

I frequently blacked out for split seconds in elementary school. The blackouts were likely Absence Seizures, a type of seizure that looks like daydreaming. Even though the blackouts happened on a regular basis, they were almost impossible to spot with an untrained eye.

In a Grade Three art class, I blacked out and knocked over a cup of water that contained a few paint brushes. At the time, no one realised it was a Partial Seizure. When I came to, my teacher asked me why I had done that. She told me it was a disturbance to the class and I needed to watch my behaviour.

I had never even heard the word “seizure” before the age of 11. Without a reference point, these incidents in school seemed normal to me. As far as I was concerned, I didn’t have seizures; I just needed to control my behaviour so I would stop getting in trouble at school.

There was no information about raising a child with Generalized Seizures available to families living with epilepsy in the late-’90s. My family and my teachers didn’t know anyone with epilepsy who could help them figure it out. There were no community epilepsy agencies in our area at the time. Without available resources, we felt left in the dark.

Without a clear understanding of epilepsy as I grew up, it became difficult for me to talk about it with others in my life. As a young adult, I would often avoid discussing it with boyfriends, new employers, and new friends.” [Source: Undiagnosed Epilepsy Made People Think I Was Acting Out

Globally, one in 100 people are diagnosed with epilepsy. It is one of the most common neurological conditions worldwide, yet public knowledge is extremely limited. Many people with epilepsy never talk publicly about their diagnosis fearing discrimination. Seizures and seizure first aid on television are often inaccurate. Myths and misconceptions about epilepsy persist.

Epilepsy is a chronic disorder characterised by recurrent seizures, which may vary from a brief lapse of attention or muscle jerks to severe and prolonged convulsions. The seizures are caused by sudden, usually brief, excessive electrical discharges in a group of brain cells (neurones). In most cases, epilepsy can be successfully treated with anti-epileptic drugs. [Source: http://www.who.int/topics/epilepsy/en/


File:Opisthotonus in a patient suffering from tetanus - Painting by Sir Charles Bell - 1809.jpg

Painting by Sir Charles Bell (1809) showing opisthotonos (in a patient suffering from tetanus.  Opisthotonus (धनुर्वात), Tetanus (धनुस्तम्भ)

Imitators of Epilepsy

  • Fainting (syncope)
  • Mini-strokes (transient ischemic attacks or TIAs)
  • Hypoglycemia (low blood sugar)
  • Migraine with confusion
  • Sleep disorders, such as narcolepsy and others
  • Movement disorders: tics, tremors, dystonia
  • Fluctuating problems with body metabolism
  • Panic attacks
  • Nonepileptic (psychogenic) seizures


What is a Seizure?

A seizure is a brief disruption in normal brain activity that interferes with brain function.

The brain is made up of billions of cells called neurones which communicate by sending electrical messages. Brain activity is a rhythmic process characterised by groups of neurones communicating with other groups of neurones. During a seizure, large groups of brain cells send messages simultaneously (known as “hypersynchrony”) which temporarily disrupts normal brain function in the regions where the seizure activity is occurring.

Seizures can cause temporary changes or impairments in a wide range of functions. Any function that the brain has can potentially be affected by a seizure, such as behaviour, sensory perception (vision, hearing, taste, touch, smell), attention, movement, emotion, language function, posture, memory, alertness, and/or consciousness. Not all seizures are the same. Some seizures may only affect one or two discrete functions, other seizures affect a wide range of brain functions.

Most people associate a seizure with a loss of consciousness and rhythmic jerking movements. Some seizures do cause convulsive body movements and a loss of consciousness, but not all. There are many different kinds of seizures. A temporary uncontrollable twitching of a body part could be due to a seizure. A sudden, brief change in feeling or a strange sensation could be due to a seizure.

Most seizures are brief events that last from several seconds to a couple of minutes and normal brain function will return after the seizure ends. Recovery time following a seizure will vary. Sometimes recovery is immediate as soon as the seizure is over. Other types of seizures are associated with an initial period of confusion afterwards. Following some types of seizures, there may be a more prolonged period of fatigue and/or mood changes.

What is the Difference Between a Seizure and Epilepsy?

A seizure is a brief episode caused by a transient disruption in brain activity that interferes with one or more brain functions.

Epilepsy is a brain disorder associated with an increased susceptibility to seizures.

When a person experiences a seizure it does not necessarily indicate that they have epilepsy, there are many possible reasons that a seizure could happen. When someone has been diagnosed with epilepsy it indicates that they have had a seizure (usually 2 or more) and they are considered to have an increased risk of future seizures due to a brain-related cause.

Causes of Epilepsy

Just as there are many different types of epilepsy there are many different causes too, which include:

  • a brain injury or damage to the brain – Anything that can injure the brain is a potential cause of epilepsy including head trauma; stroke; brain injury during birth; neurodegenerative diseases; brain tumours; and many others. Epilepsy may begin weeks, months or years after an injury to the brain.
  • structural abnormalities that arise during brain development – Sometimes these structural changes in the brain are visible on a brain scan (such as an MRI), other times there could be subtle changes in brain structure that are not easy to detect with current imaging techniques. Epilepsy due to a structural abnormality may begin early in life, during adolescence or in adulthood.
  • genetic factors
    Some genetic causes of epilepsy are inherited and there may be other family members with epilepsy, while other genetic factors that cause epilepsy occur at random.
  • a combination of two or more of the above factors
  • Infections, including brain abscess, meningitis, encephalitis, and HIV/AIDS

For many people with epilepsy, the cause of their seizures is unknown. It is hoped that research and new developments in diagnostic testing will provide more answers for people with epilepsy and their families.

Epilepsy that does not get better after two or three anti-seizure drugs have been tried is called “medically refractory epilepsy.” In this case, the doctor may recommend surgery to:

  • Remove the abnormal brain cells causing the seizures.
  • Place a vagal nerve stimulator (VNS). This device is similar to a heart pacemaker. It can help reduce the number of seizures.

Opportunity is Here And Now: A Lesson That Can be Learned From Pandit Madan Mohan Malaviya

I came across a very interesting article from a Newspaper ‘New Indian Express’ published in India, I thought I should share it on my blog.

 “Opportunity is here and now”

It’s not the lack of opportunities that prevent a person from succeeding in life.

Not using what you have on hand is a roadblock that impedes one’s success in his/her endeavours.

I do not wish to work under someone. I want to run my own business.

For that purpose, I need capital and experience. So I am working as a sales representative in an organisation. But in this profession, I have to go from house to house; organisation to organisation.

In order to meet a person, I have to wait for hours together. Even to get an appointment to see someone, I have to visit the place several times. Many look down upon me as a ‘nuisance’ and treat me so.

Because of this, my self­ esteem has suffered severe blows.

Sometimes, I feel why at all should I get into any business.

Why can’t I get employed as a clerk in a company?

When someone praises us as capable, clever, what do we think?

This person says I am intelligent. He thinks I know a lot. He calls me clever. He compares me with Chanakya. He feels that I am highly skilful. He is astounded at my intelligence…

In this manner, we create a heap of a thousand words of praise from a single word of appreciation.

Similarly, if someone calls us a fool, we add a thousand words of insult and feel depressed.

We would not look into every possible interpretation of the word, and create meanings where none exist!

Pandit Madan Mohan Malaviya was the founder of The Banaras Hindu University (B.H.U), in North India.

B.H.U is one of the largest residential universities in Asia, with over 20,000 students.

Pandit Madan Mohan Malaviya

In the first decade of the 20th Century, the country (India) was in abysmal depths and independence appeared like a distant dream. The total number of colleges in the country had gone up from 27 in 1857 to just 72 in 1882 and the total number of B. A. graduates in twenty-five years was 3284. Literacy was an unbelievable low of about 6% in 1900 and the educational facilities were meagre. All the five Universities which existed at that time in Calcutta, Bombay, Madras, Lahore and Allahabad, were mainly examining Universities. While India had only five Universities at that time, U.K had eighteen, France– fifteen, Italy– twenty-one, Germany-twenty two, and USA– 134 Universities.

Under these conditions, it would have looked foolhardy and vain to think or even dream of the ‘post-independent India’. However, at that time, Malaviyaji started looking beyond the current milieu and the forthcoming independence. He saw from the depths/from the dark abyss into the distant future and visualized a ‘Resurgent Modern India’!!

Malaviyaji realised that ‘Modern India’ can be built by engineers, doctors, scientists & artists, only when they are imbued with high character, probity and honour. He strongly felt that all of them could be nurtured in a beautiful, big garden called the ‘University’, which should be an extension and modified version of the gurukul. Hence, in order to meet the future immense needs of the ‘Resurgent Modern India’, he visualized a ‘Modern University’ that combines the best thought and culture of the East with the best Science & Technology of the West. Source: http://www.mahamana.org/biography-.html

“Everyone knows that there is no great beggar than Pandit Malaviyaji on the face of the earth. He has never begged for himself; by the grace of God he has never been in want, but he became a voluntary beggar for causes he has made his own, and God has always filled his bowl in an over-flowing measure. But he had an insatiable appetite and although he got the crore he wanted he is still asking for more.”

Mahatma Gandhi, Silver Jubilee Adress, 21st Jan 1942.

Pandit Madan Mohan Malviya worked with determination to start the University.

There was a crisis for funds, but he did not get disheartened. He went from town to town, met many rich men and traders to collect donations.

Malaviyaji undertook frequent tours to request and persuade the rulers and rich men of various states to donate to the noble cause.

It took the Prince of Beggars, as Malaviyaji was popularly known, nearly two years from 15th July 1911 to 28th April 1913 to collect the minimum required the amount of Rs (I.N.R) 50 lakhs to start serious negotiations with the representatives of the British Government of India. It is not only the rich but also the poor and the lowly responded generously to Pandit Madan  Mohan Malaviya’s call. It is said that a woman offered her bangles for the cause and a courtesan her day’s earnings! [Source: http://www.mahamana.org/about-bhu.html%5D

He went to the Nizam of Hyderabad to request him for funds.

The last Nizam was well known for his huge wealth and jewellery collection; he had been the richest man in the world until the end of his reign

The Nizam was furious,

“How dare you come to me for funds… that too for a Hindu University?” he roared with anger and took off his footwear and flung them at Malviya.

Malviya picked up the footwear and left silently. He came directly to the marketplace and began to auction the footwear. As it was the Nizam’s footwear, many came forward to buy it. The price went up. When the Nizam heard of this, he became uneasy. He thought it would be an insult if his footwear were to be bought by someone for a pittance. So he sent one of his attendants with the instruction,

“Buy that footwear no matter what the bidding price be!”

Thus, Malviya managed to sell the Nizam’s own footwear to him, for a huge amount. He used that money to build the Banaras Hindu University!

The Benares Hindu University Act was passed on 1st October 1915 and came into force from 1st April 1916. The foundation stone was laid on 4th February 1916 by H.E.Lord Hardinge, the then Viceroy & Governor General of India. The first colleges to be started were: The Central Hindu College (Oct 1917), The College of Oriental Learning (July 1918), The Teachers Training College (Aug 1918) and The Engineering College (Aug 1919). [https://en.wikipedia.org/wiki/Banaras_Hindu_University]

I only wish to tell this to all those young men who are without an ideal or a goal in life.

Do you know what prevents a person from succeeding?

It is not his lack of skills or qualifications.

It is not what you have, but it is how you use what you have, which makes a difference in your life.

The greatness of the Vision depends mostly on its far-sightedness, it’s clarity, it’s magnitude, and it’s wide canvas.

Normally, the farther one looks into the future, hazier is the picture.  

While the ordinary see nothing but the dark clouds, the visionary sees a bright star shining in the distance.

He/She then paints it for others with all the clarity on a wide canvas.

Do not give up under the impression that ‘Opportunity is No Where!’ Take that sentence in the right spirit that ‘Opportunity is Now Here!’ and move forward with your life!

“No aspect of Malaviya ji is hidden from me. I am well aware of his simplicity, purity, tenderness, and love. From all these virtues of him, you must take as much as you (students & teachers) can. If someone can not take the warmth of Sun, even being in the open, it is not the fault of Sun. Sun itself gives warmth to one and all. If someone does not want to take it and shivers in cold then what can Sun do? Being so close to Malaviyaji, if you cannot learn from his life simplicity, sacrifice, patriotism, large-heartedness, universal love and other virtues, then who can be a greater unlucky person than you?”     

Mahatma Gandhi

“Patriotism and service to the motherland is food for Malaviya Ji. He can never, ever leave it, just as it is impossible to leave daily recitation of BhagwadGita. Patriotism and service to motherland together is the breath of life for him. That is why till he breathes he will ceaselessly continue to serve motherland and humanity.” 

Mahatma Gandhi, from monthly periodical ‘VishwaJyoti’, Jan 1962.

When I returned to my Country, I first went to Lokamanya Tilak. He appeared tall like the Himalayas. I thought it was not possible for me to scale the heights and returned. Then I went to Deshbandhu Gokhale. He appeared deep like the Ocean. I saw that it was not possible for me to gauge the depth and returned. Finally, I went to Mahamana Malaviya and he appeared like the pure flow of Ganga. I saw it was possible to take bath in the sacred flow.      

Mahatma Gandhi

His personality cannot be condensed in a few words. Mahatma Gandhi called him “praatah smaraniyal”, a pious person whose name when remembered in the morning would lift one out of the mire of one’s sordid self. Gandhiji compared Tilak to the lofty Himalayas, Gokhale to the deep seas and Malaviyaji to the crystal clear sacred river in which he decided to have ablution! Malaviyaji’s gentle, sweet, soft and graceful nature was a true reflection of his abundant love for humanity. A British official commented that Malaviyaji ‘wore the white flower of a blameless life’.

Edgar Snow, a journalist, wrote that his personality radiated ‘the sweetness and simplicity of a child, yet his words carried the strength and conviction of a man with a settled philosophy of life’. For all his sweetness he could still be tougher than the toughest when occasion demanded it. Dr S. Radhakrishnan said                             “Pandit Malaviyaji is a Karmayogi. He is not only a representative of Hinduism but the soul of Hinduism. He had strived all through his life for the Hindu ideals and we see the combination of idealism and practical wisdom……. While preserving the imperishable treasures of our past, he is keen on moving forward with the times”.

Malaviyaji visualized the importance of education and the hardships of the students early in life. He set up the ‘MacDonald Hindu Boarding House to accommodate 230 students in 1903 in Allahabad, by collecting a public donation of Rs (I.N.R) 1.3 lakhs. This appears to be the precursor for his grand vision of the Banaras Hindu University, which he built up from a vision in 1900 to a reality in 1916. These examples show his keen analysis of a problem, ability to think of a workable solution, motivate a team to work, collect a large number of funds for a public cause and realize the dream.

Gopala Krishna Gokhale said

“Malaviyaji’s sacrifice is a real one. Born in a poor family, he started earning thousands monthly. He tasted luxury and wealth but giving heed to the call of the nation, renouncing all he again embraced poverty”.

Adapted from

‘Swami Sukhabodhananda’- The New Indian Express. 


Published Date: Sep 27, 2012, 10:28 AM

23/01/2016 Opportunity is here and now http://www.newindianexpress.com/cities/chennai/article1274340

Neural Stem Cells – Promise and Perils

One of the most highly publicized issues in biology over the past several years has been the use of stem cells as a possible way of treating a variety of neurodegenerative conditions, including Parkinson’s, Huntington’s, and Alzheimer’s diseases.

Amidst the social, political, and ethical debate set off by the promise of stem cell therapies, an issue that tends to get lost is…

What, exactly, is a stem cell?

Neural stem cells are an example of a broader class of stem cells called somatic stem cells. These cells are found in various tissues, either during development or in the adult.

All somatic stem cells share two fundamental characteristics:

  1. they are self-renewing, and
  2. upon terminal division and differentiation they can give rise to the full range of cell classes within the relevant tissue.

Thus, a neural stem cell can give rise to another neural stem cell or to any of the main cell classes found in the central and peripheral nervous system (inhibitory and excitatory neurons, astrocytes, and oligodendrocytes; Figure A).

A neural stem cell is therefore distinct from a progenitor cell, which is incapable of continuing self-renewal and usually has the capacity to give rise to only one class of differentiated progeny.

  • An oligodendroglial progenitor, for example, continues to give rise to oligodendrocytes until it’s mitotic capacity is exhausted;
  • a neural stem cell, in contrast, can generate more stem cells as well as a full range of differentiated neural cell classes, presumably indefinitely.

Neural stem cells, and indeed all classes of somatic stem cells, are distinct from embryonic stem cells.

Embryonic stem cells (also known as ES cells) are derived from pre-gastrula embryos. ES cells also have the potential for infinite self-renewal and can give rise to all tissue and cell types throughout the organism including germ cells that can generate gametes (recall that somatic stem cells can only generate tissue specific cell types). Stem cells

There is some debate about the capacity of somatic stem cells to assume embryonic stem cell properties.

Some experiments with hematopoetic and neural stem cells indicate that these cells can give rise to appropriately differentiated cells in other tissues; however, some of these experiments have not been replicated.

The ultimate therapeutic promise of stem cells—neural or other types—is their ability to generate newly differentiated cell classes to replace those that may have been lost due to disease or injury.

Such therapies have been imagined for some forms of diabetes (replacement of islet cells that secrete insulin) and some hematopoetic diseases. In the nervous system, stem cell therapies have been suggested for replacement of dopaminergic cells lost to Parkinson’s disease and replacing lost neurons in other degenerative disorders.

While intriguing, this projected use of stem cell technology raises some significant perils.

  • These include insuring the controlled division of stem cells when introduced into mature tissue, and
  • identifying the appropriate molecular instructions to achieve differentiation of the desired cell class.

Clearly, the latter challenge will need to be met with a fuller understanding of the signalling and transcriptional regulatory steps used during development to guide differentiation of relevant neuron classes in the embryo.

At present, there is no clinically validated use of stem cells for human therapeutic applications in the nervous system. Nevertheless, some promising work in mice and other experimental animals indicates that both somatic and ES cells can acquire distinct identities if given appropriate instructions in vitro (i.e., prior to introduction into the host), and if delivered into a supportive host environment.

For example, ES cells grown in the presence of platelet-derived growth factor, which biases progenitors toward glial fates, can generate oligodendroglial cells that can myelinate axons in myelindeficient rats. Similarly, ES cells pretreated with retinoic acid matured into motor neurons when introduced into the developing spinal cord (Figure below).

While such experiments suggest that a combination of proper instruction and correct placement can lead to appropriate differentiation, there are still many issues to be resolved before the promise of stem cells for nervous system repair becomes a reality.

Schematic of the injection of fluorescently labeled embryonic stem (ES) cells into the spinal cord of a host chicken embryo.

ES cells integrate into the host spinal cord and apparently extendaxons.

the progeny of the grafted ES cells are seen in the ventral horn of the spinal cord. They have motor neuron-like morphologies, and their axons extend into the ventral root. (From Wichterle et al., 2002.)

Source: Neuroscience, 3rd edition
Editors: Dale Purves, George J Augustine, David Fitzpatrick, Lawrence C Katz, Anthony-Samuel LaMantia, James O McNamara, and S Mark Williams.
Sunderland (MA): Sinauer Associates; 2004.
ISBN 0-87893-725-0

What is your definition of ethics?

Ethics — described briefly as the norms by which acceptable and unacceptable behaviours are measured–has been the concern, and perhaps the great dilemma, of sentient humans since Socrates subjected it to philosophical inquiry almost 2500 years ago. Socrates believed, without universal acceptance, that the most pertinent issues people must deal with are related to how we live our lives, what actions are and are not righteous, and how people should live together peacefully and harmoniously.

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Image Source: http://quotesvil.com/ethics-quotes.html


A vast parade of philosophers, religious leaders, politicians, professors, and self-help gurus have followed Socrates’ lead through the ensuing centuries; it’s a popular and enduring subject, perhaps because it is so complex, intriguing, and pervasive in every facet of our lives.

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Image Source: http://mattdickenson.com/2012/08/06/statistics-ethics-and-open-data/


Today, ethics dominates our news in the form of anti-ethics. The headlines in newspapers and the lead stories on TV, radio, and Internet news are typically about such abhorrent behaviour as lying, stealing, revenge, convictions for corruption, gratuitous murder, and misuse of public or other people’s funds for personal gain. Readers, viewers, and listeners can hardly be faulted for thinking that we live in a corrupt society, exactly what Socrates and others did not want or envision. Perhaps the anti-ethical stance of the media is the most anti-ethical part of our society.
Nevertheless, the battle for a more ethical society rages unchecked and unabated.

Ethics In Leadership

Image Source: http://www.theexpressivepress.com/everyday-ethics-from-everyday-folks/


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Image Source: https://ethicsforadversaries.com/2011/02/17/the-inevitable-gap-between-whats-legal-and-whats-ethical/



Bad circumstances are not excuses for making bad choices.
Values and ethics are not just designed for good times, but also to get you through bad times. They are like the laws of the land— you need them when circumstances are good, but they’re even more valuable to protect you from the bad.
Most choices are not ethical choices. 
For example, what clothes to buy or what TV to get are personal choices based on what is appropriate for your situation. They are not ethical choices. Personal choices are subjective, not objective. Even though these are not ethical issues they certainly involve responsibility. 

Image Source: http://www.becomeaparalegal.org/blog/ethical-dilemmas-in-the-paralegal-field-and-life/

Ethical choices reflect the objective choice between right and wrong. That is why your conscience hurts when making an unethical choice and does not hurt when you make a wrong personal choice—– because in ethical matters there is a clear right choice. 

Image Source: http://swapsushias.blogspot.in/2013/10/ethics-vs-morals-understanding-crux-of.html#.V8aMsfl9600

Just as with a mathematics test, who takes it and whatever answer they give varies, but what makes it right is not the choice, but the actual correctness of the answer. 

Being a nice person is not the same thing as being a good and ethical person.

A person can be socially nice yet be a cheat and a liar. That makes him nice but unethical. However, niceness reflects social acceptability. Nice does not mean good.

Unfortunately, many of our choices today seem to be based on:

1.   Our desire for convenience, comfort and pleasure.
2.  Our feelings- the criteria is to feel good rather than do what is responsible.
3.  Social fads and ads- the philosophy that everyone else is doing it, so why shouldn’t I?
It is a common belief that ethics and ethical choices are confusing. 
The big question is to whom?
Only to those with unclear values. 

Source: https://sites.psu.edu/leadership/2014/02/14/ethics-trait-or-skill/


Image Source: http://centers.scb.rit.edu/ethics/fun-with-ethics/

Those who believe that ethics cannot be generalised but vary with every situation, come up with justification and keep changing their ethics from situation to situation, and person to person. 

This is called SITUATIONAL ETHICS. This is the ethics of convenience rather than conviction.

You'd think she'd have seen that coming.

Image Source: http://eqcomics.com/2012/07/17/super-ethics/


There’s harmony and inner peace to be found in following a moral compass that points in the same direction, regardless of fashion or trend —–Ted Koppel

Why do we have standards? 
 Standards are a measure. 
 One Metre in Europe is One Metre in Asia. 
One Kilogramme of flour is One Kilogramme of flour wherever you go.

Image Source: http://www.chicagonow.com/quark-in-the-road/2014/11/ethics-in-a-nutshell-for-a-short-attention-span-age/

People who do not want to adhere to any moral standards, keep changing the definition of morality by saying nothing is right or wrong, that one’s thinking makes it so. They put the onus in interpretation rather than on their behaviour. 

They feel “my behaviour is okay, your interpretation was faulty.”

Image Source: http://ethicsforadversaries.com/2011/02/17/the-inevitable-gap-between-whats-legal-and-whats-ethical/

For example,
Adolf Hitler could have believed he was right. 
But the big question is, “Was he right?” 
Giving food to the hungry is right but at the same time giving food everytime a person becomes hungry is not, teach him/her how to learn and earn.
The generalisation sets the benchmark; the exception is the situation. 
For example, murder is wrong. That is a general statement and a generalised truth, and ethical standard. Unless it is in self-defence. 

This doesn’t mean it is okay to murder if the weather is good or if you feel like it.

Our standard of ethics is revealed by the advisors we hire, the superiors we choose to work with, the friends we like to hang out with, the suppliers we choose, the buyers we deal with, as much as how we spend our leisure time. 

Image Source: http://www.paigntonacademy.org/ethics-revision-sessions/

Opinions vary from culture to culture. But values such as fairness, justice, integrity and commitment are universal and eternal. 
They have nothing to do with culture. Never has there been a time when society has not respected courage over cowardice.
Ethics and justice involve the following:
·       Empathy
·       Fairness
·       Compassion for the injured, the ill, and the aged.
·       The larger interests of the society.

Just because a majority of people agree on something doesn’t make it right.

If the citizens of a country voted to disenfranchise all blue-eyed people, that doesn’t make it a right decision.

Image Source: http://grow3.com/category/ethical-leadership-2/

 Basic ethics are pretty universal. Just as freedom without discipline leads to destruction, similarly, a society without a set of principles destroys itself.
If values were so subjective, no criminal should be in jail.
A society becomes good or bad, based on the ethical values of individuals. And what gives a society it’s strength is it’s underlying ethical values.
People who believe in the relativity of ethics get stuck in their own paradox. 
They say, “Everything is relative.” 
The statement is itself is an absolute truth. It is self-contradictory. The distinction between right and wrong, dishonesty and honesty, presupposes their existence. Changing terminology does not change the meaning.
Just like changing labels does not change the contents. Low moral values become more accepted by giving them new names, though the result is the same. 
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Image Source: Ethics Training

Sometimes even the media glamorises immorality— liars are called extroverts with imagination.

The price of apathy is to be ruled by evil men Plato
To educate a man, and not in morals, is to educate a menace to society. 
                                                                                                   —-Theodore Roosevelt

Image Source: http://edition.cnn.com/2013/05/15/business/women-work-ethics/


When Michael Severn, the President of Columbia University resigned in 1993, a reporter asked him if there was any task left incomplete.
“YES”, replied Severn.
“It sounds complacent, but there is really only one.” 
He referred to the lack of instruction in ‘Ethics’:
“The average undergraduate, however, gets no training in these areas. Most educators are afraid to touch the subject. The subject of ethics is usually left to parents to address. The result is that young people who need moral and ethical training than ever are getting less than ever. Moral and ethics are not religion. They are logical, sensible principles of good conduct that we need for a peaceful society.”
[Source: John Beckley, “Isn’t it time to Wake Up?” In the Best of….Bits and Pieces, Economics Press, Fairfield, NJ, 1994, p.129]


Image Source: http://www.nasw-michigan.org/?page=Ethics

Let no man be sorry he has done good, because others have done evil! If a man has acted right, he has done well, though alone; if wrong, the sanction of all mankind will not justify him.

                                                                                                               —–Henry Fielding

Most will agree that legality and ethics are not the same things. What may be ethical may or may not be legal, and vice-versa.
For example:
1.   An insurance salesperson more concerned with getting a larger commission than selling the best policy for that particular client sells an unsuitable policy. This may be legal but it is unethical.
2.  A young executive is driving over the speed limit, trying to reach the hospital with his bleeding child in the back seat of his car. Hardly anyone would question the breaking of law in this situation. It would be unethical not to get medical help to save the child’s life, even if it meant breaking the law.
 Legality establishes minimum standards, whereas ethics and values go beyond standards. Ethics and values are about fairness and justice. They are not about pleasing and displeasing people. They are about respecting people’s needs and rights.

Image Source: https://www.asme.org/engineering-topics/articles/engineering-ethics/embedding-ethics-in-engineering-education


Image Source:  http://peopleforethicalliving.com/ethical-living-ethical-choices/

There are many kinds of desires

the desire for success;
the desire to do one’s duty even at the cost of pleasure;
the desire for purpose—something worth dying for which gives meaning to life.
What good is it if you gain the whole world and lose your conscience?
A purposeless life is a living death.
What is your purpose?
Do you have one?
Purpose brings passion.
Find or create a purpose and then pursue it with passion and perseverance.
Every day we need to ask ourselves:
“Am I getting any closer to my purpose in life? Do you have one? 
Purpose brings passion. Find or create a purpose and then pursue it with passion and perseverance.

Image Source: http://econwatson.blogspot.in/2010/10/lighter-side-food-safety-and-ethics.html

 Adapted from ‘You Can Win’
by Shiv Khera.