Essays - Winter 2010

My Brain on My Mind

The ABCs of the thrumming, plastic mystery that allows us to think, feel, and remember

By Priscilla Long | December 1, 2009


Walter Long was a writer and he was my grandfather. He was courteous, charming, chivalrous, handsome, well-spoken, well-shaven, well-dressed, and completely senile. His mental decline began when I was a girl. In the end he didn’t know me, and he didn’t know his own son, my father. He was born in 1884. He wrote for four or five decades until, starting sometime in the 1950s, dementia destroyed his writing process. We have a photo of Granddad writing with a dip pen at a slant-top writing table. He was a tall, thin man with a high forehead and a classic, almost Grecian, nose. He was a metropolitan reporter for Philadelphia’s leading newspaper, The Philadelphia Bulletin, before the era of regular bylines. What remains of his five decades of reportage? Nothing. His words have been obliterated, eradicated, annihilated. And what do we know about his brain? About his neurons, or ex-neurons? Almost nothing. Before me, my grandfather was the writer in the family. This abecedarium is dedicated to him. To his memory.


Alphabets are an awe-inspiring invention of the Homo sapiens brain. Consider these sound symbols lining up before your eyes. Our 26 letters can create in English one to two million words. (The range has to do with what you consider a word. Are brain and brainy the same word?)

Where in our brain do we keep our ABCs? How does our brain provide us with the use of alphabetic characters without thought? I am handwriting this sentence in my writer’s notebook. The letters flow out of my pen as if they were a fluid flowing from my fingertips rather like sweat. Nothing for which I really have to use my brain.


My brain boggles my mind. Its mystery. Its moody monologue.

I walk down Bagley Avenue this fine April day. The Seattle sky is blue. The Brain, wrote Emily Dickinson, is wider than the Sky, since it contains both Sky and You. My own brain contains this blue sky plus six cherry trees in full bloom. Plus the memory of my granddad’s face. Plus bungalow yards and rock gardens bright with tulips, violets, camellias, and azaleas. The passing scene enters my eyes in the form of light waves. Neurons in my retina convert these light waves into electrical impulses that travel farther back into my brain.

Our brain contains 100 billion neurons (nerve cells). Our gray matter. Each neuron has an axon—a little arm—that transmits information in the form of electrical impulses to the dendrites—receivers—of nearby neurons. Dendrites branch twig-like from each neuron. Between axon and dendrite, the synapse is the point of connection. Axons commune with dendrites across the synaptic gap.

When neurons “fire,” they emit a rat-a-tat-tat of electrical pulses that travel down the axon and arrive at its terminal endings, which secrete from tiny pockets a neurotransmitter (dopamine, say, or serotonin). The neuro­transmitter ferries the message across the synaptic abyss and binds to the synapse, whereupon the synapse converts it back into an electrical pulse . . .

What blows my mind is this: a single neuron can make between 1,000 and 10,000 connections. At this moment our neurons are making, it could be, a million billion connections.

What this electrical/chemical transaction gives us is culture: nail polish, Poland, comic books. Otis Redding belting out “Try a Little Tenderness” at the 1967 Monterey International Pop Music Festival, along with its memory, its YouTube reenactment, its recordings and coverings and remixings, its moment in history.

The geography of the brain ought to be taught in school, like the countries of the world. The deeply folded cortex forms the outer layer. There are the twin hemispheres, right brain and left brain. (We may be of two minds.) There are the four lobes: frontal in front, occipital (visual cortex) in back, parietal (motor cortex) on top, and temporal behind the ears. There’s the limbic system (seat of emotion and memory) at the center. There’s the brain stem, whose structures keep us awake (required for consciousness) or put us to sleep (required for regeneration of neurotransmitters).

The brain also has glial cells, white matter. Glial cells surround and support neurons, carry nutrients to neurons, and eat dead neurons. Some glial cells regulate transmission and pulverize post-transmission neurotransmitters. Others produce myelin, which surrounds and protects axons. Glial cells are no longer thought to be mere glue. When stimulated, they make, not electricity as neurons do, but waves of calcium atoms. They also produce neurotransmitters—glutamate (excitatory) and adenosine (inhibitory). We may not know what they are up to, but we know they’re up to something.

So there you have the brain: a three-pound bagful of neurons, electrical pulses, chemical messengers, glial cells. There, too, you have the biological basis of the mind. “Anything can happen,” says the poet C. D. Wright, “in the strange cities of the mind.” And whatever does happen—any thought, mood, song, perception, delusion—is provided to us by this throbbing sack of cells and cerebral substances.

But what, then, is consciousness?


Consciousness, according to neuroscientists Francis Crick and Christof Koch, is “attention times working memory.” “Working memory” being the type of memory that holds online whatever you are attending to right now. Add to “attention times working memory” a third element of consciousness—the sense of self, the sense of “I” as distinct from the object of perception. If I am conscious of something, I “know” it. I am “aware” of it. As neurobiologist António Damásio puts it in The Feeling of What Happens, “Consciousness goes beyond being awake and attentive: it requires an inner sense of the self in the act of knowing.” (It also requires the neurotransmitter acetylcholine.)

There is another theory of consciousness, the quantum physics theory of consciousness, in which quarks, a fundamental particle, have proto­consciousness. This theory is said to have an aggregation problem—how would zillions of protoconscious particles make a conscious being? It puts consciousness outside life forms and into moonrocks and spoons. I will leave that theory right here.

In dreamless sleep, we are not conscious. Under anesthesia, we are not conscious. Walking down the street in a daze, we are barely conscious. Consciousness may involve what neuroscientist Jean-Pierre Changeux postulates is a “global workspace”—a metaphorical space of thought, feeling, and attention. He thinks it’s created by the firing of batches of neurons originating in the brain stem whose extra-long axons fan up and down the brain and back and forth through both hemispheres, connecting reciprocally with neurons in the thalamus (sensory relay station) and in the cerebral cortex. These neurons are focusing attention, receiving sensory news and assessing it, repressing the irrelevant, reactivating long-term memory circuits, and, by comparing the new and the known, registering a felt sense of “satisfaction” or “truth,” which is brought home by a surge of the reward system (mainly dopamine).

Crick and Koch propose, rather, that the part of our gray matter necessary for consciousness is the claustrum, a structure flat as a sheet located deep in the brain on both sides. Looked at face-on, it is shaped a bit like the United States. This claustrum maintains busy connections to most other parts of the brain (necessary for any conductor role). It also has a type of neuron internal to itself, able to rise up with others of its kind and fire synchronously. This may be the claustrum’s way of creating coherence out of the informational cacophony passing through. For consciousness feels coherent. Never mind that your brain at this moment is processing a zillion different data bits.

Gerald Edelman’s (global) theory of consciousness sees it resulting from neuronal activity all over the brain. Edelman (along with Changeux and others) applies the theory of evolution to populations of neurons. Beginning early in an individual’s development, neurons firing and connecting with other neurons form shifting populations as they interact with input from the environment. The brain’s reward system mediates which populations survive as the fittest. Edelman’s theory speaks to the fact that no two brains are exactly alike; even identical twins do not have identical brains.

How, in Edelman’s scheme, does consciousness achieve its coherence? By the recirculation of parallel signals. If you are a neuron, you receive a signal, say from a light wave, then relay it to the next neuron via an electrical pulse. Imagine a Fourth of July fireworks, a starburst in the night sky. Different groups of neurons register the light, the shape, the boom. After receiving their respective signals, populations of neurons pass them back and forth to other populations of neurons. What emerges is one glorious starburst.

I myself do not have a theory of consciousness. Still, I am a conscious (occasionally) being. My sense of myself, my sense of an “I,” has some sort of neuronal correlate. I am conscious (aware) of the fact that I am teaching a writing seminar (observed object with neuronal correlate) on the literary form known as the abecedarium (observed object with neuronal correlate). I am conscious (aware) that I will be submitting my own abecedarium—this one—to the brainy writers in the class. Because I can imagine the future, because I can plan ahead (thanks in part to my frontal lobes), I feel apprehensive. How crazy! To imagine I could comprehend the Homo sapiens brain, the most complex object in the known universe, within the 26 compartments of an abecedarium.

I will try. I will color the cones and rods and convoluted lobes printed in black outline in my anatomy coloring book. I will teach my neurons to know themselves. As I write this, I picture our class seated around our big table. I can picture the face of each writer at the table. To each face I can attach a name. This is proof that, as of today, I have dodged dementia.


Dementia dooms a life. It doomed my grandfather’s life. Even today, when Alzheimer’s disease—just one type of dementia—afflicts as many as 5.3 million Americans, including one in four of all persons age 85 or older, we know far too little about it. It’s not clear what kind of dementia Walter Long had. He may not have had Alzheimer’s. He may have had Lewy body dementia. He may have had small strokes. Whatever it was, it doomed his brain, it doomed his body, it doomed his body of work—including a novel, never published, which must have existed as a typescript. Upon his death following years of senility, this novel was discarded. For me, the disappearance of my grandfather’s writing is a distressing enigma. Not an easy problem.


Easy Problem. Philosopher’s lingo for the problem in neuroscience of comprehending the neuronal correlates of consciousness. When you see red, what exactly are your neurons doing? When you remember your grand­father’s face, what are your neurons doing? It may be difficult to parse the answer but in principle we can do it. It’s easy. The Hard Problem is the mystery of subjective experience. When long light waves stimulate our neural pathways, why do we experience the color red? And what survival benefit caused our brains to develop, through eons of evolution, an ability to experience a “sense of self,” a self able to see itself as special or heroic or smart or not so smart—as, on occasion, a complete failure?


Failure to learn new things kills neurons. People who vegetate before the TV are killing their neurons. People who never do anything new or meet anyone new are killing their neurons. People who never read or learn a new game or build a model airplane or cook up a new recipe or learn a new language are killing their neurons. Mind you, many middle-aged professionals are killing their neurons. They’re doing what they are good at, what they already know, what they learned to do years ago. They’re pursuing careers, raising children, cooking dinner, returning phone calls, reading the newspaper. They are busy and accomplished, but they are not learning anything new. If you are not learning anything new, you are killing your neurons. To keep your neurons, learn something new every day. Begin now. Doing so requires no particular genius.


Genius is nothing you can be born with. No one is born with it. Not Mozart, not Picasso, not Tolstoy. In any field, world-class achievement demands at least 10,000 hours of practice. According to Daniel J. Levitin in This Is Your Brain on Music, dozens of cognition studies have produced the same result: geniuses practice more. Neural pathways require repeated stimulation to attain a “genius” level of mastery. The neurons must be stimulated and restimulated, over and again. Essential to this learning process, to this process of achieving supreme mastery, is the hippocampus.


The hippocampus is at the core of what is known as declarative memory—memory of facts and events that can be recalled later for conscious reflection. Memories of what you did this morning, of which candidate you voted for, of whether you were supposed to bring home milk or eggs, all depend on the hippocampus. In Alzheimer’s, the hippocampus is gradually destroyed. The sea horse–shaped structure is located above the eye, about an inch behind the forehead. It is part of the limbic system, chief purveyor of emotion.

We remember what is emotional. Fear, essential for survival, is provided to us by our almond-shaped amygdalae, also part of the limbic system. Fearful events fire up the amygdala and the amygdala sends its projections all over the brain, but especially to the hippocampus. The amygdala can smell a rat. It receives sensations directly from the nose and sets off alarms with no intervening cognition. We remember what we fear.

And we remember what we like, what we want, what we love, what triggers our reward system, dopamine, serotonin. We attend to what is meaningful, what is emotionally resonant, whether positive or negative. We remember what we pay attention to.

Hippocampal activity is not essential for procedural memory—what the body knows. You don’t need your hippocampi to ride a bike or get out of bed or even play the piano if you are a pianist. The hippocampus is not essential for semantic memory—facts and words. It’s not even essential for working memory—remembering a phone number long enough to dial it. But it’s the brain’s transformer of short-term memory into long-term memory. What you lose when you lose your hippocampi is your ability to make new long-term memories.

Such was the fate of the much-studied “HM,” Henry Gustav Molaison (1926–2008). His tragic case gave us much of what we know about memory. In 1953 a neurosurgeon, attempting to halt the young man’s frequent epileptic seizures, removed most of Henry’s hippocampi, his amygdalae, and some surrounding tissue of the temporal lobe. The seizures stopped. And HM could still speak and make perfect sense (semantic memory). He could remember his old skills and even learn new skills (though he couldn’t remember learning them). He retained long-term memories, including vivid childhood scenes. He retained his high IQ. What he lost—in terms of a life, almost everything—was the capacity to turn new short-term memories into long-term memories. He could not remember what happened yesterday. He could not remember what happened this morning. He could not remember the scientists who studied him for 40 years; he met them anew at each encounter. After the surgery he could no longer care for himself and lived in a nursing home. “HM’s case,” writes neurologist Oliver Sacks in Musicophilia: Tales of Music and the Brain, “made it clear that two very different sorts of memory could exist: a conscious memory of events (episodic memory) and an unconscious memory for procedures—and that such procedural memory is unimpaired in amnesia.”

The conscious memory of events: How we take it for granted! It enables us to plan, to pursue a goal, to work, to cook, to read. It enables us to enjoy long talks and lazy days and nights out on the town. It enables storytelling, art, imagination.


Imagination depends on the conscious memory of events. How could I imagine a purple cow if I could not remember the cows of my childhood switching their tails against the horseflies? How could I imagine a purple cow if I could not remember purple crayons, purple potatoes, purple grape juice? Persons with impaired memories have impaired imaginations. Amnesiacs, writes science reporter Benedict Carey, “live in a mental universe at least as strange as fiction: new research suggests that they are marooned in the present, as helpless at imagining future experiences as they are at retrieving old ones.” Images made by functional magnetic resonance imaging (fMRI) technology show that remembering and imagining send blood to identical parts of the brain.

What does this say about the goal of living in the present?

But for most of us, the phenomena of the present (just now Miles Davis playing “Red China Blues” on YouTube) connect in our mind with previous analogous experiences. Recognition involves memory: comparing what is seen with what was seen.

My grandfather had, I think, anterograde amnesia: He couldn’t form new memories. He could re­mem­ber the long ago but not yesterday. He would get dressed in his suit and tie, don his fedora, dapper as ever, and head out the door.

“Walter! Where are you going?” Gran would ask.

“I’m going to work.” Granddad would say.

“You’re not going to work! You’re retired!” Gran would cry out.

Granddad lived, I think, in a state of perpetual churning anxiety. He felt it was time to go to work. He felt lost. He wondered out loud who these “nice people” were, sitting in his living room. (That would be us, his family.)

In the process of losing his memory, did Major Walter Long lose his pride in being decorated for “exceptional bravery under shellfire” in 1918 France during the Great War? Did he forget the trauma of war, his killed comrades? Did he forget the pleasure of composing a paragraph? Did he forget love? Did he forget joy?


Joy, happiness, contentment, the feeling of safety, the feeling of being loved, the act of loving, the feeling of respecting another and of being respected, all these feeling states are produced within the brain. The pursuit of happiness might be construed as the pursuit of more dopamine and/or serotonin flooding our synaptic clefts. Add norepinephrine to the mix—energy, the constricting of blood vessels, jumping up and down. Norepinephrine is a hormone when produced by the adrenal gland along with epinephrine (adrenaline). It’s a neurotransmitter when produced by neurons in the brain. Certain racers, bikers, fistfighters, bank robbers, pickpockets, and other daring devils may be addicted to the intoxicating rush of norepinephrine-epinephrine.

Normally, these neurotransmitters spread out and do their job, after which they break down within the synaptic clefts or are returned to their home neurons by reuptake molecules. Antidepressants like Prozac or Zoloft (SSRIs—selective serotonin reuptake inhibitors) bind to serotonin reuptake molecules, preventing them from doing their ferrying duty. This leaves serotonin flooding the synaptic gaps, free to continue stimulating the receptor molecules in the dendrites of the receiving neurons.

Cocaine binds to both serotonin and dopamine reuptake molecules, leaving the synaptic gaps awash in both. Whee! But then the crash. Receptor molecules in the dendrites are switches. When stimulated they switch on; when overstimulated they switch off. (With his or her receptors desensitized, the addict needs more and more.) And, because the neurotransmitters never get returned to their neurons, the dopaminergic and serotonergic systems get depleted, drawn down, drained out. Quite soon the system itself becomes deranged. Many addicts, whether using or recovering, have damaged brains. Tragically, lacking crack, they can feel no pleasure.

I’m no addict, but I do get migraines. This means I likely have a low supply of norepinephrine, an excitatory neurotransmitter that counter­­balances dopamine. Under migrainous conditions, dopamine flooding my synaptic clefts leads not to a high but to the worst kind of low—killer headaches.


Killer headaches—including nausea, vomiting, light-stabs to the eyes, repulsive odors, excruciating head pain, a total sense of despair—are under study by me when I’m not having one. Migraine is cousin to epilepsy. It may be in part genetic, although Pamela, my monozygotic twin sister, does not get them. Migraine begins with an electrical storm in the brain stem, seat of the autonomic nervous system, controller of heartbeat and sleep, dilator of pupils, regulator of airways. This brainstorm spreads widely throughout the brain. Firing neurons require oxygen, carried by blood, and during the brain­storm, 300 times the normal amount of blood rushes to your head. Now, we migraineurs (according to researcher Stephen J. Peroutka) possess an insufficient supply of norepinephrine, not only during the dread headache but also all the time. Firing neurons secrete norepinephrine, which constricts the blood vessels in the head. So far, no pain. But, alas, our meager supply of norepinephrine gets drawn down, and dopamine (along with its rogue co-conspirators adenosine and prostaglandin), which acts oppositely and in balance with norepinephrine, runs amok. Dopamine distends cerebral blood vessels, which activates the trigeminal (cranial) nerves. Excruciating pain. Dopamine also stirs up the neurons in the stomach lining (we have 100 million of these), creating nausea leading to violent retching.

Triggers: too much sleep, too little sleep, dark microbrews (the more delicious, the more deadly), too much company throughout a long day, most red wines, MSG, air travel, dark chocolate combined with red wine (requires immediate hospitalization), too much caffeine, too little caffeine. Some women get migraines in sync with their menstrual cycle. Pickles will do it. Sulfites, sulfates, sunlight. Too much exertion. Too little exertion.

Mostly I adore Oliver Sacks’s disquisitions on the brain, but I ingested his tome Migraine with flutters of anxiety. Might Migraine trigger a migraine?

Sacks inquires: What is the usefulness of the migraine to the migraineur?


There’s the alleged migraine personality. Migraineur Joan Didion speaks (in “In Bed”) of the compulsive worker, the perfectionist writer. This is the type who slaves over sentences that nonetheless ooze mediocrity like a bad odor. That would be me.

A migraine forces you to stop. Your day ends—bam! A migraine performs approximately the same service as being run over by a train.

Sacks thinks the profound despair brought on by a migraine is part of the migraine, the result of neurons firing out of control throughout the limbic system.

But what sets off the brainstorm? Why do triggers differ from one person to the next? Why do migraines occur on only one side of the head? And why does my personal miracle drug, Maxalt (rizatriptan benzoate)—which binds to serotonin receptors, which then release serotonin, which constricts blood vessels—cost $70 per headache?

And why me, Lord?

Is my brain sending my body some sort of sick, twisted message, some sort of poison-pen letter?


Letters—our ABCs—are meaningless squiggles until we learn our alphabet. Here’s a letter I remember. I am 4 or 5 years old. I’m sitting on the davenport in the living room. I’m holding this letter in my hands. Pale blue letter paper. Blue ink. Gran, my Scottish grandmother, has written this letter to Mummy. I turn it over. I turn it around. I turn it every which way. I put it close to my face. I hold it far from my face. I turn it upside down. I’m filled with longing. I long to know its secrets. I long to read this letter. But I cannot read. Mummy comes into the living room and takes the letter from me. Foiled! And with the letter she takes the letter’s letters. I am completely exasperated!

What part of the brain does this desperate desire to read come from? And where does the brain keep it—the long-since-satisfied longing to learn to read retained as a memory?


Memory is nothing like a scrapbook, a photo album, an attic, or a movie. Think of a broom. Remember broom. Different bits of the brain’s broom are stored in different parts of the brain. The hickory broomstick. The weight of the broom in the hand. The straw head. The color of straw. The sound of sweeping. The purpose of sweeping. The sound of the word broom. The shape of the word broom. The fact that a broom is a cleaning tool and not a glass of wine or a plate of spaghetti. (Thoughts of sweeping, for those who sweep, activate a pre-motor area, ready to lift the hand.) Memory brings all these disparate bits together, makes them cohere. The puzzle of how the brain achieves coherent perceptions out of its widespread data bits is known as the binding problem.

Memory is a mental event, this we know. Mental events work by the transmission of neural impulses at different rates. Memory is stored not in one place but all over the place, as data bits. Memory, says António Damásio, likely involves “retro-activation”—the refiring of neurons activated during an original perception or experience. An association, either external or from within, may stir up a memory.

Types of memory: procedural (how to sweep the floor); semantic (facts, words, the word broom and what it refers to); working (being used at this moment to consider the concept of a broom); episodic (personal memories, the time you swept up your diamond with the dirt); declarative (remembering facts and events that become available for later conscious reflection).

Lost to everyone’s declarative memory is the name of Walter Long’s first wife, a girl he married in 1914. This girl died of tuberculosis a year or two after she married the young man who would become my grandfather. After her death, Walter went off to fight in the Great War. He was proud of his service (my father said). He received the Croix de Guerre. Toward the end of the war, he got the mumps, requiring nursing. In 1919 he married his nurse, a young Scottish war widow with a small child. This young mother, Annie McIlwrick Humphrey, became my Gran.

But Granddad’s first wife, the girl he married in 1914 when he was 31—who was she? When I asked around a few years ago, no one in the family could remember her name, if they ever knew her name. She had gone from this world, gone from memory, gone from history. This girl, whoever she was, went from being somebody—with her looks, her likes and dislikes, with her passion for Walter Long, with a favorite pair of boots perhaps, or a love of pickles—to being nobody. Her dreams died along with her name along with her neurons.


Neurons commune with other neurons. But keep this in mind: a straightforward algorithmic connection from A to B to C is not enough for the brains of human beings or other beings to learn from experience. Rather, neurons act in assemblies that have subsets which act like cliques. Shifting perceptions are made by shifting transitory assemblies of neurons. In one type of assembly, various neurons receive input at the same time and send their output to the same place. In another type, neurons in different locations fire simultaneously. Assemblies often stack up in columns, with a single column containing perhaps 100,000 neurons.

Cliques compete with other cliques, recruiting neurons and losing them to the competition. Let’s say you are trying to remember a name, but the wrong name comes to mind. The rogue clique, the clique pulsing the memory of that wrong name, is in competition with the clique you want-want-want-want. Eventually you dredge up the right name from the mind’s murky sea. Attention is the net. Attention may be a function of feedback loops (“reentrant connections”), neurons firing from the frontal cortex back to the sensory relay station, the thalamus, to suppress irrelevant stimuli.

Certain neurons work as feature detectors. Neuroscientist Joe Tsien and his team subjected a mouse to an earthquake while recording the activity of some 200 hippocampal neurons. (Their ingenious lab inventions enable them to observe very few neurons at a time.) The earthquake caused the rodent’s neurons to fire in a particular pattern, with different cliques reacting to different aspects. There was a startle clique, a motion-disturbance clique, a clique that reacted to where this event took place (a black box). With the mouse in the same black box, when a different event (an elevator fall) occurred, the startle clique and the motion-disturbance clique both fired again. The cliques of firing neurons were organized in a hierarchy from abstract to specific. (Startle is abstract: any number of different events could fire this clique. Where is more specific: a red box will not excite black-box neurons.) Memory occurs when, after the event, the same assembly of neurons refires, although less strongly.

The mystery is this: Where does the sense of mystery come from? What about tranquility or annoyance or curiosity or philosophy? Which neurons project ambition or fascination or frustration? Where does the sense of awe come from? What about the sense of the sacred, the sense of God or of deus in res? Are these states of being a matter of brain chemistry? Are they nothing more than electrical charges pulsing, thrumming, oscillating?


Oscillating is what the living brain does. It emits brain waves. Neurons emit electrical charges in a rhythmic pattern; they fire even with no stimulation from the outside world. The brain puts out its own energy. I think of this-this-this-this as a kind of humming. Hooked up to the electroencephalograph, the sleeping person’s brain discharges mainly high-amplitude, low-frequency oscillations in the delta band (0.5 to 3 cycles per second). The barely awake or deeply meditating person’s neurons tend to discharge theta waves (4 to 7 cycles per second). The awake but resting or meditating person’s neurons tend to discharge alpha waves (8 to 12 cycles per second). Beta waves (15 to 25 cycles per second) begin when initiating purposeful activity. The gamma band (30 or more cycles per second) is linked to cognitive activity. But, like a great many statements about how the brain works, this one is oversimplified. In actuality, different brain areas are thrumming at different rates simultaneously. In actuality, the brains of some meditating persons are not in theta or in alpha. In actuality, the brains of persons in a TV-watching stupor are in alpha. In actuality, the electroencephalograph gets a lot of interference: with its electrodes stuck not on the brain but on the scalp, it may be a dull instrument. A thick, delicious book, James H. Austin’s Zen and the Brain, states that more important than the alpha state is synchronicity. Different parts of the brain begin oscillating in unison like the Rockettes at Radio City Music Hall. Bliss may result. But how little we know: our brain has barely begun to comprehend itself. And how wrong it can be. Until the late 1990s the dogma prevailed that neurons do not regenerate, that brain injuries are more or less permanent, that a devastating stroke represents irreparable loss. Then a new insight hit neuroscience like a tsunami—the brain’s plasticity.


Plasticity brings hope to the stroke victim, the brain-injured, the autistic, the amputee in phantom pain, the palsied, the deranged, the old. The brain is plastic, not fixed. Brain structures do not have rigid job descriptions. Brain maps—those synaptically interconnected networks of neurons whose pulses produce a function or a memory—have shifting borders. Also, stem cells exist within the brain, particularly within the hippocampus. Brain stem cells can generate new brain cells, perhaps maintaining a balance with dying cells. Plasticity has exploded our notions of how to rehabilitate a stroke victim. Edward Taub, working on macaques, discovered that when one hand is disabled, say by stroke, the brain map for the good hand begins to expand. It is precisely this—the brain’s compensatory ability to remap itself—that dooms the paralyzed hand. Taub’s strategy is to render the good hand moot by confining it to a sling, and then to force the paralyzed hand to practice—to pick up and drop, pick up and drop, pick up and drop—beginning at the baby stage, putting square pegs into square holes eight hours a day. In this way, new brain maps form in remaining healthy tissue to work the limp hand. Taub’s results, according to Norman Doidge in The Brain That Changes Itself, have ranged from good to spectacular. Plasticity means that old people can learn, that slow people can raise their IQ, that memory loss can be prevented or reversed.

Learning changes the brain. Gary Wayman and his team discovered that dendrites contain a growth-inhibiting protein. Synaptic activity (learning) moves that protein out of the way. Synaptic activity (learning) also makes the neuron manufacture an RNA molecule (micro RNA 132) that suppresses the manufacture of more inhibitor, allowing the dendrite to grow. Learning changes the brain by making new pathways and by growing new dendrites. And cognitive activity, according to psychopharmacologist Ste­phen Stahl, is the only intervention known to consistently diminish the risk of Mild Cognitive Impairment or Alz­heimer’s or to slow their terrible progression.

Then again, the propensity to develop late-onset Alzheimer’s has a powerful genetic component. On chromosome 19 there’s a gene (the E gene) that codes for a glycoprotein (a protein containing a carbohydrate) whose work involves cholesterol transport and metabolism. When it works, it cleans out those waxy amyloid plaques that otherwise clog thoughts and kill neurons. Persons born without a certain allele (alternative form) of this gene (the allele termed ApoE4) are in little danger of developing Alzheimer’s. Persons born with one copy of this awful allele are four times as likely to get Alzheimer’s as compared to the general population. Persons born with two copies of ApoE4 are eight times more likely to develop Alzheimer’s. Very well, but here’s the question: What is different about persons who carry two copies of ApoE4 (the worst case) who do not develop Alzheimer’s? And there are other questions.


Questions. What is it about our brain that makes us human? What is it that makes us different? Is it self-knowledge? Is it, as neuroscientist V. S. Ramachandran puts it, that we have a self that is self-reflexive, a self aware of itself? Is it knowing who we are? Is it our ability to explore our past and to imagine our future? Is it our spirituality, our brain’s ability to imagine a soul, a higher being? Is it our propensity to make music, to make poetry? And what if we lose all of it, as Walter Long did? What if we lose all that seems intrinsic to our human nature, to our own selves? Who are we then? Who are we if we can’t remember?


Remember as you would be remembered. In 2007 my father, Winslow Long, in the process of moving to Seattle, passes on to me a box of old letters and documents. In this battered cardboard carton I discover a booklet titled The Family Records of Winslows and Their Descendants in America. We Longs descend from the Winslows. The yellowed, shiny pages of this booklet reveal that my grandfather Walter Long (son of Clara Winslow Long) married Lillian Gorsuch, of Baltimore, on June 10, 1914. I hereby restore to everyone’s neurons the name of Granddad’s first wife. Did Lillian have tuberculosis at the time of their courtship? Did they know it? Did the start of the war in Europe during the 1914 summer of their wedding cause them to feel anxiety? Distress?


Stress shrinks the brain. Not normal stress or necessary stress, but chronic stress—chronic anxiety or clinical depression. The view that chronic stress destroys dendrites, neural pathways, and even entire neurons, especially in the hippocampus, is gaining acceptance as studies go forward.

Stress revs up the adrenal gland to pump glucocorticoids such as cortisol. Cortisol sparks the production of epinephrine (adrenaline), which tenses muscles, narrows blood vessels, and prepares you to kick butt or run for your life. But then the emergency ends and cortisol subsides. All is well. But in chronic stress, the emergency never ends. Cortisol bathes the hippocampus continuously, killing its neurons.

And there’s more. The brain produces a protein known as brain-derived neurotrophic factor (BDNF), which protects neurons. Chronic stress may repress the gene that expresses BDNF. After which hippocampal neurons, which thirst for BDNF, which require BDNF, which can’t go on without BDNF, shrink or balk or die.

Experimental animals subjected to stress, according to Stahl’s Essential Psychopharmacology, turn off their genes for BDNF and as a result lose synapses as well as whole neurons.

On the other hand, exercise stimulates the growth of BDNF. So insists molecular biologist John Medina in Brain Rules.

So get out and walk. And stop your constant worrying. Stop stressing out over every little thing. Stop imagining the worst. Dementia begins there.


“There is no need for temples, no need for complicated philosophy. Our own brain, our own heart is our temple; the philosophy is kindness.” So says the Dalai Lama. But in our world, violence, murder, war, and torture may be as common as kindness. Perhaps we have a deep inner need to kill, a devil in our unconscious.


Unconscious memories, unconscious wishes, unconscious fears, hates, loves. The very notion is strange. Strange to think that we have memories we can’t remember, wishes we don’t wish for, desires we don’t feel. But that we have an unconscious is told by our brain’s brilliance at doing things with no help from our conscious mind. We walk, chat, purchase potatoes, sweep, drive, read, talk on the phone, all without “thinking.” We just do it. Our brain directs the process, whatever the process is. We have reactions to people and events—a sudden mistrust or a sudden affection—that may be based on implicit, that is non-conscious, memories of something similar. The admonition “trust your gut” translates “trust your brain, trust its implicit memories.”

Blindsight also argues for the existence of the unconscious. Blindsight proves that we do not necessarily know what the brain knows. A blindsighted person is a brain-injured person. This person’s visual cortex has been damaged. He is blind, in his own opinion. Yet ask him to take a guess as to where some particular object is—say a pencil held up—and he will point right to it. The brain sees it. The brain knows where it is. But to the conscious mind, it is unknown. What is broken is the wiring that connects the part of the brain that sees to the part that knows it is seeing. To the person, the world has gone dark. To his brain, the world remains a carnival of shape and color—visual.


Visual arts are unique to our species. By means of culture we have created an external visual cortex—paintings, sculptures, billboards. We have created an external long-term memory—writing. We have created external dreams—films, plays, TV dramas. We tell stories to recall the past and we look through telescopes to see the past. We write in part to stop time, to hold onto the present as it becomes the past as we grow into the future.

I can picture my grandfather’s face. I can remember, just barely, a time when he could still be counted among the cognoscenti. He had retired with our Scottish grandmother to a Bucks County, Pennsylvania, farm, the old farmhouse built of whitewashed brick. Granddad used to take us small children out to the barn to show us a sleek black buggy, polished but parked in desuetude. I can see in my mind’s eye the barn, the buggy, the big doll I was allowed to play with. I see Walter Long’s life as a tragedy, but maybe he didn’t see it that way. He had good work while he could do it, and he had love and ambition, and at least some of his dreams came true. He reportedly reported on the sinking of the luxury ocean liner Morro Castle in 1934 and on the Lindbergh kidnapping trial of 1935. I once spent three days searching The Philadelphia Bulletin amid the massive coverage of the Lindbergh tragedy for any sign of my grandfather’s hand. No luck. But some years later he himself was featured in the paper, in a sidebar, with his picture, here quoted in full (the ellipses appear in the original):

Walter Long . . . The Zoning Board of Adjustment goes into session . . . hearing pro and con on whether a new apartment site shall be approved . . . News is being made . . . and Walter Long’s there . . . accurately recording the builders’ arguments, the opponents’ vigorous stand . . . For 15 years Walter Long has been one of The Bulletin’s experts in municipal affairs . . . He roams the City Hall annex . . . drops in daily on the Board of Health . . . keeps tab on the Department of Supplies and Purchases . . . and distinguishes himself with his detailed reporting of the City Housing Rent Commission Hearings.

There he is. My grandfather. Not in his own words but in someone’s words. Kind reader, if you were to utter the name of Walter Long, it would stay longer in this world. It would enter into your Wernicke’s area.


Wernicke’s area is where the brain comprehends and interprets language. Persons with damage to their Wernicke’s area (who have Wernicke’s aphasia) can speak, but their words pouring out make no sense. Neither do these persons comprehend a single word spoken to them. Broca’s area produces spoken speech. Persons with Broca’s aphasia may be able to speak within their own minds, but when they attempt to voice their thoughts, they fail to produce normal speech. Wernicke’s area is associated with hearing, whereas Broca’s area is associated with the neurons that activate the muscles of the larynx. Relations between Wernicke’s and Broca’s areas are intensely xenial.


Xenial (pronounced ZEE-nial) relations, friendly communicating relations, transpire among many neurons throughout many parts of the brain. Consider the binding problem, worked on most brilliantly by psychologist Anne Treisman. As we know, different aspects of the scene before us are carried into our brain by different neurons. Some neurons signal red; others black or yellow; others the news that what is before us is vertical or horizontal; others that an object is located in our upper-right quadrant or our lower-left quadrant. How then do we reconstruct a coherent picture? How come, when we see a black-and-white cow with a red ribbon around its neck, the cow doesn’t come out red, the ribbon black and white, since separate neurons have projected separate features of this beribboned bovine into our brain? The answer comes from the observation that persons with stroke-injured parietal lobes may indeed see the cow as red, the ribbon as Holstein. Think of it this way: it’s spatial attention that puts the red on the red ribbon (both originate from the same point in space). Spatial attention emanates, it seems, from the parietal lobes. Red-perceiving neurons and ribbon-perceiving neurons are getting together, communing, enjoying xenial relations, rather like people at a cocktail party going yackety-yak.


Yackety-yak. We are a yackety-yak people. We are quidnuncs, busybodies. Who did what to whom, who went out with whom, who slept with another’s whom, who won the lottery, who won the game, who lost his shirt. Gossip, it turns out, takes up more than half of all human discourse. We concern ourselves with the business of others, and others concern themselves with our business, and all this sordid business is aired on reality TV, not to mention in cafés and over dinner and upon falling asleep and during morning coffee and later at the bar. Yackety-yak. We social primates evolved within an increasingly elaborate social framework, much dependent on our frontal-lobe-located mirror neurons. When you smile, I want to smile. When you cry, I want to cry. When you laugh, you activate my funny bone. We are inherently at home in social interaction. We can gossip for hours, even if doing so reduces the items crossed off our To Do list to zero.


Zero is an awe-inspiring invention of the Homo sapiens brain. Zero is intrinsic to our human society, though we seldom give it a thought. All by itself, zero is nothing. So when does nothing become something? Nothing becomes something when you put it next to a 1, as in 10. Now this nothing is holding a place for nothing in the units place. Then if you put two nothings together with a 1 to make a 100, your little nothings are suddenly holding two places: a place for nothing in the units place and a place for nothing in the tens place. The zeros make the 1 mean not 1 but one hundred ones. Think about it. That little nothing, zero, put with only 9 other numerals, makes possible any number of numbers. The story of zero is a Homo sapiens story, invented by the Sumerians in ancient Babylonia and again by the Mayans in ancient Mexico.

Now, we also have other sorts of zeros. We have Ground Zero. We have zero population growth. We have the number of extant sentences written by Walter Long. Zero. No paper with Granddad’s handwriting on it. No paper typed by him. No article bylined by him (at least none that I’ve found). So here was a writer, my grandfather, who wrote for five decades, who lost his memory, who lost, with his memory, his entire output.

How could this have happened? It’s a mystery I ponder even as I hoard every word I write, even as I donate my own scribblings—60 boxes so far—to a university archives, even as I try to write more and more each day, as if that would overcome the oblivion that for certain lies in the future. Considering everything—wars and famines, families, feasts, births and deaths, the great loves and the great losses, considering the miracle of natural selection that evolved our brains—the loss of my grandfather’s writing is a small thing. But for me it’s a big thing. I can’t get it out of my mind. It leaves me speechless, notwithstanding the two-million-word capacity of our alphabet.

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