The Ravenous Brain: How the New Science of Consciousness Explains Our Insatiable Search for Meaning (44 page)

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Authors: Daniel Bor

BOOK: The Ravenous Brain: How the New Science of Consciousness Explains Our Insatiable Search for Meaning
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There is also circumstantial, though no less intriguing, evidence to link sleep issues with a diminished working memory. Just as light therapy helps wake up psychiatric patients, improving their symptoms in the process, in normal participants it boosts performance on a range of attention and working memory tasks.
So, from a broad range of sources, it’s clear that sleep problems do indeed reduce working memory capacity, and, in line with this, the core cortical regions of consciousness are underpowered when sleep problems are present.
In ADHD children working memory levels are especially low. How do they cope with this dwarfish holder for conscious contents? They tend to do all they can to avoid tasks that will strain their limited conscious resources—they shy away from difficult school problems and flit between many tasks, because they can’t maintain a single goal in working memory for long. And they behave in impulsive, sometimes violent ways, since it can require considerable conscious effort to suppress primitive impulses and act in a controlled, reasonable manner.
But it doesn’t take much for control in any of us to be impaired because of a deflated consciousness, as indexed by reduced working memory space. In one striking experiment, by Baba Shiv and Alexander Fedorikhin, undergraduate students were given either a seven-digit or a two-digit number to memorize. While holding this number in working memory, they were shown their reward for participating—a cart of snacks. They could either choose fruit salad—a healthy but not particularly indulgent option—or a piece of chocolate cake, which looked delicious and sweet, but also fattening. Students who were rehearsing the difficult seven-digit number were far more likely to choose the chocolate cake. It’s as if their working memory, filled up by the demanding seven-digit number, didn’t have sufficient space left to carry out normal, mature control over their feeding habits.
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If such clear results can be obtained in healthy adults, simply by remembering a longer number, it’s not hard to see how ADHD children, with such a diminished consciousness, will behave far more impulsively and appear out of control.
 
Another psychiatric group marked by a considerably reduced working memory capacity is schizophrenia. In fact, this is such a pronounced trait that some theorists have suggested that diminished working memory space is the prime psychological cause of much or all of the various nightmarish symptoms that schizophrenics endure. And, like ADHD patients, schizophrenics also have a dysfunctional prefrontal cortex.
A reduced working memory and shrunken consciousness have many knock-on effects. Effortful, taxing tasks requiring a deep understanding or a firm control over oneself must seem an impossibly high mountain to climb for ADHD patients, so they simply avoid such activity. Schizophrenics, with their distinct suite of genetic abnormalities, react differently to the problem, not even having the mental space inside an episode to notice their cognitive limitations. Instead of developing strategies to avoid the information overload, as ADHD patients do, I suspect that schizophrenics embrace this saturation of mental details and constantly strive to discover the hidden structures within their broken conscious stream. Autistics also search for patterns incessantly, usually with great success, and in a way that may help alleviate their suffering. Normal people do as well, of course, but we are prone to jumping to conclusions and to succumbing to superstitious beliefs as we make too much of too little data. Schizophrenics, via their misfiring awareness and paucity of working memory space, take these flaws of insight and magnify them a hundredfold. The result is usually an elaborate, heartbreaking edifice of delusions and hallucinations that schizophrenics have no hope of correcting with their deficient pattern-spotting consciousness.
CHEMICAL CASCADES UNBALANCING AWARENESS
 
If a reduced working memory is a core feature of both ADHD and schizophrenia, what treatments can target this, boosting working memory and consciousness while simultaneously alleviating symptoms?
Drug treatments for ADHD tend to rely on the assumption that the prefrontal cortex is underperforming. For instance, the stimulant drug Ritalin acts by increasing available amounts of the neurotransmitter dopamine. This neurotransmitter is vital for normal prefrontal parietal network function. If healthy, mentally well subjects are given Ritalin, and then receive brain scans, it is found not only that their working memory performance improves (especially if they started with a low working memory capacity), but that their prefrontal parietal network functions more efficiently. Ritalin may therefore help ADHD sufferers by flooding the consciousness network with a brain chemical it somewhat lacks, and in this way ramping awareness, in terms of working memory capacity, back up to near normal levels.
Unfortunately, though, most of these stimulant drugs do not work at all for schizophrenics, who already have an overabundance of prefrontal dopamine (in fact, giving the ADHD drug of choice, Ritalin, to schizophrenics is a reliable way to create psychotic symptoms). For optimal working memory, you actually need a medium amount of dopamine in the prefrontal cortex—too much or too little, and working memory shrinks.
For many years it has been assumed that correcting the prefrontal dopamine imbalance is the key to treatment for both ADHD and schizophrenia. Indeed, most antipsychotic drugs used for schizophrenia are designed to reduce dopamine levels. Although treatments targeting dopamine levels largely seem to fit for ADHD, emerging research is suggesting that for schizophrenia, scientists have been centering on the wrong chemical all along. Instead, the evidence now points the finger at glutamate, the most common neurotransmitter in the brain, whose purpose is mainly to cause neurons to fire and maintain consciousness.
While autistics have a supercharged glutamate system, their genetic opposite, schizophrenics, have severely deficient glutamate signaling, which has a knock-on effect on dopamine activity in the prefrontal cortex. So while ADHD patients have a reduced working memory primarily because of a lack of dopamine in the prefrontal cortex, schizophrenics’ similar working memory problems have their source in much broader chemical imbalances that limit proper conscious function throughout the entire system. This probably means that schizophrenics also have a badly disrupted attentional system, so that all manner of unhelpful, unwanted feelings and ideas can gate-crash into consciousness. This feature, combined with a shrunken capacity to store such information within awareness, ever more readily creates a fractured, disorganized information overload.
One intriguing clue that has helped to shift the research perspective away from seeing schizophrenia as primarily a dopamine disorder comes from anesthesia. Ketamine is a general anesthetic that removes consciousness by suppressing a key part of the glutamate system, and with less of this neuron-activating chemical pathway, the brain’s activity dramatically drops. But if given in lower doses to normal people, ketamine can, for the short while that the drug flows through their brains, effectively turn them into schizophrenics, as well as reduce their working memory capacity. For instance, otherwise mentally healthy volunteers will start to hear imaginary popping sounds, or become convinced that the study is being run by aliens. If given to schizophrenics in these low doses, ketamine can greatly exacerbate all their symptoms, and patients will say it is like being back in an acute episode. So here’s a drug that if given in low doses dampens neuronal activity in a certain way, but not quite enough to make people unconscious. But consciousness is nevertheless still reduced, working memory drops, and the result is that normal people temporarily turn into schizophrenics.
Therefore schizophrenia, with such vivid, active, disturbing symptoms, may on the surface appear to have little to do with a reduced consciousness. But dig deeper, and on any level you care to examine—with a diminished working memory, prefrontal dysfunction, and glutamate at semi-anesthetized levels—it becomes clear that a reduced consciousness is exactly how you should characterize this illness.
 
A new perspective on schizophrenia is particularly vital because the sad fact is that the current crop of drugs given to schizophrenics, still centering on the dopamine system, are poor at helping these patients. They seem to improve matters not so much by removing the various delusions and hallucinations, but largely by acting as a partial sedative, so that the tormenting symptoms are blunted. As might be expected from drugs that are only targeting a secondary neurotransmitter imbalance (an overabundance of dopamine), rather than the underfunctioning chemical ringleader (glutamate), only about 40 percent of schizophrenics gain any benefit from them. In contrast, far more robust figures can be obtained when examining significant adverse side effects: Approximately 67 percent of schizophrenic patients report these, with excessive sleepiness one of the most common problems. There is even anecdotal evidence that some schizophrenics function better in the long term if they’ve never been prescribed antipsychotics.
What is needed instead are drugs that focus on the root cause—abnormal glutamate activity. If a medication could ensure normal levels of this neurotransmitter, it might also indirectly generate a more functional dopamine system in the prefrontal cortex and in the process restore normal consciousness and improve working memory. Although as yet only at the research stage, new forms of medication along these lines are being developed. For instance, Sandeep Patil and colleagues, of the pharmaceutical company Eli Lilly, have created a drug that targets a specific part of the glutamate system thought to be dysfunctional in schizophrenics (this drug’s mechanism, incidentally, is largely the opposite of that of arbaclofen, a drug currently in trials to treat autistic sufferers). In early trials, schizophrenics showed a positive response to the drug, and it is hoped that these and similarly acting medications will soon arrive in the clinic and allow schizophrenics to lead a more normal life than is currently possible.
As a more general point, many mental illnesses are relatively poorly treated with medication. Developing new drugs is only part of the problem. Drugs already exist that can individually target many of the neurotransmitters in the brain. But psychiatrists have little means to assess what is wrong with their patients on the level of brain chemistry and do not really know how the patient might react to a given form of medication before it is provided.
When accompanying my wife to her psychiatric appointments, I found that the main focus of the doctors each time was to reconfirm her diagnosis and then prescribe the standard medications for that imprecise condition. They would start with the most popular drug and, as each successive pill failed to help her in any way, work their way down the list, trying a new one every six months or so. Then, when they were beginning to exhaust single treatments, they would start combining drugs. I would ask the doctors what they knew about how each cocktail of drugs interacted on the brain’s chemistry. They would tell us that the combination of drugs had not been shown to be harmful, but they believed that no one understood what happened to the brain when you combined such drugs. All they knew each time was that such combinations had been helpful for some patients.
These experiences illustrated to me where the main pressure point of imprecise neuroscientific knowledge lies. We are making great strides in our scientific understanding of the human brain, and there are some relatively clear cases, such as schizophrenia and the neurotransmitter glutamate, where a previous approach was missing the point, and a new, more accurate viewpoint may provide striking benefits. But, on the whole, neural complexities are utterly daunting. The more we learn, the more complicated the microcircuitry of neural communication appears. There isn’t just the tricky issue of how one neurotransmitter will interact with others. On a smaller scale, single genes can have many different effects in the brain and can be turned on or off by small sections of RNA; other short sections of DNA, not part of any gene, and previously classed just as “junk DNA,” can nevertheless indirectly change neurotransmitter function as well.
So clinicians in this field have an almost impossible lot. Their job is to treat the debilitating mental symptoms of the patient, but the true problem is happening somewhere in the brain, probably relating to a dysfunctional neurotransmitter system—though there could also be anatomical abnormalities, with brain regions not built quite right in the first place. And even if the neurotransmitters are faulty, the cause of this could be one of a hundred biomechanical possibilities.
Thus, on the one hand, it’s entirely understandable that psychiatrists remain primarily concerned with uncovering psychological problems and making pragmatic, admittedly crude attempts to alleviate those symptoms with one or a few of their arsenal of possible pharmaceutical weapons. On the other hand, absolutely any attempt in the future to edge closer to the locus of the problem by detecting brain abnormalities in these mentally ill patients, and to use more targeted solutions based on those clues, would almost certainly be of great benefit.
Already there are important successes emerging in this direction as scientists try to untangle the dizzying complexities of the brain in areas relevant to psychiatry. Some of these results could soon find their way into the clinic to aid diagnosis. For instance, an increasing number of genes coding for dopamine and prefrontal function are being associated with psychiatric conditions. Such results reinforce the view that consciousness should be the main context by which investigators should search for clues to mental illnesses. Other genes have been discovered whose variants determine whether or not you will respond to SSRIs, or whether such drugs will even pass the blood-brain barrier and flow where it really matters. Researchers are also looking for chemical markers in the blood or spinal column, which can help pinpoint dysfunctional components in the brain. And novel brain-scanning methods can measure neurotransmitter changes as a result of medication or mental illness.

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