No One Cares About Crazy People Read online

  The cost to America’s human treasury—the miasma of disabling personal agony, bewilderment, and social ostracism felt by a victim and his or her loved ones—is beyond any system of counting. Yet the abstraction of “human treasury” tends to distract one from contemplating the ruined uniqueness and hopes of individual lives.

  What if you raised a child who grew up sunny, loved, and loving, perhaps unaccountably talented, a source of family joy, only to watch that child slowly transform in adolescence into a mysterious stranger, shorn of affect, dull of gaze, unresponsive to communication—and perhaps worse?

  What if you grew to understand that this stranger was indeed communicating—but with no one whom you could see or hear?

  What if you were forced to commence the lifelong process of reckoning with the likelihood that this child you thought you knew might persist in living, yet would never really return?

  What if this transformation deepened and grew malign? What if this offspring of yours believed that you meant him harm—or intended to harm you? Or wanted to harm others? Or herself?

  What if all of this misfortune were compounded by primal fear and judgmental withdrawal on the part of friends and even relatives? What if you picked up on gossip, as you surely would, among these friends, and relatives, and casual acquaintances, that your child’s madness was just an extension of his unhappiness, or weak character—or your own failures as a parent?

  As if the symptoms of schizophrenia were not devastating enough in themselves, nature has added a cruel joke, a seemingly valueless yet powerful barrier between the sufferer and professionals reaching out to help. The cruel joke is called anosognosia. Anosognosia, a Greek term connoting a blockage of insight into one’s self (literally, “without knowledge”), is the false conviction within a person that nothing is wrong with his mind. It stems from a physiological by-product of psychosis, and accompanies about 50 percent of schizophrenia occurrences and 40 percent of bipolar cases. Anosognosia disrupts the parietal lobe’s capacity to interpret sensory information from around the body. It may also be present in victims of strokes or of physical trauma to the brain.

  Kevin would never admit that he suffered from mental illness. The closest term that he would tolerate was “a condition.” As his illness deepened, so did his anosognosia. At the outset of his treatment, he consented to a prescribed regimen of oral medications. But nearly three years later—when the end was near—he decided that he did not need them, and he calmly informed us that he was going to stop taking them. We could not budge him from this insistence. Predictably, his refusal to take his pills led to another break, which led to another of his several hospitalizations. After that, he agreed to resume his regimen of meds, or so we’d thought. But after his death we discovered some of these drugs concealed or scattered in our basement.

  It was not until nearly a decade after Kevin’s death that my family learned—far too late—that our son’s suicidal impulses might have been suppressed by a well-established, but underused, alternative method of administering antipsychotic medications. This is the so-called “depot” method—“depot” from the French sense of “place of deposit.” More recently the concept has been rebranded as LAIs, for “long-acting injectables.”

  “Depot” was introduced in the late 1960s precisely to neutralize anosognosia. It involves a periodic injection performed by a clinician, rather than a self-administered daily oral dosage, of the prescribed medication. (Not all antipsychotic meds, particularly among the “second generation” ones that will be examined in chapter 15, can be transferred from the oral to the depot method.) The deposit usually goes into the muscled tissue of the patient’s buttocks. The density of the muscle tissue ensures that the injected substance will flow into the patient’s system gradually, and in consistent quantities, over a period of time—usually about a month. The clinician serves as an outside monitor who keeps track of the patient’s cooperation. Oral meds, on the other hand, must be taken daily, and the responsibility usually falls on the patient. And therein lies the biggest rub.

  Among the most notoriously feckless and forgetful populations in the world is that of mid-adolescents. Stir in with those traits the twin poisons of schizophrenia and anosognosia, and you have what seems to be a near-guarantee of catastrophe.

  The biggest question when comparing “depot” over oral dosage is whether that intuitive response is valid: whether “depots” actually reduce incidences of relapse into psychosis, as they were designed to do.

  Advocates of the depot method tend to feel certain that the answer is yes. In 2007, two British investigators, Maxine Patel of the Institute of Psychiatry in London and Mark Taylor, lead clinician at Springpark Centre, Glasgow, made a flat assertion: “Depots overcome overt, covert, and unintentional nonadherence” to patients’ medical regimens.5 Statistical studies, however, have been less categorical. In 2011, a team of investigators reviewed ten recent studies of 1,700 participants and concluded: “Depot antipsychotic drugs significantly reduced relapse,” pointing to “relative and absolute risk reductions” of 30 and 10 percent.6 Another review of studies pointed out that most schizophrenia patients stopped taking their meds at some point—75 percent after only two years—and asserted that no strong evidence pointed to a decisive benefit of the depot method.7

  As for the Powers family, we endured our own “study,” one we would have given anything to avoid. Our younger son, Kevin, was prescribed oral antipsychotics by a series of psychiatrists over three years; he loathed taking them yet pretended not to; he went off them; eventually hiding the ones he assured us he’d taken; and destroyed himself in the midst of a psychotic break. Our older son, Dean, some years and some resistance later, accepted the shrewdly constructed arguments of his psychiatrist, agreed to “depot” injections of Haldol, and has lived, and has improved.

  In the decade or so before the end of the nineteenth century, mind science was still struggling to free itself from the last tangles of superstition, supernatural explanation, and the use of metaphor as a means of explaining madness. The young Viennese thinker Sigmund Freud was building upon innovative work by his European contemporaries to give humankind a sophisticated if fanciful conceptual scaffold on which to build rational understanding of the irrational. Freud classified aspects and functions of the mind, introducing such new terms as “the unconscious,” “libido,” “repression,” “denial,” “catharsis,” “parapraxis,” “transference,” “dream interpretation”; and “the id,” “the ego,” and “the superego.” He hypnotized his patients and got them to recall things they didn’t know they remembered. Exploring these recovered memories often relieved those patients of their symptoms of depression, hysteria, or compulsive behavior.

  Freud’s methods seemed to work, at least for a small and select circle of patients. He was thought a revolutionary; he had created something where nothing had existed before, a sweeping model of the mind, built upon internally consistent components. No one had ever previously attempted a unified theory of human thought and its intricacies. Yet the changing times were pleading for such a theory; the Western world was hurtling from rural to urban, religious to secular, uncritical assumption to sharp analytic skepticism. “Progress,” founded on questioning the verities of received thought and wisdom, was becoming the new secular god. People were losing patience with the blandishments that until the late nineteenth century fed the hunger for comprehending the mind’s mysteries: blandishments such as demons, “humours,” planetary gravity, “energy,” Scrooge’s undigested bit of beef. All these faded before Freud’s dense nosologies.

  The problem remained that Freud’s constructs were metaphors. They were intended to alleviate compulsive preoccupations of the mind—neuroses—via painstakingly coaxing memories from the patient: “psychoanalysis.” Freud’s categories did not describe anything physical, visible, tactile. Nothing he said was verifiable via the scientific method. His scaffolding, if powerfully persuasive, was a scaffolding of words, employed to extract wo
rds.

  Much of what we believe about “the mind” we must express through metaphor. The mind is itself a metaphor. The brain, where the corporeal answers resided, lay inaccessible, surrounded by a hard layer of protective bone, the skull. Unlike blood or bodily tissue, it could not be extracted for inspection without killing the patient. Or without waiting until the patient was dead.

  The only way into the brain, for millennia, was via autopsy. As the practice of dissecting dead bodies grew in sophistication, it proved invaluable in advancing medical knowledge, as when the German Rudolf Ludwig Carl Virchow used it to discover a large quantity of white cells in the body of a fifty-year-old woman; he called this condition leukämie.

  Inevitably, autopsy led doctors to explore the most complex organ in the body, thanks to Emil Kraepelin, who was the first psychiatrist to apply empirical science to evaluate the brain. Almost no laypeople in America today would recognize his name, yet many in the profession still consider him to be the father of modern psychiatry instead of Freud, whose theories Kraepelin detested.

  Born in 1856, the same year as Freud, Kraepelin made his mark early, in 1883, when at age twenty-seven he published his foundational Compendium der Psychiatrie, arguing his case for the organic causes of mental illness and setting out his groundbreaking systems of classification. He charged headlong at the established masters of “mind-cure.” His great text dismissed the idea that a given illness could be inferred from a given symptom. Instead, it was constituted of particular, observable combinations of symptoms that became evident as the illness progressed and pointed to its specific nature. Kraepelin drew this conclusion from poring over thousands of medical case studies. As for psychiatry, he concluded it should be joined to medical science, given that severe mental illness was the result of flawed biological processes in the brain—measurable through the steady deterioration of the patient’s thought processes and behavior in ways unprompted by external experiences. From his studies in biology he assembled his pioneering classifications of mental affliction in essentially two overall categories. One he called the exogenous, which stemmed from the reversals of fortune that life can bring to people, of the kinds that many people brought to Freud. These patients, Kraepelin agreed, could be treated. He assigned this category the umbrella designation manic-depressive. The second classification was incalculably more foreboding, and what it described set Kraepelin apart from previous psychiatric thought—even, and especially, from his great contemporary—and bête noire—Sigmund Freud. This was the endogenous, the inner region of the physical brain. Here lay the zone of organic brain damage (unacknowledged by the Viennese master) that was caused by flawed organic patterns and deteriorating tissue.

  The organic deterioration Kraepelin postulated was, and is, associated with extreme old age. It is called dementia. But Kraepelin noticed from the case studies that a significant number of patients had begun showing symptoms of dementia in their teens and early twenties. Something was going wrong with the brains of these young people, and it was going wrong decades ahead of normal expectations. What could it be?

  In 1896, Kraepelin introduced a term to define his answer to that question: “dementia praecox.” (That same year Freud coined “psychoanalysis.”) This Latinate word has references to “precocious” and “premature.” Kraepelin had no hesitation about defining this form of illness as biological in origin, the result, perhaps, of “toxic” secretions from the sex glands (take that, Sigmund!) or the intestines.

  Other psychiatrists soon gravitated to the biological point of view. In 1903, a thirty-nine-year-old doctor left his practice in Frankfurt to join Kraepelin as an assistant at the Munich medical school. Alois Alzheimer had admired the Munich doctor’s work from afar, and he saw that it converged with some of his own. Alzheimer was then treating a fifty-one-year-old woman who was beset by delusions, hallucinations, paranoia, and bursts of violent behavior—classic symptoms of senile dementia, for which she was, statistically, too young. Alzheimer had never seen a case like this. When the woman died in 1906 at age fifty-five, Alzheimer obtained consent from her family to examine her brain. What he found in his autopsy—peering at thinly sliced slivers of cortex matter—were deposits of plaque and decayed strands of nerve cells: common flaws in the brain of, say, a ninety-year-old, but virtually unheard of in someone so young.

  Alzheimer’s disease,* as it became known, is similar to senile dementia, though its onset before age sixty-five was and remains extremely rare. In a grossly unfair example of “unintended consequences,” its frequency has greatly expanded exactly because of medical progress, which has eliminated or deferred the onset of many lethal diseases, thus allowing people to live longer, and thus bringing more and more of them into the age range for this excruciating, slowly progressing affliction. And it remains irreversible.

  The scientific value of Kraepelin’s and Alzheimer’s discoveries is immense. They decisively ratified the existence of physical causes of mental illness, and thus legitimized decades of development of neurotechnology—culminating, thus far at least, in CAT and PET scans, EEGs, MRIs, and MEGs†—methods, all, of providing information about what is happening in the living brain, whether the presence of tumors, evidence of epilepsy, or—eventually—the glimmerings of the causes of schizophrenia.

  A figure even more important than Alzheimer in building upon Kraepelin’s ideas (often, paradoxically, by taking issue with them) was the Swiss psychiatrist Eugen Bleuler. Bleuler was born in 1857, a year after Kraepelin and Freud. Unlike the emotionally remote Kraepelin with his dependence upon case studies, Bleuler plunged directly into the lives of his psychiatric patients. Not only did he conduct analytical interviews with them, which partly rebridged the gap that Kraepelin had marked off from Freud, but he socialized with them, accompanied them on hikes, arranged theater productions in which he acted along with them, and sometimes supervised their financial interests.8 These intimate encounters allowed Bleuler to gather analytic insights unavailable through the filter of abstract assessment. He came to believe that mental illnesses covered an even wider and more complex range than the types Kraepelin had laid out—that they could include not just organic but environmental components, such as the ravages of abuse, traumatic shock, stress, all events that roughly corresponded to Kraepelin’s “exogenous” category.

  Here was the essence of what would become the “spectrum” concept of differentiated mental disorders, and with ever-improving diagnostic technology, its principles were to light the way for tremendous gains in brain science.* But Bleuler left himself open for years of second-guessing, not least because of a single word choice. Perhaps a little dazzled by the promise of his own refinements, he persuaded his colleagues to drop “dementia praecox” from the lexicon and replace it with a word of his own. Getting rid of Kraepelin’s term was not a bad idea in itself: Bleuler had grown convinced that it was not dementia that psychiatrists were seeing in young patients, but something else, something a great deal more complicated. In 1908 he summed up this something else with the term “schizophrenia.” This was not a wise choice. The word’s literal meaning, drawing upon the Greek, meant “a splitting of the mind.” Its ambiguity practically pleaded for misinterpretation, especially among laypeople. By “split,” Bleuler meant a “loosening of associations”—the associations being the physical conductors that unify thoughts and behavior. (In important ways, this term anticipates Julian Jaynes’s formulations.) In other words, psychosis did not always arise from “dementia,” or decaying cells and tissue. In people who were not decrepit, it usually was triggered by a cluster of genetic flaws, often the result of heredity.

  Yet “a loosening of associations” was for many just a short step from “split personality,” which itself was but a short step from the old, largely discarded ghost of demonic possession. The times were rife with images of it, especially from the Gothic precincts of the British Isles. The Scotsman Robert Louis Stevenson published The Strange Case of Dr Jekyll and Mr Hyde in 1886. In 1897,
the Irish novelist Bram Stoker published Dracula. Even Freud, from far-off Vienna, joined the fun—albeit unintentionally—with his 1918 paper on the patient he called “the Wolf Man.” The Wolf Man was not in fact a shape-shifter; he was a depressive Russian aristocrat who, while very young, had witnessed his parents having sex, started having dreams of trees filled with white wolves, and from then on never felt really great, though he lived until 1979. It may not be entirely insignificant that the parents were using a sex technique that involved canine resonances.

  Bleuler accepted Freud’s emphasis on the unconscious, his use of hypnotism, and his strong diagnostic interest in hysteria. But he held back from accepting psychoanalysis as the cure-all for mental illness. He posited that the affliction, or afflictions, presented both basic and accessory symptoms. Basic symptoms, probably passed along through heredity, involved the deterioration and ultimate breakdown of the ability to think. Accessory symptoms were manifestations of that breakdown: delusions and hallucinations. The fundamentals of his formulation retain their diagnostic dimensions today.

  Both Kraepelin and Bleuler (despite their differences) seem to have possessed great gifts, including extraordinary intuition. As has been remarked, decades would have to pass before neurotechnology came along to ratify and fine-tune their pioneering proposals about physical contributors—lesions, in a word—to madness. The basics of brain formation, so inaccessible to their generation, are by now familiar to most educated people. Still, a brief summary here may help the reader comprehend the inception of schizophrenia as we presently understand it, following Kraepelin’s and Bleuler’s beacon.

  The prefrontal cortex is a complex, fragile region of the brain. In its healthy state, it directs human impulses toward rational choices and away from destructive or self-destructive behavior. It allows us to deal with the present moment while storing plans for the future. Yet as the newest part of the brain to develop in human evolution, the prefrontal cortex is also the region that takes the longest time to reach maturity, or maximum operating efficiency. It will not be fully functional until the person is past the age of twenty.