In 1887, only a few years after Koller’s great announcement, the young doctor—Arthur Conan Doyle—published his first major novel, entitled A Study in Scarlet, in a now forgotten magazine called Beeton’s Christmas Annual. The tale introduced the world to Sherlock Holmes, the pipe-smoking sleuth who employed a method he called “deductive reasoning,” which was based on the diagnostic approach of a physician. As Conan Doyle’s legion of readers would learn in subsequent episodes, Sherlock enjoyed injecting a 7 percent solution of cocaine as a means of escape after particular trying cases. Parenthetically, it is too rich to neglect to mention that one of Conan Doyle’s most avid readers was Sigmund Freud. As Freud’s now famous patient Sergius Pankejeff (better known as “the Wolf-Man”) recalled: “Once we happened to speak of Conan Doyle and his creation, Sherlock Holmes. I had thought that Freud would have no use for this type of light reading matter, and was surprised to find that this was not at all the case and that Freud read this author attentively.”
Arthur Conan Doyle, M.D.: the creator of Sherlock Holmes, 1894. (photo credit 5.4)
Three years after Sherlock Holmes’s debut, in 1890, a second novel, A Sign of the Four, was published to great acclaim. Conan Doyle’s precise description of Holmes’s cocaine self-administration in this novel could just as easily be applied to Halsted’s technique and mottled arm:
Sherlock Holmes took his bottle from the corner of the mantel-piece and his hypodermic syringe from its neat morocco case. With his long, white, nervous fingers he adjusted the delicate needle, and rolled back his left shirt-cuff. For some little time his eyes rested thoughtfully upon the sinewy forearm and wrist all dotted and scarred with innumerable puncture-marks. Finally he thrust the sharp point home, pressed down the tiny piston, and sank back into the velvet-lined arm-chair with a long sigh of satisfaction.
Like the fictional detective, Halsted was instantly struck by how marvelous the drug made him feel. An injection of cocaine guaranteed freedom from all vicissitudes and slights, release from resentments and pain, and a sense of utter satisfaction so strong and compelling, exhilarating and calming that he would eventually risk or sacrifice anything just to be under its power again.
IN A MATTER OF WEEKS Halsted and his immediate circle were transformed from an elite cadre of doctors into active cocaine abusers. Tragically, some of the medical students, resident physicians, and surgeons who participated in these experiments were decimated by the drug and died early deaths. Most poignant was the fate of Halsted’s close colleague, assistant, and friend Richard J. Hall. The two first met in medical school and spent time together in Vienna in 1879. Upon returning to New York, they were each appointed to the faculty of their alma mater. Present at the start of Halsted’s precipitous love affair with cocaine in 1884, Hall recorded some of their earliest experiments in the New York Medical Journal. Unfortunately, Hall became so addicted to cocaine that he was forced to “dry out” at a sanatorium in Santa Barbara, California. In 1895, a rehabilitated Hall wrote Halsted a rambling letter boasting of a new surgical practice and explaining his long silence:
My dear Halsted; It is now quite a long time since I received a long letter from you and a very kind one. I am not sure that I ever answered it, for at that time I was only pulling myself together, after a long period of misery, the causes of which I do not need to describe.
Two years later, Richard Hall died at the age of forty-four of unclear causes, though many suspect he never truly beat his demons down. William may have narrowly avoided the ultimate cocaine oblivion that took his friend at such an early age, but he hardly escaped unscathed.
CHAPTER 6
Cocaine Damnation
WHY IS COCAINE SO PLEASURABLE, so compelling, and, ultimately, so addictive?
With most substances of abuse, rapid delivery of the drug to the brain is critical. The faster the absorption, the more intense is the high. Paradoxically, the faster the absorption, the shorter is the duration of action, often inspiring the desire for more drugs. During the late nineteenth century, many cocaine fans took their drug in the form of laced teas, tonics, alcohol-based elixirs, and soft drinks. Yet the twists and turns of the stomach and intestines are simply too circuitous a path to the bloodstream and brain to yield cocaine’s most explosive effects. And if there is one thing most experienced drug users seek, it is the quickest and most potent means of getting high.
Once cocaine became available in crystalline form, some, like Freud, drank it mixed in a small amount of water or dabbed on the tongue. Many others, however, began to snort or sniff a carefully ground-up dose into the nostrils, using a tiny spoonlike device or a straw-shaped object. The experienced cocaine user quickly learns the importance of grinding down the crystals with a sharp-edged instrument, such as a razor blade, into a fine powder, to avoid large pellets, which do not dissolve well and can erode or ulcerate the wet, sensitive mucus membranes that line the interior of the nose. Of greater distress to the avid cocaine user is the issue of waste: more times than not, large pieces of cocaine simply fall out at the first blow or shake of the nose. Those users who do take the time to finely chop their drug are eventually rewarded. Beneath the inner lining of the nose are thousands of tiny capillaries, which lead to larger and larger still blood vessels. The effects from such ingestions may last fifteen to thirty minutes.
A more efficient and addictive means of using cocaine is to smoke it after the drug has been chemically altered. If one smokes ordinary cocaine hydrochloride, much of the active ingredient is destroyed. To counteract this loss, in the mid-1980s drug dealers began “cooking” the cocaine in a pan laced with water and baking soda. The resulting chemical reaction frees the cocaine molecules from the attached hydrochloride salt and produces a loud popping or cracking noise—hence the drug’s odd name, crack cocaine. Cocaine users soon flocked to purchase this substance from their dealers because smoking it guaranteed remarkably intense, albeit short-lived highs.
Once cocaine is chemically manipulated and smoked, psychoactive molecules are released and inhaled into tiny air sacs, called alveoli, in the inner recesses of the lungs. These are the structures where the real work of respiration takes place; molecules of life-giving oxygen are absorbed into the bloodstream and waste molecules of carbon dioxide are readied for exhalation. Surrounding the alveoli is an intricate network of blood vessels called arterioles and capillaries. In terms of surface area, these arterioles equal the square footage of a football field. As a result, the molecules of inhaled cocaine easily cross the membrane-thin layer of the alveoli and instantly enter the bloodstream, the body’s equivalent of the autobahn, with a direct route to the brain.
Unlike with morphine and other opiates, relatively few cocaine addicts choose to inject the drug into their veins, although Halsted and Fleischl-Marxow may have occasionally done so. This method, alas, is dangerous, potentially painful, and highly addictive. Nevertheless, injecting cocaine rewards the addict in generating a speedy and intense high.
Whether tasted, sniffed, smoked, or injected, once inside the bloodstream, the cocaine molecules travel rapidly to other critical organs as well. Most noticeable is the drug’s arrival in the heart, the central pumping and distribution system that directs the blood into the lungs in order for it to grab an allotment of nourishing oxygen before being sent to the rest of the body. Cardiac muscle is exquisitely vulnerable to cocaine’s powers. Under its influence, the heart pumps harder and faster. Blood vessels will constrict, or tighten, leading to an alarming increase of blood pressure. More troubling, the drug can provoke serious disturbances in how the heart beats and may even incite a heart attack or stroke. Cocaine can also wreak havoc on the liver, spleen, and kidneys, altering those organs’ functions and potentially causing serious damage.
A sagittal view of the brain, showing a neuron with connections to the prefrontal cortex and its pleasure enters, the nucleus accumbens, and the ventral tegmental area. (photo credit 6.1)
After arriving at the brain’s prefrontal corte
x, cocaine travels to the ventral tegmental area (VTA), which has a direct pathway to a nearby region called the nucleus accumbens, thought to be a key pleasure center. Just about every gratifying act known to man, whether drinking a cold glass of water on a hot day, enjoying a delicious meal, feeling the warmth of the sun or the closeness of a loved one, sexual arousal and the rollicking climaxes we refer to as orgasms, the satisfaction experienced with an achievement or acquisition, or delighting in a harvest moon—essentially every experience that makes life worth living—is registered, recorded, anticipated, and mediated in this part of the brain. From this “pleasure center,” these experiences are quickly translated into the recognizable signs of contentment, from a smile to a sense of well-being.
If nature set out to design an addictive drug, it could hardly do better than cocaine. This is because the drug brilliantly fools the neurons ending in the nucleus accumbens into sensing a virtual abundance of enjoyable feelings and sensations.
The predominant chemical effect of a dose of cocaine is a massive flood of receptor neurons with dopamine, the neurotransmitter that helps govern pleasure, motivation, and reward. Such synaptic flooding also occurs with two other major neurotransmitters that contribute to one’s mood, serotonin and norepinephrine. Under normal circumstances, transporter proteins at the nerve endings remove these neurotransmitters from the synapse (the microscopic gap between two neurons) and recycle them back into vesicles (the transmitting neuron’s storage centers). But with cocaine molecules on the scene, the transporter proteins are, essentially, jammed up. Consequently, the receiving neurons sense far more dopamine (as well as serotonin and norepinephrine) than usual and interpret this excess as extreme pleasure or a “rush” of euphoria. A pharmacological version of the legendary Trojan horse, cocaine essentially sneaks through the gates into the brain’s finely honed reward system before seizing control.
The synapse between a transmitting neuron and a receiving neuron and the release of dopamine. The figure demonstrates normal dopamine transporter uptake (left) and blocked dopamine transporter uptake (right) under the influence of cocaine. (photo credit 6.2)
Within a few moments of smoking, injecting, or sniffing cocaine, a sense of exhilarating delight begins. This is not the slaphappy, “I love everyone” kind of joy that transpires after a few belts of whiskey. When under the influence of cocaine, one feels supremely confident, almost electrically charged with faster thoughts, better ideas (at least in one’s own mind at the time of the high), an increased speed of speaking, and a greater appreciation of such sensations as sight, sound, and touch. This energy burst also decreases the need to eat and sleep, allowing a user to stay awake all night if he consumes enough of the stuff.
And if a drug-induced sexual experience is the aim, many swear by cocaine’s ability to increase desire and focus on that pursuit. Yet it is precisely in the sexual arena where one of cocaine’s many perverse powers emerges. While cocaine may, indeed, catapult a person’s quest for sexual stimulation and climax, the drug blocks the neurons’ ability to reabsorb serotonin in the synapse. It causes vasoconstriction of the blood vessels in the penis, thus interfering with a man’s ability to maintain an erection. Moreover, for both men and women, cocaine interrupts the brain’s physiological processes for achieving an orgasm. Ecstatic arousal and desire are jet-propelled, but the fuel to finish the journey is defiantly lacking long before the first orbit is complete.
Cocaine, of course, also contains a brutally negative force. When the drug is metabolized and inactive in the brain, the transporter molecules begin to function again and absorb all the excess neurotransmitters in the synapse. This mop-up effort results in a shortage of these critical mood-regulating chemicals in the brain. In turn, that shortage causes the pleasure circuits to abruptly cease their orgiastic firing, a situation known all too well by experienced cocaine abusers as a “crash.” Specifically, such crashes are awful, dramatic lows that occur immediately following the cocaine high; unfortunately, their effects linger far, far after the intensely pleasurable sensations are over. To make matters worse, as an individual successively fools the neurons to release, deplete, and replenish their stores of dopamine, serotonin, and norepinephrine with repeated doses of cocaine, he requires greater amounts of the drug to achieve the same levels of satisfaction, forming a perfect endless loop of addictive and destructive behavior.
In time, cocaine abuse yields significant damage not only in the brain’s pleasure centers but also in the frontal cortex, the region of the brain that facilitates decision making. The extent of this neurological derangement was most starkly demonstrated during the late 1960s. Scientists gave one set of laboratory rats ample food and water, and open access to heroin; the other group was given the same food and water but the bar was serving cocaine. The heroin rats certainly became addicted to their drug, but its narcotic effects curtailed their consumption to specific times during the day. Basically, they got stoned and fell asleep, awoke, drank water and ate, and then started all over again. On the other side of the caged neighborhood, the cocaine rats did nothing but consume more cocaine. At various points some of these rats would collapse with nervous exhaustion, but once they awoke, they routinely pursued more cocaine. A month later, the heroin rats were surviving nicely, albeit addicted to narcotics; the cocaine rats were all dead.
AT THE TIME DR. HALSTED began experimenting with cocaine, he enjoyed a comfortable home life with his companion and roommate, Thomas Alexander McBride, a former medical school classmate. McBride, handsome and well-spoken, was considered quite the man about town. He maintained a prosperous carriage trade practice in addition to his duties as a clinical assistant in internal medicine at the College of Physicians and Surgeons. McBride and Halsted lived in a “luxuriously furnished” flat on Twenty-fifth Street between Madison Avenue and Fourth Avenue (now Park Avenue South) that served as the unofficial clubhouse for an expanding cadre of medical students and doctors. McBride was said to have spent “lavishly” on his roommate, but the precise contours of their domestic arrangement remain unclear. It was likely a close and loving relationship, though one that would have attracted little attention or comment in an era when discreet and separate social spheres existed for men and women, not to mention a decided aversion to publicly discussing sexuality.
In a matter of months, cocaine completely took over Halsted’s life. First he missed only occasional lectures or perhaps an appointment with a colleague. Soon enough, he was referring patients to other surgeons to avoid the operating room. Although he made a somewhat confused appearance at the evening meeting of the New York Surgical Society on April 28, 1885, for most of that spring, William engaged in few, if any, clinical activities. His last recorded operations at Bellevue took place on March 23, an amputation of a laborer’s leg above the knee for gangrene resulting from a crush injury and an excision of a vaginal-cutaneous sinus tract in a woman. On May 5, 1885, he ceased to be a doctor and surgeon, the path to which he had devoted the last intense decade of his life. After examining a laborer suffering from a compound fracture of the tibia, a thin, haggard, and addicted Halsted abruptly exited Bellevue Hospital to nervously hibernate and consume alarmingly large amounts of cocaine in his Manhattan town house.
Always a prolific medical correspondent with a precise literary style, the years 1885 and 1886 signaled Halsted’s most fallow period as a writer. As proof, one need only consult the memorial edition of the surgeon’s scientific, surgical, and academic papers, a chock-filled two volumes containing more than 150 contributions. His now famous paper on cocaine that did appear in print in 1885 was all but excised from Halsted’s clothbound Surgical Papers. Instead, the editor lists only the paper’s title and bibliographic citation, accompanied by the terse comment that it “would require such reediting as is not deemed expedient.”
In fact, “Practical Comments on the Use and Abuse of Cocaine Suggested by Its Invariably Successful Employment in More Than a Thousand Minor Surgical Operations” both advanced su
rgical technique and informs a retrospective diagnosis of William’s condition. Many medical historians credit the article, which appeared in the September 12, 1885, issue of the New York Medical Journal, with introducing the world to local anesthetic by nerve blockade. The paper also demonstrated the ease with which cocaine could be injected into the skin to achieve the desired results, the means of diluting cocaine solutions to avoid toxicity and still numb the surgical area, and ways of prolonging the anesthetic effects by reducing the flow of blood to the operative site. Still, the paper is presented in a prose so disjointed, hyperactive, and overwrought that it was almost certainly written under the influence of cocaine.
Neither indifferent as to which of how many possibilities may best explain, not yet at a loss to comprehend, why surgeons have, and that so many, quite without discredit, could have scarcely any interest in what, as a local anesthetic, had been supposed, if not declared, by most so very sure to prove, especially to them. Attractive, still I do not think that this circumstance, or some sense of obligation to rescue fragmentary reputation for surgeons rather than the belief that an opportunity existed for assisting others to an appreciable extent, induced me, several months ago to write on the subject in hand the greater part of somewhat comprehensive paper, which poor health disinclined me to complete.
Even the most experienced consumer of the medical literature is forced to scratch his head when reading this seminal publication. The paper ends with the promise of more data to be published in a subsequent issue, but Halsted never wrote a “Part II.”
In the summer of 1885, shortly after sending his cocaine study off to the New York Medical Journal, Halsted made a return trip to Vienna in search of rest and recreation. While there, he demonstrated his cocaine-injection technique for local anesthesia to his mentor Anton Wölfler and an American dentist named Thomas. Although the dentist was thrilled by the method, Wölfler declared it to be useless. Dr. Wölfler subsequently published an enthusiastic article on it in one of the daily newspapers, but without mentioning Halsted’s name. To the end of his life, the surgeon recalled this slight. One person William did not record meeting with while in Vienna was Sigmund Freud.
An Anatomy of Addiction Page 11
