Blindsight

The cocaine shot into Duncan Andrews’ antecubital vein in a concentrated bolus after having been propelled by the plunger of a syringe. Chemical alarms sounded immediately. A number of the blood cells and plasma enzymes recognized the cocaine molecules as being part of a family of compounds called alkaloids, which are manufactured by plants and include such physiologically active substances as caffeine, morphine, strychnine, and nicotine.

In a desperate but vain attempt to protect the body from this sudden invasion, plasma enzymes called cholesterases attacked the cocaine, splitting some of the foreign molecules into physiologically inert fragments. But the cocaine dose was overwhelming. Within seconds the cocaine was streaking through the right side of the heart, spreading through the lungs, and then heading out into Duncan’s body.

The pharmacologic effects of the drug began almost instantly. Some of the cocaine molecules tumbled into the coronary arteries and began constricting them and reducing blood flow to the heart. At the same time the cocaine began to diffuse out of the coronary vessels into the extracellular fluid, bathing the hardworking heart muscle fibers. There the foreign compound began to interrupt the movement of sodium ions through the heart cells’ membranes, a critical part of the heart muscle contractile function. The result was that cardiac conductivity and contractility began to fall.

Simultaneously the cocaine molecules fanned out throughout the brain, having coursed up into the skull through the carotid arteries. Like knives through butter, the cocaine penetrated the blood brain barrier. Once inside the brain, the cocaine bathed the defenseless brain cells, pooling in spaces called synapses across which the nerve cells communicated.

Within the synapses the cocaine began to exert its most perverse effects. It became an impersonator. By an ironic twist of chemical fate, an outer portion of the cocaine molecule was erroneously recognized by the nerve cells as a neurotransmitter, either epinephrine, norepinephrine, or dopamine. Like skeleton keys, the cocaine molecules insinuated themselves into the molecular pumps responsible for absorbing these neurotransmitters, locking them, and bringing the pumps to a sudden halt.

The result was predictable. Since the reabsorption of the neurotransmitters was blocked, the neurotransmitters’ stimulative effect was preserved. And the stimulation caused the release of more neurotransmitters in an upward spiral of self-fulfilling excitation. Nerve cells that would have normally reverted to quiescence and serenity began to fire frantically.

The brain progressively brimmed with activity, particularly the pleasure centers deeply embedded below the cerebral cortex. Here dopamine was the principal neurotransmitter. With a perverse predilection the cocaine blocked the dopamine pumps, and the dopamine concentration soared. Circuits of nerve cells divinely wired to ensure the survival of the species rang with excitement and filled afferent pathways running up to the cortex with ecstatic messages.

But the pleasure centers were not the only areas of Duncan’s brain to be affected, just some of the first. Soon the darker side of the cocaine invasion began to exert its effect. Phylogenetically older, more caudal centers of the brain involving functions like muscle coordination and the regulation of breathing began to be affected. Even the thermoregulatory area began to be stimulated, as well as the part of the brain responsible for vomiting.

Thus all was not well. In the middle of the rush of pleasurable impulses, an ominous condition was in the making. A dark cloud was forming on the horizon, auguring a horrible neurological storm. The cocaine was about to reveal its true deceitful self: a minion of death disguised in an aura of beguiling pleasure.