Seizures may occur in any part of the brain; their point of origin often can be mapped. Some occur as a result of lesions in specific domains. Nineteenth-century doctor John Hughlings Jackson, an aloof but meticulous researcher, posited that lesions would produce two effects. He based this belief on the idea that most of the neurotransmitters in the brain at any given moment inhibit action. A minority of neurons at anyone time release neurotransmitters that bind to receptors. Others do nothing. Thus, Jackson said lesions would produce negative reactions because of the destruction of brain tissue. However, they also would have the opposite reaction of freeing other, healthy areas of the brain, which previously had been suppressed.

Four ions-sodium, potassium, calcium, and chloride-regulate electrical charges in synapses.

The minus and plus aspects of brain damage appeared to match the observed effects of a brain tumor in a teenage girl named Bhagawhandi in the 1970s. A neuroscientist who observed the girl diagnosed a malignant brain tumor. As the tumor grew to press on her temporal lobe and her brain started to swell, she suffered a series of seizures. They grew more frequent. However, whereas her initial seizures were intense grand mal convulsions, her new manifestations, localized in the temporal lobe, were weaker. She began experiencing dreamy states in which she saw visions of her home in India. Far from being unpleasant, they made her happy-“They take me back home,” she said. She remained peaceful and lucid during her episodes. The seizures killed her in a few weeks, but doctors often noted the rapt expression on her face as she moved deeper into her visions. Only a few diseases of the central nervous system produce pleasure. Anything that pushes the brain out of homeostasis is more likely to bring pain and discomfort to the body.

A photomicrograph of L-dopa, suggestive of an abstract painting, hints at the complex world of neurochemistry.
A photomicrograph of L-dopa, suggestive of an abstract painting, hints at the complex world of neurochemistry.

The beauty of L-dopa lay in aseemingly simple but startling idea for treatment: If the neurons’ ability to make dopamine had dramatically decreased, why not merely supplement the supply of the drug in the brain? Not only did L-dopa help the encephalitis lethargica patients, it also became a popular treatment for a far more common disease, Parkinson’s disease, marked by muscle rigidity and loss of motor control.

Despite its ability to ease suffering, though, L-dopa is no “magiC bullet,” no magic cure. Sacks’s patients began relapsing into their former patterns of tics and frenzies. Parkinson’s sufferers also found that over time, L-dopa lost some of its power to help them. Still, the tangible results of L-dopa treatments have encouraged neuroscientists to seek the right combination of medications to restore balance to brain chemistry for a variety of illnesses.

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