In 1957, a Swedish scientist named Arvid Carlsson was experimenting with a new antipsycholtc drug called reserpine. Injection of the drug to rabbits temporarily paralyzed them. Carlsson speculated that the reserpine blocked a key neurotransmitter in the brain, resulting a chemical imbalance causing the symptoms. He expected a chemical called levodopa, or L-dopa, could be converted into noradrenaline in the brain to restore the chemical imbalance. It worked – the rabbits became alert and moved normally. But when he examined the chemicals in their brain, he discovered that the L-dopa had been converted not into noradrenaline, but into a different compound called dopamine.
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Most neurologists at the time regarded dopamine as an unimportant chemical, but Carlsson was convinced that dopamine was an essential neurotransmitter for the brain to function. He suggested that dopamine deficiency was the reason for Parkinson’s disease.
Carlsson’s suggestion inspired two Austrian researchers, Herbert Ehringer, and Oleh Hornykiewicz. They examined autopsied brains and found that parkinsonian brains had virtually no dopamine. Teaming up with physician Walther Birkmayer, Hornykiewicz proved that, besides the black stuff, dopamine was also missing from the substantia nigra region.
Their work formed the basis of a new dopamine-centered theory of PD. This theory suggested a possible cure for PD. Because if dopamine deficiency causes PD, then the logical solution is to replace the missing chemical. But getting the drug into the brain is not as simple as taking a pill. The brain is protected by the “blood-brain barrier,” which blocks certain neurotransmitters like dopamine from directly reaching the brain. Instead, the brain manufactures its own dopamine from chemicals like L-dopa, which can pass through the blood-brain barrier as Carlsson had shown with his rabbits experiment. Birkmayer and Hornkiewicz administered small quantities of L-dopa intravenously into 20 patients with advanced Parkinson’s disease and found L-dopa worked. The patients could now walk, talk and stand up like normal.
But many scientists were unconvinced, thinking it was a placebo effect. In 1966, a controlled double-blind trial of the drug concluded that the drug had no effect on Parkinson’s symptoms. Worse, one-third of patients suffered serious side effects such as high blood pressure and nausea.
Despite the skepticism, a few scientists believed L-dopa might be effective once the correct dose was determined. In 1967, Swiss chemists discovered that adding carbidopa, an enzyme block, enabled more of the L-dopa to reach the bloodstream rather than being broken down in the bloodstream. With this new regimen for carbidopa-levodopa, the US scientist George Cotzias found that a group of 18 patients made spectacular improvements in their motor function.
In the late 1960s, a neuroscientist named Roger Duvoisin was experimenting with L-dopa to treat PD. He treated his first case with carbidopa-levodopa in December 1967. The effect was so dramatic he was quickly convinced. He videotaped his patients before and after each treatment. The transformation of the patients before and after the treatment was so convincing that the Food and Drug Administration quickly approved the drug for the routine treatment of PD.
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But clinicians soon discovered that after starting L-dopa for a month or two, the patients displayed new disabling motor side effects such as involuntary writhing movements called dyskinesias (Greek for “bad movements”). And the drug became less effective over time. Sometimes, the power of the drug suddenly vanished without warning. And some patients suffered side effects like confusion, agitation, paranoia, and hallucinations. Neurologists called these side effects “motor complications.”
Because of these side effects of L-dopa, many neurologists start patients with a less powerful class of drugs called dopamine agonists. Discovered in the 1970s, dopamine agonists work by “pretending” to be dopamine. While the brain isn’t actually receiving dopamine, it “thinks” it is and reacts accordingly. They are half as effective as L-dopa and have their own set of side effects, ranging from nausea to sleep attacks to compulsions.Â Research shows that one in ten patients are susceptible to impulse-control disorder (ICD).
PD patients are very lucky to have L-dopa. There are no equivalent for other neurodegenerative illnesses such as Huntington’s, Lou Gehrig’s, or Alzheimer’s. L-dopa turned Parkinson’s from a rapid slide into immobility and death condition into a chronic disease with the gradual trajectory of decline.
By the late 1960s, scientists had made enormous progress since James Parkinson’s 1817 essay. They could diagnose the disease and characterize its underlying pathology. They also discovered drugs that can relieve the symptoms, albeit temporarily. But what about its causes? Is it genetic or is it caused by something in the environment? Understanding the cause might well lead to a cure.
- In 1957, Arvid Carlsson discovered that L-dopa converts into dopamine in the brain of rabbits. He suggested that dopamine deficiency was the reason for Parkinson’s disease.
- Herbert Ehringer, Oleh Hornykiewicz, and Walther Birkmayer discovered that dopamine was missing from the substantia nigra of the brains of PD patients. Their work formed the basis of a new dopamine-centered theory of PD.
- By the late 1960s, Walther Birkmayer, Oleh Hornykiewics, George Cotzias, and Roger Duvoisin showed that levodopa could temporarilyÂ relieve parkinsonian symptoms in humans.
- After starting levodopa for a month or two, PD patients experience levodopa-induced side effects called “motor complications.”
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