believed that human narcoleptics have mutations in the genes which produce this neurotransmitter. Additionally, most narcoleptics show no sign of a genetic link. Because of this researchers believe that narcolepsy is influenced by environmental conditions. It has been hypothesized that narcolepsy is an autoimmune disease in which the bodys immune system attacks part of the nervous system. In a study on HLA type in narcoleptic people it was shown that the HLA type was not important in inducing narcolepsy; however, it does affect susceptibility to narcolepsy. Furthermore, researchers have been unable to prove that narcoleptics immune systems are attacking their hypocretin/orexin receptors. Research is being focused on the brains of narcoleptic patients. However, after death the results are inconclusive since the damaged neurons would have been removed throughout the lifetime of the individual. The disease plateaus at a point and is therefore unprogressive. Although there have been some differences noted in the brains of narcoleptics it cannot be determined if these are the cause or effect of the disease. In order to alleviate the problem of the brain removing damaged neurons before death, Siegel experimented on live dogs. He injected a stain into the cerebral spinal fluid at the onset of narcoleptic symptoms. The stain used only stains damaged tissue. Degeneration could be seen in parts of the brain until six months of age when no more degeneration could be observed. Much of the degeneration appears to occur in the amygdala. Nevertheless, this information has just sparked more questions. Siegels article was easy to read and provided some useful information. However, much of the research in his paper was not his own research. Siegel relied heavily on other researchers data and seemed to have performed only a couple of the mentioned experiments. Moreover, Siegels article leaves the reader with many questions left unanswered at the end of t...
