A patient presented with symptoms that suggested she may be schizophrenic. Because many conditions mimicked schizophrenia, the doctor reviewed the family's notes and noted that the patient had missed an eye doctor appointment. The doctor, well aware that a test could confirm or deny a diagnosis, requested that an eye examination be performed. Kayser-Fleischer rings were present in the cornea of ​​his eyes. These rings are deposits of copper and sulfur granules and are green-gold in color. They are not always present; however, when they are, they are a classic identifier of Wilson's disease. (Holtz, 2006, pp.108-109) Therefore, the eye exam confirmed a diagnosis of Wilson's disease for this patient. While working in England in the early 1900s, Alexander Kinnear Wilson, an American neurologist, described the disease. (Schilsky & Brewer, 2009) As with many things, since he originally described it, it is named after him. Wilson's disease is also called hepatolenticular degeneration. (Mayo Clinic, 2009). It is a chronic genetic disease that accumulates excess copper in the liver. The accumulation of excess copper begins at birth. (Pittsburg Children's Hospital, 2010) Copper is an essential trace metal, vital to human health, requiring a small, regular intake to maintain homeostasis. According to Copperinfo (2011), “At least 20 enzymes contain copper and at least 10 of these require copper to function.” The brain, skin, heart and immune system all need copper. Ingested copper is absorbed in the stomach and small intestine. From there it enters the bloodstream, making its way to the liver. (Copperinfo, 2011) A healthy liver acts as a filter. Part of its functionality is to metabolize carbohydrates...... middle of paper ......cinnati Children's Hospital, 2009). A normal liver adequately filters and eliminates toxins from the body through urine or bile. Lack of copper homeostasis in a diseased and damaged liver hinders this process. This excessive accumulation of copper in the liver is Wilson's disease. Inherited mutated genes, one from each parent, cause the disease. If only one mutated gene is passed on, the individual is simply a carrier and will never be diagnosed with Wilson's disease. It is widespread throughout the world, including several ethnic groups. It most often affects children and adolescents aged 10 to 20. Occasionally there are exceptions and we see Wilson diagnoses in children as young as three and in adults over the age of 50. There is a treatment available that, if continued throughout life, will maintain copper homeostasis and the patient will live a good life..