Creutzfeldt-Jakob Disease Case Study

At this point, coordination is at a point where falls are often major risks, and considering many cases of the disease occur in the elderly, this can become a fatal risk. Close relatives are soon to become unrecognizable and the long term memory of the individual begins to fade as the disease worsens. It is often that at this point of the disease, the patient is put into a care center, as they may become a burden to the family members around them. Emotions swing and become entirely unpredictable and often resistance to care will occur as the patients lose awareness of their condition and become confused with their surroundings.

“Korsakoff syndrome is a preventable memory disorder that usually emerges (although not always) in the outcome of an episode of Wernicke 's encephalopathy, therefore the chronic disorder is sometimes known as Wernicke- Korsakoff syndrome.” Wernicke encephalopathy is an acute brain reaction to severe lack of thiamine. Wernicke encephalopathy is a medical emergency that causes life-threatening brain disruption, confusion, staggering and stumbling, lack of coordination, and abnormal involuntary eye movements.”

There is now strong scientific suspicion that the agent responsible for the outbreak of prion disease in cows, bovine spongiform encephalopathy (BSE or 'mad cow' disease), is the same agent responsible for the outbreak of vCJD in humans. Variant CJD (vCJD) is not the same disease as classic CJD It has different clinical and pathologic characteristics. Each disease also has a particular genetic profile of the prion protein gene. Both disorders are fatal brain diseases with unusually long periods measured in years, and are caused by a transmissible agent called a

Creutzfeldt-Jakob disease (vCJD) is a mad cow human disease which is believed to be caused by eating beef products contaminated with central nervous system tissue, such as brain and spinal cord, from cattle infected with mad cow disease. For this reason, the many

Regardless of which occur first, affected individuals will generally experience most of the symptoms as the disease progresses. Specifically, symptoms that include difficulty swallowing, moving, forming words, tight muscles, spasticity, and/or exaggerated reflexes occur when the upper motor neurons have been damaged. When lower motor neurons are damaged, symptoms such as muscle weakness, atrophy, cramping, and twitching will occur. In some cases, a few of the muscle neurons that

The third stage is deterioration or disturbance. This stage altitude is between 11400 to 20000ft.(3) In this stage obvious symptoms is begin, but not everyone can recognize the symptoms of this stage. (1) (2) And there is some of these symptoms shortness of breath/air hunger, incoordination, cyanosis, difficulty with simple tasks, drowsiness, diminished vision, headache, tingling, euphoria, numbness, aggression, hot/cold flashes, and poor judgement.(1) The arterial oxygen saturations in this phase is between 70 to 80 percent.(10)

In Ronald Bailey’s article “Transhumanism: The Most Dangerous Idea? Why Striving to Be More Human Is Human”, Bailey poses an underlying question about which ideas, if embraced, would pose the greatest threat to the welfare of humanity? In particular, Bailey posed the question to 8 of the most prominent policy intellectuals editors of the “foreign policy” from the September and October issue. Of the 8 editors, the answer that caught Bailey’s attention the most was that of editor Francis Fukuyama. Fukuyama proposed in his Foreign “Policy article”, that the world’s most dangerous idea was that of Transhumanism.

Acute disseminated encephalomyelitis is an immune-mediated inflammatory demyelinating condition that affects the white matter of the brain and spinal cord. ADEM also attacks the nerves of the central nervous system and damages their myelin insulation, which destroys the white matter. It is often triggered after the patient has received a viral infection or sometimes exceedingly rarely specific non-routine vaccinations. It affects children more than adults but can affect anyone. More than half of patients have an illness usually an infection two to four weeks before developing ADEM. Most of these illnesses are viral or bacterial, often no more than an upper respiratory tract infection. In children with ADEM, prolonged and severe headaches occur. In addition, the patient develops fevers during the ADEM course.

This disease gets its name from the German neurologist Hans Gerhard Creutzfeldt and Alfons Maria Jakob that first identified this disease. (Victor, 2015) VCJD is primarily found in the brain of the cattle. Abnormal proteins called prions have thought to be the cause of this disease in both cattle and in humans. These prions cause tiny holes that look like a sponge under a microscope. (Melissa Conrad Stöppler, 2015) Unlike most viruses and bacteria these prions unfortunately do not die when exposed to heat, ultraviolet light, and radiation. Disinfectants that are usually used to kill viruses and bacteria also do not work to kill prions. Even cooking the meat very well will not lower the risk of prions in the

In the early 1900’s, the Fore tribe was struck with an epidemic of Kuru, a brain eating disorder that causes shaking, and furthermore the name “Kuru” in the means shaking or trembling in a literal sense. The Fore spread this disease a fair bit, specifically due to their cannibalistic funeral practices of eating the remains of the dead, and specifically the brain (Bichell, Rae Ellen 2016). However, the presence of Prions have been around for eras, but the discovery in the Fore tribe spearheaded the movement to learn more about them. Eventually in 1982, the “Prion protein” was discovered by Stanley Prusiner, eventually earning him the Nobel Prize in 1997 for his proof of the lack of DNA or RNA in the protein, juxtaposed to bacteria and viruses (Prion Alliance, 2016). As the amount of diseases discovered increased, it became eerily known that the Prion disease in humans and animals were all caused by one original misfolded protein, PrPsc. Despite a common origin, pinning down a solution to the problems of Prions is an extremely complex issue. With an extreme resistance to everything, Prions opens the question of sanitization in hospitals. If a doctor were to be working with a Prion-contaminated sample, the tools used may be thought to be completely clean, yet Prions being highly resistant would persevere against normal

KD is a very rare disorder, the prevalence thought to be 2 per 100,000 people according to the Cell and Tissue Research article. It is thought that KD is often misdiagnosis as amyotrophic lateral sclerosis (ALS). The first case ever recorded of KD came from a patient who was previously diagnosis with ALS and wanted a seconded opinion. The onset for KD is usually midlife, the range being from 30-60 years of age. The onset is often preceded by non-specific

This week may be the last week I write to you. In my last letter to you, you may have noticed that I seemed depressed and not like myself. I wasn’t completely truthful in that letter. I’m not just having a bad day, I’m diseased with an incurable, fatal disease.

Transmissible spongiform encephalopathies (TSEs) are neurodegenerative diseases that are thought to be caused by the misfolding of prion proteins. Prions are able to replicate in the absence of nucleic acids. TSEs include: scrapie, bovine spongiform encephalopathy, Creutzfeldt-Jakob disease, kuru, Gerstmann-Straussler-Scheinker disease, and Fatal Familial Insomnia. They can affect many different animals, including humans. Currently, there are no ways to diagnose, treat, or cure TSEs, as much more research is needed before these diseases are completely understood.

Genetic instability refers to temporary or permanent unscheduled alterations within the genome occur and can occur both at chromosomal or nucleotide level. Instability at nucleotide level consists of increased frequency of base-pair mutation or amplified number of nucleotide repeat units such as trinucleotide repeats (TNR) in a gene which will show altered expression and malfunction of RNA and/or protein (Castel et al., 2010).

CJD is a serious neurodegenerative disorder, a rare form of rapidly progressive dementia, with a 100% fatality within one to two years of onset. CJD belongs to a family of human and animal diseases known as the transmissible spongiform encephalopathies (TSEs). It is believed to be caused by an abnormal isoform of a cellular glycoprotein known as the prion protein that becomes toxic in an abnormal form (CDC) although Dr. Campellone suggest other proteins may play a role in this disease as well. Although, it is so rare that only between one to every one million people worldwide are diagnosed.