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Essay: Creutzfeldt-Jakob Disease (CJD): Types, Prevention, & Symptoms

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  • Published: 26 February 2023*
  • Last Modified: 22 July 2024
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Creutzfeldt-Jakob Disease

Introduction

Aging is a process that everyone needs to come to terms with, and with that also means understanding that you are at an increased risk to develop a variety of diseases. That being said, no one is ever prepared to get a diagnosis like Creutzfeldt-Jakob Disease (CJD). While this disease is extremely rare, it has an ‘estimated incidence of 1 in 1 million throughout the world every year and only affects 350 people in the US each year’ (Appleby, Manuelidis, 2018), it is fast and fatal and difficult for any family to handle. This is a disease where the cause is widely unknown, and anyone can develop it. This disease comes from a family of both human and animal diseases known as Transmissible Spongiform Encephalopathies (TSE). It is also called prion disease because it is caused by an abnormal isoform of a cellular glycoprotein known as the prion protein (CDC, 2018). It is important to note that humans have naturally occurring prion proteins in their body, it is when these proteins spontaneously mutate that the disease occurs.

Types and History of Creutzfeldt-Jakob Disease

There are 3 different types of Creutzfeldt-Jakob Disease. The most common type of CJD is Sporadic. This type accounts for approximately 85% of cases for this disease and is named as such because the cause of it is unknown (CDC, 2018). Another type of CJD is Hereditary, which accounts for 10-15% of CJD cases. This type is caused by a gene mutation, which ‘children have a 50% chance of getting if this disease runs in their family’ (Appleby, Manuelidis, 2018). This mutation only needs to be passed on by one parent for the child to be at an increased risk of developing it later on in life. Last, there is acquired Creutzfeldt-Jakob disease. This is the rarest, and least likely way someone will develop the disease. Acquired cases only account for 1% of those with CJD since the disease was discovered in 1920 (Ricketts, et al., 1997). In 1997, a retrospective study was done through the Montreal Neurological Institute that confirmed that transplanting tissue could cause CJD, within this study they found 4 cases starting in 1974 that fit this criterion. The causes included, corneal transplant from animals and humans infected, electrodes that were previously used on patients with suspected CJD, and cadaver-extracted pituitary growth hormone (Ricketts, et al., 1997). There is also an acquired CJD called variant Creutzfeldt-Jakob Disease which is ‘contracted when someone eats meat from cattle that has Bovine Spongiform Encephalopathy (BSE) or ‘mad cow disease’’ (Appleby, Manuelidis, 2018). It is extremely rare for someone in the US to have vCJD, and if they do it is because they contracted it while traveling abroad.

Risk Factors and Demographics

Most cases of CJD occur for unknown reasons, that being said, there are no risk factors for the disease that can be identified. While there are no risk factors that are certain associations that are related to the different types of the disease. The main association is age, with most having illness onset at a median age of 60. Genetics are also an association for the disease. If the gene mutation runs in the family, there is a 50% chance of passing it on and there only needs to be one copy of the gene from a parent in order to be affected by the disease (Mayoclinic, 2018). There is also an association with exposure to contaminated tissue and acquired CJD. This is not something that likely occurs today because of the extensive measures put into place to prevent acquired CJD from occurring, these are still important to note. Those who have received Human Growth Hormone (HGH) from human pituitary glands or grafts of tissue such as the dura mater that cover the brain may have a risk of contracting the disease (Ae, et al, 2018). If someone eats cattle that have BSE, also may develop variant CJD (Mayoclinic, 2018). There are also no demographic predispositions for this disease other than age, which means that individuals over 50 have an increased chance of getting it, but gender and race are not predisposing factors.

Symptoms

When looking at the symptoms of Creutzfeldt-Jakob Disease, many can confuse it with other dementia-like brain disorders such as Alzheimer’s (Mayoclinic, 2018). The big difference between other disorders and this disease is the rapid progression of mental deterioration within the first few months of illness onset (CDC, 2018). When looking for signs and symptoms of an individual with CJD, they will present with personality changes, anxiety, depression, memory loss, impaired thinking, blurred vision/ blindness, insomnia, difficulty speaking, difficulty swallowing, and sudden, jerky movements (Mayoclinic, 2018). As the disease progresses, ‘mental symptoms will worsen, and most individuals eventually lapse into a coma’ (Mayoclinic, 2018). Creutzfeldt-Jakob Disease itself is not usually the cause of death. Individuals will often die from heart failure, respiratory failure, pneumonia, or other infections (Appleby, et al., 2009).

Prevention, Testing, Diagnosis and Treatment

There is no known way to prevent this disease if it is sporadic or hereditary. If it is acquired CJD some prevention methods have been developed. There is now an exclusive use of synthetic HGH, surgical instruments are destroyed if they are used on the brain or nervous tissue of someone who is known to or suspected to have the disease, and lumbar punctures are now done with single use kits (Mayoclinic, 2018). When testing for CJD in order to come to a diagnosis, there are a few steps that need to be taken first. To start, there needs to be at least 2 clinical features that represent rapidly progressing dementia. These include, myoclonus (spasmodic jerky contraction of groups of muscles), visual or cerebellar signs, pyramidal/ extra pyramidal signs (both sets of signs show that portions of the brain are deteriorating, affecting physical things like memory and speech), and akinetic mutism (lack of mobility and speech).  There also needs to be at least 1 positive laboratory test which includes a typical EEG with periodical sharp wave complexes, MRI with high signal abnormalities in caudate nucleus and/or putamen on diffusion-weighted imaging or fluid attenuated inversion recovery, and a spinal tap test (this will allow doctors to see if there are abnormal prion proteins in the spinal fluid). Lastly, there needs to be no routine investigations indicating an alternative diagnosis (Mayoclinic, 2018). There is currently no treatment for this disease. Most of the treatment is focused on making the individual as comfortable as possible. These treatments include opiates for pain, clonazepam (sedative) and sodium valproate (anticonvulsant) to treat spasms, and as the disease progresses there may be a need for IV fluids and artificial feeding with a nasogastric or G-tube (Appleby, Manuelidis, 2018).

This is a fatal disease that currently has no treatment or prevention. With dementia-like brain disorders already affecting so many families, this is often a wrench because it is so rapidly progressing. It is important to make sure that those that are diagnosed with this disease are made comfortable and enjoy time with their families, because their life expectancies are only about a year after the diagnosis, with all individuals with the disease passing away quickly. There may not be a cure now, but lets hope with advancements, there can be some in the future.

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