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Creutzfeldt–Jakob disease

Common variable immunodeficiency (CVID) is a group of disorders characterized by low levels of a type of protein known as immunoglobulins (Ig). Because of low level of Ig, the immune system cannot make antibodies that fight bacteria, viruses or other toxins in the body. This leads to frequent infections, particularly in the sinuses, lungs, and digestive tract

Prevalence

1 / 1 000 000

1 - 1.5 / 1,000,000

US Estimated

1 - 2 / 1,000,000

Europe Estimated

Age of Onset

adults - older adults

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ICD-10

A81.0

Inheritance Pattern

Autosomal dominant

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Autosomal recessive

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Mitochondrial/Multigenic

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X-linked dominant

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X-linked recessive

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Rare View

Creutzfeldt-Jakob disease (CJD) is a rapidly progressive, invariably fatal neurodegenerative disorder believed to be caused by an abnormal isoform of a cellular glycoprotein known as the prion protein.

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5 Facts you should know

FACT

1

Creutzfeldt–Jakob disease (CJD) is a neurodegenerative disease that is incurable and invariably fatal

FACT

2

Infection with this disease leads to death usually within 1 year of onset of illness

FACT

3

CJD is at times called a human form of mad cow disease (bovine spongiform encephalopathy or BSE)

FACT

4

CJD is caused by an infectious agent called a prion

FACT

5

CJD causes the brain tissue to degenerate rapidly, and as the disease destroys the brain, the brain develops holes and the texture changes to resemble that of a sponge

Creutzfeldt–Jakob disease is also known as...

Creutzfeldt–Jakob disease is also known as:

  • CJD

  • Subacute spongiform encephalopathy

  • Neurocognitive disorder due to prion disease

What’s your Rare IQ?

Creutzfeldt-Jakob Disease (CJD) is a rare, degenerative, and fatal brain disorder. What is a key pathological feature of Creutzfeldt-Jakob Disease?

 

Common signs & symptoms

Rapidly progressive dementia, typically evolving over weeks to months

Cognitive decline with behavioral or personality changes

Myoclonus, often stimulus-induced

Cerebellar ataxia (gait instability, dysarthria)

Visual disturbances, including cortical blindness

Pyramidal and extrapyramidal signs (rigidity, bradykinesia)

Akinetic mutism in advanced stages

Current treatments

No curative or disease-modifying treatment currently available

Supportive and palliative management

Symptom control (myoclonus, agitation, pain)

Nutritional and hydration support

Prevention of complications (aspiration, infections)

Early palliative care involvement

Advance care planning and goals-of-care discussions

Family counseling and psychosocial support

Infection control and prevention

Strict prion decontamination procedures for medical instruments

Adherence to institutional prion-handling protocols

Management is focused on comfort, safety, and quality of life, given the uniformly progressive and fatal nature of the disease.