Creutzfeldt - Jakob disease pathophysiology
Classic CJD is a human prion disease. It is a neurodegenerative disorder with characteristic clinical and diagnostic features. This disease is rapidly progressive and always fatal. Infection with this disease leads to death usually within 1 year of onset of illness. Creutzfeldt-Jakob (KROITS-felt YAH-kobe) disease is a degenerative brain disorder that leads to dementia and, ultimately, death. Symptoms of Creutzfeldt-Jakob disease (CJD) can resemble those of other dementia-like brain disorders, such as Alzheimer's. But Creutzfeldt-Jakob disease usually progresses much more rapidly. There are different types of CJD: variant (vCJD), sporadic (sCJD), familial (fCJD), iatrogenic. Symptoms of CJD are rapidly progressive dementia, leading to memory loss, personality changes, and hallucinations, anxiety, depression, paranoia, obsessive-compulsive symptoms, and psychosis. Various causes of CJD are: Transmission, Blood donor restrictions, Sperm donor restrictions. Diagnosis of CJD includes: Electroencephalography, Cerebrospinal fluid analysis for 14-3-3 protein, MRI of the brain.
Creutzfeldt - Jakob disease Statistics
These statistics are calculated extrapolations of various prevalence or incidence rates against the populations of country. The approximate number of patients encountered with Creutzfeldt - Jakob disease in Israel is 6.
Creutzfeldt - Jakob disease Treatment
Currently, there is no cure for Creutzfeldt-Jakob disease. Treatment is aimed at alleviating symptoms and making the patient as comfortable as possible. Drugs can help relieve pain if it occurs. The drugs clonazepam and sodium valproate may help relieve myoclonus or irregular, jerking movements.
Creutzfeldt - Jakob disease ongoing research
Some ongoing research studies on Creutzfeldt - Jakob disease in Israel are CSF tau correlates with CJD disease severity and cognitive decline, Familial Creutzfeldt-Jakob disease with the E200K mutation: longitudinal neuroimaging from asymptomatic to symptomatic CJD, Characterization of sleep disorders in patients with E200K familial Creutzfeldt-Jakob disease.