User:Nphilip/sandbox

This is my sandbox. For my Intro Neuro Class I am working with my partner to update this page, Posterior cortical atrophy.

My draft for the PCA Page

=Overview=

Posterior Cortical Atrophy (PCA) is neurodegenerative disease that causes cognitive impairments due to atrophy in the parietal cerebral area. PCA patients have progressive cognitive impairments of visuospacial and visuoperceptual skills. PCA is considered a from of dementia, Alzheimer’s disease is a common underlying cause for most but not all PCA patients. In 1988, D. Frank Benson first reported PCA symptoms, Posterior Cortical Atrophy is also referred to as Benson’ s syndrome.

=Diagnosis=

To date, there is no fully accepted diagnostic criteria for PCA. This is partially due to the gradual onset of PCA symptoms, the variety of symptoms, the rare nature of the disease and younger age of patients. In 2012, the first international conference on PCA was held in Vancouver, Canada. Continued research and testing will hopefully result in a accepted and standardized criteria for diagnosis.

PCA patients are often initially misdiagnosed with an anxiety disorder or  depression; this may be a cause of personal insight that leads to fear of their visual impairments. The early visual impairments of a PCA patient have often led to a referral to an Ophthalmologist, which can result in unnecessary cataract surgery.

Due to the lack of biological marks of PCA, neuropsychological examinations should be used for diagnosis. Neuroimaging can assist in diagnosis of PCA, often though the comparison of images of PCA patients with AD patients in relation to the atrophy of the brain. Magnetic Resonance Imaging (MRI's) taken of a PCA patient during the early stages of the disease can show brain atrophy in the right posterior lobe and occipital gyrus. PCA imaging can contradict the common MRI images of AD patients, which shows atrophy in the medial temporal cortex. Single-photon emission computed tomography and Positron emission tomography studies can also be used. PCA patients may show a lost of grey matter in the posterior and occipital temporal cortices mainly in the right hemisphere. Some neuroimaging methods may not be conclusive in the diagnosis of a PCA patient, therefore, careful observation of a patient can also assist in diagnosis. The variation and lack of organized clinical testing lead to continued difficulties and delays in the diagnosis of PCA in patients.

'''An updated version of the previous paragraph. A peer comment suggested that I rework the paragraph; adding more clarity and making it more asscible a reader who does not have previous neuroscience background.'''

Due to the lack of biological marks of PCA, neuropsychological examinations should be used for diagnosis. Neuroimaging can also assist in diagnosis of PCA. The common tools used for Neuroimaging of both PCA and AD patients are Magnetic Resonance Imaging (MRI's), as well as Single-photon emission computed tomography and Positron emission tomography images. Images of PCA patient’s brains are often compared to AD patient images to assist diagnosis. Due to the early onset of PCA in comparison to AD, images taken at the early stages of the disease will vary from brain images of AD patients. At this early stage PCA patients will show brain atrophy more centrally located in the right posterior lobe and occipital gyrus, while AD brain images show the majority of atrophy in the medial temporal cortex. This variation within the images will assist in early diagnosis of PCA; however, as the years go on the images will become increasingly similar, due to the majority of PCA patients also having AD later in life because of continued brain atrophy. A key aspect found through brain imaging of PCA patients is a loss of grey matter (collections of neuronal cell bodies) in the posterior and occipital temporal cortices within the right hemisphere. For some PCA patients, neuroimaging may not result with a clear diagnosis; therefore, careful observation of the patient in relation to PCA symptoms can also assist in the diagnosis of the patient. The variation and lack of organized clinical testing has lead to continued difficulties and delays in the diagnosis of PCA in patients.

temporal cortex

=Treatment= Specific and accepted scientific treatment for PCA has yet to be discovered; this may be due to the rarity and variations of the disease. At times PCA patients are treated with prescriptions originally created for treatment of AD such as cholinesterase inhibitors, memantine, donepezil, rivastigmine and glantamine. Antidepressant drugs have also provided some positive effects. Patients may find success with non-prescription treatments such as psychological treatments. PCA patients may find assistance in meeting with an occupational therapist or sensory team for aid in adapting to the PCA symptoms, especially for visual changes. No study to date has been definitive to provide accepted conclusive analysis on treatment options.