Lobar atrophy

Pick's disease is a specific pathology that is one of the causes of frontotemporal lobar degeneration. It is also known as Pick disease and PiD (not to be confused with pelvic inflammatory disease or Parkinson's disease ). A defining characteristic of the disease is build-up of tau proteins in neurons, accumulating into silver-staining, spherical aggregations known as 'Pick bodies'. Common symptoms noticed early are personality and emotional changes and deterioration of language.The symptoms of Pick's disease include difficulty in language and thinking, efforts to dissociate from family, behavioral changes, unwarranted anxiety, irrational fears, compulsive buying disorder (CBD or oniomania), impaired regulation of social conduct (e.g., breaches of etiquette, vulgar language, tactlessness, disinhibition, misperception), passivity, low motivation (aboulia), inertia, overactivity, pacing, and wandering. A characteristic of Pick’s disease is that dysfunctional, argumentative, or hostile social conduct is initially exhibited towards family members and not initially exhibited in a workplace or neutral environment. PiD is highly hereditary. The changes in personality allow doctors to distinguish between PiD and AD. Pick's disease is one of the causes of the clinical syndrome of frontotemporal lobar degeneration, which has three subtypes. PiD pathology is associated more with the frontotemporal dementia and progressive nonfluent aphasia subtypes than the semantic dementia subtype.While other pathologies causing frontotemporal lobar degeneration are associated with a genetic cause, evidence is not conclusive in modern research on whether classical PiD pathology has or does not have a direct genetic link, or whether it has been shown to run in families or certain ethnic- or gender-specific subgroups. However, excess of a protein called β-amyloid (Aβ) in neural cells has been linked to neural degeneration. A buildup of Aβ within cells causes inflammation, leading to cell destruction by the immune system. Proteins associated with Pick's disease are present in all nerve cells, but those with the disease have an abnormal amount.PiD was first recognized as a distinct disease separate from other neurodegenerative diseases because of the presence of large, dark-staining aggregates of proteins in neurological tissue, as well as the aforementioned ballooned cells, which are known as Pick cells. Pick bodies are almost universally present in patients with PiD, but some new cases of atypical PiD have come to light that lack noticeable Pick bodies. A variety of stains can aid in the visualization of Pick bodies and Pick cells, but immunohistochemical staining using anti-tau and anti-ubiquitin antibodies have proven the most efficient and specific. Hematoxylin and eosin staining allows visualization of another population of Pick cells, which are both tau and ubiquitin protein negative. Several silver impregnation stains have been used, including the Bielschowsky, Bodian, and Gallyas methods. The latter two techniques are sensitive enough to allow PiD to be distinguished from AD, as the Bodian will bind preferentially to cells with PiD as compared to the Gallyas method, which preferentially binds to the cells with Alzheimer's.The confirmatory diagnosis is made by brain biopsy, but other tests can be used to help, such as MRI, EEG, CT, and physical examination and history.Pick's disease, unfortunately, has a rapidly progressing, insidious course with steady deterioration over roughly 4 years. This time can vary by individual, but many patients' quality of life decreases and fatality generally occurring (on average) 4 years from diagnosis. No known cure exists for Pick's disease and many AD treatments have less utility in this patient population. Treatment is symptomatic with different physicians using different treatment regimens for the illness; some recommend no treatment so as to do no harm. Other physicians may recommend a trial of a medication to improve mood symptoms, and cognitive exercises to attempt to slow decline.PiD is named after Arnold Pick, a professor of psychiatry from Charles University in Prague, who first discovered and described the disease in 1892 by examining the brain tissue of several deceased patients with histories of dementia. As a result, the characteristic histological feature of this disease—a protein tangle that appears as a large body in neuronal tissue—is named a Pick body. In 1911, Alois Alzheimer noted the complete absence of senile plaques and neurofilbrillary tangles, as well as the presence of Pick bodies and occasional ballooned neurons.