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First of all, a preliminary examination should reveal the inadequacy of actions and a violation of social behavior. To assess the state of the brain, the following methods are prescribed:

This type of diagnostics allows you to getlayer-by-layer high-precision images of indomethacin pills. CT allows you to determine the degree of progression of the process and identify the most affected part of the brain.

It usually develops during sleep and disappears during physical activity

In Pick's disease, a mandatory differential diagnosis is shown with such diseases as Alzheimer's disease, Huntington's chorea, brain cancer, mental disorders in diffuse atherosclerosis. Etiotropic therapy that eliminates Pick's disease does not yet exist. Unfortunately, at the moment, no therapy has been developed to stop the progression of the disease at least at any stage. First of indocin pills, people with Pick's disease need care and constant care. In view of such a deplorable state, they are not only unable to live independently, but they can also carry a certain danger for others and themselves personally (open without setting fire to household gas, etc.).

This method is based on the ability of special equipment to capture the minimum electrical impulses that appear in the human brain during the conduction of signals.

  • Data on the received impulses are displayed on a sheet of paper in the form of a set of curves.
  • With Pick's disease, the cortex becomes thinner, respectively, there are much fewer processes in it, which, accordingly, is displayed by the electroencephalogram.
  • MRI or magnetic resonance imaging is of the same diagnostic value as CT.
  • The patient is prescribed to take those substances that are not produced in the brain due to atrophy (antidepressants, MAO inhibitors, acetylcholinesterase inhibitors, etc.).
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Physical therapist assisting little boy sitting on gym ball during rehabilitation in children hospital

Pharmacocorrection of existing mental disorders. Drugs that reduce aggression, antidepressants are used.

  • They stimulate brain cells, improving their metabolic processes, thereby helping to slow down the death of neurons, followed by atrophy of the cerebral cortex.
  • Patients participate in special trainings aimed at slowing the progression of the disease.
  • The prognosis of later life in Pick's disease is unfavorable.
  • Five to ten years after the onset of the disease, a complete mental and moral decomposition of the patient's personality occurs, cachexia and insanity occur.

Man is completely lost to society. The average life expectancy for Pick's disease is about six to eight years. Patients require mandatory permanent full care, which is best done in a specialized psychiatric hospital. The information provided in this article is for informational purposes only and cannot replace professional advice and qualified medical assistance. At the slightest suspicion of the presence of this disease, be sure to consult a doctor!

Pick's disease is a rare pathology that affects the central nervous system and occurs mainly in a chronic progressive form.

A specific feature of the disease is the development of progressive destructive and atrophic processes in the cerebral cortex (especially the frontal and temporal lobes).

Symptoms of the disease are manifested by presenile dementia and a rough, rapid intellectual disintegration of the personality. Pick's disease develops after the age of fifty, with a median age of onset of 54 years. The ratio of men with Pick's disease to women with this disease is 1:2.

At the moment, Pick's disease is considered as a severe type of lobar degeneration, leading to severe progressive dementia of the frontotemporal type. Frontotemporal dementias account for 1/5 of all early cases of age-related dementias (in addition to Pick's disease, this group of indocin also includes primary progressive aphasia). For reference. Unlike Alzheimer's disease or Lewy body dementia, Pick's disease is considered presenile dementia, as it develops predominantly in people between the ages of fifty and sixty.

The causes of Pick's disease are similar to those of Alzheimer's, but the dementia in Pick's disease is more malignant. The average life expectancy in patients with Pick's disease is 6-10 years from the onset of the first symptoms of the disease.

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Morphologically, atrophic processes are determined in the frontal and temporal lobes of the brain, often more pronounced in the dominant hemisphere. Atrophy affects both the cortex and subcortical structures. There are no inflammatory changes. Vascular disorders are not typical or mild. Senile plaques and neurofibrillary tangles typical of Alzheimer's disease are absent. Intraneuronal argentophilic inclusions are considered pathognomonic for Pick's disease.

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This also includes the use of anesthesia, especially in cases of its frequent use or inadequate dosing. Some authors believe that Pick's disease may develop in connection with a previous mental disorder. For reference. Along with this, researchers are inclined to believe that factors such as intoxication, traumatic brain injury, infections, mental disorders, hypovitaminosis of vitamins gr. They play only a provocative role.

However, sporadic cases are observed much more often than familial cases, and brothers and sisters are more likely to get sick within the same family than relatives in different generations. Among the possible etiofactors are long-term effects on the brain of harmful chemicals.

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In this regard, Pick's disease is referred to as taupathies (together with progressing tonuclear palsy and corticobasal degeneration). For reference. An important and specific feature of Pick's disease is also considered a hereditary predisposition to the development of frontotemporal dementia. In more than half of the cases, the pathology runs in a family form and is inherited. In the presence of genes associated with Pick's disease (MART, GRN, C9ORF72), the risk of developing the disease is more than fifty percent.

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The main signs of the disease are: frontal atrophy; dilated anterior horns of the lateral ventricles; thinned and smoothed furrows; expanded subarachnoid spaces; decrease in the density of the medulla in atrophied areas. The exact causes and mechanism of development of frontotemporal dementia are still poorly understood. It is believed that the main role in the development of the disease is played by the impaired metabolism of tau protein, which is part of the nerve cells.