Sick Fedez. Demyelination can be the basis of various diseases, including multiple sclerosis
Sick Fedez. Shock announcement on social media. Fedez suffers from demyelinationa phenomenon that causes the disappearance of the myelin sheaths of nerve fibers and which can be the basis of various diseases, including multiple sclerosis.
“I’m here to tell you that unfortunately I have been found a health problem, fortunately with great timing, which involves a path. An important path that I will have to take and that I feel like telling. Not now, not at this moment in which I have I need to cling to my family, to my children. But that I feel like telling in the future because when I discovered what I discovered, reading other people’s stories gave me comfort “. Fedez, 32, shared his concern about the disease he suffers on social media. You did not specify which pathology you are dealing with but in December 2019, a guest at La Confessione sul Nove, Fedez he said: “I have found something called demyelination in my head, I am at risk of multiple sclerosis.”
For demyelination we mean a pathological process that leads to the disappearance of the myelin sheaths of the nerve fibers and to the reactive proliferation of neurlia cells (supporting tissue placed inside the brain and spinal cord). Demyelination often occurs when there are pathologies of the nervous system: in all lesions of the white matter, or the part of the brain that contains nerve fibers (heart attacks, hemorrhages, tumors), and especially in the so-called demyelinating diseases. Myelin surrounds the axons, or extensions of neurons, and is divided into central and peripheral. Central myelin is that of the central nervous system (CNS) and is made up of oligodendrocytes. Peripheral myelin is that of the peripheral nervous system (PNS) and is produced by so-called Schwann cells.
There demyelination it can be central or peripheral. The most famous of the CNS demyelinating diseases is multiple sclerosis. It was once said that in this disease only the myelin sheath is altered due to inflammatory processes, while the axons are little affected or initially remain intact. It was believed that only after so many years of myelin destruction did the axons begin to suffer. Today, however, it is known that there is an early axonal degeneration that involves the death of the neuron due to the propagation of the lesion, up to the cell body. An outbreak of demyelination causes a decrease in conduction speed and if there is also damage to the axon, conduction is altered or blocked. At the onset of multiple sclerosis, myelin swells and fragments due to acute inflammatory phenomena. At this stage of the disease there is minimal axonal damage.
Over time – as stated on the website of the Corriere della Sera – the lost myelin is replaced by the proliferation of astrocytes (constitutive elements of neurlia), with a scarring that leads to stretching and fragmentation of the axons. When the axon is not yet damaged, repair is possible as myelin can regenerate. At the beginning of the disease the number of degenerated axons is not high, so there are moments with functional deficits due exclusively to myelin inflammation. When the inflammation subsides, the patient recovers. Gradually, however, the axonal damage accumulates, until it exceeds a certain threshold: at that point the patient no longer recovers as before, and the disease takes on a so-called progressive course.
Another example of demyelinating disease is Schilder’s disease (or diffuse cerebral sclerosis). The process of demyelination it can manifest itself with different symptoms in relation to the area of the nervous system affected, but these are in any case symptoms related to the loss of function of the axons without the myelin sheath. Even in leukodystrophies there are alterations of myelin: these pathologies, however, are linked to congenital enzymatic alterations, which determine alteration of the synthesis or metabolism of myelin. As for the demyelinating diseases of the PNS, an example is the Guillain-Barré syndrome.
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