[Nervism].

Stress proteins are constitutively expressed in normal CNS tissues, in a variety of cell types (oligodendrocytes, astrocytes and neurons). Their function is uncertain but they may be critical during nervous system development and may protect cells from various stresses, such as hypoxia, anoxia, and excessive excitatory stimulation. Increased amounts of stress proteins are expressed in various cells of the CNS during acute toxic-metabolic states and in more chronic degenerative diseases. Increased expression of stress proteins may constitute a sensitive marker of cell injury. Antibodies to mycobacterial stress proteins bind to normal human myelin and to oligodendrocytes in regions of MS demyelination. Cellular immune responses to stress proteins occur with increased frequency and magnitude in persons with MS, especially those with recent onset of disease. In addition, there are populations of T cells expressing gamma/delta T cells in the brains and CSF of persons with MS, suggesting an in situ immune response to hsp. Humoral immune responses to stress proteins are found in CSF, but no disease specificity has been documented. Some myelin proteins have sequence homology with particular stress proteins. One instance is the homology between a peptide of mycobacterial hsp65 and the myelin protein CNP. Preliminary observations suggest that immune responses to such cross-reactive epitopes modify the course of EAE. All in all, these data support the hypothesis that an immune response to the stress proteins of an infectious agent could result in a cross-reactive immune response to CNS myelin, resulting in demyelination. This may be an especially important mechanism in MS.

Central Nervous System↗

PubMed1994

[The neurology of terminal states].

The paper gives a theoretical justification of CNS abnormality developing in patients who have a history of critical and terminal states, including clinical death. The most significant abnormality is that which is termed posthypoxic and/or postresuscitation encephalopathies whose nature has not been elucidated particularly at the cellular and molecular levels. It is emphasized that this involves brain abnormalities, which is a sequela of hypoxia or ischemia of systemic origin, rather than primary brain damages. In some patients who have sustained a severe hypoxic episode of any nature and recovered their psychoneurological status ever rapidly and rather fully, there may be an abrupt progressive deterioration of their neurological status in some days or months, which results in death or grave irreversible disability. It is concluded that not only do reparative and compensatory processes occur, but also there are phenomena of progressive degenerative changes in a primarily successfully resuscitated person or experimental animal in the central nervous system in the postresuscitation period. A classification of psychoneurological disorders in patients in the early postresuscitation period has been made and ways of their prevention or alleviation have been indicated.

Central Nervous System↗