myelin-basic-protein and Craniocerebral-Trauma

Multiple sclerosis (MS) is acquired as a systemic "trait" by individuals who are genetically susceptible. This condition does not involve the central nervous system (CNS) and is characterized by a state of hyperactive immunocompetent responsiveness. It develops as the result of an antigenic challenge by a viral protein, either from a viral infection or a vaccination. In order for MS to become a disease affecting the CNS, it is necessary for the blood-brain barrier's (BBB) impermeability to be altered. This is now a fully recognized fact. As a result of this change, the MS lesion, which consists of edema and inflammation occurs. It may but need not lead to demyelination. Several mechanisms can cause this increased permeability of the BBB. The role of the immune system, and in particular of T lymphocytes in initiating and continuing the process of lesion formation remains extremely controversial. In fact, there are unanswered questions regarding the actual target of MS: is it the myelin sheath itself or its forming cell, the oligodendrocyte, or is it the BBB itself leading to bystander demyelination? The role of mild, concussional trauma to the CNS in producing the alteration of the BBB and therefore acting as a trigger or facilitator in the development or enlargement of MS lesions in the CNS, is based on considerable clinical, neuropathological and experimental evidence. Along with another viral infection, it must be one of the commonest causes of progression of MS, and quite often leads to the onset of the clinical manifestations of an hitherto asymptomatic condition.

Topics: Amino Acid Sequence; Animals; Blood-Brain Barrier; Craniocerebral Trauma; Genetic Predisposition to Disease; Humans; Immune System; Molecular Sequence Data; Multiple Sclerosis; Myelin Basic Protein; Sequence Homology, Amino Acid; Viral Proteins

Murine models of CNS injury show auto-reactive T cell responses directed at myelin antigens, associated with improved neuronal survival and functional recovery. This pilot study shows, for the first time, that similar immune responses against myelin occur in human traumatic brain injury (TBI), with an expansion of lymphocytes recognising myelin basic protein observed in 40% of patients studied. "Reactive" patients did not have greater contusion volume on imaging, but were younger than the "unreactive" subgroup and tended towards a more favorable outcome. These findings are consistent with the concept of "beneficial autoimmunity".

Topics: Adult; Age Factors; Autoimmunity; Case-Control Studies; Cell Proliferation; Craniocerebral Trauma; Cytokines; Female; Glasgow Coma Scale; Humans; Lymphocytes; Magnetic Resonance Imaging; Male; Middle Aged; Myelin Basic Protein; Pilot Projects; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Time Factors

A double antibody sequential radioimmunoassay for human myelin basic protein (MBP) has been developed. The assay utilizes a rabbit antibody to human MBP and purified rabbit MBP as the radiolabelled antigen. This assay was used to analyze cerebrospinal fluid (CSF) from 22 patients with severe head injury, 61 other cases of various neurological disorders, and 106 normal controls. The results showed that closed head trauma caused moderate to severe elevations in CSF MBP, and elevated CSF MBP was detectable in several diseases which involve CNS myelin.

Topics: Craniocerebral Trauma; Humans; Multiple Sclerosis; Myelin Basic Protein; Nervous System Diseases; Radioimmunoassay

Serum levels of myelin basic protein (M.B.P.), a nervous-system-specific protein, were measured in 157 patients after head injury and related both to the type of brain damage and to the clinical outcome assessed three months after injury. Mean concentrations of M.B.P. in patients with severe intracerebral damage, with or without associated extracerebral haematoma, were significantly raised at the time of admission and remained high for two weeks after injury. In patients with extracerebral haematoma not associated with severe intracerebral damage mean M.B.P. values rose four to six days after injury and were significantly raised only in patients with poor eventual outcome. Mean serum-M.B.P. concentrations in patients with a good outcome after injury were similar to those in controls. In patients with a poor outcome the mean M.B.P. levels between two and six days after injury were significantly higher than in those with a good outcome. The assay of serum-M.B.P. may be valuable in assessment of severity of brain damage in patients after head injury and in prediction of outcome.

Topics: Blood-Brain Barrier; Brain Diseases; Brain Injuries; Brain Neoplasms; Cerebrovascular Disorders; Craniocerebral Trauma; Hematoma; Humans; Myelin Basic Protein; Prognosis