myelin-basic-protein and Brain-Edema

After head injury, many complex neurochemical events occur locally, at the site of initial injury, and globally, as a result of secondary phenomena. Neurochemical alterations in the cerebrospinal fluid after injury can be utilized to reflect these events. The authors review the role of the cerebrospinal fluid in the treatment of head injury as it relates to the diagnosis, prognosis, and further elucidation of the pathophysiological manifestations of head injury at the cellular and biochemical level.

Topics: Acetylcholine; Brain Edema; Brain Injuries; Calcium; Cerebrospinal Fluid Proteins; Dopamine; Fatty Acids, Unsaturated; Histamine; Humans; Kallikreins; Kinins; Lactates; Lactic Acid; Myelin Basic Protein; Neurotransmitter Agents; Norepinephrine; Potassium; Prostaglandins; Pyruvates; Pyruvic Acid; Serotonin

Hypoxic-ischemic (HI) injury to the developing brain remains a major cause of morbidity. To date, few therapeutic strategies could provide complete neuroprotection. Erythropoietin (EPO) has been shown to be beneficial in several models of neonatal HI. This study examines the effect of treatment with erythropoietin on postnatal day 2 (P2) rats introduced with HI injury.. Rats at P2 were randomized into four groups: sham, bilateral carotid artery occlusion (BCAO), BCAO + early EPO, and BCAO + late EPO groups. Pups in each group were injected with either saline or EPO (5000U/kg) intraperitoneally once at immediately (early) or 48h (late) after HI induction. Body weight was assessed at P2 before and day 7 after HI. Mortality Rate was assessed at 24h, 48h and 72h after HI and brain water content was assessed at 72h. Brain weight and expression of myelin basic protein (MBP) were assessed at day 7 and day 14. At day 31 to 35 following HI insult, neurological behavior function was assessed via Morris water maze (MWM) test.. HI cause significant higher mortality in male than in female (P=0.0445). Among the surviving animal, HI affect significantly the body growth, brain growth, MBP expression, and neurological behavior. EPO treatments at both early and late time points significantly benefit the rats in injury recovery, in which they promoted weight gains, reduced brain edema, as well as improved spatial learning ability and memory.. We demonstrated a single dose of EPO at 5000U/kg immediately or 48h after HI injury had significant benefit for the P2 rats in injury recovery, and there was no adverse effect associated with either EPO treatment.

Topics: Age Factors; Analysis of Variance; Animals; Animals, Newborn; Body Weight; Brain Edema; Developmental Disabilities; Disease Models, Animal; Erythropoietin; Hypoxia-Ischemia, Brain; Maze Learning; Myelin Basic Protein; Neuroprotective Agents; Rats; Rats, Sprague-Dawley

Intracranial surgery causes cortical injury from incisions, hemorrhage, retraction, and electrocautery. The term "surgical brain injury" (SBI) has been developed to categorize this injury inherent to the procedure. Neuroinflammation plays a significant role in SBI. Traditional antiinflammatory therapies are often limited by their immunosuppressive side effects and poor CNS penetration. This study uses mucosal tolerance to develop an immune system that is tolerant to brain myelin basic protein (MBP) so that inflammation can be suppressed in a timely and site-specific manner following surgical disruption of the blood-brain barrier.. A standard SBI model using CD57 mice was used. Nasopharyngeal mucosa was exposed to vehicle, ovalbumin, or MBP to develop mucosal tolerance to these antigens. Immunological tolerance to MBP was confirmed in vivo through hypersensitivity testing. Neurological scores, cerebral edema, and interleukin (IL)-1β and transforming growth factor (TGF)-β1 cytokine levels were measured 48 hours postoperatively.. Hypersensitivity testing confirmed the development of immune tolerance to MBP. Myelin basic protein-tolerant mice demonstrated reduced neurological injury, less cerebral edema, decreased levels of IL-1β, and increased levels of TGFβ1 following SBI.. Developing preoperative immunological tolerance to brain antigens through mucosal tolerance provides neuroprotection, reduces brain edema, and modulates neuroinflammation following SBI.

Topics: Animals; Brain; Brain Edema; Brain Injuries; Cytokines; Encephalitis; Immune Tolerance; Immunity, Mucosal; Mice; Myelin Basic Protein

This study describes morphological abnormalities of brain cells during acute methamphetamine (METH) intoxication in the rat and demonstrates the role of hyperthermia, disruption of the blood-brain barrier (BBB) and edema in their development. Rats with chronically implanted brain, muscle and skin temperature probes and an intravenous (i.v.) catheter were exposed to METH (9 mg/kg) at standard (23 degrees C) and warm (29 degrees C) ambient temperatures, allowing for the observation of hyperthermia ranging from mild to pathological (38-42 degrees C). When brain temperature peaked or reached a level suggestive of possible lethality (>41.5 degrees C), rats were injected with Evans blue (EB), rapidly anesthetized, perfused, and their brains were taken for further analyses. Four brain areas (cortex, hippocampus, thalamus and hypothalamus) were analyzed for EB extravasation, water and electrolyte (Na(+), K(+), Cl(-)) contents, immunostained for albumin and glial fibrillary acidic protein (GFAP), and examined for neuronal, glial and axonal alterations using standard light and electron microscopy. These examinations revealed profound abnormalities in neuronal, glial, and endothelial cells, which were stronger with METH administered at 29 degrees C than 23 degrees C and tightly correlated with brain and body hyperthermia. These changes had some structural specificity, but in each structure they tightly correlated with increases in EB levels, the numbers of albumin-positive cells, and water and ion contents, suggesting leakage of the BBB, acutely developing brain edema, and serious shifts in brain ion homeostasis as leading factors underlying brain abnormalities. While most of these acute structural and functional abnormalities appear to be reversible, they could trigger subsequent cellular alterations in the brain and accelerate neurodegeneration-the most dangerous complication of chronic amphetamine-like drug abuse.

Topics: Albumins; Animals; Blood-Brain Barrier; Brain; Brain Edema; Capillary Permeability; Central Nervous System Stimulants; Electrolytes; Endothelial Cells; Endothelium, Vascular; Epithelial Cells; Fever; Glial Fibrillary Acidic Protein; Male; Methamphetamine; Myelin Basic Protein; Nerve Tissue Proteins; Neuroglia; Neurons; Rats; Rats, Long-Evans; Transcription Factors

A total of 21 patients with postmeasles and 26 patients with postvaricella C.N.S. complications were studied. In both groups, males were predominant than females. The C.N.S. manifestations included disturbed level of consciousness, coma, seizures, motor deficits, ataxia and myoclonus. The sequelae were more frequent in postmeasles cases and ranged from behavioral abnormalities to motor deficits. C.S.F. examination showed that most of the cases demonstrated increase in the protein content (45-100mg) and pleocytosis. Myelin protein was detected in 8 samples and 6 samples of postmeasles and varicella C.S.F. out of 12 samples in Tested in each group. Specific virus IgG antibody was detected significantly in 8 paired C.S.F. samples of postvaricella group and only one sample of postmeasles out of 12 paired samples tested in each group. C-T. scan examination revealed that the most common finding was the brain oedema (13 in measles, and 21 in varicella group).

Topics: Adolescent; Adult; Brain Diseases; Brain Edema; Chickenpox; Child; Female; Humans; Immunoglobulin A; Immunoglobulin G; Immunoglobulin M; Male; Measles; Myelin Basic Protein; Serum Albumin

Trauma to the spinal cord induces a series of electrophysiological, immunological and biochemical events, but it is still unclear how such reactions are initiated and maintained. Most likely release of neurochemicals, breakdown of microvascular permeability and the formation of vasogenic edema play important roles in the pathophysiology of spinal cord trauma. In an animal model we have focused the attention to the possible involvement of endogenous serotonin, prostaglandins and opioid peptides in the formation of edema and associated disturbances of vascular permeability. The trauma was produced in anesthetized rats by making a focal lesion in the right dorsal horn at the T10-11 segments. This injury resulted in a profound increase in the microvascular permeability to 131I-sodium and an elevation of water content in the rostral T9 and caudal T12 segments as measured 5 h after the onset of the injury. Light microscopy of the perifocal changes in the T9-T12 segments using Nissl stain and immunohistochemistry to glial fibrillary acidic protein (GFAP) and myelin basic protein (MBP) showed profound cellular changes which were most severe in the ipsilateral ventral horn. Many nerve cell bodies were shrunken and the tissue had a spongy edematous appearance. There was a marked increase of GFAP immunoreactivity as well as a significant diminution of MBP staining. Pre-treatment with p-chlorophenylalanine (p-CPA, an endogenous serotonin depletor and synthesis inhibitor) or indomethacin (an endogenous prostaglandin synthesis inhibitor) or naloxone (an opioid receptor antagonist) significantly reduced the permeability changes and the edema formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Blood Pressure; Body Water; Brain Edema; Capillary Permeability; Carbon Dioxide; Fenclonine; Glial Fibrillary Acidic Protein; Indomethacin; Male; Myelin Basic Protein; Naloxone; Oxygen; Partial Pressure; Rats; Rats, Wistar; Spinal Cord; Spinal Cord Injuries

Topics: Animals; Autolysis; Brain; Brain Edema; Central Nervous System; Demyelinating Diseases; Edema; Female; Lipid Metabolism; Myelin Basic Protein; Myelin Proteins; Myelin Sheath; Rats; Spinal Cord; Spinal Cord Diseases; Time Factors; Triethyltin Compounds

Topics: Animals; Basophils; Brain Edema; Cerebral Cortex; Cyclophosphamide; Disease Models, Animal; Encephalomyelitis, Autoimmune, Experimental; Endothelium; Extracellular Space; Fibrin; Freund's Adjuvant; Immunization, Passive; Inflammation; Intercellular Junctions; Lymphocytes; Macrophages; Microscopy, Electron; Myelin Basic Protein; Neutrophils; Pertussis Vaccine; Rats