Central nervous system , trauma

Braughler, J.M, and Hall, E.D. (1989). Central nervous system trauma and stroke. I. Biochemical considerations for oxygen radical formation and lipid peroxidation. Free Rad. Biol. Med. 6, 289-301. 

Isolated seizures that are not epilepsy can be caused by stroke, central nervous system trauma, central nervous system infections, metabolic disturbances (e.g., hyponatremia and hypoglycemia), and hypoxia. If these underlying causes of seizures are not corrected, they may lead to the development of recurrent seizures I or epilepsy. Medications can also cause seizures. Some drugs that are commonly associated with seizures include tramadol, bupropion, theophylline, some antidepressants, some antipsy-chotics, amphetamines, cocaine, imipenem, lithium, excessive doses of penicillins or cephalosporins, and sympathomimetics or stimulants. 

Braughler JM, Hall ED, Jacobsen EJ, et al The 21 aminosteroids potent inhibitors of lipid peroxidation for the treatment of central nervous system trauma and ischemia. Drug Future 14 143-152, 1989... 

Schwartz, M., Protective autoimmunity as a T-cell response to central nervous system trauma prospects for therapeutic vaccines. Prog Neurobiol, 2001. 65(5) 489-96. 

In summarizing evidence for the participation of deranged sympatho-adrenal ( neurogenic ) factors in human hypertension, it must be concluded that such factors have been conclusively demonstrated only in cases of pheochromocytoma, central nervous system trauma, and increased intracranial pressure. There is presumptive evidence that neurogenic factors may be important during the early, labile phases of essential hypertension and that the effects of this early sympatho-adrenal activity may lead to a persistent hypertension on a renal basis later in life. However, the development of hypertension through this or any other mechanism occurs only in individuals predisposed by some completely unknown, but probably hereditary, influence. 

Young, W. (1985) Blood flow, metabolic and neurophysiological mechanisms in spinal cord injury, In Central Nervous System Trauma Status Report (Becker, D.B. and Povlishock, J.T., Eds.), pp. 463-474, National Institutes of Health, Bethesda, MD. 

Hall, E.D., McCall, J.M. Chase, R.L., Yonkers, P.A. and Braughler, J.M. (1987) A nonglucocorticoid steroid analog of methylprednisolone duplicates its high-dose pharmacology in models of central nervous system trauma and neuronal membrane damage, J. Pharmacol. Exp. 242, 137-142. 

Faden AI (1996) Pharmacological treatment of central nervous system trauma. Pharmacol Toxicol 78 12-17. 

Hirschberg DL, Moalem G, He J, Mor F, Cohen IR, Schwartz M (1998) Accumulation of passively transferred primed T cells independently of then antigen specificity following central nervous system trauma. J Neuroimmunol 89 88-96. 

Central nervous system trauma, for example, post-stroke Metabolic disorders such as hjrperthyroidism Infectious diseases such as encephalitis Seizure disorders Central nervous system tumor... 

Mocchetti, I. and Wrathall, J. R., Neurotrophic factors in central nervous system trauma, J. Neurotrauma, 12, 853, 1995. 

Jacobsen, E.J., McCall, J.M., Ayer, D.E., Van Doornik, F.J., Palmer, J.R., Belonga. K.L., Braughler, J.M., Hall, E.D., Houser, D.J., Krook, M.A. and Runge, T.A. (1990) Novel 21-aminosteroids that inhibit iron-dependent lipid peroxidation and protect against central nervous system trauma. J. Med. Chem. 33 1145-1151. 

Bakay, R. A., K. M. Sweeney, and M. D. Wood. 1986. Pathophysiology of cerebrospinal fluid in head injury Part 2. Biochemical markers for central nervous system trauma. Neurosurgery 18 376-382. 

Therapeutic Potential of the Lazaroids (21-Aminosteroids) in Acute Central Nervous System Trauma, Ischemia, and Subarachnoid Hemorrhage Edward D. Hull, John M. McCall and Eugene D. Means... 

Anderson DK, HaU ED (1994) lipid hydrolysis and free radical formation in central nervous system trauma. In Salzman SK, Faden AI (eds) The neuiobiology of central nervous system trauma. Oxford University Press, Oxford, pp 131-138 Ao Q, Wang AJ, Chen GO, Wang ST, Zuo HC, Zhang XF (2007) Combined transplantation of neural stem ceUs and olfactory ensheathing ceUs for the repair of spinal cord injuries. Med Hypotheses 69 1234-1237... 

In clinical chemistry, the variations of the Na concentration level in the extracellular fluid are interpreted as follows [3] (1) The level of Na" is elevated in dehydration (water deficit), central nervous system trauma or disease, and hyperadrenocorticism with hyperaldosteronism or corticosterone of corticosteroid excess. (2) A decrement of the Na level is observed in adrenal insufficiency, in renal insufficiency (especially with inadequate Na intake), in renal tubular acidosis as a physiological response to trauma and bums (Na shifts into cells), in unusual losses via the gastrointestinal tract as in acute or chronic diarrhea or intestinal obstruction or fistula, and in unusual sweating with inadequate sodium replacement. In some patients with edema associated with cardiac or renal disease, seram Na concentration is low, even though total body sodium content is greater than normal water retention (excess antidiuretic hormone, ADH) and abnormal distribution of sodium between intracellular and extracellular fluid contribute to this paradoxical situation. Hyperglycemia occasionally results in a shift of intracellular water to the extracellular... 

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