And brain trauma

Bramlett H. M. and Dietrich W. D. (2004). Pathophysiology of cerebral ischemia and brain trauma Similarities and differences. J. Cereb. Blood Flow Metab. 24 133-150. 

These agents have obvious therapeutic utility in the treatment of opioid overdose. As the understanding of the role of endogenous opioid systems in pathophysiological states e.g., shock, stroke, spinal cord and brain trauma) increases, additional therapeutic indications for these antagonists may develop. 

Bramlett HM, Dietrich WD (2004) Pathophysiology of cerebral ischemia and brain trauma similarities and differences. J Cereb Blood Flow Metab 24 133-150 Brown TP, Rumsby PC, Capleton AC, Rushton L, Levy LS (2006) Pesticides and Parkinson s disease - is there a link Environ Health Perspect 114 156-164 Butler D, Bendiske J, Michaelis ML, Karanian DA, Bahr BA (2007) Microtubule-stabilizing agent prevents protein accumulation-induced loss of synaptic markers. Eur J Pharmacol 562 20-27 Campbell A, Smith MA, Sayre LM, Bondy SC, Perry G (2001) Mechanisms by which metals promote events connected to neurodegenerative diseases. Brain Res Bull 55 125-132... 

It has been revealed that cannabinoids exhibit neuroprotectant activities in both in vitro and in vivo models [249]. The neuroprotective effects are mainly based on regulation of transmitter release, modulation of calcium homeostasis, anti-oxidant properties and modulation of immune responses. A number of neurological disorders, including brain trauma, cerebral ischaemia, Parkinson s disease and Alzheimer s disease represent possible therapeutic areas for cannabinoids with neuroprotective properties. Cannabinoids are also suggested to have potential against glaucoma due to their neuroprotective nature and lowering of intraocular pressure [250]. 

Free arachidonic acid, along with diacylglycerols and free docosahexaenoic acid, is a product of membrane lipid breakdown at the onset of cerebral ischemia, seizures and other forms of brain trauma 585... 

Under physiologic conditions, the balance of membrane lipid metabolism, particularly that of arachidonoyl and docosahexaenoyl chains, favors a very small and tightly controlled cellular pool of free arachidonic acid (AA, 20 4n-3) and docosahexaenoic acid (DHA, 22 6n-3), but levels increase very rapidly upon cell activation, cerebral ischemia, seizures and other types of brain trauma [1, 2], Other free fatty acids (FFAs) in addition to AA, released during cell activation and the initial stages of focal and global cerebral ischemia, are stearic acid (18 0), palmitic acid (16 0) and oleic acid (18 1). 

Phospholipids in synaptic membranes are an important target in seizures, head injury, neurodegenerative diseases and cerebral ischemia. Synaptic membranes are excitable membranes enriched in phospholipids esterified with the polyunsaturated fatty acids AA and DHA which form a significant proportion of the FFAs rapidly released during ischemia, seizure activity and other brain trauma. 

Free arachidonic acid, along with diacylglycerols and free docosahexaenoic acid, is a product of membrane lipid breakdown at the onset of cerebral ischemia, seizures and other forms of brain trauma. Because polyunsaturated fatty acids are the predominant FFA pool components that accumulate under these conditions, this further supports the notion that fatty acids released from the C2 position of membrane phospholipids are major contributors to the FFA pool, implicating PLA2 activation as the critical step in FFA release [1,2] (Fig. 33-6). 

HETE and acute cerebral blood flow drop after brain trauma in rats (Kehl et al.,... 

Most of the contraindications specific to pentazocine stem from its excitatory effects. Other contraindications are similar to those for morphine. Pentazocine is contraindicated in patients with myocardial infarction because it increases heart rate and cardiac load. Similarly, it is contraindicated in epileptic patients because it decreases seizure threshold. In addition, in head trauma patients, it can increase intracranial pressure and brain injury. Pentazocine use in patients with psychoses is contraindicated because of its psychotomimetic side effects. 

R. Vink, T. K. McIntosh, P. Demediuk, M. W. Weiner and A. I. Faden, Decline in intracellular free Mg " " is associated with irreversible tissue injury after brain trauma. /. Biol. Chem., 1988,263,757-761. 

Ritalin and related generic methylphenidate drugs are available by prescription for individuals six years and older. Ritalin is distributed in 5, 10, and 20 mg tablets. In addition to ADHD, methylphenidate is used for several other medical conditions. It continues to be used for narcolepsy. It has also been used in treating depression, especially in elderly populations. Methylphenidate has been suggested for use in the treatment of brain injury from stroke or brain trauma it has also been suggested to improve appetite and the mood of cancer and HIV patients. Another use is for pain control and/or sedation for patients using opiates. 

Designer drugs" include amphetamines which have been modified for heightened psychoactive effects. The use of MDMA or Ecstasy has become popular over the past few years, especially after some psychiatrists attested to its beneficial use in alleviating anxiety and emotional trauma in their patients. MDA, a structural sister to MDMA, has been found to produce destruction of serotonergic neurons in rat brain. 

Saito et al., 1993) and Parkinson s diseases (Vanderklish and Bahr, 2000). The list could continue to include organ ischemia, stroke, brain trauma, various platelet syndromes, hypertension, liver dysfunction, and some types of cancer Table 1 offers a panorama of the diseases that have most frequently been linked to calpains. A role for these proteases in the genesis of these conditions has been generally inferred from... 

Because of its involvement in the encoding of short-term memories and their conversion into long-term memories, the hippocampus has been the subject of numerous studies on the memory loss that occurs in the elderly, especially those affected with Alzheimer s disease. The majority of these studies have shown that new neurons develop in the hippocampus of adult and old humans as well as of experimental animals1415 these studies have also determined what influences their genesis, survival, and integration in the brain. For example, neurogenesis may be stimulated by learning, physical activity, optimal nutrition, etc. to replace lost neurons or to facilitate recovery after brain trauma (e.g., stroke).14-19... 

In term infants, acute hypoxic-ischemic injury and birth trauma appear to be more significant events in the evolution of brain injury (64). It has been widely recognized, however, that although many neonates who ultimately develop CP sustain their injury during birth or in the NICU, most CP patients do not have evidence of acute neonatal events capable of producing permanent injury (65-67). In term neonates, the large majority of infants with CP have no clearly discernible asphyxial event to which the injury can be attributed. 

Pathological activation of glutamate receptors is a common feature and one of the primary causes of neuronal death in acute neuronal injury (such as trauma, epilepsy, and brain ischemia) and chronic neurodegenerative diseases (such as Parkinson s disease, Alzheimer diseases, amyotrophic lateral sclerosis, and AIDS dementia) (Choi, 1988 Doble, 1999 Lipton and Rosemberg, 1994). In particular, elevation of extracellular glutamate level is a key factor in the development of neuronal damage under ischemic conditions. 

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