Brain injury, traumatic seizures

SSRI selective sCTotonin reuptake inhibitor (class of drugs used to treat d ression, e.g., sCTtraline) SSS sick sinus s5mdrome stat immediately (Latin statim ) supl supplement or supplied supp suppository Susp suspension SVT supraventricular tachycardia Sx s5mptom S5md syndrome Sz seizure tab/tabs tablet/tablets tach tachycardia TB tubCTCulosis TBI traumatic brain injury TCA tricyclic antidqjressant (class of drugs commonly used to treat d ression, e.g., amitriptyline) TCP transcutaneous pacing TD transdermal TFT thyroid function test TEA transient ischemic attack tid three times a day (Latin ter in die ) tine tincture TMP trimethoprim (type of antibiotic)... 

Schierhout G, Roberts I. Anti-epileptic drugs for preventing seizures following acute traumatic brain injury. Cochrane Database Syst Rev 2001. 

As previously discussed, the COX-2 inhibitors have selectivity for inhibition of the COX-2 enzyme, which has low constitutive activity but is highly inducible at sites of tissue injury. In addition to the peripheral role of COX-2 in inflammation, COX-2 may play an important role in the CNS. COX-2 is expressed constitutively in some excitatory neurons in the brain and spinal cord and is induced in traumatic brain injury such as that induced by ischemia and seizures. It has been hypothesized that COX-2 may also be involved in neurodegen-erative diseases, since COX-2 inhibitors have shown some positive effects in Alzheimer s disease. Thus, the mechanism of action of COX-2 inhibitors may involve brain and spinal cord sites as well as local sites of injury. 

Keywords Alzheimer disease Brain Cytokines Glial cells Huntington s disease Ik IkB kinase Ischemic and traumatic brain injury Learning Memory Multiple sclerosis Neuronal Plasticity Neuroprotection NF-kB Nuclear factor Parkinson s disease Rel family Seizures Synaptic transmission Therapeutic target Transcription factor... 

Traumatic brain injury, simulated by a model of closed head injury to mice, had also been shown to result in disruption of the BBB. The temporal resolution of this disruption was monitored by MRI in rats subjected to closed head injury. Blood-brain barrier disruption appeared immediately after the impact, and declined gradually, until full reversal to control levels 30 min post-injury. Opening of the BBB was similarly demonstrated in response to acute anticholinesterase exposure, however, low-level exposure has not yet been tested. BBB disruption under anticholinesterase exposure was proven to be seizure-dependent, as it could be blocked by the use of anticonvulsant agents. The anticholinesterase effect on BBB ultrastructure did not impair endothelial tight junctions. Yet, an increased number of endothelial vesicles were observed, suggesting increased transcytosis as the mechanism involved. ... 

Hall, E.D., Kupina, N.C., and Althaus, J.S. 1999. Peroxynitrite scavengers for the acute treatment of traumatic brain injury. Ann N Y Acad Sci 890 462-468 Handforth, A., and Ackermann, R.F. 1995. Mapping of limbic seizure progressions utilizing the electrogenic status epilepticus model and the 14C-2-deoxyglucose method. Brain Res Brain Res Rev 20(1) 1-23... 

Vespa, P.M., Miller, C., McArthur, D., et al, 2007. Nonconvulsive electrographic seizures after traumatic brain injury result in a delayed, prolonged increase in intracranial pressure and metabolic crisis. Grit. Care Med. 35, 2830-2836. 

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