Abstract | OBJECTIVE: METHODS: RESULTS: Both phenytoin and carbamazepine significantly improved the clinical course of the disease. Withdrawal of phenytoin resulted in acute exacerbation, accompanied by a significantly increased inflammatory infiltrate within the central nervous system and the death of nearly 60% of EAE mice. There were no clinical worsening or deaths in control mice after withdrawal of phenytoin. Withdrawal of carbamazepine led to acute worsening of EAE symptoms, increased inflammatory infiltrate, and was associated with the death of 8% of mice. INTERPRETATION:
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Authors | Joel A Black, Shujun Liu, Michael Carrithers, Lisette M Carrithers, Stephen G Waxman |
Journal | Annals of neurology
(Ann Neurol)
Vol. 62
Issue 1
Pg. 21-33
(Jul 2007)
ISSN: 0364-5134 [Print] United States |
PMID | 17654737
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, Non-P.H.S.)
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Chemical References |
- Anticonvulsants
- Antigens, CD
- Glycoproteins
- Myelin-Oligodendrocyte Glycoprotein
- NAV1.6 Voltage-Gated Sodium Channel
- Nerve Tissue Proteins
- Peptide Fragments
- Scn8a protein, mouse
- Sodium Channels
- myelin oligodendrocyte glycoprotein (35-55)
- Carbamazepine
- Phenytoin
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Topics |
- Animals
- Anticonvulsants
(adverse effects)
- Antigens, CD
(metabolism)
- Axons
(drug effects, metabolism, pathology)
- Carbamazepine
(adverse effects)
- Cell Count
(methods)
- Disease Models, Animal
- Encephalomyelitis, Autoimmune, Experimental
(chemically induced, drug therapy, physiopathology)
- Flow Cytometry
(methods)
- Gene Expression Regulation
(drug effects)
- Glycoproteins
- Mice
- Mice, Inbred C57BL
- Myelin-Oligodendrocyte Glycoprotein
- NAV1.6 Voltage-Gated Sodium Channel
- Nerve Tissue Proteins
(metabolism)
- Peptide Fragments
- Phenytoin
(adverse effects)
- Pyramidal Tracts
(drug effects, metabolism, pathology)
- Severity of Illness Index
- Sodium Channels
(metabolism)
- Substance Withdrawal Syndrome
(etiology)
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