| Chapter title |
Toxicity of Antiepileptic Drugs to Mitochondria
|
|---|---|
| Chapter number | 2 |
| Book title |
Pharmacology of Mitochondria
|
| Published in |
Handbook of experimental pharmacology, January 2016
|
| DOI | 10.1007/164_2016_2 |
| Pubmed ID | |
| Book ISBNs |
978-3-31-957311-3, 978-3-31-957313-7
|
| Authors |
Josef Finsterer, Finsterer, Josef |
| Abstract |
Some of the side and beneficial effects of antiepileptic drugs (AEDs) are mediated via the influence on mitochondria. This is of particular importance in patients requiring AED treatment for mitochondrial epilepsy. AED treatment in patients with mitochondrial disorders should rely on the known influences of AEDs on these organelles. AEDs may influence various mitochondrial functions or structures in a beneficial or detrimental way. There are AEDs in which the toxic effect outweighs the beneficial effect, such as valproic acid (VPA), carbamazepine (CBZ), phenytoin (PHT), or phenobarbital (PB). There are, however, also AEDs in which the beneficial effect on mitochondria outweighs the mitochondrion-toxic effect, such as gabapentin (GBT), lamotrigine (LTG), levetiracetam (LEV), or zonisamide (ZNS). In the majority of the AEDs, however, information about their influence of mitochondria is lacking. In clinical practice mitochondrial epilepsy should be initially treated with AEDs with low mitochondrion-toxic potential. Only in cases of ineffectivity or severe mitochondrial epilepsy, mitochondrion-toxic AEDs should be given. This applies for AEDs given orally or intravenously. |
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Mendeley readers
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