Anticonvulsants (also known as antiepileptic drugs, antiseizure drugs, or anti-seizure medications (ASM)) are a diverse group of pharmacological agents used in the treatment of epilepticseizures.[1] Anticonvulsants are also increasingly being used in the treatment of bipolar disorder[2][3] and borderline personality disorder,[4] since many seem to act as mood stabilizers, and for the treatment of neuropathic pain.[5] Anticonvulsants suppress the excessive rapid firing of neurons during seizures.[6] Anticonvulsants also prevent the spread of the seizure within the brain.[7]
Conventional antiepileptic drugs may block sodium channels or enhance γ-aminobutyric acid (GABA) function. Several antiepileptic drugs have multiple or uncertain mechanisms of action.[8] Next to the voltage-gated sodium channels and components of the GABA system, their targets include GABAA receptors, the GABA transporter type 1, and GABA transaminase.[9] Additional targets include voltage-gated calcium channels, SV2A, and α2δ.[10][11] By blocking sodium or calcium channels, antiepileptic drugs reduce the release of excitatory glutamate, whose release is considered to be elevated in epilepsy, but also that of GABA.[12] This is probably a side effect or even the actual mechanism of action for some antiepileptic drugs, since GABA can itself, directly or indirectly, act proconvulsively.[12] Another potential target of antiepileptic drugs is the peroxisome proliferator-activated receptor alpha.[13][14][15][16][17][18][19]
Some anticonvulsants have shown antiepileptogenic effects in animal models of epilepsy.[20] That is, they either prevent the development of epilepsy or can halt or reverse the progression of epilepsy. However, no drug has been shown in human trials to prevent epileptogenesis (the development of epilepsy in an individual at risk, such as after a head injury).[21]
^Joshi A, Bow A, Agius M (2019). "Pharmacological Therapies in Bipolar Disorder: a Review of Current Treatment Options". Psychiatria Danubina. 31 (Suppl 3): 595–603. ISSN0353-5053. PMID31488797.
^Keck PE Jr, McElroy SL, Strakowski SM (1998). "Anticonvulsants and antipsychotics in the treatment of bipolar disorder". The Journal of Clinical Psychiatry. 59 (Suppl 6): 74–82. PMID9674940.
^American Psychiatric Association, and American Psychiatric Association. Work Group on Borderline Personality Disorder. Practice guideline for the treatment of patients with borderline personality disorder. American Psychiatric Pub, 2001.
^McLean MJ, Macdonald RL (June 1986). "Sodium valproate, but not ethosuximide, produces use- and voltage-dependent limitation of high frequency repetitive firing of action potentials of mouse central neurons in cell culture". Journal of Pharmacology and Experimental Therapeutics. 237 (3): 1001–1011. PMID3086538.
^ abKammerer M, Rassner, M. P., Freiman, T. M., Feuerstein, T. J. (2 May 2011). "Effects of antiepileptic drugs on GABA release from rat and human neocortical synaptosomes". Naunyn-Schmiedeberg's Archives of Pharmacology. 384 (1): 47–57. doi:10.1007/s00210-011-0636-8. PMID21533993. S2CID1388805.
^Citraro R, et al. (2013). "Antiepileptic action of N-palmitoylethanolamine through CB1 and PPAR-α receptor activation in a genetic model of absence epilepsy". Neuropharmacology. 69: 115–26. doi:10.1016/j.neuropharm.2012.11.017. PMID23206503. S2CID27701532.
^Lampen A, Carlberg C, Nau H (2001). "Peroxisome proliferator-activated receptor delta is a specific sensor for teratogenic valproic acid derivatives". Eur J Pharmacol. 431 (1): 25–33. doi:10.1016/S0014-2999(01)01423-6. PMID11716839.
^Maguire JH, Murthy AR, Hall IH (1985). "Hypolipidemic activity of antiepileptic 5-phenylhydantoins in mice". Eur J Pharmacol. 117 (1): 135–8. doi:10.1016/0014-2999(85)90483-2. PMID4085542.
^Hall IH, Patrick MA, Maguire JH (1990). "Hypolipidemic activity in rodents of phenobarbital and related derivatives". Archiv der Pharmazie. 323 (9): 579–86. doi:10.1002/ardp.19903230905. PMID2288480. S2CID46002731.
^Frigerio F, Chaffard G, Berwaer M, Maechler P (2006). "The antiepileptic drug topiramate preserves metabolism-secretion coupling in insulin secreting cells chronically exposed to the fatty acid oleate". Biochem Pharmacol. 72 (8): 965–73. doi:10.1016/j.bcp.2006.07.013. PMID16934763.