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use recreational drugs (同)do drugs
administer a drug to; "They drugged the kidnapped tourist" (同)dose
a substance that is used as a medicine or narcotic
a drug used to treat or prevent convulsions (as in epilepsy) (同)anticonvulsant_drug, antiepileptic, antiepileptic_drug

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/03/17 17:54:44」(JST)

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Anticonvulsants (also commonly known as antiepileptic drugs or as antiseizure drugs) are a diverse group of pharmacological agents used in the treatment of epileptic seizures. Anticonvulsants are also increasingly being used in the treatment of bipolar disorder^[1] and borderline personality disorder,^[2] since many seem to act as mood stabilizers, and for the treatment of neuropathic pain.^[3] Anticonvulsants suppress the rapid and excessive firing of neurons during seizures.^[4] Anticonvulsants also prevent the spread of the seizure within the brain.^[5] Some investigators have observed that anticonvulsants themselves may cause reduced IQ in children.^[6] However these adverse effects must be balanced against the significant risk epileptic seizures pose to children and the distinct possibility of death and devastating neurological sequelae secondary to seizures. Anticonvulsants are more accurately called antiepileptic drugs (abbreviated "AEDs"), and are often referred to as antiseizure drugs because they provide symptomatic treatment only and have not been demonstrated to alter the course of epilepsy.

Conventional antiepileptic drugs may block sodium channels or enhance γ-aminobutyric acid (GABA) function. Several antiepileptic drugs have multiple or uncertain mechanisms of action.^[7] Next to the voltage-gated sodium channels and components of the GABA system, their targets include GABA_A receptors, the GAT-1 GABA transporter, and GABA transaminase.^[8] Additional targets include voltage-gated calcium channels, SV2A, and α2δ.^[9]^[10] 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.^[11] 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.^[11] Another potential target of antiepileptic drugs is the peroxisome proliferator-activated receptor alpha.^[12]^[13]^[14]^[15]^[16]^[17]^[18] The drug class was the 5th-best-selling in the US in 2007.^[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]

1 Approval
2 Drugs
- 2.1 Aldehydes
- 2.2 Aromatic allylic alcohols
- 2.3 Barbiturates
- 2.4 Benzodiazepines
- 2.5 Bromides
- 2.6 Carbamates
- 2.7 Carboxamides
- 2.8 Fatty acids
- 2.9 Fructose derivatives
- 2.10 GABA analogs
- 2.11 Hydantoins
- 2.12 Oxazolidinediones
- 2.13 Propionates
- 2.14 Pyrimidinediones
- 2.15 Pyrrolidines
- 2.16 Succinimides
- 2.17 Sulfonamides
- 2.18 Triazines
- 2.19 Ureas
- 2.20 Valproylamides (amide derivatives of valproate)
- 2.21 Other
3 Non-medical anticonvulsants
4 Treatment guidelines
5 History
- 5.1 Marketing approval history
6 Use in pregnancy
7 See also
8 References
9 Further reading
10 External links

Approval

The usual method of achieving approval for a drug is to show it is effective when compared against placebo, or that it is more effective than an existing drug. In monotherapy (where only one drug is taken) it is considered unethical by most to conduct a trial with placebo on a new drug of uncertain efficacy. This is because untreated epilepsy leaves the patient at significant risk of death. Therefore, almost all new epilepsy drugs are initially approved only as adjunctive (add-on) therapies. Patients whose epilepsy is currently uncontrolled by their medication (i.e., it is refractory to treatment) are selected to see if supplementing the medication with the new drug leads to an improvement in seizure control. Any reduction in the frequency of seizures is compared against a placebo.^[21] The lack of superiority over existing treatment, combined with lacking placebo-controlled trials, means that few modern drugs have earned FDA approval as initial monotherapy. In contrast, Europe only requires equivalence to existing treatments, and has approved many more. Despite their lack of FDA approval, the American Academy of Neurology and the American Epilepsy Society still recommend a number of these new drugs as initial monotherapy.^[21]

Drugs

In the following list, the dates in parentheses are the earliest approved use of the drug.

Aldehydes

Paraldehyde (1882). One of the earliest anticonvulsants. It is still used to treat status epilepticus, particularly where there are no resuscitation facilities.

Aromatic allylic alcohols

Stiripentol (2001 - limited availability). Indicated for the treatment of Dravet syndrome.^[22]^[23]

Barbiturates

Barbiturates are drugs that act as central nervous system (CNS) depressants, and by virtue of this they produce a wide spectrum of effects, from mild sedation to anesthesia. The following are classified as anticonvulsants:

Phenobarbital (1912). See also the related drug primidone.
Methylphenobarbital (1935). Known as mephobarbital in the US. No longer marketed in the UK
Barbexaclone (1982). Only available in some European countries.

Phenobarbital was the main anticonvulsant from 1912 until the development of phenytoin in 1938. Today, phenobarbital is rarely used to treat epilepsy in new patients since there are other effective drugs that are less sedating. Phenobarbital sodium injection can be used to stop acute convulsions or status epilepticus, but a benzodiazepine such as lorazepam, diazepam or midazolam is usually tried first. Other barbiturates only have an anticonvulsant effect at anaesthetic doses.

Benzodiazepines

The benzodiazepines are a class of drugs with hypnotic, anxiolytic, anticonvulsive, amnestic and muscle relaxant properties. Benzodiazepines act as a central nervous system depressant. The relative strength of each of these properties in any given benzodiazepine varies greatly and influences the indications for which it is prescribed. Long-term use can be problematic due to the development of tolerance to the anticonvulsant effects and dependency.^[24]^[25]^[26]^[27] Of the many drugs in this class, only a few are used to treat epilepsy:

Clobazam (1979). Notably used on a short-term basis around menstruation in women with catamenial epilepsy.
Clonazepam (1974).
Clorazepate (1972).

The following benzodiazepines are used to treat status epilepticus:

Diazepam (1963). Can be given rectally by trained care-givers.
Midazolam (N/A). Increasingly being used as an alternative to diazepam. This water-soluble drug is squirted into the side of the mouth but not swallowed. It is rapidly absorbed by the buccal mucosa.
Lorazepam (1972). Given by injection in hospital.

Nitrazepam, temazepam, and especially nimetazepam are powerful anticonvulsant agents, however their use is rare due to an increased incidence of side effects and strong sedative and motor-impairing properties.

Bromides

Potassium bromide (1857). The earliest effective treatment for epilepsy. There would not be a better drug until phenobarbital in 1912. It is still used as an anticonvulsant for dogs and cats.

Carbamates

Felbamate (1993). This effective anticonvulsant has had its usage severely restricted due to rare but life-threatening side effects.^[28]^[29]^[30]

Carboxamides

Carbamazepine

The following are carboxamides:

Carbamazepine (1963). A popular anticonvulsant that is available in generic formulations.
Oxcarbazepine (1990). A derivative of carbamazepine that has similar efficacy but is better tolerated and is also available generically.
Eslicarbazepine acetate (2009)

Fatty acids

The following are fatty-acids:

The valproates — valproic acid, sodium valproate, and divalproex sodium (1967).
Vigabatrin (1989).
Progabide
Tiagabine (1996).

Vigabatrin and progabide are also analogs of GABA.

Fructose derivatives

Topiramate (1995).

GABA analogs

Gabapentin (1993).
Pregabalin (2004).

Hydantoins

The following are hydantoins:

Ethotoin (1957).
Phenytoin (1938).
Mephenytoin
Fosphenytoin (1996).

Oxazolidinediones

The following are oxazolidinediones:

Paramethadione
Trimethadione (1946).
Ethadione

Propionates

Beclamide

Pyrimidinediones

Primidone (1952).

Pyrrolidines

Brivaracetam
Levetiracetam (1999).
Seletracetam

Succinimides

The following are succinimides:

Ethosuximide (1955).
Phensuximide
Mesuximide

Sulfonamides

Acetazolamide (1953).
Sultiame
Methazolamide
Zonisamide (2000).

Triazines

Lamotrigine (1990).

Ureas

Pheneturide
Phenacemide

Valproylamides (amide derivatives of valproate)

Valpromide
Valnoctamide

Other

Perampanel

Non-medical anticonvulsants

Sometimes, ketogenic diet or vagus nerve stimulation are described as "anticonvulsant" therapies as well.

Treatment guidelines

According to guidelines by the AAN and AES,^[31] mainly based on a major article review in 2004,^[32] patients with newly diagnosed epilepsy who require treatment can be initiated on standard anticonvulsants such as carbamazepine, phenytoin, valproic acid/valproate semisodium, phenobarbital, or on the newer anticonvulsants gabapentin, lamotrigine, oxcarbazepine or topiramate. The choice of anticonvulsants depends on individual patient characteristics.^[31] Both newer and older drugs are generally equally effective in new onset epilepsy.^[31] The newer drugs tend to have fewer side effects.^[31] For newly diagnosed partial or mixed seizures, there is evidence for using gabapentin, lamotrigine, oxcarbazepine or topiramate as monotherapy.^[31] Lamotrigine can be included in the options for children with newly diagnosed absence seizures.^[31]

History

The first anticonvulsant was bromide, suggested in 1857 by Charles Locock who used it to treat women with "hysterical epilepsy" (probably catamenial epilepsy). Bromides are effective against epilepsy, and also cause impotence, which is not related to its anti-epileptic effects. Bromide also suffered from the way it affected behaviour, introducing the idea of the 'epileptic personality' which was actually a result of medication. Phenobarbital was first used in 1912 for both its sedative and antiepileptic properties. By the 1930s, the development of animal models in epilepsy research led to the development of phenytoin by Tracy Putnam and H. Houston Merritt, which had the distinct advantage of treating epileptic seizures with less sedation.^[33] By the 1970s, a National Institutes of Health initiative, the Anticonvulsant Screening Program, headed by J. Kiffin Penry, served as a mechanism for drawing the interest and abilities of pharmaceutical companies in the development of new anticonvulsant medications.

Marketing approval history

The following table lists anticonvulsant drugs together with the date their marketing was approved in the US, UK and France. Data for the UK and France are incomplete. In recent years, the European Medicines Agency has approved drugs throughout the European Union. Some of the drugs are no longer marketed.

Drug	Brand	US	UK	France
acetazolamide	Diamox	1953-07-2727 July 1953^[34]	1988^[35]
carbamazepine	Tegretol	1974-07-1515 July 1974^[36]^[37]	1965^[35]	1963^[38]
clobazam	Frisium		1979^[35]
clonazepam	Klonopin/Rivotril	1975-06-044 June 1975^[39]	1974^[35]
diazepam	Valium	1963-11-1515 November 1963^[40]
divalproex sodium	Depakote	1983-03-1010 March 1983^[41]
eslicarbazepine		Data needed
ethosuximide	Zarontin	1960-11-022 November 1960^[42]	1955^[35]	1962^[38]
ethotoin	Peganone	1957-04-2222 April 1957^[43]
felbamate	Felbatol	1993-07-2929 July 1993^[44]
fosphenytoin	Cerebyx	1996-08-055 August 1996^[45]
gabapentin	Neurontin	1993-12-3030 December 1993^[46]	1993-05May 1993^[35]^[38]	1994-10October 1994^[38]
lamotrigine	Lamictal	1994-12-2727 December 1994^[47]	1991-10October 1991^[35]^[38]	1995-05May 1995^[38]
lacosamide	Vimpat	2008-10-2828 October 2008^[48]
levetiracetam	Keppra	1999-11-3030 November 1999^[49]	2000-09-2929 September 2000^[35]^[50]	2000-09-2929 September 2000^[50]
mephenytoin	Mesantoin	1946-10-2323 October 1946^[51]
metharbital	Gemonil	1952^[52]^[53]
methsuximide	Celontin	1957-02-088 February 1957^[54]
methazolamide	Neptazane	1959-01-2626 January 1959^[55]
oxcarbazepine	Trileptal	2000-01-1414 January 2000^[56]	2000^[35]
phenobarbital			1912^[35]	1920^[38]
phenytoin	Dilantin/Epanutin	1938^[38]^[57]	1938^[35]	1941^[38]
phensuximide	Milontin	1953^[58]^[59]
pregabalin	Lyrica	2004-12-3030 December 2004^[60]	2004-07-066 July 2004^[35]^[61]	2004-07-066 July 2004^[61]
primidone	Mysoline	1954-03-088 March 1954^[62]	1952^[35]	1953^[38]
sodium valproate	Epilim		1977-12December 1977^[38]	1967-06June 1967^[38]
stiripentol	Diacomit		2001-12-055 December 2001^[63]	2001-12-055 December 2001^[63]
tiagabine	Gabitril	1997-09-3030 September 1997^[64]^[65]	1998^[35]	1997-11November 1997^[38]
topiramate	Topamax	1996-12-2424 December 1996^[66]	1995^[35]
trimethadione	Tridione	1946-01-2525 January 1946^[67]
valproic acid	Depakene/Convulex	1978-02-2828 February 1978^[68]	1993^[35]
vigabatrin	Sabril	2009-08-2121 August 2009^[69]	1989^[35]
zonisamide	Zonegran	2000-03-2727 March 2000^[70]	2005-03-1010 March 2005^[35]^[71]	2005-03-1010 March 2005^[71]

Use in pregnancy

During pregnancy, the metabolism of several anticonvulsants is affected. There may be an increase in the clearance and resultant decrease in the blood concentration of lamotrigine, phenytoin, and to a lesser extent carbamazepine, and possibly decreases the level of levetiracetam and the active oxcarbazepine metabolite, the monohydroxy derivative.^[72] Therefore, these drugs should be monitored during use in pregnancy.^[72]

Valproic acid, and its derivatives such as sodium valproate and divalproex sodium, causes cognitive deficit in the child, with an increased dose causing decreased intelligence quotient.^[73] On the other hand, evidence is conflicting for carbamazepine regarding any increased risk of congenital physical anomalies or neurodevelopmental disorders by intrauterine exposure.^[73] Similarly, children exposed lamotrigine or phenytoin in the womb do not seem to differ in their skills compared to those who were exposed to carbamazepine.^[73]

There is inadequate evidence to determine if newborns of women with epilepsy taking anticonvulsants have a substantially increased risk of hemorrhagic disease of the newborn.^[72]

Regarding breastfeeding, some anticonvulsants probably pass into breast milk in clinically significant amounts, including primidone and levetiracetam.^[72] On the other hand, valproate, phenobarbital, phenytoin, and carbamazepine probably are not transferred into breast milk in clinically important amounts.^[72]

In animal models, several anticonvulsant drugs have been demonstrated to induce neuronal apoptosis in the developing brain.^[74]^[75]^[76]^[77]^[78]

References

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^ 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.
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^ Harden, C. L. (1 May 1994). "New antiepileptic drugs". Neurology 44 (5): 787–787. doi:10.1212/WNL.44.5.787.
^ Loring, David W (1 September 2005). "Cognitive Side Effects of Antiepileptic Drugs in Children". Psychiatric Times XXII (10).
^ https://www.neurology.wisc.edu/publications/2010%20pubs/stafstrom-4.pdf
^ Rogawski MA, Löscher W; Löscher (July 2004). "The neurobiology of antiepileptic drugs". Nature Reviews Neuroscience 5 (7): 553–64. doi:10.1038/nrn1430. PMID 15208697.
^ Rogawski MA, Bazil CW; Bazil (July 2008). "New molecular targets for antiepileptic drugs: alpha(2)delta, SV2A, and K(v)7/KCNQ/M potassium channels". Curr Neurol Neurosci Rep 8 (4): 345–52. doi:10.1007/s11910-008-0053-7. PMC 2587091. PMID 18590620.
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^ "Public summary of positive opinion for orpphan opinion for orphan designation of stiripentol for the treatment of severe myoclonic epilepsy in infancy" (PDF). European Medicines Agency. 30 July 2007. Retrieved 19 May 2013. Doc.Ref.: EMEA/COMP/269/04
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^ French, J; Smith, M; Faught, E; Brown, L (12 May 1999). "Practice advisory: The use of felbamate in the treatment of patients with intractable epilepsy: report of the Quality Standards Subcommittee of the American Academy of Neurology and the American Epilepsy Society". Neurology 52 (8): 1540–5. doi:10.1212/WNL.52.8.1540. PMID 10331676.
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^ NDA 017533
^ NDA 013263
^ NDA 018723
^ NDA 012380
^ NDA 010841
^ NDA 020189
^ NDA 020450
^ NDA 020235
^ NDA 020241
^ NDA 022253
^ NDA 021035
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^ NDA 006008
^ NDA 008322
^ Dodson, W. Edwin; Giuliano Avanzini; Shorvon, Simon D.; Fish, David R.; Emilio Perucca (2004). The treatment of epilepsy. Oxford: Blackwell Science. xxviii. ISBN 0-632-06046-8.
^ NDA 010596
^ NDA 011721
^ NDA 021014
^ NDA 008762 (Marketed in 1938, approved 1953)
^ NDA 008855
^ Kutt, Henn; Resor, Stanley R. (1992). The Medical treatment of epilepsy. New York: Dekker. p. 385. ISBN 0-8247-8549-5. (first usage)
^ NDA 021446
^ ^a ^b EPAR: Lyrica Retrieved on 1 November 2007.
^ NDA 009170
^ ^a ^b EPAR: Diacomit. Orphan designation: 5 December 2001, full authorisation: 4 January 2007 Retrieved on 1 November 2007.
^ NDA 020646
^ "NDA: 020646". DrugPatentWatch. Retrieved 19 May 2013.
^ NDA 020505
^ NDA 005856
^ NDA 018081
^ Lundbeck Press Release
^ NDA 020789
^ ^a ^b EPAR: Zonegran. Retrieved on 1 November 2007
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^ ^a ^b ^c Bromley, Rebecca; Weston, Jennifer; Adab, Naghme; Greenhalgh, Janette; Sanniti, Anna; McKay, Andrew J; Tudur Smith, Catrin; Marson, Anthony G (2014). "Treatment for epilepsy in pregnancy: neurodevelopmental outcomes in the child". doi:10.1002/14651858.CD010236.pub2.
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^ Manthey D, Asimiadou S; et al. (Jun 2005). "Sulthiame but not levetiracetam exerts neurotoxic effect in the developing rat brain". Exp Neurol 193 (2): 497–503. doi:10.1016/j.expneurol.2005.01.006. PMID 15869952.
^ Katz I, Kim J; et al. (Aug 2007). "Effects of lamotrigine alone and in combination with MK-801, phenobarbital, or phenytoin on cell death in the neonatal rat brain". J Pharmacol Exp Ther 322 (2): 494–500. doi:10.1124/jpet.107.123133. PMID 17483293.
^ Kim J, Kondratyev A, and Gale K (Oct 2007). "Antiepileptic drug-induced neuronal cell death in the immature brain: effects of carbamazepine, topiramate, and levetiracetam as monotherapy versus polytherapy". J Pharmacol Exp Ther 323 (1): 165–73. doi:10.1124/jpet.107.126250. PMC 2789311. PMID 17636003.
^ Forcelli PA, Kim J; et al. (Dec 2011). "Pattern of antiepileptic drug-induced cell death in limbic regions of the neonatal rat brain". Epilepsia 52 (12): e207–11. doi:10.1111/j.1528-1167.2011.03297.x. PMC 3230752. PMID 22050285.

External links

eMedicine: Antiepileptic Drugs: an overview
NINDS: Anticonvulsant Screening Program
Use of Anticonvulsants in Pharmacotherapy of Bronchial Asthma
MDNG: Anticonvulsants and Bone Health
Miami Children's Brain Institute - Anticonvulsants
Drug Reference for FDA Approved Epilepsy Drugs
Epilepsy Action: UK Anti-Epileptic Drugs List

UpToDate Contents

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1. 抗てんかん剤：作用機序、薬理学、および有害事象 antiepileptic drugs mechanism of action pharmacology and adverse effects
2. 成人におけるてんかんのマネージメントの概要 overview of the management of epilepsy in adults
3. 成人におけるてんかんの初期治療 initial treatment of epilepsy in adults
4. 小児における痙攣およびてんかん：初期治療およびモニタリング seizures and epilepsy in children initial treatment and monitoring
5. 成人におけるてんかんの外科的治療 surgical treatment of epilepsy in adults

English Journal

A DFT investigation of structure, spectroscopic properties and tautomerism of the anticonvulsant drug Lyrica.

Sadeghzade Z1, Beyramabadi SA2, Morsali A1.
Spectrochimica acta. Part A, Molecular and biomolecular spectroscopy.Spectrochim Acta A Mol Biomol Spectrosc.2015 Mar 5;138:637-42. doi: 10.1016/j.saa.2014.11.069. Epub 2014 Dec 9.
The Lyrica (Pregabalin) is a novel anticonvulsant and neuropathic pain drug, which could exist as four possible conformers. Herein, employing density functional theory (DFT), and handling the solvent effects with the PCM model, the structural parameters, energetic behavior, natural bond orbital anal
PMID 25541402

Role of the adenosine system and glucose restriction in the acute anticonvulsant effect of caprylic acid in the 6Hz psychomotor seizure test in mice.

Socała K1, Nieoczym D2, Pieróg M2, Wlaź P2.
Progress in neuro-psychopharmacology & biological psychiatry.Prog Neuropsychopharmacol Biol Psychiatry.2015 Mar 3;57:44-51. doi: 10.1016/j.pnpbp.2014.10.006. Epub 2014 Oct 27.
Although several studies have reported the acute anticonvulsant activity of caprylic acid in animal seizure models, little is known about the mechanism underlying this effect. Recently, the role of adenosine in the efficacy of the ketogenic diet has been postulated. Therefore, the present study aime
PMID 25455587

Japanese Journal

てんかん (特集麻酔前の評価・準備と予後予測(2)) -- (神経・筋疾患)

須藤貴史,齋藤繁
麻酔 59(9), 1096-1099, 2010-09
NAID 40017289316

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★リンクテーブル★

リンク元	「antiseizure drug」「antiepileptic agent」「anticonvulsant agent」「抗痙攣剤」「抗けいれん剤」
関連記事	「anticonvulsants」「anticonvulsant」「drug」