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Lamotrigine, sold as the brand name Lamictal among others, is an anticonvulsant medication used to treat epilepsy and bipolar disorder.
Common side effects include sleepiness, headache, vomiting, trouble with coordination, and rash.
Lamotrigine was first marketed in the United Kingdom in 1991 and approved for use in the United States in 1994.
1 Medical uses
1.1 Epilepsy
1.2 Bipolar disorder
1.3 Other uses
2 Side effects
2.1 Women
2.2 Pregnancy and breastfeeding
2.3 Other types of effects
3 Pharmacology
3.1 Mechanism of action
3.2 Pharmacokinetics
4 History
5 Trade names
6 References
7 External links
Medical uses
Lamotrigine is used for the treatment of partial seizures.
It is also appropriate for the treatment of Lennox–Gastaut syndrome.
Bipolar disorder
Lamotrigine is approved in the US for maintenance treatment of bipolar I disorder and bipolar II disorder.
There is less evidence of therapeutic benefit when lamotrigine is used to treat a current mood episode. It has not demonstrated effectiveness in treating acute mania,
A 2013 review about lamotrigine concluded that it is recommended in bipolar maintenance when depression is prominent and that more research is needed in regard to its role in the treatment of acute bipolar depression and unipolar depression. Furthermore, no information to recommend its use in other psychiatric disorders was found.
Other uses
Off-label uses include the treatment of peripheral neuropathy, trigeminal neuralgia, cluster headaches, migraines, and reducing neuropathic pain,
Side effects
Lamotrigine prescribing information has a black box warning about life-threatening skin reactions, including Stevens–Johnson syndrome (SJS), DRESS syndrome and toxic epidermal necrolysis (TEN).
There is also an increased incidence of these eruptions in patients who are currently on, or recently discontinued a valproate -type anticonvulsant drug, as these medications interact in such a way that the clearance of both is decreased and the effective dose of lamotrigine is increased.
Side effects such as rash, fever, and fatigue are very serious, as they may indicate incipient Stevens–Johnson syndrome, toxic epidermal necrolysis, DRESS syndrome or aseptic meningitis.
Other side effects include loss of balance or coordination, double vision, crossed eyes, pupil constriction, blurred vision, dizziness and lack of coordination, drowsiness, insomnia, anxiety, vivid dreams or nightmares, dry mouth, mouth ulcers, memory problems, mood changes, itchiness, runny nose, cough, nausea, indigestion, abdominal pain, weight loss, missed or painful menstrual periods, and vaginitis. The side effect profile varies for different patient populations.
Lamotrigine has been associated with a decrease in white blood cell count ( leukopenia ).
Cases of lamotrigine-induced neuroleptic malignant syndrome have been reported.
In 2018 the FDA required a new warning for the risk of hemophagocytic lymphohistiocytosis (HLH). This reaction can occur between days to weeks after starting the treatment.
Women are more likely than men to have side-effects. This is the opposite of most other anticonvulsants.
There is evidence showing interactions between lamotrigine and female hormones, which can be of particular concern for women on estrogen-containing hormonal contraceptives. Ethinylestradiol, the ingredient of such contraceptives, has been shown to decrease serum levels of lamotrigine.
Pregnancy and breastfeeding
Many studies have found no association between lamotrigine exposure in utero and birth defects, while those that have found an association have found only slight associations with minor malformations like cleft palates.
Lamotrigine is expressed in breast milk ; the manufacturer does not recommend breastfeeding during treatment. In “Medications and Mothers’ Milk,” a frequently updated review of scientific literature, lamotrigine is rated as L3: moderately safe.
Other types of effects
Lamotrigine binds to melanin -containing tissues such as the iris of the eye. The long-term consequences of this are unknown.
Some patients have reported experiencing a loss of concentration, even with very small doses. Lamotrigine has been implicated in the apoptotic neurodegeneration of the developing brain.
Lamotrigine is known to affect sleep. Studies with small numbers of patients (10-15) reported that lamotrigine increases sleep stability (increases the duration of REM sleep, decreases the number of phase shifts and decreases the duration of slow-wave sleep ),
Lamotrigine can induce a type of seizure known as a myoclonic jerk, which tends to happen soon after the use of the medication.
In overdose, lamotrigine can cause uncontrolled seizures in most people. Reported results in overdoses involving up to 15 grams include increased seizures, coma and death.
Mechanism of action
Lamotrigine is a member of the sodium channel blocking class of antiepileptic drugs.
It is a triazine derivate that inhibits voltage-sensitive sodium channels, leading to stabilization of neuronal membranes. It also blocks L-, N-, and P-type calcium channels and has weak 5-hydroxytryptamine-3 (5-HT3) receptor inhibition. These actions are thought to inhibit release of glutamate at cortical projections in the ventral striatum limbic areas,
Lamotrigine does not have pronounced effects on any of the usual neurotransmitter receptors that anticonvulsants effect ( adrenergic, dopamine D1 and D2, muscarinic, GABA, histaminergic H1, serotonin 5-HT2, and N-methyl-D-aspartate ). Inhibitory effects on 5-HT, norepinephrine, and dopamine transporters are weak.
These studies suggested that lamotrigine acts presynaptically on voltage-gated sodium channels to decrease glutamate release. Several electrophysiological studies have investigated the effects of lamotrigine on voltage-dependent sodium channels. For example, lamotrigine blocked sustained repetitive firing in cultured mouse spinal cord neurons in a concentration-dependent manner, at concentrations that are therapeutically relevant in the treatment of human seizures. In cultured hippocampal neurons, lamotrigine reduced sodium currents in a voltage-dependent manner, and at depolarised potentials showed a small frequency-dependent inhibition. These and a variety of other results indicate that the antiepileptic effect of lamotrigine, like that of phenytoin and carbamazepine, is at least in part due to use- and voltage-dependent modulation of fast voltage-dependent sodium currents. However, lamotrigine has a broader clinical spectrum of activity than phenytoin and carbamazepine and is recognised to be protective against generalised absence epilepsy and other generalised epilepsy syndromes, including primary generalised tonic–clonic seizures, juvenile myoclonic epilepsy, and Lennox-Gastaut syndrome.
The basis for this broader spectrum of activity of lamotrigine is unknown, but could relate to actions of the drug on voltage-activated calcium channels. Lamotrigine blocks T-type calcium channels weakly, if at all. However, it does inhibit native and recombinant high-voltage–activated calcium channels (N- and P/Q/R-types) at therapeutic concentrations. Whether this activity on calcium channels accounts for lamotrigine’s broader clinical spectrum of activity in comparison with phenytoin and carbamazepine remains to be determined.
It antagonises the following receptors with the following IC 50 values:
5-HT 3, IC 50 =18μM
σ receptors, IC 50 =145μM
The pharmacokinetics of lamotrigine follow first-order kinetics, with a half-life of 29 hours and volume of distribution of 1.36 L/kg.
Lamotrigine is inactivated by glucuronidation in the liver.
Lamotrigine has fewer drug interactions than many anticonvulsant drugs, although pharmacokinetic interactions with carbamazepine, phenytoin and other hepatic enzyme inducing medications may shorten half-life.
The capacity of available tests to detect potentially adverse consequences of melanin binding is unknown. Clinical trials excluded subtle effects and optimal duration of treatment. There are no specific recommendations for periodic ophthalmological monitoring. Lamotrigine binds to the eye and melanin-containing tissues which can accumulate over time and may cause toxicity. Prescribers should be aware of the possibility of long-term ophthalmologic effects and base treatment on clinical response. Patient compliance should be periodically reassessed with lab and medical testing of liver and kidney function to monitor progress or side effects.
1991 – Lamotrigine is first used in the United Kingdom as an anticonvulsant medication
December 1994 — lamotrigine was first approved for use in the United States and, that for the treatment of partial seizures.
August 1998 — for use as adjunctive treatment of Lennox-Gastaut syndrome in pediatric and adult patients, new dosage form: chewable dispersible tablets.
December 1998 — for use as monotherapy for treatment of partial seizures in adult patients when converting from a single enzyme-inducing anticonvulsant drug.
January 2003 — for use as adjunctive therapy for partial seizures in pediatric patients as young as two years of age.
June 2003 — approved for maintenance treatment of Bipolar II disorder ; the first such medication since lithium.
January 2004 — for use as monotherapy for treatment of partial seizures in adult patients when converting from the anti-epileptic drug valproate [including valproic acid ( Depakene ); sodium valproate ( Epilim ) and divalproex sodium ( Depakote )].
Trade names
Lamotrigine, 150 mg tablet.
Lamictal 200 mg tablets
Lamotrigine was originally brought to market by GlaxoSmithKline, trademarked as Lamictal; it also available in generic form under many brand names worldwide.

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