Lamotriginesold 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 and approved for use in the United States in Lamotrigine is used for the treatment of partial seizures.
It is also used as an alternative medication for absence seizure and atypical absence, myoclonic, and atonic seizures. It is also appropriate for the lamictal and lithium of Lennox—Gastaut syndrome. Lamotrigine reduces the frequency of LGS seizures, and is one of two medications known to decrease the severity of drop attacks.
Lamotrigine is approved in the US for maintenance treatment of bipolar I disorder and bipolar II disorder. The drug seems ineffective in the treatment of current rapid-cycling, acute mania, or acute depression in bipolar disorder; however, it is effective at prevention of or delaying of manic, depressive, or rapid cycling episodes.
There is less evidence of therapeutic benefit when lamotrigine is used to treat a current mood episode, lamictal and lithium. A review about lamotrigine concluded that it is recommended in bipolar maintenance when depression is prominent and that more research is needed in regards 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. Off-label uses include the treatment of peripheral neuropathytrigeminal neuralgiacluster headachesmigrainesand reducing neuropathic pain   although a systematic review conducted in concluded that well-designed clinical trials have shown no benefit for lamotrigine in neuropathic pain. Rash and other skin reactions are more common in children, so this medication is often reserved for adults.
For patients whose lamotrigine has been stopped after development of a rash, re-challenge with lamotrigine is also a viable option. However, it is not applicable for lamictal and lithium serious cases. 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 lamictal and lithium is increased, lamictal and lithium.
Side-effects such as rash, fever, lamictal and lithium, and fatigue are very serious, as they mental illness and addiction indicate incipient Stevens—Johnson syndrome, toxic epidermal necrolysis, DRESS syndrome or aseptic meningitis. Other side-effects include loss of lamictal and lithium or coordination; double vision ; crossed lamictal and lithium ; pupil constriction; blurred vision; dizziness and lack of coordination; drowsiness, insomnia ; anxiety; vivid dreams or nightmares ; dry mouthmouth ulcers;  memory problems; mood changes; itchiness; runny nose; cough; nauseaindigestion, 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, lamictal and lithium. Cases of lamotrigine-induced neuroleptic malignant syndrome have been reported.
This reaction can occur between days to weeks lamictal and lithium starting the treatment. Women are more likely than men to have side-effects. There is evidence showing interactions between lamotrigine and female hormones, which can be of particular concern for women on estrogen-containing hormonal contraceptives.
Ethinylestradiolthe ingredient of such contraceptives, has been shown to decrease serum levels of lamotrigine. Likewise, women may experience an increase in lamotrigine side-effects upon discontinuation of the pill.
This may include the "pill-free" week where lamotrigine serum levels have been shown to increase twofold. 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.
Lamotrigine binds to melanin -containing lamictal and lithium 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 lamictal and lithium neurodegeneration of the developing brain.
No detrimental effects on cognitive function were observed; however, the only statistical improvement in core ADHD symptoms was an improvement on a Paced Auditory Serial Addition Test PASAT that measures auditory processing speed and calculation ability. Lamotrigine is known to affect sleep, lamictal and lithium. Studies with small numbers 10—15 of patients reported that lamotrigine increases sleep stability increases the duration of REM sleepdecreases the number of phase shifts and decreases the duration of slow-wave sleep and that there was no effect on vigilance,  and daytime somnolence and cognitive function.
Lamotrigine can induce a type of seizure known as a myoclonic jerkwhich tends to happen soon after the use of the medication. It can also cause myoclonic status epilepticus. In overdose, lamotrigine can cause uncontrolled seizures in most people. Reported results lamictal and lithium overdoses involving up to 15 g include increased seizures, lamictal and lithium, coma and death. Lamotrigine is a member of the sodium channel blocking class of antiepileptic drugs.
In addition, lamotrigine shares few side-effects lamictal and lithium other, unrelated anticonvulsants known to inhibit sodium channels, which further emphasises its unique properties. It is a triazine derivate that inhibits voltage-sensitive sodium channelslamictal and lithium, 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 and its neuroprotective and antiglutamatergic effects have been pointed out as promising contributors to its mood stabilizing activity. Lamotrigine does not have pronounced effects on any of the usual neurotransmitter receptors that anticonvulsants effect adrenergicdopamine D1 and D2muscarinicGABAhistaminergic H1serotonin 5-HT2and N-methyl-D-aspartate.
Inhibitory effects on 5-HTlamictal and lithium, norepinephrineand dopamine transporters are weak. As is the case for antiepileptic drugs that act on voltage-dependent sodium channelslamotrigine thereby inhibits the release of glutamate and aspartatewhich is evoked by the sodium-channel activator veratrineand was less effective in the inhibition of acetylcholine or GABA release.
At high concentrations, it had no lamictal and lithium on spontaneous or potassium evoked amino acid release. 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, lamictal and lithium.
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 carbamazepineis 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 epilepsyand 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. It antagonises the following receptors with the following IC 50 values: The pharmacokinetics of lamotrigine follow first-order kineticswith a half-life of 29 hours and volume of distribution of 1.
Available data indicate that its bioavailability is not affected by food. Estimate of the mean apparent volume of distribution of lamotrigine following oral administration ranges from 0.
This is independent of dose and is similar following single and multiple doses in both patients with epilepsy lamictal and lithium in healthy volunteers. Lamotrigine is inactivated by glucuronidation in the liver. Its major metabolite is an lamictal and lithium 2-n-glucuronide conjugate. 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.
Lamotrigine was originally brought to market by GlaxoSmithKlinetrademarked as Lamictal; it also available in generic form under many brand names worldwide. From Wikipedia, lamictal and lithium, the free encyclopedia.
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