Nicotine as an Antiepileptic Agent in ADNFLE: An N‐of‐One Study

Willoughby, John O.; Pope, Kenneth J.; Eaton, Vaughn

doi:10.1046/j.1528-1157.2003.11903.x

Cited by 22 publications

(29 citation statements)

References 4 publications

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“…They usually respond to antiepileptic drug treatment, with carbamazepine being particularly effective [5,36,51]; acetazolamide has also been reported as effective in resistant cases [52]. In a single patient with a known α4 nicotinic acetylcholine receptor subunit, nicotine (administered via patch) was found to result in a significant reduction in seizure frequency [53]; however, nicotine has not been used in larger trials in ADNFLE.…”

Section: Clinical Features Of Adnflementioning

confidence: 99%

The Sleep Manifestations of Frontal Lobe Epilepsy

Derry

2011

Curr Neurol Neurosci Rep

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Frontal lobe seizures have a tendency to occur from sleep, and in some cases occur exclusively (or almost exclusively) from sleep; these individuals are said to have nocturnal frontal lobe epilepsy (NFLE). NFLE can be difficult to distinguish clinically from various other sleep disorders, particularly parasomnias, which also present with paroxysmal motor activity in sleep. Here, the manifestations of frontal lobe epilepsy are reviewed in detail, with particular reference to the influence of sleep and the characteristics of NFLE. Key aspects of differential diagnosis are also considered, and the underlying mechanisms involved in NFLE discussed.

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Section: Clinical Features Of Adnflementioning

confidence: 99%

The Sleep Manifestations of Frontal Lobe Epilepsy

Derry

2011

Curr Neurol Neurosci Rep

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“…Recently, in case reports a reduction or a complete control of nocturnal seizures has been reported with acetazolamide (ACZ), 500 mg at night [103], or with nicotine patches [111]. Both treatments were added to carbamazepine or other antiepileptic drugs.…”

Section: Response To Treatmentmentioning

confidence: 99%

Autosomal dominant nocturnal frontal lobe epilepsy

et al. 2004

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Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is an idiopathic epilepsy, with a spectrum of clinical manifestations, ranging from brief, stereotyped, sudden arousals to more complex dystonic-dyskinetic seizures. Video-polysomnography allows a correct differential diagnosis. There is no difference between sporadic nocturnal frontal lobe epilepsy (NFLE) and ADNFLE in the clinical and neurophysiological findings. ADNFLE is the first idiopathic epilepsy for which a genetic basis has been identified. Mutations have been found in two genes (CHRNA4 and CHRNB2) coding for neuronal nicotinic receptor subunits (alpha4 and beta2, respectively). Contrasting data have been reported on the effect of these mutations on the functionality of the receptor.Moreover, the incomplete data on the neuronal network/s in which this receptor is involved, make difficult the understanding of the genotype-phenotype correlation. This is an overview on the clinical and genetic aspects of ADNFLE including a discussion of some open questions on the role of the neuronal nicotinic receptor subunit mutations in the pathogenesis of this form of epilepsy.

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“…The beneficial effect of nicotine on seizure frequency was later reported in 9 out of 22 subjects from two ADNFLE Norwegian pedigrees with CHRNA4 mutations [14]. These data suggest that nicotine consumption is an environmental factor reducing susceptibility to seizures in ADNFLE patients and, hence, that transdermal nicotine should be considered in pharmacoresistant NFLE cases [13,14].…”

Section: Introductionmentioning

confidence: 81%

“…Willoughby et al [13] described one ADNFLE patient with a CHRNA4 mutation whose seizures were refractory to standard antiepileptic therapy and improved after treatment with nicotine transdermal patches. The beneficial effect of nicotine on seizure frequency was later reported in 9 out of 22 subjects from two ADNFLE Norwegian pedigrees with CHRNA4 mutations [14].…”

Section: Introductionmentioning

confidence: 99%

“…This might suggest that nicotinic 'overactivity' of the mutated receptors is responsible for the arousal phenomena in humans and would contradict the idea of a therapeutic effect of nicotine. However, the chronic use of nicotine has been documented to desensitize nAChR [17], and this would account for the beneficial effect demonstrated in ADNFLE patients with known nAChR mutations [13,14].…”

Section: Introductionmentioning

confidence: 99%

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