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Frontal Lobe Epilepsy (Epilepsy, Supplementary Motor)

140  relevant articles (2 outcomes, 4 trials/studies) found for this Disease

Description: A localization-related (focal) form of epilepsy characterized by seizures which arise in the frontal lobe. A variety of clinical syndromes exist depending on the exact location of the seizure focus. Simple or complex motor movements may occur, and most commonly involve the face and upper extremities. Seizures in the anterior frontal regions may be associated with head and eye turning, typically away from the side of origin of the seizure. Frontal lobe seizures may be idiopathic (cryptogenic) or caused by an identifiable disease process such as traumatic injuries, neoplasms, or other macroscopic or microscopic lesions of the frontal lobes (symptomatic frontal lobe seizures). (From Adams et al., Principles of Neurology, 6th ed, pp318-9)

Also Known As:
Epilepsy, Supplementary Motor; Epilepsy, Frontal Lobe; Benign Frontal Childhood Epilepsy; Childhood Benign Frontal Epilepsy; Epilepsy, Anterior Fronto-Polar; Epilepsy, Benign Frontal, Childhood; Epilepsy, Cingulate; Epilepsy, Opercular; Epilepsy, Orbito-Frontal; Anterior Fronto-Polar Epilepsies; Anterior Fronto-Polar Epilepsy; Cingulate Epilepsies; Cingulate Epilepsy; Epilepsies, Anterior Fronto-Polar; Epilepsies, Cingulate; Epilepsies, Orbito-Frontal; Epilepsies, Supplementary Motor; Epilepsy, Anterior Fronto Polar; Epilepsy, Orbito Frontal; Frontal Lobe Epilepsies; Fronto-Polar Epilepsies, Anterior; Fronto-Polar Epilepsy, Anterior; Motor Epilepsies, Supplementary; Opercular Epilepsies; Opercular Epilepsy; Orbito-Frontal Epilepsies; Orbito-Frontal Epilepsy; Supplementary Motor Epilepsies; Supplementary Motor Epilepsy; Frontal Epilepsy, Benign, Childhood

Relationship Network

Disease Context: Research Results

Related Diseases

1. Seizures (Seizure)
2. Epilepsy (Aura)
3. Partial Epilepsies (Epilepsy, Partial)
4. Temporal Lobe Epilepsy
5. Benign Neonatal Epilepsy (Benign Familial Neonatal Convulsions)

Experts

1. Ferini-Strambi, Luigi: 5 articles (09/2008 - 04/2002)
2. Combi, Romina: 3 articles (09/2008 - 08/2002)
3. Tenchini, Maria Luisa: 3 articles (09/2008 - 04/2002)
4. Oldani, Alessandro: 3 articles (12/2006 - 04/2002)
5. Zucconi, Marco: 3 articles (12/2006 - 04/2002)
6. Dalprà, Leda: 3 articles (12/2005 - 04/2002)
7. Berkovic, Samuel F: 2 articles (08/2008 - 09/2007)
8. Lester, Henry A: 2 articles (09/2007 - 08/2005)
9. Cohen, Bruce N: 2 articles (09/2007 - 08/2005)
10. Malcovati, Massimo: 2 articles (08/2002 - 04/2002)

Drugs and Biologics

Drugs and Important Biological Agents (IBA) related to Frontal Lobe Epilepsy:
1. oxcarbazepine (Trileptal)FDA LinkGeneric
2. Anticonvulsants (Antiepileptic Drugs)IBA
3. topiramate (Topamax)FDA Link
4. Acetylcholine (Acetylcholine Chloride)FDA Link
5. Guanfacine (Tenex)FDA LinkGeneric
6. Nicotinic Receptors (Nicotinic Acetylcholine Receptor)IBA
7. Ion Channels (Ion Channel)IBA
06/01/2000 - "DEVELOPMENT: We studied the main ion channel disorders related to simply inherited idiopathic epileptic syndromes in which four genes have been codified to date: benign familial neonatal convulsions, generalized epilepsy with febrile seizures plus and autosomal dominant nocturnal frontal lobe epilepsy"
12/01/2006 - "Thus, the discovery of KCNQ2 mutations in benign familial neonatal convulsions, SCN1A mutations in severe myoclonic epilepsy of infancy and in generalized epilepsy with febrile seizures plus, and CHRA4 and CHRB2 mutations in autosomal-dominant nocturnal frontal lobe epilepsy, has led to the establishment of epilepsy as a disorder of ion channel function and, furthermore, has led to the introduction of genetic tests that are available clinically to aid in diagnosis and treatment"
12/01/2000 - "Recently, gene defects underlying four monogenic epilepsies (generalized epilepsy with febrile seizures, autosomal dominant nocturnal frontal lobe epilepsy, benign familial neonatal convulsions and episodic ataxia type 1 with partial seizures) have been identified, shedding new light on the pathophysiology of epilepsy as these diseases are caused by ion channel mutations"
10/01/1999 - "Unique among reviews of this topic is that all known human hereditary diseases of voltage-gated ion channels are described covering various fields of medicine such as neurology (nocturnal frontal lobe epilepsy, benign neonatal convulsions, episodic ataxia, hemiplegic migraine, deafness, stationary night blindness), nephrology (X-linked recessive nephrolithiasis, Bartter), myology (hypokalemic and hyperkalemic periodic paralysis, myotonia congenita, paramyotonia, malignant hyperthermia), cardiology (LQT syndrome), and interesting parallels in mechanisms of disease emphasized"
08/01/2008 - "Human nocturnal frontal lobe epilepsy: pharmocogenomic profiles of pathogenic nicotinic acetylcholine receptor beta-subunit mutations outside the ion channel pore."
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8. Voltage-Gated Potassium Channels (Voltage-Gated Potassium Channel)IBA
05/20/2004 - "Mutations of the nicotinic acetylcholine receptor subunits are found in familial nocturnal frontal lobe epilepsy, while defects in the voltage gated potassium channels (KCNQ2 and KCNQ3) have been identified in benign familial neonatal convulsions"
01/01/2002 - "Mutations in the CHRNA4 or CHRNB subunits of the neuronal nicotinic acetylcholine receptor lead to familial nocturnal frontal lobe epilepsy, while defects in the voltage-gated potassium channels KCNQ2 and KCNQ3 have recently been found to cause benign familial neonatal convulsions"
01/01/2001 - "So far, the genetic defects underlying three different idiopathic epilepsy syndromes have been identified: mutations in the CHRNA4- or CHRNB subunits of the neuronal nicotinic acetylcholine receptor are found in familial nocturnal frontal lobe epilepsy, while defects in the voltage-gated potassium channels KCNQ2 and KCNQ3 have recently been identified in benign familial neonatal convulsions"
11/01/1997 - "weakness), particularly in response to lowered serum potassium (hypokalemic periodic paralysis); despite the recently discovered etiology of the disease, the pathogenesis of the weakness is still unknown; iv) dominant mutations in a voltage-gated potassium channel expressed in the CNS cause episodic ataxia type 1 presumably by antagonizing repolarization of the cell membrane; v) dominant mutations in a neuronal calcium channel alpha-subunit may cause either episodic ataxia type II or familial hemiplegic migraine by a so far unknown pathomechanism; vi) the first mutation in an ion channel associated with an inherited form of epilepsy, nocturnal frontal lobe epilepsy, was found in the alpha(4)-subunit of a neuronal nicotinic acetylcholine receptor."
01/01/2001 - "Consequently, mutations in ion channel encoding genes are found in a variety of inherited diseases associated with hyper- or hypoexcitability of the affected tissue, the so-called 'channelopathies.' An increasing number of epileptic syndromes belongs to this group of rare disorders: Autosomal dominant nocturnal frontal lobe epilepsy is caused by mutations in a neuronal nicotinic acetylcholine receptor (affected genes: CHRNA4, CHRNB2), benign familial neonatal convulsions by mutations in potassium channels constituting the M-current (KCNQ2, KCNQ3), generalized epilepsy with febrile seizures plus by mutations in subunits of the voltage-gated sodium channel or the GABA(A) receptor (SCN1B, SCN1A, GABRG2), and episodic ataxia type 1-which is associated with epilepsy in a few patients--by mutations within another voltage-gated potassium channel (KCNA1)"
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9. Carbamazepine (Tegretol)FDA LinkGeneric
10. Potassium Channels (Potassium Channel)IBA
01/01/1999 - "Disease gene identification, such as the two potassium ion channels (KCNQ2 and KCNQ3) for the two forms of benign familial neonatal seizures (BFNC) and the alpha4 subunit of the nicotinic receptor for autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE), however, should yield significant advances in drug discoveries"
01/01/1999 - "In humans, three autosomal-dominant disorders--benign familial neonatal convulsions, nocturnal frontal lobe epilepsy, and "generalized epilepsy with febrile seizures plus"--result from mutations affecting voltage-sensitive potassium channels, a central nicotinic acetylcholine receptor, and a voltage-sensitive sodium channel, respectively"
05/01/2001 - "Generalized epilepsy with febrile seizures plus (GEFS+), benign familial neonatal convulsions and nocturnal frontal lobe epilepsy, three autosomal dominant idiopathic epilepsies, result from mutations affecting voltage-gated sodium and potassium channels, and nicotinic acetylcholine receptors, respectively"
01/01/2001 - "Consequently, mutations in ion channel encoding genes are found in a variety of inherited diseases associated with hyper- or hypoexcitability of the affected tissue, the so-called 'channelopathies.' An increasing number of epileptic syndromes belongs to this group of rare disorders: Autosomal dominant nocturnal frontal lobe epilepsy is caused by mutations in a neuronal nicotinic acetylcholine receptor (affected genes: CHRNA4, CHRNB2), benign familial neonatal convulsions by mutations in potassium channels constituting the M-current (KCNQ2, KCNQ3), generalized epilepsy with febrile seizures plus by mutations in subunits of the voltage-gated sodium channel or the GABA(A) receptor (SCN1B, SCN1A, GABRG2), and episodic ataxia type 1-which is associated with epilepsy in a few patients--by mutations within another voltage-gated potassium channel (KCNA1)"
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Therapies and Procedures

1. Electrodes (Electrode)
2. Deep Brain Stimulation
3. Continuous Positive Airway Pressure
4. Drug Therapy (Chemotherapy)

Best Treatments:
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