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Nocturnal seizures

MedGen UID:
581539
Concept ID:
C0393719
Disease or Syndrome
Synonyms: Night seizure; Nocturnal epilepsy; Sleep related epilepsy; Sleep seizure; Sleep seizures; Sleep-related epilepsy
SNOMED CT: Sleep related epilepsy (230445007); Nocturnal epilepsy (230445007); Sleep-related epilepsy (230445007); Night seizure (230445007); Sleep seizure (230445007)
 
HPO: HP:0031951

Definition

Seizures that occur while the affected individual is sleeping. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVNocturnal seizures

Conditions with this feature

Autosomal dominant nocturnal frontal lobe epilepsy 4
MedGen UID:
332082
Concept ID:
C1835905
Disease or Syndrome
Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is characterized by clusters of nocturnal motor seizures, which are often stereotyped and brief (5 seconds to 5 minutes). They vary from simple arousals from sleep to dramatic, often bizarre hyperkinetic events with tonic or dystonic features. Affected individuals may experience aura. Retained awareness during seizures is common. A minority of individuals experience daytime seizures. Onset ranges from infancy to adulthood. About 80% of individuals develop ADNFLE in the first two decades of life; mean age of onset is ten years. Clinical neurologic examination is normal and intellect is usually preserved, but reduced intellect, psychiatric comorbidity, or cognitive deficits may occur. Within a family, the manifestations of the disorder may vary considerably. ADNFLE is lifelong but not progressive. As an individual reaches middle age, attacks may become milder and less frequent.
Benign Rolandic epilepsy
MedGen UID:
432274
Concept ID:
C2363129
Disease or Syndrome
Benign epilepsy of childhood with centrotemporal spikes (BECTS) or sharp waves, also known as rolandic epilepsy, is the most common idiopathic childhood epilepsy syndrome (Neubauer et al., 1998). It is termed 'rolandic' epilepsy because of the characteristic features of partial seizures involving the region around the lower portion of the central gyrus of Rolando. This results in classic focal seizures that affect the vocal tract, beginning with guttural sounds at the larynx and sensorimotor symptoms that progress to the tongue, mouth, and face, resulting in hypersalivation and speech arrest. Seizures most often occur in sleep shortly before awakening. The disorder occurs more often in boys than in girls (3:2). Rolandic epilepsy is considered a neurodevelopmental disorder, affecting 0.2% of the population. Affected individuals may have learning disabilities or behavioral problems; however, the seizures and accompanying problems usually remit during adolescence (summary by Strug et al., 2009). See also focal epilepsy and speech disorder (FESD; 245570), which is caused by mutation in the GRIN2A gene (138253) on chromosome 16p13. Some patients with GRIN2A mutations show features consistent with a clinical diagnosis of BECTS. Some patients with DEPDC5 (614191) mutations may show features consistent with rolandic epilepsy (see FFEVF, 604364).
Neurodevelopmental disorder with epilepsy, cataracts, feeding difficulties, and delayed brain myelination
MedGen UID:
1377894
Concept ID:
C4479333
Disease or Syndrome
Neurodevelopmental disorder with epilepsy, cataracts, feeding difficulties, and delayed brain myelination is a syndromic form of severe to profound intellectual disability with onset of delayed psychomotor development and seizures in infancy. Affected children have hypotonia, feeding difficulties resulting in failure to thrive, and inability to speak or walk, and they tend to show repetitive stereotypic behaviors. Brain imaging shows cerebral atrophy and delayed myelination (summary by Schoch et al., 2017).
Hyperekplexia 1
MedGen UID:
1647581
Concept ID:
C4551954
Disease or Syndrome
Hyperekplexia is an early-onset neurologic disorder characterized by an exaggerated startle response to sudden, unexpected auditory or tactile stimuli. Affected individuals have brief episodes of intense, generalized hypertonia in response to stimulation. Neonates may have prolonged periods of rigidity and are at risk for sudden death from apnea or aspiration. Many affected infants have inguinal hernias. The symptoms tend to resolve after infancy, but adults may have increased startle-induced falls and/or experience nocturnal muscle jerks (summary by Ryan et al., 1992). Genetic Heterogeneity of Hyperekplexia See also HKPX2 (614619), caused by mutation in the GLRB gene (138492) on chromosome 4q31; HKPX3 (614618), caused by mutation in the GLYT2 gene (SLC6A5; 604159) on chromosome 11p15; and HKPX4 (618011), caused by mutation in the ATAD1 gene (614452) on chromosome 10q23. Hyperekplexia can also occur in developmental and epileptic encephalopathy-8 (DEE8; 300607), caused by mutation in the ARHGEF9 gene (300429). See also sporadic stiff-man syndrome (184850) and the 'Jumping Frenchmen of Maine' (244100).
Epilepsy, familial focal, with variable foci 1
MedGen UID:
1641798
Concept ID:
C4551983
Disease or Syndrome
DEPDC5-related epilepsy encompasses a range of epilepsy syndromes, almost all of which are characterized by focal seizures, with seizure onset in a discrete area of the brain. While most individuals with DEPDC5-related epilepsy have a normal brain MRI, some have epilepsy associated with a cortical malformation, usually focal cortical dysplasia. Seizure syndromes include familial focal epilepsy with variable foci (FFEVF), autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE), familial mesial temporal lobe epilepsies (FMTLE), autosomal dominant epilepsy with auditory features (ADEAF), and infantile spasms. Although psychomotor development is usually normal, intellectual disability or autism spectrum disorder has been reported in some individuals.
Kohlschutter-Tonz syndrome-like
MedGen UID:
1781649
Concept ID:
C5543202
Disease or Syndrome
Den Hoed-de Boer-Voisin syndrome (DHDBV) is characterized by global developmental delay with moderately to severely impaired intellectual development, poor or absent speech, and delayed motor skills. Although the severity of the disorder varies, many patients are nonverbal and have hypotonia with inability to sit or walk. Early-onset epilepsy is common and may be refractory to treatment, leading to epileptic encephalopathy and further interruption of developmental progress. Most patients have feeding difficulties with poor overall growth and dysmorphic facial features, as well as significant dental anomalies resembling amelogenesis imperfecta. The phenotype is reminiscent of Kohlschutter-Tonz syndrome (KTZS; 226750). More variable features of DHDBV include visual defects, behavioral abnormalities, and nonspecific involvement of other organ systems (summary by den Hoed et al., 2021).
Developmental delay, impaired speech, and behavioral abnormalities
MedGen UID:
1794167
Concept ID:
C5561957
Disease or Syndrome
Developmental delay, impaired speech, and behavioral abnormalities (DDISBA) is characterized by global developmental delay apparent from early childhood. Intellectual disability can range from mild to severe. Additional variable features may include dysmorphic facial features, seizures, hypotonia, motor abnormalities such as Tourette syndrome or dystonia, and hearing loss (summary by Cousin et al., 2021).
Neurodevelopmental disorder with or without variable movement or behavioral abnormalities
MedGen UID:
1802087
Concept ID:
C5676908
Disease or Syndrome
Neurodevelopmental disorder with or without variable movement or behavioral abnormalities (NEDMAB) is an autosomal dominant disorder characterized by mildly to severely impaired intellectual development and, in some patients, movement abnormalities consisting of tremors, cerebellar ataxia, or extrapyramidal symptoms. Movement abnormalities have onset in childhood or adolescence. Other variable features include autism spectrum disorder or autistic features and epilepsy.

Professional guidelines

PubMed

Liu G, Slater N, Perkins A
Am Fam Physician 2017 Jul 15;96(2):87-96. PMID: 28762701
Eliashiv D, Avidan AY
Crit Care Clin 2015 Jul;31(3):511-31. doi: 10.1016/j.ccc.2015.03.009. PMID: 26118918
Tinuper P, Bisulli F, Provini F
Epilepsia 2012 Dec;53 Suppl 7:12-9. doi: 10.1111/j.1528-1167.2012.03710.x. PMID: 23153205

Recent clinical studies

Etiology

Whitney R, Jones KC, Sharma S, RamachandranNair R
Epilepsia 2023 Jun;64(6):1424-1431. Epub 2023 Apr 21 doi: 10.1111/epi.17617. PMID: 37039574
Beghi E
Neuroepidemiology 2020;54(2):185-191. Epub 2019 Dec 18 doi: 10.1159/000503831. PMID: 31852003
Rundo JV, Downey R 3rd
Handb Clin Neurol 2019;160:381-392. doi: 10.1016/B978-0-444-64032-1.00025-4. PMID: 31277862
Liu G, Slater N, Perkins A
Am Fam Physician 2017 Jul 15;96(2):87-96. PMID: 28762701
Bergey GK
Continuum (Minneap Minn) 2016 Feb;22(1 Epilepsy):38-50. doi: 10.1212/CON.0000000000000271. PMID: 26844729

Diagnosis

Eiser AS
Sleep Med Clin 2024 Mar;19(1):159-167. Epub 2023 Nov 22 doi: 10.1016/j.jsmc.2023.10.003. PMID: 38368062
Gigliotti F, Esposito D, Basile C, Cesario S, Bruni O
Pediatr Pulmonol 2022 Aug;57(8):1869-1878. Epub 2021 Mar 1 doi: 10.1002/ppul.25304. PMID: 33647192
Beghi E
Neuroepidemiology 2020;54(2):185-191. Epub 2019 Dec 18 doi: 10.1159/000503831. PMID: 31852003
Rundo JV, Downey R 3rd
Handb Clin Neurol 2019;160:381-392. doi: 10.1016/B978-0-444-64032-1.00025-4. PMID: 31277862
Bergey GK
Continuum (Minneap Minn) 2016 Feb;22(1 Epilepsy):38-50. doi: 10.1212/CON.0000000000000271. PMID: 26844729

Therapy

Armand Larsen S, Terney D, Østerkjerhuus T, Vinding Merinder T, Annala K, Knight A, Beniczky S
Brain Behav 2022 Sep;12(9):e2737. Epub 2022 Aug 8 doi: 10.1002/brb3.2737. PMID: 35939047Free PMC Article
Gibbon FM, Maccormac E, Gringras P
Arch Dis Child 2019 Feb;104(2):189-192. Epub 2018 Sep 28 doi: 10.1136/archdischild-2017-313421. PMID: 30266875Free PMC Article
Liu G, Slater N, Perkins A
Am Fam Physician 2017 Jul 15;96(2):87-96. PMID: 28762701
Bergey GK
Continuum (Minneap Minn) 2016 Feb;22(1 Epilepsy):38-50. doi: 10.1212/CON.0000000000000271. PMID: 26844729
Eriksson SH
Curr Opin Neurol 2011 Apr;24(2):171-6. doi: 10.1097/WCO.0b013e3283445355. PMID: 21386677

Prognosis

Eichelberger H, Nelson ALA
Curr Probl Pediatr Adolesc Health Care 2020 Dec;50(12):100893. Epub 2020 Nov 1 doi: 10.1016/j.cppeds.2020.100893. PMID: 33139210
Beghi E
Neuroepidemiology 2020;54(2):185-191. Epub 2019 Dec 18 doi: 10.1159/000503831. PMID: 31852003
Somboon T, Grigg-Damberger MM, Foldvary-Schaefer N
Chest 2019 Jul;156(1):172-181. Epub 2019 Jan 31 doi: 10.1016/j.chest.2019.01.016. PMID: 30711481
van der Lende M, Hesdorffer DC, Sander JW, Thijs RD
Neurology 2018 Oct 16;91(16):e1508-e1518. Epub 2018 Sep 21 doi: 10.1212/WNL.0000000000006356. PMID: 30242018
Capovilla G, Striano P, Beccaria F
Epilepsia 2009 May;50 Suppl 5:45-8. doi: 10.1111/j.1528-1167.2009.02120.x. PMID: 19469846

Clinical prediction guides

Tan B, Liu Q, Qin Y, Chen Q, Chen R, Jin Y, Li M, Jia X, Xu X, Zhang Q
Epilepsy Behav 2024 Jan;150:109559. Epub 2023 Nov 29 doi: 10.1016/j.yebeh.2023.109559. PMID: 38035537
Bijlenga D, Fronczek R, Gorter EJ, Thijs RD
Epilepsy Res 2023 Nov;197:107238. Epub 2023 Oct 10 doi: 10.1016/j.eplepsyres.2023.107238. PMID: 37839340
Karapinar E, YunusoĞlu C, Tekin B, Dede HÖ, Bebek N, Baykan B, GÜrses C
Arq Neuropsiquiatr 2020 Dec;78(12):772-777. doi: 10.1590/0004-282X20200064. PMID: 33331513
Somboon T, Grigg-Damberger MM, Foldvary-Schaefer N
Chest 2019 Jul;156(1):172-181. Epub 2019 Jan 31 doi: 10.1016/j.chest.2019.01.016. PMID: 30711481
Hesdorffer DC, Tomson T
CNS Drugs 2013 Feb;27(2):113-9. doi: 10.1007/s40263-012-0006-1. PMID: 23109241

Recent systematic reviews

Ali A, Wu S, Issa NP, Rose S, Towle VL, Warnke P, Tao JX
Epilepsy Behav 2017 Nov;76:1-6. Epub 2017 Sep 13 doi: 10.1016/j.yebeh.2017.08.021. PMID: 28917499

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