K-complexk-complex in sleep cycle, k-complexes
A K-complex is an electroencephalography EEG waveform that occurs during stage 2 of NREM sleep It is the "largest event in healthy human EEG"1 They are more frequent in the first sleep cycles
K-complexes have two proposed functions:1 first, suppressing cortical arousal in response to stimuli that the sleeping brain evaluates not to signal danger, and second, aiding sleep-based memory consolidation
The K-complex was discovered in 1937 in the private laboratories of Alfred Lee Loomis2
- 1 Neurophysiology
- 2 Development
- 3 Clinical
- 31 Epilepsy
- 32 Restless legs syndrome
- 33 Obstructive sleep apnea
- 4 Notes
K-complex consists of a brief negative high-voltage peak, usually greater than 100 µV, followed by a slower positive complex around 350 and 550 ms and at 900 ms a final negative peak K-complexes occur roughly every 10–17 minutes and are often followed by bursts of sleep spindles They occur spontaneously1 but also occur in response to external stimuli such as sounds, touches on the skin3 and internal ones such as inspiratory interruptions4 They are generated in widespread cortical locations1 though they tend to predominate over the frontal parts of the brain5
Both K-complex and delta wave activity in stage 2 sleep create slow-wave 08 Hz and delta 16–40 Hz oscillations However, their topographical distribution is different, and the delta power of K-complexes is higher6
They are created by the occurrence in widespread cortical areas of outward dendritic currents from the middle III to the upper I layers of the cerebral cortex This is accompanied by a decrease in broadband EEG power including gamma wave activity This produces "down-states" of neuronal silence in which neural network activity is reduced1 The activity of K-complexes is transferred to the thalamus where it synchronizes the thalamocortical network during sleep, producing sleep oscillations such as spindles and delta waves7 It has been observed that they are indeed identical in the "laminar distributions of transmembrane currents" to the slow waves of slow-wave sleep1
K-complexes have been suggested both to protect sleep and also to engage in information processing, as they are both an essential part of the synchronization of NREM sleep, while they also respond to both internal and external stimuli in a reactive manner8 This would be consistent with a function in suppressing cortical arousal in response to stimuli that the brain needs to initially process in regard to whether it is dangerous or not1
Another suggested function is aiding the activation homeostasis of synapses9 and memory consolidation The activation thresholds of cortical synapses become lowered during wakefulness as they process information, making them more responsive, and so need to be adjusted back to preserve their signal-to-noise ratio9 The down-state provided by K-complexes does this by reducing the strengths of synaptic connections that occur while an individual is awake1 Further, the recovery from the down-state they induce allows that "cortical firing 'reboots' in a systematic order" so that memory engrams encoded during neuronal firing can be "repeatedly practiced and thus consolidated"1
They are present in the sleep of 5-month-old infants, and develop with age Between 3 and 5 years of age a faster negative component appears and continues to increase until adolescence Another change occurs in adults: before 30 years of age their frequency and amplitude is higher than in older people particularly those over 50 years of age10 This parallels the decrease in other components of sleep such as sleep spindle density and delta power10
In individuals with idiopathic generalized epilepsy, K-complex induced synchronization can trigger spike-and-wave discharges This tends to happen most between the shift between waking and NREM, and between NREM and REM sleep11 In autosomal dominant nocturnal frontal lobe epilepsy, K-complexes are almost invariably present at the start of seizures12
Restless legs syndromeedit
Individuals with restless legs syndrome have increased numbers of K-complexes and these are associated with and often precede leg movements Dopamine enhancing drugs such as L-DOPA that reduce leg movements do not reduce the K-complex suggesting that they are primary and the leg movements secondary to them Failure of such drugs to reduce K-complexes in spite of reducing the leg movements has been suggested to be why patients after such treatment still continue to complain of non-restorative sleep13 Clonazepam is another treatment for RLS; like other benzodiazepines, it inhibits REM sleep by enhancing levels of GABA This inhibition of REM sleep significantly decreases K-complex count, and unlike L-DOPA treatment, clonazepam studies report improvement in sleep restoration14 Therefore, drugs that inhibit REM sleep also decrease K-complex count
Obstructive sleep apneaedit
Obstructive sleep apnea syndrome is associated with inspiratory occlusions evoking fewer K-complexes during NREM sleep even though K-complexes are evoked normally to auditory stimuli and such individuals react normally to respiratory interruptions when awake This suggests a link between such sleep apnea and a sleep specific blunted cortical response to respiratory problems151617
- ^ a b c d e f g h i Cash SS; Halgren E; Dehghani N; et al 2009 "Human K-Complex Represents an Isolated Cortical Down-State" Science 324 5930: 1084–87 doi:101126/science1169626 PMID 19461004
- ^ Loomis AL; Harvey EN; Hobart GA 1937 "Cerebral states during sleep as studies by human brain potentials" J Exp Psychol 21: 127–44 doi:101037/h0057431
- ^ Roth M; Shaw J; Green J 1956 "The form, voltage distribution and physiological significance of the K-complex" Electroenceph Clin Neurophysiol 8 3: 385–402 PMID 13330651
- ^ Webster KE; Colrain IM 1998 "Multichannel EEG analysis of respiratory evoked-potential components during wakefulness and NREM sleep" J Appl Physiol 85 5: 1727–35
- ^ McCormick L, Nielsen T, Nicolas A, Ptito M, Montplaisir J 1997 "Topographical distribution of spindles and K-complexes in normal subjects" Sleep 20 11: 939–41 PMID 9456457
- ^ Happe S; Anderer P; Gruber G; Klösch G; Saletu B; Zeitlhofer J 2002 "Scalp topography of the spontaneous K-complex and of delta-waves in human sleep" Brain Topogr 15 1: 43–9 doi:101023/A:1019992523246 PMID 12371676
- ^ Amzica F; Steriade M 1998 "Cellular substrates and laminar profile of sleep K-complex" Neuroscience 82 3: 671–86 doi:101016/s0306-45229700319-9 PMID 9483527
- ^ Halász P 2005 "K-complex, a reactive EEG graphoelement of NREM sleep: an old chap in a new garment" Sleep Med Rev 9 5: 391–412 doi:101016/jsmrv200504003 PMID 16122950
- ^ a b Tononi G; Cirelli C 2006 "Sleep function and synaptic homeostasis" Sleep Med Rev 10 1: 49–62 doi:101016/jsmrv200505002 PMID 16376591
- ^ a b Wauquier A October 1993 "Aging and changes in phasic events during sleep" Physiol Behav 54 4: 803–6 doi:101016/0031-93849390095-w PMID 8248360
- ^ Steriade M; Amzica F 1998 "Slow sleep oscillation, rhythmic K-complexes, and their paroxysmal developments" J Sleep Res 7 S1: 30–5 doi:101046/j1365-28697s14x PMID 9682191
- ^ El Helou J; Navarro V; Depienne C; Fedirko E; LeGuern E; Baulac M; An-Gourfinkel I; Adam C 2008 "K-complex-induced seizures in autosomal dominant nocturnal frontal lobe epilepsy" Clin Neurophysiol 119 10: 2201–4 doi:101016/jclinph200807212 PMID 18762450
- ^ Montplaisir J; Boucher S; Gosselin A; Poirier G; Lavigne G 1996 "Persistence of repetitive EEG arousals K-alpha complexes in RLS patients treated with L-DOPA" Sleep 19 3: 196–9 PMID 8723375
- ^ Saletu M 2001 "Restless legs syndrome RLS and periodic limb movement disorder PLMD acute placebo-controlled sleep laboratory studies with clonazepam" European Neuropsychopharmacology 11 2: 153–161 doi:101016/s0924-977x0100080-3
- ^ Huang J; Colrain IM; Melendres MC; Karamessinis LR; Pepe ME; Samuel JM; Abi-Raad RF; Trescher WH; Marcus CL 2008 "Cortical processing of respiratory afferent stimuli during sleep in children with the obstructive sleep apnea syndrome" Sleep 31 3: 403–10 PMC 2276751 PMID 18363317
- ^ Gora J, Trinder J, Pierce R, Colrain IM November 2002 "Evidence of a sleep-specific blunted cortical response to inspiratory occlusions in mild obstructive sleep apnea syndrome" Am J Respir Crit Care Med 166 9: 1225–34 doi:101164/rccm2106005 PMID 12403692
- ^ Afifi L; Guilleminault C; Colrain IM 2003 "Sleep and respiratory stimulus specific dampening of cortical responsiveness in OSAS" Respir Physiol Neurobiol 136 2–3: 221–34 doi:101016/s1569-90480300084-3 PMID 12853013
|Evoked potentials||Negativity Bereitschaftspotential ELAN N100 Visual N1 N170 N200 N2pc N400 Contingent negative variation CNV Mismatch negativity Positivity C1 & P1 P50 P200 P300 P3a P3b P600 late positivity Late positive component|
k-complex, k-complex definition, k-complex eeg, k-complex in sleep cycle, k-complex sleep, k-complex stimulation, k-complex waves, k-complexes, k-complexes and sleep spindles
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