Introduction

Sleep is a swiftly reversible state of decreased metabolism, responsiveness and, motor activity, which is broadly categorized into rapid eye movement (REM) and non-rapid eye movement (NREM).[1] The NREM sleep phase again subdivides into stage N1, stage N2, and stage N3. The K-Complex is a waveform identified on electroencephalography (EEG), which primarily occurs during Stage 2 (N2) of NREM sleep, along with sleep spindles, which make up the two distinct features seen in this stage.

The K-complex (KC) is a sharp, well-delineated, high-voltage, biphasic wave that lasts for more than 0.5 seconds and has been termed as the largest event in a healthy human EEG.[2] On EEG, it was described by Laurino et al. as having a short positive voltage peak, which is usually at 200 milliseconds, followed by a large negative complex at around 550 milliseconds and finally, a long-lasting positive peak at 900 milliseconds.[3] However, the initial short positive peak may not always be present. The occurrence of K-complexes may be spontaneous (spontaneous K-complex [SKC]), as a response to an internal stimulus such as a respiratory interruption or in response to an external stimulus like a touch on the skin (evoked K-complex [EKC]). Though K-complexes are generated in widespread areas of the cortex, they are seen maximally over the frontal and superior frontal cortices.[3]

Issues of Concern

The EEG is a technique of electrophysiological monitoring that involves electrodes attached to the scalp to measure the amplitude and frequency of electrical activity in the brain. The K-complex is a waveform seen on electroencephalography during the second stage (N2) of NREM sleep. An EEG conducted during a sleep study helps in the identification of the various waveforms and phases of sleep architecture. The second stage of NREM sleep on EEG shows theta waves, which, along with K-complexes and sleep spindles, are the defining characteristics of this stage. Any abnormalities in these waveforms are therefore picked up on EEG.

When performing a functional MRI of the brain in conjunction with the EEG, the K-complex corresponds with increased signals in the paracentral gyri, thalami, medial region of the parietal, and frontal lobes and superior temporal lobes.[4] The increased activity in these regions during the K-complex indicates the brain activity and thus could point towards the possible functions of this phenomenon.

Development

The presence of K-complexes has been seen during sleep in the EEG of infants as young as 5 months old. When the child is about 3 to 5 years old, a faster negative component develops which continues to increase well into adolescence. During adulthood, there are changes observed at around 30 years of age. There is a decrease in the frequency and amplitude of the K-complex in those more than 50 years of age, seen especially in the elderly.[5]

Function

Although the exact function of the K-complex during sleep is not precisely known, there are a few theories. In more recent times, it has been said to have seemingly contrasting functions when it comes to sleep promotion and arousal. Some of its proposed functions are as follows.

1. Maintenance of sleep: During sleep, certain stimuli can be dangerous and require arousal from sleep while others are harmless. The K-complexes function to suppress cortical activity and arousal to maintain sleep when encountered with a stimulus that the brain evaluates as harmless.[6]
2. Arousal from sleep: When the brain interprets a particular stimulus as potentially dangerous, the K-complex has also shown to help in arousal from sleep.[7][8]
3. Memory consolidation: An important proposed function of sleep is to aid in the conversion of short term memory into the long term. The ‘down-state’ produced by the K-complex aids in the function of memory consolidation.[2]
4. Maintenance of synapse homeostasis: The K-complex creates a sort of ‘reboot’ for the neural connections to keep them in homeostasis.[2][9]

Clinical Significance

Though the exact function and clinical significance of the K-complex is still a matter of debate and mystery, some disease states do show documented changes in the waveform.

Alzheimer Disease

The neurocognitive decline in Alzheimer disease based on MMSE scores is associated with a significant decrease in the frequency of K-complexes in the frontal region; this indicates that the neurodegenerative process of Alzheimer disease is maximal in the frontal lobes as well based on the location of K-complex changes.[10] Spontaneous K-complexes also decrease with amnestic mild cognitive impairment and aging.[11]

Insomnia

Given the sleep protective role of the K-complex by inhibiting cortical arousal, the postulate is that they must be reduced in insomnia and is especially associated with increased night-time awakenings. However, in one study, there was no deficiency in the frequency and density of K-complexes in those who have chronic psychophysiological insomnia.[12]

Epilepsy

Since seizures are associated with abnormal neuronal discharges, changes may be seen in the K-complex, too, since it is also a phenomenon of electrical brain activity. Most individuals with primary generalized epilepsy suffer from epileptiform discharges and clinical seizures induced by a faulty arousal system. When a polyspike or spike discharge overlaps on a K-complex, it is termed as an epileptiform K-complex and occurs in focal and generalized epilepsy. The polyspike/spike is more frequent and sharper in generalized epilepsy when compared to a normal epileptiform K-complex. Nocturnal frontal lobe epilepsy is an autosomal dominant disorder in which K-complexes not only increase but are almost always present at the start of a clinical seizure.[13] This presentation is reflective of an unstable sleep condition and suggests a link between K-complexes and epilepsy.[14]

Restless Legs Syndrome

Restless legs syndrome (RLS) is a neurologic, sleep-related movement disorder marked by an uncontrollable urge to move the legs, particularly when they are at rest with partial relief obtained after performing leg movement. Patients with this condition have an increased number of K-complexes, which often precede the leg movement. The dopamine enhancing drugs used to treat it reduce the leg movements but not the K-complexes, which suggests that the movement of the legs occurs secondary to the increased K-complexes, which is the primary event.

Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) is a condition caused by the repetitive collapse of the airway during sleep, which leads to episodes of apnea and hypopnea. When compared with healthy individuals, the K-complex in patients of OSA has shorter durations, smaller amplitudes, and rougher positive waves.[15] In patients with OSA who are on continuous positive airway pressure (CPAP) treatment, researchers observed a significant decrease in the K-complex amplitudes during the night, which is comparable to that seen in normal individuals. Patients with untreated OSA have no similar observable decrease in the K-complex amplitudes as the night progresses. Research has also observed that mild airflow limitation, irrespective of having OSA, leads to an increase in K-complex frequency and the N550 amplitude, which could have implications for sleep time airflow limitations, as seen with snoring as well as OSA.[7]