In this review, two major factors were found to contribute to the high frequency of sleep issues co-occurring with ADHD. The major inducer of sleep disturbance in ADHD patients was found to be explained by the direct effect of the underactivity of the inhibitory pathways within the prefrontal cortex (PFC) of the brain. The underactive PFC directly effects input to the suprachiasmatic nucleus and causes underactivity of the basal forebrain, dampening both major sleep-inducing pathways. Additionally, the prevalence of the evening chronotype genes to be found in 73-78% of ADHD patients further describes an abnormal circadian rhythm seen in these patients. The sleep issues observed in these subjects ultimately causes short sleep and sleep deprivation, resulting in decreased functionality in the patients’ daily lives, regardless of underlying etiology.

In studying the neurological mechanisms through which ADHD and sleep disturbances function, it can be understood how the condition of ADHD can affect sleep directly. It is understood that the major mechanism causative of ADHD symptomatology is a lack of NE, DA and other catecholamines acting in the prefrontal cortex (PFC). These neurotransmitters primarily function to maintain inhibitory functions of the PFC to other areas of the brain. In their absence, the brain struggles to: focus on the understanding and consolidation of important, but not necessarily intuitive information, to block out both internal and external distractions and to inhibit inappropriate behaviors. 11.

Additionally, it has been found that the basal ganglia, an important structure linking the PFC and hypothalamus, is also dysfunctional in ADHD patients13. Pathological support for this understanding is shown in how MRI studies have demonstrated reduced volume in the PFC, basal ganglia, dorsal anterior cingulate cortex, corpus callosum, and the cerebellum in ADHD patients5. Additionally, diffusion tensor imaging (DTI) those with ADHD has revealed evidence of decreased myelination in the axons of these pathways, demonstrating a decrease in the speed of neuronal communication in inhibitory pathways due to low catecholamines5. The basal ganglia function to help facilitate attention based on the processing of important visual cues. Later we will discuss how damage to this region would affect the retino-hypothalamic tract and thus sleep patterns.

There are two major ways through which sleepiness is achieved in the individual, and the induction of these align with light input from the sun s 24-hour cycle resulting in proper circadian rhythm. The primary pathway which aids in sleep includes the suprachiasmatic nucleus (SCN) within the hypothalamus which, when it ceases to be stimulated by light by glutaminergic input through the retino-hypothalamic pathway, ceases to exert GABAergic input to the superior cervical ganglion (SCG), allowing for the SCG to then become active. Norepinephrine release from the SCG then induces melatonin release from the pineal gland, initiating sleepiness3.

Additionally, it is known that sleep is also induced by adenosine release from the basal forebrain which quiets the activity of the midbrain (an arousal center) thus allowing for sleep to occur by helping to turn off the arousal center 11. It is important here to note that the basal forebrain consists of many structures but most importantly, this region contains the medial forebrain bundle 12. The combination of the induction of these two pathways beginning a few hours before bedtime and persisting consistently and in a strong enough manner until sleep occurs, is how one falls asleep.

Underactive input to the hypothalamus from the PFC could directly result in underactivity of the hypothalamus, where the SCN resides. Since it is through a buildup of signals from the PFC to the SCN that the SCN is eventually silenced and melatonin secretion is ultimately induced, underactivity of input from the PFC to the hypothalamus would likely inhibit this sleep-inducing pathway. The underactivity of the PFC would equate to an increased duration of time needed to mount a proper sleep-inducing response from the pineal gland. This is because underactivity of the PFC would translate directly to a lower frequency of signals sent to the hypothalamus and thus increased latency in the time it takes to induce pineal gland activity. This interaction can be observed symptomatically as the increased sleep latency often noted in ADHD patients.

It is known that The ventromedial PFC monitors and inhibits emotions and emotional habits through extensive projections to the amygdala, hypothalamus, and nucleus accumbens, as well as to brainstem nuclei mediating the stress response. 1.So, since the entire PFC is underactive in ADHD due to the lack of proper dopaminergic and catecholaminergic activity, the ventromedial PFC (part of the basal forebrain) is directly understood to be underactive as well. This indicates an effectual underactivity of secretion of adenosine by the basal forebrain to quiet the midbrain, thus hindering the process of the body transitioning from awake to sleep through ceasing of the midbrain activity. Additionally, underactivity of the nucleus accumbens, (part of the basal forebrain) and hypothalamus due to decreased input to the region by the PFC, secondary to global underactivity of the PFC, will further result in a lack of adenosine secreted by the basal forebrain. Thus, further supporting the idea that the arousal signals from the midbrain would fail to be inhibited, furthering the awake state in an individual.

Lastly, dysfunction in the basal ganglia directly as is discussed earlier in this paper in regard to damaged structures seen in the brains of ADHD patients, can influence sleep. Dysfunction in the basal ganglia indicates further dysfunction of the basal forebrain-midbrain pathway resulting in poor sleep through inability to quiet signals of arousal. Additionally, as signal travels through the basal ganglia when coursing through the retino-hypothalamic tract, altered input to the SCN through this tract could cause abnormality in the sleep/wake cycle when there is dysfunction in the basal ganglia.

Research shows that between 73-78% of people with ADHD have the evening chronotype 8. This chronotype causes increased sleep latency and habitually leads to increased short sleep , two sleep issues commonly described by those afflicted with ADHD, leading to chronic sleep debt in these individuals 7. The gene mutations attributed to this chronotype include: 3111C allele on the CLOCK gene, as well as mutations in the PER3 gene while the gene mutations attributed to the ADHD phenotype include chromosomal regions 5p13, 16p13 and 17p11 9. While there is virtually no overlap in the genetic source of each issue, comorbidity of these problems is still high, pointing to a correlation without a common cause, unlike the neurological pathways discussed earlier. 

These two highly comorbid conditions likely impact each other greatly as the exacerbation of one could certainly be understood to worsen the phenotype of the opposing condition. The evening chronotype causes individuals to not be able to fully fall asleep until late into the night with many patients describing the inability to fully fall asleep until about 3-4 am most nights. As the average person s workday starts around 8 am or 9 am, the patient with the evening chronotype is often forced to then wake up from a deep sleep only hours after finally falling asleep, resulting in less restorative sleep. They habitually experience sleep deprivation through consistent nights of short sleep which is all shown to increase mortality in a variety of ways 10. While some may catch up on lost hours of sleep during the weekends, many cannot recover fully from the level of sleep deprivation they experience with such a sleeping pattern. This deprivation of sleep leads to the cognitive and attention difficulties we know result from a lack of sleep which only worsens the already existing impulsivity and attention deficit phenotype seen in ADHD patients.

Furthermore, it is known that many people with the evening chronotype do not experience peak performance in terms of focus and cognitive functioning until later in the day 8. As most jobs require peak functioning in the morning and then allow for a steady decline into the evening, the patient with an evening chronotype is already at a disadvantage before the further deficits from ADHD in this realm of functioning is factored in 8. The anxiety that then comes from the inability to focus at work secondary to ADHD symptomatology further perpetuates the inability to calm racing thoughts in the evening and worsens the ability to sleep. The distraction of stress over the inability to sleep then causes further distraction and exacerbation of ADHD symptoms at work and as such the vicious cycle repeats itself resulting in sleep impairment nightly and attention impairments daily for the patient.