Exploring the Connection Between ADHD and Sleep Disorders: Pathophysiology, Treatment, and Clinical Implications (2024)

4 DOMAIN CONCEPTUALISATION OF THE LINK BETWEEN ADHD AND SLEEP DISTURBANCES

The 4 Domain Conceptual Model of Interactions of ADHD and Sleep postulates that sleep problems can be causes, effects, or intrinsic features of ADHD. [Hvolby, 2015]

1. Hyperactivity as a Cause of Sleep Problems:

• ADHD leads directly to sleep issues due to hyperactivity, nocturnal motricity, or bedtime resistance.
• This is more common in hyperactive than inattentive ADHD.
• Stimulant treatment can help manage symptoms and improve sleep, though symptom rebound at bedtime is possible.

2. Sleep Problems as a Cause of ADHD Symptoms:

• Disturbed sleep can lead to daytime symptoms and functional impairments characteristic of ADHD.

3. Bidirectional Relationship:

• Sleep disturbances and ADHD may exacerbate each other in a feed-forward loop.
• Children with ADHD are more vulnerable to sleep disturbances, and psychiatric comorbidities can further complicate treatment.
• Poor sleep negatively impacts emotional regulation and attentional functioning, particularly in children with anxiety disorders.

Common Neurobiological Mechanisms:

• ADHD and sleep disturbances may share overlapping neurobiological mechanisms, such as circadian rhythm and sleep/wake disorders.
• There may be a genetic predisposition to sleep dysregulation in ADHD individuals.
• Both ADHD and sleep issues exhibit intra-individual variability, volatility and unpredictability in neuropsychological tasks and sleep patterns.
• One significant finding is that a more rapid decline in sleep duration (which decreases during development) at ages 3–5 has been identified as a significant predictor of subsequent ADHD, suggesting that disruptions in sleep patterns during early childhood could be an early indicator of ADHD. [Scottet al., 2013]

Proposed Diagnostic Subtype – ADHD-SOM:

• Based on the close link between ADHD and sleep dysregulation, some authors have proposed a diagnostic subtype, ADHD-SOM (from ‘Somnus’, Latin for sleep), where sleep disorders significantly contribute to ADHD symptomatology. [Bijlenga et al., 2019]
• Awareness of this diagnostic subtype emphasises the importance of sleep assessment in ADHD assessment to differentiate symptoms caused by sleep issues from those directly related to ADHD.

PATHOPHYSIOLOGY OF SLEEP DYSFUNCTION IN ADHD: AN INTEGRATIVE VIEW

1. Neurobiology of Sleep-Wake Cycles:

Attention-Deficit/Hyperactivity Disorder (ADHD) and sleep disturbances share common neural correlates, including structural changes in the frontoparietal network (FPN), also known as the ventral attention system, and the frontostriatal circuitry.

Additionally, the default mode network (DMN), which is active during rest and mind wandering, is significantly impacted in individuals with ADHD. The DMN mediates ruminations that affect the ability to fall asleep and is further influenced by sleep deprivation.

Neurobiology of Attention Deficit Hyperactivity Disorder (ADHD) – A Primer

Primer on Neurobiology and Neuropsychiatry of Sleep – Application to Clinical Practice

Studies have identified lower grey matter volumes in key brain regions such as the middle frontal gyrus, inferior frontal gyrus, amygdala, striatum, and insula in individuals with ADHD.

These structural changes are associated with ADHD symptoms and sleep dysregulation. It is hypothesised that these alterations mediate the relationship between ADHD and sleep problems through mechanisms involving altered neurotransmitter function and circadian rhythm disruption. [Scarpelli et al., 2019]

Studies have demonstrated that structural alterations in the aforementioned brain regions, particularly reduced grey matter volume, correlate with the severity of ADHD symptoms and the extent of sleep disruptions. [Krause et al., 2017; Shen et al., 2020]

The dorsolateral prefrontal cortex (DLPFC), medial prefrontal cortex (mPFC), and posterior cingulate cortex (PCC) show functional alterations due to inadequate sleep, which may, in turn, exacerbate ADHD symptoms. [Morin et al., 2015]

This suggests that the interplay between brain structure and function is crucial in understanding the link between ADHD and sleep disturbances. [Krause et al., 2017;Shen et al., 2020]

2. Neurotransmitter Systems:

Dopamine and noradrenaline are critical in the regulation of both sleep and wakefulness. Dysregulation of these neurotransmitter systems is a central feature in ADHD, contributing to sleep architecture disturbances and affecting the sleep-wake cycle and circadian rhythms. [Weiss et al., 2015]

Read more about neurotransmitters and sleep.

3. Phenotypic Overlap:

The behavioural, mood, and cognitive manifestations of disrupted or insufficient sleep often mimic the symptoms observed in ADHD.

Both conditions demonstrate hypoarousal and excessive daytime sleepiness, complicating the differentiation and management of ADHD. [Owens et al., 2013]

4. Genetic and Neurobiological Underpinnings:

Research points towards a genetic correlation between ADHD and alterations in circadian rhythm, implicating genes such as CLOCK, BMAL1, and PER2.

These genes are crucial for maintaining circadian rhythm and exhibit altered expression in individuals with ADHD, suggesting a potential genetic basis for the observed disruptions in sleep timing. [Benedetti et al., 2003; Baird et al., 2012]

5. Circadian Rhythms and ADHD:

A substantial proportion of both children and adults with ADHD exhibit a delayed sleep-wake phase disorder, characterised by a pronounced delay in the timing of sleep, wakefulness, and peak alertness times.

The prevalence of Delayed Sleep Phase Syndrome (DSPS) in ADHD is between 26%-78%, which is significantly higher than the general population. [Coogan and McGowan, 2017;Snitselaar et al., 2017; Craig et al., 2017]

External signals, such as light exposure and social rhythms, significantly influence sleep patterns in individuals with ADHD. Disruptions in these external cues can exacerbate the circadian misalignment commonly observed in ADHD, leading to further complications in sleep quality and duration. [Weiss et al., 2015]

6. Visual System and Circadian Regulation:

The visual system plays an important role in regulating circadian rhythms through light perception.

Studies indicate that individuals with ADHD may have unique visual system characteristics, such as reduced visual acuity and a higher prevalence of refractive errors, which could influence light perception and circadian regulation.

Furthermore, the melanopsin-containing intrinsically photosensitive retinal ganglion cells (ipRGCs), which are crucial for light-induced regulation of melatonin and dopamine, may function suboptimally in individuals with ADHD. [Mezer and Wygnanski-Jaffe, 2012; Kim et al., 2014]

This dysfunction might be a key factor in the circadian misalignment observed in many patients with ADHD.

Moreover, retinal dopamine dysfunction, implicated in the neurodevelopmental growth of the eye, could explain the frequent refractive errors observed in this group, further complicating the sensory challenges associated with ADHD. [Bijlenga et al., 2019]

Adults with ADHD show a significant prevalence of light sensitivity, with 69% reporting an oversensitivity to bright light compared to 24% in the non-ADHD population.

This hypersensitivity often leads to extended use of sunglasses, potentially further desynchronising the biological clock from natural daylight cycles, which influences circadian rhythms. [Kooij and Bijlenga, 2014]

SLEEP ARCHITECTURE IN CHILDREN WITH ADHD

A systematic review highlighted that children with ADHD tend to spend more time in the N1 sleep stage—characterised as a lighter, less restorative phase of sleep—compared to neurotypical controls.

This alteration in sleep architecture could contribute to the increased daytime sleepiness observed in this population, suggesting a fundamental alteration in sleep quality and structure that might exacerbate or even mimic ADHD symptoms. [Díaz-Román et al., 2016; Bijlenga et al., 2019]

Examining microstructural EEG signatures has yielded more specific insights, revealing altered slow wave activity (SWA) and theta oscillations in children with ADHD.

The alterations in SWA and theta activity may be indicative of higher sleep pressure, which is thought to reflect a state of chronic sleep deprivation in children with ADHD.

These changes are predominantly observed in frontocentral regions of the brain, suggesting a disruption in the front-limbic circuits, which are crucial for emotional and cognitive regulation. [Díaz-Román et al., 2016]

This correlation supports the hypothesis that chronic sleep debt could play a formative role in the development or exacerbation of ADHD symptoms.

Overall, while there are some distinctions in the sleep architecture of children with ADHD compared to healthy controls (HC), these differences are generally minor. [Díaz-Román et al., 2016]

ADHD, SLEEP AND ADOLESCENCE – DEVELOPMENTAL NEUROBIOLOGY

Adolescence is a crucial period for the maturation of the prefrontal cortex (PFC), during which the development of higher-order cognitive networks is essential for behavioural regulation and executive functioning.

Sleep, a vital component of neurodevelopment, significantly influences the maturation of these cognitive networks. Sleep disruptions, commonly observed in ADHD, can hinder the normal developmental trajectory of the PFC, potentially resulting in prolonged cognitive and behavioural dysfunction. [Anastasiades et al., 2022]

During adolescence, there is a prominent shift in neural connectivity balance from the limbic regions to the PFC.

This shift typically supports the development of emotional regulation and decision-making abilities.

However, in ADHD, sleep deprivation may exacerbate the dominance of limbic influences, thereby delaying or disrupting the maturation of PFC networks.

This limbic predominance is characterised by a reduction in glutamatergic synapse density and heightened limbic connectivity, affecting emotional and behavioural responses. [Mills et al., 2018]

Chronic sleep restriction, increasingly prevalent in modern societies, further complicates the neurodevelopmental landscape during adolescence.

Research indicates that adolescents today sleep significantly less than those a century ago, which has implications for PFC development.

Reduced sleep impairs the PFC’s inhibitory control over the amygdala and diminishes its excitatory drive to the striatum, potentially reversing developmental gains achieved during this critical period. [Matricciani et al., 2012]

Sleep deprivation may thus contribute to the distinctive pattern of brain network interactions observed in ADHD, specifically decoupling the default mode network (DMN) and the frontoparietal network (FPN).

This decoupling results in a weaker negative correlation between these networks, which is necessary for attentional control and thus contributes to the attentional dysfunctions observed in ADHD. [Mills et al., 2018]

SLEEP DISTURBANCES IN ADHD AND ASD

When Autism Spectrum Disorder (ASD) and Attention-Deficit/Hyperactivity Disorder (ADHD) occur together, they tend to produce more significant functional challenges than when either condition exists alone. This compounded effect is particularly evident in sleep disturbances.

Clinically, there is a high incidence of ADHD among patients with ASD who experience sleep disruptions, and similarly, a significant presence of ASD symptoms in those diagnosed with ADHD. Traditionally, these overlapping issues have been managed as separate conditions. [Shanahan et al., 2021]

Neurobiological Mechanisms of Insomnia in Comorbid ADHD and ASD:

Recent hypotheses propose that insomnia in individuals with ASD and ADHD broadly involves:

1. Increased activity of the orexinergic system
2. Reduced activity in the melatonergic systems
3. Reduced activity in the serotonergic systems
4. Decrease in REM sleep phases.

These alterations contribute to dysregulated sleep patterns, manifesting as difficulty initiating and maintaining sleep. [Kohyama, 2016]

1. Circadian Rhythm and Melatonin Dysregulation:

Both ASD and ADHD are associated with disturbances in core circadian clock genes, which may contribute to sleep-wake cycle irregularities observed in these populations.

Abnormalities in Neurexins and neuroligins, synaptic cell-adhesion molecules that mediate trans-synaptic signalling and shape neural network properties, are vulnerability factors in ASD. [Geoffray et al. 2016]

Furthermore, the nocturnal production of melatonin has been shown to be significantly reduced in patients with ASD. [Tordjman et al 2005]

Melatonin levels are decreased in 65% of persons with ASD due to the enzyme acetylserotonin O-methyltransferase (ASMT) dysfunction. An ASMT polymorphism causes up to a 50% drop in melatonin concentration. [Pagan et al., 2017]

Approximately two-thirds of patients with ASD show altered melatonin production, further compounded by abnormal synthesis, concentrations, release patterns, and melatonin metabolism. [Wu et al., 2020]

2. Serotonergic and Orexinergic Dysregulation:

It is proposed that increased orexinergic system activity and reduced 5-hydroxytryptamine activity contribute to prolonged wakefulness and insomnia in autism spectrum disorders and attention-deficit/hyperactivity disorder (ADHD). [Kohyama, 2016]

Prolonged wakefulness has been shown to reduce medial prefrontal cortex activity and disinhibit functional amygdala activity in ASD, leading to further stimulation of wakefulness.

3. Impact of Neurodevelopmental and Immune System Interactions:

Both ASD and ADHD are associated with immunological dysfunction, which contributes to disturbed signalling of intracellular melatonin receptor type 1A and peripheral and central inflammation, which may exacerbate sleep disturbances.

ADHD and Autism Comorbidity: A Comprehensive Review Based on Expert Consensus Recommendations and Latest Research Findings

4. Endocannabinoid System Abnormalities:

Emerging research also points to abnormalities in the endocannabinoid system (ECS) as potentially significant in both ASD and ADHD.

Alterations in the expression of cannabinoid receptor genes (CNR1, CNR2) and CNS changes in regions like the cerebellum, basal ganglia, and hippocampus suggest that ECS dysregulation could influence sleep patterns.

PSYCHIATRIC COMORBIDITIES, ADHD AND SLEEP DYSFUNCTION

The presence of psychiatric comorbidities in individuals with ADHD complicates the clinical picture mediating the relationship between ADHD and sleep dysfunction.

Behavioural problems and symptoms of hyperactivity and inattention typical of ADHD contribute to increased arousal levels, thereby delaying sleep onset. [Cohen et al., 2014]

Moreover, the co-occurrence of anxiety and depression, which are known to affect sleep architecture and latency adversely, results in greater sleep disturbances in ADHD patients with these comorbid conditions compared to those with ADHD alone. [Accardo et al., 2012]

Furthermore, the interrelations between ADHD and other comorbid psychiatric disorders, such as substance abuse and personality disorders, are significant.

These comorbidities are associated with a higher insomnia disorder prevalence. [Fadeuilhe et al., 2021]

SPECIFIC SLEEP DISORDERS IN ADHD

Clinical Phenotypes of Sleep Dysfunction in ADHD:

Sleep disturbances associated with ADHD are heterogeneous, identifying distinct sleep-related phenotypes that mimic conditions like narcolepsy, delayed-onset insomnia, obstructive sleep apnea (OSA), periodic limb movement disorder, and sleep-related epileptiform discharges.

These findings suggest that sleep problems in ADHD patients are not monolithic but vary widely, potentially influencing the choice of treatment strategies. [Miano et al., 2019]

ADHD AND RESTLESS LEGS SYNDROME (RLS)

RLS Diagnostic Criteria: [Walters and Zee, 2023]

1. An urge to move the legs often accompanied by uncomfortable leg sensations. These sensations are often described as “creeping, crawling, tingling, pulling, or painful” feelings deep within the limbs, affecting areas such as the knees, ankles, or even the entire lower limbs. [Trenkwalder et al., 2005]
2. Symptoms are worse at rest, i.e., lying or sitting
3. There is a least partial and temporary relief of symptoms by activity, e.g., walking or stretching or bending the legs
4. Symptoms are worse later in the day or at night
5. Mimics of RLS such as leg cramps and positional discomfort should be excluded by history and physical.
6. Restless Legs Syndrome (RLS) presents as an intense compulsion to move the body in an effort to alleviate uncomfortable sensations, typically experienced when the individual is resting, sitting, or sleeping.

RLS is often associated with insomnia due to the need for continual movement to relieve discomfort.

Studies indicate that up to 44% of children with ADHD experience RLS, and approximately 26% of those diagnosed with RLS exhibit ADHD or symptoms similar to ADHD. [Owens, 2009]

Children diagnosed with both conditions exhibit overlapping symptoms such as alterations in diurnal activities, inattention, mood regulation difficulties, hyperactivity paroxysms, and poor school performance.

Pathophysiology of the association between ADHD and RLS:

From a neurobiological perspective, it is postulated that ADHD and RLS/PLMD may share a common pathophysiology involving dopamine deficiency and low iron stores.

Iron deficiency, frequently associated with ADHD and RLS, is a critical cofactor for tyrosine hydroxylase, the rate-limiting enzyme in dopamine synthesis, directly influencing the dopamine pathway. [Konofal et al., 2010]

The hallmark of RLS is brain iron deficiency, as evidenced by low cerebrospinal fluid (CSF) ferritin levels in RLS patients. [Vlasie et al., 2022]

This deficiency is explained by insufficient iron crossing the blood-brain barrier and inadequate iron import into critical neuronal cells, such as the neuromelanin cells of the substantia nigra.

Iron deficiency can reduce extracellular dopamine levels, the dopamine transporter (DAT), and the D1 and D2 receptors, further affecting dopaminergic transmission.

Dopamine levels are under the regulation of the circadian clock. For instance, in the retina, dopamine synthesis and receptors are adjusted in response to light, and dopamine signalling influences the expression of clock genes. Both MAO-A and Tyrosine hydroxylase are influenced by the circadian clock. Dopamine levels follow a circadian rhythm, with levels tending to be higher during the daytime and decreasing in the evening. [Verwey et al., 2016]

RLS is best conceptualised as a condition involving dysregulation of the circadian rhythm in dopaminergic activity.

Thus, in RLS, the post-synaptic response is adequate for daytime, but at night, the dopaminergic deficit results in the circadian pattern of night-time RLS symptoms, alternating with arousal and alertness in the morning that prevents the expected sleepiness of a fragmented RLS sleep pathophysiology. [Vlasie et al., 2022]

The disruption of sleep caused by RLS can lead to or exacerbate ADHD symptoms, with daytime RLS manifestations such as restlessness and inattention often mirroring those of ADHD.

Additionally, the involvement of the MEIS1 gene in the risk of insomnia may be confounded by its associations with other sleep-related disorders, such as RLS and periodic leg movements during sleep (PLMS). This raises the possibility that reported insomnia linked to MEIS1 may actually be related to underlying conditions like RLS or PLMS rather than primary insomnia.

Restless Sleep Disorder (RSD) in Children: [DelRosso et al., 2022]

Restless Sleep Disorder (RSD) is a new sleep disorder diagnosed in 7.7% of children referred to a pediatric sleep centre and is closely linked to both Restless Legs Syndrome (RLS) and Attention-Deficit/Hyperactivity Disorder (ADHD).

Children with RSD experience frequent nightly movements during sleep for at least three months, resulting in daytime symptoms such as excessive sleepiness, hyperactivity, and irritability.

This disorder shares common features with RLS, including increased sympathetic predominance, NREM sleep instability, and iron deficiency. Additionally, there is a higher prevalence of parasomnias and ADHD in children with RSD.

Severe insomnia with nocturnal hyperactivity may indicate an early expression of undiagnosed or late-diagnosed RLS or RSD itself. [DelRosso et al., 2022]

ADHD AND INSOMNIA

Insomnia – Neurobiology | Pathophysiology | Assessment and Management

Insomnia is a sleep disorder characterised by difficulty falling asleep, staying asleep, or experiencing early-morning awakenings and being unable to return to sleep. [Riemann et al., 2023]

These nighttime sleep difficulties are accompanied by significant daytime problems, such as fatigue, low mood or irritability, and attention or concentration issues. To be diagnosed with insomnia disorder, these symptoms must occur at least several times a week for a period of three months.

Insomnia is particularly prevalent in the ADHD population, affecting 73.3% of children and 66.8% of adults with ADHD, rates significantly higher than those in the general population. [Wajszilber et al., 2018]

Common symptoms of ADHD-related insomnia include prolonged sleep onset, frequent night awakenings, and significant resistance to bedtime.

These issues are often compounded by unhealthy sleep practices and a lack of routines.

Insomnia in ADHD can lead to increased daytime sleepiness and is often associated with other visual and sensory sensitivities, such as an oversensitivity to light, which can further disrupt sleep patterns.

DELAYED SLEEP-WAKE PHASE DISORDER (DSPD) / DELAYED SLEEP PHASE SYNDROME (DSPS) IN ADHD

Delayed Sleep-Wake Phase Disorder (DSWPD), also known as Delayed Sleep Phase Syndrome (DSPS), is commonly associated with ADHD, particularly in adolescents and adults.

This disorder is characterised by a shift in the natural sleep period to a later time, resulting in delayed sleep onset and wake times. [Wajszilber et al., 2018]

DSPS may be associated with a late chronotype, which is common to many patients with ADHD.

This chronotype is associated with a delayed circadian preference and potentially delayed melatonin release, which impacts their sleep-wake cycles.

Besides the biological aspects, poor sleep hygiene and difficulties with impulse control in ADHD can hinder the winding-down process necessary for sleep initiation, leading to resistance at bedtime and delayed sleep onset.

ADHD, NARCOLEPSY AND CATAPLEXY

Patients with narcolepsy exhibit a higher predisposition to ADHD than the general population, suggesting underlying neurobiological links between these disorders. [Wilenius and Partinen, 2020]

There are two primary types of Narcolepsy:

• Type 1 Narcolepsy is diagnosed through the presence of cataplexy and/or significantly low levels of hypocretin.
• Type 2 Narcolepsy is characterised by excessive daytime sleepiness (EDS) without cataplexy and with normal hypocretin levels.

A meta-analysis involving 839 narcolepsy patients reported a pooled prevalence of ADHD at 25%, highlighting a significant difference in prevalence between narcolepsy type 1 (20%) and type 2 (46%).[Ren et al., 2023]

Compared to healthy controls, the odds of having ADHD in the narcolepsy population are dramatically higher (odds ratio 9.59), suggesting an inherent neurobiological linkage.[Ren et al., 2023]

Over 30% of individuals with narcolepsy experience comorbid Attention-Deficit/Hyperactivity Disorder (ADHD), with this comorbidity more pronounced in those without cataplexy (30%) compared to those with cataplexy (15%). [Lecendreux et al., 2015]

Genetic factors link narcolepsy and ADHD, with individuals displaying shorter REM latencies fitting type 2 narcolepsy criteria and often lacking the DQB1*06:02 allele. This suggests a possible subtype within type 2 narcolepsy that includes ADHD and hypersomnia, providing a genetic basis for these clinical manifestations. [Ito et al., 2018]

The overlap in symptoms between ADHD and narcolepsy can lead to diagnostic confusion, as both disorders exhibit features like inattention and impaired executive function.

EDS in children with narcolepsy can present as attention problems, behaviours resembling hyperactivity, and emotional lability, leading to a misdiagnosis of ADHD. [Szabo et al., 2019]

NEUROBIOLOGY OF ADHD AND NARCOLEPSY

Narcolepsy is marked by a loss of hypocretin/orexin (Hcrt/Orx) signalling, which normally inhibits Rapid Eye Movement (REM) sleep during wakefulness.

The absence of this signalling leads to immediate transitions from wakefulness directly into REM sleep, associated with symptoms such as excessive daytime sleepiness (EDS) and fragmented sleep. [Kumar and Sagili, 2014]

Additionally, the lack of adequate excitatory drive to wake-promoting neurons due to the absence of orexins results in reduced arousal and disinhibition of sleep-promoting pathways, contributing further to the sleep disturbances observed in narcolepsy.

The neurobiological framework of narcolepsy and ADHD extends to the functionality of dopaminergic (DA) neurons in the ventral tegmental area (VTA) and the dorsal raphe (DR) nucleus, which have important implications for sleep/wake regulation. [Szabo et al., 2019]

VTA DA neurons, which form the crux of the mesolimbic pathway and project to forebrain structures like the nucleus accumbens, play a vital role in reward processing and cataplexy.

These neurons also influence the activity of serotoninergic (5-HT) neurons in the Dorsal Raphe (DR) and noradrenergic (NA) neurons in the locus coeruleus (LC).

DA is a precursor for NA synthesis, and LC neurons have recently been documented to release DA and NA.

Restful REM sleep is characterised by a phenomenon known as NA time out, achieved through silencing of the locus coeruleus (LC).

During REM sleep, monoaminergic neurons such as 5HT (serotonin), histamine (HA), noradrenaline (NA), and orexin are silenced, while dopamine (DA) neurons remain active and contribute to the dreaming that occurs in REM sleep. Dopamine, via activation of D2 receptors, plays an important role in modulating REM sleep by inhibiting NA neuron activity through autoinhibitory α2-adrenoceptors. [Takeuchi et al., 2016]

Understanding the stimulatory and inhibitory interactions among DA, NE, and 5-HT neurons is crucial for addressing narcolepsy symptoms, particularly excessive daytime sleepiness (EDS) and cataplexy.[Szabo et al., 2019]

Cataplexy and ADHD:

Cataplexy, a hallmark of narcolepsy, particularly type 1, where orexin (hypocretin) deficiency is evident, is characterised by sudden, transient episodes of muscle weakness triggered by strong emotions.

During wakefulness, orexin is critical in stimulating various neuron groups, including monoaminergic neurons and the ventrolateral periaqueductal grey/lateral pontine tegmentum (vlPAG/LPT).

These systems, in turn, exert inhibitory control over the sublaterodorsal nucleus (SLD), preventing muscle atonia during REM sleep by activating GABAergic pathways in the ventromedial medulla and spinal cord.

However, during REM sleep, inhibition of the vlPAG/LPT occurs due to the action of melanin-concentrating hormone (MCH) and other neurotransmitters. This leads to the activation of SLD neurons, causing the release of GABA and glycine, which induce atonia by inhibiting motor neurons.

In the context of cataplexy, the loss of orexinergic neurons means that vlPAG/LPT and GABAergic inputs can no longer effectively inhibit the SLD to prevent atonia.

This results in unchecked activation of atonia-producing pathways during emotional triggers, leading to the sudden loss of muscle tone characteristic of cataplexy.

Emotional stimuli, particularly positive emotions, activate the medial prefrontal cortex (mPFC), stimulating GABAergic projections in the central amygdala (CeA). These projections inhibit noradrenergic centres like the locus coeruleus (LC) and the vlPAG/LPT, promoting muscle atonia via disinhibition of the SLD.

In non-narcoleptic individuals, orexin neurons typically maintain muscle tone by exciting these regions and preventing SLD disinhibition.

ADHD AND OBSTRUCTIVE SLEEP APNOEA (OSA)

Sleep-disordered breathing (SDB), prevalent among individuals with ADHD, affects psychological outcomes through various mechanisms, including hypoxic insults, stress/inflammation in the brain, and repeated arousal-based sleep disruptions.

Research indicates a robust link between Obstructive Sleep Apnea (OSA) and Attention-Deficit/Hyperactivity Disorder (ADHD), particularly in childhood.

A history of snoring or potential OSA during childhood is associated with a twofold increase in the likelihood of an ADHD diagnosis or symptoms. [Constantin et al., 2014]

Moreover, OSA is hypothesized as one of five sleep phenotypes associated with ADHD, alongside hyperarousal, delayed sleep onset insomnia, restless legs syndrome/periodic limb movements during sleep, and sleep EEG epileptiform discharges. [Miano et al., 2019]

These mechanisms can affect prefrontal cortex functioning, leading to neurobehavioral deficits that underpin ADHD symptoms.

Elevated levels of high-sensitivity C-reactive protein (hsCRP) observed in children with OSA [Gozal et al., 2006] suggest that hsCRP testing may be useful for monitoring the development of neurocognitive deficits in this group. [Chang and Chae, 2010]

Pathophysiological link between OSA and ADHD:

ADHD and OSA exist in a reciprocal relationship where each condition exacerbates the symptoms of the other. Attention deficits are reported in up to 95% of pediatric OSA patients. [Nguyen-Ngoc-Quynh et al., 2023]

The connection between ADHD and Obstructive Sleep Apnea (OSA) involves several key factors affecting upper airway patency:

1. Central Ventilatory Drive: Increased during childhood, leading to stronger upper airway reflexes and less collapsibility compared to adults. This drive declines with age.
2. Obstructive Hypoventilation: Children exhibit a pattern of obstructive hypoventilation rather than the cyclic obstructions seen in adults.
3. Arousal Threshold: Higher in children, making them less likely to wake from upper airway obstruction, preserving sleep architecture but masking OSA symptoms.
4. Nasal Mucosal Edema: Allergic rhinitis can increase nasal resistance, exacerbating sleep-breathing disorders.
5. Untreated OSA Consequences: Can lead to neurobehavioral issues (overlapping with ADHD symptoms), cardiovascular problems, and growth impairments. [Chang and Chae, 2010]
6. REM Sleep and Apnea: Higher apnea-hypopnea indices during REM sleep correlate with more nightmares, which improve with positive airway pressure therapy. ADHD, often comorbid with insomnia, leads to frequent nocturnal awakenings and negative dreams. [Siclari et al., 2020]
7. Neuromuscular Control: Neuromuscular control of the upper airway is crucial in OSA. The genioglossus muscle, an important upper airway dilator, is innervated by the hypoglossal motoneuron. Neurotransmitters such as noradrenaline and serotonin excite orofacial motoneurons, including those that innervate upper airway muscles. The genioglossus muscle, crucial for upper airway patency, is less active during sleep due to reduced noradrenaline and serotonin, leading to airway hypotonia. Animal models have shown these neurotransmittersto reduce their activity during slow-wave sleep and cease firing during REM sleep, contributing to sleep-related upper airway hypotonia.

DIAGNOSIS AND MANAGEMENT OF SLEEP DISORDERS IN ADHD

Read more on the assessment of Insomnia.

1. Sleep History: The 3P model [Spielman et al., 1987] can help the clinician focus on a sleep history

• Predisposing Factors: Genetic and personality traits that contribute to physiological and cognitive hyperarousal.
• Precipitating Factors: Immediate triggers such as grief or significant stressors.
• Perpetuating Factors: Conditions or habits that maintain insomnia, such as poor sleep hygiene.

2. Diagnosis and Clinical Evaluation:

• Onset of the Problem: Whether acute or chronic.
• Duration and Severity: Both subjective and objective measures.
• Pattern of Insomnia: Constant or episodic, with details on frequency and any seasonal or situation-specific variations.
• Impact: Effects on behaviour, mood, cognitive functioning, and academic or occupational performance.

3. Nature of Sleep Disturbance:

• Sleep Onset Latency: Difficulty falling asleep.
• Sleep Architecture: Time in bed, duration of sleep, number and duration of awakenings, morning wake time, and any changes in sleep timing.
• Symptoms: Daytime napping, sleepiness, restlessness, leg discomfort, nightmares, unusual behaviours at night, night terrors, sleep paralysis, and breathing difficulties.

4. Additional Contributing Factors:

• Diet and Substance Use: Influence of food timing, caffeine, allergies, alcohol, and illicit substances.
• Lifestyle and Environment: Effects of travel, jet lag, shift work, sleep-interfering behaviours, and sleeping environment (noise, light, temperature).

5. Comorbidities:

• Physical and Mental Health Issues: Assessment of physical illnesses (like pain, cardiac or respiratory conditions) and mental health issues (such as depression and anxiety).
• Medications: Review of all medications, including those potentially causing insomnia.

6. Psychosocial Factors:

• Stressors and Lifestyle: Examination of life stressors, late-night responsibilities, and social obligations.

7. Risk Assessment:

• Safety Concerns: Assess risks such as sleepiness while driving or operating machinery.

8. Tools for Assessment:

Children:

• Bespoke sleep diary (1-week minimum).
• Sleep Disturbance Index (SDI): a four-item, parent-rated questionnaire that covers settling problems, night waking and parental involvement at night.
• Children’s Sleep Habits Questionnaire (CSHQ): a 45-item, parent-rated questionnaire that assesses the frequency of behaviours associated with common paediatric sleep disorders.
• Paediatric Daytime Sleepiness Scale (PDSS): a self-report questionnaire designed to assess sleepiness in 11- to 15- year-olds.

Adults:

• Bespoke sleep diary (1 week minimum).
• Epworth Sleepiness Scale (ESS): a self-administered questionnaire with eight questions. Respondents are asked to rate, on a four-point scale (0–3), their usual chances of dozing off or falling asleep while engaged in eight different activities.
• Pittsburgh Sleep Quality Index (PSQI) is a self-report questionnaire that assesses sleep quality over a one-month period.
• STOP-Bang Questionnaire: an eight-item questionnaire that determines the risk for sleep apnoea. It is one of the most widely accepted screening tools for obstructive sleep apnoea.
• Morningness–Eveningness Questionnaire (MEQ): a self-assessment questionnaire to measure whether a person’s circadian rhythm (biological clock) produces peak alertness in the morning, in the evening or in between.

9. Objective Evaluation Tools:

Actigraphy:

• Actigraphy is a wrist-worn device that records movement and employs an algorithm to estimate sleep and wake periods.
• It has satisfactory reliability with the “gold standard” polysomnography in good sleepers who spend little time awake and still but not in those with sleep difficulties where significant periods of waking stillness occur. It is often combined with a light sensor to estimate the latency from lights out to sleep onset.
• Actigraphy can be useful for a patient whose sleep history is unreliable or when circadian disorders are suspected.

Personal Monitoring devices:

• Commercial devices measuring sleep are available but do not accurately reflect sleep architecture, efficiency, or latency and tend to overestimate sleep duration in normal sleepers.
• They are not recommended to make clinical decisions until rigorous studies are conducted.

Polysomnography (PSG): [Rundo and Downey, 2019]

• The gold standard to measure sleep objectively
• Considered to be the gold standard for diagnosing sleep-related breathing disorders, which include obstructive sleep apnea (OSA), central sleep apnea, and sleep-related hypoventilation/hypoxia.
• It can also be used to evaluate for other sleep disorders, including nocturnal seizures, narcolepsy, periodic limb movement disorder, and rapid eye movement sleep behaviour disorder.
• It can be helpful to rule out other possible explanations for poor sleep, such as sleep apnea or periodic leg movement disorder.

10. Treatment Evaluation:

• Treatment History and Response: Review past and current treatments, including effectiveness and patient satisfaction.
• Future Management Plans: Strategies based on comprehensive evaluation and risk assessment.

MANAGEMENT OF INSOMNIA IN ADHD

General Principles:

1. Monitoring and Medication Review:

• Monitoring Insomnia: Observe if insomnia associated with stimulants may attenuate after 1–2 months. [Lecendreux and Cortese 2007]
• Consider if it is possible to stop the medication or reduce the stimulant dose.
• Switching to an alternative class of stimulant
• Switching to an alternative stimulant formulation.

Behavioural and Lifestyle Modifications:

• Implementing consistent sleep hygiene and behavioural measures to promote better sleep.
• Assess and review the possible underlying causes of sleep problems, including environmental and lifestyle factors.

Treatment Strategies:

• Treat specific sleep-related disorders such as Restless Legs Syndrome (RLS).
• Add small, short-acting stimulant doses in the early evening if a rebound effect occurs.
• Consider the use of non-stimulant options like atomoxetine for managing ADHD without exacerbating sleep issues.

4. Supplemental Approaches:

• Evaluate the appropriateness and potential benefits of using melatonin to aid sleep.

PSYCHOLOGICAL AND NON-MEDICATION STRATEGIES FOR MANAGING SLEEP DISTURBANCES IN ADHD

Psychoeducation

• Psychoeducation to patients and their families about the importance of sleep and how it affects health and behaviour.
• Information provided includes the impact of sleep deprivation and the benefits of regular sleep patterns.
• Educators emphasise the role of the bedroom as a sleep-only environment, advocating for eliminating all non-sleep activities to strengthen the psychological association between the bedroom and sleep.

Educational Sessions

• Provide practical strategies on sleep hygiene and relaxation techniques.
• Interactive sessions allowing caregivers and adolescents with ADHD to engage actively with the material, apply it in real-time, and discuss challenges and successes.
• Homework assignments reinforcing these strategies, ensuring that lessons extend beyond the clinical setting into daily routines, thereby improving sleep latency and efficiency significantly. [Loring et al., 2018; Cortesi et al., 2012]

Sleep Hygiene

Sleep hygiene practices are customised to individual needs, focusing on establishing a conducive sleeping environment.

Key strategies include:

• Consistent sleep and wake times
• Using the bed for sleep only
• Control of environmental factors such as light, noise, and temperature.
• Patients are advised to leave the bedroom if unable to sleep within 15 minutes, engaging in a quiet activity until feeling sleepy. This method helps prevent the frustration associated with insomnia from compounding, promoting a healthy sleep-wake cycle.

Behavioural Interventions

Behavioural interventions for insomnia in ADHD include techniques like graduated extinction, where disruptive behaviours are ignored for a predetermined period to discourage them, and bedtime fading, which involves setting a later bedtime initially that gradually moves earlier.

While effective in establishing sleep routines, these strategies often need more direct impacts on ADHD symptoms, highlighting the necessity for a multifaceted approach in treatment plans. [Mindell et al., 2006; Vriend and Corkum, 2011]

Addressing circadian rhythm disruptions in ADHD can involve multiple approaches, including the use of light therapy to advance the circadian phase, sleep hygiene measures, and pharmacological interventions like melatonin supplementation. [Kooij and Bijlenga, 2013]

Ball Blankets

Ball blankets, designed with loose balls that apply gentle pressure across the body, stimulate sensory receptors that promote relaxation and sensory integration.

Studies have demonstrated that using ball blankets at bedtime can significantly reduce sleep onset latency and minimise night-time awakenings in children with ADHD, offering a non-invasive method to enhance sleep quality. [Hvolby and Bilenberg 2011]

Chronotherapy

• Chronotherapy is tailored to adjust the internal biological clock through strategic exposure to light and the use of melatonin supplements.
• It involves administering low-dose melatonin in the late afternoon or early evening to advance the sleep phase or using bright light therapy in the morning to delay it, depending on the specific circadian rhythm disorder being treated.
• This approach has been shown to be effective in synchronising sleep patterns with natural environmental cues, thereby improving both sleep quality and daytime alertness. [Kooij and Bijlenga 2013; Burgess and Emens, 2016]

Light Therapy

• Light therapy involves using a 10,000-lux light box to mimic natural sunlight, which helps regulate melatonin production and manage circadian rhythm disorders.
• Sessions typically occur in the morning to help advance delayed sleep phases or in the evening to treat advanced sleep phases.
• This method not only helps in adjusting sleep times but also contributes to the reduction of ADHD symptoms by stabilising daily rhythms. [Fargason et al., 2017; Rybak et al., 2006]

Neurofeedback

• Neurofeedback targets specific brain wave frequencies to enhance sleep quality. Using sensorimotor rhythm (SMR) neurofeedback, practitioners aim to increase the density of sleep spindles—a type of brain wave associated with tranquil sleep and sensory shielding from external stimuli.
• This approach has been shown to decrease sleep latency, increase total sleep time, and, importantly, normalise sleep onset.
• Long-term benefits include improved attention and cognitive functions in individuals with ADHD, demonstrating the broad impact of well-regulated sleep on overall health. [Sterman et al., 1970; Hoedlmoser et al., 2008; Arns et al., 2014a]

Neurofeedback and The Role of Sleep in Psychiatric Disorders – Dr. Martjin Arns

ADHD Treatment via QEEG-Informed Neurofeedback Treatment Stratification and Predictors of Response: Awaiting Multi-Centre Replication

CBT-I

Cognitive Behavioural Therapy for Insomnia (CBT-I) has demonstrated efficacy in improving self-rated insomnia severity, sleep onset latency, wake time after sleep onset, and even daytime symptoms in patients with insomnia without psychiatric comorbidities. It is effective both in conventional settings and when administered via the Internet. [Hertenstein et al., 2022]

However, there is a gap in evidence-based CBT specifically tailored for individuals with ADHD.

Although proof of principle exists for CBT in children with ADHD, typically developing adolescents, and adults with ADHD experiencing sleep problems, these interventions often do not comprehensively address the multifaceted sleep difficulties seen in ADHD.

The newly developed CBT-i/ADHD protocol represents a tailored behavioural treatment that integrates classic CBT-i principles with modifications to better suit individuals with ADHD.

This approach has been shown to significantly reduce insomnia severity.

There was also a modest improvement in ADHD symptoms noted three months post-treatment. The protocol has proved feasible in clinical settings, suggesting its potential for broader clinical application. [Jernelöv et al., 2019]

Another initiative, the Sleep IntervEntion as Symptom Treatment for ADHD (SIESTA) project, was specifically designed for adolescents with ADHD to tackle their sleep challenges.

This blended CBT sleep intervention aims to enhance sleep quality, reduce ADHD symptoms, and address related difficulties. A protocol has been outlined for a randomised controlled trial to validate its efficacy and applicability in real-world settings. [Keuppens et al., 2023]

PHARMACOTHERAPEUTIC INTERVENTIONS

The relationship between ADHD medications and sleep is complex, requiring thorough evaluation before starting treatment.

Effects of Stimulants on Sleep:

ADHD pharmacotherapy often significantly impacts sleep patterns, as these medications can alter sleep latency, total sleep time, and overall sleep architecture. Thus, they can improve and worsen sleep architecture.

Guidelines suggest a detailed assessment of sleep before initiating any ADHD medication regimen due to these potential impacts. [Graham et al., 2011; Wolraich et al., 2011]

In patients with ADHD, stimulants are often associated with disrupted sleep, including difficulties in sleep onset and decreased overall sleep duration. [Hvolby, 2015]

However, there is also evidence that stimulants can sometimes paradoxically calm patients, improving sleep. [Hvolby, 2015]

Clinical experiences also suggest that careful management of dosing times and formulations can mitigate some adverse sleep effects, with an additional dose of a short-acting stimulant in the evening sometimes beneficial to counteract symptom rebound as drug concentrations wane. [Carlson and Kelly, 2003; Cortese et al., 2013]

Long-acting stimulants like osmotic-release oral system methylphenidate (OROS-MPH) and lisdexamfetamine (LDX) offer the benefits of smoother drug levels throughout the day, which can help minimise sleep disturbances.

Evidence also suggests that adults with ADHD on stable treatment had lower rates of insomnia disorder compared to those untreated. [Fadeuilhe et al., 2021]

Effect of Methylphenidate on Sleep:

In clinical settings, immediate-release methylphenidate has been reported to increase sleep onset latency and decrease total sleep time, with varied effects on sleep quality across studies. [Boonstra et al., 2007; Sangal et al., 2006]

OROS-MPH combines immediate and extended-release mechanisms to maintain a steady therapeutic level, reduce night-time awakenings, and positively influence sleep stage distributions. [Kim et al., 2010; Lee et al., 2012]

Polysomnographic studies have documented that OROS-MPH reduces the number of night-time awakenings and increases the proportion of stage 2 sleep, compared to baseline measurements before treatment initiation. [Kim et al., 2010]

Evidence also suggests that sleep quality is maintained in children with ADHD taking OROS-MPH. [Wolraich et al., 2001]

Long-term observations further support these outcomes, with parental reports indicating sustained good to excellent sleep quality after one and twelve months of ongoing OROS-MPH treatment. [Wilens et al., 2003]

However, the effects in the short term may differ. Sleep diaries maintained by parents indicate that OROS-MPH, along with another extended-release methylphenidate formulation, markedly decreases total sleep time within the first one to four weeks post-treatment initiation. [Lee et al., 2012]

Effect of Amphetamines on Sleep:

Lisdexamfetamine (LDX) does not appear to affect sleep quality or quantity adversely based on objective sleep measures in both adults and children diagnosed with ADHD. [Adler et al., 2009a; Surman and Roth, 2011]

Modifications in dosing or switching to different stimulant formulations, such as extended-release versions, have been used to reduce these adverse effects. [Konofal et al., 2010]

Effect of Non-stimulant ADHD medication on Sleep:

Non-stimulant medications such as atomoxetine and guanfacine typically induce somnolence, which can be strategically utilised by dosing in the evening to minimise daytime sleepiness and potentially improve nocturnal sleep quality. [Block et al., 2009; Garnock-Jones and Keating, 2009]

Atomoxetine, for instance, has been shown to have a less disruptive effect on sleep architecture compared to stimulants, causing fewer instances of insomnia and a higher frequency of somnolence. [Sangal et al., 2006; Dittmann et al., 2013]

Atomoxetine, commonly used for ADHD, shows improved tolerability when dosed in the evening, effectively reducing daytime somnolence. [Block et al., 2009]

Others:

Off-label use of hypnotic agents like zolpidem, mirtazapine, trazodone, and antihistamines is prevalent in treating insomnia in children with ADHD. However, such practices are not universally endorsed in clinical guidelines.

Additionally, clonidine is suggested for managing stimulant-associated sleep onset delays, typically in its immediate-release form, to avoid exacerbating sleep disturbances. [Prince et al., 1996; Wilens et al., 1994]

Clonidine has been shown to significantly improve subjective sleep quality, sleep latency, and sleep disturbances in children and adolescents with sleep difficulties. This effect is particularly pronounced in children and adolescents with ADHD. [Jang et al., 2022]

SPECIFIC STRATEGIES:

Melatonin Supplementation:

• Melatonin is recognised for its utility in managing circadian rhythm disruptions commonly seen in ADHD patients.
• Similarly, melatonin has gained recognition for its efficacy in improving sleep quality in individuals with ASD and ADHD.
• Complementing melatonin with cognitive behavioural therapy (CBT) has been shown to enhance sleep duration further and decrease sleep onset latency. [Maras et al., 2018]
• Supplementation has been shown to improve sleep onset latency, efficiency, and overall sleep duration, particularly in pediatric populations with ADHD. [Maras et al., 2018]
• Low doses of melatonin (1 mg) can increase Total Sleep Time (TST) in children and adolescents with ADHD receiving treatment with psychostimulants with an adequate tolerability profile.[Checa-Ros et al., 2023]
• In adults, melatonin may be considered a first-line treatment for shifting sleep time, using lower doses 4–6 hrs before bedtime to establish biological evening and/or higher doses before bedtime for sleep initiation. [Surman and Walsh, 2021]

While this article does not focus on ASD and sleep dysfunction, recommendations for melatonin use in ASD and comorbid ADHD can be extrapolated to clinical practice. [Petti et al., 2023]

• For children with difficulty initiating sleep, immediate-release melatonin, 1–3 mg, administered 30 minutes before bedtime, is recommended. The same dose of sustained-release melatonin is advised for children struggling to maintain sleep.
• When used as a chronobiotic, melatonin should be given 3–4 hours before sleep.
• Consensus-determined doses for melatonin are 1–2 mg for children aged 3–5, 2–3 mg for children aged 6–12, and up to 5 mg for adolescents and adults. When melatonin efficacy wanes, switching brands or lots is advised, with pharmaceutical-grade melatonin being preferred when available.
• Although generally safe, melatonin was the most frequently ingested substance reported to poison control centres by youth aged ≤19 years in 2020, highlighting the importance of cautious use and monitoring.

Iron supplementation in RLS:

Iron therapy is beneficial for treating Restless Leg Syndrome in ADHD, improving both sleep quality and ADHD symptoms due to enhanced dopamine neurotransmission. [Trotti and Becker, 2019; Konofal et al., 2008]

Oral iron supplementation for 12 weeks should be considered for patients with RLS with low ferritin levels (<75 μg/l) and transferrin saturation <45%.

A drop in serum ferritin is seen only in 10-20% of patients with RLS. [Manconi et al., 2021]

An updated algorithm considered intravenous administration of ferric carboxymaltose if transferrin saturation was <45%, and one of the following: [Manconi et al., 2021]

• Serum ferritin concentration <100 μg/l and a more rapid response than that with oral iron is desired
• Oral iron cannot be adequately absorbed owing to gastrointestinal disorders, bariatric surgery or chronic inflammatory conditions.
• Oral iron is not tolerated.
• RLS does not improve despite an adequate trial of oral intake of iron.

Treatment of children with RLS with dopamine agonists has been shown to result not only in improved sleep quality and quantity but also in improvement in “ADHD” behaviours previously resistant to treatment with psychostimulants.[Vlasie et al., 2022]

Key Principles in the Treatment of RLS:

Treatment guidelines for Restless Legs Syndrome (RLS) recommend starting therapy with low doses of dopamine agonists or α2δ ligands, such as pregabalin, in severe cases. Dopamine’s circadian rhythm, which increases in the morning and decreases in the evening and night, complicates treatment.

Administering low doses of dopamine at night may provide initial relief but can lead to a “slippery-slope” effect, where increasing doses are required to achieve the same effect, ultimately worsening the underlying pathology due to receptor downregulation and augmentation. [Vlasie et al., 2022]

Dopaminergic agents like levodopa, pramipexole, ropinirole, and rotigotine temporarily enhance dopamine’s effect on postsynaptic receptors but also contribute to the irreversible reduction of dopamine receptors. [Zeng et al., 2023]

Overall, the downregulation of inhibitory D3Rs and upregulation of excitatory D1Rs seem to contribute to the augmentation of RLS.

This results in tolerance and worsened daytime symptoms, leading to dependence on medication.

Long-acting medications, such as transdermal rotigotine, are recommended to reduce the risk of augmentation. Additionally, using low doses of medication helps minimise the augmentation effect, making dopamine therapy a limited but necessary option for managing RLS. [Zeng et al., 2023]

Sleep Breathing Disorders:

Surgical interventions, such as the removal of adenoids or tonsils, are recommended as first-line treatments for children with Sleep Disordered Breathing (SDB).

Treatment such as adenotonsillectomy is commonly used for pediatric OSA and has been shown to improve ADHD symptoms significantly. [Urbano et al., 2021]

Adults with Obstructive Sleep Apnea (OSA) may benefit from the use of positive airway pressure devices, oral appliances, or surgical solutions.

A recent trial showed that Solriamfetol, a selective dopamine and noradrenaline reuptake inhibitor approved in the USA as a treatment for excessive daytime sleepiness (hypersomnia) associated with narcolepsy and obstructive sleep apnoea (OSA) in adults, may also be a novel and effective option for managing ADHD in adults, further supporting the connection between the two conditions. [Surman et al., 2023]

Delayed Sleep Phase Syndrome (DSPS):

Treatments for individuals with Delayed Sleep Phase Syndrome (DSPS) include light therapy and chronotherapy to adjust the sleep-wake cycle, supplemented by timed melatonin administration to facilitate sleep onset and synchronisation of circadian rhythms.

For delayed sleep phase syndrome in children and adolescents: Lower doses, typically 0.2 mg to 0.5 mg, are administered 6 to 8 hours before the desired bedtime. [Rana et al., 2021]

In adults, evidence suggests that chronotherapy with melatonin (0.5 mg/day) can advance the dim-light melatonin onset (DLMO) by 1.5 hours and reduce ADHD symptoms by 14%. However, combining melatonin with bright light therapy (BLT) advances the DLMO by 2 hours without affecting ADHD symptoms, indicating that behavioural coaching is necessary to improve sleep timing and further alleviate ADHD symptoms. [van Andel et al., 2022]

NEUROMODULATION

Repetitive transcranial magnetic stimulation (rTMS) shows promise as a non-pharmacological therapy to improve sleep disorders in preschool-aged children with ADHD. [Yilin et al., 2023]

Interventions such as transcranial direct current stimulation (tDCS) during NREM sleep may enhance slow frontal oscillations, improving declarative memory performance and behavioural inhibition in children with ADHD.

These findings propose a promising avenue for targeted interventions that address both sleep disturbances and cognitive deficits associated with ADHD. [Díaz-Román et al., 2016]

CONCLUSION

Sleep, an indispensable aspect of human life, constitutes about one-third of our existence and is crucial for maintaining optimal physical and psychological health. The consequences of chronic sleep deprivation are severe, increasing the risk of psychiatric illnesses, diabetes, cardiovascular diseases, and stroke.

This is particularly pertinent in populations with neurodevelopmental disorders such as attention-deficit hyperactivity disorder (ADHD), where the prevalence of sleep disorders significantly exceeds that of the general population.

ADHD is associated with a diverse spectrum of sleep disorders, which complicates the diagnosis and management of ADHD.

While this article primarily focuses on ADHD and sleep disorders, it’s essential to acknowledge the significant overlap with Autism Spectrum Disorder (ASD). We will cover the specifics of ASD and sleep disorders in another article.

By integrating knowledge from sleep medicine into routine psychiatric practice, clinicians can offer integrated care to their patients, ultimately leading to better health outcomes.