Cookie Preferences
By clicking, you agree to store cookies on your device to enhance navigation, analyze usage, and support marketing. More Info
Thank you! Your submission has been received!
Oops! Something went wrong while submitting the form.
X
Background:
Sleep is more than simple rest. When discussing sleep, we tend to focus on the quantity rather than the quality, how many hours of sleep we get versus the quality or depth of sleep. Duration is an important part of the picture, but understanding the stages of sleep and how certain mental health disorders affect those stages is a crucial part of the discussion.
Sleep is an active mental process where the brain goes through distinct phases of complex electrical rhythms. These phases can be broken down into non-rapid eye movement (NREM) and rapid eye movement (REM). The non-rapid eye movement phase consists of three stages of the four stages of sleep, referred to as N1, N2(light sleep), and N3(deep sleep). N4 is the REM phase, during which time vivid dreaming typically occurs.
Two of the most important measurable brain rhythms occur during non-rapid eye movement (NREM) sleep. These electrical rhythms are referred to as slow waves and sleep spindles. Slow waves reflect deep, restorative sleep, while spindles are brief bursts of brain activity that support memory and learning.
The Study:
A new research review has compiled data on how these sleep oscillations differ across psychiatric conditions. The findings suggest that subtle changes in nightly brain rhythms may hold important clues about a range of disorders, from ADHD to schizophrenia.
The Results:
People with ADHD showed increased slow-spindle activity, meaning those brief bursts of NREM activity were more frequent or stronger than in people without ADHD. Why this happens isn’t fully understood, but it may reflect differences in how the ADHD brain organizes information during sleep. Evidence for slow-wave abnormalities was mixed, suggesting that deep sleep disruption is not a consistent hallmark of ADHD.
Among individuals with autism spectrum disorder (ASD), results were less consistent. However, some studies pointed to lower “spindle chirp” (the subtle shift in spindle frequency over time) and reduced slow-wave amplitude. Lower amplitude suggests that the brain’s deep-sleep signals may be weaker or less synchronized. Researchers are still working to understand how these patterns relate to sensory processing, learning differences, or daytime behavior.
People with depression tended to show reduced slow-wave activity and fewer or weaker sleep spindles, but this pattern appeared most strongly in patients taking antidepressant medications. Since antidepressants can influence sleep architecture, researchers are careful not to overinterpret the changes. Nevertheless, these changes raise interesting questions about how both depression and its treatments shape the sleeping brain.
In post-traumatic stress disorder (PTSD), the trend moved in the opposite direction. Patients showed higher spindle frequency and activity, and these changes were linked to symptom severity which suggests that the brain may be “overactive” during sleep in ways that relate to hyperarousal or intrusive memories. This strengthens the idea that sleep physiology plays a role in how traumatic memories are processed.
The clearest and most reliable findings emerged in psychotic disorders, including schizophrenia. Across multiple studies, individuals showed: Lower spindle density (fewer spindles overall), reduced spindle amplitude and duration, correlations with symptom severity, and cognitive deficits.
Lower slow-wave activity also appeared, especially in the early phases of illness. These results echo earlier research suggesting that sleep spindles, which are generated by thalamocortical circuits, might offer a window into the neural disruptions that underlie psychosis.
The Take-Away:
The review concludes with a key message: While sleep disturbances are clearly present across psychiatric conditions, the field needs larger, better-standardized, and more longitudinal studies. With more consistent methods and longer follow-ups, researchers may be able to determine whether these oscillations can serve as reliable biomarkers or future treatment targets.
For now, the take-home message is that the effects of these mental health disorders on sleep are real and measurable.
Mayeli A, Sanguineti C, Ferrarelli F. Recent Evidence of Non-Rapid Eye Movement Sleep Oscillation Abnormalities in Psychiatric Disorders. Curr Psychiatry Rep. 2025 Dec;27(12):765-781. doi: 10.1007/s11920-024-01544-x. Epub 2024 Oct 14. PMID: 39400693.
Sleep disorders are one of the most commonly self-reported comorbidities of adults with ADHD, affecting 50 to 70 percent of them. A team of British researchers set out to see whether this association could be further confirmed with objective sleep measures, using cognitive function tests and electroencephalography (EEG).
Measured as theta/beta ratio, EEG slowing is a widely used indicator in ADHD research. While it occurs normally in non-ADHD adults at the conclusion of a day, during the day it signals excessive sleepiness, whether from obstructive sleep apnea or from neurodegenerative and neurodevelopmental disorders. Coffee reverses EEG slowing, as do ADHD stimulant medications.
Study participants were either on stable treatment with ADHD medication (stimulant or non-stimulant medication), or on no medication. Participants had to refrain from taking any stimulant medications for at least 48 hours prior to taking the tests. Persons with IQ below 80 or with recurrent depression or undergoing a depressive episode were excluded.
The team administered a cognitive function test, The Sustained Attention to Response Task (SART). Observers rated on-task sleepiness using videos from the cognitive testing sessions. They wired participants for EEG monitoring.
Observer-rated sleepiness was found to be moderately higher in the ADHD group than in controls. Although sleep quality was slightly lower in the sleepy group than in the ADHD group, and symptom severity slightly greater in the ADHD group than the sleepy group, neither difference was statistically significant, indicating extensive overlap.
Omission errors in the SART were strongly correlated with sleepiness level, and the strength of this correlation was independent of ADHD symptom severity. EEG slowing in all regions of the brain was more than 50 percent higher in the ADHD group than in the control group and was highest in the frontal cortex.
Treating the sleepy group as a third group, EEG slowing was highest for the ADHD group, followed closely by the sleepy group, and more distantly by the neurotypical group. The gaps between the ADHD and sleepy groups on the one hand, and the neurotypical group on the other, were both large and statistically significant, whereas the gap between the ADHD and sleepy groups was not. EEG slowing was both a significant predictor of ADHD and of ADHD symptom severity.
The authors concluded, These findings indicate that the cognitive performance deficits routinely attributed to ADHD are largely due to on-task sleepiness and not exclusively due to ADHD symptom severity. We would like to propose a simple working hypothesis that daytime sleepiness plays a major role in cognitive functioning of adults with ADHD. As adults with ADHD are more severely sleep deprived compared to neurotypical control subjects and are more vulnerable to sleep deprivation, in various neurocognitive tasks they should manifest larger sleepiness-related reductions in cognitive performance. One clear testable prediction of the working hypothesis would be that carefully controlling for sleepiness, time of day and/or individual circadian rhythms, would result in substantial reduction in the neurocognitive deficits in replications of classic ADHD studies.
A team of Spanish researchers performed a systematic search of the medical literature and found 28 studies that could be included in a series of meta-analyses of specific measures of sleep impairment. Except for a single meta-analysis with eight studies and 1,713 participants, however, all involved just three to five studies apiece, with anywhere from 121 to just over a thousand participants.
The team examined three sorts of measures:
· Subjective measures, based on self-reporting by ADHD patients.
· Polysomnography is an objective sleep study in which the subject is wired up and studied by technicians in a lab, usually overnight, monitoring multiple body functions, such as brain activity, eye movements, muscle activation, and heart rhythm.
· Actigraphy, a non-invasive objective means of monitoring sleep. The subject wears an actimetry monitor, which is usually worn like a wristwatch on the non-dominant arm. Because it is minimally intrusive, the subject may wear it for a week or more while engaging in normal activities.
In the subjective measures, adults with ADHD generally reported substantially higher sleep impairments than non-ADHD controls. In the largest meta-analysis, covering eight studies and 1,713 participants, adults with ADHD reported moderately longer latency times for falling asleep than controls. In meta-analyses of five studies with between 834 and 1,130 participants, they also reported moderately poorer sleep quality, more frequent night awakenings, being moderately less rested upon awakening in the morning, and moderate-to-strongly greater daytime sleepiness. There was no significant difference in perceived sleep duration.
Polysomnography measures, on the other hand, failed to confirm these subjective impressions. No significant differences were found between adults with ADHD and controls for the initial latency period until onset of sleep, sleep efficiency, waking after the onset of sleep, total sleep time, stage one or stage two sleep, slow-wave sleep, REM (rapid eye movement) sleep, and latency period until REM sleep.
As mentioned above, polysomnography is conducted in lab settings, and therefore inevitably diverges from normal patterns of behavior. Actigraphy helps bridge that gap, by monitoring normal behavior, though with more limited types and precision of data analysis.
And indeed, a meta-analysis of four studies with 222 participants confirmed self-reports that sleep efficiency was moderate to strongly lower in adults with ADHD and that the latency period until the onset of sleep was markedly longer. On the other hand, it found no significant difference in true sleep.
The researchers also looked at prevalence statistics. Whereas the prevalence of sleep-onset insomnia in the general population has been reported in the range of 13 to 15 percent, a meta-analysis of four studies with 466 participants found fully two-thirds of adults with ADHD reporting insomnia, a greater than four-to-one ratio. Similarly, a meta-analysis of three studies with 458 participants found one-third reporting daytime sleepiness, which is twice the rate reported in the general population.
There was no sign of publication bias in any of these results. The authors cautioned, however, about the small number of studies involved, stating this "compromises the generalizability of the findings." Also, some studies included patients undergoing pharmacological treatment for ADHD, "increasing the risk of confounding results."
Moreover, "Sleep onset latency and sleep efficiency were not significantly impaired in the polysomnography, which was incongruent with the actigraphy results. This may be due to a difference in the evaluation context. Whereas polysomnography is considered the gold-standard measure to objectively assess sleep architecture, actigraphy shows a more ecological approach, with the evaluation being conducted in a more naturalistic context for a longer period. However, actigraphy has more environmental influence, which can compromise the data recorded and the interpretation of the results, whereas, in polysomnography, multiple variables can be controlled in the laboratory setting to increase the internal validity of the results. On the contrary, polysomnography studies can produce artifacts due to the unusual circumstances in the setting, so results may need to be interpreted with caution."
The authors concluded, "The results found in the present study show the relevance of addressing sleep concerns in adult populations diagnosed with neurodevelopmental conditions."
We are only beginning to explore how ADHD affects sleep in adults. A team of European researchers recently published the first meta-analysis on the subject, drawing on thirteen studies with 1,439 participants. They examined both subjective evaluations from sleep questionnaires and objective measurements from actigraphy and polysomnography. However, due to differences among the studies, only two to seven could be combined for any single topic, generally with considerably fewer participants (88 to 873).
Several patterns emerged. Looking at results from sleep questionnaires, they found that adults with ADHD were far more likely to report general sleep problems (very large SMD effect size 1.55). Getting more specific, they were also more likely to report frequent night awakenings(medium effect size 0.56), taking longer to get to sleep (medium-to-large effect size 0.67), lower sleep quality (medium-to-large effect size 0.69), lower sleep efficiency (medium effect size 0.55), and feeling sleepy during the daytime(large effect size 0.75).
There was little to no sign of publication bias, though considerable heterogeneity on all but night awakenings and sleep quality.
Actigraphy readings confirmed some subjective reports. On average, adults with ADHD took longer to get to sleep (large effect size 0.80) and had lower sleep efficiency (medium-to-large effect size 0.68). They also spent more time awake (small-to-medium effect size 0.40). There was little to no sign of publication bias and there was little heterogeneity among studies.
None of the polysomnography measurements, however, found any significant differences between adults with and without ADHD. All effect sizes were small (under 0.20), and none came close to being statistically significant.
There were four instances where measurement criteria overlapped those from actigraphy and self-reporting, with varying degrees of agreement and divergence. There was no significant difference in total sleep time, matching findings from both the questionnaires and actigraphy. On percent time spent awake, polysomnography found little to no effect size with no statistical significance, whereas actigraphy found a small-to-medium effect size that did not quite reach significance, and self-reporting came up with a medium effect size that was statistically significant. Sleep onset latency and sleep efficiency, for which questionnaires and actigraphy found medium-to-large effects, the polysomnography measurements found little to none, with no statistical significance.
Polysomnography found no significant differences in stage 1-sleep, stage 2-sleep, slow-wave sleep, and REM sleep. Except for slow-wave sleep, there was no sign of publication bias. Heterogeneity was generally minimal.
One problem with the extant literature is that many studies did not take medication status into account.
The authors concluded, "future studies should be conducted in medicatio- naïve samples of adults with and without ADHD matched for comorbid psychiatric disorders and other relevant demographic variables."
In summary, these findings provide robust evidence that ADHD adults report a variety of sleep problems. In contrast, objective demonstrations of sleep abnormalities have not been consistently demonstrated. More work in medication-naïve samples is needed to confirm these conclusions.
Background:
Sleep is more than simple rest. When discussing sleep, we tend to focus on the quantity rather than the quality, how many hours of sleep we get versus the quality or depth of sleep. Duration is an important part of the picture, but understanding the stages of sleep and how certain mental health disorders affect those stages is a crucial part of the discussion.
Sleep is an active mental process where the brain goes through distinct phases of complex electrical rhythms. These phases can be broken down into non-rapid eye movement (NREM) and rapid eye movement (REM). The non-rapid eye movement phase consists of three stages of the four stages of sleep, referred to as N1, N2(light sleep), and N3(deep sleep). N4 is the REM phase, during which time vivid dreaming typically occurs.
Two of the most important measurable brain rhythms occur during non-rapid eye movement (NREM) sleep. These electrical rhythms are referred to as slow waves and sleep spindles. Slow waves reflect deep, restorative sleep, while spindles are brief bursts of brain activity that support memory and learning.
The Study:
A new research review has compiled data on how these sleep oscillations differ across psychiatric conditions. The findings suggest that subtle changes in nightly brain rhythms may hold important clues about a range of disorders, from ADHD to schizophrenia.
The Results:
People with ADHD showed increased slow-spindle activity, meaning those brief bursts of NREM activity were more frequent or stronger than in people without ADHD. Why this happens isn’t fully understood, but it may reflect differences in how the ADHD brain organizes information during sleep. Evidence for slow-wave abnormalities was mixed, suggesting that deep sleep disruption is not a consistent hallmark of ADHD.
Among individuals with autism spectrum disorder (ASD), results were less consistent. However, some studies pointed to lower “spindle chirp” (the subtle shift in spindle frequency over time) and reduced slow-wave amplitude. Lower amplitude suggests that the brain’s deep-sleep signals may be weaker or less synchronized. Researchers are still working to understand how these patterns relate to sensory processing, learning differences, or daytime behavior.
People with depression tended to show reduced slow-wave activity and fewer or weaker sleep spindles, but this pattern appeared most strongly in patients taking antidepressant medications. Since antidepressants can influence sleep architecture, researchers are careful not to overinterpret the changes. Nevertheless, these changes raise interesting questions about how both depression and its treatments shape the sleeping brain.
In post-traumatic stress disorder (PTSD), the trend moved in the opposite direction. Patients showed higher spindle frequency and activity, and these changes were linked to symptom severity which suggests that the brain may be “overactive” during sleep in ways that relate to hyperarousal or intrusive memories. This strengthens the idea that sleep physiology plays a role in how traumatic memories are processed.
The clearest and most reliable findings emerged in psychotic disorders, including schizophrenia. Across multiple studies, individuals showed: Lower spindle density (fewer spindles overall), reduced spindle amplitude and duration, correlations with symptom severity, and cognitive deficits.
Lower slow-wave activity also appeared, especially in the early phases of illness. These results echo earlier research suggesting that sleep spindles, which are generated by thalamocortical circuits, might offer a window into the neural disruptions that underlie psychosis.
The Take-Away:
The review concludes with a key message: While sleep disturbances are clearly present across psychiatric conditions, the field needs larger, better-standardized, and more longitudinal studies. With more consistent methods and longer follow-ups, researchers may be able to determine whether these oscillations can serve as reliable biomarkers or future treatment targets.
For now, the take-home message is that the effects of these mental health disorders on sleep are real and measurable.
Many studies have shown that ADHD is associated with increased risks of suicidal behavior, substance misuse, injuries, and criminality. As we often discuss in our blogs, treatments for ADHD include medication and non-medication options, such as CBT (Cognitive Behavioral Therapy). While non-drug approaches are often used for young children or mild cases of ADHD, medications – both stimulants and non-stimulants – are common for adolescents and adults.
Global prescriptions for ADHD drugs have risen significantly in recent years, raising questions about their safety and effectiveness. Randomized controlled trials have demonstrated that medication can help reduce the core symptoms of ADHD. However, research from these trials still offers limited or inconclusive insights into wider and more significant clinical outcomes, such as suicidal behavior and substance use disorder.
An international study team conducted a nationwide population study using the Swedish national registers. Sweden has a single-payer national health insurance system, which covers nearly every resident, enabling such studies. The researchers examined all Swedish residents aged 6 to 64 who received their first ADHD diagnosis between 2007 and 2018. Analyses of criminal behavior and transport accidents focused on a subgroup aged 15 to 64, since individuals in Sweden must be at least 15 years old to be legally accountable for crimes or to drive.
The team controlled for confounding factors, including demographics (age at ADHD diagnosis, calendar year, sex, country of birth, highest education (using parental education for those under 25), psychiatric and physical diagnoses, dispensations of psychotropic drugs, and health care use (outpatient visits and hospital admissions for both psychiatric and non-psychiatric reasons).
Time-varying covariates from the previous month covered diagnoses, medication dispensations, and healthcare use. During the study, ADHD treatments licensed in Sweden included amphetamine, atomoxetine, dexamphetamine, guanfacine, lisdexamphetamine, and methylphenidate.
After accounting for covariates, individuals diagnosed with ADHD who received medication treatment showed better outcomes than those who did not. Specifically:
-Suicidal behaviors dropped by roughly 15% in both first-time and recurrent cases.
-Initial criminal activity decreased by 13%, with repeated offences falling by 25%.
-Substance abuse initiation declined by 15%, while recurring substance abuse was reduced
by 25%.
-First automotive crashes were down 12%, and subsequent crashes fell by 16%.
There was no notable reduction in first-time accidental injuries, and only a marginally significant 4% decrease in repeated injuries.
The team concluded, “Drug treatment for ADHD was associated with beneficial effects in reducing the risks of suicidal behaviours, substance misuse, transport accidents, and criminality, but not accidental injuries when considering first event rate. The risk reductions were more pronounced for recurrent events, with reduced rates for all five outcomes.”
.png)
Background:
Pharmacotherapies, such as methylphenidate, are highly effective for short-term ADHD management, but issues remain with medication tolerability and adherence. Some patients experience unwanted side effects from stimulant medications, leaving them searching for alternative ADHD treatments. Alternative treatments such as cognitive training, behavioral therapies, psychological interventions, neurofeedback, and dietary changes have, so far, shown limited success. Thus, there is a critical need for non-pharmacological options that boost neurocognitive performance and address core ADHD symptoms.
First— What Are NIBS (Non-Invasive Brain Stimulation) Techniques?
Non-invasive brain stimulation (NIBS) techniques, including transcranial direct current stimulation (tDCS), transcranial random noise stimulation (tRNS), transcranial alternating current stimulation (tACS), and repetitive transcranial magnetic stimulation (rTMS) are generating growing attention within the scientific community.
NIBS techniques are methods that use external stimulation, such as magnets or electrical currents, to affect brain activity without any invasive procedures. In transcranial alternating current stimulation (tACS), for example, small electrodes are placed on the scalp of the patient, and a weak electrical current is administered.
The theory behind these techniques is that when a direct current is applied between two or more electrodes placed on specific areas of the head, it makes certain neurons more or less likely to fire. This technique has been successfully used to treat conditions like depression and anxiety, and to aid recovery from stroke or brain injury.
The Study:
Previous meta-analyses have produced conflicting indications of efficacy. A Chinese research team consisting of sports and rehabilitative medicine professionals has just published a network meta-analysis to explore this further, through direct comparison of five critical outcome domains: inhibitory control, working memory, cognitive flexibility, inattention, hyperactivity and impulsivity.
To be included, randomized controlled trials needed to have participants diagnosed with ADHD, use sham control groups, and assess ADHD symptoms and executive functions – such as inhibitory control, working memory, cognitive flexibility, inattention, hyperactivity, and impulsivity – using standardized tests.
A total of thirty-seven studies encompassing 1,615 participants satisfied the inclusion criteria. It is worth noting, however, that the authors did not specify the number of randomized controlled trials nor the number of participants included in each arm of the network meta-analysis.
Furthermore, the team stated, “We checked for potential small study effects and publication bias by conducting comparison-adjusted funnel plots,” but did not share their findings. They also did not provide information on outcome variation (heterogeneity) among the RCTs.
Results:
Ultimately, none of the interventions produced significant improvements in ADHD symptoms, whether in inattention symptoms or hyperactivity/impulsivity symptoms. Likewise, none of the interventions produced significant improvements in inhibitory control. Some tDCS interventions enhanced working memory and cognitive flexibility, but details about trial numbers and participants were missing. The team concluded, “none of the NIBS interventions significantly improved inhibitory control compared to sham controls. … In terms of working memory, anodal tDCS over the left DLPFC plus cathodal tDCS over the right DLPFC … and anodal tDCS over the right inferior frontal cortex (rIFC) plus cathodal tDCS over the right supraorbital area ... were associated with significant improvements compared to sham stimulation. For cognitive flexibility, only anodal tDCS over the left DLPFC plus cathodal tDCS over the right supraorbital area demonstrated a statistically significant benefit relative to sham. ... Compared to the sham controls, none of the NIBS interventions significantly improved inattention. ... Compared to the sham controls, none of the NIBS interventions significantly improved hyperactivity and impulsivity.”
How Should We Interpret These Results?
In a word, skeptically.
If one were to read just the study’s abstract, which states, “The dual-tDCS and a-tDCS may be considered among the preferred NIBS interventions for improving cognitive function in ADHD”, it might seem that the takeaway from this study is that this combination of brain stimulation techniques might be a viable treatment option for those with ADHD. Upon closer inspection, however, the results do not suggest that any of these methods significantly improve ADHD symptoms. Additionally, this study suffers from quite a few methodological flaws, so any results should be viewed critically.
_logo%201.svg)
