W5: Insomnia, sleep and mental health and Respiratory control & panic disorder

What is Insomnia Disorder and how is it diagnosed?

Insomnia Disorder involves difficulty initiating or maintaining sleep, or waking too early, despite adequate opportunity. Diagnosis requires ≥3 nights per week for ≥4 weeks plus daytime impairment (fatigue, cognitive difficulty, low mood) and distress about sleep. SOL or WASO >30 minutes typically indicates clinically significant sleep disturbance.

Describe the relationship between insomnia and mental health.

Insomnia and mental health are bidirectionally linked: insomnia increases risk for future depression and anxiety, while psychiatric disorders frequently include insomnia symptoms. Around 50% of individuals with mental health disorders experience insomnia. If you have insomnia and go to work, there is loss in productivity and money.

What evidence supports hyperarousal as a mechanism underlying insomnia?

Insomnia involves 24-hour hyperarousal, shown through the eeg and MSLT. If they cant fall asleep every 2 hour sleep opportunity in 24 hours, they are hyper aroused. EEG shows increased high power frequency during NREM (beta) and REM; event-related potentials reveal greater sensitivity to auditory stimuli. Subjectively perceived high cognitive activity like a racing mind.

What is hyper arousal in terms of insomnia?

Increased sympathetic autonomic response to stress.

What are some types of elevated physiological arousal symptoms/

Physiologically, individuals show elevated heart rate, increased sympathetic activation, reduced HR variability, higher metabolic rate, increased core temperature, and elevated nighttime cortisol. These reflect a chronic fight-or-flight state.

What treatments exist for insomnia and why is CBT-I preferred over medication?

Clinical guidelines recommend CBT-I as first-line treatment because it is as effective as sleep medication short-term but better for long-term. Medications like benzodiazepines or zolpidem offer temporary relief but cause dependence and do not fix underlying problems. Despite this, 90% of Australian GP visits resulted in medication rather than behavioral treatment.

How does insomnia treatment influence depression outcomes?

Treating insomnia significantly improves depression. In Manber et al. (2008), individuals with MDD and insomnia receiving CBT-I plus antidepressants had nearly double the remission rate compared to controls, when insomnia is treated. This suggests insomnia interferes with mood recovery and that targeting sleep can meaningfully enhance treatment response in depressive disorders.

What are the different aspects of CBTI for insomnia?

Sleep hygiene, stimulus control, sleep restriction, relaxation, cognitive, wrap up

What is the evidence for insomnia being a risk factor for persistent depression?

Meaklim (2023) did a study during covid. It showed that insomnia is a key risk factor for persistent anxiety and depressive symptoms. Also 50% of depressed individuals have insomnia.

What are some major sleep effects in depressed people?

Reduced TST, SE, and SW%. Increased SOL, REM%. Reduced REM latency

How does sleep change across bipolar disorder and why is this important?

Bipolar disorder shows prominent sleep disruption: reduced need for sleep during mania, and insomnia or hypersomnia during depressive episodes. Sleep disturbance is a major prodrome of mania and a common prodrome of depression. Sleep deprivation can trigger manic episodes, making sleep regulation central in bipolar management. Less muscle movement during manic episode

What sleep abnormalities occur in schizophrenia?

~45% of people with schizophrenia have comorbid insomnia. PSG studies show reduced TST, SE, and increased SOL, with inconsistent findings regarding SWS. A robust finding is reduced sleep spindles, which may impair memory consolidation. Sleep problems may also precede schizophrenia.

Describe circadian disruptions in schizophrenia and their clinical relevance.

People with schizophrenia often show delayed or unstable (free-running) circadian rhythms. Antipsychotics normalize circadian timing in only about half of cases, and sleep disturbances persist even when rhythm stabilizes. Free running means it changes day to day

Summarise sleep abnormalities in PTSD based on Zhang et al. (2019).

Also a bidirectional relationship. PTSD shows reduced TST, SE, and SWS, with increased WASO. REM% reductions appear mainly in individuals under 30. These people will be hypersroused and vigilant, affecting sleep. WASO changes are stronger in women. Whether controls have trauma exposure affects differences. PSG abnormalities persist regardless of other psychiatric comorbidities. All these effects not persisted when the type was combat exposure, perhaps due to training for this.

Why does adolescence increase vulnerability to sleep problems and mental health issues? Include a discussion of changes in brain activity.

Adolescence includes major neural reorganisation—synaptic pruning and changes in delta/theta EEG activity. Theta wave reduction, which is important for sleep onset and for mindfulness. There is also a reduced delta wave, so reduced restorative sleep. Reduced restorative sleep can be interpreted as a slower increase in sleep drive.

What is the adolescent circadian phase delay and how was it demonstrated?

Taylor et al. (2005) showed later melatonin onset and slower sleepiness buildup in Tanner stage 5 adolescents compared to Tanner stage 1 children during a 36-hour constant routine. Older adolescents stayed alert longer, demonstrating a biologically driven circadian delay independent of behaviour or environment. At 10:30 the older group took longer to fall asleep. 

How do social and cultural factors interact with biological changes to worsen adolescent sleep?

Evening socialising, screen use, homework, and artificial lighting encourage later bedtimes. Light exposure further delays the circadian clock. Because school wake times remain fixed, sleep duration shortens, creating weekday sleep debt. Adolescents compensate with weekend “rebound” sleep, reinforcing irregular sleep patterns and circadian misalignment.

Summarise the SENSE Study and its main findings.

The SENSE Study tested a CBT- and mindfulness-based group sleep intervention in at-risk adolescents. Compared to education controls, the intervention improved subjective sleepiness, reduced SOL and daytime sleepiness, improved sleep knowledge, and reduced anxiety/OC symptoms. At two-year follow-up, benefits persisted, including reductions in depression and anxiety trajectories.

Describe the anatomy and basic process of gas exchange in the lungs.

Air travels through the oronasal cavity → trachea → bronchi → bronchioles → alveoli, where gas exchange occurs. Venous blood arrives by the pulmonary artery high in CO₂ and low in O₂; diffusion across the capillary membrane oxygenates blood and removes CO₂. Exhaled air contains ~13% O₂ and ~5% CO₂.

Explain how inspiratory and expiratory muscles function in breathing.

Inspiration is active: diaphragm contraction flattens the thoracic floor while external intercostals lift the ribs, increasing lung volume and reducing pressure. Resting expiration is passive, relying on lung recoil once inspiratory muscles relax. Accessory muscles (sternocleidomastoid, scalenes, abdominals, internal intercostals) engage during forced or laboured breathing. to get that last bit of air

Describe the neural innervation of respiratory muscles and why this matters clinically.

Breathing relies on spinally-innervated muscles: diaphragm (phrenic nerve, C3–C5), intercostals (T1–T11), scalenes (C3–C8), sternocleidomastoid (C2–C3), and abdominals (T7–12, L1). Damage at different spinal levels impairs different components of breathing. Cervical lesions above C5 can eliminate diaphragmatic function, threatening ventilation.

What are the major brainstem structures controlling breathing and their roles?

The medulla’s dorsal respiratory group (DRG) generates rhythmic, quiet breathing, controlling diaphragm and intercostals. When it stops firing it allows for passive expiration. The ventral respiratory group (VRG) regulates forced breathing via accessory muscles. Pontine respiratory groups fine-tune rhythm, while rhythm generators (preBötzinger, RTN) and chemosensitive areas adjust breathing to CO₂ and O₂ changes.

Explain the roles of the preBötzinger complex and retrotrapezoid nucleus in breathing.

The preBötzinger complex are the respiratory pacemaker cells, continuously signaling the phrenic nerve (to contract the inspiration muscles) to drive inspiration. This are important for the rythm of breath. And interacts with PRG and DRG. The RTN generates expiratory rhythm during forced breathing and interacts with PRG DRG and VRG to inhibit inspiration. Both structures are chemosensitive—responding to CO₂-driven pH changes—and integrate with DRG/VRG and pontine centres to stabilize breathing.

What inputs to the respiratory centres influence breathing, and how?

Peripheral chemoreceptors (carotid bodies, aortic arch) respond rapidly to blood CO₂/O₂ changes. This can elicit quicker response from central chemoreceptors.

Mechanoreceptors detect stretch in pulmonary , irritants, like smoke dust and pollen, sending vagal signals to modify breathing—e.g., smoke stops inspiration via DRG inhibition.

Describe the bidirectional relationship between breathing and emotions.

The amygdala directly influences respiratory centres, increasing breathing rate and depth during fear or anxiety. Conversely, altered CO₂ levels can activate the amygdala and evoke fear responses. Thus emotions modulate respiratory drive, while changes in breathing—especially CO₂—can trigger or amplify emotional states. trigger a panic attack. Basolateral amygdala and hypothalamus are also CO2 sensitive. So changes in that, can trigger fear response

Where does the amygdala directly link?

Prg, Increase respiratory rates. DRG to increase the inspired volume.

What symptoms arise from abnormal CO₂ levels and why?

produces dizziness, tingling, weakness, palpitations, shortness of breath, visual disturbances, sweating, and panic-like sensations. These symptoms reflect CO₂’s role in pH regulation, cerebral blood flow, neuromuscular excitability, and autonomic output. Many panic symptoms mimic physiological responses to altered CO₂.

What characterises a panic attack and panic disorder?

A panic attack is a sudden period (~30 minutes) of intense fear with physical symptoms such as palpitations, dyspnea, dizziness, and feelings of suffocation. Panic Disorder involves recurrent attacks paired with persistent worry and avoidance behaviours. Symptoms can escalate without external threat, reflecting dysregulated fear and respiratory systems.

Explain the CO₂ hypersensitivity (suffocation false alarm) theory of panic disorder.

This theory proposes that individuals with Panic Disorder have an overreactive suffocation alarm system. Their brainstem and limbic circuits misinterpret small CO₂ increases as life-threatening, triggering panic. Evidence includes heightened CO₂ challenge responses, increased sighing, and central apneas that lower CO₂ due to increased breathing during sleep.

Why is paper-bag breathing no longer recommended for panic attacks?

Paper-bag breathing increases inhaled CO₂ to counteract hypocapnia, but it can dangerously elevate CO₂ in people with asthma, cardiac conditions. Safer alternatives—including CBT-based breathing retraining and Pharmacological treatments (antidepressants, benzodiazepines) are effective.

What are breath-holding spells in toddlers and what do they reveal?

Breath-holding spells are involuntary episodes during tantrums where toddlers stop breathing, turn blue, and may faint or seize. Breathing resumes spontaneously. Occurring in ~5% of children, these episodes demonstrate the powerful emotional influence on respiratory control mechanisms even in early development.

Summarise Sharma et al. (2016) on mood effects on dyspnea.

In healthy adults performing exercise while viewing mood-inducing images, negative images increased arousal and worsened perceived dyspnea.

Whats dyspnea?

A term for the discomfort associated with being short of breath. 

How does deep breathing influence stress physiology?

Deep, slow breathing practices from yoga, tai chi, and meditation increase parasympathetic activity and reduce cortisol. Relaxation components also contribute. These techniques modulate vagal tone, lowering sympathetic activation and improving emotional regulation and reducing cortisol secretion. You are increasing vagal nerve activity.

What were the findings of Busch et al. (2012) regarding breathing vs relaxation?

Busch et al. compared guided (effortful) vs relaxed deep breathing. Relaxed breathing reduced sympathetic tone and lowered pain and thermal thresholds, whereas both techniques reduced negative mood similarly.