W6: Sleep Apnea and motor control

What is sleep apnea and how is it diagnosed?

Sleep apnea involves repeated apneas (no airflow >10 s) or hypopneas (>50% airflow reduction with desaturation or arousal). Severity is measured by the Apnea–Hypopnea Index (AHI): <5 normal anything above is concerning. Consequences include oxygen desaturation, CO₂ rise, and repeated arousals.

Distinguish obstructive vs central sleep apnea.

Obstructive sleep apnea involves continued respiratory effort but a physically blocked airway. Central sleep apnea reflects absent respiratory effort due to impaired brainstem drive. OSA is mechanical; CSA is neurological/chemosensory. Both cause fragmented sleep, hypoxia, and physiological stress during sleep.

Describe conditions associated with central sleep apnea.

CSA occurs in congenital central hypoventilation syndrome (impaired CO₂ response), opioid use (preBötzinger suppression) which slows the pacemaker cells which are already slow in sleep, and congestive heart failure (slow circulatory feedback causing unstable respiratory timing). Also worse as CO2 is already higher in sleep. Each condition interrupts chemosensory regulation, leading to absent drive during sleep when automatic respiration is essential.

What is the Congenital central hypoventilation syndrome?

Genetic condition of the RTN.

Why does congestive heart failure cause central apnea?

CHF slows blood circulation, slower rates of diffusion also increases co2, delaying CO₂ information reaching brainstem chemoreceptors. Blood is not as oxygenated as it should be. By the time the signal is getting to your brain, its signaling you to stop breathing entirely.

What causes obstructive sleep apnea, and what role does airway anatomy play?

OSA results from repetitive upper airway collapse during sleep. The airway lacks rigid bony support and relies on dilator muscles—especially the genioglossus, the tongue muscle. This is Neuromuscular compensation.  OSA patients typically have smaller upper airways and insufficient neuromuscular compensation to counter collapsing forces when muscle tone drops during sleep.

What are the consequences and treatments for CSA?

" Congestive Heart Failure: Sleepiness, disturbed sleep.

" Congenital Central Hypoventilation Syndrome: death or serious brain

damage.

. Opioids: death (accidental overdose).

> Treatments

" Congestive Heart Failure: optimise heart function, artificial ventilation.

. Congenital Central Hypoventilation Syndrome: artificial ventilation.

Opioids: reduce opioids, artificial ventilation.

What is the sleep architecture for OSA people?

Because of so many arousals the dont have deep SWS. And less REM.

What is neuromuscular compensation in OSA?

OSA patients show increased genioglossus activation while awake to keep the airway open. When transitioning into sleep, this compensatory activity drops sharply, precipitating airway collapse. In deeper sleep stages, activation returns but remains inadequate, revealing a sleep-state-dependent vulnerability of the upper airway.

What do single motor unit recordings show about upper airway control?

Recordings from genioglossus motor units reveal that many respiratory-related motor units stop firing at sleep onset. Loss of rhythmic drive reduces airway muscle tone, enabling obstruction.

Summarise the pathophysiology of obstructive sleep apnea.

Sleep reduces dilator muscle activity → airway collapses → hypoxia and CO₂ rise → respiratory drive increases → arousal restores muscle tone → airway reopens. Repeated cycles cause fragmentation of sleep, hypoxia, mental health

What neurocognitive deficits are associated with OSA?

OSA leads to excessive daytime sleepiness, attention and vigilance deficits, slower reaction times, memory impairment, and potential hippocampal volume reduction due to chronic intermittent hypoxia. Severity varies individually—just as seen experimentally with sleep loss—revealing differential vulnerability to cognitive effects.

Explain links between OSA and mental health.

OSA is a risk factor for depression, anxiety, and PTSD. Around 40% of OSA patients show depressive symptoms. PTSD patients have very high OSA prevalence (~76%), possibly due to hyperarousal leading to frequent awakenings before airway compensation occurs. OSA may worsen emotional regulation and stress tolerance.

Describe main treatments for obstructive and central sleep apnea.

OSA treatments include CPAP (most effective), mandibular advancement splints, hypoglossal nerve stimulation, and airway surgeries. CSA treatment targets the underlying cause: optimise heart failure, reduce opioids, or use artificial ventilation in congenital hypoventilation. All aim to restore stable ventilation during sleep.

What do Locked-In Syndrome and the sea squirt example illustrate about the brain?

The sea squirt digests its brain once movement is unnecessary, suggesting the brain evolved for behavioural interaction. Locked-In Syndrome shows intact cognition despite inability to move. Together, these examples highlight that the brain’s primary adaptive function is to control movement and interact with the environment.

What is Locked in syndrome and the symptoms

Due to damage to the pons. This is damage to the connection between the brain and spinal cord. Completely paralysed, unable to breathe without a ventilator, normal wake and sleep, intact cognition.

What is blindsight and what does it reveal about motor pathways?

Blindsight allows cortically blind individuals to respond accurately to unseen visual stimuli. type 1 includes guessing the aspects of visual stimuli like colour above chance. And type is when patient claims to feel that objects in their blind area have moved.

Describe smooth, skeletal, and cardiac muscle.

Smooth muscle controls involuntary movements in the gut, arteries, and reproductive organs. Next are the striated muscles. Skeletal muscle enables voluntary posture and movement through tendon attachments to bones. Cardiac muscle powers the heart’s rhythmic contractions. Only skeletal muscle is under voluntary CNS control, making it central in motor behaviour.

Explain skeletal muscle structure and the role of motor units.

Each alpha motor neuron innervates multiple muscle fibres, forming a motor unit. Fine-control muscles (eyes) have few fibres per motor neuron, while gross muscles (back, limbs) have many. Force is modulated by recruiting additional motor units and altering firing rate (rate coding). Flexion and extension is both down by the contraction of a muscle.

Describe the sliding filament mechanism of muscle contraction.

An action potential triggers acetylcholine release at the neuromuscular junction. These bind to receptors that trigger influx of sodium in the muscle membrane and cause an action potential. Then T-tubules transmit this signal, releasing calcium from the sarcoplasmic reticulum. Calcium enables myosin to bind to actin and form cross-bridges, causing sliding toward the M-line. Through pulling of actin by myosin. Repeated cycling produces contraction until neural signalling stops.

What are Myofibrils?

Run the length of the muscle and are made up of thick and thin filaments that give the striated appearnece. These are the contracting parts. 

How do we modulate force?

We can recruit more motor units for gross movements. We can change the rate of AP discharge to the muscle. Rapid firing produces more forceful contraction due to multiple twitches. 

Why are muscle spindles important?

These are embedded in the extrafusal muscles. Intrafusal muscles wrapped around a sheath. Spindles have sensory axons (1a afferents). Direct stimulation of the alpha motor neuron from the 1a afferent neuron causes the muscle to contract, this is the reflex arc. bypasses to keep you safe

What is the stretch reflex and why is it useful?

Muscle spindles detect stretch and send 1a afferent signals to the spinal cord, triggering alpha motor neuron activation and reflexive contraction of the same muscle. Simultaneously, antagonists are inhibited. that is the hammies contraction is inhibited. This reflex maintains posture, corrects unexpected and stabilises limb position.

What are Golgi tendon organs and how do they prevent injury?

Golgi tendon organs in tendons sense muscle tension via Ib afferents. Excess tension activates inhibitory interneurons that reduce alpha motor neuron firing, decreasing contraction. This protective reflex prevents muscle damage by limiting dangerously over contracting.

How does tetrodotoxin affect motor control?

Tetrodotoxin blocks voltage-gated sodium channels, preventing action potentials in nerves. This causes complete paralysis because skeletal muscles cannot receive neural commands. Venomous species like pufferfish and blue-ringed octopus use TTX, demonstrating how critical sodium channels are to motor function.