Apnea in newborns is most commonly caused by an immature brainstem that hasn’t yet developed reliable control over breathing. Nearly all infants born before 29 weeks gestation experience apnea, and even babies born closer to full term can have episodes triggered by infections, metabolic problems, or airway obstructions. Understanding why these pauses happen helps make sense of the monitoring and treatments your baby may need in the hospital.
Three Types of Newborn Apnea
Not all apnea looks the same. There are three distinct types, and each has a different underlying mechanism.
Central apnea happens when the brain’s respiratory center simply stops sending signals to the breathing muscles. The baby makes no effort to breathe at all. This is the type most directly linked to brainstem immaturity.
Obstructive apnea occurs when the airway is physically blocked. The baby may be trying to breathe, but air can’t get through. Neck position, a small jaw, or excess soft tissue in the throat can all contribute.
Mixed apnea combines both: a period of no breathing effort from the brain, typically followed by an airway obstruction. This is the most common type in premature infants.
Why Premature Brains Struggle to Control Breathing
The brainstem region that controls breathing rhythm is one of the last parts of the nervous system to fully mature. In a preterm infant, the neurons responsible for respiratory drive are incompletely organized, with fewer synaptic connections than a full-term baby would have. Research using auditory brainstem tests has shown that infants with apnea have measurably slower nerve conduction in the brainstem compared to premature infants of the same age without apnea, confirming that the issue is neurological immaturity beyond what’s expected for their age.
This immaturity shows up in a paradoxical way: when oxygen levels drop, adults and older children automatically breathe faster and harder. Newborns do the opposite. They may briefly speed up, but then their breathing slows and can stop entirely. The brain’s response to low oxygen is essentially to shut down rather than ramp up, which makes apnea episodes self-reinforcing if not interrupted.
Brain chemicals play a role too. GABA, a neurotransmitter that normally helps regulate brain activity, appears to be overly active in the respiratory centers of preterm infants. It suppresses breathing rate and blunts the baby’s ability to respond to rising carbon dioxide levels, both of which make apnea more likely.
Prematurity Is the Biggest Risk Factor
The earlier a baby is born, the higher the chance of apnea. The numbers follow a steep curve: about 7% of infants born at 34 to 35 weeks gestation develop apnea, rising to 15% at 32 to 33 weeks, 54% at 30 to 31 weeks, and nearly 100% of those born before 29 weeks or weighing under 1,000 grams. The relationship is straightforward: less time in the womb means less brainstem development, which means less reliable breathing control.
Medical Conditions That Trigger Apnea
Even when a baby’s brainstem is the underlying vulnerability, specific medical problems can push an otherwise stable infant into apnea episodes. Because the respiratory control centers are so sensitive, they can be overwhelmed by stressors that a mature brain would handle easily.
- Infection and sepsis: One of the most important triggers. New-onset apnea in a newborn who was previously stable is often the first sign of a serious infection, sometimes appearing before fever or other symptoms do.
- Anemia: When the blood carries less oxygen, the brain’s paradoxical response to low oxygen can kick in, suppressing breathing rather than increasing it.
- Low blood sugar (hypoglycemia): The brain needs a steady supply of glucose to function. When levels drop, the respiratory center is among the first areas affected.
- Temperature instability: Both overheating and getting too cold can depress the breathing center. Maintaining a stable temperature in an incubator is partly about preventing apnea.
- Toxin or drug exposure: Medications given to the mother before birth, or substances the baby was exposed to in utero, can suppress respiratory drive.
When apnea appears suddenly in a baby who wasn’t having episodes before, the medical team will typically look for one of these secondary causes rather than assuming it’s simply prematurity-related.
Feeding and Airway Reflexes
Feeding is a surprisingly common trigger. Newborns have to coordinate sucking, swallowing, and breathing simultaneously, and premature infants often can’t manage all three at once. When swallowing interrupts the breathing rhythm, the pause can become long enough to count as apnea.
Making this worse, newborns have exaggerated protective reflexes in the throat. When liquid touches the larynx, the brain triggers a reflex that shuts down breathing to prevent aspiration. In a full-term baby this reflex is brief and well-controlled. In a preterm infant, it can cause a prolonged pause because the immature brainstem overreacts to the stimulus and takes longer to restart normal breathing.
Anatomical Causes of Airway Obstruction
Some babies have structural features that make their airway more likely to collapse or narrow. Conditions involving a very small jaw (micrognathia), craniofacial differences, or abnormalities of the larynx can cause obstructive apnea that’s distinct from the brainstem-driven type. Babies with Pierre Robin sequence, for instance, have a recessed jaw that allows the tongue to fall back and block the airway, particularly in certain positions. Research shows that about 61% of these infants have worsened obstruction with positional changes, and supine (face-up) positioning is a common aggravator.
Even in babies without structural abnormalities, the chest wall itself is part of the problem. A newborn’s rib cage is extremely pliable, and in premature infants, the chest can actually collapse inward during breathing efforts. This forces the tiny muscles between the ribs to work much harder, and when those muscles tire out, breathing can stop.
How Apnea Is Treated
Caffeine is the cornerstone treatment for apnea of prematurity. It works by blocking adenosine receptors in the brain. Adenosine naturally slows neural activity, so blocking it keeps the respiratory center more alert and active. Caffeine has been used as a respiratory stimulant in preterm infants for over 30 years, and it remains one of the most commonly prescribed medications in neonatal intensive care.
Beyond caffeine, the approach depends on the cause. If infection is the trigger, treating the infection resolves the apnea. If anemia is contributing, a blood transfusion may help. For obstructive causes, positioning adjustments or, in more severe structural cases, surgical intervention may be needed. Babies on monitors will have alarms set to alert nurses when breathing pauses, heart rate drops, or oxygen saturation falls, so that gentle stimulation (like rubbing the baby’s back or repositioning) can restart breathing before the episode becomes dangerous.
When Apnea Resolves
For most premature infants, apnea goes away on its own as the brain matures. Several studies suggest that the majority of babies are free of apnea episodes by 37 to 40 weeks postmenstrual age (that is, counting from the mother’s last menstrual period, not from the date of birth). One study of 91 infants born before 32 weeks found their last apnea event occurred at an average of about 38 weeks postmenstrual age.
The most extremely premature babies may take longer. Infants born at the lowest gestational ages sometimes continue to have episodes until around 43 weeks postmenstrual age, which can be several weeks after their original due date. This extended timeline is one reason very premature infants stay in the hospital longer: they need to demonstrate a sustained period without apnea episodes before they can safely go home.