The sudden interruption of breathing, or choking, occurs when a foreign object lodges in the throat or windpipe, blocking the flow of air into the lungs. This obstruction rapidly leads to oxygen deprivation, a state the brain is highly sensitive to. The resulting lack of oxygen can trigger a cascade of neurological reactions, potentially including seizure activity.
How Oxygen Deprivation Triggers Seizures
Severe oxygen deprivation, or hypoxia, can directly lead to seizure activity in the brain. The brain is an obligate consumer of oxygen and glucose, and even a brief interruption to this supply profoundly impacts its function. The severity and duration of oxygen loss dictate the neurological response, ranging from confusion to convulsive episodes.
When the airway is completely blocked, the body enters a state of asphyxia, rapidly depleting oxygen stores. This sudden starvation of oxygen to the brain, called hypoxic ischemic encephalopathy (HIE), causes injury to brain cells. Seizures associated with HIE are essentially the brain’s electrical system malfunctioning under extreme stress.
The immediate effect of oxygen loss is a widespread metabolic crisis within the neurons. This electrical disturbance can manifest as a seizure, an episode of uncontrolled, abnormal electrical firing in the brain. Case reports involving self-induced hypoxia, such as “the choking game,” confirm that external obstruction leading to hypoxia is a sufficient trigger for this neurological event.
The Brain’s Immediate Reaction to Hypoxia
The brain relies on oxygen primarily for the production of adenosine triphosphate (ATP). When oxygen supply stops, ATP production ceases, causing the failure of energy-dependent systems, most notably the sodium-potassium pumps. These pumps maintain the ion balance across the neuronal membrane necessary for normal electrical signaling. Pump failure leads to a dramatic redistribution of ions, including an influx of sodium and calcium.
This ion imbalance results in “anoxic depolarization,” a massive electrical shutdown of neural activity. A consequence is the excessive release of glutamate, the brain’s main excitatory neurotransmitter. In excess, glutamate becomes toxic, a process known as excitotoxicity.
The flood of glutamate overstimulates its corresponding receptors, particularly the N-methyl-D-aspartate (NMDA) receptors. This drives an uncontrolled influx of calcium ions into the neurons. The excessive calcium triggers cellular damage and promotes uncontrolled neural firing, which is the physiological basis of seizure activity.
Emergency Protocol for Hypoxic Events
The priority during a choking incident is to rapidly clear the obstruction and restore breathing. For a conscious adult or child, the standard protocol involves alternating between five back blows and five abdominal thrusts (the Heimlich maneuver). If the person becomes unresponsive, they should be lowered to the floor, and standard cardiopulmonary resuscitation (CPR) should be initiated, starting with chest compressions. Emergency medical services should be called immediately while first aid is administered.
If the person begins to seize after breathing is restored, the focus shifts to seizure first aid.
Seizure First Aid
- Gently ease the person to the floor and turn them onto their side to keep the airway clear.
- Clear the surrounding area of any hard or sharp objects that could cause injury.
- Place a soft, flat object, such as a folded jacket, under the head for protection.
- Time the seizure; if it lasts longer than five minutes, or if the person has trouble breathing or waking up afterward, call emergency services again.
- Never attempt to put anything into the person’s mouth or restrain their movements during the seizure.