What Happens to Your Pupils When You Die?

The pupil is the dark center of the eye, an aperture that allows light to pass through to the retina. It is surrounded by the iris, the colored part of the eye, which contains involuntary muscles that act like a camera’s diaphragm. The purpose of this system is to regulate the amount of light striking the light-sensitive tissues at the back of the eye. A functional pupillary light reflex—where the pupil constricts in bright light and widens in dim light—is a reliable indicator of an active brainstem.

The Living Pupil: Autonomic Nervous System Control

The size of the pupil is continuously adjusted by two opposing sets of smooth muscles within the iris, regulated involuntarily by the autonomic nervous system. This dual control system ensures swift adjustments to changes in ambient light and psychological state. The parasympathetic nervous system governs the sphincter pupillae muscle, which is arranged circularly around the pupil. When this muscle contracts, it causes the pupil to constrict (miosis), limiting the amount of light entering the eye.

The sympathetic nervous system controls the dilator pupillae muscle, whose fibers radiate outward. Activation of this system causes these radial muscles to contract, resulting in pupillary dilation (mydriasis). This dynamic balance is maintained by specific nerve pathways originating in the brainstem. The parasympathetic pathway stems from the Edinger-Westphal nucleus, while the sympathetic pathway originates in the hypothalamus and travels down the spinal cord before ascending to the eye.

Immediate Fixation: The Loss of the Light Reflex

The swift cessation of the pupillary light reflex is one of the earliest changes observed following clinical death. This reflex pathway is dependent on oxygen and continuous neural activity within the brainstem. Once circulation stops, the lack of oxygen (anoxia) immediately causes the brainstem centers that mediate the parasympathetic constriction reflex to fail.

The parasympathetic signal, which normally causes the pupil to constrict, is lost almost instantaneously. Without this inhibitory force, the pupil assumes a fixed, dilated state because the dilator muscle is no longer actively opposed by the sphincter muscle. Studies show that pupils become non-reactive to light in a matter of seconds following circulatory arrest.

Pupils in brain-dead patients are classically described as fixed and dilated, meaning they do not change size in response to light. The typical size in this state is four millimeters or larger. The fixed, non-reactive pupil is a recognized sign used in emergency medicine and forensic specialists to confirm the absence of brainstem function. In some cases of cardiac arrest, the pupil may dilate further immediately following the event, linked to a transient burst of peripheral sympathetic activity or the release of stored norepinephrine.

Post-Mortem Physical Alterations of the Eye

Beyond the functional loss of the light reflex, the eyes undergo a series of physical changes hours after death utilized in forensic pathology. One of the first alterations is a rapid decrease in intraocular pressure (IOP) as internal metabolic processes cease. The eye loses its normal firmness and becomes noticeably softer, with internal pressure potentially halving within three hours after death.

The cornea, the clear outer layer, begins to lose its transparency and becomes hazy (corneal clouding or opacity). This change occurs because the cornea requires a continuous supply of nutrients and oxygen, which is cut off after death, and due to surface dehydration. If the eyelids remain open, clouding can begin within minutes to a few hours, but it may be delayed if the eyelids are closed and the environment is humid.

A separate post-mortem sign that occurs when the eyes are open is the formation of Tache Noire Sclerae, or “black spot of the sclera.” This appears as a dark, reddish-brown to black band on the sclera where it is exposed to the air. The discoloration is caused by the drying and desiccation of the exposed tissue, and it can develop in one to two hours if the eyelids are left ajar.