Alcohol acts as a central nervous system depressant, slowing down neurological signaling throughout the body. The eyes, with their complex system of muscles, nerves, and vessels, provide immediate and observable indicators of intoxication. These effects manifest in the physical appearance, movement, and function of the eyes. This article details the specific changes caused by alcohol consumption.
Visible External Changes
One of the most recognized signs of intoxication is the appearance of bloodshot eyes. This reddening occurs because alcohol is a vasodilator, causing the small blood vessels in the conjunctiva—the thin, clear membrane covering the white part of the eye—to widen. The increased blood flow makes these capillaries larger and more prominent, leading to the characteristic red look.
Alcohol frequently causes the eyes to take on a watery or “glassy” appearance. This effect is linked to dehydration, as alcohol is a diuretic that reduces the body’s moisture availability for tear production. Ethanol is also secreted into the tears, increasing their salt concentration and shortening the tear film break-up time, which leads to a compromised and unstable tear film. This disruption can result in dry eye symptoms and irritation.
The depressant effect of alcohol on the central nervous system also affects the muscles surrounding the eyes. Ptosis, or drooping of the upper eyelids, can occur due to the relaxation and weakening of the muscles responsible for lifting them. This muscle relaxation contributes to the heavy, tired appearance associated with intoxication.
Disruption of Eye Movement and Coordination
Alcohol severely impairs the oculomotor system, which controls precise eye movements, leading to observable involuntary motions. The most common of these is nystagmus, defined as rapid, rhythmic, and involuntary oscillation of the eyes.
A common form is horizontal gaze nystagmus (HGN), where the eye involuntarily jerks as it moves toward the side. This occurs because alcohol inhibits the cerebellum, the area of the brain responsible for fine-tuning coordination and balance, including the ability to hold the eyes steady at an eccentric gaze. When the brain struggles to maintain a fixed position, the eye drifts slowly away from the target and then rapidly jerks back in a corrective movement.
The brain also loses its ability to perform smooth pursuit, the mechanism that allows the eyes to smoothly track a moving object. Under the influence of alcohol, this motion breaks down, replaced by a series of small, jerky movements called saccades. This impairment reflects the systematic disruption of oculomotor functioning. Another form, positional alcohol nystagmus (PAN), is triggered by changes in head position because alcohol alters the density of the fluid in the inner ear’s vestibular system, which controls balance and spatial orientation.
Alcohol’s Impact on Visual Acuity
Beyond affecting the eyes’ appearance and movement, alcohol directly compromises the quality of vision. Blurred vision and double vision, or diplopia, are common consequences of intoxication. The impairment of eye muscle coordination makes it difficult for both eyes to align and focus on the same point simultaneously, causing the brain to receive two slightly different images.
Alcohol also slows down the reaction time of the pupils, the openings that control the amount of light entering the eye. Normally, the iris muscles quickly constrict or dilate the pupil in response to changes in light, but alcohol causes these muscles to relax and react more sluggishly. This slowed response makes it challenging to rapidly adjust to varying light conditions, such as adapting to oncoming headlights during night driving.
Additionally, alcohol impairs depth perception, the ability to accurately judge the distance and spatial relationship between objects. When communication between the eyes and the brain is slowed, the brain struggles to process the visual information needed to create a three-dimensional view of the environment. This functional deficit is compounded by a reduction in contrast sensitivity, making it harder to distinguish objects based on subtle differences in lightness and darkness.
The Underlying Physiology
The effects on the eyes are fundamentally rooted in alcohol’s action as a central nervous system depressant. Alcohol slows neurological signaling by interacting with various neurotransmitter systems in the brain. Specifically, alcohol enhances the effects of gamma-aminobutyric acid (GABA), the brain’s primary inhibitory neurotransmitter.
By increasing the inhibitory activity of GABA, alcohol effectively slows down communication across the brain, leading to the sedative effects associated with intoxication. This generalized slowing affects the brainstem, which controls involuntary actions like pupil response and basic muscle function, and the cerebellum, which manages coordination and balance. The poor motor coordination observed in eye movements, such as nystagmus, is a direct manifestation of this cerebellar inhibition.
This physiological mechanism links the generalized slowing of the nervous system back to the specific observable ocular effects. For instance, the relaxation of the iris muscles and the resulting slow pupil response are due to impaired signaling in the brainstem. Similarly, uncoordinated eye movements that cause double vision stem from the slowed communication between the brain and the ocular muscles.