Today I awoke feeling hopeless, disconnected from my body and my thoughts. All I could sense was the void that my vision loss represented. I kept thinking how beautiful it would be to see clearly, as I opened my eyes to a world submerged in gray fog. Suddenly, the room began to distort. The shadows slowly transformed into figures, men and women trying to pull off my legs were manifesting and then, out of nowhere, a tiger, vibrant and terrifying, ran through the mist of my bedroom. I kept telling myself: This is only a dream. But why was I chosen to endure these hallucinations, which grew more vivid as my world grew darker?
The paradox of seeing more while seeing less
This paradox (seeing more as you see less) is the hallmark of Charles Bonnet syndrome (CBS). Named after the Swiss naturalist who, in 1760, described the vivid visions of his grandfather (who was nearly blind from cataracts), CBS remains one of the most haunting intersections of ophthalmology and neurology in which patients with visual impairment experience hallucinations despite not being psychiatrically or psychologically impaired.
The deafferentation theory: a starved brain
To understand why a brain deprived of light creates all of these hallucinations, we must look at the deafferentation theory. In a healthy visual system, the retina constantly sends a stream of electrochemical signals to the visual cortex in the occipital lobe. This constant stimulus acts as a regulatory mechanism. When conditions like age-related macular degeneration (AMD), glaucoma, diabetic retinopathy, retinal vein occlusion, or cataracts cut off this stream of information, the visual cortex becomes “starved”; this is known as denervation supersensitivity.
The neurons in the ventral stream which are responsible for recognizing objects and faces begin to suffer spontaneously. Without the presence of incoming light, the brain opens its own library of stored memories and images, projecting them into the external world. This is similar to phantom limb syndrome; just as an amputee feels pain in a missing leg, the visually impaired person “sees” with a missing eye.
Specific hallucinations and brain anatomy
The specific nature of the hallucinations is directly related to areas of the brain that are hyperexcitable. If the fusiform gyrus is spontaneously active, the patient sees complex faces. If the parahippocampal gyrus is affected, the patient may see landscapes or buildings.
Beyond ocular pathology, CBS is also linked to neurological disruptions. Occipital lobe strokes or low cerebral perfusion pressure can mimic the effects of peripheral vision loss by damaging the primary visual processing centers. In both cases, the result is a dissociation between the eye’s inability to capture light and the brain’s desperate attempt to interpret images.
Management and hope
One of the most tragic aspects of CBS is that it occurs in individuals who are psychiatrically or psychologically intact, unlike those with schizophrenia or dementia. Many patients remain silent, fearing a psychiatric diagnosis, which only exacerbates isolation. Currently, there is no definitive cure; however, the management focuses on two principal pillars, such as treating the underlying cause (cataract surgery) and cognitive/behavioral therapy.
Other techniques like rapid eye movements (blinking or moving eyes left to right) can sometimes reset the hyperexcited neurons and clear the visual field. Charles Bonnet syndrome is evidence of the brain’s incredible plasticity and physiology, but is also a reminder that “seeing” is not just a biological function of the eyes, but a complex construction of the mind.
Ceres Alhelí Otero Peniche is a medical student in Mexico.
