Sir,
We read with interest the excellent article by Drs Ross and Rahman, describing visual hallucinations in a patient following enucleation.1 These hallucinations were characteristic of Charles Bonnet syndrome (CBS) and, interestingly, disappeared with eye closure. We would like to propose a possible pathophysiologic mechanism to explain this observation.
A visual acuity of 6/6 in the patient's other eye is not incompatible with the diagnosis of CBS, which has been described both in people with good visual acuity in the fellow eye2, 3 and in patients who have visual field defects and good central visual acuity in the affected eye.2, 4, 5 Shiraishi et al6 proposed that it is the dynamic reduction in visual acuity, rather than the actual visual acuity, that has a greater impact on CBS.2, 7
This case is intriguing because the hallucinations ceased when the patient's eyes were closed, only to return when he opened his eyes. Although it is well known that eye closure may terminate hallucinations in patients with CBS, this is the first case in which it appears that transient reduction of light perception on closure of the fellow eye is associated with its cessation. The enucleated eye constantly has no light perception and lid closure will not have any additional effect. It is possible, as the authors suggest, that closing the eyes results in secondary normalization of sensory input, thus abolishing the abnormal independent impulses and resultant complex imagery.1 Another possibility might be that deafferentation induced changes in the cortical neurons, resulting in reorganization of the receptive field and increased sensitivity to sensory input.8 Stimulation of these hypersensitive areas by normal sensory impulses (in this case from the left eye) may trigger visual hallucinations.7, 9, 10 However, a minimum amount of sensory input is required in order to trigger the hallucinations. Therefore, when the patient closes both his eyes, normal input is abolished and the hallucinations cease, only to return when he opens his eyes. This theory would also explain why some hallucinations cease when patients eventually lose all light perception. This possibility is illustrated in another patient who experienced CBS following cortical resection for cortical dysplasia.5 In this patient, the hallucinations diminished with eye closure, and varied in intensity with blinking, light intensity, and the sight of moving objects—factors that vary the intensity of the visual stimulation.
Regardless of the mechanism, we agree with the authors that it is important to recognize CBS and its possible occurrence following sudden loss of vision.
References
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Tan CS, Lim VS, Ho DY, Yeo E, Ng BY, Au Eong KG . Charles Bonnet syndrome in Asian patients in a tertiary ophthalmic centre. Br J Ophthalmol 2004; 88: 1325–1329.
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Choi EJ, Lee JK, Kang JK, Lee SA . Complex visual hallucinations after occipital cortical resection in a patient with epilepsy due to cortical dysplasia. Arch Neurol 2005; 62 (3): 481–484.
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Tan CS, Sabel BA . Dynamic changes in visual acuity as the pathophysiologic mechanism in Charles Bonnet syndrome (visual hallucinations). Eur Arch Psychiatr Clin Neurosci 2005 August 4 (E-pub ahead of print).
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Tan CS, Sabel BA . Charles Bonnet syndrome in patients with visual field defects—are hallucinations good or bad? J Neurosurg 2005; 103 (1): 193–195 (author reply 195).
Tan CS, Sabel BA . Charles Bonnet syndrome after occipital cortical resection for cortical dysplasia may be related to denervation supersensitivity. Arch Neurol 2005; 62 (9): 1479–1480.
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Tan, C., Sabel, B. & Eong, KG. Charles Bonnet syndrome (visual hallucinations) following enucleation. Eye 20, 1394–1395 (2006). https://doi.org/10.1038/sj.eye.6702236
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DOI: https://doi.org/10.1038/sj.eye.6702236