Charles Bonnet syndrome and the association with dementia

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a r c h s o c e s p o f t a l m o l . 2 0 1 4;8 9(1):42–44
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Fig. 1 – Patient with complete intraretinal fluid resolution after the intravitreal injection of aflibercept. Five previous
injections of ranibizumab. (A) Preaflibercept and (B) postaflibercept.
studies including the present one has proven to be effective
with a single injection for treating refractory cases of the said
disease.
R.E. Cervera ∗ , V. Castro, J. Montero, C. Torralba, A. Gracia
Servicio de Oftalmología, Hospital General Universitario, Valencia,
Spain
reference
∗ Corresponding author.
E-mail address: Cervera enr@gva.es (R.E. Cervera).
1. Heier JS, Brown DM, Chong V, Korobelnik JF, Kaiser PK, Nguyen
QD, et al. Intravitreal aflibercept (VEGF trap-eye) in wet
age-related macular degeneration. Ophthalmology.
2012;119:2537–48.
2173-5794/$ – see front matter
© 2013 Sociedad Española de Oftalmología. Published by
Elsevier España, S.L. All rights reserved.
Charles Bonnet syndrome and the association
with dementia夽
Síndrome de Charles Bonnet y la asociación con demencia
Dear Sir:
The Charles Bonnet syndrome (CBS) is a clinical condition
characterized by the appearance of visual hallucinations in
patients with major visual deterioration and preserved cognitive conditions. It is estimated that the prevalence of visual
hallucinations could exceed 50% in patients with severe
eyesight conditions. However, case studies demonstrate a
prevalence of 1.84–3.15% due to lack of knowledge by the
physician and the fear patients have of being considered mentally deranged.1
The cause of said hallucinations is unknown. However,
there are some triggering factors such as fatigue, stress, poor
lighting and glare. In addition, CBS has been associated to
social isolation, cognitive defects, sensory deprivation and
poor quality of social contact. Various theories have been
proposed to explain the origin of hallucinations in CBS. Diminished visual acuity produces a reduction in brain cortex
stimulation which does not disappear completely as in the
case of blindness. Residual afference could trigger deafferantiation with histological, biochemical and anatomical changes
in the synapses in order to offset for stimulation, producing
hyper excitable synapses.1
Some authors have related the appearance of CBS as a
stage of evolution towards dementia.1–3 The factors that could
contribute to this evolution include the onset of cognitive
decline, sleep cycle alterations, depression and its extended
duration.4
The paper presented by the authors at the “LXV meeting of
the Neurology Society of Spain (Barcelona, November 19–23,
2013) under the title “Cognitive Deterioration Incidence Study in
Charles Bonnet Syndrome Patients”, analyzed the evolution of
Please cite this article as: Santos-Bueso E, Porta-Etessam J, Sáenz-Francés F, Serrador-García M, García-Sánchez J. Síndrome de Charles
Bonnet y la asociación con demencia. Arch Soc Esp Oftalmol. 2014;89:43–44.
夽
Documento descargado de http://www.elsevier.es el 20/11/2016. Copia para uso personal, se prohíbe la transmisión de este documento por cualquier medio o formato.
44
a r c h s o c e s p o f t a l m o l . 2 0 1 4;8 9(1):42–44
24 diagnosed CBS cases in the Neuroophthalmology Unit
of the San Carlos Clinic Hospital of Madrid. The CBS diagnostic was reached by Ophthalmology, Neurology and Psychiatry
and was reviewed after one and 2 years with anamnesis, complete exploration and specific neurological tests. Some of the
conclusions of said study emphasize that the rate of cognitive decline incidence was 25 times higher than the rate of the
Spanish population for the same age range, with statistically
significant differences.
To conclude, knowledge of CBS and cooperation with Neurology and Psychiatry are of crucial importance to preempt
incorrect diagnostics and treatments. Referring patients to
these specialties is essential to obtain an early diagnostic of
cognitive decline in many of them and prescribe adequate and
specific treatments to contribute to substantial improvements
in their life quality and expectancy.
2. Guerra-García H. Charles Bonnet syndrome and early
dementia. J Am Geriatr Soc. 1997;45:893–4.
3. Terao T, Collinson S. Charles Bonnet syndrome and dementia.
Lancet. 2000;355:2168.
4. Fenelon G, Mahleux F, Huon R, Ziegle M. Hallucinations in
Parkinson’ disease: prevalence, phenomenology and risk
factors. Brain. 2000;123:733–45.
E. Santos-Bueso a,∗ , J. Porta-Etessam b , F. Sáenz-Francés a ,
M. Serrador-García a , J. García-Sánchez a
a Unidad de Neurooftalmología, Servicio de Oftalmología,
Instituto de Investigación Sanitaria, Hospital Clínico San Carlos
(IdISSC), Madrid, Spain
b
Servicio de Neurología, Hospital Clínico San Carlos, Madrid, Spain
∗ Corresponding
reference
author.
E-mail address: esbueso@hotmail.com
(E. Santos-Bueso).
1. Schadlu AP, Schadlu R, Shepherd JB. Charles Bonnet syndrome:
a review. Curr Opin Ophthalmol. 2009;20:219–22.
2173-5794/$ – see front matter
© 2013 Sociedad Española de Oftalmología. Published by
Elsevier España, S.L. All rights reserved.