Case ReportEpileptic mechanisms in Charles Bonnet syndrome
Introduction
Charles Bonnet syndrome (CBS) is characterized by persistent or repetitive complex visual hallucinations (CVHs) occurring in the context of intact cognitive status and consciousness, with preserved insight (pseudo-hallucinations) [1], [2]. The eponym CBS has recently been applied to CVHs arising within the hemianopic field in lateralized central visual pathway lesions [3], [4]. Although CVHs, sometimes lateralized, can be a component of focal epileptic seizures [5], [6], [7], epileptic activity has generally not been found to be the cause of CBS hallucinosis [4]. We describe a patient whose CBS clinical course was closely associated with epileptic phenomena.
Section snippets
Case report
A 65-year-old, right-handed woman with hypertension and type II diabetes mellitus was referred with a 6-day history of progressive worsening of existing gait disturbances, resulting from a right parietal intraparenchymal hemorrhage, caused by hypertension, that occurred 4 months earlier. This event had been complicated by tonic–clonic epileptic status and eventually resulted in a left hemiparesis, mild gait ataxia, and marginal left hemianopia. Seizures had since been controlled with valproate
Discussion
The case we describe suggests that epileptic mechanisms (right-sided PLEDs plus associated with focal seizures) can play a role in the occurrence of recurrent CVHs that meet diagnostic criteria for CBS [1], [2].
Our patient's CBS occurred in the context of worsened neurological status with new neurological signs, 4 months after a right parietal hemorrhage. Two types of hallucinatory experiences occurred: CHVs and delayed palinopsia (the delayed hallucinatory return of real objects to the visual
Acknowledgment
The authors wish to thank Professor Ian McKeith for his helpful suggestions on the article.
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The utility and application of electrophysiological methods in the study of visual hallucinations
2018, Clinical NeurophysiologyCitation Excerpt :Slowing in posterior and occipital regions in the absence of epileptiform discharge has also been observed in a patient with seizures and another patient with CBS during complex VH (Josephson and Kirsch, 2006). Furthermore, epileptiform discharges in conjunction with complex VH have been observed over right-sided centro-parietal regions in a patient with CBS, with both epileptic activity and VH diminishing following antiepileptic treatment (Ossola et al., 2010). However, slowing is not a consistently reported phenomena; both intermittent and continuous periodic occipital and temporal sharp and spike waves have been observed in occipital epilepsy with elementary VH (Yalçin et al., 2000; Oishi et al., 2003; Alves-Leon et al., 2011), while epileptic mechanisms including generalised periodic synchronous discharges have also been observed in conjunction with complex VH and cognitive dysfunction in DLB (Sun et al., 2014).
Palinopsia revamped: A systematic review of the literature
2015, Survey of OphthalmologyCitation Excerpt :Epileptic discharges are commonly associated with palinopsia, but the seizure is usually secondary to an easily diagnosable cortical lesion or metabolic disturbance (Sections 3.1 and 3.2). There are six cases of palinopsia from idiopathic seizures,17,75,107,115,133,141 five of which reported hallucinatory palinopsia (Appendix). There are nine cases of palinopsia from diffuse cortical pathology: three from multiple sclerosis8,71,117 (MS), three from posterior cortical atrophy (PCA) variant of Alzheimer disease,33,145 one from a primary B-cell lymphoma with unremarkable neuroimaging,135 one from Creutzfeld-Jacob disease (CJD),119 and one from an epileptic ion channel mutation42 (Appendix).
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