Parkinson's Disease With Visual Hallucinations Is Associated With Epileptiform Activity on EEG

Background: Visual hallucinations (VHs) in Parkinson's disease (PD) are the cardinal symptoms which declare the onset of PD psychosis (PDP). The anthropomorphic and zoomorphic VHs of PD resemble those of Charles Bonnet syndrome and temporal lobe epilepsy. In both of these disorders electroencephalography (EEG) abnormalities have been described. We therefore sought to examine whether VHs in PD were associated with similar EEG abnormalities.Methods: This retrospective observational study searched the medical records of 300 PD patients and filtered for those containing clinical 20-min scalp EEGs. Remaining records were separated into two groups: patients with reported VHs and those without. The prevalence of epileptiform discharges in the EEGs of both groups was identified.Results: Epileptiform discharges were present in 5 of 13 (38.5%) PD patients with VHs; all localized to the temporal lobe. No epileptiform discharges were observed in the EEGs of the 31 PD patients without VHs.Conclusion: The significantly high incidence of temporal lobe epileptiform discharges in PD patients with VHs as compared to those without VHs lends to the possibility of an association visual cortex epileptogenic focus. Accordingly, for treatment-refractory patients, antiepileptic drugs might be considered, as in the case of Charles Bonnet syndrome, temporal lobe epilepsy and migraine with visual aura. Future prospective studies involving larger samples and multi-center cohorts are required to validate these observational findings.

Charles Bonnet syndrome as first manifestation of occipital infarction

Purpose To describe a case of Charles Bonnet syndrome as the first manifestation of occipital infarction in a patient with preserved visual acuity. Observations We report a 78-year-old man followed in our department with a two-month-long history of visual hallucinations based on the vision of flowers and fruits intermittently, being perceived as unreal images. Best-corrected visual acuity was stable in the follow-up time being 20/20 in the right eye and 20/25 in the left eye. Extraocular muscle function testing, pupillary reflexes, biomicroscopy, fundus and optical coherence tomography examinations did not reveal any interesting findings. In order to rule out occipital pathology, orbital-cerebral magnetic resonance imaging was performed, showing an image compatible with the chronic ischemic right occipital lesion. The patient was diagnosed with Charles Bonnet syndrome secondary to occipital infarction and neurology decided that no treatment was required. 24-2 and 10-2 visual field tests showed no remarkable alterations and Full-field 120 point screening test showed nonspecific peripheral defects. Hallucinations improved over the months, being described as not annoying and increasingly infrequent. Conclusions and Importance Charles Bonnet syndrome is a condition characterized by the presence of recurrent and complex visual hallucinations in patients with visual pathway pathologic defects. Visual acuity or visual field loss is not a requirement for diagnosis. Charles Bonnet syndrome should be suspected in all patients with non-disturbing visual hallucinations, even though they present good visual acuteness. It will be essential to perform complementary explorations to identify the underlying pathology that allows the starting of a correct treatment option.

A Case Study on Polypharmacy and Depression in a 75-Year-Old Woman with Visual Deficits and Charles Bonnet Syndrome

Depression is one of the most prevalent pathologies in older adults. Its diagnosis and treatment are complex due to different factors that intervene in its development and progression, including intercurrent organic diseases, perceptual deficits, use of drugs, and psycho-social conditions associated with the aging process. We present the case of a 75-year-old woman (who lives in the community) with a diagnosis of major depression with more than 10 years of history, analyzing her evolution and therapeutic approach.

Abstract 1122‐000107: Charles Bonnet Syndrome Secondary to Massive Dural Arteriovenous Fistula Disguised as Extensive Venous Sinus Thrombosis

Introduction : Charles Bonnet Syndrome is characterized by visual hallucinations that can occur following severe visual insult, rarely due to dural arteriovenous fistulas (DAVF) or cerebral venous sinus thrombosis (CVST). Prompt differentiation between DAVF and CVST is important since treatments may differ and inadequate treatment may result in blindness. We highlight a patient who presented with Charles Bonnet Syndrome initially misdiagnosed with CVST by MR venography and later correctly diagnosed with a massive DAVF with superimposed CVST by digital subtraction angiography and underwent DAVF embolization with complete resolution. Methods : Case Report. Results : A 78 year‐old man with hypertension and hyperlipidemia presented with three weeks of bilateral vision loss associated with formed hallucinations exacerbated by dark rooms. Neurological exam revealed decreased visual acuity of 20/400 and grade five papilledema bilaterally. Non‐Contrast (TOF) MR venogram revealed lack of flow in the superior sagittal sinus (SSS), straight sinus (SS) and deep venous system, and partial flow of the left transverse and sigmoid sinus and left jugular vein. MR brain without gadolinium was unremarkable. Cerebral angiography revealed a high‐grade DAVF predominantly supplied by the occipital branch of the left external carotid artery [Figure 1; A‐C], with retrograde flow into the left sigmoid, transverse, superior sagittal, and straight sinuses, as well as retrograde flow into the right vein of Trolard [Figure 1; A‐D]. The left distal sigmoid sinus and left jugular bulb were occluded. The left transverse and proximal left sigmoid venous sinuses were compartmentalized from non‐occlusive thrombus, while the SSS and bilateral transverse sinuses where patent [Figure 1; A, B]. Embolization using coils and onyx was performed with complete occlusion of the left transverse and sigmoid sinuses, the points of main drainage of the fistula, as there was no single trans arterial pedicle suitable for embolization. Postembolization angiography demonstrated a Cognard Grade 1 fistula with some residual fistulous shunting of the occipital artery to the torcula. Follow up angiogram at six weeks showed interval occlusion of the residual shunt. He had minimal improvement in his vision at three months of follow up. Conclusions : This case highlights a patient with Charles Bonnet Syndrome due to a high flow DAVF. The MR venogram failed to capture the DAVF since the retrograde flow was interpreted as thrombosis on MRV. DAVF and CVST have a complex cause‐effect relationship, since thrombosis may open up venous channels that can lead to a fistula and sluggish blood flow from a fistula may stimulate thrombus formation. Treatments between CVST and DAVF differ since high grade DAVF often require endovascular embolization and anticoagulation may increase the risk of intracerebral hemorrhage in a subset of patients. Digital subtraction angiography and/or contrast enhanced MRV should be considered in cases of suspected extensive thrombosis to help differentiate between thrombosis and DAVF.