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Table of Contents    
Year : 2014  |  Volume : 62  |  Issue : 5  |  Page : 557-559

Charles Bonnet syndrome in a case of cerebral venous thrombosis with fMRI-EEG correlation

1 Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore, Karnataka, India
2 Department of Neuroimaging and Interventional Radiology, National Institute of Mental Health and Neurosciences, Bangalore, Karnataka, India

Date of Submission07-Aug-2014
Date of Decision08-Aug-2014
Date of Acceptance28-Sep-2014
Date of Web Publication12-Nov-2014

Correspondence Address:
R Subasree
Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.144489

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How to cite this article:
Subasree R, Kulkarni GB, Kumar M V, Bharath RD, Sandhya M, Yadav R, Modi S, Kumar N, Panda R. Charles Bonnet syndrome in a case of cerebral venous thrombosis with fMRI-EEG correlation. Neurol India 2014;62:557-9

How to cite this URL:
Subasree R, Kulkarni GB, Kumar M V, Bharath RD, Sandhya M, Yadav R, Modi S, Kumar N, Panda R. Charles Bonnet syndrome in a case of cerebral venous thrombosis with fMRI-EEG correlation. Neurol India [serial online] 2014 [cited 2023 Dec 2];62:557-9. Available from:


Charles Bonnet syndrome (CBS) is characterised by complex visual hallucinations with preserved insight in a patient with impaired vision or organic brain pathology. Occipital cortical and other cerebral resections, stroke, multiple sclerosis and temporal arteritis are the organic brain diseases associated with CBS. CBS in cerebral venous thrombosis (CVT) is not yet documented in English literature.

A 27-year-old labourer presented with 4 days history of headache, recurrent vomiting and gradual onset of painless bilateral vision loss. He complained of seeing transient images of vivid human figures like men in uniform, lady combing her hair, lady standing with a shawl, a crying baby, landscapes, buildings and also animals like cat. They lasted only for few seconds to minutes and occurred infrequently almost daily. Patient was aware these were non-existent. They occurred more often in dim light and in evenings. The complex visual hallucinations (VH) disappeared on looking at them and when someone talked to him. There was no past history of psychiatric illness. He had no perception of light in left eye and visual acuity was 3/60 in the right eye. Fundus revealed florid papilledema with haemorrhage and macular exudates. Perimetry revealed enlarged blind spot with concentric constriction of visual fields. There were no other neurological deficits. Computed tomography (CT) brain showed hyper dense superior sagittal sinuses with empty delta sign. [Figure 1]a and b. Magnetic resonance imaging (MRI) showed filling defect in superior sagittal sinus and right transverse sinus and loss of flow void in superior sagittal sinus in T2. MR-venogram revealed thrombosis of superior sagittal sinus, right transverse and straight sinus and few cortical veins [Figure 2]b. Repeat imaging (10 days after onset) showed additional appearance of parenchymal bleed in right inferior frontal gyrus, left temporal region and multiple micro bleeds in susceptibility weighted images. [Figure 3]a-c. Resting functional MR-images (fMRI) were acquired using a 3T scanner (Skyra, Siemens, Erlangen, Germany). For design specification and model of the fMRI the patient was asked to press the start response button at the onset of hallucination and press the end response button at the end of hallucination so as to record the onset and duration of hallucination. 3 sets of visual hallucination in fMRI scan of 9 minutes were recorded. Analysis was performed using statistical parametric mapping (SPM8; Welcome Department of Cognitive Neurology, London). EEG data were recorded using a 32-channel MR compatible EEG system (Brain Products, Gilching, Germany). Functional MRI acquired during hallucination revealed activation of bilateral parietal and temporal cortex. [Figure 2]a. Electroencephalography during rest and visual hallucinations was normal.
Figure 1: (a and b) Hyper dense superior sagittal sinus in plain and empty delta sign on contrast scan respectively

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Figure 2: (a) FMRI showing activation of bilateral (more on dominant side) parietal and temporal regions and (b) MR Venography showing non visualisation of superior sagittal sinus and right transverse sinus

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Figure 3: (a) T1 Sagittal view showing frontal sub acute bleed with loss of flow void in right transverse sinus. (b and c) susceptibility weighted images showing right frontal, left temporal bleeds and micro bleeds with spared parietal lobe

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He also had prothrombotic risk factors like alcoholism, low B12 levels, hyper homocysteinemia and polycythaemia. Patient was started on low dose subcutaneous heparin 5000 U 6 hourly for 7 days overlapped later with acenocoumarol. Visual acuity was monitored regularly and repeat MR-venogram after 2 weeks showed resolution of parenchymal bleed. His follow up perimeter revealed improvement in the visual field. Acuity gradually improved over next 2 weeks to 6/12 in right eye and 6/24 in left eye. As his vision started improving, his hallucinations disappeared over the next 2 weeks period.

CVT presents with a wide spectrum of neurologic features. [1] Acute vision loss with papilledema was described in a patient with severe occipital lobe oedema secondary to venous congestion, pseudo tumour cerebri and cortical venous thrombosis. [2] Intracranial venous sinus thrombosis leading to intracranial hypertension is uncommon. [3] Severe visual loss due to CVT rarely occurs (2% to 4%). On studying 624 cases, Ferro et al. [4] found that persistent visual loss (visual field defects in 6 patients and decreased visual acuity in 21 patients) was more frequent in patients diagnosed as CVT with raised ICT with a delay of more than 4 days from onset of symptoms. Purvin et al. [1] described reduced visual acuity in ten patients of cerebral venous thrombosis with raised ICT.

Several pathologic conditions like focal epilepsy, migraine, diffuse lewy body disease, brainstem or thalamic lesions can cause complex hallucinations. Mechanisms hypothesised are epileptic hallucinations due to irritative process on the cortical centres, visual pathway lesions causing defective visual input and defective visual processing and brainstem lesions affecting various neurotransmitters. [5] Central to the genesis of complex visual forms in man is the visual association (extra striate) cortex. [5],[6]

Manford et al. [5] described two cases of visual hallucinations in abnormal visual field in posterior cerebral infarct involving the occipital cortex. He proposed the "deafferentation" theory and "perceptual release" theory. Ffytch et al. [7] and Santhouse et al. [8] linked certain regions of fMRI signal activation to specific hallucinatory experiences. There was no occipital cortex lesion in our patient and epileptic activity was ruled out by EEG. Vision loss was due to raised ICT with Cerebral venous thrombosis. Hence we hypothesise, that the VH and CBS seen in our patient was probably due to venous congestion and sensory deprivation of visual cortex with subsequent cortical release of extrastriate cortex as evident by FMRI -EEG studies. Management of CBS is supportive and few drugs like sodium valproate, gabapentin, olanzapine and carbamazepine can alleviate symptoms. The CBS in our patient resolved with management of CVT.

 » References Top

Purvin VA, Trobe JD, Kosmorsky G. Neuro-ophthalmic features of cerebral venous obstruction. Arch Neurol 1995;52:880-5.  Back to cited text no. 1
Ko YC, Chen WT, Lin PK, Hsu WM, Liu JH. Cerebral venous thrombosis presenting as acute visual loss. Br J Ophthalmol 2001;85:1140-1.  Back to cited text no. 2
Couban S, Maxner CE. Cerebral venous sinus thrombosis presenting as idiopathic intracranial hypertension. CMAJ 1991;145:657-9.  Back to cited text no. 3
Ferro JM, Canhão P, Stam J, Bousser MG, Barinagarrementeria F, Massaro A, et al. ISCVT Investigators. Delay in the diagnosis of cerebral vein and dural sinus thrombosis: Influence on outcome. Stroke 2009;40:3133-8.  Back to cited text no. 4
Manford M, Andermann F. Complex visual hallucinations. Clinical and neurobiological insights. Brain 1998;121 (Pt 10):1819-40.  Back to cited text no. 5
Burke W. The neural basis of Charles Bonnet hallucinations: A hypothesis. J Neurol Neurosurg Psychiatry 2002;73:535-41.  Back to cited text no. 6
Ffytche DH, Howard RJ, Brammer MJ, David A, Woodruff P, Williams S. The anatomy of conscious vision: An fMRI study of visual hallucinations. Nat Neurosci 1998;1:738-42.  Back to cited text no. 7
Santhouse AM, Howard RJ, ffytche DH. Visual hallucinatory syndromes and the anatomy of the visual brain. Brain 2000;123 (Pt 10):2055-64.  Back to cited text no. 8


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