Clinical Neurology and Neurosurgery 125 (2014) 207–209

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Case Report

Palinopsia without visual field defect: Case report and minireview S. Praveen-kumar ∗ , A. Rajesh Department of Neurology, Bowring & Lady Curzon Hospitals, Bangalore, India

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Article history: Received 16 October 2013 Received in revised form 2 April 2014 Accepted 18 July 2014 Available online 20 August 2014 Keywords: Palinopsia Visual after-images Visual field defects Oligodendroglioma Non-dominant temporo-occipital region

1. Introduction Palinopsia (Greek palin, again and opsis, vision) is a distortion of processing in the visual system in which images persist or recur after the visual stimulus has been removed [1]. Palinopsia typically localizes to a lesion in the non-dominant occipitotemporal cortex and most cases of palinopsia due to posteriorly placed cerebral lesions have an associated visual field defect [1]. There are only rare reports of palinopsia with visual pathway lesions but without such field defects [2]. In such cases, the lesion is presumed to spare the geniculocalcarine radiations. We hereby report a patient who presented with the sole complaint of palinopsia. He had normal visual fields and no neurological deficits. MRI brain revealed a glioma in the temporo-occipital region. The tumour was surgically decompressed and subsequently the palinopsia disappeared. 2. Case report A 47 year old right handed gentleman presented with a week long history of unusual transient visual disturbances. He described seeing persistent images of the persons or objects long after the actual disappearance of the same from his visual field. He had seen repeatedly the images of the saluting posture of a person whom he

∗ Corresponding author at: Department of Neurology, Bowring & Lady Curzon Hospitals, Shivajinagar, Bangalore 560001, Karnataka, India. Tel.: +91 9448685155. E-mail addresses: [email protected] (S. Praveen-kumar), [email protected] (A. Rajesh). 0303-8467/© 2014 Elsevier B.V. All rights reserved.

had seen saluting in front of a temple shrine a few minutes before, he continued to see such images being incorporated in other persons and objects even after that person had already left from the temple; those images were in normal colours and exactly simulating the real persons or objects he has seen some time before, so much so that the patient went to converse with those persons or handling those objects. While driving in his scooter and having crossed the traffic signals, he saw an oblique row of red and green lights in his central vision till he reached his office; having watched his son eat a pastry at home, he noticed other persons on the road and in his office also eating pastries. These visual symptoms would last for few minutes. No emotional response or confusion accompanied these visual disturbances. He had mild heaviness of head for the past 1 week which was not associated with nausea or vomiting. He was a known case of diabetes and hypertension which were fairly well controlled with medications for the same. He had no past history of migraines, epilepsy or any psychiatric illnesses in the past. There was no history of any recent or chronic medication intake. On examination, his general physical examination was normal; pulse was 70 per minute and BP was 130/84 mmHg. Neurologically, he was conscious and oriented. Behaviour and mood were normal. No focal neurological deficits were noted. He underwent formal visual testing. His visual acuity (corrected) was 6/6 bilateral; visual fields on confrontation and formal perimetry were normal. Fundoscopy did not reveal papilloedema. Other systemic examination was normal. Investigations revealed normal routine haematological parameters. Blood glucose and other biochemical parameters were normal. Magnetic resonance imaging of the brain revealed right


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3. Discussion

Fig. 1. T2 weighted MRI brain image revealed right temporo-occipital well circumscribed mass lesion without midline shift.

temporo-occipital well circumscribed mass lesion without midline shift (Fig. 1). The lesion was enhancing on contrast and magnetic resonance spectroscopy showed increased choline peak. The imaging findings were suggestive of glioma. He was started on carbamazepine, but the transient visual symptoms persisted. He underwent right temporo-occipital craniotomy with decompression of the lesion. Post-operative period was uneventful and he did not complain of any such visual disturbances. The resected tissue on histopathological examination showed anaplastic oligodendroglioma WHO grade III. He was then shifted to the care of the oncologist for further radiotherapy and chemotherapy and palliative care.

Palinopsia is a visual after-effect which is usually missed and often misdiagnosed. Much of the difficulty in diagnosing the causes of palinopsia is due in part to its rare and transient occurrence. The physiological basis may be visual after-sensations, a component of normal vision. Visual after-imagery occurs in visual perception. In palinopsia, the illusory image often becomes incorporated appropriately into the visual scene being perceived. Palinopsia is a symptom distinct from the physiological after-image in which images of an object persist or reappear after the person has stopped looking at the object [1]. Bender et al. [1] have compared the similarities and differences between palinopsia and normal visual after-images and these are summarized in Table 1. Though Bender et al. [1] have proposed four possible mechanisms of palinopsia, namely, visual after-sensations, sensory seizures, hallucinations and psychogenic elaborations or fantasies, the exact mechanism is not known. More than one factor may be involved in any single patient. The palinopsia caused by seizures has several characteristic features, including accompanying signs of seizure activity, absence of hemianopia and spread of palinoptic images to involve the whole visual field and response to antiepileptic therapy [1]. There was nothing in the history or symptoms to suggest seizures in our patient and the palinoptic symptoms persisted in spite of starting carbamazepine. Several drugs sharing a 5-HT2-receptor activity or having serotonergic activity like trazodone, lysergic acid diethylamide, risperidone, mirtazepine, topiramate and zonisamide have been documented as causing palinopsia [3]. However, none of these reported drugs were being taken by our patient. Palinopsia typically localizes to a lesion in the non-dominant occipitotemporal cortex [1]. This posterior hemispheric location suggests that it could be due to abnormal cortical or subcortical control of visual synthesis. Since palinoptic imagery is a vivid visual memory of previously viewed scenes, it could be attributed to defective visual information processing in the occipital lobe. Palinopsia may be the result of disordered temporal synthesis of observed visual information, but the precise mechanism remains obscure. Remaining normal occipital cortex may soon compensate for defective temporal integrate, making palinopsia a relatively transient phenomenon [1]. This case demonstrates palinopsia with accompanying lesion of the posterior visual pathway but without any visual field defects. Such reports are sparsely published in literature [2]. Most reported visual pathway lesions associated with palinopsia are right hemisphere lesions and are accompanied by an incomplete

Table 1 The similarities and differences between palinopsia and normal visual after-images [1]. Characteristics

Physiologic after-images

Palinoptic images

Intensity and duration Size

Determined by that of initial visual stimulus Linearly related to the distance from the subject of the background on which it is visualized (Emmert’s law)

Not affected by that of initial visual stimulus Larger when visualized against a distant background

Negative (colours are complementary to those of original object) Positive (corresponds to the original colours) Prolonged or reappear

Same colours as original object (positive) or black and white Same colours as original object (positive) or black and white No effect

May form in both central and peripheral field; several after-images may form concomitantly Perceived binocularly

Multiple images may form in different portions of defective visual field Perceived binocularly

Move in the direction of active eye movements Remain stationary or appear to move in a direction opposite to the movement of the environment

Move in the direction of active eye movements Appear to move in a direction opposite to the movement of the environment

Background against which objects are viewed Light Dark Response to blink/wave of hand in front of eyes/stroboscopic flash Visual fields Response to a stimulus applied to one eye Response to eye movements Active Passive

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left homonymous hemianopia [1]. It occurs during the progressive evolution or resolution of a homonymous visual field defect; the imagery usually appears in the region of altered perception. Palinopsia with cerebral lesions is often [1] but not always [2] associated with visual field defects. Although visual processing circuitry is implicated, the precise neural substrates of palinopsia remain elusive. According to Pelaez, pattern completion in a neural network model of the thalamus and a biologically plausible model of synaptic plasticity are key concepts for analysing cognitive disorders that involve hallucinations of several kinds including visual hallucinations due to psychedelic drug consumption. It has been suggested that all these types of hallucinations are the result of pattern completion dynamics in thalamic deafferented areas [4]. Methods of localizing lesions suspected of inducing palinopsia include CT and MRI brain. However, palinopsia can occur in the presence of normal imaging. By cross-correlating an fMRI time series with hallucinatory events, hallucinatory cerebral activity can be mapped into areas of increased activity, with affected areas defining the type of hallucinatory experience reported [5]. To characterize the functional neuroanatomy mediating perseveratory after-images, Goldstein et al. conducted an fMRI study and concluded that the after-images can be associated with activation of a distinct neural network and the findings of this study potentially offer insight into neural mechanisms mediating a broad range of paroxysmal sensory phenomena (e.g., “flashback”), particularly


those involving disturbances of visual perception of “where” and “when.” Further, these findings may have implications for elucidating the neural mechanisms by which inflammatory mediators (e.g., cytokines) can affect neuropsychiatric function [5]. 4. Conclusion This case upholds the importance of not overlooking rare symptoms, even though they are transient, especially when they are the sole symptoms at presentation. Our case reiterates the fact that posterior visual pathway lesions may cause palinopsia even when formal visual field testing does not disclose hemianopic defects. Presumably the lesions, though in proximity, selectively spare the cerebral visual pathway. Brain imaging should be performed for unexplained palinopsia even when formal visual field testing is normal. References [1] Bender MB, Feldman M, Sobin AJ. Palinopsia. Brain 1968;91:321–8. [2] Ritsema ME, Marjorie A, Murphy MA. Palinopsia from posterior visual pathway lesions without visual field defects. J Neuroophthalmol 2007;27:115–7. [3] Sierra-Hidalgo F, de Pablo-Fernandez E. Palinopsia induced by topiramate and zonisamide in a patient with migraine. Clin Neuropharmacol 2013;36(2):63–4. [4] Pelaez JR. Towards a neural network based therapy for hallucinatory disorders. Neural Netw 2000;13:1047–61. [5] Goldstein MA, Silverman ME, Wang AK, Tuescher O. An fMRI study of the neural mechanisms of palinopsia. J Neuropsychiatry Clin Neurosci 2007;19(2):223–4.

Palinopsia without visual field defect: case report and minireview.

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