Article ID: WMC003210 ISSN 2046-1690

Transient Recurrent Acquired Delayed Eidetic Memory: TRADEM Syndrome-Remembering the Present

Corresponding Author: Dr. Daniel E Jacome, MD, Dartmouth Hitchcock Medical Center Department of Neurology, One Burnham Street, Suite 2, 01376 - United States of America

Submitting Author: Dr. Daniel E Jacome, MD, Dartmouth Hitchcock Medical Center Department of Neurology, One Burnham Street, Suite 2, 01376 - United States of America

Article ID: WMC003210 Article Type: Case Report Submitted on:03-Apr-2012, 02:08:18 AM GMT Published on: 03-Apr-2012, 05:47:21 PM GMT Article URL: http://www.webmedcentral.com/article_view/3210 Subject Categories:NEUROLOGY Keywords:Optic neuritis, Visual hallucinations, Influenza vaccination, Synesthesia, Palinopsia How to cite the article:Jacome DE. Transient Recurrent Acquired Delayed Eidetic Memory: TRADEM Syndrome-Remembering the Present . WebmedCentral NEUROLOGY 2012;3(4):WMC003210 Copyright: This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Source(s) of Funding: Self supported

Competing Interests: None

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Transient Recurrent Acquired Delayed Eidetic Memory: TRADEM Syndrome-Remembering the Present

Author(s): Jacome DE

Abstract myelinolysis (CPM) [2]. In synesthesia the simultaneous engagement of the senses is normally induced by external stimuli, with the exception of ictal epileptic synesthesia [3]. Although never submitted to A seventy eight year old psychiatrist developed rigorous scientific validation, there are similarities recurrent transient episodes of sectoral visual colorful between synesthesia and psychotic behavior. The and detailed memories, as the actual identical events psychotic experience has “a life of its own” or even that have occurred in real life and registered by him in exists as alter ego, albeit detached from reality and previous hours, resurrecting the actual original internally accepted as tangible-real, suggesting the experience in a clear sensorium. He had no additional presence of an internal generator for dissociation and symptoms. In contrast to a previously reported patient “synesthesic re-association”. A unique case of with multiple sclerosis, these “remembered volitional miniature (“lilliputian”) monocular sectoral hallucinations” were not under volitional control and synesthesia in a patient with multiple sclerosis was were mute. They differed from palinopsia because its reported by this author [4]. The patient could voluntary complexity, its vivid detailed overtones, its delayed recall and replayed images of past experiences or presentation, their logical evolving concatenation, and faces with sound, over the right eye only. Yet, no because they were not precipitated by external visual dialogue or direct interaction was established with the cues but originated from within. They could be false images. suppressed by eye movement and by eye closure but A patient with intact cognition, bilateral not by blinking. They were also clinically distinct from post-vaccination retrobulbar optic neuropathy and the hallucinations of Charles Bonnet syndrome. recurrent episodes of eidetic imagery occurring in a Symptoms followed influenza vaccination and clear sensorium is described. He exhibited no signs of dissipated after four months, to never return. psychosis and had no history of migraine. Extensive neurological investigations revealed only the presence of bilateral retro-bulbar optic neuropathy, Case Report suggesting a peripheral visual pathogenic mechanism for the replayed eidetic memories. Introduction A seventy year old retired psychiatrist was seen in neurological consultation for multiple recurrent visual hallucinations in a clear sensorium, in the absence of additional concurrent symptoms of three months Eidetic memory refers to a normally inherited ability to duration. The episodes lasted from three to five recall in vivid detail visual information, with or without minutes. Although the hallucinations were colorful, other senses participation. Eidetic memory can be they were not mobile or shifted, yet, “they were not subdivided: When vivid recall is solely visual, is more frozen in time”. They tended to occupy the upper strictly labeled as “photographic memory” or “eidetic visual fields on both eyes and simulated the playback imagery”. If other senses participate, it constitutes of a silent movie already watched, in luxury of detail. eidetic memory proper, in where the actual recollection There was a delay of up to a few hours in the conforms in its entirety to the original experience [1]. appearance of the hallucinations that spontaneously Modifying factors of the eidetic phenomenon includes reproduced a living scene that took place earlier. For duration, repetition, intensity and affective salience of instance, the national news watched on television the original life experience that is later recalled in great hours earlier, would appeared silently again in front of or greater detail, as “déjà-vécu” [1]. his eyes. Closing either eye did not suppress the Some overlapping exists between synesthesia and visual phenomena but shifting his gaze or closing both eidetic memory proper. Synesthesia may be inherited eyes simultaneously suppressed them. Head position as a unique ability or be acquired, as in the case of changes made no difference in either inducing or bimodal synesthesia secondary to central pontine

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abolishing the hallucinations. They began after appearance. There were no orbital lesions or signs of experiencing severe flu symptoms following routine sinusitis. The optic nerves show no signs of annual influenza vaccination. He never had similar inflammation. His EEG showed a normal background symptoms in the past. He had no headache, nausea, in the absence of focal slowing, periodic complexes or double vision, unilateral weakness and numbness or signs of epilepsy. His visual evoked potentials (VEPs) a near syncope sensation along with the visual revealed poorly formed waves with delayed main symptoms. His partner did not observe any changes in deflection latencies [“P 100”] at several degree check his demeanor, speech fluency and comprehension sizes and up to 140 milliseconds delay at 64 degree during the reported episodes. He had no droopy check sizes on both eyes. No medication was eyelids. He was never confused or acted prescribed. After four months the hallucinations inappropriate. He had no warnings including slurred remitted completed and have not recurred after three speech or tunnel vision. Although he had mild years. depression it was stable and it was never accompanied of any hallucinations. He took bupropion Discussions and conclusion 50 mg and escitalopram 20 mg a day reporting no side effects. He also took atorvastatin, levothyroxine, valsartan, amlodipine, allopurinol, hydrochlorothiazide Visual hallucinations arising from abnormal peripheral and metoprolol at standard doses. Additional history visual pathways are not uncommon. Lepore reported included hypertension, hypothyroidism, mild renal fifty seven patients with visual loss of peripheral origin failure following successful complete resection of renal that had experienced spontaneous visual phenomena cell carcinoma of the left kidney, localized prostate [5]. In 21% of his series the hallucinations were cancer, prostate hypertrophy, gout, obstructive sleep complex in nature. Palinopsia is a visual phenomenon apnea, coronary artery disease, compensated chronic of perseveration. It may be secondary to cerebral obstructive lung disease and coronary artery disease. lesions or may originate in the most peripheral visual One daughter was bipolar and there was family history pathways including the optic nerves. To illustrate this meningioma. He did not smoke or abused alcohol. His clinical occurrence in greater detail, refer to this review of system was significant for high pitched author’s description of a patient with MS, palinopsia tinnitus, nocturia, dyspnea with exertion and for rare and visual extinction on fixation due to retrobulbar ON, angina pectoris. His general physical examination was and to Pomeranz and Lessell review on the subject [6, not contributory. His blood pressure was 132/64 mm 7]. The latter authors reported palinopsia in addition to Hg, heart rate 54, regular and he was afebrile. His was polyopia, in eight patients lacking cerebral lesions. alert and oriented. He did not exhibit attention, Two patients of the latter group had optic nerve language or memory disturbance. Mood and affect involvement (one had optic neuritis and a second were normal. His visual acuity corrected was 20/20. Leber’s hereditary optic neuropathy). A third patient Color perception was accurate. There was no tilting of had macular edema [7]. Palinopsia in patients with the horizon or defects in depth perception. Pupils were peripheral visual pathways compromise is explained irregular from remote cataract surgery. No visual field on basis of occipital cortical release or deficits were identified. He had no conjunctival “deafferentiation” [5, 6, 7]. injection or erythema of the eyelids. There were no The hallucinations of Charles Bonnet syndrome are retinal exudates or hemorrhages on his also complex but somewhat capricious, may be mobile ophtalmoscopic examination. His optic nerves were or stationary and include metamorphosic details or slightly pale. Eye movements were complete and figures lacking internal cohesion, i.e., “having a story symmetric. He had no nystagmus. He had no ptosis or within the story” [8 ]. Conversely, they may present as proptosis and no cranial nerve findings otherwise. He simple hallucinations, i.e., periodic monocular had normal strength and balance. Gait was normal. achromatopsia (personal observation, unpublished). His muscle tone was not increase and there were no They develop in a clear sensorium in subjects with tremors of the hands with held postures, with action or visual defects, more often due to macular at rest. Sedimentation rate, creatine phosphokinase, degeneration and less frequently following optic antinuclear antibody, C-reactive protein and serum neuritis [8 ]. protein electrophoresis were normal. Head CT showed A patient with sectoral, “TV-like”, or “picture within a no acute lesions, bleeding, or hydrocephalus. White picture” spontaneous visual hallucinations involving matter changes indicative of micro-angiopathy and the left inferior visual field was reported by Benegas, expected for age group were identified on his MRI of et, al [9]. She had a right parieto-occipital lobe stroke the brain. The pituitary gland was of normal size and and a left inferior quadrantanopia [9]. Of relevance, the

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patient herein described had no volitional control on Uremia rarely causes ON [21]. Several categories of his hallucinations as in the case of lilliputian monocular uremic related ON may be identified: hallucinations mentioned above, yet, eye movements 1. Anterior ischemic ON due to anemia and transient (shifting gaze and refocusing) and bilateral eye closure recurrent hypotension sometimes precipitated by extinguished the “re-lived memories”. Visual dialysis. hallucinations only during eye closure, hence 2. Demyelinating ON. suppressed by opening of the eyes, may occur 3. Non inflammatory “toxic” axonal ON due to uremia following general anesthesia, and constitutes a rare, or medication adverse effects. transient, post-operative complication of 4. Atrophic ON secondary to uremia related chronic cardiovascular and orthopedic surgery [10, 11]. The idiopathic intracranial hypertension and papilledema opposite is even more exotic; one patient with [21]. monocular quadrantanopic complex visual It is very unlikely that uremic encephalopathy caused hallucinations due to non-arteritic anterior ischemic this patient’s visual hallucination given he had only a optic neuropathy, abolished by closure of the affected mild elevation of his BUN and creatinine, exhibited no eye and gaze aversion, was reported by Toosy, et al. clinical cognitive impairment and had a normal EEG. [12]. His hallucinations were not related to immediate Furthermore, there was electrophysiological evidence or recent events and posed no logic or recognizable of abnormal signal conduction trough his optic nerves. context. He had visual loss congruous with the Given his history, I propose this patient represents a location of his hallucinations [12]. The authors equated clinical example of post influenza vaccination optic the effect of closure of the eye with poor vision, as the neuropathy, first described by Hull and Bates in a restorative mechanism for normal occipital cortical patient with bilateral ON recurring twice, within two activation, once the afferent defective information was weeks of exposure to the annual standard vaccination excluded from central computation [12]. [22]. Blinking on the patient been discussed, did not Recently a construct in the formation, sustenance, interrupt his displayed sectoral visual memories, even modification (“editing”) and expression of memories that blinking, albeit briefly, may interfere with visual into the conscious real was presented by Meyer [23]. recognition in normal circumstances [13]. According to his hypothesis, the present is the past in Disappearance of epileptic occipital hallucinations with process of actualization, where memories contained in “fixation off” (changing the target of fixation) is the the “converging-diverging zone”, are played back into hallmark of epileptic “fixation off sensitivity” (FOS) but “the screen” of the special senses, i.e., the retina and this patient had no occipital lesions, no history of optic nerves. Following this reasoning, a defective seizures and his EEG was normal [14 ]. Although he peripheral sensor occasionally could result in bizarre had history of depression he was never psychotic, his recreations, when the retrieved information from the depression was stable, and he took only small doses cortical convergent-divergent zones supersedes and of escitalopram and bupropion, drugs that rarely may masks the current life images been observed by the cause hallucinations [15][16]. Although under individual. Finally, of speculative philosophical exceptional circumstances synesthesia and palinopsia significance (i.e., time is an illusion created by the constitute migraine manifestations, this patient had no brain), the rare clinical phenomenon of TRADEM, may history of migraine and his hallucinations were not represent a neuro-chronological disorder of time flow, associated or followed by headache [17, 18]. in where past is also the present but only kept It is unclear why the hallucinations were sectoral on “undercover” until it becomes unmasked at the wrong this case, and not assigned to a fixed quadratanopic time and for the wrong reasons [24]. defect, as is in the highly unusual example of sectoral palinopsia [19]. In the absence of hemianopsia his References hallucinations did not constitute visual “mirror” allesthesia, where objects visualized in the normal field transferred, albeit incompletely, to the 1. Stromeyer CF, Psotka, J (1970). “The detailed quadrantanopic “blind” visual field [20]. texture of eidetic images”. Nature 225:346-349. The diagnosis of non-inflammatory retrobulbar optic 2. Jacome DE (2011). Sound induced photisms in neuropathy may be missed in patient with normal or pontine and extrapontine myelinolysis. Clin Neurol near normal visual acuity, or when it develops in Neurosurg 113:503-505. isolation. Its diagnosis is best established by 3. Jacome DE, Gumnit RJ (1979). Audioalgesic and performing visual evoked potentials (VEPs) since MRI audiovisuoalgesic synesthesias: epileptic of the orbits will fail to show acute demyelination. manifestation. Neurology 29:1050-1053.

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4.Jacome DE (1999). Volitional monocular lliliputian 21. Winkelmayer WC, Eigner M, Berger O, Grisold W, visual hallucinations and synesthesia. Eur Neurol Leithner C (2001). Optic neuropathy in uremia: An 41:54-56. interdisciplinary emergency. Am J Kidney Dis 37: E23. 5. Lepore FE (1990). Spontaneous visual phenomena with visual loss. Neurology 40:444-447. 22. Hull TP, Bates JH (1997). Optic neuritis after 6. Jacome DE (1985). Palinopsia and bilateral visual influenza vaccination. Am J of Ophtalmol 124: 703-704. extinction on fixation. Ann Ophtalmol 17:251-252. 23. Meyer K (2012). Another remembered present. 7.Pomeranz HD, Lessell S (2000). Palinopsia and Science 335: 415-416. polyopia in the absence of drugs or cerebral disease. 24. Callender C (2012). Is time an illusion? Scientific Neurology 54: 855-859. American 21: 14-21. 8. Komeima K, Kameyama T, Miyake Y (2005). Charles Bonnet syndrome associated with a first attack of multiple sclerosis. Jpn J Ophtalmol 49:533-534. 9. Benegas NM, Liu GT, Volpe NJ, Galetta SI (1996). “Picture within a picture” visual hallucinations. Neurology 47: 1347-1348. 10. Laloux P, Osseman M (1992). Visual hallucinations on eye closure after cardiovascular surgery. J Clin Neuroophtalmol 12: 242-244. 11. Otomo S, Sugita M, Yano T (2008). Visual hallucinations on eye closure after orthopedic surgery under general anesthesia. J Anesth 22: 439-442. 12. Toosy AT, Roberton BJ, Jayaram H, Plant GT (2006). Monocular complex visual hallucinations and their suppression by eye closure. Eye 20: 732-733. 13. Thomas LE, Irwin DE (2006). Voluntary eye blinks disrupt iconic memory. Percept Psychophys 68:475-488. 14. Kurth C, Bittermann HJ, Wegerer V, Bleich S, Steinhoff BJ (2001). Fixation-off sensitivity in an adult with symptomatic occipital epilepsy. Epilepsia 42: 947-949. 15. Capaldi VF, Carr RB (2010). Citalopram-induced hallucinations and delusions in a young adult. Gen Hosp Psychiatry 32: 648. 16. Ames D, Wirsching WC, Szuba MP (1992). Organic mental disorders associated with bupropion in three patients. J Clin Psychiatry 53: 53-55. 17. Alstadhaug KB, Benjaminsen E. (2010). Synesthesia and migraine: case report. BMC Neurology 10: 121-123. 18. Belcastro V, Cupini LM, Corbelli I, Pieroni A, D’Amore C, Caproni S, Gorgone G, Feriazzo E, Di Palma F, Sarchielli P, Calabresi P (2011). Palinopsia in patients with migraine: a case-control study. Cephalalgia 31: 999-1004. 19. Nagata T, Yamashita Y, Hada H, Sogabe T (2001). A case of visual perseveration attack caused by transverse-sigmoid sinus dural arteriovenous fistula. Rinsho Shinkeigaku 41: 498-502. 20. Kasten E, Poggel DA (2006). A mirror in the mind: a case of visual allesthesia in homonymous hemianopia. Neurocase 12: 98-106.

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