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Show Journal of Clinical Neuro- ophthalmology 10( 2): 103- 110, 1990. Visual Illusions Associated with Previous Drug Abuse Leah Levi, M. D., and Neil R. Miller, M. D. © 1990 Raven Press, Ltd., New York We describe the visual illusions experienced by five patients with a history of previous use of hallucinogens, marijuana, or both. Symptoms included shimmering of images, illusory movement of images, visual perseveration of stationary objects, streaking of moving objects, and moving objects appearing as a consecutive series of stationary images. In all cases, the symptoms had persisted or recurred after periods of drug abstinence ranging from several months to several years. Despite thorough and repeated examinations and investigations, there was no evidence of neurologic ophthalmologic disease in these patients. When patients present with these and other visual illusions, a thorough drug history may afford the answer, provided that other recognized causes of these visual symptoms, such as migraine, epilepsy, and intracranial lesions have been excluded. Key Words: Visual illusions-- Drug abuse. From the Neuro- Ophthalmology Unit, The Wilmer Eye Institute, The Johns Hopkins Medical Institutions, Baltimore, Maryland. Address correspondence and reprint requests to Dr. MilIe~ at Maumenee B- 109, The Wilmer Institute, The Johns Hopkins Hospital, 601 N. Wolfe Street, Baltimore, MD 21205, U. S. A. 103 Ophthalmologists and neuroophthalmologists are often asked to evaluate patients with visual difficulties that seem to defy explanation. The complaints may seem vague and perceptual in nature, and a complete neuroophthalmologic examination usually yields no clues. Referral for neurologic examination and neuroimaging is typically unrewarding, and finally the patient is thought to have either a nonorganic problem or to be hyperaware of what are probably normal visual sensations. There are, however, patients with a history of drug abuse in whom the unusual visual symptoms seem to be related to previous use of illicit drugs. These patients are not " hard- core" drug users but have used drugs " recreationally." Such patients do not readily admit to the physician that they have used illicit drugs, even when questioned directly. In view of the severe problem with illicit drugs in the United States and the attempt by the Federal Government to prevent children and adolescents from using these drugs, it seems appropriate to review the findings in six such patients that we have evaluated and to emphasize their visual difficulties. CASE REPORTS Patient 1 An otherwise healthy 19- year- old man complained of visual difficulties that had begun 8 months earlier. He was a daily user of marijuana at the time his symptoms began. On one occasion, while high on marijuana, he noticed that the environment surrounding his point of fixation would seem to move from side to side. Friends smoking marijuana obtained from the same dealer at the same time did not notice any unusual visual effects. The patient's visual disturbance persisted, even though he eventually stopped using marijuana. It was present during both monocular and binocular viewing, and it was particularly trouble- 104 L. LEVI AND N. R. MILLER some during reading. The patient denied any use of lysergic acid diethylamide ( LSD), but he had ingested an hallucinogenic mushroom - 1 year before the onset of visual symptoms. Before referral to the Neuro- ophthalmology Unit of the Johns Hopkins Hospital, he had been examined by several physicians, including a neurologist and an ophthalmologist, and he had undergone testing of visual evoked responses, a head computed tomographic ( CT) scan, magnetic resonance ( MR) imaging, and toxicology screening. Results of all examinations and tests were normal, including rapid plasma reagin ( RPR), fluorescent treponemal antibody absorption ( FTA- Abs), and human immunodeficiency syndrome ( HIV) serum testing. A complete neuroophthalmologic examination, including static and kinetic perimetry and tests of fusional amplitudes, was normal. The patient had no nystagmus or any other disorder of ocular motility. Patient 2 A healthy 27- year- old man complained of intermittent visual disturbances dating from midadolescence. He had used marijuana almost daily from age 14 to 16, but he denied having used any other drugs, including LSD or similar hallucinogens. His visual difficulties began when, while smoking marijuana, he experienced loss of depth perception, as well as a " strobe light effect" characterized by seeing a moving object as if it were a series of still pictures. When people talked, it seemed to the patient that the movements of their mouths were not synchronized with their voices. Friends who were smoking marijuana obtained from the same dealer at the same time did not report any similar visual disturbances. This experience so frightened the patient that he never again used marijuana or any other illicit drug. For the next year, however, he experienced similar visual episodes, lasting - 1 h and occurring up to several times a day. The patient had no headache or nausea preceding, during, or following any of these episodes, nor did he have any past history of migraine. The episodes could be precipitated by describing the experience to others, by stress, or by being near others who were smoking marijuana. Over time, the " strobelight effect" recurred less frequently, but lack of depth perception remained a constant symptom. The patient was evaluated by numerous physicians, including ophthalmologists, none of whom found any abnormalities. A recent electroencephalogram ( EEG) and CT scan of the head were normal. Toxicology screening was negative as were PPR f: T/, Abc ,~'" ld HIV ,,~ says. J Llul j .. tUici l"' r/ lfluillif.';, , I,'; i'l j ""," 1 The only abnormality found in a complete neuroophthalmologic examination was stereoacuity of only 140 s of arc, despite normal visual acuity, color vision, and visual fields tested kinetically. There was no evidence of strabismus or amblyopia. Patient 3 A 29- year- old man presented with a 4- year history of visual disturbance, consisting of the constant shimmering of images, as if he were looking through " heat waves." The disturbance occurred during both binocular and monocular viewing. The patient had no history of migraine or epilepsy, but about 10 years previously, he had used marijuana, cocaine, and LSD, although he denied having used these substances for several years. At about the time of onset of visual symptoms, the patient also developed severe depression and was treated with a tricyclic antidepressant. The patient experienced gradual improvement in both depression and visual symptoms over the next 2 years. Both the visual symptoms and the depression recurred after he was involved in a hang- gliding accident, but an opthalmologic examination, head computed tomographic CT scan, and EEG at that time were normal. The depression was subsequently treated successfully with electroshock therapy, but this did not change the visual disturbance. Just before his evaluation in the Neuroophthalmology Unit, he had been given a medication containing epinephrine by his dentist, and he thought that this had improved his visual symptoms. A recent tOxicology screen was negative. A complete neuroophthalmologic examination including both static and kinetic visual field testing was normal, as were the results of a VEP. Serologic tests, including RPR, FTA- Abs, and HIV assay were negative. MR imaging and positron emission tomographic ( PET) scanning, performed while the patient was experiencing his symptoms, were also normal. Patient 4 A 31- year- old man related a 13- year history of visual problems. He had smoked marijuana at least every other day, and he also admitted to amphetamine and barbiturate usage. He had taken LSD on one occasion. Two years after his last drug use, he noticed that moving light sources in a dark environment appeared as long streaks, similar to the effect of a long- exposure photograph. He could not recall noticing this effect during his past drug experiences, but he admitted that he had usually VISUAL ILLUSIONS AND PREVIOUS DRUG ABUSE 105 kept his eyes closed. He subsequently observed that after looking at any object, a clear and life- like image would persist for several seconds to several minutes, even if he closed his eyes. Over several years, these symptoms had become so prominent that he was no longer able to read or to watch television. The streaking appearance of moving objects also persisted. He had seen a number of neurologists, ophthalmologists, and neuroophthalmologists over a period of at least 10 years, none of whom had found any abnormalities. In addition, past and recent EEG's, a head CT scan, MR imaging, and a variety of serologic studies ( e. g., serologic tests for syphilis, assay for antinuclear antibodies, HIV titers) were normal as were two separate toxicology screening examinations. A complete neuroophthalmologic examination including both static and kinetic visual field testing was normal. The patient subsequently underwent acupuncture and hypnosis, neither of which were successful in alleviating his symptoms. Patient 5 A 31- year- old man complained of visual difficulties that began at about age 25. The difficulties were characterized by episodes in which images of viewed objects would " speed up" as if the patient were watching a " motion picture at fast speed." The patient was evaluated by a neurologist who performed an EEG that was normal. The patient was told that his visual problem was " emotionaL" The symptoms initially improved but recurred about 9 months later, at which time the patient also noted that actual moving objects seemed to have " disjointed movements." The patient was aware that these perceptions were essentially hallucinations, and this realization frightened him. He began seeing a psychologist who thought that he had problems with " self- image." About 1 year after his visual symptoms began, the patient began to experience " flashbacks." He became confused about temporal events, and he began to notice changes in his personality. He began to believe that if he stared in certain ways at objects, they would change their appearance and movement. He experienced macropsia and micropsia when looking at objects. The patient saw several psychiatrists who told him he was too " emotional" and that he was having a " nervous breakdown." He was placed on tricyclic antidepressant agents without improvement in his symptoms. He was then seen by one neurologist who thought he was experiencing partial complex seizures even though an EEG was normal. He was placed on carbe-mazepine without improvement. A second neurologist thought his visual disturbances might be caused by migraine and placed the patient on propranolol, again without improvement. Because of the difference in opinions between the two neurologists, the patient was referred to the NeuroOphthalmology Unit of the Johns Hopkins Hospital. The patient initially denied any history of drug abuse; however, after repeated questioning, he admitted to having used a variety of illicit drugs on several occasions beginning - 1- 2 years before the onset of visual symptoms. He had smoked marijuana on several occasions, he thought he had used cocaine once, and he " might" have used crack cocaine on at least one occasion. In addition, he stated that he had attended a party during which he unknowingly ingested some type of hallucinogenic substance. The patient's mother stated that she had seen her son the day after this party and that he was very confused and had difficulty with his recent memory. The patient stated that he had not used any illicit drugs for the last 4 years, but he thought that at least once while he was smoking marijuana, he experienced disturbances of visual perception similar to those that he was currently experiencing. A complete neuroopthalmologic examination that included both static and kinetic visual field testing and testing of stereoacuity gave normal results. The patient underwent a CT scan, MR imaging, testing of visual evoked responses, and another EEG. All of these studies gave normal results. Toxicology screening was negative, as were serologic tests for syphilis and HIV. Patient 6 A 36- year- old man had noticed " streaking" of moving objects for 2 years. This visual disturbance occurred if an object moved across his visual field, but not if he directly tracked the object. The effect was most dramatic at night with car lights, which would appear as long streaks. The patient denied any formed or unformed hallucinations, nor did he experience any formed afterimages or oscillopsia. He did, however, develop motion sickness whenever there was motion in the visual periphery, such as when he was driving a car or watching a movie containing moving objects on a large screen. This latter symptom did not occur with selfmotion. The patient denied any other neurologic symptoms, including headache. He initially denied use of illegal drugs, but he later admitted to almost identical experiences after ingesting LSD in 1elin Neuro- ophtlullmol, Vol. 10, No. 2, 1990 106 L. LEVI AND N. R. MILLER the late 1960s, about 20 years previously. In fact, he and his companions had regularly used the " streaking" of moving objects as an indication that the drug had begun to take effect. He had not used hallUcinogens for the last 10 years, but he had used numerous other drugs, including marijuana, hashish, amphetamines, and cocaine up to 5 years before his present visual difficulties. None of these drugs caused visual symptoms similar to his current complaints. The onset of symptoms occurred during a period of great stress, but they did not resolve when the stress abated. Ophthalmologic and neurologic evaluations performed 2 years before his referral, including a head CT scan and an EEG, had shown no abnormalities. A recent otolaryngologic examination was also normal. Complete systemic, neurologic, and neuroophthalmologic evaluations at The Johns Hopkins Hospital, including quantitative eye movement recordings, serologic tests for syphilis, screening for HIV, and a toxicology screen were normal. MR imaging of the brain was also normal. COMMENT Although popular lore emphasizes the spectacular hallucinations that may accompany the use of LSD, the dominant effects are abnormal visual perceptions rather than true hallucinations ( 1,2), prompting the term " illusionogen" to characterize this and comparable drugs ( 2). Visual flashbacks have been estimated to occur in about 5% of hallucinogen users ( 3,4), most of the visual complaints consisting of disturbances of visual perception. Included in these visual illusions are alterations of color perception, positive and negative afterimages, illusions of movement, haloes around objects, shimmering of images, micropsia, macropsia, metamorphopsia, teleopsia, and palinopsia or visual perseveration ( 2,3,5- 9). What is often not appreciated, by either the clinician or the patient, is that these phenomena are not dose- related ( 4,9), may occur after only one exposure to LSD ( 2,3,9), and may begin long after the cessation of drug taking ( 10,11). In addition, both marijuana and hashish can induce flashbacks at the time of use or shortly thereafter in subjects who have previously used LSD ( 3,9,12- 14). In fact, it has been stated that the factor that correlates best with the occurences of flashbacks in LSD users is previous use of marijuana ( 14). Visual flashbacks also have been reported after the use of marijuana alone ( 4,14,15); however, given the frequent impurity and contamination of illicit drugs, and questions about the re-liability of the accounts of some of these patients, it is difficult to completely exclude the possibility of exposure to an hallucinogen in these cases. Since many of the illusions interfere with visually demanding activities such as reading, driving, or watching television, the likelihood is high that the patient will present initially to the ophthalmologist. There may be a great deal of reluctance at the first encounter to volunteer a history of past drug abuse, even if the patient is specifically questioned about it; however, even if the relationship between previous drug use and the visual symptoms seems clear, it is important that this possible cause be considered a diagnosis of exclusion. Patients with acquired nystagmus and oscillopsia, or with an acquired mild or intermittent strabismus frequently describe apparent movement of images and of reading material. In addition, patients with refractive errors, particularly undercorrected hyperopia or presbyopia, or patients with poor fusional amplitudes often have vague complaints of letters merging together or print moving about when they attempt to read. A thorough history and ophthalmologic examination will usually identify the cause in these cases, but in some patients the symptoms may be difficult to differentiate from illusory movement of the environment ( described by patient 1 when reading) or visual perseveration of printed words ( described by patient 4 when reading). Of perhaps greater significance is that all the visual illusions associated with LSD or marijuana use have also been described in patients with migraine, with epilepsy, and with intracranial lesions, particularly tumors and infarcts in the parieto- occipital region. In cases of migraine ( 16- 18) and epilepsy ( 16,19- 21), the episodic nature of the symptoms and the associated features suggest the diagnosis, and most patients with disorders such as tumors or vascular malformations ( 20,22- 26), traumatic damage ( 19), or hemisphere stroke ( 20,23,27,28), also have a homonymous hemianopic visual field defect. Since these clinical features are not invariate, however ( 20,27,29,30), it is imperative that these causes be excluded with a complete history and neuroophthalmologic examination, and with investigations such as EEG and appropriate neuroimaging studies, before ascribing the symptoms to the effects of past drug exposure. To underscore this point, one of the patients initially reported by Abraham as having LSD- related visual illusions ( 9) proved later to have temporal lobe epilepsy that was responsive to carbemazepine ( 16). All six of our cases presented with visual per-j '_ 1", ,., . oIli · " I" ltfUI/," .. ' , !. r" VISUAL ILLUSIONS AND PREVIOUS DRUG ABUSE 107 ceptual difficulties, and all had been evaluated and investigated extensively, generally over a period of several years ( Table 1). With the exception of the decreased stereopsis in patient 2, no abnormalities had ever been found in any of the patients. The three patients who had also used cocaine in the past ( patients 3, 5, and 6) had no evidence of cerebral infarction by CT scanning or MR imaging. In all cases, visual symptoms had persisted or recurred despite a drug- free interval of up to several years. In four of the patients ( patients 1, 2, 5, and 6), visual symptoms were first experienced during drug use. For patients 1 and 2, and probably patient 5, the drug being used at the time of visual symptoms was marijuana, whereas patient 6 first noted a visual disturbance as a typical effect of LSD. In the other two patients ( 3 and 4), it was less clear whether the visual symptoms had occurred during drug use: Patient 3 admitted that he had usually kept his eyes closed during drug intoxication. However, their complaints were identical to those previously reported as occurring in flashbacks, and there was no evidence of any other ophthalmologic, neurologic, or neurosurgical cause. Both patients had used marijuana extensively in the past and had also used LSD. The patients described a number of visual illusions typical of drug- related flashbacks: Patient 1 noted that the environment around his point of fixation would appear to move ( 2,9,11); patient 2 saw a series of successive still images when viewing a moving object ( 7,8), and he had decreased depth perception ( 5); patient 3 described shimmering images ( 3,6,11); patient 4 saw moving objects as streaks ( 9), and he experienced visual persevera- Age TABLE 1. Patient summary Patient 2 3 4 5 6 19 27 29 31 31 36 Drug Marijuana, mushroom Marijuana Marijuana, LSD, cocaine Marijuana, LSD Marijuana, cocaine, crack. hallucinogenic substance (?) Marijuana, LSD. cocaine, hashish, numerous others Effect Movement of images Strobe light effect, loss of stereopsis Shimmering Streaking effect, palinopsia Speeding up of moving images, macropsia. micropsia Streaking effect tion of stationary objects ( 5); patient 5 experienced inappropriate speeding up of moving images, and he also experienced micropsia and macropsia when he stared at objects; and patient 6 saw moving objects as streaks ( 9). In addition to these difficulties, patient 6 experienced motion sickness when objects moved in the visual periphery. To our knowledge, this complaint has not been previously reported in association with drug abuse. The visual illusions associated with drug abuse have been dismissed as being merely increased awareness of normal phenomena ( 6). Support for this theory comes from the work by Heron et al. ( 31), who reported that some patients experience identical symptoms after prolonged isolation. Nevertheless, since identical symptoms also have been described in patients with known intracranial lesions and since the individual complaints are so stereotyped, we believe that the visual illusions reported by our patients reflect true organic defects. Some speculation may even be possible as to the sites of the lesions responsible for these symptoms. The streaking of moving objects, described by patients 4 and 6, and indeed by about 44% of subjects who have used LSD at least once, has been termed " the trailing effect" and has been defined as " formed positive afterimages that remain immediately behind an object as it moves across the subject's visual field" ( 9). To confuse the terminology, " the trailing effect" has also been defined as " seeing a moving object ... in serial momentary stationary positions" ( 7). This latter description is like the " strobe light effect" reported by patient 2, and is distinct from the streaking effect seen by patients 4 and 6. We do not think that it is appropriate to use the term " trailing effect" for both types of experience. Streaking is most likely a manifestation of the perseveration of each successive image of the moving object, the subject appreciating nevertheless that the object is moving smoothly. Indeed, patient 4 perseverated stationary objects in addition to seeing streaking of moving objects. Visual perseveration, or palinopsia, has been described in patients with tumors of the parietooccipital region ( 19,22- 25,27,28), especially in the nondominant hemisphere, in patients with migraine ( 17,18), and in patients with temporal lobe epilepsy ( 21). Long- term effects on the parietooccipital or temporal regions may be the cause of visual perseveration in past drug users. In the strobe light effect, on the other hand, the object does not seem to move smoothly, but appears to complete its trajectory via a succession of J( lin Neuro- ophlhalmol, Vol. lO, No. 2, 1990 108 L. LEVI AND N. R. MILLER still images, none of which persists. This is clearly a motion perception defect rather than visual perseveration, although there have been some cases where both mechanisms seem to operate and create an image like " a stroboscopic photograph with multiple exposures" ( 8). It is most interesting that in patient 2 the strobe light effect was accompanied by a subjective and objective loss of depth perception, an observation which allows us to conjecture about the anatomical location of this patient's problem. The symptoms experienced by patient 2 are similar to those reported by Zihl et al. ( 29) in a patient who developed a sagittal sinus thrombosis that resulted in bilateral infarcts of the temporoparietal and occipital periventricular white matter. The patient's only complaint was that moving objects would appear as two or more still images. Psychophysical testing confirmed that the patient had a severe defect in motion perception. Like our patient 2, the patient had moderately decreased stereopsis, but the remainder of the neuroophthalmologic examination, including visual field testing, was completely normal. The similarities between patient 2 and this case support our belief that patient 2' s complaints were caused by altered motion perception rather than by visual perseveration. In a study of head injuries causing damage to one or both parietooccipital regions, it was reported that many of these patients would see moving objects as a series of stills and that all had defective motion perception by psychophysical testing ( 25). Abnormal motion perception also seems to be responsible for the increased speed of moving images observed by patient 5. This patient complained that the environment moved as if he were viewing a motion picture running at fast speed. This disturbance is essentially the opposite of that experienced by patient 2. Experimental studies attempting to define the anatomic basis for visual motion perception have shown that area medial- temporal ( MT), located along the dorsal third of the posterior bank of the middle temporal sulcus, is important in visual motion processing in the monkey ( 32,33). It is relevant to the patient described by Zihl et al. ( 29) and to our patient 2 that, in monkeys, MT also contains cells that code for binocular disparity ( 34). It could be speculated that marijuana, or an hallucinogenic contaminant, may have affected the human homologue of area MT, possibly in the temporoparietal region, leading to both the strobe- light effect and the decreased stereopsis reported by patient 2. These drugs may be of interest as a potential means of studying the neurophysiology of motion pprcpntinn The shimmering of images described by patient 3 has been reported with a mass of the right occipital lobe ( 23), after an injury to the " left posterior hemisphere ( 27)," and in a patient with migraine ( 17). The apparent movement of images reported by patient 1 has been also described in patients with bilateral parietooccipital infarctions ( 20), bilateral occipital lobe ischemia ( 3D), and injury to the " left posterior hemisphere" ( 27). A complaint not mentioned in the literature concerning drug abuse is motion sickness when images of objects move in the visual periphery, described by patient 6, a past user of LSD. This symptom may represent an increased sensitivity to stimuli that would normally induce a sensation of self- motion. The sensation of self- motion, or vection, is a byproduct of sensory signals during optokinetic stimulation which, in conjunction with vestibular signals, are thought to give the brain stem an estimate of head velocity so that appropriate compensatory eye movements may be generated ( 35). Perhaps because of an alteration in motion perception, this visual- vestibular interaction has been disturbed in patient 6 and has not adapted appropriately, leading to motion sickness when there is movement in the visual periphery. It has been observed that serotonin- depleted rabbits are no longer able to use visual cues ( OKN) to adapt their vestibuloocular reflex ( 36), indicating that serotonin may playa role in visual- vestibular interactions. A similar explanation may underlie the motion sickness described by patient 6, since at least some of the effects of LSD result from its interactions with brain serotonin receptors. The visual illusory phenomena described by our patients may be roughly localized to the parietooccipital or temporoparietal regions. Whether the effects on these areas are direct or a result of altered neuronal output from other regions is not clear. Although much is known about the pharmacology of hallucinogens, particularly LSD, the exact basis for their immediate hallucinatory and illusory effects has not been determined, let alone why these effects may recur long after the cessation of drug use. What is evident is that there is a relationship between LSD and the serotonergic system ( 37). The hallucinogenic effects once were thought to be caused by inhibition of serotonergic neurons in the dorsal raphe nuclei of the mesencephalon, producing disinhibition of postsynaptic sites innervated by these inhibitory axons, such as the visual and limbic systems ( 38). However, not only is this inhibitory action of LSD much shorter than the hallucinatory effect, but a closely related drug, lisuride, an even more potent inhibitor of dorsal raphe VISUAL ILLUSIONS AND PREVIOUS DRUG ABUSE 109 firing than LSD, does not result in hallucinations ( 38,39). Moreover, serotonin receptor blockers, although preventing the behavioral effects of LSD in cats, do not block the raphe inhibitory effects ( 40). Recently, it has been found that LSD enhances receptor sensitivity to neurotransmitters such as serotonin and norepinephrine in the facial motor nucleus, whereas lisuride does not ( 38). If this also occurs at sites conceivably involved in hallucinatory activity, this could explain how this drug produces hallucinations. This facilitatory effect of LSD outlasts the exposure time to the drug ( 38,40), but whether or not the receptors remain sensitized for prolonged periods, so that stress or certain medications are able to precipitate a recurrence of drug effects, is not known. In addition, it is not clear whether the same mechanisms that produce hallucinations also produce visual illusions. In a case of LSD flashbacks reported by Anderson ( 8), the visual illusions responded to trifluoperazine, whereas the hallucinations did not. It was suggested by Anderson that some of the illusory phenomena associated with the use of hallucinogens may, in fact, have a different basis than the hallucinatory experiences. In summary, we describe six patients who experienced various visual illusions after previous occasional drug abuse. Other causes such as migraine, epilepsy and intracranial pathology were excluded by careful history, complete neuroophthalmologic examination, and extensive laboratory and neuroimaging investigations, many of which were performed repeatedly over several years. None of the patients was abusing drugs at the time of the examination, nor did toxicologic screening studies detect the presence of any abnormal substances in the urine or serum of these patients. Since a history of drug abuse usually is not volunteered initially by the patient even after direct questioning and since these visual illusions may occur after an extensive drug- free interval, it is incumbent upon the clinician to maintain a high level of vigilance and persist with appropriate inquiries, particularly when other lesions have been excluded. The visual illusions associated with past use of illicit drugs may be caused by damage to the parietooccipital or temporoparietal regions of the brain. 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