J Neurol (1992) 239 : 89-90 Journal of Neurology © Springer-Verlag 1992 Peduncular hailucinosis associated with posterior thalamic infarction J. Serra Catafau, F. Rubio, and J. Peres Serra Department of Neurology, Hospital de Bellvitge "Princeps d'Espanya", Feixa Llarga s/n, L'Hospitalet de Llobregat, E-08907 Barcelona, Spain Received January 2, 1991 / Received in revised form April 29, 1991 / Accepted May 7, 1991 Summary. P e d u n c u l a r h a l l u c i n a t i o n s a r e g e n e r a l l y assoc i a t e d w i t h lesions o f t h e m i d b r a i n . W e d e s c r i b e a 68y e a r - o l d m a n w h o d e v e l o p e d left h e m i p a r e s i s , p a r a e s thesias o n t h e left side a n d vivid visual h a l l u c i n a t i o n s , suggesting p e d u n c u l a r hallucinosis. M R I d e m o n s t r a t e d a right p o s t e r i o r t h a l a m i c infarct as t h e sole lesion. For 3 days he complained of vivid visual hallucinations in his left visual field. He saw houses, bulls, horses, turtles and a young woman. The images were animated, without any logical sense, almost always in black and white but sometimes in faint colours. The images were normal in size and appeared and disappeared very Key words: P e d u n c u l a r hallucinosis - S t r o k e - T h a l a m u s Introduction I n 1922, L ' H e r m i t t e [12] r e p o r t e d a 7 2 - y e a r - o l d w o m a n w i t h a n e u r o l o g i c a l deficit i n d i c a t i v e o f a m e s e n c e p h a l i c lesion, w h o d e v e l o p e d vivid visual hallucinations. I n 1927, V a n B o g a e r t [18] d e s c r i b e d a similar case w i t h a n a t o m i cal v e r i f i c a t i o n of an infarct affecting t h e c e r e b r a l p e duncles, H e n a m e d this s y n d r o m e p e d u n c u l a r hallucinosis ( P H ) . Case report A 68-year-old right-handed man was admitted to hospital complaining of the abrupt onset of difficulty in using his left limbs and paraesthesias on the left side. About 20 min thereafter he complained of vivid visual hallucinations. He saw a variety of animals in his room, including "lions jumping in through the window" and "men's heads". Examination on admission disclosed the following: blood pressure 190/110mmHg, pulse 80 beats/min, axillary temperature 37°C. Heart, pulmonary and abdominal examination was normal. He was alert, correctly oriented, with normal speech and normal visual fields. He had mild left hemiparesis. Sensation was normal, although he complained of left numbness. He had left dysmetria, increased deep tendon reflexes on his left side and no Babinski sign. He described seeing images of a large number of animals in movement, always in his left visual field. Routine laboratory studies showed slightly elevated serum levels of cholesterol. ECG and chest radiograph were normal. CT of the brain showed cortical atrophy. The EEG showed low-voltage waves with diffuse fast rhythms and superimposition of theta waves in the right temporal region. MRI on the 10th day in hospital (Fig. 1) revealed an area of increased T2 signal affecting the right posterior thalamocapsular region, consistent with an ischaemic lesion. It affected the lateral portion of the right pulvinar, laternal geniculate body, posterior portion of the ventral thalamic nuclei, nucleus reticularis and a zone of the posterior limb of the internal capsule (Fig. 2). Offprint requests to: J. Serra Catafau Fig. 1. MRI showing increased T2 signal from area in right posterior thalamocapsular region. (Field 1.5 T, TR 2200, TE 40, General Electric "Signa") ~--4 v " • ,,'" .'.::. • /4 :+., .." J: ;5 " Fig. 2. 1 Nucleus ventralis anterior, 2 nucleus dorsomedialis, 3 nucleus ventralis lateralis, 4 nucleus ventralis posterior pars medialis, 5 nucleus ventralis posterior pars lateralis, 6 nucleus pulvinaris 90 quickly. He correctly identified them as hallucinations and was aware of the unreality of the phenomena. The visual hallucinations eventually disappeared, although when discharged he still showed mild left hemiparesis and had developed thalamic pain affecting his left arm. flowing from the cortex to the thalamus; thus its lesion might have caused an imbalance resulting in a release p h e n o m e n o n . Ours appears to be the first case of P H due to a posterior thalamic lesion described during life using MRI. Discussion Hallucinations are perceptions in the absence of external stimuli. F r o m Cogan [4], visual hallucinations have been divided into release and irritative p h e n o m e n a . Irritative p h e n o m e n a are paroxysmal and stereotyped hallucinations that m a y have some value in the localization of a lesion [11]. Release p h e n o m e n a are continuous hallucinations in which the images are complex and m a y change from one episode to the next, influenced by the cultural background of each patient. They are attributed to complete or partial absence of normal visual input, occur with lesions at any level of the visual pathways, and have no localizing value. P H involves a form of release phen o m e n a with vivid, usually coloured, visual images of people, animals, plants, scenes or geometric patterns and possessing all the qualities of a true sensorial perception. Nevertheless, patients correctly identify the hallucinations and are aware of their unreality. L ' H e r m i t t e [12, 13] and Van Bogaert [17, 18] were the first to associate the signs and symptoms of a mesencephalic infarct with the onset of visual hallucinations. Since then, there have been reports in other clinical situations [1, 3, 7, 9, 16]. Most of the descriptions are associated with lesions affecting the cerebral peduncles or related areas. Nevertheless, hallucinations have been described in patients with proved lesions in other cerebral areas [2, 5, 6, 8, 15]. The pathogenesis of this syndrome has not b e e n well established. This is partly due to the variety of lesional localizations capable of producing PH. M c K e e et al. [14] suggested that the destruction of the substantia nigra pars reticulata was the cause of the process, but this hypothesis could not explain either our case or others [8]. Most of the described cases of P H only have in c o m m o n the fact that the lesion affected the reticular substance. We think that the hallucinations seen in our patient m a y be caused by a lesion of the nucleus reticularis (NR), which is in relation to the reticular formation. Fibres running from a particular nucleus of the dorsal thalamus (e.g. the pulvinar) to specific cortical areas (e.g. areas 18 and 19) give collaterals ending in particular areas of the NR. Conversely, corticothalamic fibres that project to that particular nucleus of the dorsal thalamus give colaterals to the same area of the NR. Cells f r o m the part of the N R project to the thalamic nucleus, from which it receives afferent fibres [10]. The N R is strategically situated to analyse the neural activity References 1. Alajouanine T, Copcevitch M (1928) Hallucinose prdhypnique, automatisme ambulatoire et verbal nocturne, 6clipses confusionelles paroxystiques chez une malade atteinte d'un syndrome parkinsonien postencdphalitique, avec syndrome de Parinaud respectant les mouvements automaticordflexes, et crises toniques des membres ~t type de crampes vesp6rales. Rev Neurol (Paris) 50 : 714-718 2. 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