J Neurol (1991) 238:457-459
Journal of
Neurology © Springer-Verlag 1991
Peduncular hallucinations Hans W. K61mel
Neurologische Abteilung, Universit~itsklinikum Rudolf Virchow, Augustenburger Platz 1, W-1000 Berlin 65, Federal Republic of Germany Received November 30, 1990 ! Received in revised form March 7, 1991 / Accepted March 14, 1991
S u m m a r y . P e d u n c u l a r hallucinations usually present as visual disorders and are often genuine hallucinations associated with thalamic and/or mesencephalic lesions. I n this case r e p o r t we describe the clinical findings in a patient with hallucinations. M a g n e t i c resonance imaging d e m o n s t r a t e d bilateral ischaemic lesions in the thalamus and in the m e s e n c e p h a l o n . T h e pathogenesis o f hallucinations in these disorders is discussed in the light of the findings p r o v i d e d by imaging techniques.
daylight hours for the previous 3 days. Initial neurological examination confirmed rapid changes in the level of consciousness. It was possible to arouse the patient, but he fell asleep repeatedly during the examination. His appreciation of time, place and situation' could vary from adequacy to total disorientation within a few minutes. Neurological examination revealed complete vertical gaze palsy in both directions. The vertical component of the vestibulo-ocular reflex was absent. Horizontal eye movements were saccadic and limited. There was failure of convergence. The patient reported inconsistent diplopia. The pupils were round and
K e y words: H a l l u c i n a t i o n - T h a l a m u s - M e s e n c e p h a l o n
- Infarction
Introduction
In 1922 J e a n L h e r m i t t e [15] described a patient w h o suffered f r o m vivid visual hallucinations. Neurological examination suggested a lesion in the m e s e n c e p h a l o n and the pontine region, and L h e r m i t t e c o n t e n d e d that the mesencephalic lesion was the cause of this particular type o f hallucination. Five years later V a n B o g a e r t [20] r e p o r t e d a similar clinical picture as well as pathologicalanatomical findings which led him to term this disorder " p e d u n c u l a r hallucination". N e i t h e r L h e r m i t t e nor van B o g a e r t i n t e n d e d to describe a m e c h a n i s m of disease with this term; b o t h merely referred to the possible origin o f the hallucinations in the m e s e n c e p h a l o n . Similar visual hallucinations and comparable neurological findings have also b e e n r e p o r t e d in patients with p r e d o m i n a n t l y thalamic lesions [5] and it is p r o b a b l e that the thalamus, which is c o n n e c t e d to the visual cortex by a n u m b e r of pathways, is m o r e important in g e n e r a t i o n o f these p h e n o m e n a than are the cerebral peduncles [2]. W e present the case of a patient with " p e d u n c u l a r hallucinations" and discuss the p h e n o m e n a in the light of information o b t a i n e d by magnetic reson a n c e imaging.
C a s e report
This 56-year-old man was admitted to the hospital because he had suffered sudden and unexplained attacks of somnolence during
Fig. la, b. Magnetic resonance imaging demonstrates recent vascular lesions on both sides of the thalamus and in the left pulvinar (a) and symmetrical lesions (arrow) on the rostra1 part of both red nuclei in the midbrain (b)
458 equal, while the reaction to light was sluggish and limited. There was no disorder of visual acuity or limitation of the visual fields. With the exception of thalamic amnesia and slight bilateral limb ataxia the rest of the examination was normal. The patient complained of insomnia, but periods of normal consciousness during daylight hours became progressively longer, and it was possible to converse with him normally for extended periods. He attributed his heart disease and the current disorder to a lifetime of hard work. One evening after approximately a week on the ward the patient had an outburst in which he threw all available objects about his room. He was visibly aroused and so afraid that it was difficult to calm him. He reported that two strangers, one large and one small, dressed in dark clothes had crept into his room and threatened him with clubs. After observing them for several seconds, he had heard them whisper that they would "take care of him", and he had then attempted to defend himself. The attackers appeared to withdraw and then disappeared from the room. It was difficult to convince the patient that he had suffered a hallucination. Three days later, in the evening, the same two men appeared again, this time accompanied by a third man, and all three were armed with clubs. Once again the patient had the impression that the three intended to kill him, and he attempted to defend himself as he had the night before. The figures disappeared. The patient was given a moderate dose of a neuroleptic agent, which calmed him adequately. Soon after he developed a normal sleep/wake cycle. The vertical gaze palsy did not resolve completely. CT studies on the brain were normal, but magnetic resonance imaging demonstrated small recent lesions in the midportion of the thalamus bilaterally, in the left caudal portion of the thalamus and symmetrically in the mesencephalon, mediodorsal from the rostral pole of the red nuclei (Fig. la, b). The EEG recorded slight generalized changes. Visual and acoustic evoked potentials were normal.
Discussion P e d u n c u l a r hallucinations have b e e n described in conjunction with a variety of illnesses [8, 17-19] t h o u g h they are m o s t c o m m o n l y associated with infarction. These vivid hallucinations are almost always complex and possess a n u m b e r of c o m m o n characteristics: 1. Visual hallucinations occur most often, but other senses m a y be involved. 2. T h e y usually e n c o m p a s s the whole visual field. 3. T h e y are vivid and full of m o t i o n but only slightly coloured. 4. Their c o n t e n t is quite varied. 5. T h e y occur over a period of days to several weeks. 6. It is not k n o w n w h e t h e r ocular m o t i o n affects them. 7. Most episodes last for a few seconds and generally occur at twilight, in the evening or in the dark. Visual acuity and the visual fields are uneffected. P e d u n cular hallucination should not be diagnosed in patients with peripheral or central visual disorders associated with visual field defects or m a r k e d l y r e d u c e d visual acuity. Hallucinations often associated with these visual disorders are release p h e n o m e n a [4], which m a y not be the case in p e d u n c u l a r hallucinations, although this possibility has b e e n considered [2, 8]. Only the fact that pedun-
cular hallucinations occur in obscure light, w h e n vision is impaired suggests the possibility of a release mechanism. It m a y be that thalamic and mesencephalic disorders do not have their full effects when visual inputs are n o r m a l u n d e r daylight conditions but b e c o m e a p p a r e n t when the latter are reduced. This suggests some relation to hypnagogic hallucinations. Some patients are unable to appreciate that they are suffering f r o m hallucinations. It is not true that these are pseudo-hallucinations, as Rozanski [17] believed. In contrast to visual hallucinations in h e m i a n o p i c fields [12], peduncular hallucinations are usually genuine, at least initially. T h e r e f o r e , patients do not always enjoy their hallucinations, as R o z a n s k i [17] claimed, and m a y suffer considerable anxiety [20]. Hallucinations must be differentiated f r o m c o m m o n confabulation, which does not occur sporadically and which is well integrated into daily life. In the K o r s a k o w s y n d r o m e confabulation usually helps to fill gaps in m e m o r y . Peduncular hallucinations must also be differentiated f r o m hallucinosis - a long-lasting, often auditive hallucination without neurological deficit. Little is k n o w n about the incidence of these hallucinations, and there are no systematic studies in the literature. T h e disorders are not m e n t i o n e d in large series on unilateral or bilateral thalamic and midbrain infarcts [3, 10, 11]. H o w e v e r , it is k n o w n that patients suffering from hallucinations rarely report t h e m [13], and it is to be expected that such p h e n o m e n a would be m e n t i o n e d m o r e often if reports were elicited. T h e following neurological s y m p t o m s and signs are almost always present: impaired ocular m o v e m e n t , disturbance of the sleep/wake cycle, variation in the level of consciousness and coordination disorders. Vertical gaze palsy predominates, suggesting a lesion of the mesencephalic interstitial nucleus [14]. Disturbed sleep/wake cycles, somnolence and changes in the level of consciousness occur with lesions in the mesencephalic reticular formation, which has connections with the thalamic midline nuclei. Disturbed coordination is attributable to lesions in the thalamus, the red nucleus and the cerebellar peduncles. Clinical findings in our patient and most reports in the literature suggest the presence of bilateral vascular lesions, at least in the midbrain. T h e y usually escape detection in cranial C T and m a y be missed in careful pathological-anatomical preparations. H o w e v e r , magnetic resonance imaging is usually capable of d e m o n s t r a t i n g these findings. The bilateral lesions in the rostral m e s e n c e p h a l o n and the thalamus in our patient p r o b a b l y occurred simultaneously. These regions are served by branches of the posterior cerebral artery or by a unique thalamic artery described by P e r c h e r o n [16]. Gentilini et al. [10] reported 48 bilateral thalamic infarcts from their own experience and the literature. Lhermitte [15] t h o u g h t that the disturbed sleep/wake cycle was the decisive pathogenetic factor in the disorder, and a n u m b e r of other authors adopted this position. D u r i n g periods of somnolence dream-like images similar to those in hypnagogic states m a y develop. Twilight con-
459 ditions r e d u c e physiological visual inputs and p r o m o t e expression of internal images. It is possible that an additional thalamic lesion in the region o f the pulvinar is also involved. D e Morsier [5, 6] believed that the thalamic lesion was principally responsible for the d e v e l o p m e n t of this type of hallucinations. A n imbalance in n e u r o t r a n s m i t t e r c o n c e n t r a t i o n s might p r o v i d e an additional explanation for this disorder. P e d u n c u l a r hallucinations a p p e a r to be related to those o b s e r v e d in patients with parkinsonian s y n d r o m e s [1]. It is possible that an imbalance b e t w e e n serotoninergic and d o p a m i n e r g i c activity in the m i d p o r t i o n and posterior region o f the thalamus and in the mesencephalic reticular f o r m a t i o n [9] causes these disorders. T h e g o o d response o f o u r patient to a neuroleptic agent m a y support this hypothesis. Finally it should be n o t e d that disturbances of ocular m o v e m e n t are present in almost all of these patients. Limited eye m o v e m e n t reduces input to the retina as well as to the proprioceptors of the extraocular muscles. These impulses have inhibitory effects t h r o u g h the visual pathw a y or the superior colliculi, as D o n a l d s o n and L o n g [7] were able to d e m o n s t r a t e in cats. It is likely that these impulses inhibit the d e v e l o p m e n t of internal images or sounds. R e d u c e d inhibitory activity w o u l d result in mobilization of internal images in the f o r m o f hallucinations.
References 1. Alajouanine T, Copcevitch M (1928) Hallucinose pr6hypnique avec syndrome de Parinaud chez une malade atteinte de parkinsonisme post-enc6phalitique. Rev Neurol 11 : 714-718 2. Caplan LR (1980) "Top of the basilar" syndrome. Neurology 30 : 72-79 3. Castaigne P, Lherrnitte F, Buge A, Escourolle R, Hauw JJ, Lyon-Caen O (1981) Paramedian thalamic and midbrain infarcts: clinical and neuropathological study. Ann Neurol 10: 127-148
4. Cogan DG (1973) Visual hallucinations as release phenomena. Graefes Arch Clin Exp Ophthalmol 188 : 139-150 5. De Morsier G (1935) Pathog6nie de l'hallucinose p6donculaire. Apropos d'un nouveau cas. Rev Neurol 64 : 606-624 6. De Morsier G (1969) Les hallucinations visuelles dienc6phaliques. Psychiatr Clin 2 : 167-184 7. Donaldson IMI, Long AC (1980) Interaction between extraocular proprioceptive and visual signals in the superior colliculus of the cat. J Physiol (Lond) 298 : 85-110 8. Dunn DW, Weisberg LA, Nadell J (1983) Peduncular hallucinations caused by brainstem compression. Neurology 33: 1360-1361 9. Felten DL, Laties AM, Carpenter MB (1974) Monoaminecontaining cell bodies in the squirrel monkey brain. Am J Anat 139 : 153-166 10. Gentilini O, De Renzi E, Crisi G (1987) Bilateral paramedian thalamic artery infarcts: report of eight cases. J Neurol Neurosurg Psychiatry 50: 900-909 11. Guberman A, Stuss D (1983) The syndrome of bilateral paramedian thalamic infarction. Neurology 33 : 540-546 12. K61mel HW (1984) Visuelle Halluzinationen im hemianopen Feld. (Schriftenreihe Neurologie, vo126) Springer, Berlin Heidelberg NewYork 13. KOlmel HW (1985) Complex visual hallucinations in the hemianopic field. J Neurol Neurosurg Psychiatry 48: 29-38 14. K6mpf D, Oppermann J, K6nig F, Talman-Gros S, Babaian E (1984) Vertikale Blickparese und thalamische Demenz. Syndrom der posterioren thalamosubthalamischen paramedianen Arterie. Nervenarzt 55 : 625-636 15. Lhermitte J (1922) Syndrome de la calotte p6donculaire. Les troubles psychosensorielles dans les 16sions du m6senc6phale. Rev Neurol 38:1359-1365 16. Percheron G (1976) Les art~res du thalamus humain. Rev Neurol 132 : 297-307,309-324 17. Rozanski J (1952) Peduncular hallucinosis following vertebral angiography. Neurology 2 : 341-349 18. Silverman SM, Bergman PS, Bender MB (1961) The dynamics of transient cerebral blindness. Arch Neurol 4 : 333-348 19. Smith RA, Gelles DB, Vanderhaeghen JJ (1971 Subcortical visual hallucinations. Cortex 7:162-168 20. Van Bogaert L (1927) L'hallucinose p6donculaire. Rev Neurol 47 : 608-617
Journal of
Neurology © Springer-Verlag 1991
Peduncular hallucinations Hans W. K61mel
Neurologische Abteilung, Universit~itsklinikum Rudolf Virchow, Augustenburger Platz 1, W-1000 Berlin 65, Federal Republic of Germany Received November 30, 1990 ! Received in revised form March 7, 1991 / Accepted March 14, 1991
S u m m a r y . P e d u n c u l a r hallucinations usually present as visual disorders and are often genuine hallucinations associated with thalamic and/or mesencephalic lesions. I n this case r e p o r t we describe the clinical findings in a patient with hallucinations. M a g n e t i c resonance imaging d e m o n s t r a t e d bilateral ischaemic lesions in the thalamus and in the m e s e n c e p h a l o n . T h e pathogenesis o f hallucinations in these disorders is discussed in the light of the findings p r o v i d e d by imaging techniques.
daylight hours for the previous 3 days. Initial neurological examination confirmed rapid changes in the level of consciousness. It was possible to arouse the patient, but he fell asleep repeatedly during the examination. His appreciation of time, place and situation' could vary from adequacy to total disorientation within a few minutes. Neurological examination revealed complete vertical gaze palsy in both directions. The vertical component of the vestibulo-ocular reflex was absent. Horizontal eye movements were saccadic and limited. There was failure of convergence. The patient reported inconsistent diplopia. The pupils were round and
K e y words: H a l l u c i n a t i o n - T h a l a m u s - M e s e n c e p h a l o n
- Infarction
Introduction
In 1922 J e a n L h e r m i t t e [15] described a patient w h o suffered f r o m vivid visual hallucinations. Neurological examination suggested a lesion in the m e s e n c e p h a l o n and the pontine region, and L h e r m i t t e c o n t e n d e d that the mesencephalic lesion was the cause of this particular type o f hallucination. Five years later V a n B o g a e r t [20] r e p o r t e d a similar clinical picture as well as pathologicalanatomical findings which led him to term this disorder " p e d u n c u l a r hallucination". N e i t h e r L h e r m i t t e nor van B o g a e r t i n t e n d e d to describe a m e c h a n i s m of disease with this term; b o t h merely referred to the possible origin o f the hallucinations in the m e s e n c e p h a l o n . Similar visual hallucinations and comparable neurological findings have also b e e n r e p o r t e d in patients with p r e d o m i n a n t l y thalamic lesions [5] and it is p r o b a b l e that the thalamus, which is c o n n e c t e d to the visual cortex by a n u m b e r of pathways, is m o r e important in g e n e r a t i o n o f these p h e n o m e n a than are the cerebral peduncles [2]. W e present the case of a patient with " p e d u n c u l a r hallucinations" and discuss the p h e n o m e n a in the light of information o b t a i n e d by magnetic reson a n c e imaging.
C a s e report
This 56-year-old man was admitted to the hospital because he had suffered sudden and unexplained attacks of somnolence during
Fig. la, b. Magnetic resonance imaging demonstrates recent vascular lesions on both sides of the thalamus and in the left pulvinar (a) and symmetrical lesions (arrow) on the rostra1 part of both red nuclei in the midbrain (b)
458 equal, while the reaction to light was sluggish and limited. There was no disorder of visual acuity or limitation of the visual fields. With the exception of thalamic amnesia and slight bilateral limb ataxia the rest of the examination was normal. The patient complained of insomnia, but periods of normal consciousness during daylight hours became progressively longer, and it was possible to converse with him normally for extended periods. He attributed his heart disease and the current disorder to a lifetime of hard work. One evening after approximately a week on the ward the patient had an outburst in which he threw all available objects about his room. He was visibly aroused and so afraid that it was difficult to calm him. He reported that two strangers, one large and one small, dressed in dark clothes had crept into his room and threatened him with clubs. After observing them for several seconds, he had heard them whisper that they would "take care of him", and he had then attempted to defend himself. The attackers appeared to withdraw and then disappeared from the room. It was difficult to convince the patient that he had suffered a hallucination. Three days later, in the evening, the same two men appeared again, this time accompanied by a third man, and all three were armed with clubs. Once again the patient had the impression that the three intended to kill him, and he attempted to defend himself as he had the night before. The figures disappeared. The patient was given a moderate dose of a neuroleptic agent, which calmed him adequately. Soon after he developed a normal sleep/wake cycle. The vertical gaze palsy did not resolve completely. CT studies on the brain were normal, but magnetic resonance imaging demonstrated small recent lesions in the midportion of the thalamus bilaterally, in the left caudal portion of the thalamus and symmetrically in the mesencephalon, mediodorsal from the rostral pole of the red nuclei (Fig. la, b). The EEG recorded slight generalized changes. Visual and acoustic evoked potentials were normal.
Discussion P e d u n c u l a r hallucinations have b e e n described in conjunction with a variety of illnesses [8, 17-19] t h o u g h they are m o s t c o m m o n l y associated with infarction. These vivid hallucinations are almost always complex and possess a n u m b e r of c o m m o n characteristics: 1. Visual hallucinations occur most often, but other senses m a y be involved. 2. T h e y usually e n c o m p a s s the whole visual field. 3. T h e y are vivid and full of m o t i o n but only slightly coloured. 4. Their c o n t e n t is quite varied. 5. T h e y occur over a period of days to several weeks. 6. It is not k n o w n w h e t h e r ocular m o t i o n affects them. 7. Most episodes last for a few seconds and generally occur at twilight, in the evening or in the dark. Visual acuity and the visual fields are uneffected. P e d u n cular hallucination should not be diagnosed in patients with peripheral or central visual disorders associated with visual field defects or m a r k e d l y r e d u c e d visual acuity. Hallucinations often associated with these visual disorders are release p h e n o m e n a [4], which m a y not be the case in p e d u n c u l a r hallucinations, although this possibility has b e e n considered [2, 8]. Only the fact that pedun-
cular hallucinations occur in obscure light, w h e n vision is impaired suggests the possibility of a release mechanism. It m a y be that thalamic and mesencephalic disorders do not have their full effects when visual inputs are n o r m a l u n d e r daylight conditions but b e c o m e a p p a r e n t when the latter are reduced. This suggests some relation to hypnagogic hallucinations. Some patients are unable to appreciate that they are suffering f r o m hallucinations. It is not true that these are pseudo-hallucinations, as Rozanski [17] believed. In contrast to visual hallucinations in h e m i a n o p i c fields [12], peduncular hallucinations are usually genuine, at least initially. T h e r e f o r e , patients do not always enjoy their hallucinations, as R o z a n s k i [17] claimed, and m a y suffer considerable anxiety [20]. Hallucinations must be differentiated f r o m c o m m o n confabulation, which does not occur sporadically and which is well integrated into daily life. In the K o r s a k o w s y n d r o m e confabulation usually helps to fill gaps in m e m o r y . Peduncular hallucinations must also be differentiated f r o m hallucinosis - a long-lasting, often auditive hallucination without neurological deficit. Little is k n o w n about the incidence of these hallucinations, and there are no systematic studies in the literature. T h e disorders are not m e n t i o n e d in large series on unilateral or bilateral thalamic and midbrain infarcts [3, 10, 11]. H o w e v e r , it is k n o w n that patients suffering from hallucinations rarely report t h e m [13], and it is to be expected that such p h e n o m e n a would be m e n t i o n e d m o r e often if reports were elicited. T h e following neurological s y m p t o m s and signs are almost always present: impaired ocular m o v e m e n t , disturbance of the sleep/wake cycle, variation in the level of consciousness and coordination disorders. Vertical gaze palsy predominates, suggesting a lesion of the mesencephalic interstitial nucleus [14]. Disturbed sleep/wake cycles, somnolence and changes in the level of consciousness occur with lesions in the mesencephalic reticular formation, which has connections with the thalamic midline nuclei. Disturbed coordination is attributable to lesions in the thalamus, the red nucleus and the cerebellar peduncles. Clinical findings in our patient and most reports in the literature suggest the presence of bilateral vascular lesions, at least in the midbrain. T h e y usually escape detection in cranial C T and m a y be missed in careful pathological-anatomical preparations. H o w e v e r , magnetic resonance imaging is usually capable of d e m o n s t r a t i n g these findings. The bilateral lesions in the rostral m e s e n c e p h a l o n and the thalamus in our patient p r o b a b l y occurred simultaneously. These regions are served by branches of the posterior cerebral artery or by a unique thalamic artery described by P e r c h e r o n [16]. Gentilini et al. [10] reported 48 bilateral thalamic infarcts from their own experience and the literature. Lhermitte [15] t h o u g h t that the disturbed sleep/wake cycle was the decisive pathogenetic factor in the disorder, and a n u m b e r of other authors adopted this position. D u r i n g periods of somnolence dream-like images similar to those in hypnagogic states m a y develop. Twilight con-
459 ditions r e d u c e physiological visual inputs and p r o m o t e expression of internal images. It is possible that an additional thalamic lesion in the region o f the pulvinar is also involved. D e Morsier [5, 6] believed that the thalamic lesion was principally responsible for the d e v e l o p m e n t of this type of hallucinations. A n imbalance in n e u r o t r a n s m i t t e r c o n c e n t r a t i o n s might p r o v i d e an additional explanation for this disorder. P e d u n c u l a r hallucinations a p p e a r to be related to those o b s e r v e d in patients with parkinsonian s y n d r o m e s [1]. It is possible that an imbalance b e t w e e n serotoninergic and d o p a m i n e r g i c activity in the m i d p o r t i o n and posterior region o f the thalamus and in the mesencephalic reticular f o r m a t i o n [9] causes these disorders. T h e g o o d response o f o u r patient to a neuroleptic agent m a y support this hypothesis. Finally it should be n o t e d that disturbances of ocular m o v e m e n t are present in almost all of these patients. Limited eye m o v e m e n t reduces input to the retina as well as to the proprioceptors of the extraocular muscles. These impulses have inhibitory effects t h r o u g h the visual pathw a y or the superior colliculi, as D o n a l d s o n and L o n g [7] were able to d e m o n s t r a t e in cats. It is likely that these impulses inhibit the d e v e l o p m e n t of internal images or sounds. R e d u c e d inhibitory activity w o u l d result in mobilization of internal images in the f o r m o f hallucinations.
References 1. Alajouanine T, Copcevitch M (1928) Hallucinose pr6hypnique avec syndrome de Parinaud chez une malade atteinte de parkinsonisme post-enc6phalitique. Rev Neurol 11 : 714-718 2. Caplan LR (1980) "Top of the basilar" syndrome. Neurology 30 : 72-79 3. Castaigne P, Lherrnitte F, Buge A, Escourolle R, Hauw JJ, Lyon-Caen O (1981) Paramedian thalamic and midbrain infarcts: clinical and neuropathological study. Ann Neurol 10: 127-148
4. Cogan DG (1973) Visual hallucinations as release phenomena. Graefes Arch Clin Exp Ophthalmol 188 : 139-150 5. De Morsier G (1935) Pathog6nie de l'hallucinose p6donculaire. Apropos d'un nouveau cas. Rev Neurol 64 : 606-624 6. De Morsier G (1969) Les hallucinations visuelles dienc6phaliques. Psychiatr Clin 2 : 167-184 7. Donaldson IMI, Long AC (1980) Interaction between extraocular proprioceptive and visual signals in the superior colliculus of the cat. J Physiol (Lond) 298 : 85-110 8. Dunn DW, Weisberg LA, Nadell J (1983) Peduncular hallucinations caused by brainstem compression. Neurology 33: 1360-1361 9. Felten DL, Laties AM, Carpenter MB (1974) Monoaminecontaining cell bodies in the squirrel monkey brain. Am J Anat 139 : 153-166 10. Gentilini O, De Renzi E, Crisi G (1987) Bilateral paramedian thalamic artery infarcts: report of eight cases. J Neurol Neurosurg Psychiatry 50: 900-909 11. Guberman A, Stuss D (1983) The syndrome of bilateral paramedian thalamic infarction. Neurology 33 : 540-546 12. K61mel HW (1984) Visuelle Halluzinationen im hemianopen Feld. (Schriftenreihe Neurologie, vo126) Springer, Berlin Heidelberg NewYork 13. KOlmel HW (1985) Complex visual hallucinations in the hemianopic field. J Neurol Neurosurg Psychiatry 48: 29-38 14. K6mpf D, Oppermann J, K6nig F, Talman-Gros S, Babaian E (1984) Vertikale Blickparese und thalamische Demenz. Syndrom der posterioren thalamosubthalamischen paramedianen Arterie. Nervenarzt 55 : 625-636 15. Lhermitte J (1922) Syndrome de la calotte p6donculaire. Les troubles psychosensorielles dans les 16sions du m6senc6phale. Rev Neurol 38:1359-1365 16. Percheron G (1976) Les art~res du thalamus humain. Rev Neurol 132 : 297-307,309-324 17. Rozanski J (1952) Peduncular hallucinosis following vertebral angiography. Neurology 2 : 341-349 18. Silverman SM, Bergman PS, Bender MB (1961) The dynamics of transient cerebral blindness. Arch Neurol 4 : 333-348 19. Smith RA, Gelles DB, Vanderhaeghen JJ (1971 Subcortical visual hallucinations. Cortex 7:162-168 20. Van Bogaert L (1927) L'hallucinose p6donculaire. Rev Neurol 47 : 608-617
