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)

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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-

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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.

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