Copyright Ó Munksgaard 2002

Acta Neurol Scand 2002: 105: 228–231
Printed in UK. All rights reserved

ACTA NEUROLOGICA
SCANDINAVICA
ISSN 0001-6314

Case report

Palinopsia and perilesional hyperperfusion
following subcortical hemorrhage
Hayashi R, Shimizu S, Watanabe R, Katsumata Y, Mimura M.
Palinopsia and perilesional hyperperfusion following subcortical
hemorrhage.
Acta Neurol Scand 2002: 105: 228–231. Ó Munksgaard 2002.
We report a patient who exhibited transient palinopsia and visual
hallucinations. Disturbances initially included an auditory component
and increasingly were localized to the left visual field. These events
occurred during recovery from a right subcortical hematoma with left
homonymous hemianopia. Single-photon emission computed
tomography (SPECT) demonstrated extensive perilesional
hyperperfusion involving parts of the right parietal, temporal, and
occipital cortex. Perilesional hyperperfusion disappeared as the visual
abnormalities diminished. We believe that excitatory neuronal
activation in perilesional cortex during recovery contributed
importantly to the transient abnormal perceptions.

R. Hayashi1,3, S. Shimizu3,
R. Watanabe1, Y. Katsumata2,
M. Mimura4
Departments of 1Neurology and 2Radiology, Yokohama
City Hospital, Yokohama, Japan,3Department of
Neurology, Yokohama Stroke and Brain Center,
Yokohama, Japan,4Department of Neuropsychiatry,
Showa University School of Medicine, Tokyo, Japan

Key words: palinopsia; single-photon emission computed
tomography; hyperperfusion; subcortical hematoma
Ryuichiro Hayashi, Department of Neurology, Yokohama
Stroke and Brain Center, 1-2-1 Takigashira, Isogo-ku,
235-0012, Japan
Tel.: +81-45-753-2500
Fax: +81-45-753-2879
e-mail: ryuich@m1.interq.or.jp
Accepted for publication August 16, 2001

Palinopsia, defined as visual images that persist or
recur after the stimulating object is removed,
usually is associated with a right-sided posterior
cerebral lesion (1). The underlying mechanism
remains a subject of debate. We report a patient
who presented with palinopsia and vivid visual
hallucinations in the left visual field occurring in
association with a right-sided subcortial
hematoma. Single-photon emission computed tomography (SPECT) with 99mTc-hexamethylpropyleneamine oxime (HMPAO) demonstrated
extensive perilesional hyperperfusion, suggesting
an excitatory mechanism underlying our patients’
abnormal visual phenomena.
Case report

On 1 February 1999, while walking on the street, a
59-year-old, right-handed man suddenly experienced nausea and gait disturbance. No visual
symptoms were present. He was admitted to our
hospital. The patient had a past history of
hypertension, but did not take any medication.
Five years previously he experienced numbness in
his right hand; diagnosed with left thalamic
228

hemorrhage at another hospital, he recovered
completely and returned to his job as a taxi
driver without significant residual symptoms or
disability.
On admission the blood pressure was 201/
101 mmHg and the pulse was 74/min. On neurologic examination the patient was alert and oriented. Left homonymous hemianopia, left
hemihypesthesia, and left hemiparesis were present. Visual and auditory acuity were intact. No
unilateral spatial neglect, no auditory or visual
extinction, and no motor impersistence could be
demonstrated. Laboratory findings were normal.
An electrocardiogram showed a normal rhythm
but was suggestive of left ventricular hypertrophy.
Computed tomography (CT) of the brain performed approximately 3 h after onset revealed a
subcortical hematoma beneath the right parietal
cortex (Fig. 1).
Beginning on the second hospital day, palinopsia
involving specific persistent and recurrent visual
images became apparent, mainly in the left visual
field. Subsequently, visual hallucinations in the left
visual field were also noted. Left hemianopia,

Palinopsia and perilesional hyperperfusion

Figure 1. Computed tomography reveals a subcortical hematoma located in the parietal region (angular gyrus).

hemihypesthesia, and hemiparesis gradually
decreased, until the fourth hospital day when
they had almost disappeared. In conjunction with
recovery from these neurologic abnormalities, the
abnormal perceptions cleared by the fourth hospital day.
The first persistent image was noted during
confrontation visual field testing on the second
hospital day when the examiner presented moving
fingers in both fields simultaneously. After the
examiner ceased presentation of fingers, the patient
continued to point alternately to either side, saying
‘‘Yes, I can see your fingers’’. He maintained that
he could see the examiner’s fingers on both sides
for approximately 15 min after they had been
withdrawn. Persistent finger images were more
clearly seen and more frequent on the left than on
the right side. The image initially was accompanied
by the examiner’s voice, saying ‘‘Can you see this?’’
The patient claimed that he could see an image
whether he opened or closed his eyes. On the third
hospital day, the finger image also remained after
visual stimulation was removed, but this time the
image was seen only on the left and was no longer
accompanied by the examiner’s voice. This finger
image occasionally recurred in the absence of any
visual stimuli.
The second abnormal visual image that the
patient experienced was his wife’s hand beckoning
from his left side. His wife denied any such
movement, either shortly before or during these
perceptions. The patient became aware that this
hand was not real upon failure of his attempts to
grasp at it. Like the images of the examiner’s
fingers, those of the wife’s hand appeared normal
in size and color.
The third image, a colorful whirling object like a
pinwheel, was seen on the left side. The patient felt

that the image was familiar to him, but he could
not recall exactly where he had seen it.
None of the abnormal visual images evoked any
emotional reaction. All images included appropriate movement and were increasingly located in the
left visual field. The images were superimposed
upon the background actually viewed, which could
be seen through the images. All three images
described above gradually became less frequent,
subsequently recurring only with eyes closed and
finally disappearing.
The patient’s orientation and ability to calculate
were intact during occurrence of visual symptoms.
He did not experience migraine or convulsive
seizures. The SPECT using 99mTc HMPAO,
performed on the fourth hospital day, demonstrated a defect secondary to the hematoma; this was
surrounded by a broad hyperperfused region
including portions of temporal, parietal, and
occipital cortex (Fig. 2A). On a follow-up SPECT
examination on the 12th hospital day, the surrounding
hyperperfusion
had
disappeared
(Fig. 2B). Magnetic resonance imaging (MRI) on
the 10th hospital day revealed a right parietal
hematoma and the old left thalamic hemorrhage.
Signal intensities around the right parietal
hematoma were normal (Fig. 3).
Electroencephalography performed on the ninth
hospital day showed no abnormalities.
Discussion

We report a patient who presented with palinopsia
and visual hallucinations occurring during recovery from subcortical hemorrhage with hemianopia,
from approximately the second to the fourth day
after initial symptoms. In these occurrences of
palinopsia, visual images were relatively simple and
stereotyped, appeared to be in motion, appeared
during the recovery phase of hemianopia, were
located primarily in the hemianopic visual field,
and initially were accompanied by related auditory
phenomena. The SPECT demonstrated hyperperfusion of cortical areas surrounding the hematoma
that disappeared as visual abnormalities diminished, suggesting that perilesional cortical hyperactivity was related to the patients’ visual
symptoms.
The pathophysiology associated with the SPECT
finding of hyperperfusion is unclear. Mayer et al.
(2) recently reported perilesional delayed cortical
hyperemia in areas surrounding lobar hemorrhage
that appeared normal by CT. These authors
suggested that this phenomenon reflects either a
local inflammatory response or a disorder of
autoregulation. Similar abnormal events may
229

Hayashi et al.

Figure 3. Magnetic resonance imaging reveals a parietal
hematoma with intact surrounding cortex.

Figure 2. A. Hyperfusion in the temporal, parietal, and occipital regions surrounds the defect from the hematoma on the
fifth hospital day B. On the 12th hospital day, SPECT no
longer shows hyperperfusion. 99mTc-HMPAO, hexamethylpropyleneamine oxime, SPECT, single-photon emission computed tomography.

have occurred in our patient. Another plausible
explanation might involve hemorrhagic infarction,
which was pointed out by Bogousslavsky et al. (3)
as being difficult to differentiate from primary
cerebral hemorrhage. In such an occurrence transient ischemia is followed by early reperfusion that
results in hemorrhagic infarction and also a
surrounding area of early postischemic hyperperfusion (4). In any events, a small hematoma
beneath the parietal cortex might not account for
all of our patients’ initial symptoms, which
230

included hemianopia, hemihypesthesia, and
hemiparesis. More widespread diffuse ischemia
followed by post-ischemic hyperperfusion is more
likely to explain both the early deficits and the
recovery-phase phenomena.
Bender et al. (1) proposed four possible mechanisms of palinopsia: visual aftersensations, sensory
seizures, hallucinations, and psychogenic elaborations or fantasies. These authors noted similarities
between normal afterimages and palinoptic images
and considered many occurrences of palinopsia to
be visual aftersensations generated at the cerebral
level. In the present patient, palinopsia initially
appeared immediately after visual stimuli. Accordingly, accentuated normal after images at the
cerebral level may explain his initial palinopsia.
However, the same images subsequently recurred
without preceding stimuli. In addition, the images
initially were accompanied by an auditory sensation of the examiner’s voice. Thus, our patient’s
symptoms cannot be explained as visual aftersensations alone. The patient was not confused, and
his consciousness remained clear. His mentation
and behavior otherwise appeared normal, which
argued against a general confusional state or
psychogenic elaboration and fantasy.
Cummings et al. (5) considered palinopsia to be a
type of release hallucination resulting from loss or
suppression of normal visual input, and emphasized the need to distinguish it from ictal visual
perseveration caused by seizures. Palinopsia caused
by seizures has several characteristic features,

Palinopsia and perilesional hyperperfusion
including accompanying signs of seizure activity,
absence of hemianopia, and spread of palinoptic
images to involve the whole visual field (5–7). In the
present patient palinopsia appeared primarily in the
left visual field and was associated with transient
hemianopia, this supports release hallucinations
rather than seizure phenomena as an explanation.
Simple formed hallucinations in the hemianopic
field sometimes are accompanied by palinopsia (8).
Lance considered this type of hallucination to be
an irritative phenomenon of the visual association
cortex involving interruption of normal afferent
inflow from the calcarine cortex. On the other
hand, Wunderlich et al. (9) reported a case with
complex visual hallucinations during recovery
from prolonged cortical blindness. In this case,
visual hallucinations led to increases in regional
cerebral blood flow in the hypometabolic parietooccipital and lateral temporal cortex, and the
reporting authors considered the visual hallucinations to be related to transient cortical hyperexcitability in the presence of partial damage and
dysfunction. In our present case, a broad hyperperfused area surrounding the hematoma might
indicate cortical instability and excitatory neuronal
activation in these areas during recovery from
hemianopia. Therefore, cortical dysfunction itself,

rather than ‘‘release’’ of cortex as a result of
deprivation of normal visual output, might have
caused palinopsia, associated visual hallucinations,
and auditory phenomena in the present patient.
References
1. BENDER MB, FELDMAN M, SOBIN AJ. Palinopsia Brain
1968;91:321–38.
2. MAYER SA, LIGNELLI A, FINK ME et al. Perilesional blood
flow and edema formation in acute intracerebral hemorrhage: a SPECT study. Stroke 1998;29:1791–8.
3. BOGOUSSLAVSKY J, REGLI F, USKÉ A, MAEDER P. Early
spontaneous hematoma in cerebral infarct: is primary
cerebral
hemorrhage
overdiagnosed?
Neurology
1991;41:837–40.
4. MARCHAL G, YOUNG AR, BARON JC. Early postischemic
hyperperfusion: pathophysiologic insights from positron
emission tomography. J Cereb Blood Flow Metab
1999;19:467–82.
5. CUMMINGS JL, SYNDULKO K, GOLDBERG Z, TREIMAN DM.
Palinopsia reconsidered. Neurology 1982;32:444–7.
6. SWASH M. Visual perseveration in temporal lobe epilepsy.
J Neurol Neurosurg Psychiatry 1979;42:569–71.
7. LEFÈBRE C, KöLMEL HW. Palinopsia as an epileptic phenomenon. Eur Neurol 1989;29:323–7.
8. LANCE JW. Simple formed hallucinations confined to the
area of a specific visual defect. Brain 1976;99:719–34.
9. WUNDERLICH G, SUCHAN B, VOLKMANN J, HERZOG H,
HöMBERG B, SEITZ RJ. Visual hallucinations recovery from
cortical blindness. Arch Neurol 2000;57:561–5.

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