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Transient Visuospatial Disorder From Angiographic Contrast
Michael P. Merchut, MD;
Bunnie Richie, DO
Arch Neurol. 2002;59:851-854.
ABSTRACT
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Background The blood-brain barrier may be permeable under the clinical settings
of uncontrolled hypertension, renal insufficiency, immunosuppressive drugs,
and intravascular radiographic contrast. Some reversible neurological complications
after angiography are caused by cortical penetration of contrast media detected
on brain computed tomographic (CT) scans.
Objectives To describe the first report of a transient visuospatial disorder having
elements of Balint syndrome, and caused by angiographic contrast penetration
of the bilateral parieto-occipital cortex; and to review cases published between
1980 and 2001 of cortical contrast penetration, documented by CT.
Results Simultanagnosia, optic ataxia, and ocular apraxia occurred in a 74-year-old
woman who received nonionic contrast media during a failed renal angioplasty.
Contrast noted in the bilateral parieto-occipital cortex on the initial CT
scan disappeared after 4 days with clinical resolution.
Conclusions Angiographic contrast tends to breach the blood-brain barrier of the
vertebrobasilar circulation, penetrating the occipital cortex and leading
to transient, localizable syndromes of cortical blindness or abnormal visuospatial
processing.
INTRODUCTION
CATHETER-related vasospasm, intimal tears, or emboli occasionally cause
focal deficits during arteriography. Other patients experience confusion,
delirium, seizures, or cortical blindness that are typically reversible after
several hours to a few days. In these instances, intra-arterial contrast apparently
penetrates the blood-brain barrier by opening tight capillary junctions or
enhancing endothelial pinocytosis. It then enters the cerebral cortex and
adversely affects neuronal membranes. Contrast neurotoxicity seems to be related
to the chemical or ionic properties of the contrast medium and its hyperosmolarity,
lipid solubility, and viscosity.1-2
The reduced clearance of intravascular contrast in renal failure may be an
additional clinical factor,3-4
but it is difficult to demonstrate in an experimental model.4
There are several reports of angiographic contrast entering the occipital
cortex and causing cortical blindness, sometimes with denial of visual deficit
(Anton syndrome).3-9
The following is the first case report, to our knowledge, of angiographic
contrast causing a transient visuospatial or visual processing disorder having
elements of Balint syndrome.
REPORT OF A CASE
A hypertensive 74-year-old right-handed woman developed renal insufficiency
from bilateral renal artery stenosis. There was no prior history of transient
focal neurological deficit, stroke, seizure, or substance abuse. She underwent
an unsuccessful percutaneous renal angioplasty, receiving a total of 415 mL
of iopamidol (Isovue 370; Bracco Diagnostics, Princeton, NJ) contrast. By
the next morning, her family found her to be clumsy. She would reach with
her hand too far, or not far enough, when trying to grasp nearby objects.
On examination that afternoon, she was afebrile with a blood pressure of 170/70
mm Hg and a pulse of 68 beats per minute. She was repeatedly using a knife
and fork to "cut" on an empty dinner plate, having great difficulty focusing
on, or attending to, other food items on her dinner tray, despite being verbally
directed to their location. By bedside confrontation visual field testing,
she was not blind and had no extinction to simultaneous, bilateral visual
stimuli. She was more inattentive to the most peripherally located visual
targets. Ocular movements were full, either when suddenly looking toward a
noise, or tracking a target; though the latter required many attempts with
continuous encouragement. Her pupillary light reaction was normal.
In attempting to get more comfortably seated, she struggled to pull
herself up in bed, grasping the tray table and other objects, but not the
raised siderail. Multiple attempts were needed to reach and grasp her telephone,
but once it was in her hands, she was able to use it properly. After finally
focusing on a vegetable or fruit item on the left or right of her tray, she
could not accurately spoon or stab it with her fork. Likewise, finger-nose-finger
testing was clumsily performed with either hand, but no tremor was seen. Bilateral
asterixis was present.
When shown a magazine advertisement of several dancers, with a wristwatch
(the largest object) in the foreground, she could only identify "people."
She could only read or spell words 4 to 5 letters long, and she refused to
write or draw. However, she remained alert, oriented, and cooperative, and
she successfully performed 3-step commands. Verbal fluency, comprehension,
and repetition were normal and without paraphasic errors. Although a few common
objects were visually identified, she could not name certain food items such
as a cookie, despite accurately describing their shape and color. Touching
these same items, however, allowed her to correctly name them. A picture of
rock star Elvis Presley was easily identified. She had finger agnosia and
trouble with calculations, but was able to distinguish left from right. She
appropriately followed commands to "salute the flag as if a parade marched
by" and "brush your teeth as if you had a toothbrush in your hand." Chronic
findings from an idiopathic peripheral neuropathy included distally weak (4/5),
areflexic lower limbs with decreased pinprick and proprioception. There was
extinction to double-simultaneous tactile stimulation on the left limbs, but
graphesthesia was intact. An uninfused computed tomographic scan of the brain
(Figure 1) showed persistent intravascular
contrast, especially in the circle of Willis, plus bilateral gyral enhancement
of the occipital and posterior parietal lobes. Hemodialysis was begun for
acute oliguric renal failure.
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Figure 1. Angiographic contrast in the bilateral
parieto-occipital cortex. Initial brain computed tomographic scan with iodinated
contrast persisting in blood vessels and in the gyri of bilateral occipital
and posterior parietal lobes.
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Three days later, her visual fields were easily tested and full to confrontation.
Spoken language, reading, and repetition were normal. When viewing a picture
of people seated at a table with a background of a fountain and city skyline,
she could only identify "people." She was unable to reach and grasp a glass
of water. She described the colors of a pen ("gold and black") and knew "ink
comes out of it," but could only name "pen" after touching it. However, other
common items were named easily by sight.
On the fourth day, she could interpret and identify all musicians and
their instruments in a picture of an orchestra, and described various cosmetics
illustrated in a magazine advertisement. Visual fields, visual tracking, reading,
and comprehension remained normal. There was no asterixis, and finger-nose-finger
tests and other limb maneuvers were performed well. A repeated uninfused computed
tomography brain scan was now normal (Figure
2). She remained neurologically normal the next 3 days and was discharged
home.
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Figure 2. Disappearance of bilateral parieto-occipital
contrast media. Follow-up brain computed tomographic scan taken 4 days later,
with resolution of intravascular and gyral contrast. No ischemic infarction
is seen.
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COMMENT
Simultanagnosia is a visual processing problem in which only one object
from an array is "seen" at one time, with the inability of the individual
to maintain visual awareness of the other objects. This occurs despite relatively
intact visual fields and acuity, normal language, and unrestricted head and
eye movements.10-11 Our patient
was readily able to describe or name "people," but she remained oblivious
to the wristwatch, fountain, or city skyline in the pictures shown to her.
After 4 days, she could name all the items in a complex picture to the finest
detail, without any constriction of her visual attention. Bilateral superior
occipital lesions may produce simultanagnosia in isolation, whereas bilateral
parieto-occipital lesions may create visuospatial deficits, in addition to
simultanagnosia.12
Our patient also had great difficulty moving her eyes, on command, to
a peripheral target such as the other items on her dinner tray. This did not
seem to be due to simultanagnosia since she was asked to "find the bowl of
carrots on your right," or "look next to your left hand for the plate of bread,"
and would only find these items after several suggestions and directions prompting
many attempts. Reflexive visual saccades, as when quickly looking in the direction
of a loud noise, appeared normal. This deficit seems to be that of ocular
apraxia, which was described as "psychic paralysis of gaze" and "spasm of
fixation."12-13
The first deficit noted in our patient was her impaired ability to reach
and grasp objects that she wanted. Despite seeing the telephone, she had trouble
getting her hand on it, reaching beyond its location or not reaching far enough.
After finally visually locating, on command, a specific food item on her tray,
she could not spoon it up or pierce it with a fork. Such erratic reaching
under visual guidance represents optic ataxia.12-13
After 3 days, she could accurately grasp, raise, and drink a glass of water.
Balint syndrome, consisting of simultanagnosia, optic ataxia, and ocular
apraxia, is typically associated with bilateral lesions in the superior parieto-occipital
lobes.12-13 Some have argued that
these deficits may be produced by lesions elsewhere, and that this clinical
triad may not exist as cohesively as previously assumed.11
Nevertheless, we feel our case has great similarity, both clinically and neuroanatomically,
to the historical syndrome of Balint. Our patient exhibited simultanagnosia
and optic ataxia, and probably ocular apraxia. These deficits often coexist
as a result of bilateral lesions in the parieto-occipital, dorsal visual association
areas, which in general comprise the "where" visual system, dealing with the
accurate location of objects. The temporo-occipital, ventral visual association
areas constitute the "what" system, or the identification and recognition
of objects.14 Although she could name several
items, our patient could not name a "cookie" or "pen," unless she touched
them. Her partial visual agnosia shows that there was some involvement of
these temporo-occipital areas as well. The presence of some elements of the
Gerstmann syndrome (finger agnosia and impaired calculations) also suggests
lesion extension into the dominant angular gyrus.15
Whether or not our patient manifested Balint syndrome, if indeed it
specifically or uniquely exists, she did have a reversible syndrome of abnormal
visual processing due to penetration of angiographic contrast media into the
bilateral parieto-occipital cortex. Angiographic contrast is neurotoxic, and
its presence within brain parenchyma makes it unlikely that other mechanisms,
such as arterial emboli or vasospasm induced by the angiographic procedure,
were causative. Contrast may even appear in the occipital lobes following
intra-arterial injection as remote as the abdominal aorta or renal arteries
as noted in our case and in one other report.4
In addition to our report, there are 14 other cases of contrast penetration
in the cerebral cortex documented by computed tomography scan. Twelve of these
15 cases involved the occipital cortex, with transient cortical blindness
in 10 cases (Table 1). Some of
these cases were exposed to relatively less toxic nonionic contrast media,
and the amounts of contrast injected varied greatly. Renal insufficiency,
delaying clearance of intravascular contrast and prolonging its exposure to
the blood-brain barrier, was an additional factor in our case and in 2 others.3-4 Cortical blindness has occurred after
contrast injection into the aorta, or the renal, subclavian, coronary, carotid,
or vertebral arteries. This apparently increased frequency of contrast permeating
the occipital cortex suggests that the blood-brain barrier is more vulnerable
in the posterior circulation.
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Table 1. CT-Confirmed Cortical Penetration of Angiographic Contrast*
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The sympathetic innervation of the vertebrobasilar arterial system is
not as extensive or complete as that of the carotid arterial system.19 Thus, a relative lack of protective, sympathetically
mediated arteriolar vasoconstriction during severe hypertension may account
for the predominance of posterior hemisphere lesions in eclampsia or hypertensive
encephalopathy.20-21 A reversible
posterior leukoencephalopathy syndrome seems to be related to transplant immunosuppressive
treatment and renal insufficiency, as well as hypertension.21-22
Early on, vascular permeability presumably creates edematous lesions, which
often resolve upon control of blood pressure or reduction of immunosuppressive
drugs. Clinically, cortical blindness is common in this syndrome, and is often
accompanied by agitated delirium or seizures, making the bedside examination
difficult. If the visual system could be examined thoroughly, perhaps more
subtle deficits in visual processing would be detected.
The blood-brain barrier of the vertebrobasilar system thus seems breachable
in the setting of several conditions that may coexist, including hypertension,
renal insufficiency, immunosuppressive drugs, and angiographic contrast. Ionic
or nonionic contrast tends to selectively penetrate the occipital cortex,
causing transient syndromes from dramatic cortical blindness to more subtle
visuospatial processing disorders.
AUTHOR INFORMATION
Accepted for publication December 3, 2001.
Author contributions: Both authors had equal
responsibility for the work.
Corresponding author: Michael P. Merchut, MD, Department of Neurology,
Loyola University Medical Center, 2160 S First Avenue, Maywood, IL 60153 (e-mail: mmerchu{at}lumc.edu).
From the Department of Neurology, Loyola University Medical Center,
Maywood, Ill.
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