Kee Hyun Chang, Man Chung Han,
MD MD
#{149} Moon
Hee
Han,
MD
#{149} Hak
Soo Kim,
Delayed Encephalopathy Monoxide Intoxication: Distribution ofCerebral Magnetic resonance (MR) images obtained in 15 patients with delayed encephalopathy after acute carbon monoxide (CO) intoxication were reviewed. Images had been obtained 4-9 weeks after exposure to CO, during the relapse of neuropsychiatric symptoms
after
initial
recovery.
Bi-
lateral symmetric confluent high signal intensity in the periventricular white matter and centrum semiovale was ages
seen
(n
on long-repetition-time
im-
The high intensity extended into the corpus callosum (n = 11), subcortical U fibers (n = 12), and external (n 9) and internal (n = 7) capsules. Bilateral diffuse low-intensity signal in the thalamus and putamen on T2-weighted images, =
15).
suggesting
iron
onstrated
was
in 10 patients.
ischemia pallidus
three
deposition,
of four
extent
and
patients
with
studies,
a decrease
signal
matter lesions ing of clinical
Index
of the terms:
cerebral
Radiology
I
white
RSNA,
1992
morning,
which encephaneurologic
of the
findings
of CO
some
cases
intoxica-
magnetic findings associated
have
been
en-
rea).
resonance
(MR) encephaintoxica-
documented
in only
#{149} Brain,
a
patients (14-17). In this article, we describe the MR imaging appearance of delayed encephalopathy associated with acute CO intoxication, and emphasize the distribution of the cerebral white mat-
ter lesion.
AND
Twenty
Radiol-
brain
MR
METHODS
images
of 15 patients
(five men, 10 women; age range, 25-71 years) with delayed encephalopathy of acute CO intoxication were retrospectively reviewed. Four patients underwent more than one MR imaging examination. Of those four, one underwent MR imaging three times, and three underwent imaging twice. In all patients, the diagnosis of acute CO intoxication was made on the basis of circumstantial evidence. In Korea, there are hundreds of victims of acute CO intoxication every winter in Korea as a main
(2,16). fuel
confirmed
because
of aggra-
symptoms
unit
(Goldstar,
Proton-density-
after
plane
ters:
2,500
were
by using and
Seoul,
and
images
axial
obtained
the
in the
following
3,000/30
Ko-
T2-weighted
and
parame-
80 (repetition
time [TR] msec/echo time msec), one signal average, 5-mm section thickness, and 2-mm gap with the 2.0-T imager; and 2,000/30 7-mm 0.5-T
and
100,
thickness, imager.
matrix
imaging
special corpus
signal
of 256
findings
attention callosum,
ternal the
two
and 3-mm Ti-weighted
averages, gap with spin-echo
the im-
(400-600/30; two to four signal averwere obtained in the sagittal plane. field of view was 20-25 cm, with an
ages ages) The MR
10.5912
of Diagnostic
CO exposure,
acquisition
MATERIALS
room
of neuropsychiatric
spin-echo
mailer.
10.5912
emergency
perconducting
de-
of delayed with CO
oxygen
a period of initial recovery. Follow-up MR images were obtained in four patients 1-9 months after the initial MR imaging examination. MR imaging was performed with either a 2.0-T (n = 12) or 0.5-T (n = 3) su-
intoxication,
have been well To our knowledge,
at the
following vation
of the globi tomogra-
of delayed
hyperbaric
in
the diagnosis. The COHb was not measured in the other four patients. Prior to the acute insult, all patients had been normal neurologically. MR imaging was performed 4-9 weeks
periventricular
and necrosis The computed
underwent
arrival
of
(CO)
and
therapy, and then awakened within 72 hours. In 11 patients (cases 1-11 in Tables 1 and 2), elevated blood levels of carboxyhemoglobin (COHb) measured soon after
occasevere
characteristic
monoxide
matter (3-8).
imaging lopathy few
ogy (K.H.C., M.H.H., H.S.K., M.C.H.) and Neurology (B.A.W.), Seoul National University Hospital and College of Medicine, 28 Yongon-dong Chongno-gu, Seoul, 110-744, Korea. From the 1990 RSNA scientific assembly. Received September 25, 1991; revision requested October 21; revision received January 27, 1992; accepted February 24. Supported in part by a grant from the faculty practice research fund of Seoul National University Hospital (1992). Address reprint requests to K.H.C. ©
are more carbon
(CT)
of white
1992; 184:117-122
From the Departments
patients
Carbon Features Lesions’
into the bedroom through cracks the floor. All the patients of the present series were found unconscious in the
tion than of other types of anoxia (2). The basic neuropathologic features of CO intoxication are known to be
tion
lessenThese
matter,
acute
in
white
Brain, diseases,
MR. 10.1214 #{149} Brain, Carbon monoxide
sequelae
cephalopathy, scribed (8-13).
results suggest that the main pathologic feature of delayed encephalopathy associated with CO intoxication is a reversible demyelinating process
however,
MD
leaks
severe coma, pa-
sionally will again undergo neuropsychiatric deterioration, is called postanoxic delayed lopathy (1). These delayed
including
In
Ae Wie,
may recover in 24-48 hours. varying intervals of apparent
normality,
phy
follow-up
intensity
accompanied symptoms.
tients After
however,
or necrosis of the globus was seen in nine patients.
MR imaging
an anoxic episode enough to produce
FTER
white pallidi
Bilateral
#{149} Bong
after Acute MR Imaging White Matter
degeneration
dem-
MD
capsule pattern
x 200-256.
were
reviewed
with
to the involvement subcortical U fibers, and
of the
internal white
capsule, matter
The of the exand
abnormali-
ties. In addition, the signal intensity basal ganglia and thalami was also ated.
of the evalu-
RESULTS The ings
clinical in the
and
MR imaging
15 patients
are
rized in Tables 1 and The most common symptoms
at the
time
find-
summa-
2. neurologic of MR
imaging
Since coal is used for under-the-floor
home heating systems, acute CO intoxication is occasionally caused by accidental inhalation of CO-containing coal gas that
Abbreviations: TR = repetition
CoHb time.
=
carboxyhemoglobin,
117
were mental dysfunction, including memory impairment, disorientation, abnormal etc. Other
nary
behavior, symptoms
and/or
Table
fecal
incontinence,
1
Associated
par-
trum
semiovale
1!54/M
7
2
Disorientation; behavior;
2/35/F
5
1
Confusion; urinary
In nine
there
however,
cept
for two
both confluent lesions were
matter
4 and
were
losum (Figs
The
three
body,
into
patients
eight. The
and
was
seen
in the
putamen
extensive
than
in the
in these
five patients
basal
ganglia
noted
in nine
ganglia pallidus usually 118
(Figs
3
urinary
continence;
parkinsonism
Disorientation;
5
2
10/58/F
6
3
in-
im-
memory parkinsonism
Memory impairment; abnormal behavior; urinary incontinence; improved at 7-mo follow-up Stuporousness; parkinsonism Memory impairment; disori-
5
2
and fe-
urinary
Dementia;
4
12/58/F
2.5
mutism;
urinary
Memory impairment; abnormal behavior; urinary incontinence;
parkinsonism;
fluctuation
of clinical at 5-mo fol-
symptoms
13/53/F
4
2
14/63/M
4
2
15/48/F
6
4
low-up Confusion; disorientation; urinary incontinence Abnormal behavior; memory impairment
cal-
Disorientation;
memory
pairment;
havior;
MR imaging
was performed
with
a 0.5-1
abnormal
unbe-
parkinsonism
unit.
finding of the thaIimages, sug(Figs 1-3, 5),
Among also
in six and
ranged in
10 patients
without
the
2, 4, 5), which
All the
was
basal
lesions involved the globus bilaterally. The lesions were round or oval in shape and
#{149} Radiology
4
malbehavior;
incontinence
finding at MR or infarct of the
patients.
4
11/54/F*
hypointensity.
The third common imaging was ischemia
incon-
cal incontinence
the caudate nucleus in two (Figs 1, 3). Three of the 10 patients were less than 40 years old. Associated white matter abnormalities tended to be more
9
in
which was seen in 10 patients. the 10 patients, hypointensity was
6!57/M*
9/71/F
in
diffuse
conspicuous
was diffuse hypointensity amus on T2-weighted gesting iron deposition
4
entation;
*
second
6
the
corpus
or splenium
urinary
disorientation; parkinsonism; improved at 1-mo follow-up Memory impairment; disori. entation; urinary incontinence; parkinsonism Memory impairment; disorientation; parkinsonism Memory impairment; abnor-
ex-
was involved in ii patients 2, 3, 5); the lesion was localized
in the genu,
5/56/F
4
patchy white
extended
respectively.
2
8
subcortical U fibers (Figs 2-4), external capsules (Figs 3, 4), and internal capsules (Fig 3) in 12, nine, and seven
patients,
8
8/62/F
9), in whom
and multifocal combined. The
lesions
Confusion;
the
in all patients
(cases
disorientation, and fecal inconti-
pairment;
lesion was more extensive and prominent in the frontal lobes than in the other regions. The lesions were difconfluent
4/58/MS
7/25/F
diffuse
maining
and
2
cen-
of the lesion white matter, sites. In the re-
fuse
4
images. was
abnormal urinary inconti-
nence; parkinsonism; improved at 1-mo follow-up; almost recovered at 9.mo follow-up 3!39!M
uniform distribution throughout the deep with no predilection six patients,
Major Clinical Findings
nence
on proton-density-
patients,
Lucid Interval (wk)
tience;
of the matter and
on Ti-weighted
Encephalopathy
CO Exposure and MR Imaging (wk)
and T2-weighted images (Fig 1), which was seen in all patients. The hyperintensity varied in degree from slight to severe. The abnormality appeared as slight hypointensity or
isointensity
Delayed
Case No.! Age (y)!Gender
The most common and charactenistic MR imaging finding was bilateral hyperintensity white
with
Interval between
kinsonism, gait disturbance, and speech disturbance. The symptoms that developed were preceded by an interval of apparent normality (the “lucid interval”) after initial recovery from the comatose state of acute CO intoxication. The lucid interval varied from 1 to 4 weeks in duration, and was 2 weeks long in most patients.
symmetric periventnicular
of Clinical Features in 15 Patients with CO Intoxication
Summary
and confusion, included un-
from
a few
millimeters
to 1
centimeter in size. In one patient, focal hemorrhage was associated in the right
glohus
men
(Fig 4).
In four
pallidus
and
left
puta-
(cases
4, 5, 9, and
suggestive were in the
putamen,
occipital
respectively. Diffuse
cerebral
cortex,
and
of ischthalami, and
pons,
cerebellar
atro-
phy was obvious in four patients (cases 2, 6, 8, and 9). On follow-up MR imaging studies obtained in four patients, three (cases 2, 3, and 8) showed decrease of the
matter
symptoms, whereas (case 12) demonstrated
nal intensity
patients
14), the findings emia or infarct
white
and signal intensity, which coincided with decreasing severity of clinical
lesions
in both
extent
the
of the
tion with fluctuating toms. In one patient
lesion
fourth increased
patient sig-
in associa-
clinical symp(case 2), the
white matter lesions were markedly diminished in association with diffuse brain atrophy, and the lesions of the globus
pallidus
the 1-month white matter small
foci
had
follow-up lesions
in the
disappeared
study, remained
centrum
on
but the as
semiovale
on the 9-month follow-up study (Fig 2). The hypointensity of the thalamus seen on the i-month follow-up irnJuly
1992
Table 2 Summary
of MR Imaging
Features
in 15 Patients
Delayed
with Lesion
Case No.
PVWM and CS
Examination
Corpus Callosum
Encephalopathy
Associated
CO Intoxication
with
Locations*
Subcortical U Fibers
External Capsule
Internal Capsule
Ischemia or Necrosis of Globi Pallidi
Increased Iron Deposition Thalami, putamen, caudate nucleus No Thalami
Other Findings None
I
Initial
Yes
Yes
No
Yes
Yes
No
2
Initial Follow-upi
Yest Yes
Yes No
Yes No
No No
No No
Yes No
3
Initial
Yes
Yes
Yes
Yes
Yes
No
Thalami, putamen, caudate nucleus
4#
Initial
Yes
Yes
Yes
No
No
Yes
Thalami, putamen
Ischemia or infarct: putamen, white matter
5
Initial
Yes
No
Yes
Yes
No
Yes**
Thalami
Ischemia infarct: occipital cortex
6#
Initial
Yest
No
No
No
No
Yes
Thalami
7 8
Initial Initial
Yes Yes
Yes Yes
Yes No
Yes No
Yes Yes
Yes Yes
Thalami No
9
Follow-up Initial
Yes Yes
No No
No Yes
No Yes
No Yes
Yes No
No No
Cerebralcerebellar atrophy None Cerebralcerebellar atrophy Same Multifocal ischemia infarct: thalami, PVWM; cerebralcerebellar atrophy None None
10 11#
Initial Initial
Yes Yes
Yes Yes
Yes Yes
No Yes
No Yes
Yes No
l2tt 13
Initial Initial
Yest Yes
Yes Yes
Yes Yes
Yes Yes
No Yes
Yes No
14
Initial
Yes
No
Yes
Yes
No
No
15
Initial
Yest
Yes
Yes
No
No
Yes
Note-CS * Abnormality t Abnormality
=
centrum semiovale, shown as confluent was more prominent
PVWM = periventncular hyperintensity on long in the frontal lobes.
white matter. TR images and
Lesions extended to caudate nucleus and putamen. Findings did not change at second follow-up examination. t Findings slightly improved at follow-up examination. I MR imaging was performed with a 0.5-T unit. ** Lesions associated with focal hemorrhages in right globus tt Findings increased in intensity at follow-up imaging.
isointensity
or slight
hypointensity
None Cerebralcerebellar atrophy None
No Thalami, putamen No Thalami, putamen No
or
None None Ischemiainfarct: pons None
Thalami, putamen
on short
or
TR images.
S
ages 9-month
showed
no change
follow-up
on the
images.
DISCUSSION
cases)
for
acute
usually
older
(18).
1
11.8%
are middle-aged The
lucid
(65
nence,
interval
lence,
parkinsonism,
and the
mutism duration
of
hospitalized The pa-
gait
age interval,
lucid
22
distur-
(2). The
the
clinical
symptoms
series
are
in the the same
almost
as
those reported previously. A variety of cerebral morphologic changes caused by CO intoxication
or
of
and present
varies
2 to 40 days in length (mean, days). The most frequent symptoms are mental deterioration, inconti-
bance,
#{149} Number
in
the patients CO intoxication. of
tients
cases) (2,18).
184
left putamen.
occurred
549
from
Volume
and
cephalopathy
The incidence of delayed encephalopathy following acute CO intoxication is small, ranging from 0.06% (13 of 2,100 cases) to 2.8% (65 of 2,360
of all cases of CO intoxication In one study (2), delayed en-
pallidus
preva-
have
include
been
well ischemia
documented. or necrosis
globus pallidus, demyelination crosis of the cerebral white spongy necrosis of cerebral and
necrosis
of the
These of the
or nematter, cortices,
hippocampus
Radiology
(3-
#{149} 119
8). Of these, the lesions of cerebral white matter are the most characteristic of and clinically corresponding to the delayed encephalopathy with CO intoxication (3-5,8,1 1).
CO-related
white
matter
abnormal-
have
been categorized into three groups, although there is much overlap among the groups. The first category consists of multiple small necrotic foci in the centrum semiovale ities
and interhemispheric The second category consists of extensive, of necrosis periventricular
throughout white
logically,
the
axonal merous
show
consists
with relative in the deep
may
sions
are
and
to be spared.
is the
type
patients lopathy
The
of demyelina-
a.
b.
Figure
of axThe le-
1. Case
year-old centrum
1.
(a, b) Axial T2-weighted
man show semiovale.
bilateral
confluent
(2,500/80) high
intensity
MR images obtained in the periventricular
at 2.0 T in a 54white matter and
discrete,
or even confluent. The lemost prominent in the fronSubcortical arcuate U fibers
tal lobes.
tend
nu-
preservation white matter.
be small
extensive,
extensive
and contain macrophages.
category
sions
the deep matter. Histo-
lesions
destruction lipid-laden
third tion ons
commissures. of the lesions confluent areas
that
This
third
is seen
most
with delayed or the so-called
category often
in
encephabiphasic
“myelinopathy” of Grinker (3-5). Lapresle and Fardeau (3) correlated the remitting-and-relapsing clinical course with the Grinker type of white
matter lesions cases.
in six of their
seven
According to Ginsberg et al (5), “it appears likely that the differences described among the various morphologic categories represent gradations in intensity of a pathologic process rather than reflecting fundamental distinctions in pathogenesis.” In an
a.
b.
experimental study of CO intoxication in primates (5), one animal that exhibited a relapsing course had white matter lesions similar to those of the animals that showed immediate and nonrelapsing deficits. The animal brains extensively damaged demonstrated the white matter lesions extending into the corpus callosum, internal capsule, and subcortical U fibers
in several
zones
(5).
The pathologic findings of white matter lesions are represented by low attenuation on CT scans (8-13) and by high sity-
signal intensity and T2-weighted
on
proton-denMR images
(14-17). The previous reports and MR imaging of patients
on CT with CO
intoxication,
not
cluded
however,
a detailed
distribution
matter sions
description
and
lesion. delineated
the the
present findings
120
#{149} Radiology
have
The
pattern
white with
MR
inwhite
matter
le-
imaging
series generally matched described in the prior
Figure
2. Case 2. (a, b) Initial at 2.0 T in a 35-year-old
obtained
lar white
of the of the
d.
C.
fibers.
in
matter
Subtle
and putamen plete resolution
and
high
centrum
intensity
and
(c, d) follow-up axial woman. (a, b) A massive
semiovale is also
seen
extends in the
T2-weighted confluent
into the corpus globus
pallidus
(2,500/80) MR images lesion of the periventricu-
callosum bilaterally
and and
subcortical caudate
in the right side. (c, d) Images obtained 9 months later demonstrate of the white matter abnormality, except for some residual lesion
trum serniovale. In c, notice the low signal intensity creased iron deposition in the thalami. Hemosiderin role in the low signal intensity.
suggesting and mineral
axonal injury-related deposition may
U
nucleus
almost cornin the cenalso
inplay
July
a
1992
the production of neuropathologic lesions (1). Higher prevalence in the aged patients suggests that preexisting smallvessel arteriosclerotic changes might also contribute to the development of the lesion to some degree. Multifocal lesions in the white matter (cases 4 and 9) and lesions in the thalamus, putamen, and pons (cases 4, 9, and 14) were found in the elderly patients and might have been caused by small vessel
b. 3. Case
3. (a) Initial and (b) follow-up at 2.0 1 in a 39-year-old man. (a) Diffuse
Figure
tamed
periventricular white matter sule, and subcortical U fibers. the thalamus, putamen, and decrease of the signal intensity bers.
axial T2-weighted confluent high
(3,000/80)
signal
intensity
MR images obthroughout the
extends into the corpus callosum, external capsule, internal capThe low signal intensity caused by iron accumulation is seen in caudate nucleus bilaterally. (b) One month later, there is slight in the corpus callosum, external capsule, and subcortical U fi-
disease
rather
than
CO
cation itself. To our knowledge, the intensity in the thalamus often, in the putamen and nucleus) on T2-weighted not been described in the CO intoxication. Drayer et al (19) described duced signal intensity in and putamen, suggesting mulation, was noticed in 42 cases)
of multiple
intoxi-
low signal (and, less caudate images has literature on that rethe thalamus iron accu60% (25 of
sclerosis
patients
and correlated with the degree of white matter abnormality. Dietrich al (20) also reported increased iron deposition in the basal ganglia and thalamus in children with hypoxicanoxic
leukoencephalopathy.
et
They
explained that interruption of normal axonal transportation of nonheme iron caused by white matter abnormality might lead to increased accumulation of iron at the basal ganglia and thalamus. Additional iron deposition might occur more rapidly due to direct cell injury. Increased iron deposition
has
tients
with
also
is believed
a. Figure
4. Case
Ti-weighted basal
ing
b. 5.
MR
(500/30)
ganglia.
(b) On
images
image the
obtained
reveals
at 2.0 T in a 56-year-old
a 1.5-cm-sized
12-weighted
(2,500/70)
woman.
hemorrhage axial
image,
with
(a) Left
high
asymmetric
foci
in the left
of high
are seen in the basal ganglia bilaterally. There is confluent high intensity of mild degree throughout the penventricular white matter, extending into the subcortical U fibers and nal capsule. Focal ischemia or infarct is also seen in the left occipital cortex.
pathologic studies of CO encephalopathy (1,4,8). The frequent involvement of the subcortical U fibers in our
ure was believed to have contributed to the development of the cerebral white matter lesions in dogs. Gins-
series,
berg
however,
was
in contradiction
to the pathologic description, in which the U fibers were relatively spared (4,5). This discrepancy might have been related to the reversible demyelination of the U fibers, but the exact cause is unknown. The pathogenesis of the delayed leukoencephalopathy with CO intoxication remains
and other uncertain.
anoxic
conditions
Preziosi et al (6) reported vation of cerebral venous sendondary to right-sided Volume
184
#{149} Number
I
that elepressure heart fail-
et al (1,5)
tion between matter lesions abolic acidosis sion
than
with
observed
closer
extent
exter-
correla-
CO exposure, hemoconcentration. effect due cytochromes
COHb
level, Direct
MR
the
iron
that
imaging
deposition
is not
pathologic
condition,
it should
be regarded
common
pathway
(21).
Our
hypothesis,
It
find-
to axonal
results
although
support iron
deposi-
that
to binding of CO to brain may also contribute to
are
no
cephalopathy
substantial
differ-
associated
toxication. The ischemia
hyof
acidosis, cytotoxic
there
ences in clinical course in patients with and without increased iron deposition. Further studies are needed to determine whether the presence of increased iron deposition portends a different prognosis in delayed en-
of hypoxia
the degree of systemic but not with duration
this
(21).
that
tion at the basal ganglia in elderly patients might be mainly due to the aging process. In the present series, although the white matter lesion appeared to be more extensive in the patients with iron deposition, it seems
per se. Meanwhile, Okeda et al (7) described that the severity of the white matter damage correlated well only with potension,
rather
disruption
the size of the white and the degree of metand systolic hypotenthe
but
in pa-
infarctions
to any
as a final
intensity
been
of increased
specific
parasagittal
intensity
described
cerebral
or
bus
pallidus
with
or necrosis is another
CO
in-
of the
gb-
characteristic
of CO intoxication, whether delayed
regardless encephabopathy
of
velops
lesion
gbobus
(3-8).
The
of the
Radiology
de-
#{149} 121
pallidus has ganic hallmark
poxic
been
process
that
are
considered an of the ischemic-hy-
observed
in many
by
circulatory
bance of the arterial (8,10). In the present acteristic was seen
border series, in 60%
cases).
of the
dus
caused
The
lesions
in CO
intoxication
ischemic
may
be hemorrhagic,
5. Unilateral lidus served
The pus had
lesions
focal
and been
zone this (nine
palliconsist
(3-5),
but
as in case
of the
globus
nucleus
necroses
charof 15
gbobus
necrosis
or lentiform (13).
states distur-
usually
of bilateral rarely
or-
may
of the
the substantia well documented
palbe ob-
hippocam-
which in the pathologic specimens (3-7), were not observed in any cases of the present series. This was presumably due either to the lesions being small or to the limited image quality of the present series. Diffuse cerebral and cerebellar atrophy noted in our four patients might result from either the aging process and/or CO-related injury to the granular layer of the cerebral cortex and
Purkinje layer brain atrophy woman)
of the cerebellum. in case 2 (35-year-old
probably
related
nigra,
reflected
the
Figure 5. Case 4. (a, b) Axial T2-weighted (2,500/100) MR images obtained at 0.5 T in a 58year-old man. Small round areas of high intensity in the globus pallidus are evident bilaterally. On a Ti-weighted sagittal image (not shown), the lesions appeared as low intensity, mdicating ischemic necrosis. Periventricular white matter and centrum semiovale show slightly high intensity, with subtle extension into U fibers and corpus callosurn. There is low intensity in parts of the thalamus and putamen. A few foci of high intensity, suggesting ischemia or infarcts, are also seen in the left putamen and right high frontal subcortical white matter.
The
References 1.
CO-
injury.
The outcome and prognosis of the delayed encephabopathy with CO intoxication is relatively good. According to one clinical study (2), 75%
(27 of 36 patients) recovered year, but some of them had sequelae,
including
turbance tively
and good
and
mild
imaging, patients, ter lesions
as seen suggest consist
elination
rather
crosis
and
within
axonal
In summary,
2.
1
with
The
rela-
others
(2)
4.
in three of our four that most white matof reversible demy-
5.
at follow-up
than
MR
irreversible
ne-
destruction.
MR imaging
findings
of bilateral symmetric confluent abnormality in the periventricular white matter and centrum semiovale, frequently extending into the corpus callosum, internal capsule, external capsule, and subcortical U fibers (regardless of bilateral basal ganglia necrosis), is considered to be typical of delayed encephabopathy of acute CO
intoxication. tion in the probably
Increased thalamus caused
transport
by
iron deposiand putamen, interruption
of nonheme
#{149} Radiology
6.
7.
8.
of
iron
sec-
to the diffuse white matter lesion, is commonly associated. The reversible demyelination may be mainly responsible for the development of delayed encephabopathy following acute CO intoxication. U
122
3.
persistent memory dis-
parkinsonism. prognosis
improvement
axonal ondary
b.
a.
9.
10.
Ginsberg MD. Delayed neurological deterioration following hypoxia. In: Davis JN, Rowland LP, eds. Cerebral hypoxia and its consequences. New York: Raven, 1979; 2144. Choi IS. Delayed neurologic sequelae in carbon monoxide intoxication. Arch Neurol 1983; 40:433-435. Lapresle J, Fardeau M. The central nervous system and carbon monoxide poisoning. II. Anatomical study of brain lesions following intoxication with carbon monoxide (22 cases). Prog Brain Res 1967; 24:3175. Schochet SS. Exogenous toxic-metabolic disease including vitamin deficiency. In: Davis RL, Robertson DM, eds. Textbook of neuropathology. 1st ed. Baltimore: Wilhams & Wilkins, 1985; 372-402. Ginsberg MD, Myers RE, McDonagh BF. Experimental carbon monoxide encephalopathy in the primate. II. Clinical aspects, neuropathology, and physiologic correlation. Arch Neurol 1974; 30:209-216. Preziosi TJ, Lindenberg R, Levy D, Christenson M. An experimental investigation in animals of the functional and morphologic effects of single and repeated exposures to high and low concentrations of carbon monoxide. Ann NY Acad Sci 1970; 174:369-384. Okeda R, Funata N, Takano T, et al. The pathogenesis of carbon monoxide encephalopathy in the acute phase: physiological and morphological correlation. Acta Neuropathol 1981; 54:1-10. Kobayashi K, Isaki K, Fukutani Y, et al. CT findings of the interval form of carbon monoxide poisoning compared with neuropathological findings. Eur Neurol 1984; 23:34-43. Nardizzi LR. Computerized tomographic correlate of carbon monoxide poisoning. Arch Neurol 1979; 36:38-39. Kim KS, Weinberg PE, Suh JH, Ho SU. Acute carbon monoxide poisoning: computed tomography of the brain. AJNR 1980; 1:399-402.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
Miura T, Mitomo M, Kawai R, Harada K. CT of the brain in acute carbon monoxide intoxication: characteristic features and prognosis. AJNR 1985; 6:739-742. Zeiss J, Brinker R. Role of contrast enhancement in cerebral CT of carbon monoxide poisoning. J Comput Assist Tomogr 1988; 12:341-343. Taylor R, Holgate RC. Carbon monoxide poisoning: asymmetric and unilateral changes on CT. AJNR 1988; 9:975-977. Davis PL. The magnetic resonance imaging appearances of basal ganglia lesions in carbon monoxide poisoning. Magn Reson Imaging 1986; 4:489-490. Vion-DuryJ, Jiddane M, Van Bunnen Y, Rumeau C, Lavielle J. Sequelae of carbon monoxide poisoning: an MRI study of two cases. J Neuroradiol 1987; 14:60-65. Horowitz AL, Kaplan R, Sarpel G. Carbon monoxide toxicity: MR imaging in the brain. Radiology 1987; 162:787-788. Tuchman RF, Moser FG, Moshe SL. Carbon monoxide poisoning: bilateral lesions in the thalamus on MR imaging of the brain. Pediatr Radiol 1990; 20:478-479. Lee MH. Clinical studies on delayed sequelae of carbon monoxide intoxication. Korean Neuropsychiatr Assoc 1978; 15:374385. Drayer B, Burger P. Hurwitz B, Dawson D, Cain J. Reduced signal intensity on MR images of thalamus and putamen in multipIe sclerosis: increased iron content? AJNR 1987; 8:413-419. Dietrich RB, Bradley WG Jr. Iron accumulation in the basal ganglia following severe ischemic-anoxic insults in children. Radiology 1988; 168:203-206. Cross PA, Atlas SW, Grossman RI. MR evaluation of brain iron in children with cerebral infarction. AJNR 1990; 11:341-348.
July
1992
MD MD
#{149} Moon
Hee
Han,
MD
#{149} Hak
Soo Kim,
Delayed Encephalopathy Monoxide Intoxication: Distribution ofCerebral Magnetic resonance (MR) images obtained in 15 patients with delayed encephalopathy after acute carbon monoxide (CO) intoxication were reviewed. Images had been obtained 4-9 weeks after exposure to CO, during the relapse of neuropsychiatric symptoms
after
initial
recovery.
Bi-
lateral symmetric confluent high signal intensity in the periventricular white matter and centrum semiovale was ages
seen
(n
on long-repetition-time
im-
The high intensity extended into the corpus callosum (n = 11), subcortical U fibers (n = 12), and external (n 9) and internal (n = 7) capsules. Bilateral diffuse low-intensity signal in the thalamus and putamen on T2-weighted images, =
15).
suggesting
iron
onstrated
was
in 10 patients.
ischemia pallidus
three
deposition,
of four
extent
and
patients
with
studies,
a decrease
signal
matter lesions ing of clinical
Index
of the terms:
cerebral
Radiology
I
white
RSNA,
1992
morning,
which encephaneurologic
of the
findings
of CO
some
cases
intoxica-
magnetic findings associated
have
been
en-
rea).
resonance
(MR) encephaintoxica-
documented
in only
#{149} Brain,
a
patients (14-17). In this article, we describe the MR imaging appearance of delayed encephalopathy associated with acute CO intoxication, and emphasize the distribution of the cerebral white mat-
ter lesion.
AND
Twenty
Radiol-
brain
MR
METHODS
images
of 15 patients
(five men, 10 women; age range, 25-71 years) with delayed encephalopathy of acute CO intoxication were retrospectively reviewed. Four patients underwent more than one MR imaging examination. Of those four, one underwent MR imaging three times, and three underwent imaging twice. In all patients, the diagnosis of acute CO intoxication was made on the basis of circumstantial evidence. In Korea, there are hundreds of victims of acute CO intoxication every winter in Korea as a main
(2,16). fuel
confirmed
because
of aggra-
symptoms
unit
(Goldstar,
Proton-density-
after
plane
ters:
2,500
were
by using and
Seoul,
and
images
axial
obtained
the
in the
following
3,000/30
Ko-
T2-weighted
and
parame-
80 (repetition
time [TR] msec/echo time msec), one signal average, 5-mm section thickness, and 2-mm gap with the 2.0-T imager; and 2,000/30 7-mm 0.5-T
and
100,
thickness, imager.
matrix
imaging
special corpus
signal
of 256
findings
attention callosum,
ternal the
two
and 3-mm Ti-weighted
averages, gap with spin-echo
the im-
(400-600/30; two to four signal averwere obtained in the sagittal plane. field of view was 20-25 cm, with an
ages ages) The MR
10.5912
of Diagnostic
CO exposure,
acquisition
MATERIALS
room
of neuropsychiatric
spin-echo
mailer.
10.5912
emergency
perconducting
de-
of delayed with CO
oxygen
a period of initial recovery. Follow-up MR images were obtained in four patients 1-9 months after the initial MR imaging examination. MR imaging was performed with either a 2.0-T (n = 12) or 0.5-T (n = 3) su-
intoxication,
have been well To our knowledge,
at the
following vation
of the globi tomogra-
of delayed
hyperbaric
in
the diagnosis. The COHb was not measured in the other four patients. Prior to the acute insult, all patients had been normal neurologically. MR imaging was performed 4-9 weeks
periventricular
and necrosis The computed
underwent
arrival
of
(CO)
and
therapy, and then awakened within 72 hours. In 11 patients (cases 1-11 in Tables 1 and 2), elevated blood levels of carboxyhemoglobin (COHb) measured soon after
occasevere
characteristic
monoxide
matter (3-8).
imaging lopathy few
ogy (K.H.C., M.H.H., H.S.K., M.C.H.) and Neurology (B.A.W.), Seoul National University Hospital and College of Medicine, 28 Yongon-dong Chongno-gu, Seoul, 110-744, Korea. From the 1990 RSNA scientific assembly. Received September 25, 1991; revision requested October 21; revision received January 27, 1992; accepted February 24. Supported in part by a grant from the faculty practice research fund of Seoul National University Hospital (1992). Address reprint requests to K.H.C. ©
are more carbon
(CT)
of white
1992; 184:117-122
From the Departments
patients
Carbon Features Lesions’
into the bedroom through cracks the floor. All the patients of the present series were found unconscious in the
tion than of other types of anoxia (2). The basic neuropathologic features of CO intoxication are known to be
tion
lessenThese
matter,
acute
in
white
Brain, diseases,
MR. 10.1214 #{149} Brain, Carbon monoxide
sequelae
cephalopathy, scribed (8-13).
results suggest that the main pathologic feature of delayed encephalopathy associated with CO intoxication is a reversible demyelinating process
however,
MD
leaks
severe coma, pa-
sionally will again undergo neuropsychiatric deterioration, is called postanoxic delayed lopathy (1). These delayed
including
In
Ae Wie,
may recover in 24-48 hours. varying intervals of apparent
normality,
phy
follow-up
intensity
accompanied symptoms.
tients After
however,
or necrosis of the globus was seen in nine patients.
MR imaging
an anoxic episode enough to produce
FTER
white pallidi
Bilateral
#{149} Bong
after Acute MR Imaging White Matter
degeneration
dem-
MD
capsule pattern
x 200-256.
were
reviewed
with
to the involvement subcortical U fibers, and
of the
internal white
capsule, matter
The of the exand
abnormali-
ties. In addition, the signal intensity basal ganglia and thalami was also ated.
of the evalu-
RESULTS The ings
clinical in the
and
MR imaging
15 patients
are
rized in Tables 1 and The most common symptoms
at the
time
find-
summa-
2. neurologic of MR
imaging
Since coal is used for under-the-floor
home heating systems, acute CO intoxication is occasionally caused by accidental inhalation of CO-containing coal gas that
Abbreviations: TR = repetition
CoHb time.
=
carboxyhemoglobin,
117
were mental dysfunction, including memory impairment, disorientation, abnormal etc. Other
nary
behavior, symptoms
and/or
Table
fecal
incontinence,
1
Associated
par-
trum
semiovale
1!54/M
7
2
Disorientation; behavior;
2/35/F
5
1
Confusion; urinary
In nine
there
however,
cept
for two
both confluent lesions were
matter
4 and
were
losum (Figs
The
three
body,
into
patients
eight. The
and
was
seen
in the
putamen
extensive
than
in the
in these
five patients
basal
ganglia
noted
in nine
ganglia pallidus usually 118
(Figs
3
urinary
continence;
parkinsonism
Disorientation;
5
2
10/58/F
6
3
in-
im-
memory parkinsonism
Memory impairment; abnormal behavior; urinary incontinence; improved at 7-mo follow-up Stuporousness; parkinsonism Memory impairment; disori-
5
2
and fe-
urinary
Dementia;
4
12/58/F
2.5
mutism;
urinary
Memory impairment; abnormal behavior; urinary incontinence;
parkinsonism;
fluctuation
of clinical at 5-mo fol-
symptoms
13/53/F
4
2
14/63/M
4
2
15/48/F
6
4
low-up Confusion; disorientation; urinary incontinence Abnormal behavior; memory impairment
cal-
Disorientation;
memory
pairment;
havior;
MR imaging
was performed
with
a 0.5-1
abnormal
unbe-
parkinsonism
unit.
finding of the thaIimages, sug(Figs 1-3, 5),
Among also
in six and
ranged in
10 patients
without
the
2, 4, 5), which
All the
was
basal
lesions involved the globus bilaterally. The lesions were round or oval in shape and
#{149} Radiology
4
malbehavior;
incontinence
finding at MR or infarct of the
patients.
4
11/54/F*
hypointensity.
The third common imaging was ischemia
incon-
cal incontinence
the caudate nucleus in two (Figs 1, 3). Three of the 10 patients were less than 40 years old. Associated white matter abnormalities tended to be more
9
in
which was seen in 10 patients. the 10 patients, hypointensity was
6!57/M*
9/71/F
in
diffuse
conspicuous
was diffuse hypointensity amus on T2-weighted gesting iron deposition
4
entation;
*
second
6
the
corpus
or splenium
urinary
disorientation; parkinsonism; improved at 1-mo follow-up Memory impairment; disori. entation; urinary incontinence; parkinsonism Memory impairment; disorientation; parkinsonism Memory impairment; abnor-
ex-
was involved in ii patients 2, 3, 5); the lesion was localized
in the genu,
5/56/F
4
patchy white
extended
respectively.
2
8
subcortical U fibers (Figs 2-4), external capsules (Figs 3, 4), and internal capsules (Fig 3) in 12, nine, and seven
patients,
8
8/62/F
9), in whom
and multifocal combined. The
lesions
Confusion;
the
in all patients
(cases
disorientation, and fecal inconti-
pairment;
lesion was more extensive and prominent in the frontal lobes than in the other regions. The lesions were difconfluent
4/58/MS
7/25/F
diffuse
maining
and
2
cen-
of the lesion white matter, sites. In the re-
fuse
4
images. was
abnormal urinary inconti-
nence; parkinsonism; improved at 1-mo follow-up; almost recovered at 9.mo follow-up 3!39!M
uniform distribution throughout the deep with no predilection six patients,
Major Clinical Findings
nence
on proton-density-
patients,
Lucid Interval (wk)
tience;
of the matter and
on Ti-weighted
Encephalopathy
CO Exposure and MR Imaging (wk)
and T2-weighted images (Fig 1), which was seen in all patients. The hyperintensity varied in degree from slight to severe. The abnormality appeared as slight hypointensity or
isointensity
Delayed
Case No.! Age (y)!Gender
The most common and charactenistic MR imaging finding was bilateral hyperintensity white
with
Interval between
kinsonism, gait disturbance, and speech disturbance. The symptoms that developed were preceded by an interval of apparent normality (the “lucid interval”) after initial recovery from the comatose state of acute CO intoxication. The lucid interval varied from 1 to 4 weeks in duration, and was 2 weeks long in most patients.
symmetric periventnicular
of Clinical Features in 15 Patients with CO Intoxication
Summary
and confusion, included un-
from
a few
millimeters
to 1
centimeter in size. In one patient, focal hemorrhage was associated in the right
glohus
men
(Fig 4).
In four
pallidus
and
left
puta-
(cases
4, 5, 9, and
suggestive were in the
putamen,
occipital
respectively. Diffuse
cerebral
cortex,
and
of ischthalami, and
pons,
cerebellar
atro-
phy was obvious in four patients (cases 2, 6, 8, and 9). On follow-up MR imaging studies obtained in four patients, three (cases 2, 3, and 8) showed decrease of the
matter
symptoms, whereas (case 12) demonstrated
nal intensity
patients
14), the findings emia or infarct
white
and signal intensity, which coincided with decreasing severity of clinical
lesions
in both
extent
the
of the
tion with fluctuating toms. In one patient
lesion
fourth increased
patient sig-
in associa-
clinical symp(case 2), the
white matter lesions were markedly diminished in association with diffuse brain atrophy, and the lesions of the globus
pallidus
the 1-month white matter small
foci
had
follow-up lesions
in the
disappeared
study, remained
centrum
on
but the as
semiovale
on the 9-month follow-up study (Fig 2). The hypointensity of the thalamus seen on the i-month follow-up irnJuly
1992
Table 2 Summary
of MR Imaging
Features
in 15 Patients
Delayed
with Lesion
Case No.
PVWM and CS
Examination
Corpus Callosum
Encephalopathy
Associated
CO Intoxication
with
Locations*
Subcortical U Fibers
External Capsule
Internal Capsule
Ischemia or Necrosis of Globi Pallidi
Increased Iron Deposition Thalami, putamen, caudate nucleus No Thalami
Other Findings None
I
Initial
Yes
Yes
No
Yes
Yes
No
2
Initial Follow-upi
Yest Yes
Yes No
Yes No
No No
No No
Yes No
3
Initial
Yes
Yes
Yes
Yes
Yes
No
Thalami, putamen, caudate nucleus
4#
Initial
Yes
Yes
Yes
No
No
Yes
Thalami, putamen
Ischemia or infarct: putamen, white matter
5
Initial
Yes
No
Yes
Yes
No
Yes**
Thalami
Ischemia infarct: occipital cortex
6#
Initial
Yest
No
No
No
No
Yes
Thalami
7 8
Initial Initial
Yes Yes
Yes Yes
Yes No
Yes No
Yes Yes
Yes Yes
Thalami No
9
Follow-up Initial
Yes Yes
No No
No Yes
No Yes
No Yes
Yes No
No No
Cerebralcerebellar atrophy None Cerebralcerebellar atrophy Same Multifocal ischemia infarct: thalami, PVWM; cerebralcerebellar atrophy None None
10 11#
Initial Initial
Yes Yes
Yes Yes
Yes Yes
No Yes
No Yes
Yes No
l2tt 13
Initial Initial
Yest Yes
Yes Yes
Yes Yes
Yes Yes
No Yes
Yes No
14
Initial
Yes
No
Yes
Yes
No
No
15
Initial
Yest
Yes
Yes
No
No
Yes
Note-CS * Abnormality t Abnormality
=
centrum semiovale, shown as confluent was more prominent
PVWM = periventncular hyperintensity on long in the frontal lobes.
white matter. TR images and
Lesions extended to caudate nucleus and putamen. Findings did not change at second follow-up examination. t Findings slightly improved at follow-up examination. I MR imaging was performed with a 0.5-T unit. ** Lesions associated with focal hemorrhages in right globus tt Findings increased in intensity at follow-up imaging.
isointensity
or slight
hypointensity
None Cerebralcerebellar atrophy None
No Thalami, putamen No Thalami, putamen No
or
None None Ischemiainfarct: pons None
Thalami, putamen
on short
or
TR images.
S
ages 9-month
showed
no change
follow-up
on the
images.
DISCUSSION
cases)
for
acute
usually
older
(18).
1
11.8%
are middle-aged The
lucid
(65
nence,
interval
lence,
parkinsonism,
and the
mutism duration
of
hospitalized The pa-
gait
age interval,
lucid
22
distur-
(2). The
the
clinical
symptoms
series
are
in the the same
almost
as
those reported previously. A variety of cerebral morphologic changes caused by CO intoxication
or
of
and present
varies
2 to 40 days in length (mean, days). The most frequent symptoms are mental deterioration, inconti-
bance,
#{149} Number
in
the patients CO intoxication. of
tients
cases) (2,18).
184
left putamen.
occurred
549
from
Volume
and
cephalopathy
The incidence of delayed encephalopathy following acute CO intoxication is small, ranging from 0.06% (13 of 2,100 cases) to 2.8% (65 of 2,360
of all cases of CO intoxication In one study (2), delayed en-
pallidus
preva-
have
include
been
well ischemia
documented. or necrosis
globus pallidus, demyelination crosis of the cerebral white spongy necrosis of cerebral and
necrosis
of the
These of the
or nematter, cortices,
hippocampus
Radiology
(3-
#{149} 119
8). Of these, the lesions of cerebral white matter are the most characteristic of and clinically corresponding to the delayed encephalopathy with CO intoxication (3-5,8,1 1).
CO-related
white
matter
abnormal-
have
been categorized into three groups, although there is much overlap among the groups. The first category consists of multiple small necrotic foci in the centrum semiovale ities
and interhemispheric The second category consists of extensive, of necrosis periventricular
throughout white
logically,
the
axonal merous
show
consists
with relative in the deep
may
sions
are
and
to be spared.
is the
type
patients lopathy
The
of demyelina-
a.
b.
Figure
of axThe le-
1. Case
year-old centrum
1.
(a, b) Axial T2-weighted
man show semiovale.
bilateral
confluent
(2,500/80) high
intensity
MR images obtained in the periventricular
at 2.0 T in a 54white matter and
discrete,
or even confluent. The lemost prominent in the fronSubcortical arcuate U fibers
tal lobes.
tend
nu-
preservation white matter.
be small
extensive,
extensive
and contain macrophages.
category
sions
the deep matter. Histo-
lesions
destruction lipid-laden
third tion ons
commissures. of the lesions confluent areas
that
This
third
is seen
most
with delayed or the so-called
category often
in
encephabiphasic
“myelinopathy” of Grinker (3-5). Lapresle and Fardeau (3) correlated the remitting-and-relapsing clinical course with the Grinker type of white
matter lesions cases.
in six of their
seven
According to Ginsberg et al (5), “it appears likely that the differences described among the various morphologic categories represent gradations in intensity of a pathologic process rather than reflecting fundamental distinctions in pathogenesis.” In an
a.
b.
experimental study of CO intoxication in primates (5), one animal that exhibited a relapsing course had white matter lesions similar to those of the animals that showed immediate and nonrelapsing deficits. The animal brains extensively damaged demonstrated the white matter lesions extending into the corpus callosum, internal capsule, and subcortical U fibers
in several
zones
(5).
The pathologic findings of white matter lesions are represented by low attenuation on CT scans (8-13) and by high sity-
signal intensity and T2-weighted
on
proton-denMR images
(14-17). The previous reports and MR imaging of patients
on CT with CO
intoxication,
not
cluded
however,
a detailed
distribution
matter sions
description
and
lesion. delineated
the the
present findings
120
#{149} Radiology
have
The
pattern
white with
MR
inwhite
matter
le-
imaging
series generally matched described in the prior
Figure
2. Case 2. (a, b) Initial at 2.0 T in a 35-year-old
obtained
lar white
of the of the
d.
C.
fibers.
in
matter
Subtle
and putamen plete resolution
and
high
centrum
intensity
and
(c, d) follow-up axial woman. (a, b) A massive
semiovale is also
seen
extends in the
T2-weighted confluent
into the corpus globus
pallidus
(2,500/80) MR images lesion of the periventricu-
callosum bilaterally
and and
subcortical caudate
in the right side. (c, d) Images obtained 9 months later demonstrate of the white matter abnormality, except for some residual lesion
trum serniovale. In c, notice the low signal intensity creased iron deposition in the thalami. Hemosiderin role in the low signal intensity.
suggesting and mineral
axonal injury-related deposition may
U
nucleus
almost cornin the cenalso
inplay
July
a
1992
the production of neuropathologic lesions (1). Higher prevalence in the aged patients suggests that preexisting smallvessel arteriosclerotic changes might also contribute to the development of the lesion to some degree. Multifocal lesions in the white matter (cases 4 and 9) and lesions in the thalamus, putamen, and pons (cases 4, 9, and 14) were found in the elderly patients and might have been caused by small vessel
b. 3. Case
3. (a) Initial and (b) follow-up at 2.0 1 in a 39-year-old man. (a) Diffuse
Figure
tamed
periventricular white matter sule, and subcortical U fibers. the thalamus, putamen, and decrease of the signal intensity bers.
axial T2-weighted confluent high
(3,000/80)
signal
intensity
MR images obthroughout the
extends into the corpus callosum, external capsule, internal capThe low signal intensity caused by iron accumulation is seen in caudate nucleus bilaterally. (b) One month later, there is slight in the corpus callosum, external capsule, and subcortical U fi-
disease
rather
than
CO
cation itself. To our knowledge, the intensity in the thalamus often, in the putamen and nucleus) on T2-weighted not been described in the CO intoxication. Drayer et al (19) described duced signal intensity in and putamen, suggesting mulation, was noticed in 42 cases)
of multiple
intoxi-
low signal (and, less caudate images has literature on that rethe thalamus iron accu60% (25 of
sclerosis
patients
and correlated with the degree of white matter abnormality. Dietrich al (20) also reported increased iron deposition in the basal ganglia and thalamus in children with hypoxicanoxic
leukoencephalopathy.
et
They
explained that interruption of normal axonal transportation of nonheme iron caused by white matter abnormality might lead to increased accumulation of iron at the basal ganglia and thalamus. Additional iron deposition might occur more rapidly due to direct cell injury. Increased iron deposition
has
tients
with
also
is believed
a. Figure
4. Case
Ti-weighted basal
ing
b. 5.
MR
(500/30)
ganglia.
(b) On
images
image the
obtained
reveals
at 2.0 T in a 56-year-old
a 1.5-cm-sized
12-weighted
(2,500/70)
woman.
hemorrhage axial
image,
with
(a) Left
high
asymmetric
foci
in the left
of high
are seen in the basal ganglia bilaterally. There is confluent high intensity of mild degree throughout the penventricular white matter, extending into the subcortical U fibers and nal capsule. Focal ischemia or infarct is also seen in the left occipital cortex.
pathologic studies of CO encephalopathy (1,4,8). The frequent involvement of the subcortical U fibers in our
ure was believed to have contributed to the development of the cerebral white matter lesions in dogs. Gins-
series,
berg
however,
was
in contradiction
to the pathologic description, in which the U fibers were relatively spared (4,5). This discrepancy might have been related to the reversible demyelination of the U fibers, but the exact cause is unknown. The pathogenesis of the delayed leukoencephalopathy with CO intoxication remains
and other uncertain.
anoxic
conditions
Preziosi et al (6) reported vation of cerebral venous sendondary to right-sided Volume
184
#{149} Number
I
that elepressure heart fail-
et al (1,5)
tion between matter lesions abolic acidosis sion
than
with
observed
closer
extent
exter-
correla-
CO exposure, hemoconcentration. effect due cytochromes
COHb
level, Direct
MR
the
iron
that
imaging
deposition
is not
pathologic
condition,
it should
be regarded
common
pathway
(21).
Our
hypothesis,
It
find-
to axonal
results
although
support iron
deposi-
that
to binding of CO to brain may also contribute to
are
no
cephalopathy
substantial
differ-
associated
toxication. The ischemia
hyof
acidosis, cytotoxic
there
ences in clinical course in patients with and without increased iron deposition. Further studies are needed to determine whether the presence of increased iron deposition portends a different prognosis in delayed en-
of hypoxia
the degree of systemic but not with duration
this
(21).
that
tion at the basal ganglia in elderly patients might be mainly due to the aging process. In the present series, although the white matter lesion appeared to be more extensive in the patients with iron deposition, it seems
per se. Meanwhile, Okeda et al (7) described that the severity of the white matter damage correlated well only with potension,
rather
disruption
the size of the white and the degree of metand systolic hypotenthe
but
in pa-
infarctions
to any
as a final
intensity
been
of increased
specific
parasagittal
intensity
described
cerebral
or
bus
pallidus
with
or necrosis is another
CO
in-
of the
gb-
characteristic
of CO intoxication, whether delayed
regardless encephabopathy
of
velops
lesion
gbobus
(3-8).
The
of the
Radiology
de-
#{149} 121
pallidus has ganic hallmark
poxic
been
process
that
are
considered an of the ischemic-hy-
observed
in many
by
circulatory
bance of the arterial (8,10). In the present acteristic was seen
border series, in 60%
cases).
of the
dus
caused
The
lesions
in CO
intoxication
ischemic
may
be hemorrhagic,
5. Unilateral lidus served
The pus had
lesions
focal
and been
zone this (nine
palliconsist
(3-5),
but
as in case
of the
globus
nucleus
necroses
charof 15
gbobus
necrosis
or lentiform (13).
states distur-
usually
of bilateral rarely
or-
may
of the
the substantia well documented
palbe ob-
hippocam-
which in the pathologic specimens (3-7), were not observed in any cases of the present series. This was presumably due either to the lesions being small or to the limited image quality of the present series. Diffuse cerebral and cerebellar atrophy noted in our four patients might result from either the aging process and/or CO-related injury to the granular layer of the cerebral cortex and
Purkinje layer brain atrophy woman)
of the cerebellum. in case 2 (35-year-old
probably
related
nigra,
reflected
the
Figure 5. Case 4. (a, b) Axial T2-weighted (2,500/100) MR images obtained at 0.5 T in a 58year-old man. Small round areas of high intensity in the globus pallidus are evident bilaterally. On a Ti-weighted sagittal image (not shown), the lesions appeared as low intensity, mdicating ischemic necrosis. Periventricular white matter and centrum semiovale show slightly high intensity, with subtle extension into U fibers and corpus callosurn. There is low intensity in parts of the thalamus and putamen. A few foci of high intensity, suggesting ischemia or infarcts, are also seen in the left putamen and right high frontal subcortical white matter.
The
References 1.
CO-
injury.
The outcome and prognosis of the delayed encephabopathy with CO intoxication is relatively good. According to one clinical study (2), 75%
(27 of 36 patients) recovered year, but some of them had sequelae,
including
turbance tively
and good
and
mild
imaging, patients, ter lesions
as seen suggest consist
elination
rather
crosis
and
within
axonal
In summary,
2.
1
with
The
rela-
others
(2)
4.
in three of our four that most white matof reversible demy-
5.
at follow-up
than
MR
irreversible
ne-
destruction.
MR imaging
findings
of bilateral symmetric confluent abnormality in the periventricular white matter and centrum semiovale, frequently extending into the corpus callosum, internal capsule, external capsule, and subcortical U fibers (regardless of bilateral basal ganglia necrosis), is considered to be typical of delayed encephabopathy of acute CO
intoxication. tion in the probably
Increased thalamus caused
transport
by
iron deposiand putamen, interruption
of nonheme
#{149} Radiology
6.
7.
8.
of
iron
sec-
to the diffuse white matter lesion, is commonly associated. The reversible demyelination may be mainly responsible for the development of delayed encephabopathy following acute CO intoxication. U
122
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improvement
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10.
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Miura T, Mitomo M, Kawai R, Harada K. CT of the brain in acute carbon monoxide intoxication: characteristic features and prognosis. AJNR 1985; 6:739-742. Zeiss J, Brinker R. Role of contrast enhancement in cerebral CT of carbon monoxide poisoning. J Comput Assist Tomogr 1988; 12:341-343. Taylor R, Holgate RC. Carbon monoxide poisoning: asymmetric and unilateral changes on CT. AJNR 1988; 9:975-977. Davis PL. The magnetic resonance imaging appearances of basal ganglia lesions in carbon monoxide poisoning. Magn Reson Imaging 1986; 4:489-490. Vion-DuryJ, Jiddane M, Van Bunnen Y, Rumeau C, Lavielle J. Sequelae of carbon monoxide poisoning: an MRI study of two cases. J Neuroradiol 1987; 14:60-65. Horowitz AL, Kaplan R, Sarpel G. Carbon monoxide toxicity: MR imaging in the brain. Radiology 1987; 162:787-788. Tuchman RF, Moser FG, Moshe SL. Carbon monoxide poisoning: bilateral lesions in the thalamus on MR imaging of the brain. Pediatr Radiol 1990; 20:478-479. Lee MH. Clinical studies on delayed sequelae of carbon monoxide intoxication. Korean Neuropsychiatr Assoc 1978; 15:374385. Drayer B, Burger P. Hurwitz B, Dawson D, Cain J. Reduced signal intensity on MR images of thalamus and putamen in multipIe sclerosis: increased iron content? AJNR 1987; 8:413-419. Dietrich RB, Bradley WG Jr. Iron accumulation in the basal ganglia following severe ischemic-anoxic insults in children. Radiology 1988; 168:203-206. Cross PA, Atlas SW, Grossman RI. MR evaluation of brain iron in children with cerebral infarction. AJNR 1990; 11:341-348.
July
1992
