DOI:10.2214/AJR.07.2425
AJR 2007; 189:W205-W211
© American Roentgen Ray Society
Brain Injury After Acute Carbon Monoxide Poisoning: Early and Late Complications
Chung-Ping Lo1,
Shao-Yuan Chen2,
Kwo-Whei Lee1,3,
Wei-Liang Chen3,
Cheng-Yu Chen1,
Chun-Jen Hsueh1 and
Guo-Shu Huang1
1 Department of Radiology, Tri-Service General Hospital and, National Defense
Medical Center, 325, Section 2, Cheng-Kung Rd., Neihu District, Taipei, Taiwan
114, Republic of China.
2 Department of Undersea and Hyperbaric Medicine, TriService General Hospital
and National Defense Medical Center, Taipei, Taiwan, Republic of China.
3 Department of Medical Imaging, Changhua Christian Hospital, Changhua, Taiwan,
Republic of China.
Received January 18, 2007;
accepted after revision May 13, 2007.
Address correspondence to C. P. Lo
(rain2343{at}ms22.hinet.net).
Partially supported by the Tri-Service General Hospital Research Funds
TSGH-C95-3-S06.
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Abstract
OBJECTIVE. The purposes of this article are to illustrate the
variable CT and MRI features of carbon monoxide–induced brain injury and
to discuss the underlying pathogenesis.
CONCLUSION. Carbon monoxide can produce different patterns of brain
injury in the acute and delayed stages. CT and MRI are valuable in the
delineation of disease extent and helpful for understanding the
pathophysiologic mechanisms.
Keywords: brain injury • carbon monoxide poisoning • CT • MRI
Introduction
Carbon monoxide (CO) is a colorless and odorless toxic gas produced as a
by-product of incomplete combustion of carbon-based fuels and substances. It
is the most common lethal poison worldwide, and neurologic sequelae are the
most frequent form of morbidity
[1–3].
The pathophysiologic mechanisms of CO toxicity can be divided into hypoxic and
cellular theories [1,
4]. The affinity of CO for heme
protein is approximately 250 times that of oxygen, and the formation of
carboxyhemoglobin reduces the oxygen-carrying capacity of blood, causing
tissue hypoxia [1,
5]. CO inhibits the
mitochondrial electron transport enzyme system and activates polymorphonuclear
leukocytes, which undergo diapedesis and cause brain lipid peroxidation,
leading to the delayed effects of CO poisoning
[2,
3,
5]. The clinical presentations
and imaging features of CO poisoning are diverse. The purpose of this essay is
to illustrate the spectrum of brain injury patterns after CO inhalation.
Diffuse Hypoxic–Ischemic Encephalopathy and Focal Cortical Injury
Acute brain injury in CO-exposed patients appears to arise largely from
hypoxia. Studies with mice, however, have shown that cerebral blood flow
initially increases within minutes of CO exposure. Blood flow remains elevated
until loss of consciousness, when transient cardiac compromise causes blood
pressure to decrease [2,
6]. Because of this,
autoregulation until cardiovascular homeostasis is exhausted and asphyxia or
apnea begins; brain hypoxia is probably not an initial feature of CO poisoning
[3]. Neurons are the cells in
the CNS most vulnerable to hypoxic–ischemic insult, and they have the
highest oxygen and glucose demands. Acute and intense CO poisoning can lead
directly to diffuse hypoxic–ischemic encephalopathy predominantly
involving the gray matter (Fig.
1A,
1B). Acute CO poisoning that
focally involves the cerebral cortex has been reported far less frequently
[5]. There is a predilection
for the temporal lobe and the hippocampus
[5]. The injury can be
transient vasogenic edema or frank necrosis (infarction) without occlusion of
cerebral arteries. Diffusion-weighted MRI is helpful for differentiating these
two conditions (Fig. 2A,
2B,
2C,
2D,
2E).
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Fig. 1A —31-year-old woman with carbon monoxide–induced acute
hypoxic–ischemic change. Unenhanced CT scans of brain show diffuse
hypodensity of gray matter involving cerebral cortex and basal ganglia. White
matter is relatively spared.
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Fig. 1B —31-year-old woman with carbon monoxide–induced acute
hypoxic–ischemic change. Unenhanced CT scans of brain show diffuse
hypodensity of gray matter involving cerebral cortex and basal ganglia. White
matter is relatively spared.
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Fig. 2A —29-year-old woman with carbon monoxide–induced focal
cortical necrosis. Axial MR image obtained with FLAIR sequence (TR/TE,
9,000/110; inversion time, 2,500 milliseconds) on day of carbon monoxide
exposure shows bilateral cortical hyperintensity involving temporal lobes,
including medial temporal lobes with predominance on right side.
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Fig. 2B —29-year-old woman with carbon monoxide–induced focal
cortical necrosis. Diffusion-weighted MR image (5,000/120; b = 0 and 1,000
s/mm2) (B) and corresponding apparent diffusion coefficient
map (C) show restricted water diffusion, indicating cytotoxic
edema.
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Fig. 2C —29-year-old woman with carbon monoxide–induced focal
cortical necrosis. Diffusion-weighted MR image (5,000/120; b = 0 and 1,000
s/mm2) (B) and corresponding apparent diffusion coefficient
map (C) show restricted water diffusion, indicating cytotoxic
edema.
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Fig. 2E —29-year-old woman with carbon monoxide–induced focal
cortical necrosis. T1-weighted image (600/14) obtained 2 months after carbon
monoxide exposure shows cortical necrosis with brain tissue loss and gyriform
hyperintensity (lamellar necrosis) over right temporal lobe.
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Necrosis of the Globus Pallidus
The globus pallidus is the most common site of involvement in CO poisoning
[5,
7]. The damage usually occurs
immediately [7]. The
predilection for the globus pallidus is unclear but may be related to the
hypotensive effects of CO poisoning in the watershed territory of the arterial
supply or to CO binding to the iron-rich globus pallidus
[7,
8]. Necrosis of the globus
pallidus is not necessarily related to the development of parkinsonism and
vice versa [4], probably
because the damage to the nigrostriatal pathway is incomplete. CT usually
shows symmetric hypodensity. On MRI, the medial portions of the globus
pallidus appear as bilateral areas of low signal intensity on T1-weighted
images and of high signal intensity on T2-weighted and FLAIR images. In the
acute stage of CO poisoning, contrast-enhanced T1-weighted images may show
patchy or peripheral enhancement in the necrotic areas (Fig.
3A,
3B,
3C,
3D,
3E). Diffusion-weighted MRI
and apparent diffusion coefficient maps show restriction of water diffusivity
due to cytotoxic edema from acute tissue necrosis
[8].
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Fig. 3A —29-year-old woman with acute carbon monoxide poisoning.
Unenhanced (A) and contrast-enhanced (B) T1-weighted images show
hypointensity with bilateral patchy enhancement in globi pallidi
(arrows, B).
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Fig. 3B —29-year-old woman with acute carbon monoxide poisoning.
Unenhanced (A) and contrast-enhanced (B) T1-weighted images show
hypointensity with bilateral patchy enhancement in globi pallidi
(arrows, B).
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Injury to Other Basal Ganglia, Thalamus, Brainstem, and Cerebellum
The caudate nucleus, putamen, and thalamus occasionally are involved in CO
poisoning but less so than the globus pallidus. The lesions usually appear as
asymmetric hyperintense foci on T2-weighted and FLAIR images
[5]. Involvement of the
brainstem and cerebellum may be a reflection of more severe poisoning because
the posterior structures are more resistant to hypoxia
[5] (Figs.
4A,
4B and
5A,
5B,
5C,
5D).
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Fig. 4A —30-year-old woman with carbon monoxide–induced
cerebellar lesions. FLAIR MR image obtained on day after carbon monoxide
exposure shows bilateral areas of increased signal intensity (arrows)
in cerebellar hemispheres.
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Fig. 4B —30-year-old woman with carbon monoxide–induced
cerebellar lesions. FLAIR MR image obtained 6 months after carbon monoxide
exposure shows area of abnormal signal intensity has disappeared.
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Fig. 5A —30-year-old woman with carbon monoxide–induced
brainstem lesion. Axial unenhanced (A) and contrast-enhanced (B)
T1-weighted images obtained on day after carbon monoxide exposure show
bilateral areas (arrows, B) of mild enhancement over cerebral
peduncles of midbrain.
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Fig. 5B —30-year-old woman with carbon monoxide–induced
brainstem lesion. Axial unenhanced (A) and contrast-enhanced (B)
T1-weighted images obtained on day after carbon monoxide exposure show
bilateral areas (arrows, B) of mild enhancement over cerebral
peduncles of midbrain.
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Fig. 5C —30-year-old woman with carbon monoxide–induced
brainstem lesion. Unenhanced T1-weighted image obtained 6 months after carbon
monoxide exposure shows hyperintense foci over previous lesion sites, possibly
owing to necrosis with dystrophic microcalcification.
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Fig. 5D —30-year-old woman with carbon monoxide–induced
brainstem lesion. MR image obtained with gray matter suppression sequence
(TR/TE, 2,000/30; inversion time, 420 milliseconds) 6 months after carbon
monoxide exposure shows bilateral blurring of pars compacta (arrows)
of substantia nigra. Marked Parkinson's disease–like symptoms did not
develop.
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Diffuse Brain Atrophy
Energy production and mitochondrial function are restored after
carboxyhemoglobin levels decrease, but the transient changes can cause
neuronal necrosis and apoptotic death, which lead to diffuse brain atrophy
[1–3,
9] (Fig.
6A,
6B,
6C,
6D). CT and MRI show interval
enlargement of the sulcal CSF space and an increased ventricle-to-brain ratio.
Porter et al. [10] used
quantitative MRI to assess atrophy of the corpus callosum. Those investigators
found that marked atrophic change had occurred in 80% of cases within 6 months
of CO exposure and that cognitive impairment had developed in one half of the
patients. The atrophic change, however, did not correlate well with the
cognitive impairment.
Cerebral White Matter Demyelination
Demyelination of the cerebral white matter is usually not a feature of the
acute stage of CO poisoning
[5]. The most commonly involved
areas are the periventricular white matter and centrum semiovale
[5,
11]. In severe cases, however,
demyelination can extend to the subcortical white matter, corpus callosum, and
external and internal capsules
[11]. CT usually shows diffuse
and confluent hypodensity in these areas. The MRI finding of hypointensity on
T1-weighted images and hyperintensity on T2-weighted and FLAIR images may
reflect the demyelination process (Figs.
7A,
7B,
7C,
7D and
8A,
8B). Some results
[2,
3,
5] have suggested that the
underlying mechanism is most likely diapedesis of the polymorphonuclear
leukocytes, which causes lipid peroxidation and myelin breakdown.
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Fig. 7A —35-year-old woman with carbon monoxide–induced delayed
neuropsychiatric syndrome. Axial FLAIR MR images obtained 6 days (A), 2
months (B), 3 months (C), and 6 months (D) after insult
show abnormal area of high signal intensity in bilateral periventricular white
matter, which may be due to demyelination, not evident early (A) but
prominent at 2 months (B) with gradual attenuation.
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Fig. 7B —35-year-old woman with carbon monoxide–induced delayed
neuropsychiatric syndrome. Axial FLAIR MR images obtained 6 days (A), 2
months (B), 3 months (C), and 6 months (D) after insult
show abnormal area of high signal intensity in bilateral periventricular white
matter, which may be due to demyelination, not evident early (A) but
prominent at 2 months (B) with gradual attenuation.
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Fig. 7C —35-year-old woman with carbon monoxide–induced delayed
neuropsychiatric syndrome. Axial FLAIR MR images obtained 6 days (A), 2
months (B), 3 months (C), and 6 months (D) after insult
show abnormal area of high signal intensity in bilateral periventricular white
matter, which may be due to demyelination, not evident early (A) but
prominent at 2 months (B) with gradual attenuation.
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Fig. 7D —35-year-old woman with carbon monoxide–induced delayed
neuropsychiatric syndrome. Axial FLAIR MR images obtained 6 days (A), 2
months (B), 3 months (C), and 6 months (D) after insult
show abnormal area of high signal intensity in bilateral periventricular white
matter, which may be due to demyelination, not evident early (A) but
prominent at 2 months (B) with gradual attenuation.
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Fig. 8A —31-year-old man with carbon monoxide inhalation. Axial FLAIR
MR images obtained 3 days (A) and 1 month (B) after carbon
monoxide exposure show diffuse and progressive white matter hyperintensity
that extends to subcortical white matter.
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Fig. 8B —31-year-old man with carbon monoxide inhalation. Axial FLAIR
MR images obtained 3 days (A) and 1 month (B) after carbon
monoxide exposure show diffuse and progressive white matter hyperintensity
that extends to subcortical white matter.
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White matter demyelination is believed to be responsible for delayed
neuropsychiatric syndrome
[11–13].
After acute CO poisoning, a small proportion of patients who recover
consciousness within minutes to hours of exposure appear to have no persisting
neurologic deficit initially but experience delayed neuropsychiatric syndrome
after a lucid interval [5,
11–14].
The most frequent symptoms of delayed neuropsychiatric syndrome are mental
deterioration (amnesia, cognitive dysfunction), emotional disorder
(depression, anxiety, mutism), urinary and fecal incontinence, and motor
disorder (gait disturbance, Parkinson's disease–like symptoms)
[11]. Diffusion-weighted MRI
and apparent diffusion coefficient maps
[7,
12,
13] of patients with CO
poisoning have shown the development of delayed and slowly progressive
cytotoxic edema in the cerebral white matter, possibly as the result of
delayed cell death and demyelination (Fig.
9A,
9B). The interval also
parallels the development of delayed neuropsychiatric syndrome
[13]. In animal studies,
hyperbaric oxygen therapy has been found to prevent the lipid peroxidation
process, and this therapy may prevent the development of delayed
neuropsychiatric syndrome
[2–4,
10,
15].
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Fig. 9A —35-year-old woman who attempted suicide by burning charcoal.
Diffusion-weighted MR image (A) and corresponding apparent diffusion
coefficient map (B) obtained 2 months after carbon monoxide exposure
show restricted water diffusion over bilateral centrum semiovale, indicating
delayed cytotoxic edema.
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Fig. 9B —35-year-old woman who attempted suicide by burning charcoal.
Diffusion-weighted MR image (A) and corresponding apparent diffusion
coefficient map (B) obtained 2 months after carbon monoxide exposure
show restricted water diffusion over bilateral centrum semiovale, indicating
delayed cytotoxic edema.
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Conclusion
As a result of various pathophysiologic mechanisms, a number of patterns of
brain injury can be seen in patients with CO poisoning. CT and MRI help to
show the extent of disease and are useful for understanding the
pathophysiologic mechanism.
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Abstract
Introduction
