Brain Injury After Acute Carbon Monoxide Poisoning: Early and Late Complications

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1 T and MRI of arbon Monoxide Poisoning Neuroradiology Pictorial Essay ownloaded from by on 02/28/18 from IP address opyright RRS. For personal use only; all rights reserved hung-ping Lo 1 Shao-Yuan hen 2 Kwo-Whei Lee 1,3 Wei-Liang hen 3 heng-yu hen 1 hun-jen Hsueh 1 Guo-Shu Huang 1 Lo P, hen SY, Lee KW, et al. Keywords: brain injury, carbon monoxide poisoning, T, MRI OI: /JR Received January 18, 2007; accepted after revision May 13, Partially supported by the Tri-Service General Hospital Research Funds TSGH-95-3-S06. 1 epartment of Radiology, Tri-Service General Hospital and, National efense Medical enter, 325, Section 2, heng-kung Rd., Neihu istrict, Taipei, Taiwan 114, Republic of hina. ddress correspondence to. P. Lo (rain2343@ms22.hinet.net). 2 epartment of Undersea and Hyperbaric Medicine, Tri- Service General Hospital and National efense Medical enter, Taipei, Taiwan, Republic of hina. 3 epartment of Medical Imaging, hanghua hristian Hospital, hanghua, Taiwan, Republic of hina. WE This is a Web exclusive article. JR 2007; 189:W205 W X/07/1894 W205 merican Roentgen Ray Society rain Injury fter cute arbon Monoxide Poisoning: Early and Late omplications OJETIVE. The purposes of this article are to illustrate the variable T and MRI features of carbon monoxide induced brain injury and to discuss the underlying pathogenesis. ONLUSION. arbon monoxide can produce different patterns of brain injury in the acute and delayed stages. T and MRI are valuable in the delineation of disease extent and helpful for understanding the pathophysiologic mechanisms. arbon monoxide (O) 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 O toxicity can be divided into hypoxic and cellular theories [1, 4]. The affinity of O 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]. O 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 O poisoning [2, 3, 5]. The clinical presentations and imaging features of O poisoning are diverse. The purpose of this essay is to illustrate the spectrum of brain injury patterns after O inhalation. iffuse Hypoxic Ischemic Encephalopathy and Focal ortical Injury cute brain injury in O-exposed patients appears to arise largely from hypoxia. Studies with mice, however, have shown that cerebral blood flow initially increases within minutes of O exposure. lood flow remains elevated until loss of consciousness, when transient cardiac compromise causes blood pressure to decrease [2, 6]. ecause of this, autoregulation until cardiovascular homeostasis is exhausted and asphyxia or apnea begins; brain hypoxia is probably not an initial feature of O poisoning [3]. Neurons are the cells in the NS most vulnerable to hypoxic ischemic insult, and they have the highest oxygen and glucose demands. cute and intense O poisoning can lead directly to diffuse hypoxic ischemic encephalopathy predominantly involving the gray matter (Fig. 1). cute O 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. iffusion-weighted MRI is helpful for differentiating these two conditions (Fig. 2). Necrosis of the Globus Pallidus The globus pallidus is the most common site of involvement in O 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 O poisoning in the watershed territory of the arterial supply or to O 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. T 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 FLIR images. In the acute stage of O poisoning, contrast-enhanced T1-weighted images may show patchy or peripheral enhancement in the necrotic areas (Fig. 3). iffusion-weighted MRI and apparent diffusion coefficient maps show restriction of water diffusivity due to cytotoxic edema from acute tissue necrosis [8]. JR:189, October 2007 W205

2 ownloaded from by on 02/28/18 from IP address opyright RRS. For personal use only; all rights reserved Injury to Other asal Ganglia, Thalamus, rainstem, and erebellum The caudate nucleus, putamen, and thalamus occasionally are involved in O poisoning but less so than the globus pallidus. The lesions usually appear as asymmetric hyperintense foci on T2-weighted and FLIR 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. 4 and 5). iffuse rain trophy 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. 6). T and MRI show interval enlargement of the sulcal SF 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 O 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. erebral White Matter emyelination emyelination of the cerebral white matter is usually not a feature of the acute stage of O 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]. T usually shows diffuse and confluent hypodensity in these areas. The MRI finding of hypointensity on T1-weighted images and hyperintensity on T2-weighted and FLIR images may reflect the demyelination process (Figs. 7 and 8). 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. White matter demyelination is believed to be responsible for delayed neuropsychiatric syndrome [11 13]. fter acute O 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]. iffusion-weighted MRI and apparent diffusion coefficient maps [7, 12, 13] of patients with O 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. 9). 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]. onclusion s a result of various pathophysiologic mechanisms, a number of patterns of brain injury can be seen in patients with O poisoning. T and MRI help to show the extent of disease and are useful for understanding the pathophysiologic mechanism. References 1. Omaye ST. Metabolic modulation of carbon monoxide toxicity. Toxicology 2002; 180: Thom SR, hopale VM, Fisher. Hyperbaric oxygen reduces delayed immune-mediated neuropathology in experimental carbon monoxide toxicity. Toxicol ppl Pharmacol 2006; 213: Gorman, rewry, Huang YL, Sames. The clinical toxicology of carbon monoxide. Toxicology 2003; 187: Prockop L. arbon monoxide brain toxicity: clinical, magnetic resonance imaging, magnetic resonance spectroscopy, and neuropsychological effects in 9 people. J Neuroimaging 2005; 15: O onnel P, uxton PJ, Pitkin, Jarvis LJ. The magnetic resonance imaging appearances of the brain in acute carbon monoxide poisoning. lin Radiol 2000; 55: Thom SR. arbon monoxide-mediated brain lipid peroxidation in the rat. J ppl Physiol 1990; 68: hu K, Jung KH, Kim HJ, Jeong SW, Kang W, Roh JK. iffusion-weighted MRI and 99m Tc-HM- PO SPET in delayed relapsing type of carbon monoxide poisoning: evidence of delayed cytotoxic edema. Eur Neurol 2004; 51: Kinoshita T, Sugihara S, Matsusue E, Fujii S, metani M, Ogawa T. Pallidoreticular damage in acute carbon monoxide poisoning: diffusion-weighted MR imaging findings. m J Neuroradiol 2005; 26: Weaver LK, Hopkins RO, han KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med 2002; 347: Porter SS, Hopkins RO, Weaver LK, igler E, latter. orpus callosum atrophy and neuropsychological outcome following carbon monoxide poisoning. rch lin Neuropsychol 2002; 17: hang KH, Han MH, Kim HS, Wie, Han M. elayed encephalopathy after carbon monoxide intoxication: MR imaging features and distribution of cerebral white matter lesions. Radiology 1992; 184: Murata T, Kimura H, Kado H, et al. Neuronal damage in the interval form of O poisoning determined by serial diffusion-weighted magnetic resonance imaging plus 1 H-magnetic resonance spectroscopy. J Neurol Neurosurg Psychiatry 2001; 71: Kim HJ, hang KH, Song I, et al. elayed encephalopathy of acute carbon monoxide intoxication: diffusivity of cerebral white matter lesions. m J Neuroradiol 2003; 24: Parkinson R, Hopkins RO, leavinger H, et al. White matter hyperintensities and neuropsychological outcome following carbon monoxide poisoning. Neurology 2002; 58: Tibbles PM, Edelsberg JS. Hyperbaric oxygen therapy. N Engl J Med 1996; 334: W206 JR:189, October 2007

3 T and MRI of arbon Monoxide Poisoning Fig year-old woman with carbon monoxide induced acute hypoxic ischemic change. and, Unenhanced T scans of brain show diffuse hypodensity of gray matter involving cerebral cortex and basal ganglia. White matter is relatively spared. ownloaded from by on 02/28/18 from IP address opyright RRS. For personal use only; all rights reserved E Fig year-old woman with carbon monoxide induced focal cortical necrosis., xial MR image obtained with FLIR 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. and, iffusion-weighted MR image (5,000/120; b = 0 and 1,000 s/mm 2 ) () and corresponding apparent diffusion coefficient map () show restricted water diffusion, indicating cytotoxic edema., Two-dimensional time-of-flight MR angiogram shows no evidence of major arterial occlusion. E, 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. JR:189, October 2007 W207

4 Fig year-old woman with acute carbon monoxide poisoning. and, Unenhanced () and contrast-enhanced () T1-weighted images show hypointensity with bilateral patchy enhancement in globi pallidi (arrows, ). E, T2-weighted images obtained 1 day (), 2 weeks (), and 2 months (E) after poisoning show gradual collapse of globi pallidi. ownloaded from by on 02/28/18 from IP address opyright RRS. For personal use only; all rights reserved E Fig year-old woman with carbon monoxide induced cerebellar lesions., FLIR MR image obtained on day after carbon monoxide exposure shows bilateral areas of increased signal intensity (arrows) in cerebellar hemispheres., FLIR MR image obtained 6 months after carbon monoxide exposure shows area of abnormal signal intensity has disappeared. W208 JR:189, October 2007

5 T and MRI of arbon Monoxide Poisoning ownloaded from by on 02/28/18 from IP address opyright RRS. For personal use only; all rights reserved Fig year-old woman with carbon monoxide induced brainstem lesion. and, xial unenhanced () and contrast-enhanced () T1-weighted images obtained on day after carbon monoxide exposure show bilateral areas (arrows, ) of mild enhancement over cerebral peduncles of midbrain., 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., 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. Fig year-old man with carbon monoxide intoxication. and, T2-weighted images obtained 1 month after carbon monoxide exposure show bilateral hyperintensity of cerebral white matter. (Fig. 6 continues on next page) JR:189, October 2007 W209

6 Fig. 6 (continued) 40-year-old man with carbon monoxide intoxication. and, T2-weighted images obtained 2 years after carbon monoxide exposure show generalized brain atrophy with enlarged SF spaces. ownloaded from by on 02/28/18 from IP address opyright RRS. For personal use only; all rights reserved Fig year-old woman with carbon monoxide induced delayed neuropsychiatric syndrome., xial FLIR MR images obtained 6 days (), 2 months (), 3 months (), and 6 months () after insult show abnormal area of high signal intensity in bilateral periventricular white matter, which may be due to demyelination, not evident early () but prominent at 2 months () with gradual attenuation. W210 JR:189, October 2007

7 T and MRI of arbon Monoxide Poisoning ownloaded from by on 02/28/18 from IP address opyright RRS. For personal use only; all rights reserved Fig year-old man with carbon monoxide inhalation. and, xial FLIR MR images obtained 3 days () and 1 month () after carbon monoxide exposure show diffuse and progressive white matter hyperintensity that extends to subcortical white matter. Fig year-old woman who attempted suicide by burning charcoal. and, iffusion-weighted MR image () and corresponding apparent diffusion coefficient map () obtained 2 months after carbon monoxide exposure show restricted water diffusion over bilateral centrum semiovale, indicating delayed cytotoxic edema. JR:189, October 2007 W211