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A delayed neurological syndrome after carbon monoxide intoxication
NEUROL-1753; No. of Pages 2 revue neurologique xxx (2017) xxx–xxx
Available online at
ScienceDirect www.sciencedirect.com
Letter to the editor
A delayed neurological syndrome after carbon monoxide intoxication 1.
Case report
A non-smoking, left-handed, 75-year-old man was hospitalized because of subacute mental delirium and behavioral problems. Two and a half months before his hospitalization, he was found unconscious near his kitchen in the presence of a leaking 1-month natural-gas tank for a fuel-efficiency oven. He was admitted to the emergency unit with a carboxyhemoglobin (COHb) level of 3.1%, but did not require hospitalization. Several weeks later, he developed confusion, amnesic issues with unpredictable phases of aggressiveness, persecution mania and apathy (no hallucinations). Nocturnal alcohol consumption and hyperphagia were observed, but with no other symptoms of disinhibition. His neurological examination was normal. A brain computed tomography (CT) scan revealed frontotemporal lobe atrophy. Magnetic resonance imaging (MRI) using a fluid-attenuated inversion recovery (FLAIR) sequence showed hyperintense lesions involving both hippocampi, but predominantly on the left side, with no contrast enhancement (Fig. 1). Extensive blood tests, including a full blood count, electrolytes, liver and thyroid function tests, C-reactive protein (CRP), vitamin B12, folate, angiotensinconverting enzyme (ACE), and Borrelia and syphilis serological studies were all either negative or normal. Cerebrospinal fluid
(CSF) analysis showed moderate elevation of CSF protein at 0.59 g/L, but glucose, culture and cytology were normal, as were the anti-neuronal antibodies in the blood and CSF. Thoracic, abdominal and pelvic CT scans, and fluorodeoxyglucose positron emission tomography (PET)/CT scans, revealed no abnormality. Electroencephalography showed normal core activity with left-sided slow waves. Confusion and behavioral problems persisted for about 6 months, leading to a severe loss of independence. The patient required psychotropic drugs and was transferred to a nursing home. Eventually, he gradually and spontaneously recovered his physical and mental status with only a few persistent memory impairments.
2.
Discussion
This report is of an unusual case of carbon monoxide intoxication (COI) with a delayed neurological syndrome (DNS). COI can lead to acute as well as delayed brain injury, but may easily be misdiagnosed as the symptoms are nonspecific. However, COHb levels > 5% in a non-smoker (> 10% in a smoker) can confirm the diagnosis, although significant COI can arise with COHb levels below these values, especially with chronic low-level exposures. Yet, COHb levels can vary
Fig. 1 – Brain magnetic resonance imaging (MRI) using a fluid-attenuated inversion recovery (FLAIR) sequence reveals, on axial views: (A) areas of hyperintensity involving both hippocampi, but predominantly on the left side, with no contrast enhancement; and (B) sparing of the basal ganglia.
Please cite this article in press as: Mouthon-Reignier C, et al. A delayed neurological syndrome after carbon monoxide intoxication. Revue neurologique (2017), http://dx.doi.org/10.1016/j.neurol.2017.03.004
NEUROL-1753; No. of Pages 2
2
revue neurologique xxx (2017) xxx–xxx
with supplemental oxygen administration, and even between the time of CO exposure and time of determination of blood COHb levels. These facts may explain the low COHb level observed in our patient. Also, while the clinical severity of COI does not correlate with COHb levels, neurological deficits and loss of consciousness are generally considered signs of severe CO poisoning [1]. After the COI, our patient showed an apparent recovery, yet delayed neuropsychiatric symptoms were seen after more than a month. Such a DNS has been described after COI as well as in other cases of prolonged cerebral anoxia, and usually appears from 2 to 40 days after recovery from the acute stage. A DNS may result from a demyelinating leukoencephalopathy due to the destruction of oligodendrocytes, which are sensitive to hypoxia. Mental deterioration, urinary incontinence and gait disturbances as well as other, neuropsychiatric symptoms are frequently seen, although two clinically characteristic presentations have been described: parkinsonism and akinetic mutism [2]. In general, hypoxic brain damage predominates in the white matter and basal ganglia (globus pallidus), although other localizations are possible, including the hippocampi as in our present case. Lasting deficits, including memory impairment, are common and correlate with brain lesions [3,4].
Disclosure of interest The authors declare that they have no competing interest.
references
[1] Prockop LD, Chichkova RI. Carbon monoxide intoxication: an updated review. J Neurol Sci 2007;262:122–30. http:// dx.doi.org/10.1016/j.jns.2007.06.037.
[2] Shprecher D, Mehta L. The syndrome of delayed posthypoxic leukoencephalopathy. Neuro Rehab 2010;26:65–72. [3] Borras L, Constant E, De Timary P, Huguelet P, Khazaal Y. [Long-term psychiatric consequences of carbon monoxide poisoning: a case report and literature review]. Rev Med Interne 2009;30:43–8. http://dx.doi.org/10.1016/ j.revmed.2008.04.014. [4] Kwon OD, Youn S-W. Hippocampal atrophy as late sequela of carbon monoxide poisoning. Eur Neurol 2011;66:331. http://dx.doi.org/10.1159/000332976.
C. Mouthon-Reigniera,* J. Biberona,b B. De Toffola,b,c K. Mondonc,d a Department of neurology, CHRU Bretonneau, 2, boulevard Tonnelle´, 37000 Tours, France b University Franc¸ ois-Rabelais, CHRU Bretonneau, 10, boulevard Tonnelle´, 37000 Tours, France c Inserm U 930, CHRU Bretonneau, 2, boulevard Tonnelle´, 37000 Tours, France d Memory center, CHRU Bretonneau, 2, boulevard Tonnelle´, 37000 Tours, France *Corresponding author. E-mail addresses: [email protected] [email protected] (C. Mouthon-Reignier) Received 28 July 2016 Received in revised form 27 November 2016 Accepted 8 March 2017 Available online xxx http://dx.doi.org/10.1016/j.neurol.2017.03.004 0035-3787/# 2017 Published by Elsevier Masson SAS.
Please cite this article in press as: Mouthon-Reignier C, et al. A delayed neurological syndrome after carbon monoxide intoxication. Revue neurologique (2017), http://dx.doi.org/10.1016/j.neurol.2017.03.004
Available online at
ScienceDirect www.sciencedirect.com
Letter to the editor
A delayed neurological syndrome after carbon monoxide intoxication 1.
Case report
A non-smoking, left-handed, 75-year-old man was hospitalized because of subacute mental delirium and behavioral problems. Two and a half months before his hospitalization, he was found unconscious near his kitchen in the presence of a leaking 1-month natural-gas tank for a fuel-efficiency oven. He was admitted to the emergency unit with a carboxyhemoglobin (COHb) level of 3.1%, but did not require hospitalization. Several weeks later, he developed confusion, amnesic issues with unpredictable phases of aggressiveness, persecution mania and apathy (no hallucinations). Nocturnal alcohol consumption and hyperphagia were observed, but with no other symptoms of disinhibition. His neurological examination was normal. A brain computed tomography (CT) scan revealed frontotemporal lobe atrophy. Magnetic resonance imaging (MRI) using a fluid-attenuated inversion recovery (FLAIR) sequence showed hyperintense lesions involving both hippocampi, but predominantly on the left side, with no contrast enhancement (Fig. 1). Extensive blood tests, including a full blood count, electrolytes, liver and thyroid function tests, C-reactive protein (CRP), vitamin B12, folate, angiotensinconverting enzyme (ACE), and Borrelia and syphilis serological studies were all either negative or normal. Cerebrospinal fluid
(CSF) analysis showed moderate elevation of CSF protein at 0.59 g/L, but glucose, culture and cytology were normal, as were the anti-neuronal antibodies in the blood and CSF. Thoracic, abdominal and pelvic CT scans, and fluorodeoxyglucose positron emission tomography (PET)/CT scans, revealed no abnormality. Electroencephalography showed normal core activity with left-sided slow waves. Confusion and behavioral problems persisted for about 6 months, leading to a severe loss of independence. The patient required psychotropic drugs and was transferred to a nursing home. Eventually, he gradually and spontaneously recovered his physical and mental status with only a few persistent memory impairments.
2.
Discussion
This report is of an unusual case of carbon monoxide intoxication (COI) with a delayed neurological syndrome (DNS). COI can lead to acute as well as delayed brain injury, but may easily be misdiagnosed as the symptoms are nonspecific. However, COHb levels > 5% in a non-smoker (> 10% in a smoker) can confirm the diagnosis, although significant COI can arise with COHb levels below these values, especially with chronic low-level exposures. Yet, COHb levels can vary
Fig. 1 – Brain magnetic resonance imaging (MRI) using a fluid-attenuated inversion recovery (FLAIR) sequence reveals, on axial views: (A) areas of hyperintensity involving both hippocampi, but predominantly on the left side, with no contrast enhancement; and (B) sparing of the basal ganglia.
Please cite this article in press as: Mouthon-Reignier C, et al. A delayed neurological syndrome after carbon monoxide intoxication. Revue neurologique (2017), http://dx.doi.org/10.1016/j.neurol.2017.03.004
NEUROL-1753; No. of Pages 2
2
revue neurologique xxx (2017) xxx–xxx
with supplemental oxygen administration, and even between the time of CO exposure and time of determination of blood COHb levels. These facts may explain the low COHb level observed in our patient. Also, while the clinical severity of COI does not correlate with COHb levels, neurological deficits and loss of consciousness are generally considered signs of severe CO poisoning [1]. After the COI, our patient showed an apparent recovery, yet delayed neuropsychiatric symptoms were seen after more than a month. Such a DNS has been described after COI as well as in other cases of prolonged cerebral anoxia, and usually appears from 2 to 40 days after recovery from the acute stage. A DNS may result from a demyelinating leukoencephalopathy due to the destruction of oligodendrocytes, which are sensitive to hypoxia. Mental deterioration, urinary incontinence and gait disturbances as well as other, neuropsychiatric symptoms are frequently seen, although two clinically characteristic presentations have been described: parkinsonism and akinetic mutism [2]. In general, hypoxic brain damage predominates in the white matter and basal ganglia (globus pallidus), although other localizations are possible, including the hippocampi as in our present case. Lasting deficits, including memory impairment, are common and correlate with brain lesions [3,4].
Disclosure of interest The authors declare that they have no competing interest.
references
[1] Prockop LD, Chichkova RI. Carbon monoxide intoxication: an updated review. J Neurol Sci 2007;262:122–30. http:// dx.doi.org/10.1016/j.jns.2007.06.037.
[2] Shprecher D, Mehta L. The syndrome of delayed posthypoxic leukoencephalopathy. Neuro Rehab 2010;26:65–72. [3] Borras L, Constant E, De Timary P, Huguelet P, Khazaal Y. [Long-term psychiatric consequences of carbon monoxide poisoning: a case report and literature review]. Rev Med Interne 2009;30:43–8. http://dx.doi.org/10.1016/ j.revmed.2008.04.014. [4] Kwon OD, Youn S-W. Hippocampal atrophy as late sequela of carbon monoxide poisoning. Eur Neurol 2011;66:331. http://dx.doi.org/10.1159/000332976.
C. Mouthon-Reigniera,* J. Biberona,b B. De Toffola,b,c K. Mondonc,d a Department of neurology, CHRU Bretonneau, 2, boulevard Tonnelle´, 37000 Tours, France b University Franc¸ ois-Rabelais, CHRU Bretonneau, 10, boulevard Tonnelle´, 37000 Tours, France c Inserm U 930, CHRU Bretonneau, 2, boulevard Tonnelle´, 37000 Tours, France d Memory center, CHRU Bretonneau, 2, boulevard Tonnelle´, 37000 Tours, France *Corresponding author. E-mail addresses: [email protected] [email protected] (C. Mouthon-Reignier) Received 28 July 2016 Received in revised form 27 November 2016 Accepted 8 March 2017 Available online xxx http://dx.doi.org/10.1016/j.neurol.2017.03.004 0035-3787/# 2017 Published by Elsevier Masson SAS.
Please cite this article in press as: Mouthon-Reignier C, et al. A delayed neurological syndrome after carbon monoxide intoxication. Revue neurologique (2017), http://dx.doi.org/10.1016/j.neurol.2017.03.004