UHM 2018, Vol. 45, No.

1 – CASE: GLOBUS PALLIDUS INFARCTS AFTER CO POISONING

Case Report
Hemiplegia and bilateral globus pallidus infarcts
after carbon monoxide poisoning: case report
Douglas G. Sward, MD 1; Travis W. Austin, MD, MA 2
Clinical Assistant Professor, Department of Emergency Medicine, University of Maryland School
1

of Medicine, Division of Hyperbaric Medicine, Program in Trauma, University of Maryland

Medical Center, Baltimore, Maryland U.S.
2 Emergency Medicine Physician, Palliative Care Fellow, Dartmouth-Hitchcock Medical Center,

Lebanon, New Hampshire U.S.

CORRESPONDING AUTHOR: Douglas G. Sward – dgsward@hotmail.com

_____________________________________________________________________________________________________________________________________________________________________

ABSTRACT In the course of her initial evaluation, blood gas

The vast clinical manifestations of carbon monoxide (CO)
poisoning can involve the neurological, neuropsychological and
cardiac systems as well as others. In this case report, we
describe our management of a 64-year-old woman exposed to CO
in her apartment. Her presentation was unusual in that she had
symmetric globus pallidus lesions, no evidence of thrombosis,
but the lateralizing neurologic manifestation of severe hemiplegia.
___________________________________________________________________________
INTRODUCTION
Carbon monoxide (CO) is known to affect the central
nervous system. Bilateral globus pallidus lesions, al-
though not pathognomonic, are considered a classic
presentation. The patient described in this report dem-
onstrated dramatic lateralizing neurologic signs in
the setting of symmetric globus pallidus lesions.
CASE REPORT
A 64-year-old woman was found unresponsive at her
apartment following an evacuation in response to a
carbon monoxide alarm. Paramedics reported that
she had vomited and had right-sided hemiparesis. The
patient’s position when found was not documented.
The ambient CO level was 130 ppm. Transcutaneous
pulse CO-oximetry levels were not obtained. As there
were no direct witnesses, it was uncertain how long
she had been unresponsive prior to being found. A
non-rebreather mask was placed on the patient before
transport to a community hospital.
analysis revealed the woman’s carboxyhemoglobin level
to be 7%, and her troponin concentration was elevated
to 3.5 ng/ml. Chart review showed no prior history
of smoking, stroke or neurologic deficit. Computed
tomography (CT) of her head showed bilateral globus
pallidus hypodensities. She had a decreased level of
consciousness and persistent right-sided hemiparesis.
She was intubated for airway protection and then
transferred to a tertiary care center with hyperbaric
oxygen resources.
On arrival at that facility, the patient had a Glasgow
Coma Scale score of 3T. Neurologic examination gave
equivocal results due to sedation for mechanical ventila-
tion, except for a positive Babinski sign in the right leg
(left leg was normal). Her carboxyhemoglobin level
had fallen to 2.1%. Initial laboratory values are presented
in Table 1. An electrocardiogram showed normal sinus
rhythm. Blood and urine toxin screens were negative.
A repeat CT scan of her head again demonstrated
hypodensities bilaterally in the globus pallidus (Figure
1). CT of her cervical spine was unremarkable.
Arrangements were made for hyperbaric oxygen
therapy. The patient received three treatments within
24 hours. In accordance with our institutional proto-
col, she received an initial hyperbaric oxygen treatment
at 2.8 atmospheres absolute (ATA) for 46 minutes.
The following day, she underwent two hyperbaric
oxygen sessions at 2.0 ATA for 90 minutes each. Dur-
ing all three sessions, she was mechanically venti-
lated with pressure control mode.

_____________________________________________________________________________________________________________________________________________________________

KEYWORDS: carbon monoxide poisoning; neurologic manifestations; globus pallidus lesions; hemiplegia

Copyright © 2018 Undersea & Hyperbaric Medical Society, Inc. 95

 UHM 2018, Vol. 45, No. 1 – CASE: GLOBUS PALLIDUS INFARCTS AFTER CO POISONING
______________________________________________________
Table 1. Patient’s initial
laboratory values
sodium 151 mEq/L
potassium 3.5 mEq/L
chloride 116 mEq/L
bicarbonate 25 mEq/L
BUN 32 mm/dL
creatinine 1.02 mg/dL
glucose 120 mg/dL
WBC 12.5 K/mcL
Hgb 8.9 g/dL
HCT 28.0%
platelets 209 K/mm3
calcium 1.12 mg/dL
magnesium 2.3 mg/dL
phosphorus 3.7 mg/dL
lactate 1.4 mmol/L
INR 1.3
PT 16.0 sec
APTT 29 sec
fibrinogen 410 mg/dl
total protein 6.5 g/dL
albumin 3.2 g/dL
total bilirubin 0.3 mg/dL
alkaline phosphatase 60 U/L
AST 92 units/L
ALT 38 U/L
anion gap 11
osmolality 312 MoM/kg
troponin 1.56 ng/ml
CPK 3593 units/L
ABG 7.38/40/346 *
tox screen negative +
______________________________________________________
* 100% FiO2 w/PEEP 10
+ acetaminophen, aspirin, EtOH,
benzodiazepines, barbiturates, TCA
After the initial hyperbaric oxygen treatment, she
grimaced in response to sternal rub but did not follow
commands. In response to pain, she withdrew with
her legs and left arm but had no movement of her
right arm. She responded to painful stimuli of her
right arm by moving her left arm. She continued to
have an upgoing right-sided Babinski sign.
Magnetic resonance imaging and angiography of her
head and neck showed bilateral globus pallidus infarc-
tions without evidence of thrombus (Figure 2). On
96
the neck images, atheromatous disease was noted in
the carotid bulbs, with approximately 20% occlusion
on the left side and 15% occlusion on the right side.
All of the images that were obtained, including the
initial outside images, were read by our staff trauma
radiologists. An electroencephalogram showed no sei-
zure activity. Transthoracic electrocardiography showed
normal left and right ventricular function.
We consulted the neurology service, which recom-
mended supportive care. They observed that the right
hemiparesis was profound, especially so early in the
clinical course. In addition, they postulated that it was
possible that the patient had an initial loss of conscious-
ness from the CO insult, followed by thrombosis and
embolization. They also considered that a spontaneous
cerebral vascular insult might have made the patient
unable to leave the premises when the CO detectors
were sounding.
The patient continued to improve slowly throughout
her hospitalization. She was extubated on the fifth day
and experienced no respiratory distress. Although she
had persistent delayed speech, she was able to com-
municate with head nods. Her neurologic examination
had improved significantly prior to discharge although
she did not return to independent living. The patient
continued to have a moderate right arm wrist drop.
She showed a left-sided preference. She had a delay in
swallowing function, but that was improving without
any indication of aspiration. However, a percutane-
ous endoscopic gastrostomy tube was inserted prior
to discharge to help her meet nutritional goals. On
Day 20, she was discharged to a rehabilitation facility.
The patient spent several weeks on the brain injury
unit of a rehabilitation facility, where she made little
progress. She remained intermittently drowsy with mod-
erate dysarthria and was essentially aphasic. She could
take thin liquids by mouth. Her right arm remained
splinted because of right hand edema, and she had bilat-
eral lower extremity edema. Follow-up CT scans of her
brain demonstrated the expected evolution of bilateral
globus pallidus lesions. She was transferred to a long-
term care facility and has since been lost to follow-up.
DISCUSSION
Hemiplegia has a broad differential diagnosis that
includes vascular, neoplastic, paraneoplastic, infectious,
inflammatory, demyelinating, metabolic, and traumatic
Sward DG, Austin TA
 UHM 2018, Vol. 45, No. 1 – CASE: GloBUS PAllIDUS INFARCTS AFTER Co PoISoNING

processes [1]. Careful consideration of stroke mimics

and chameleons is critical [2,3]. Structurally,
lesions may localize to cerebral white matter,
internal capsule, or brainstem [4].
Bilateral globus pallidus lesions are a well-
known result of CO poisoning, but they can also
be caused by a number of other insults, including
cellular respiratory toxins, hypoglycemia, hyper-
glycemia, hypoxia, and shock [5]. CO can also
injure many other areas of the central nervous
system, including the cerebral white matter [6,7].
The natural history of these lesions remains
unclear [8].
CO toxicity affects multiple pathways through
asphyxia, cellular respiration, direct toxic effects
and possibly excess sympathetic activation [9,10].
Delayed neurologic sequelae are also well-known
complications of acute CO poisoning [11], gen-
erally described as deficits in cognition, mood,
memory, and sometimes motor dysfunction [12].
Unfortunately, they can occur even in patients
FIGURe 1. Non-contrast head CT scan obtained shortly after transfer,
treated with normobaric oxygen [13]. Weaver and
demonstrating bilateral hypodensities in the globus pallidus (arrows).
associates documented a decrease in the risk of
delayed neurologic sequelae in pa-
ients with symptomatic CO toxicity
treated with three sessions of
hyperbaric oxygen within 24 hours
after presentation [14].]
Radiographically, CO poisoning
can induce abnormal findings on
MRI, quantitative MRI, and single-
photon emission computed tomo-
graphy (SPECT) [11,15]. The classic
finding is bilateral basal ganglia in-
farction [16-22]. For example, one-
fourth of the 129 patients studied by
Choi and colleagues [22] had bilateral
globus pallidus lesions, as did all
seven of the patients evaluated with
MRI by Kim and associates [18].
However, the prevalence of such
lesions might be lower than reports
indicate [8]; other CNS insults could
be more common. In a prospective
FIGURe 2. Magnetic resonance imaging of the brain, obtained within study of 73 patients with acute CO
24 hours after admission, demonstrating bilateral globus pallidus infarctions poisoning, Parkinson found only one
(arrows) without evidence of thrombus. (1.4%) with globus pallidus lesions

Sward DG, Austin TA 97

 UHM 2018, Vol. 45, No. 1 – CASE: GLOBUS PALLIDUS INFARCTS AFTER CO POISONING
and nine (12%) with white matter hypodensities [23].
The connection that has been made between bilateral
globus pallidus lesions and CO poisoning might
have been fostered by the selection bias of some
studies. Studies reporting higher rates of globus pallidus
lesions involved patients with prolonged down-times
or extended periods of unconsciousness. Several reports
were based on only two patients [17,21]. In a literature
review published in 2014, Beppu described a shift in
focus to cerebral white matter injury [6]. Additionally,
the differential diagnosis of bilateral basal ganglia
infarction is wide, encompassing many cellular respir-
ation toxins, ethyl alcohol, trauma, cardiovascular
disease, and overdose with a variety of substances [24].
For example, 3,4-methylenedioxymethamphetamine
(MDMA), manganese, cocaine, opiates and cyanide have
all been implicated in bilateral globus pallidus
lesions [25,26].
In our clinical experience, lateralizing neurologic
deficits are not a common presentation of acute CO
poisoning. Typical neurologic symptoms are headache,
dizziness, depressed mental status, and diffuse weak-
ness [12,27]. Review of the literature found a single case
report describing hemiplegia in the setting of CO
poisoning and congenitally abnormal arteries [28]. Lin
and co-workers reported on long-term cerebral vascular
risk after CO poisoning in a retrospective case control
study [29]. Their conclusion that CO poisoning is
associated with increased risk of ischemic stroke was
challenged in a persuasive letter to the editor written
by Hampson and Weaver [30].
CO has been postulated to be pro-thrombotic [31-33],
as discussed in several case reports [34-36], population-
based studies [37-39], and laboratory studies [40-42].
Senthilkumaran and colleagues [43] expanded on the
possible mechanisms of thrombosis that Ryoo and
associates had postulated [34]. Teodoro and Geraldes
described a patient who had simultaneous acute
thrombosis and cerebral infarction after being injured
by the explosion of a gas water heater [35]. Ahmad and
Sharma found no thrombosis in the cerebral vasculature
of a patient who had attempted suicide by inhaling
charcoal smoke in an enclosed area [36]. The study by
Chung’s group [39] was based on the same dataset as
Lin’s study [29], so their reports have been critiqued in
98
similar fashion. Franchini and colleagues [37] per-
formed a systematic literature review of the association
between air pollutants, including CO, but were unable
to reach definitive conclusions because of the hetero-
geneity of the data. However, a similar review by Tang
and associates suggested that air pollution is not a
risk factor for venous thrombosis [38]. Based on these
various reports, we infer that any relationship between
CO poisoning and thrombosis is tentative at best.
Our case is interesting because of the manifestation
of severe hemiplegia in the presence of bilateral infarcts
despite the absence of thrombosis. MRA of the brain
performed reasonably soon after the initial insult
showed no evidence of thrombosis. We were not able to
find any alternative cause for the bilateral basal ganglia
infarcts except the presence of CO. We acknowledge
that alternative etiologies may have played a primary role
or at least been additive. For example, uneven ischemia
in watershed distributions in the setting of CO exposure
and/or hypotension could have caused both symmetric
globus pallidus lesions and focal neurologic deficits.
Similarly, an intracerebral thrombosis could have
resolved prior to MRA imaging or simply have been
missed. We note that the initial carboxyhemoglobin
level might have been lower than expected given the
severity of illness due to the delay in measuring it dur-
ing transfer from the scene and the urgency of other
clinical interventions. Lastly and importantly, we can-
not discount the possibility that a peripheral compres-
sive neuropathy could have played a role if the patient
had been lying on the floor for an indeterminate
amount of time prior to evacuation from the scene.
However, her ongoing aphasia, gaze preference and
abnormal lower extremity reflexes support a central
rather than a peripheral cause of her symptoms.
n
Acknowledgment
The manuscript was copy-edited by Linda J. Kesselring,
MS, ELS, the technical editor/writer in the Department
of Emergency Medicine at the University of Maryland
School of Medicine.
The authors declare that no conflicts in interest exist
with this submission.
Sward DG, Austin TA
 UHM 2018, Vol. 45, No. 1 – CASE: GLOBUS PALLIDUS INFARCTS AFTER CO POISONING
_____________________________________________________________________________________________________________________________________________________________________
REFERENCES
1. Ettinger AB, Weisbrot DM. Neurologic differential diagnosis: a
case-based approach. Cambridge University Press, 2014: 509-510.
2. Fernandes PM, Whitely WN, Hart SR, Al-Shahi Salman R.
Strokes: mimic and chameleons. Pract Neurol. 2013; 13: 21-28.
3. Plummer NR, Hari-Bhaskar K. Hunting mimics and chameleons:
diagnostic difficulties in atypical acute ischaemic stroke. BMJ Case
Rep. 2014; 2014: bcr2014204222.
4. Yew DT, Kwong WH, Yu MC. Basic neuroanatomy. World
Scientific Publishing, 1996.
5. Hegde AN, Mohan S, Lath N, Lim CC. Differential diagnosis
for bilateral abnormalities of the basal ganglia and thalamus.
Radiographics. 2011; 31: 5-30.
6. Beppu T. The role of MR imaging in assessment of brain
damage from carbon monoxide poisoning: a review of the literature.
Am J Neuroradiol. 2014; 35: 625-631.
7. O’Donnell P, Buxton PJ, Pitkin A, Jarvis LJ. The magnetic
resonance imaging appearances of the brain in acute carbon
monoxide poisoning. Clin Radiol. 2000; 55: 273-280.
8. Hopkins RO, Fearing MA, Weaver LK, Foley JF. Basal ganglia
lesions following carbon monoxide poisoning. Brain Inj. 2006; 20:
273-281.
9. Goldbaum LR, Ramierz RG, Absalon KB. What is the mechanism
of carbon monoxide toxicity? Aviat Space Environ Med. 1975; 46:
1289-1291.
10. Park EJ, Min YG, Kim GW, Cho JP, Maeng WJ, Choi SC.
Pathophysiology of brain injuries in acute carbon monoxide
poisoning: a novel hypothesis. Med Hypotheses. 2014; 83: 186-189.
11. Gale SD, Hopkins RO, Weaver LK, et al. MRI, quantitative MRI,
SPECT, and neuropsychological findings following carbon monoxide
poisoning. Brain Inj. 1999; 13: 229-243.
12. Weaver LK. Hyperbaric oxygen therapy for carbon monoxide
poisoning. Undersea Hyperb Med. 2014; 41: 339-354.
13. Tibbles PM, Perrotta PL. Treatment of carbon monoxide
poisoning: a critical review of human outcomes comparing
normobaric oxygen with hyperbaric oxygen. Ann Emerg Med. 1994;
24: 269-276.
14. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen
for acute carbon monoxide poisoning. N Engl J Med. 2002; 347:
1057-1067.
15. Miura T, Mitomo M, Kawai R, Harada K. CT of the brain in
acute carbon monoxide intoxication: characteristic features and
prognosis. AJNR Am J Neuroradiol. 1985; 6: 739-742.
16. Jones JS, Lagasse J, Zimmerman G. Computed tomographic
findings after acute carbon monoxide poisoning. Am J Emerg Med.
1994; 12: 448-451.
17. Kanaya N, Imaizumi H, Nakayama M, Nagai H, Yamaya K,
Namiki A. The utility of MRI in acute stage of carbon monoxide
poisoning. Intensive Care Med. 1992; 18: 371-372.
Sward DG, Austin TA
18. Kim DM, Lee IH, Park JY, Hwang SB, Yoo DS, Song CJ.
Acute carbon monoxide poisoning: MR imaging findings with
clinical correlation. Diagn Interv Imaging. 2017; 98: 299-306.
19. Tom T, Abedon S, Clark RI, Wong W. Neuroimaging characteris-
tics in carbon monoxide toxicity. J Neuroimaging. 1996; 6: 161-166.
20. Uchino A, Hasuo K, Shida K, Matsumoto S, Yasumori K,
Masuda K. MRI of the brain in chronic carbon monoxide poisoning.
Neuroradiology. 1994; 36: 399-401.
21. Gotoh M, Kuyama H, Asari S, Ohmoto T, Akioka T, Lai MY.
Sequential changes in MR images of the brain in acute carbon
monoxide poisoning. Comput Med Imaging Graph. 1993; 17: 55-59.
22. Choi IS, Kim SK, Lee SS, Lee MS. Evaluation of outcome after
acute carbon monoxide poisoning by brain CT. J Korean Med Sci.
1993; 8: 78-83.
23. Parkinson RB, Hopkins RO, Cleavinger HB, et al. White matter
hyperintensities and neuropsychological outcome following carbon
monoxide poisoning. Neurology. 2002; 58: 1525-1532.
24. Yarid NA, Harruff RC. Globus pallidus necrosis unrelated to
carbon monoxide poisoning: retrospective analysis of 27 cases
of basal ganglia necrosis. J Forensic Sci 2015; 60: 1484-1487.
25. Alquist CR, McGoey R, Bastian F, Newman W 3rd. Bilateral
globus pallidus lesions. J La State Med Soc. 2012; 164: 145-146.
26. Albin RL. Basal ganglia neurotoxins. Neurol Clin. 2000; 18:
665-680.
27. Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med.
1998; 339: 1603-1608.
28. Goulon M, Oútin H, Beydon L, Gajdos P, Samson Y, Jerbi Z.
Hemiplegia during carbon monoxide poisoning revealing multiple
cerebral artery abnormalities including the hypoglossal artery
[article in French]. Rev Neurol (Paris) 1984; 140: 353-357.
29. Lin CW, Chen WK, Hung DZ, et al. Association between
ischemic stroke and carbon monoxide poisoning: a population-
based retrospective cohort analysis. Eur J Intern Med 2016; 29:
65-70.
30. Hampson NB, Weaver LK. Carbon monoxide poisoning and
risk for ischemic stroke. Eur J Intern Med. 2016; 31: e7.
31. Yildirim C, Gunay N, Buyukaslan H. A case of carbon monoxide
poisoning with thrombus in the heart: a case report. Inhal Toxicol.
2005; 17: 797-801.
32. Diloe PA, Tucciarone M, Castro ER, Guerrero M. Late stent
thrombosis secondary to carbon monoxide poisoning. Cardiovasc
Revasc Med. 2011; 12: 56-58.
33. Sevinc A, Savli H, Atmaca H. An interesting case of pulmonary
emboli: acute carbon monoxide poisoning. Clin Appl Thromb
Hemost. 2005; 11: 353-357.
34. Ryoo SM, Sohn CH, Kim HJ. Intracardiac thrombus formation
induced by carbon monoxide poisoning. Hum Exp Toxicol. 2013; 32:
1193-1196.
99
 UHM 2018, Vol. 45, No. 1 – CASE: GLOBUS PALLIDUS INFARCTS AFTER CO POISONING
35. Teodoro T, Geraldes R, Pinho e Melo T. Symptomatic internal
carotid artery thrombosis in acute carbon monoxide intoxication.
Am J Emerg Med. 2014; 32:684.e5-6.
36. Ahmad A, Sharma VK. Early subcortical ischemic infarction
and delayed leucoencephalopathy after carbon monoxide poisoning
[letter to the editor]. Intern Emerg Med. 2012; 7(suppl 1): S33-S34.
37. Franchini M, Mengoli C, Cruciani M, Bonfanti C, Mannucci PM.
Association between particulate air pollution and venous thrombo-
embolism: a systematic literature review. Eur J Intern Med. 2016; 27:
10-13.
38. Tang L, Wang QY, Cheng ZP, Hu B, Liu JD, Hu Y. Air pollution
and venous thrombosis: a meta-analysis. Sci Rep. 2016; 6: 32794.
39. Chung WS, Lin CL, Kao CH. Carbon monoxide poisoning and
risk of deep vein thrombosis and pulmonary embolism: a nationwide
retrospective cohort study. J Epidemiol Community Health. 2015; 69:
557-562.
100
40. Nielson VG, Kirklin JK, George JF. Carbon monoxide releasing
molecule-2 increases the velocity of thrombus growth and strength
in human plasma. Blood Coagul Fibrinolysis. 2009; 20: 377-380.
41. Malayaman SN, Cohen JB, George JF. Carbon monoxide
releasing molecule-2 enhanced alpha2-antiplasmin activity.
Blood Coagul Fibrinolysis. 2011; 22: 345-348.
42. Gawlikowski T, Gomolka E, Piekoszewski W. Acute CO poison-
ing is associated with impaired fibrinolysis and increased thrombin
generation. Basic Clin Pharmacol Toxicol. 2013; 112: 352-356.
43. Senthilkumaran S, Menezes RG, Meenakshisundaram R,
Thirumalaikolundusubramanian P. Carbon monoxide poisoning and
intracardiac thrombus formation – additional mechanisms.
Hum Exp Toxicol. 2015; 34: 333-334.
✦
Sward DG, Austin TA