Inatomi et al. Journal of Medical Case Reports
https://doi.org/10.1186/s13256-022-03300-2

(2022) 16:137

Open Access

CASE REPORT

Electroencephalographic findings
after convulsive seizures due to cerebral arterial
air embolism secondary to lung cancer: a case
report
Shinichiro Inatomi1, Tesseki Izumi1*, Nobuyuki Eura1, Ichiro Sato2, Masato Tasaki2, Shigeo Muro2 and
Kazuma Sugie1

Abstract
Background: Cerebral arterial air embolism is often associated with an invasive iatrogenic etiology and a high rate
of convulsive seizures. There are only a few descriptions of electroencephalogram findings in convulsive seizures due
to cerebral arterial air embolism of noniatrogenic etiology. Herein, we describe the case of a patient with lung cancer
and convulsive seizures with abnormalities detected on electroencephalogram caused by cerebral arterial air embolism of noniatrogenic etiology.
Case presentation: A 55-year-old Japanese man underwent radiotherapy and chemotherapy for cancer in the hilum
of the left lung that was diagnosed after hemoptysis. One year after the diagnosis, he developed fever and chest pain
that required hospitalization. At admission, he was in shock, and chest computed tomography revealed invasion of
the left atrium and left main bronchus by the hilar cancer. Chest and abdominal computed tomography revealed
small low-density areas within the tumor and around the intestinal membrane, which were interpreted as the presence of air due to invasion of the lung cancer. He was diagnosed with septic shock due to necrotic infection secondary to cancer invasion into the left atrium. The following day, he complained of difficulty in speaking and weakness
in the left side of his body. A head computed tomography scan revealed multiple small low-density areas in the right
cortex and bilateral subcortex, which were interpreted as air emboli. On day 3, he experienced generalized tonic–
clonic seizures for approximately 1 minute, followed by myoclonus-like convulsions in the left lower limb and a rightsided gaze. The electroencephalogram findings after the convulsive seizures revealed partial epilepsy-like waves with
intermittent spikes in the bilateral cerebral hemispheres and a diffuse slow wave in the left frontal lobe. He recovered
from sepsis without recurrence of convulsive seizures; however, he died of hemoptysis on day 50 after discharge.
Conclusions: Electroencephalogram findings of focal spike activities and diffuse slow waves were detected in early
seizures due to cerebral arterial air embolism of noniatrogenic etiology associated with lung cancer. Additional case
descriptions are warranted to establish patterns in electroencephalogram findings specific to cerebral arterial air
embolism.
Keywords: Seizure, Cerebral arterial air embolism, Electroencephalography, Lung cancer

*Correspondence: izumitesseki@yahoo.co.jp
1
Department of Neurology, Nara Medical University, 840 Shijo‑cho,
Kashihara, Nara 634‑8521, Japan
Full list of author information is available at the end of the article

Background
Cerebral arterial air embolism (CAE) is often associated
with an invasive iatrogenic etiology and a high rate of

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Inatomi et al. Journal of Medical Case Reports

(2022) 16:137

convulsive seizures. In this report, we describe the case
of a patient with lung cancer and convulsive seizures with
detectable electroencephalogram (EEG) abnormalities
due to CAE of noniatrogenic etiology. This case indicates
that convulsive seizures should be considered an important symptom of CAE not only from iatrogenic but also
noniatrogenic etiologies, such as lung cancer. There are
only a few descriptions of EEG findings in convulsive seizures due to CAE, and additional observational data are
required to identify relevant patterns.

Case presentation
A 55-year-old Japanese man underwent radiotherapy
and chemotherapy for cancer in the hilum of the left lung
that was diagnosed after hemoptysis. Although a biopsy
could not be performed because of the risk of complications associated with the cancer location, the cancer
was suspected to be squamous cell carcinoma based on
sputum cytology results and tumor marker levels. At
approximately 6 months after the diagnosis, he developed a severe cough, and chest computed tomography
(CT) revealed tumor growth and metastasis to the upper
left lung lobe and lymph nodes. One year after the diagnosis, he developed fever and chest pain that required
hospitalization. At admission (day 1), he was in shock

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with an altered mental state and had a blood pressure of
69/58 mmHg, pulse rate of 146/min, and respiratory rate
of 24/min (maximum). Chest CT at admission revealed
that the left lung hilar cancer had invaded the left atrium
and left main bronchus (Fig. 1A). Additionally, chest and
abdominal CT at admission revealed small low-density
areas within the tumor (Fig. 1B) and around the intestinal membrane (Fig. 1C), which were interpreted as the
presence of air due to invasion of the lung cancer. Echocardiography at admission revealed tumor invasion into
the left atrium; however, no findings indicated infective
endocarditis. Staphylococcus aureus was detected in
blood cultures on day 1. He was diagnosed with septic
shock caused by necrotic infection secondary to cancer
invasion into the left atrium. A vasopressor, noradrenaline, and antibiotics (meropenem 1 g/day for 2 days and
3 g/day for 3 days and vancomycin 2 g/day for 5 days, followed by cefazolin 6 g/day for 14 days) were administered
intravenously.
The following day before dawn (day 2), he complained
of difficulty in speaking and weakness in the left side of
his body. Neurological examination revealed normal
consciousness (Glasgow Coma scale; 15 points), left unilateral spatial neglect, left hemiparesis, and right lower
limb mild weakness. He scored 7 points on the National

Fig. 1 Chest computed tomography (CT) image showing a left pulmonary hilar mass invading the left atrium and the left main bronchus (A) and
air densities (arrow) inside the tumor (B). Abdominal CT image showing air densities (arrow) around the intestinal membrane (C). Window level/
window width: A, C: (40/300), B: (−700/1800)

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Institute of Health Stroke Scale (NIHSS; left arm motor
4 points, left leg motor 2 points, and neglect 1 point). A
head CT after neurological symptoms revealed multiple
small low-density areas in the right cortex and bilateral
subcortex, which were interpreted as air emboli (Fig. 2A,
B). Head magnetic resonance imaging (MRI) after head
CT revealed faint hyperintensity along the right parietal
cortex, subcortex, and left frontal cortex on diffusionweighted images (Fig. 2C) and a small dot-like low signal
in the right frontal cortex and left parietal subcortex on
susceptibility-weighted images (Fig. 2E, F). He was additionally diagnosed with CAE associated with invasion of
lung cancer into the left atrium, and ischemic stroke or
brain metastasis was associated with cancer progression.
On the evening of day 3, systemic tonic and clonic convulsions occurred for approximately 1 minute, followed
by myoclonus-like convulsions in the left lower limb and
a right-sided gaze. EEG performed after the episode of
convulsive seizures revealed partial epilepsy-like waves
with intermittent spikes corresponding to the bilateral
central, parietal, and occipital regions, and a diffuse slow
wave for the left frontal lobe (Fig. 3). Convulsive seizures were considered to be early seizures due to CAE, as
well as ischemic stroke. Levetiracetam (anticonvulsant)
2000 mg/day was administered for 7 days intravenously
after convulsive seizures, followed by oral administration.
The patient recovered from sepsis, and no recurrence of
convulsive seizures was observed. He was discharged on
day 28 with an NIHSS score of 4 points (left arm motor 3
points, left leg motor 1 point); however, he died of hemoptysis on day 50 after discharge.

Discussion and conclusions
CAE with convulsive seizures associated with lung cancer at the time of seizure onset [1] and 8 days after onset
[2] have been reported. In our patient, CAE detected by
head CT and MRI was assigned a noniatrogenic cause,
namely, air embolus from the invasion of lung cancer
into predominantly the left atrium, and was determined
to be the cause of acute convulsive seizures. Although we
could not establish a direct relationship between invasive
lung cancer and brain air embolism, we believe that lung
cancer led to CAE, since CAE usually occurs after septic
shock, which may happen as a consequence of invasive
lung cancer. Also, it is highly unlikely that intrapulmonary shunt lesions other than the invasive lung cancer,
such as chest arteriovenous malformations, may have
been observed in the plain and enhanced chest CT performed during the hospitalization. Notably, the EEG
findings were consistent with the changes associated with
CAE in the bilateral cerebral hemispheres. A few reports
have described EEG findings in CAE due to invasive iatrogenic or noniatrogenic etiologies, such as lung cancer

Page 3 of 6

(present case), lung transplantation, patent foramen
ovale, esophageal cancer, or scuba diving, for example,
“epileptiform electroencephalographic activities with a
spike” during cardiopulmonary bypass [3], “epileptiform
disturbance” during mitral valve replacement [4], “nonconvulsive status epileptics” in lung transplantation [5],
“focal seizure during hyperventilation” in a patient with a
bronchogenic cyst [6], and “normal EEG” after scuba diving [7]. In our patient, focal spikes and diffuse slow waves
were caused by CAE of noniatrogenic etiology, which
consists of CAE due to invasive iatrogenic mechanism
and noniatrogenic mechanisms, as reported previously.
A study that analyzed 39 patients with convulsive seizures due to CAE of “invasive iatrogenic etiology” after
cardiovascular procedures reported that the seizures
occurred during the early stages of onset [8], and we also
observed seizures within 48 hours of CAE onset. Therefore, it is possible that mechanisms leading to convulsive
seizures after CAE may be similar to those observed in
ischemic stroke, such as a decrease in epilepsy threshold due to neuronal excitotoxicity, including loss of
neurovascular/blood–brain barrier integrity, increased
release of neurotransmitters, ion channel dysfunction,
and alterations in gene expression [9]. EEG findings after
early seizures during ischemic stroke include epileptiform abnormalities, such as periodic lateralized epileptic
discharges (PLEDS) [10] and focal or diffuse slowing of
background activity, such as frontal intermittent rhythmic delta activities (FIRDA) [11]. Although PLEDS and
FIRDA were not clearly noted in the EEG of the present patient, these findings may be consistent with those
of early seizure in ischemic stroke. Interestingly, while
an analysis of 35 studies on the incidence of seizures
after ischemic stroke reported early seizure (either 1 or
2 weeks following stroke) occurrence in 3.3% of cases
[12], the incidence of seizures after CAE due to “invasive iatrogenic mechanism” ranges between 24% and 73%
[8, 13, 14], indicating greater frequency of early seizures
after CAE than after ischemic stroke [14]. Therefore, seizures associated with CAE may involve unique mechanisms, such as an inflammatory response triggered by the
bubble surface [15] or the direct effects of an air embolus
on the central nervous system, apart from processes leading to early seizure in patients with ischemic stroke.
Similar to early seizures in ischemic stroke, recurrences
of convulsive seizures after CAE may be relatively rare
[14], even though the conditions that can cause CAE are
often serious. Possible explanations for the low rate of
recurrence of convulsive seizures in CAE include properties of air emboli that change over time, absence of gliosis
typically observed with late seizures in ischemic stroke,
and the availability of anticonvulsants.

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Fig. 2 Head computed tomography (CT) image taken on day 1 showing multiple air-like densities (circle) in the right cortex and the subcortex
bilaterally (A, B). Window level/window width: (40/80). Head magnetic resonance imaging (MRI) showing faint hyperintensity (circle) along the
right parietal cortex and subcortex and the left frontal cortex (C) on diffusion-weighted images, with an apparent diffusion coefficient map (D) and
a small dot-like low signal (circle) in the right frontal cortex (E) and the left parietal subcortex (F) on susceptibility-weighted imaging. (TR/TE): C, D:
(4000/95), E, F: (49/40)

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Fig. 3 Electroencephalogram (EEG) after convulsive seizures showing spikes in C4, P4, and O2 and C3, P3, and O1, with diffuse slow waves
corresponding to the left frontal lobe

In summary, EEG findings of focal spike activities and
diffuse slow waves were detected in early seizures due
to CAE of noniatrogenic etiology associated with lung
cancer. Differential diagnosis of early onset convulsive
seizures should include CAE due to noniatrogenic or
invasive iatrogenic mechanisms. Additional case descriptions are needed to establish patterns in EEG findings
specific to CAE.
Abbreviations
CAE: Cerebral arterial air embolism; EEG: Electroencephalogram; NIHSS:
National Institute of Health Stroke Scale; CT: Computed tomography; MRI:
Magnetic resonance imaging.
Acknowledgements
Not applicable.
Authors’ contributions
All authors performed the diagnosis and medical treatment. TI was a major
contributor in writing the manuscript. All authors read and approved the final
manuscript.
Funding
Not applicable.

Availability of data and materials
Not applicable.

Declarations
Ethics approval and consent to participate
Not applicable.
Consent for publication
Written informed consent was obtained from the patient’s next of kin for
publication of this case report and any accompanying images. A copy of the
written consent is available for review by the Editor-in-Chief of this journal.
Competing interests
The authors declare that they have no competing interests.
Author details
1
Department of Neurology, Nara Medical University, 840 Shijo‑cho, Kashihara,
Nara 634‑8521, Japan. 2 Department of Respiratory Medicine, Nara Medical
University, 840 Shijo‑cho, Kashihara, Nara 634‑8521, Japan.
Received: 27 November 2021 Accepted: 31 January 2022

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