Endoscopically observed outer membrane of chronic subdural hematoma after endovascular embolization of middle meningeal artery.

Background: Embolization of the middle meningeal artery (MMA) has been established for chronic subdural hematoma (CSDH). Neuroendoscopic observation of the outer membrane of the hematoma was carried out after embolization. The treatment mechanism of embolization is discussed, focusing on the vasculature and inflammation of the membrane. Methods: Four patients with recurrent CSDH were included in this study. The MMA was embolized using Embosphere® particles in three patients. The outer membrane was observed with normal and narrow band images (NBIs). Results: The net-like vessels were not obstructed in the whole area of the outer membrane, but in a patchy fashion of embolized areas surrounded by nonembolized areas. In two patients, the nonembolized areas showed a hemorrhagic inflammatory red color. Histopathological examination confirmed hypertrophic dura with leukocyte infiltration. Dilated dural arteries and proliferated sinusoid arteries were located in the deep and superficial border cell layers. These arteries were visualized as green and brown on NBI, respectively. In the embolized area, the red membrane turned pink, indicating ischemia and subsiding inflammatory hyperemia. In the third patient, the outer membrane was white in both the nonembolized and embolized areas in endoscopic view, and the net-like vessels were sparse in both endoscopy and histology, indicating a scar inflammatory phase. The membrane transition was not observed in the patient that did not undergo embolization. Conclusion: Endoscopic observation revealed that embolization of the MMA blocked both the dural and sinusoidal arteries. Ischemic transformation causing the suppression of inflammation of the outer membrane is a suggested mechanism of MMA embolization.

Suppressive Effects of Transient Receptor Potential Melastatin 8 Agonist on Epileptiform Discharges and Epileptic Seizures.

Epilepsy is a relatively common condition, but more than 30% of patients have refractory epilepsy that is inadequately controlled by or is resistant to multiple drug treatments. Thus, new antiepileptic drugs based on newly identified mechanisms are required. A previous report revealed the suppressive effects of transient receptor potential melastatin 8 (TRPM8) activation on penicillin G-induced epileptiform discharges (EDs). However, it is unclear whether TRPM8 agonists suppress epileptic seizures or affect EDs or epileptic seizures in TRPM8 knockout (TRPM8KO) mice. We investigated the effects of TRPM8 agonist and lack of TRPM8 channels on EDs and epileptic seizures. Mice were injected with TRPM8 agonist 90 min after or 30 min before epilepsy-inducer injection, and electrocorticograms (ECoGs) were recorded under anesthesia, while behavior was monitored when awake. TRPM8 agonist suppressed EDs and epileptic seizures in wildtype (WT) mice, but not in TRPM8KO mice. In addition, TRPM8KO mice had a shorter firing latency of EDs, and EDs and epileptic seizures were deteriorated by the epilepsy inducer compared with those in WT mice, with the EDs being more easily propagated to the contralateral side. These findings suggest that TRPM8 activation in epileptic regions has anti-epileptic effects.

Combined Strategy of Burr Hole Surgery and Elective Craniotomy under Intracranial Pressure Monitoring for Severe Acute Subdural Hematoma.

Burr hole surgery in the emergency room can be lifesaving for patients with acute subdural hematoma (ASDH). In the first part of this study, a strategy of combined burr hole surgery, a period of intracranial pressure (ICP) monitoring, and then craniotomy was examined for safe and effective treatment of ASDH. Since 2012, 16 patients with severe ASDH with indications for burr hole surgery were admitted to Kenwakai Otemachi Hospital. From 2012 to 2016, craniotomy was performed immediately after burr hole surgery (emergency [EM] group, n = 10). From 2017, an ICP sensor was placed before burr hole surgery. After a period for correction of traumatic coagulopathy, craniotomy was performed when ICP increased (elective [EL] group, n = 6). Patient background, bleeding tendency, intraoperative blood transfusion, and outcomes were compared between the groups. In the second part of the study, ICP was measured before and after burr hole surgery in seven patients (including two of the six in the EL group) to assess the effect of this surgery. Activated partial thromboplastin time (APTT) and prothrombin time-international normalized ratio (PT-INR) were significantly prolonged after craniotomy in the EM group, but not in the EL group, and the EM group tended to require a higher intraoperative transfusion volume. The rate of good outcomes was significantly higher in the EL group, and ICP was significantly decreased after burr hole surgery. These results suggest the value of burr hole surgery followed by ICP monitoring in patients with severe ASDH. Craniotomy can be performed safely using this method, and this may contribute to improved outcomes.

[Effect of Antithrombotic Drugs Reversal on Geriatric Traumatic Brain Injury].

BACKGROUND: As the aging rate in the traumatic brain injury population increases, the number of patients taking antithrombotic drugs is also expected to increase among the population with traumatic brain injury; however, the utility or risk of reversal of such drugs is unclear. Therefore, we performed a retrospective cohort study of the effect of reversal of antithrombotic drugs on geriatric traumatic brain injury at our hospital. METHODS: The study subjects included 83 patients(65 years or older)with intracranial traumatic lesions or skull fractures who were admitted to our hospital during 2013-2018. According to the hospital's protocol, we performed platelet transfusion in patients taking antiplatelet drugs, prothrombin complex concentrate(PCC)administration in patients taking warfarin and direct oral anticoagulants except dabigatran: factor IX complex before January 2018 and four-factor PCC after February 2018. We administered idarucizumab in the case of dabigatran. Fresh frozen plasma transfusion was additionally performed in operative cases. RESULTS: Twenty-six patients took antithrombotic drugs. There was no significant difference in the ratio of talk and deteriorate, favorable outcome(Glasgow Outcome Scale: good recovery+moderate disability), and hospitalization period between the non-antithrombotic and antithrombotic administration groups involving reversal. The timing of antithrombotic drug resumption varied, but no major embolic event occurred during the follow-up period. CONCLUSION: This study suggests that reversal of antithrombotic drugs in geriatric traumatic brain injury may contribute to suppression of talk and deteriorate and lead to more favorable outcomes. As there are also contradictory reports about the utility of reversal, additional studies should be performed for confirmation.

Suppressive Effects of Cooling Compounds Icilin on Penicillin G-Induced Epileptiform Discharges in Anesthetized Rats.

More than 30% of patients with epilepsy are refractory and have inadequate seizure control. Focal cortical cooling (FCC) suppresses epileptiform discharges (EDs) in patients with refractory focal cortical epilepsy. However, little is known about the mechanism by which FCC inhibits seizures at 15°C, and FCC treatment is highly invasive. Therefore, new antiepileptic drugs are needed that produce the same effects as FCC but with different mechanisms of action. To address this need, we focused on transient receptor potential melastatin 8 (TRPM8), an ion channel that detects cold, which is activated at 15°C. We examined whether TRPM8 activation suppresses penicillin G (PG)-induced EDs in anesthetized rats. Icilin, a TRPM8 and TRP Ankyrin 1 agonist, was administered after PG injection, and a focal electrocorticogram (ECoG) and cortical temperature were recorded for 4 h. We measured spike amplitude, duration, firing rate, and power density in each band to evaluate the effects of icilin. PG-induced EDs and increased delta, theta, alpha, and beta power spectra were observed in the ECoG. Icilin suppressed EDs while maintaining cortical temperature. In particular, 3.0-mM icilin significantly suppressed PG-induced spike amplitude, duration, and firing rate and improved the increased power density of each band in the EDs to the level of basal activity in the ECoG. These suppressive effects of 3.0-mM icilin on EDs were antagonized by administering N-(3-aminopropyl)-2-[(3-methylphenyl) methoxy]-N-(2-thienylmethyl)-benzamide hydrochloride (AMTB), a selective TRPM8 inhibitor. Our results suggest that TRPM8 activation in epileptic brain regions may be a new therapeutic approach for patients with epilepsy.

[Predictive Factors of Intracranial Pressure Elevation in Patients with Severe Acute Subdural Hematoma].

INTRODUCTION: Elevated intracranial pressure(ICP)can cause secondary brain injury after severe traumatic brain injury(TBI), and ICP is the key factor that determines the outcome. Therefore, prediction of elevation of ICP during the course of the injury would allow for more effective care of patients with severe TBI. In this study, we investigated predictive factors for elevation of ICP in patients with severe acute subdural hematoma(ASDH). METHODS: Twenty patients with severe isolated ASDH were admitted to our hospital between January 2009 and April 2016. The patients were divided into two groups with a maximum ICP of ≥20mmHg(elevated ICP group)and <20mmHg(normal ICP group). Age, mechanism of injury, Glasgow Coma Scale score on admission, initial head computed tomography findings, vital signs, serological and blood gas examinations, initial ICP, and clinical outcome were evaluated. RESULTS: The elevated ICP group had significantly higher initial ICP(5.0±3.1 vs. 30±22.4mmHg, p<0.01), arterial oxygen pressure(151.2±68.3 vs. 314.2±197.1mmHg, p<0.05), and activated partial thromboplastin time(APTT;28.17±3.1 vs. 35.96±8.0, p<0.05)at admission, and significantly lower fibrinogen level(273.3±65.1 vs. 188.1±82.4mg/dL, p<0.05)and favorable outcome rate(p<0.01). CONCLUSIONS: Our results show that high initial ICP, APTT, and arterial oxygen and low fibrinogen levels are associated with ICP elevation in patients with severe ASDH. These factors might be useful for the indication of therapeutic methods such as decompressive craniectomy.

Risk of Deterioration of Geriatric Traumatic Brain Injury in Patients Treated with Antithrombotic Drugs.

OBJECTIVE: Developed countries have rapidly aging populations and the use of antithrombotic drugs is increasing. We investigated the effects of antithrombotic drugs and reversal of these drugs in patients with geriatric traumatic brain injury (TBI). METHODS: Age, sex, mechanism of injury, Glasgow Coma Scale on admission, head computed tomography findings, antithrombotic therapy, acute exacerbation, and outcomes at discharge were examined in 711 patients with geriatric TBI, complicated with traumatic intracranial hemorrhage using data from the Japan Neurotrauma Data Bank Project 2015 (JNTDB P2015). These items were compared between patients who did and did not receive antithrombotic therapy. We also conducted a questionnaire survey of reversal of antithrombotic therapy at hospitals participating in the JNTDB P2015. Acute exacerbation was compared in hospitals that did and did not regularly use reversal of this therapy. RESULTS: The major cause of injury was a fall. In head computed tomography, acute subdural hematoma was found in 65.7% of the subjects. Antithrombotic therapy was performed in 30.4% of subjects, and these subjects were significantly older than those who did not receive this therapy; many had a fall as the mechanism of injury, and the level of consciousness was significantly exacerbated with this therapy. In hospitals that performed regular reversal, late exacerbation of the level of consciousness was suppressed. CONCLUSIONS: Patients with geriatric TBI who are given antithrombotic drugs have a risk for late exacerbation, even if initially diagnosed with mild TBI. Therefore, there is a possibility that reversal of antithrombotic drugs is important to suppress the risk of deterioration of patients with TBI.

Probability of Soluble Tissue Factor Release Lead to the Elevation of D-dimer as a Biomarker for Traumatic Brain Injury.

d-dimer is a potential biomarker for the detection of traumatic brain injury (TBI). However, the mechanisms that trigger elevation of d-dimer in TBI remain unclear. The purpose of this study was to evaluate the reliability of d-dimer in blood as a biomarker for TBI and to determine the mechanisms involved in regulating its blood levels. Nine patients with moderate to severe isolated TBI (Glasgow Coma Scale [GCS] score 7-13) were admitted to our hospital from May 2013 to June 2014. Blood samples were collected from systemic arteries on arrival and at 1, 3, 5, and 7 days after injury. Blood levels of neuron specific enolase (NSE), d-dimer, and soluble tissue factor (sTF) were measured. NSE (33.4 ng/ml: normal <12.0 ng/ml) and d-dimer (56.1 µg/ml: normal <1.0 µg/ml) were elevated at admission and declined on day 1 after injury. At admission, there were significant correlations of d-dimer levels with NSE (R = 0.727, P = 0.026) and sTF (R = 0.803, P = 0.009) levels. The blood level of d-dimer accurately reflects the degree of brain tissue damage indicated by NSE levels. Our data suggest that release of sTF induced by brain tissue damage may activate the coagulation cascade, leading to elevation of d-dimer.

D-Dimer Elevation as a Blood Biomarker for Detection of Structural Disorder in Mild Traumatic Brain Injury.

CT scans are useful in patients with traumatic brain injury (TBI), but the potential risks associated with ionizing radiation are unknown. Further, CT scans are not commonly available in developing countries. In this study, coagulopathy and abnormal fibrinolysis were investigated as blood biomarkers for detection of structural disorder in mild traumatic brain injury (TBI). A total of 88 patients with mild and isolated TBI (Glasgow Coma Scale [GCS] score 14-15) were admitted to Kenwakai Ootemachi Hospital between October 2014 and March 2016. After exclusion of those treated with oral antiplatelet agents and anticoagulants, 73 patients were included in this study. Patients were classified into those with (lesion [+]) and without (lesion [-]) intracranial structural disorder, based on CT scans at admission and follow-up CT or MRI. Age, GCS score, and blood test findings (platelet count, international normalized ratio of prothrombin time [PT-INR], activated partial thromboplastin time [APTT], fibrinogen, fibrin/fibrinogen degradation products [FDP], and D-dimer) on admission were compared between the two groups. The lesion(+) and lesion(-) groups comprised 54 (74%) and 19 patients (26%), respectively. In multivariate logistic regression analysis, D-dimer (3.6 vs. 0.8 µg/mL) was the only significant independent risk factor for structural disorder (p < 0.001). Platelet counts (23.9 vs. 23.5 × 104 /µL), PT-INR (1.05 vs. 1.07), APTT (29.3 vs. 31.7 sec), FDP (12 vs. 2.4 µg/mL), and fibrinogen levels (260.6 vs. 231.3 mg/dL) were not associated with structural disorder. These results show that D-dimer is associated with intracranial structural disorder in mild TBI.

Directions for Use of Intracranial Pressure Monitoring in the Treatment of Severe Traumatic Brain Injury Using Data from The Japan Neurotrauma Data Bank.

Neuromonitoring can be used to observe intracranial pathological conditions in neurointensive care; however, use of intracranial pressure (ICP) monitoring is low in Japan. In this study, we retrospectively investigated the effects of ICP monitoring in the treatment of severe traumatic brain injury (TBI), using data from the Japan Neurotrauma Data Bank (JNTDB). The study was conducted in 1091 subjects enrolled in the JNTDB (Project 2009) from July 2009 to June 2011. The subjects were divided into those treated with and treated without ICP monitoring in intensive care for severe TBI. Age at admission, sex, level of consciousness (Glasgow Coma Scale [GCS] score), pupillary findings, findings on head CT, treatment, and outcome were compared between these groups. The subjects were also classified into two groups based on the outcome. Relationships among patient background factors, including ICP and clinical outcome were evaluated. The rate of ICP monitoring in treatment of severe TBI was 28%. Therapies were performed aggressively in the ICP monitoring group, and this group had a significant reduction in mortality, but no increase in the favorable outcome rate. In multivariate analysis, age, GCS, pupillary abnormalities, perimesencephalic cistern disappearance or compression, and ICP were associated with a favorable outcome, but the therapeutic method did not affect outcome. We conclude that ICP monitoring and management of ICP are both important for management and care of severe TBI. However, current therapies do not control ICP sufficiently, and more effective therapies are needed.

Decreased Flow Velocity with Transcranial Color-Coded Duplex Sonography Correlates with Delayed Cerebral Ischemia due to Peripheral Vasospasm of the Middle Cerebral Artery.

BACKGROUND AND OBJECTIVE: Despite intensive therapy, vasospasm remains a major cause of delayed cerebral ischemia (DCI) in worsening patient outcome after aneurysmal subarachnoid hemorrhage (aSAH). Transcranial Doppler (TCD) and transcranial color-coded duplex sonography (TCCS) are noninvasive modalities that can be used to assess vasospasm. However, high flow velocity does not always reflect DCI. The purpose of this study was to investigate the utility of TCD/TCCS in decreasing permanent neurological deficits. METHODS: We retrospectively enrolled patients with aSAH who were treated within 72 hours after onset. TCCS was performed every day from days 4 to 14. Peak systolic velocity (PSV), mean velocity (MV), and pulsatility index were recorded and compared between DCI and non-DCI patients. In patients with DCI, endovascular therapy was administered to improve vasospasm, which led to a documented change in velocity. RESULTS: Of the 73 patients, 7 (9.6%) exhibited DCI. In 5 of the 7 patients, DCI was caused by vasospasm of M2 or the more peripheral middle cerebral artery (MCA), and the PSV and MV of the DCI group were lower than those of the non-DCI group after day 7. Intra-arterial vasodilator therapy (IAVT) was performed for all patients with DCI immediately to increase the flow volume by the next day. CONCLUSIONS: Increasing flow velocity cannot always reveal vasospasm excluding M1. In patients with vasospasm of M2 or more distal arteries, decreasing flow velocity might be suggestive of DCI. IAVT led to increases in the flow velocity through expansion of the peripheral MCA.

Effects of Brain Temperature on Cerebrovascular Autoregulation During the Acute Stage of Severe Traumatic Brain Injury.

The pressure reactivity index (PRx) is calculated as a moving correlation coefficient between intracranial pressure (ICP) and mean arterial blood pressure (MABP), and this analytical value is viewed as reflecting a vasomotor response to MABP variability. At present, the factors influencing the PRx value during the acute stage of traumatic brain injury (TBI) are not known. We observed significant cases where changes in the calculated value of PRx seemed to be influenced by changes in brain temperature during the course of acute stage TBI. In one case, a patient was treated for 72 h with therapeutic brain hypothermia after a decompressive hemicraniectomy. During the hypothermic condition, the mean value of PRx was -0.019; however, after gradual rewarming, the value of PRx increased drastically, and the mean value during the rewarming period, when the brain temperature exceeded 35 °C, was 0.331. Similarly, in another case where the patient underwent therapeutic brain hypothermia, the PRx showed a mean value of -0.038 during the hypothermic condition, and a mean value of 0.052 during the rewarming period. In both cases, a trend toward a negative correlation between ICP and MABP during brain hypothermia shifted to a positive correlation upon rewarming.

Importance of Early Postoperative Body Temperature Management for Treatment of Subarachnoid Hemorrhage.

BACKGROUND: The importance of acute-phase brain temperature management is widely accepted for prevention of exacerbation of brain damage by a high body temperature. METHODS: In this study, we investigated the influence of body temperature in the early postoperative period on the outcomes of 62 patients with subarachnoid hemorrhage who were admitted to our department. Body temperature was measured from day 4 to day 14 after onset. The patients were divided into those treated with surgical clipping (clip group) and coil embolization (coil group), those graded I-III (mild) and IV-V (severe) based on the Hunt & Hess classification on admission, those with and without development of delayed cerebral ischemia (DCI), and those with favorable and poor outcomes. Body temperatures throughout the hospital stay were compared in each group. RESULTS: There was no significant difference in body temperature between the clip and coil groups or between the mild and severe groups, but body temperature was significantly higher in patients with DCI compared to those without DCI, and in patients with a poor outcome compared to those with a favorable outcome. CONCLUSIONS: Fever in the early postoperative period of subarachnoid hemorrhage is associated with development of DCI and a poor outcome.

Real-time ultrasound-guided endoscopic surgery for putaminal hemorrhage.

OBJECT: Endoscopic surgery plays a significant role in the treatment of intracerebral hemorrhage. However, the residual hematoma cannot be measured intraoperatively from the endoscopic view, and it is difficult to determine the precise location of the endoscope within the hematoma cavity. The authors attempted to develop real-time ultrasound-guided endoscopic surgery using a bur-hole-type probe. METHODS: From November 2012 to March 2014, patients with hypertensive putaminal hemorrhage who underwent endoscopic hematoma removal were enrolled in this study. Real-time ultrasound guidance was performed with a bur-hole-type probe that was advanced via a second bur hole, which was placed in the temporal region. Ultrasound was used to guide insertion of the endoscope sheath as well as to provide information regarding the location of the hematoma during surgical evacuation. Finally, the cavity was irrigated with artificial cerebrospinal fluid and was observed as a low-echoic space, which facilitated detection of residual hematoma. RESULTS: Ten patients with putaminal hemorrhage>30 cm3 were included in this study. Their mean age (±SD) was 60.9±8.6 years, and the mean preoperative hematoma volume was 65.2±37.1 cm3. The mean percentage of hematoma that was evacuated was 96%±3%. None of the patients exhibited rebleeding after surgery. CONCLUSIONS: This navigation method was effective in demonstrating both the real-time location of the endoscope and real-time viewing of the residual hematoma. Use of ultrasound guidance minimized the occurrence of brain injury due to hematoma evacuation.

Predictors of deterioration indicating a requirement for surgery in mild to moderate traumatic brain injury.

OBJECTIVES: Careful course observation is necessary for cases of mild to moderate traumatic brain injury even when disturbed consciousness is mild on admission. This is because delayed enlargement of hematoma and progression of cerebral swelling may occur and result in an emergency craniotomy. Here, we investigated coagulopathy and abnormal fibrinolysis as a predictive factor of "deterioration requiring surgery" in mild to moderate traumatic brain injury. PATIENTS AND METHODS: Sixty-one patients with mild to moderate (Glasgow Coma Scale (GCS) score 9-15) traumatic brain injury were admitted between June 2009 and October 2010. There were 54 subjects in the study, excluding those treated with oral antiplatelet agents and anticoagulants. Patients were classified into those with deterioration requiring surgery [op(+)] or those without deterioration requiring surgery [op(-)]. This was based on whether surgical treatment was performed for hematoma expansion, and exacerbated consciousness level within 3 days after admission. Age, GCS score on admission and blood test findings (platelet count, PT-INR, APTT, fibrinogen, FDP, and d-dimer) on admission were compared. RESULTS: The op(+) and op(-) groups comprised 7 (13.0%) and 47 patients (87.0%), respectively. Platelet counts (24.8 vs 18.5 × 10(4)/µl) were decreased, and PT-INR (1.0 vs 1.2) was higher in the op(+) group. Specially, APTT (28.6 vs 39.1s), FDP (28.9 vs 112.9 µg/ml), and D-dimer (17.3 vs 69.6 µg/ml) values were significantly higher in the op(+) group. CONCLUSIONS: Coagulopathy and abnormal fibrinolysis, which are measurable in routine medical practice, is associated with deterioration requiring surgery in mild to moderate traumatic brain injury, indicating that careful course observation is necessary.

Update on intensive neuromonitoring for patients with traumatic brain injury: a review of the literature and the current situation.

Intracranial pressure (ICP) measurements are fundamental in the present protocols for intensive care of patients during the acute stage of severe traumatic brain injury. However, the latest report of a large scale randomized clinical trial indicated no association of ICP monitoring with any significant improvement in neurological outcome in severely head injured patients. Aggressive treatment of patients with therapeutic hypothermia during the acute stage of traumatic brain injury also failed to show any significant beneficial effects on clinical outcome. This lack of significant results in clinical trials has limited the therapeutic strategies available for treatment of severe traumatic brain injury. However, combined application of different types of neuromonitoring, including ICP measurement, may have potential benefits for understanding the pathophysiology of damaged brains. The combination of monitoring techniques is expected to increase the precision of the data and aid in prevention of secondary brain damage, as well as assist in determining appropriate time periods for therapeutic interventions. In this study, we have characterized the techniques used to monitor patients during the acute severe traumatic brain injury stage, in order to establish the beneficial effects on outcome observed in clinical studies conducted in the past and to follow up any valuable clues that point to additional strategies for aggressive management of these patients.

Recent advances and future directions of hypothermia therapy for traumatic brain injury.

For severe traumatic brain injury (TBI) patients, no effective treatment method replacing hypothermia therapy has emerged, and hypothermia therapy still plays the major role. To increase its efficacy, first, early introduction is important. Since there are diverse pathologies of severe TBI, it is necessary to appropriately control the temperature in the hypothermia maintenance and rewarming phases by monitoring relative to the pathology. Currently, hypothermia is considered appropriate for severe TBI patients requiring craniotomy for removal of hematoma, while induced normothermia is appropriate for severe TBI patients with diffuse brain injury. Induced normothermia is expected to exhibit a cerebroprotective effect equivalent to hypothermia, as well as reduce the complexity of whole-body management and systemic complications. According to the Japan Neurotrauma Data Bank of the Japan Society of Neurotraumatology, the brain temperature was controlled in 43.9% of severe TBI patients (induced normothermia: 32.2%, hypothermia: 11.7%) in Japan. Brain temperature management was performed mainly in young patients, and the outcome on discharge was favorable in patients who received brain temperature management. Particularly, patients who need craniotomy for removal of hematoma were a good indication of therapeutic hypothermia. Improvement of therapeutic outcomes with widespread temperature management in TBI patients is expected.

Brain abscess associated with patent foramen ovale.

BACKGROUND: Brain abscesses can develop with Tetralogy of Fallot and pulmonary anterior venous fistula with large right-to-left shunt. However, some patients exhibit cryptogenic brain abscess (CBA) in the absence of any such congenital disease or other infections. Patent foramen ovale (PFO) is a very common disease that exhibits right-to-left shunt. This study reports the potential for concern between CBA and PFO. METHODS: We enrolled patients with CBA in our hospital between January 2003 and January 2013. Patients underwent transesophageal echocardiography (TEE) with contrast medium to investigate the presence of PFO. RESULTS: Seven patients were included. Four were females, and the mean age was 67.7 ± 9.2 years. In all patients, TEE failed to reveal any new findings, however, six patients had PFO, and another patient had pulmonary arteriovenous shunt. Four patients had odontopathy. CONCLUSION: In this study, all CBA patients exhibited right-to-left shunt. CBA might be caused by paradoxical embolization of a bacterial mass via PFO. Thus, more patients with CBA need to undergo TEE to detect PFO.