2024 Volume 11 Pages 291-296
Chronic subdural hematoma (CSDH) in posterior fossa is rare, and its pathogenesis and treatment remain unclear. In this study, we report a case of a patient with CSDH in the posterior fossa who was taking warfarin and underwent middle meningeal artery (MMA) embolization successfully. A 59-year-old man taking warfarin for a mechanical aortic valve presented with a complaint of hearing impairment. He then developed headaches and was referred to our hospital after the previous physician identified CSDH above and below the left tentorium cerebelli on computed tomography (CT). We conducted MMA embolization with n-butyl-2-cyanoacrylate while continuing anticoagulation therapy. Right after the day of the surgery, symptoms of hearing impairment and right hemiplegia immediately improved. He was discharged after 10 days of hospitalization and was able to walk independently. His symptoms disappeared 20 days after surgery. There was no recurrence 100 days after surgery. In this study, we experienced a case of a CSDH in the posterior fossa that was clinically improved by MMA embolization. MMA embolization is a useful option for nonspecific CSDH without interruption of warfarin therapy.
Chronic subdural hematoma (CSDH) is a brain condition that typically develops due to aging or trauma, and its main treatment is a surgical burr hole drainage. However, in patients receiving oral anticoagulant therapy, the choice of treatment strategy can be difficult.1) In this study, we report a case of a patient with CSDH in the posterior fossa who was taking warfarin and underwent middle meningeal artery (MMA) embolization with improvement in hearing impairment and other symptoms. This treatment may be a useful choice for nonspecific CSDH without interruption of anticoagulation. Although CSDH in the posterior fossa is rare, and its pathogenesis and appropriate treatment remain unclear,2) our case is expected to contribute to the consideration of future treatment strategies.
A 59-year-old man who had previously undergone aortic valve replacement with a mechanical valve and continued taking warfarin presented with a complaint of hearing impairment. He then developed headaches and was referred to our hospital after the previous physician identified CSDH above and below the left tentorium cerebelli on computed tomography (CT) (Fig. 1A). His consciousness was lucid, and physical examination revealed hearing impairment on the left side, severe hemiplegia on the right upper limb, and no cerebellar ataxia. On laboratory examination, prothrombin time-international normalized ratio (PT-INR) was prolonged to 1.93. Magnetic resonance imaging (MRI) revealed that there were areas of high to low signal intensities, accompanied by niveau, on T1-weighted images, suggesting chronic subdural hematoma (Fig. 1B). He wished to continue taking warfarin; thus, the indication for MMA embolization was considered. Subsequent digital subtraction angiography (DSA) revealed dilation of the meningeal artery strongly depicted from MMA, of which embolization was performed (Fig. 2A). A 4 Fr JB2 type catheter was placed into the main trunk of the left external carotid artery. A Renegade microcatheter (Boston Scientific) was inserted into the MMA, which was navigated by a CHIKAI Black microguidewire (ASAHI Intecc). After microangiography observed microcapillaries from the MMA to the surface of the dura mater, a Marathon microcatheter (Medtronic) was introduced into the peripheral anterior branch of the MMA with the guidance of a CHIKAI X010 microguidewire (ASAHI Intecc) and embolized with 30% n-butyl-2-cyanoacrylate (Fig. 2B). The Renegade microcatheter was placed into the main trunk of MMA, which was embolized with 6 HILAL 2 mm× 2 cm coils (COOK medical) (Fig. 2C). Following DSA confirmed the disappearance of the microcapillaries (Fig. 2D). Right after the day of the surgery, symptoms of hearing impairment and right hemiplegia immediately improved. We continued anticoagulation therapy during hospitalization, and he was discharged after 10 days of hospitalization and was able to walk independently. Headache and hearing loss had never appeared after surgery. There was no recurrence 100 days after surgery on CT (Fig. 3).
Preoperative cranial images. A: Computed tomography (CT) performed by the initial physician revealed iso-high-density areas observed in the left subdural and below the tentorium cerebelli. B: T1-weighted magnetic resonance imaging (MRI) scanned on our hospital revealed areas of high to low signal intensities, accompanied by niveau.
Left: Frontal views of the left external carotid artery on digital subtraction angiography (DSA). Right: Lateral views on DSA. A: Preoperative angiography revealed dilation from the middle meningeal artery (MMA) of the anterior branch (white arrows) and the posterior branch (black arrows). B: The posterior branch was embolized with 30% n-butyl-2-cyanoacrylate. C: The main trunk was embolized with coils. D: Postoperative angiography confirmed the disappearance of the microcapillaries.
A: Follow-up CT images performed a day after the surgery. B: 20 days after. C: 49 days. D: 105 days.
Although CSDH in the posterior fossa is rare, its exact frequency of occurrence remains unclear. In a study conducted before the advent of CT, only 3 out of 535 SDH cases, including both acute and chronic instances, were in the posterior fossa.3) Furthermore, CSDH in the posterior fossa has been reported in only a few cases in the literature.4-19) In a retrospective study of 329 patients with supratentorial CSDH who underwent surgery between 2006 and 2020, MRI revealed CSDH in 24 patients (7.3%). CT scans did not visualize hematomas in 20 patients (83.3%), whereas those 24 patients detected by MRI were incidental findings lacking symptoms associated with infratentorial disorders.20) One study proposed that the low incidence of CSDH in the posterior fossa may be attributed to the inadequate visualization of the posterior fossa using CT and the spontaneous resolution of smaller hematomas.18) Infratentorial SDH can occur due to direct traumatic damage to the posterior fossa, which may involve injury to the venous sinus or bridging veins. The infrequent occurrence of venous sinus injuries and the limited number of bridging veins present in the posterior fossa may contribute to the observed low incidence of CSDH in this region.21) In addition, a CSDH may develop as a transformation from an acute subdural hematoma. Acute subdural hematomas in the posterior fossa are also exceedingly rare and frequently result in fatal outcomes.10) In our case, the patient presented with a rare instance of symptomatic CSDH in the posterior fossa, which was shown through a CT scan performed by the initial physician.
The initial symptoms of CSDH in the posterior fossa are often headache, vomiting, anisocoria, dysphagia, cranial nerve palsies, nuchal rigidity, and ataxia, which may be caused by a central disorder of the vestibular connections of the central nervous system such as vestibular nuclei and tracts, cerebellum, descending tracts of cerebellum, or hydrocephalus.2,3,18) Hearing impairment in our case was an excessively rare symptom. In addition, the patient was receiving warfarin therapy due to an aortic valve replacement. Patients with mechanical heart valves are at substantial risk of thrombus formation on the valve and subsequent systemic embolism, making lifelong oral anticoagulation therapy strongly recommended.22) However, anticoagulation therapy significantly increases the risk of CSDH, particularly in older patients using vitamin K antagonists such as warfarin.23) In addition, anticoagulant therapy is considered one of the risk factors for CSDH in the posterior fossa.4,10,12,20) However, interrupting anticoagulation therapy in CSDH patients heightens the risk of arterial ischemic events due to an increased risk of ischemic stroke.24) Consequently, there is no consensus on the interruption of anticoagulation therapy during the perioperative period. In previous case reports involving symptomatic posterior fossa CSDHs, 14 patients underwent surgery that included burr hole drainage in 6 patients, lateral suboccipital craniotomy in 2, and small craniotomy in 6 (Table 1). However, there have been no reports of MMA embolization performed. Of 14 cases, 13 had higher risk factor for hemorrhage, 11 underwent antithrombotic therapy, and 2 had leukemia.
Characteristics of previously reported cases of patients with posterior fossa CSDHs who underwent surgery and of our case
Author | Year | Age, sex | Side | General condition | Symptom | Surgical intervention | Outcome |
---|---|---|---|---|---|---|---|
Kanter | 1984 | 59, F | Left | Anticoagulation therapy | Comatose | Lat. Suboccipital craniotomy | Poor |
Ashkenazi | 1994 | 65, F | Left | Leukemia (AML) | Vertigo, nystagmus | Small craniotomy | Good |
Kachkov | 1999 | 41, F | Right | Anticoagulation therapy | Ataxia | Lat. Suboccipital craniotomy | Good |
Stendel | 2002 | 70, F | Bil. | Anticoagulation therapy | Vertigo, ataxia | Burr hole | Good |
Pollo | 2003 | 52, F | Bil. | Leukemia (AML) | Tetraparesis | Burr hole | Good |
Costa | 2004 | 64, F | Right | No anticoagulative background | Somnolence | Small craniotomy | Good |
Berhouma | 2007 | 38, F | Right | Anticoagulation therapy | Vertigo, ataxia | Small craniotomy | Good |
Kurisu | 2012 | 86, F | Bil. | Anticoagulation therapy | Loss of consciousness | Burr hole | Good |
Takemoto | 2016 | 69, F | Bil. | Anticoagulation therapy | Nausea, headache Loss of consciousness |
Small craniotomy | Good |
Kochi | 2017 | 86, F | Bil. | Anticoagulation therapy | Headache | Small craniotomy | Good |
Mochizuki | 2018 | 71, F | Left | Anticoagulation therapy | Ataxia, nausea Loss of consciousness |
Small craniotomy | Good |
Inoue | 2019 | 74, M | Bil. | Anticoagulation and antiplatelet therapy | Somnolence | Burr hole | Good |
Cristaldi | 2022 | 75, F | Bil. | Anticoagulation therapy | Loss of consciousness | Burr hole | Good |
Dlaka | 2023 | 71, M | Bil. | Anticoagulation therapy | Somnolence | Burr hole | Good |
Our case | 59, M | Left | Anticoagulation therapy | Headache, hearing loss | MMA embolization | Good |
MMA embolization was recently reported as a minimally invasive treatment for CSDH.25) MMA embolization may be selected as an adjunctive treatment option to decrease the likelihood of hematoma reaccumulation, including for patients with multiple prior CSDH recurrences.26) The safety of MMA embolization for the patients receiving anticoagulation therapy has also been reported.27) It can also be performed as a sole intervention in patients considered high surgical risks. In our case, posterior burr hole surgery was considered more difficult and higher risk than calvarium burr hole surgery. However, the risk of MMA embolization is equivalent both supra- and infratentorial CSDH. We believe that MMA embolization has been a promising option in a multitude of prior cases.
Meta-analysis shows that MMA embolization was associated with lower rates of CSDH recurrence and surgical rescue compared with burr hole surgery.28) However, MMA embolization still carries risks such as ischemic complications from embolic material. Long-term durability of MMA embolization as definitive treatment for CSDH has yet to be established. It may not be suitable for patients with severely neurological deficits or those with unfavorable endovascular access.29)
In this study, we experienced a case of a CSDH in the posterior fossa that was clinically improved by MMA embolization. MMA embolization was a useful treatment for nonspecific CSDH without interruption of warfarin therapy.
The authors declare no conflict of interest regarding the materials or methods used in this study or the findings specified in this paper. The research was approved by the institutional ethics committee. The consent was obtained from all the participants.