A 70-year-old female consulted for 2-year evolution symptoms consisting of syncopal episodes, with loss of postural tone and without the presence of abnormal movements, relaxation of sphincters or other associated symptoms. She referred a frequency of approximately two to three episodes per year without consultation to the emergency services or previous study of the episodes. On the admission day to the institution, she presented an event of the same characteristics with mild traumatic brain injury (TBI) and facial trauma secondary to falling from her own height. For this reason, a simple skull computed tomography (CT) is carried out and a neurosurgery concept is requested.
During the initial evaluation, the patient is found in a Glasgow Coma Scale (GCS) as follows: GCS of 15, acceptable general condition, with vital signs within normal limits, with craniofacial trauma stigmas, bradypsychic, cranial nerves without alterations, preserved muscle strength in all 4 limbs, without sensory deficits and without the presence of pathological reflexes.
Significant vasogenic edema in the extension of the left frontal lobe with volume effect and deviation of the midline to the right is evidenced on the skull CT (Fig. 1). Findings highly suggestive of tumor lesion without clear limits in it were considered.
The study was extended with simple and contrasted brain nuclear magnetic resonance imaging (MRI) in order to characterize the lesion. The initial diagnostic impression was a metastatic lesion; therefore, extension studies were requested in order to search for possible primary neoplasm, which were negative. Anti-edema management was started with intravenous 8 mg of dexamethasone every 8 h and anticonvulsant management was managed with 500 mg of levetiracetam every 12 h.
The simple and contrasted MRI (Fig. 2) showed a lesion with well-defined intra-axial left frontal edges, isointense in T1 and T2 sequences, with homogeneous uptake of the contrast medium, without restriction to diffusion, associated with large perilesional edema, with deviation of the midline to the right and subfalcine herniation (Fig. 2).
The patient underwent surgical intervention with prior skull CT-guided surgical site marking (Fig. 3). The procedure was carried out under general anesthesia, with a left pterional craniotomy. Through intraoperative ultrasonographic guidance, the tumor lesion was identified and delimited in the left inferior frontal opercular subcortical gyrus. A corticotomy was carried out through the fissure and after 0.5 cm of depth, the lesion was identified. A blunt dissection was conducted through the capsular plane and progressive devascularization was carried out, subsequently achieving complete exeresis of the lesion. Intraoperatively, a solid encapsulated violet-colored tumor was observed, highly suggestive of meningioma.
During the postoperative follow-up, there were no motor or sensory focal neurological signs. Motor aphasia was evident, which resolved after the first 48 h. A control tomography was carried out, with evidence of postsurgical changes and decrease in vasogenic edema. The pathology report informs a lesion compatible with transitional meningioma, World Health Organization (WHO) grade I. The patient was discharged without sequels of neurological deficit, with the indication to continue the outpatient follow-up. In her first outpatient post-operative follow-up after 2 weeks, she remained asymptomatic, without neurological deficit and a healthy surgical wound.