We discuss a patient with a tumor on the anterior corpus callosum who underwent open biopsy eventually succumbing to cerebrogenic fatal arrhythmia following wounded glioma syndrome. A healthy 37-year-old female patient was admitted to our department due to a history of headache for 13 months. MRI revealed a suspicious glioma infiltrating the anterior corpus callosum. Neurologic examination only showed low cognitive assessment score (Montreal Cognitive Assessment score 20/30). ECG was normal sinus rhythm. Steroids and levetiracetam were administered prior to operation. Patient underwent right frontal craniotomy and biopsy of tumor with unremarkable events. During the first hospital day, patient had episodes of bradycardia followed by decrease in sensorium. Brain CT scan showed progression of edema without hemorrhage within the tumor bed. This was followed minutes later by two episodes of generalized tonic-clonic seizures and pulseless ventricular tachycardia. Cardiac resuscitation was done for 24 minutes but patient eventually expired. Location of the lesion and the epileptogenicity of the peritumoral cortex greatly contributed to the patient’s demise. Involvement of the frontomesial structures, particularly the insula and the cingulate cortex, and their connection to the central autonomic network, increased susceptibility to arrhythmias. Decreased seizure threshold worsened post-operative edema, further aggravating the dysregulation of the brain-heart-connection.

Glioblastoma multiforme (GBM) represents the most malignant form of brain tumor and is relatively common, comprising nearly almost 20% of all primary malignancies of the central nervous system1. GBM is a WHO grade IV tumor with several variants, depending primarily on their genetic signature and on the predominant histological architecture. Among the variants of GBM, epithelioid glioblastoma (E-GBM) has been one of the more recently described. This tumor, documented to be highly malignant and clinically aggressive, has been separated from close variants and thus differentials, pleomorphic anaplastic xanthoastrocytoma, rhabdoid GBM, small cell and giant cell GBM, GBM with neuroectodermal differentiation, and gliosarcoma2. Autoimmune diseases have been linked within creased risk of CNS complications, from the constant effects of chronic inflammatory milieu. Systemic lupus erythematosus (SLE) has been associated with several CNS abnormalities, hence the terms CNS lupus or neuropsychiatric lupus. Likewise, SLE has been repeatedly associated with CNS malignancies in several cases and case reports. To date, there is paucity in the reported cases of malignant brain tumors, especially rare variants, in patients with SLE. While it is hypothesized that the inflammatory milieu that bathes the brain in a dynamic microenvironment that influences the incidence of rare variants of GBM, clinicians should be mindful, as treatment is challenging: it may either induce exacerbation of autoimmunity or cause undertreatment of the malignancy. This complex interplay births curiosity into the enigma of autoimmunity and oncology. In this particular report, we highlight the case of a patient with SLE who developed E-GBM. We identify the clinicopathologic features of the tumor present in the patient and explore the known aspects of the crosstalk between SLE and E-GBM.
Lupus Erythematosus, Systemic ; Glioblastoma