A 24-year-old male patient presented to us with global aphasia and right-sided hemiplegia. Medical history was significant for intermittent headaches for 4 months. One month after the onset of symptoms, the patient developed an evening rise in temperatures and abdominal pain. He sought treatment at another institution where he was evaluated with ultrasound abdomen that showed splenomegaly with multiple granulomas and the findings were later confirmed with computerized tomography (CT) abdomen which also revealed periportal, para-aortic, and aortic caval lymphadenitis-like features, for which he was treated presumptively as a mycobacterial tuberculosis infection. Ten days later, the symptoms worsened and the patient developed new-onset speech difficulty along with right-sided weakness. Consequently, the patient was evaluated with a magnetic resonance imaging (MRI) brain which was suggestive of left frontal thin subdural (measuring around 2*3*2 mm, volume 6 cubic mm) and a rim of thin epidural collection, and the patient was continued on anti-tubercular treatment (ATT) presuming CNS tuberculosis.
A month later, he presented to us when complaints progressed to aphasia and hemiplegia. Physical examination was significant for altered sensorium with a Glasgow Coma Scale of E3VAM5 and right-sided hemiplegia. The patient was reevaluated with a plain and contrast MRI of the brain. On T1, isointense rim with the hypointense collection was noted in the lesion [Figures 1a and 1b], findings confirmed in T2 sequence with fluid-fluid level, also T2 and MR flair sequence shows hyperintense extra-axial/subdural collection [Figures 1c and 1d]. MRI contrast scan featured conglomerate peripheral ring-enhancing lesions [Figures 1e and 1f] in the left frontal lobe (intraparenchymal) with moderate to significant perilesional edema causing mass effect over the frontal horn and body of the ipsilateral ventricle. Diffuse weighted imaging was suggestive of diffusion restriction within the wall of the lesion and in the dependent content and debris [Figure 1g]. Magnetic resonance (MR) spectroscopy showed significantly large lipid lactate peaks in the lesion [Figure 2a]. Findings favored infective etiology with cerebral abscess, subdural empyema, and dural thickening with an intradural abscess in the left frontal region with frontal cortical vein thrombosis. Radiological findings were confirmed intra-op, subsequently was compared with post op scan which showed complete abscess evacuation [Figure 2b].
The patient underwent left fronto-temporo-parietal decompressive craniectomy and abscess evacuation. After craniectomy, adherent purulent collection was noted on the inner table of the bone flap and dura, suggestive of osteomyelitis and epidural abscess [Figure 3a]. Durotomy was performed and thick pus was noted in the subdural plane [Figure 3b] which was evacuated. Subsequently, the abscess was approached through a pial incision over the superior frontal gyrus at the point of tense thickened pia; clear differentiation was seen between the capsule and surrounding glial tissue. The capsule was incised with a stab, purulent contents were evacuated, the leftover capsular wall was excised, and hemostasis was achieved. The osteomyelitic bone and raised intracranial pressure features were indications for not replacing the bone flap. The histopathology and culture evaluation grew B. pseudomallei, subsequently, he was started on intravenous antibiotics and the postoperative contrast-enhanced CT showed complete abscess evacuation with a significant reduction of perilesional edema [Figure 2b]. Recovery was uneventful with aphasia resolution and right-sided motor power improvement. At 1-month follow-up, the patient had significant neurological improvement with no new deficits.