DOI: https://doi.org/10.36347/sjmcr.2024.v12i10.010

Pages: 1662-1664

Bilateral basal ganglia lesions can arise from a diverse range of causes, such as metabolic imbalances, toxic exposure, degenerative conditions, vascular events, inflammatory processes, infections, and tumors. We present a case involving a 66-year-old male patient who was admitted to the hospital following acute changes in behavior and psychomotor slowing. His medical history was notable for Parkinson’s disease, with a recent adjustment in L-Dopa dosage, as well as diabetes mellitus and arterial hypertension. Upon initial evaluation, the patient was hypertensive, drowsy, disoriented in both time and space, exhibited dysarthria, and displayed global bradykinesia. Diagnostic investigations revealed a brain CT scan that showed bilateral, symmetrical hypodensities in the lenticulo-caudate region without midline shift or evidence of cerebral herniation. The cerebrospinal fluid (CSF) analysis found 15 cells/μL with no other abnormalities, while laboratory tests highlighted hypernatremia (175 mEq/L), elevated creatinine (3.5 mg/dL), hyperglycemia (<300 mg/dL), along with slightly increased C-reactive protein and anticardiolipin antibodies, and thrombocytopenia (107,000/uL). Following treatment adjustments—including the correction of metabolic imbalances and discontinuation of L-Dopa—subsequent brain imaging showed improvement in the lesions, and the patient’s condition returned to baseline. The basal ganglia play a complex role in brain function, relying heavily on glucose and oxygen, which makes them particularly sensitive to metabolic disturbances. In this case, symmetrical lesions in the basal ganglia resulted in acute mental status changes, likely linked to hyperglycemia, acute kidney injury, hypertension, and potential exposure to toxic substances, including medication and environmental toxins. Full clinical recovery, alongside negative follow-up investigations and regression of the lesions, supports the proposed diagnosis.