Abstract

Acute lymphoblastic leukemia is characterized by the presence of numerous immature white blood cells or lymphocytes in the bone marrow. The utilization of L-asparaginase (L-ASNase) as a chemotherapeutic agent is crucial in the management of acute lymphoblastic leukemia (ALL). Given its anti-proliferative characteristics, L-asparaginase plays a pivotal role in ALL treatment by catalyzing the hydrolysis of asparagine into aspartic acid and ammonia at a biochemical level. As cancer cells heavily rely on asparagine for their proliferation, the depletion of this amino acid by asparaginase leads to the starvation of cancer cells, impeding their growth and eventually inducing cell death. However, L-ASNase therapy causes neurological disturbances. One of this enzyme's most frequent neurological side effects is cognitive impairment. Patients receiving this drug may experience difficulties with concentration, memory, and information processing; it may also cause other neurological symptoms, such as seizures, headaches, dizziness, confusion, and delirium. Depending on the individual and the drug dose, these symptoms may be temporary or long-lasting. This review aims to highlight the neurotoxicity problems associated with ASNase treatment in acute lymphoblastic leukemia. These include cerebrovascular events, such as posterior reversible encephalopathy syndrome, secondary brain tumors, and Central Nervous System (CNS) infiltration. Rapid recognition of etiology is essential and represents a difficult task because the neurotoxicity of antineoplastic treatments often simulates complications related to the disease itself, making it necessary to interrupt the use of the enzyme during an ongoing protocol.