Pathogenetic mechanisms and cellular pathology of common metabolic encephalopathies are discussed. Clinical considerations and anatomic bases are summarized as foundational points. Hypertensive, hypoxic/ischemic, uremic, hepatic, septic, hypoglycemic, diabetic, thiamin deficiency, osmotic demyelinative and traumatic forms of metabolic encephalopathies are considered, with relevant clinical, imaging correlates, biochemical bases and histopathological manifestations.
Pediatric encephalopathy presents a diagnostic challenge due to overlapping clinical features across multiple etiologies. Among these, inflammatory, infectious, and autoimmune causes are important as many are reversible with prompt recognition. Early, accurate diagnosis is crucial to reduce long-term neurologic sequelae risk. This article outlines a radiology-centered, pattern-based approach emphasizing clinical and imaging red flags, essential MRI protocols, and disease-specific diagnostic frameworks. Advanced MRI techniques, including diffusion-weighted imaging, perfusion imaging, and MR spectroscopy, enhance lesion characterization and guide management. Integrating these imaging insights with clinical data enables clinicians and radiologists to recognize treatable conditions rapidly and optimize outcomes in affected children.
This article provides a comprehensive review of acute encephalopathic syndromes caused by multiple therapeutic medications, emphasizing their imaging features and underlying mechanisms. It covers chemotherapeutic-related acute encephalopathies such as acute toxic leukoencephalopathy, posterior reversible encephalopathy syndrome, and neurovascular complications of chemotherapy; immunotherapy-induced neurotoxicities including immunotherapy-associated encephalitis, aseptic meningitis, cranial neuropathies, demyelination, and hypophysitis; and chimeric antigen receptor T-cell therapy-related syndromes such as cytokine release syndrome, immune effector cell-associated neurotoxicity, and tumor inflammation-associated neurotoxicity. Toxicities from non-cancer medications-metronidazole, vigabatrin, and anti-amyloid monoclonal antibodies-are also discussed.
Metabolic derangements and vitamin deficiencies represent one category of important, potentially reversible causes of acute encephalopathy, also termed "potentially reversible acute encephalopathic syndromes." This article summarizes their underlying pathophysiology and distinctive neuroimaging features, emphasizing disorders of glucose, ammonia, bilirubin, calcium-phosphorus metabolism, complex B-vitamin deficiencies, uremia, and osmotic stress. Magnetic resonance-particularly diffusion-weighted imaging-plays a pivotal role in diagnosis, prognostication, and therapeutic monitoring. Recognition of characteristic imaging patterns, such as "dark white matter" in hyperglycemia, the "lentiform fork sign" in uremia, and T1 pallidal hyperintensity in bilirubin toxicity, enables timely management and improved outcomes through an integrated clinicoradiologic approach.
Acute toxic leukoencephalopathy is characterized by white-matter injury from exposure to drugs, toxins, or environmental agents. Illicit drugs, including opioids, cocaine, amphetamines, and nitrous oxide, can cause white and gray matter damage due to lipophilicity, direct toxicity, hypoxia, and vasospasm. Environmental toxins also cause leukoencephalopathy via similar mechanisms. Different agents may manifest with specific imaging findings; therefore, imaging plays a crucial role in diagnosis, prognosis, and treatment guidance, as most cases have confusing and variable clinical presentations.
