E5073. Brain Overload: Understanding Toxic Metabolic Encephalopathy on MRI
  1. Namita Bhagat; Yale New Haven Health-Bridgeport Hospital
  2. Anisa Chowdhary; Yale New Haven Health-Bridgeport Hospital
  3. Rachana Borkar; Yale New Haven Health-Bridgeport Hospital
  4. Anish Neupane; Yale New Haven Health-Bridgeport Hospital
  5. Gaurav Cheraya; Yale New Haven Health-Bridgeport Hospital
  6. Ahmed Ragab; Yale New Haven Health-Bridgeport Hospital
  7. Ajay Malhotra; Yale New Haven Hospital
Toxic metabolic disorders are rare and can be caused by both endogenous and exogenous causes. Endogenous causes include metabolic derangements, such as uremic and hepatic encephalopathies, disorders of glucose metabolism, Vitamin B12 deficiency, and osmotic demyelination. Exogenous causes include alcohol, illicit drugs (cocaine, heroin, alcohol, amphetamines, toluene, and cannabis), various chemotherapeutic and immunosuppressive agents, prescribed medications like antiepileptics and antibiotics, as well as exposure to toxic gases and industrial agents. Drug abuse accounts for majority of cases of toxic encephalopathy. CNS complications of toxic metabolic disorders include neurovascular complications, encephalopathy, atrophy, infection, changes in the corpus callosum, and other miscellaneous changes, which produce characteristic imaging manifestations, which can be appreciated at MRI.

Educational Goals / Teaching Points
Most toxic metabolic disorders demonstrate symmetrical pattern of injury involving the deep gray nuclei and cerebral cortex. Bilateral and symmetric lesions with restricted diffusion, no or mild mass effects, and no enhancement are often depicted. It is critical for radiologists to recognize these imaging manifestations as the extent of brain involvement may predict the prognosis and guide clinical management. This exhibit will provide a brief overview of imaging manifestations of various toxic metabolic encephalopathies on MRI.

Key Anatomic/Physiologic Issues and Imaging Findings/Techniques
All toxic metabolic disorders cause excito-toxic brain injury with cytotoxic edema. Myelin, due to its high lipid content, is vulnerable to lipophilic toxic substances. The imaging features of cytotoxic cerebral edema appear primarily as changes at DWI as the entire process is a redistribution of water. As the pathologic process progresses, alterations in T2-weighted and FLAIR signal intensity and contrast enhancement appear secondarily. The basal ganglia, thalami, cortical gray matter, periventricular white matter, and corpus callosum are classical sites of predilection. These disorders are divided according to patterns of involvement, which include: 1) basal ganglia and thalami involvement; 2) symmetrical periventricular white matter involvement with gray matter sparing; 3) asymmetric white matter involvement; 4) prominent cortical involvement; 5) corpus callosum involvement; 6) corticospinal tract involvement; 7) dentate nuclei involvement; and 8) Pons involvement.

Toxic metabolic disorders present a challenging diagnosis. Knowledge of the imaging appearance in combination with clinical history can help narrow the differential diagnosis and exclude other causes. MRI plays a crucial role in early recognition and timely management of these disorders, thus leading to reduced morbidity and mortality.