E4931. Guiding the Way: Expert Navigation through the Enigma of Decoding Toxic and Metabolic Brain Disorders
Authors
Benjamin Rutta;
Columbia University Irving Medical Center
Annie Singh;
Atal Bihari Vajpayee Institute of Medical Sciences and Dr Ram Manohar Lohia Hospital
Mohammad Chaudhry;
Newark Beth Israel Medical Center
Uma Menon;
The Pingry School
Gagandeep Singh;
Columbia University Irving Medical Center
Background
Toxic and metabolic encephalopathies (TME) arise from derangements in various physiologic processes, due to endogenous dysfunction or exogenous toxins. They can be hereditary or acquired. Due to their diverse symptoms and varied clinical presentation, they are challenging to diagnose clinically, with MRI patterns being essential for identification, prognosis, and management.
Educational Goals / Teaching Points
- Identify common MRI features associated with various etiologies of TME. - Recognize imaging patterns and underlying pathophysiology, which offers insights into disease characteristics and prognosis. - Understand importance of correlating imaging features with clinical history for accurate diagnosis. - Recognize early diagnosis and treatment of TME can lead to a better prognosis and reduced complications due to the potential reversibility of many of these conditions.
Key Anatomic/Physiologic Issues and Imaging Findings/Techniques
- Imaging techniques used to visualize toxic and metabolic brain disorders include conventional CT and MRI. MRI is the modality of choice, owing to improved contrast as well as microscopic changes. - On MR, normal basal ganglia are isointense to the cortex on T1, T2, and FLAIR sequences. Symmetrical bilateral signal intensity is expected. With age, globus pallidus becomes more hypointense when compared to putamen and caudate nucleus on T2- and FLAIR-weighted images owing to micromineralization, in particular iron. - Toxic and metabolic disorders on MRI usually present as symmetric bilateral increased T2/FLAIR signal intensity and restricted diffusion in the following common general patterns: basal ganglia/thalami involvement, dentate nuclei involvement, prominent cortical gray matter involvement, symmetric periventricular white matter involvement with gray matter sparing, corticospinal tract region involvement, corpus callosum involvement, asymmetric white matter involvement resembling demyelination, parieto-occipital subcortical vasogenic edema, and central pons involvement. - Increased T1 signal intensity and T2* signal may also be seen owing to necrotic hemorrhage associated with certain toxic and metabolic brain disorders.
Conclusion
Toxic and metabolic brain disorders are a challenging entity to diagnose, given the variability and heterogeneity among the group of diseases and unspecific patterns of presentation. Though an extensive number of other etiologies and uncommon presentations are possible, common imaging features can help guide the diagnosis and management in most cases.
