Acquired Metabolic, Systemic, and Toxic Disorders



10.1055/b-0034-102657

Acquired Metabolic, Systemic, and Toxic Disorders



Acute Hypertensive Encephalopathy


This entity, also known by the term posterior reversible encephalopathy syndrome (PRES), is caused by acute severe hypertension. There is a predilection for involvement of the parietooccipital regions (the posterior circulation), with bilateral, symmetric abnormal high signal intensity (vasogenic edema) on fluid attenuated inversion recovery (FLAIR) involving the cortex and subcortical white matter in a nonvascular distribution ( Fig. 1.34 ). In prominent disease, the involvement of the cerebral hemispheres may be more extensive. Diffusion is usually not restricted. There may be accompanying involvement of the basal ganglia.

Fig. 1.34 Posterior reversible encephalopathy syndrome (PRES). In this entity, also known as acute hypertensive encephalopathy, symmetric abnormal high signal intensity is seen on FLAIR scans, consistent with vasogenic edema, posteriorly in the parietal-occipital regions involving cortical gray and subcortical white matter. On DWI, these areas are most commonly normal, but may be hyperintense (as illustrated), however, with the ADC map normal (no restricted diffusion).


Wernicke Encephalopathy


This entity is caused by thiamine deficiency, and is seen in severe malnutrition, in particular with alcohol abuse. On FLAIR, in extensive disease, abnormal bilateral hyperintensity can be noted in the mamillary bodies, around the third ventricle, and in the medial thalami, tectal plate, and periaqueductal area ( Fig. 1.35 ). Involvement of the mamillary bodies is a distinctive feature. The mamillary bodies can also have abnormal contrast enhancement, as can occur in the other involved areas.

Fig. 1.35 Wernicke encephalopathy. Involvement of the mamillary bodies, seen on FLAIR with abnormal hyperintensity (image not shown) and post-contrast with abnormal enhancement (illustrated, arrows), is the most characteristic finding in this disease from an imaging perspective.


Hepatic Encephalopathy


This entity can occur with either acute or chronic liver disease, and is characterized on MR imaging by high signal intensity bilaterally within the globus pallidus on T1-weighted images ( Fig. 1.36 ). The signal intensity characteristics are thought to reflect manganese deposition. Similar findings can be seen with hyperalimentation.

Fig. 1.36 Hepatic encephalopathy. Subtle abnormal high signal intensity (arrow, first image) is present bilaterally in the globus pallidus on a T1-weighted scan in this patient, consistent with manganese deposition. Presumably dependent on the amount of abnormal metal accumulation, the findings range in patients from somewhat subtle to striking hyperintensity. Also noted in this case is bilateral abnormal hyperintensity in the thalami (arrow, second image), which can also be seen in hepatic encephalopathy (involving any of the basal ganglia), but is less common.

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Jun 14, 2020 | Posted by in NEUROLOGICAL IMAGING | Comments Off on Acquired Metabolic, Systemic, and Toxic Disorders

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