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DOI: 10.1055/a-2552-7482
Toxische Enzephalopathien – beyond Drugs
Toxic encephalopathies – beyond drugsAuthors
Eine Enzephalopathie kann bei zahlreichen Vergiftungen auftreten. Neben den sich teilweise überlappenden bildmorphologischen Befunden infolge verschiedener Intoxikationen muss der Neuroradiologe über die Ursachen einer toxischen Enzephalopathie informiert sein. Hierzu zählen die hepatische und urämische Enzephalopathie sowie Vergiftungen durch Kohlenmonoxid, Methanol, Arsen, Blausäure, Schwermetalle und verschiedene Medikamente.
Abstract
Toxic encephalopathy can occur with numerous unintentional intoxications. In addition to exogenous poisoning, the causes also include hepatic and uremic encephalopathy, as these also lead to an unphysiological increase in the concentration of metabolites with a potentially toxic effect on the central nervous system (CNS). The neuroradiologist must also be informed about the spectrum of exogenous poisoning with possible cerebral involvement. This includes poisoning by carbon monoxide, methanol, arsenic, hydrocyanic acid (cyanides), heavy metals and various medications. In magnetic resonance imaging (MRI), the various causes of toxic encephalopathy show partially overlapping image morphological characteristics, a common feature is almost always a bilateral occurrence of the lesions. Despite overlapping imaging, there are frequent characteristic findings in some intoxications, although these are not specific for the respective cause and may be absent in individual reported cases. These include signal enhancement in the T1-weighted sequence due to the accumulation of manganese in the basal ganglia in hepatic encephalopathy, the lentiform fork sign of the basal ganglia in uremic encephalopathy, the bilateral lesion of the optic nerve in methanol poisoning, and the atrophy of the visual cortex and cerebellum in chronic mercury poisoning. Clinically, toxicologic screening of the patient is one of the main components of the diagnostics of intoxication, as is neuroradiologic MRI assessment in the case of cerebral involvement.
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Eine Enzephalopathie kann infolge vieler Intoxikationen auftreten. Der Neuroradiologe sollte neben den bildmorphologischen Befunden auch über das klinische Spektrum und über die unterschiedlichen Expositionsquellen der einzelnen Toxine informiert sein.
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Bei einer toxischen Enzephalopathie ist häufig die graue Substanz betroffen, wobei kortikale Läsionen in allen zerebralen und zerebellären Abschnitten einschließlich dem Hippocampus ebenso vorkommen wie Läsionen in der tiefen grauen Substanz. Auch die weiße Substanz insbesondere des Centrum semiovale kann betroffen sein.
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Sichere Hinweise auf die jeweilige Ursache sind bildmorphologisch nicht gegeben, da die MRT-Befunde nicht spezifisch für bestimmte Intoxikationen sind.
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Es besteht eine ausgeprägte interindividuelle Variabilität der möglichen bildgebenden ZNS-Befunde gleicher Ursache, etwa bei Kohlenmonoxidvergiftungen.
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Alle bildmorphologischen Veränderungen sind i. d. R. bilateral und weitgehend symmetrisch nachweisbar.
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Klassische Befunde einer toxischen Enzephalopathie sind eine T1-Signalanhebung der Basalganglien infolge einer lokalen Mangananreicherung bei der hepatischen Enzephalopathie, das sog. Lentiform Fork Sign bei der urämischen Enzephalopathie, die bilaterale Läsion des N. opticus infolge einer Methanolvergiftung sowie die betonte Atrophie von visuellem Kortex und Zerebellum bei einer chronischen Quecksilberintoxikation.
Schlüsselwörter
hepatische Enzephalopathie - urämische Enzephalopathie - Vergiftung - Intoxikation - KohlenmonoxidKeywords
hepatic encephalopathy - uremic encephalopathy - poisoning - intoxications - carbon monoxidePublication History
Article published online:
01 December 2025
© 2025. Thieme. All rights reserved.
Georg Thieme Verlag KG
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