Vigabatrin-associated brain abnormalities on magnetic resonance imaging (VABAM)

Toxicosis
Iatrogenic diseases

General description

Vigabatrin-associated brain abnormalities on magnetic resonance imaging (VABAM) represent a unique form of drug-induced neurotoxicity observed in patients receiving vigabatrin therapy for spasms. The pathophysiology of VABAM is closely linked to vigabatrin's mechanism of action as an irreversible inhibitor of gamma-aminobutyric acid (GABA) transaminase, which leads to increased central GABA levels.

Clinical manifestations

The clinical presentation of VABAM varies considerably, with the majority of cases being asymptomatic. When symptomatic manifestations occur, they predominantly involve extrapyramidal symptoms and movement disorders. The clinical symptoms associated with VABAM include hyperkinetic disorders, myoclonus, tremor, lethargy, and in rare cases, acute encephalopathy.

T2WI and FLAIR hyperintensity

Anatomical regions
  • Globus pallidus
  • Thalamus
  • Dentate nucleus
  • Corpus callosum
  • Anterior commissure
  • Brainstem
    Midbrain
  • Brainstem
    Pons
    Central tegmental tract
Symmetric
Bilateral
T2WI
Hyperintensity
FLAIR
Hyperintensity
DWI
Hyperintensity

MRI demonstrates T2WI/FLAIR and DWI hyperintensities in the globus pallidus, thalamus, central tegmental tract of the brainstem, and dentate nucleus. MRI abnormalities may also be seen in the anterior commissure and corpus callosum.