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|Year : 2017 | Volume
| Issue : 5 | Page : 1193
Isoniazid toxicity presenting as bilateral dentate hyperintensities
Aarthi Deepesh, Hima S Pendharkar
Department of Neuroimaging and Interventional Radiology, National Institute of Mental Health and Neuro Sciences, Bengaluru, Karnataka, India
|Date of Web Publication||6-Sep-2017|
Hima S Pendharkar
Department of Neuroimaging and Interventional Radiology, National Institute of Mental Health and Neuro Sciences, Bengaluru - 560 029, Karnataka
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Deepesh A, Pendharkar HS. Isoniazid toxicity presenting as bilateral dentate hyperintensities. Neurol India 2017;65:1193
A 29-year old female patient presented with progressive ataxia over 20 days. She was on a 4-drug antituberculosis regime (including isoniazid [INH]) for a year due to the presence of multiple central nervous system tuberculomas.
Isoniazid neurotoxicity usually manifests with seizures, encephalopathy, and peripheral neuropathy; however, cerebellar ataxia is rare. Reduction of gamma-aminobutyric acid levels and downregulation of N-methyl-D-aspartate receptors are potential mechanisms for the dentate nuclei edema, and hence, the signal changes visualised on magnetic resonance imaging [Figure 1]. In developing countries, where tuberculosis is prevalent, INH toxicity should be included in the differential diagnosis of bilateral dentate nuclei hyperintensity, among other causes such as metronidazole or methyl bromide toxicity, as well as enteroviral infections, or atypical Wernicke's encephalopathy.
|Figure 1: (a) T2 weighted image shows symmetric hyperintensity involving bilateral dentate nuclei. (b) Axial post-contrast T1 three-dimensional magnetization prepared rapid acquisition gradient reversal echo [MPRAGE] (three-dimensional inversion recovery) image did not reveal any abnormal postcontrast enhancement. There was no blooming on susceptibility weighted imaging or diffusion restriction (image not shown)|
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