Final diagnosis – Isoniazid Induced Neurotoxicity(INH) (Drug induced Cerebellitis).

Neurotoxicity  seen in chronic  kidney  patient  taking  isoniazid  due  to  reduced  clearance  of  INH.

The  mechanism  for INH  toxicity  is  due  to  energy  deprivation  and  deficiency  of  Vitamin B complex. There  is  interruption  of  pathways  responsible  for  pyridoxine  phosphorylation  resulting  in  decreased  production  of  pyridoxal 5-phosphate  required  for neurotransmission  via gamma aminobutyric acid (GABA). GABA  is  an  inhibitory  neurotransmitter in  the  central nervous  system. Deficiency  of  GABA  results  in  cerebellar  signs.

Pyridoxine  supplementation  is  always advised with INH therapy.  However,  even  with  pyridoxine  supplementation  (15–50  mg/day),  up  to  5%  of   patients  would  still  have  some  adverse  effects,  with  the  proportion  rising  fourfold  when  pyridoxine  dosage  is   inadequate.

Clinical presentation: INH neurotoxicity can present with seizures,  encephalopathy,  and  peripheral  neuropathy. Cerebellar  ataxia  is rare

Key imaging  features: T2  and  FLAIR  image  showing  symmetrical  hyperintensities  involving  bilateral  dentate  nuclei  due  to  its  toxicity-induced  edema.

Differential diagnosis  -Metronidazole  toxicity, Enteroviral  encephalopathy,  Atypical Wernicke’s  encephalopathy.

Treatment- Starting  patient  on  pyridoxine  and  ATT  regime  need  to  be modified.

References:

1.Navni Garg, Rahul Mutreja. Bilateral dentate hyperintensities: Isoniazid –induced toxicity European society of Radiology 10.1594/EURORAD/CASE.13907

2. Prashant Peter, Mary John (2014) Isoniazid-induced cerebellitis: a disguised presentation. Singapore Med J 55(1):e17–e19. (PMID: 4291918)

3.S Senthil Raj Kumar, S Shanmuga Jayanthan,G Rupesh (2020) Isoniazid: A rare drug-induced cause for bilateral dentate nuclei hyperintensity. Indian Journal of Radiology and Imaging.