Annals of Indian Psychiatry

: 2020  |  Volume : 4  |  Issue : 2  |  Page : 244--245

A child on treatment for infantile spasms with drug-induced extrapyramidal symptoms

Abhijeet Taori1, Divya Malpani2,  
1 Department of Radiology, Suyash Hospital, Indore, Madhya Pradesh, India
2 Department of Radiology, Apollo Hospitals, Indore, Madhya Pradesh, India

Correspondence Address:
Dr. Abhijeet Taori
Suyash Hospital, Indore, Madhya Pradesh

How to cite this article:
Taori A, Malpani D. A child on treatment for infantile spasms with drug-induced extrapyramidal symptoms.Ann Indian Psychiatry 2020;4:244-245

How to cite this URL:
Taori A, Malpani D. A child on treatment for infantile spasms with drug-induced extrapyramidal symptoms. Ann Indian Psychiatry [serial online] 2020 [cited 2022 Jun 27 ];4:244-245
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Full Text

An 11-month-old male infant presented with ataxia in emergency. Clinical evaluation also showed abnormal choreiform movement of the arms with intermittent seizures.

Detailed history showed that the patient was a healthy full-term infant who was born following an unremarkable pregnancy. At 7 months of age, an infantile spasm was detected which was confirmed in a corroborative electroencephalography (EEG). Vigabatrin treatment was initiated with titrated doses reaching up to 140 mg/kg/day which resulted in gradual decrease in frequency of spasm and associated EEG alterations.

After a month, the child presented with abnormal movements of hands. A subsequent magnetic resonance (MR) performed showed diffuse hyperintensity involving the bilateral globi pallidi and thalamus on T2-weighted image [Figure 1]. Axial diffusion-weighted imaging demonstrated restricted diffusion involving the bilateral globi pallidi, thalamus, and dorsal brainstem [Figure 2]. The clinical history, presentation, and imaging findings were in keeping with vigabatrin-associated toxicity.{Figure 1}{Figure 2}


Vigabatrin is an antiepileptic drug of choice in the treatment of infantile spasms. It acts by inhibition of gamma-aminobutyric acid (GABA) transaminase. The risk of developing toxicity is higher in younger patients than 1 year.[1] Pathophysiology is unclear, but it is generally believed that myelin in the developing brain is vulnerability to elevated levels of GABA.[2] Literature suggests that likelihood of developing toxicity is highly dose dependent.[3]

MR imaging abnormalities in vigabatrin-induced toxicity are reversible on cessation of the drug; thus, a high index of suspicion in an appropriate clinical scenario is essential for early recognition.[4]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


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