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Efavirenz as a cause of ataxia in children
Insights
Efavirenz toxicity can cause acute ataxia in children with HIV. This highlights the importance of considering medication side effects in pediatric patients presenting with walking unsteadiness.
Area of Science:
- Neurology
- Pediatrics
- Infectious Diseases
Background:
- Acute ataxia in children is commonly linked to toxin ingestion or post-infectious causes.
- Neurological complications are frequent in HIV-positive children, though cerebellar dysfunction is rarely documented.
- Ataxia in HIV is typically secondary to opportunistic infections, vascular issues, or neoplastic lesions.
Purpose of the Study:
- To report two cases of acute ataxia in pediatric patients with HIV.
- To highlight efavirenz toxicity as a potential cause of ataxia in this population.
- To emphasize the need to consider medication side effects in the differential diagnosis of pediatric ataxia.
Main Methods:
- Case report of two pediatric patients presenting with acute ataxia.
- Review of clinical presentation, medical history, and neurological examination findings.
- Assessment of potential causes including infections, mass lesions, and medication toxicity.
Main Results:
- Both patients presented with acute ataxia, a rare neurological complication.
- Efavirenz toxicity was identified as the cause of ataxia in both cases.
- The cases occurred within a one-month period, suggesting a potential emerging issue.
Conclusions:
- Efavirenz toxicity is an important differential diagnosis for acute ataxia in HIV-positive children.
- Clinicians should consider antiretroviral medication side effects when evaluating pediatric ataxia.
- Further investigation into the neurological side effects of efavirenz in children is warranted.
Abstract:
Acute ataxia in childhood is often caused by toxin ingestion. With the increasing number of paediatric patients on antiretroviral medication, we observe more side-effects of these drugs. Acute ataxia is defined as unsteadiness of walking or fine motor movement of <72 hours. The most common causes are postinfectious acute cerebellar ataxia, toxin ingestion and Guillain-Barré syndrome. However, the possibility of a mass lesion must always be excluded. Reported neurological abnormalities in HIV-positive children range from 10% to 68%. A South African study found the prevalence of neurological complications to be 59%, the most common of which were HIV encephalopathy and long-tract motor signs; however, no cases of cerebellar dysfunction were documented. Ataxia rarely occurs in an HIV-positive person, the chronic sequelae being neurocognitive impairment and polyneuropathy. Ataxia in the setting of HIV is generally secondary to an infectious, vascular or neoplastic cerebellar lesion. However, most infections are opportunistic and unlikely to occur when CD4 levels are adequate. The vascular or mass lesions are readily excluded with neuro-imaging. We report 2 cases of efavirenz toxicity that caused ataxia. We treated 2 children who presented in a 1-month period, which highlighted an important differential to consider in HIV-positive paediatric patients presenting with ataxia.
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