BACKGROUND: Intrathecal baclofen is widely accepted as a treatment option for severe spasticity through its γ-Aminobutyric acid-B (GABAB ) agonist properties. Abrupt cessation can lead to severe and life-threatening withdrawal characterized by altered mental status, autonomic dysreflexia, rigidity, and seizures. This symptomatic presentation is similar to alcohol withdrawal, which is mediated by modification of GABAA expression. Use of the α2-adrenergic agonist dexmedetomidine for the treatment of ethanol withdrawal has been widely reported, raising the question of its potential role in baclofen withdrawal. We present a case of the successful treatment of acute severe baclofen withdrawal with a dexmedetomidine infusion. METHODS: A 15-year-old patient with spastic quadriparesis and cerebral palsy underwent unexpected removal of his baclofen pump due to an infection that was encountered during a planned pump revision. Following removal, he was placed on high dose enteral baclofen every 6 h. Despite further benzodiazepine supplementation, he had progressive hemodynamic instability, severe rebound spasticity, and intermittent spontaneous clonus consistent with baclofen withdrawal. A dexmedetomidine infusion was titrated to a peak dose of 16 mcg per hour with successful treatment of withdrawal symptoms. RESULTS: The patient became normotensive without tachycardia. Tone and agitation improved. CONCLUSION: Dexmedetomidine is to our knowledge a previously unreported option for treatment of acute severe baclofen withdrawal. We report a case of safe and efficacious use in a patient with spastic quadriparesis on chronic intrathecal baclofen. Scientifically rigorous comparison with other options remains to be performed.
BACKGROUND: Intrathecal baclofen is widely accepted as a treatment option for severe spasticity through its γ-Aminobutyric acid-B (GABAB ) agonist properties. Abrupt cessation can lead to severe and life-threatening withdrawal characterized by altered mental status, autonomic dysreflexia, rigidity, and seizures. This symptomatic presentation is similar to alcohol withdrawal, which is mediated by modification of GABAA expression. Use of the α2-adrenergic agonist dexmedetomidine for the treatment of ethanol withdrawal has been widely reported, raising the question of its potential role in baclofen withdrawal. We present a case of the successful treatment of acute severe baclofen withdrawal with a dexmedetomidine infusion. METHODS: A 15-year-old patient with spastic quadriparesis and cerebral palsy underwent unexpected removal of his baclofen pump due to an infection that was encountered during a planned pump revision. Following removal, he was placed on high dose enteral baclofen every 6 h. Despite further benzodiazepine supplementation, he had progressive hemodynamic instability, severe rebound spasticity, and intermittent spontaneous clonus consistent with baclofen withdrawal. A dexmedetomidine infusion was titrated to a peak dose of 16 mcg per hour with successful treatment of withdrawal symptoms. RESULTS: The patient became normotensive without tachycardia. Tone and agitation improved. CONCLUSION:Dexmedetomidine is to our knowledge a previously unreported option for treatment of acute severe baclofen withdrawal. We report a case of safe and efficacious use in a patient with spastic quadriparesis on chronic intrathecal baclofen. Scientifically rigorous comparison with other options remains to be performed.
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