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Intrathecal Baclofen Therapy

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Neurosurgery for Spasticity

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Abstract

Baclofen, a γ-aminobutyric acid-B (GABA-B) receptor agonist, has a direct action on the receptors of the dorsal horn gray matter, where density of GABA-B receptors is high. Baclofen activates GABA-B presynaptic receptors that inhibit the release of excitatory neurotransmitters of the dorsal horn, particularly aspartate and glutamate. The excitability of monosynaptic and polysynaptic reflexes of the spinal cord becomes thereby reduced. Given orally, baclofen has a weak capacity to penetrate the blood–central nervous system barrier. After oral administration the drug is absorbed by more than 80 % through the intestinal mucosa the plasmatic concentration is maximal within 90–120 min; most is eliminated by urinary excretion. Failure of oral medication to produce sufficient reduction of spasticity is due to the poor passage of the drug across the blood–central nervous system barrier. In animal experiments, the concentration in the cerebrospinal fluid (CSF) was less than one-tenth of that in the plasma level. Systemic delivery would produce the same concentrations along the spinal cord and would be distributed equally to the brain, and the consequences would be somnolence or even coma. To circumvent this problem, Penn and Kroin introduced and developed the method of delivering baclofen intrathecally by subarachnoid lumbar infusion.

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  1. Department of Neurosurgery, University of Lyon 1 Hôpital Neurologique Pierre Wertheimer, GHE, Lyon, France

    Marc Sindou M.D., D.Sc., George Georgoulis M.D. & Patrick Mertens M.D., Ph.D.

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Sindou, M., Georgoulis, G., Mertens, P. (2014). Intrathecal Baclofen Therapy. In: Neurosurgery for Spasticity. Springer, Vienna. https://doi.org/10.1007/978-3-7091-1771-2_6

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