The neurochemistry of central pain: evidence from clinical studies, hypothesis and therapeutic implications.
Recent evidence suggests that central pain, i.e., pain due to central nervous system damage, may be due to a deranged neurotransmission between the sensory thalamus and sensory cortical areas. Central pain can be controlled either by opposing glutamate neurotransmission or potentiating GABAergic transmission. It is speculated that a relative hypofunction of the GABAergic inhibition both at thalamic and cortical levels leads to a sectorial excitatory hypertonus in those same areas. A blend of the two should mark each patient. A pharmacological dissection approach is provided that should optimize the treatment, up to now globally poor, of central pain.
Canavero
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S
Department of Neurosciences, Ospedale Molinette, Turin, Italy.
Bonicalzi
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D018686:Anesthetics, Intravenous / Q000008:administration & dosage; D001418:Baclofen / Q000008:administration & dosage; D002540:Cerebral Cortex / Q000737:chemistry* / Q000378:metabolism / Q000503:physiopathology; D018755:GABA Agonists / Q000008:administration & dosage; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D008297:Male; D008874:Midazolam / Q000008:administration & dosage; D008875:Middle Aged; D010146:Pain / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology*; D015742:Propofol / Q000008:administration & dosage; D013788:Thalamus / Q000737:chemistry* / Q000378:metabolism / Q000503:physiopathology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D018686:Anesthetics, Intravenous; D018755:GABA Agonists; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D001418:Baclofen; D008874:Midazolam; D015742:Propofol