Lack of effect of topiramate for central pain.
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Biomedical subjects
Publications and source records attributed to S Canavero.
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Pain syndromes due to peripheral or central nervous system damage, or both, may hinder neurorehabilitation. Control of pain may be obtained by ablative or augmentative procedures. Of the ablative modes only DREZ and Cordectomy are still being employed in cases of pain due to Brachial Plexus Avulsion and conus and cauda damage at T9-L1: in both pain is not simply due to "deafferentiation". The augmentative procedures include spinal cord, deep brain and cortical stimulation. Subarachnoid infusion of drugs (midazolam, clonidine, baclofen, etc.) is a new avenue open to control pain. Indications, results and mechanisms of action of those procedures in neuropathic pain are discussed on the basis of literature and personal experience.
We report two cases of central pain which receded completely after treatment of the inciting lesion. These cases highlight the intrinsic reversibility of central pain and the focal nature of central pain mechanisms.
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An exceptional case of long-standing central pain temporarily relieved by a focal stroke in the primary somatosensory area is reported. This case highlights the focal nature of central pain mechanisms and the possible value of selective subparietal leukotomies in the management of central pain.
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In this report, the authors describe a case in which the patient began to experience a supernumerary phantom arm after she received motor cortex stimulation for central pain. The patient had a history of right thalamocapsular stroke. It is speculated that the motor cortex activation triggered a response in the patient's parietal lobe, precipitating perception of the phantom limb. To the authors' knowledge this is the first reported case of its kind.
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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.
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