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Excerpt
The role of somatosensory cortex in the genesis of neurogenic pain has been recently emphasized.1 Exceptional cases of sudden disappearance of neurogenic pain may result from focal lesions between the parietal and pericentral somatosensory cortex and the thalamus, interrupting an out-of-balance oscillatory loop.2 We describe a patient with neurogenic pain transiently relieved following accidental subparietal ischemia. This is also an exceptional case of ipsilaterality of pain processing.
This 52-year-old woman had undergone selective left trigeminal rhizotomies in the posterior fossa for treatment of refractory trigeminal neuralgia.3 She developed drugresistant left facial anesthesia dolorosa. Neurometabolic assessment showed left (sic!) parietofrontal hypoperfusion and thalamic disactivation (Fig. 1). Her pain was 100% responsive to subhypnotic propofol infusion.3 This led to 100% analgesia with left (sic!) parietal cortex (see Fig. 1) stimulation (surgical protocol4). Unfortunately, all effect was lost within 2 months. Immediately before removal of the electrodes, a further trial of stimulation was unsuccessfully administered. At this time, 12 months after successful implantation, her response to propofol was markedly diminished, and at higher voltages, pain was worsened. Within 3 days, pain vanished. A window-adjusted computed tomographic scan demonstrated a subcortical wedge of anomalous density (Fig. 2A); Magnetic resonance imaging disclosed subparietal hypointensity plus frontal lobe hypointensity (Fig. 2B). All findings were on the left (sic!) side. SPECT showed renormalization of the primary somatosensory area (SI) and primary motor-sensory area (MI) blood flow, plus an area of nearabsent flow forward in the frontal lobe (see Fig. 1). After 3 weeks, the pain gradually reappeared.
This pain was the result of an anomalous generator in the somatosensory cortex and thalamus. This generator was GABA (propofol)-responsive, likely the result of denervation-triggered GABA decrease at central levels. In our model, central pain is subtended by a relative glutamatergic(excitatory) hypertonus following GABA decrease: this uncurbed overexcitation is responsible for both pain and cortical anomaly.5,6 In this patient, focal parietal ischemia curtailed a glutamatergic hyperdrive (from lower stations), thus renormalizing a physiologic GABA-glutamate balance at central levels (justifying why ischemia was not visible as an area of absence of flow). As ischemia subsided, so did the pain.
This case supports the notion that cortical(mainly somatosensory2,7,8) ablation can relieve central neurogenic pain: focal stereotactic lesions in the subparietal white matter may be even better for achieving pain resolution, with minimal tissue damage,2,8 as suggested by two previous studies.10,11
In conclusion, parietal lobe surgery9 needs reevaluation.
