The gate control theory of pain (Melzack and Wall, 1965) suggests that tactile stimuli can decrease the perception of pain. We have found the reverse effect: Heat at levels that induce pain can substantially suppress tactile sensitivity, independently of shifts in attention or arousal. Ten human observers were stimulated by a tonic, pain-producing heat stimulus and vibrotactile stimuli (1, 10, and 100 Hz) coincidentally presented to the right thenar eminence. Vibrotactile thresholds were assessed with the skin at a normative temperature of 31 degrees C and at higher temperatures producing pain. Increases in vibrotactile thresholds (mean change = 7.3 dB) occurred at skin temperatures just below and above those that induced pain. Furthermore, absolute-magnitude estimates of suprathreshold vibrotactile stimuli determined during the same experiments showed decreased sensitivity and psychophysical recruitment. The changes are not attributable to attentional or arousal shifts, since they were not associated with changes in auditory thresholds. Furthermore, the changes occurred just below the subjects' pain thresholds (where nociceptors are presumably activated). This over-twofold diminution of vibrotactile sensitivity suggests that heat stimuli capable of inducing pain can significantly diminish taction, perhaps through a "touch gate" in a manner similar to the gate control theory proposed for pain.

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Optimal management of symptomatic cavernous angiomas (CA) located in the thalamus and the brainstem is problematic. Clinical and radiological (MRI) follow-up series suggest that having hemorrhaged once, recurrent hemorrhage with progressive neurologic dysfunction may commonly occur. We have therefore chosen to treat these lesions when first symptomatic with stereotactic linear radiosurgery (SLR). We now report, after a median follow-up of 27 months, 12 patients with CAs (9 women, 3 men, mean age 40 years) treated in this fashion. Ten patients presented with hemorrhage (3 had more than one hemorrhage): two patients had new onset seizures. All patients had enhanced MRI/MRAs characteristic of CA. There were five brainstem and five thalamic CAs, and one each in the temporal lobe and insula. Cerebral angiograms were done in 8 patients for comparison with their respective MRAs. Only one CA was visualized in the late venous phase on cerebral angiogram and identical vascular features were appreciated on the MRA. The diameter of the CAs ranged from 1.0 to 3.0 cm with a mean of 1.6 cm. Dosimetry planning was based on MRI/CT features and the mean dose at the isocenter was 2.167 cGy (range = 2,000–2,500 cGy) delivered with a mean collimation diameter of 1.46 cm (range = 1.0–2.0 cm). All 12 patients continued to improve neurologically after SLR and had MRI-documented changes in their lesions: in general, the lesions became smaller and signal characteristics converted to methe-maglobin. However, 1 patient had an early post-SLR hemorrhage, documented by MRI, at 4.5 months. This patient''s lateral mesencephalic syndrome subsequently resolved and he was functionally improved, compared with baseline, at 22 months. Two patients developed hemiparesis at 7 and 9 months following SLR. One patient had a large pontine CA (2.0 cm) and the other a small peduncle CA (1.1 cm). Both patients had delayed brainstem radiation injury without rebleed documented on Gd-DTPA MRI. Three additional patients underwent SLR safety but have been followed less than 6 months each. Our experience suggests that radiosurgery for cavernous angioma protects against rebleed (though, as expected, not early rebleeds) as a recent study indicated a median of 12 months to recurrent hemorrhage. Delayed radiation injury may occur more frequently than expected from conventional dosimetry when this technique is used deep within the brain. We now target the lesion margins more conservatively by excluding the surrounding hemosiderin-stained parenchyma.

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