OBJECTIVE: Alexithymia has a high prevalence in patients with chronic or somatoform pain disorders. Various investigations demonstrated a hypersensitivity and low tolerance of alexithymics to touch and painful stimulation. It was argued that alexithymic characteristics may lead an individual to augment stimuli in order to prevent ignoring stimuli that might be dangerous. Therefore, there may be a relation to the reducer-augmenter construct. To test this hypothesis, cortical reactivity in response to unpleasant acoustical stimulation was measured. METHODS: Nineteen high alexithymics and 18 low alexithymics were stimulated with five series of acoustic stimuli (white noise) of different intensity levels. Evoked potentials were recorded at electroencephalogram electrodes Fz, Cz, and Pz. RESULTS: With ascending stimulus intensities, both groups showed increasing P1-N1 and N1-P2 peak-to-peak amplitudes. High alexithymics had higher P1-N1 amplitudes and a stronger intensity-dependent slope of P1-N1 amplitude. In contrast to that, N1-P2 amplitude of low alexithymics tended to decrease in response to the highest stimulus intensity level. CONCLUSION: High alexithymic subjects seem to behave like cortical augmenters. This may be due to a disturbed transmarginal inhibition, which may normally serve as a protective physiological mechanism.
OBJECTIVE: Alexithymia has a high prevalence in patients with chronic or somatoform pain disorders. Various investigations demonstrated a hypersensitivity and low tolerance of alexithymics to touch and painful stimulation. It was argued that alexithymic characteristics may lead an individual to augment stimuli in order to prevent ignoring stimuli that might be dangerous. Therefore, there may be a relation to the reducer-augmenter construct. To test this hypothesis, cortical reactivity in response to unpleasant acoustical stimulation was measured. METHODS: Nineteen high alexithymics and 18 low alexithymics were stimulated with five series of acoustic stimuli (white noise) of different intensity levels. Evoked potentials were recorded at electroencephalogram electrodes Fz, Cz, and Pz. RESULTS: With ascending stimulus intensities, both groups showed increasing P1-N1 and N1-P2 peak-to-peak amplitudes. High alexithymics had higher P1-N1 amplitudes and a stronger intensity-dependent slope of P1-N1 amplitude. In contrast to that, N1-P2 amplitude of low alexithymics tended to decrease in response to the highest stimulus intensity level. CONCLUSION: High alexithymic subjects seem to behave like cortical augmenters. This may be due to a disturbed transmarginal inhibition, which may normally serve as a protective physiological mechanism.