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Brain, Vol. 119, No. 6, 1991-2004, 1996
© 1996 Guarantors of Brain


research-article

Startle reflex and emotion modulation impairment after a right amygdala lesion

Alessandro Angrilli1,, Alessandra Mauri2, Daniela Palomba1, Herta Flor4, Niels Birbaumer1,3, Giuseppe Sartori1 and Francesco di Paola2

1Department of General Psychology, University of Padua Treviso, Italy 2Regional Hospital of Treviso Treviso, Italy 3Institute of Medical Psychology and Behavioural Neurobiology, University of Tübingen Berlin, Germany 4Department of Psychology, Humboldt-University Berlin, Germany

Correspondence to: Correspondence to: Alessandro Angrilli, Dipartimento di Psicologia Generale, Via Venezia 8, 35131 Padova, Italy

In the present study, startle responses during resting states as well as during the presentation of a set of emotive slides were recorded from a 32-year-old male patient with a rare localized lesion of the right amygdala. The startle reflex is a response modulated by affective states: it has been reliably used in the literature to measure the aversiveness of emotive stimuli. The animal literature has shown that the circuit of this reflex is directly influenced by amygdala projections. The startle responses of the patient were compared with those of eight age-matched normal subjects. The patient's startle amplitudes showed an overall impaired response and an inhibited reflex contralateral to the lesion. In addition, he failed to show the typical startle potentiation induced by an aversive emotive background. The data confirm, in the human, previous results from the literature in other species on amygdala involvement in startle and emotional responses. Furthemore, the observation of the importance of the right amygdala in the modulation of emotion is consistent with the hypothesis of right hemisphere specialization for aversive emotions. The results are discussed in the context of the literature on human amygdala lesions.

emotion; startle reflex; amygdala; right hemisphere

Received October 27, 1995. Revised June 20, 1996. Accepted August 8, 1996.


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