ItaL J. Neurol. Sci V: 77-83, 1984 Speech suppression without aphasia after bilateral perisylvian softenings (bilateral rolandic operculum damage) Villa G., Caltagirone C. Clinica Neurologica, Universit3 Cattolica del S. Cuore di Roma. The authors describe a patient who suffered two successive, right and left, strokes that caused bilateral rolandic operculum damage. The clinical picture was characterized by selective impairment of volitionalfacio-pharyngo-glosso- masticatory movements with sparing of automatic and reflex motor activity (Foix-Chavany-Marie syndrome). Though completely speechless, the patient was not aphasic. This dissociation is discussed in the light of the peculiar localization of lesions evidenced by CT-scan. Key-Words : Bilateral rolandic operculum softenings -- Foix-Chavany-Marie syndrome -- speech suppression without aphasia -- CT-scan. Introduction Bilateral destruction of the rolandic operculum caused by perisylvian infarctions may result in the so-called 'bilateral anterior opercular syn- drome' [9] or Foix-Chavany-Marie (FCM) syn- drome [5]. This uncommon neurological disord- er is characterized by the selective impairment of voluntary movements -- with preservation of automatic and reflex motor activity -- in the lower cranial nerve distributions (V, VII and IX through XII) of both sides. It was first described by Magnus in 1837 [8] and then reported almost exclusively in the French literature [1, 3, 5, 11] with some exceptions [2, 4, 9]. We report a typical case of FCM syndrome. It presented with an acute facio-pharyngo-glosso- masticatory diplegia and automatic-voluntary dissociation of the affected muscles. CT-scan showed bilateral damage: the left hemisphere lesion was confined to the rolandic operculum; in the right hemisphere the whole territory of the middle cerebral artery was involved. There are two main reasons for the present case report: Firstly, even if FCM syndrome has a localizing value, it is often misdiagnosed because the neu- rological picture is very similar to that of the more frequent bulbar and peripheral palsies. Thus, from a clinico-methodological point of view, the procedures that led to the diagnosis in our case are worth emphasizing. Briefly: a) FCM syndrome, being the cortical type of pseu- dobulbar paralysis, can be differentiated from peripheral and bulbar syndromes on the basis of clinical and electromyographic signs of supran- uclear neuronal damage; b) beyond the general characteristics of a pseudobulbar deficit, some peculiar clinical features of FCM syndrome point to a cortical localization of lesions; c) CT- scanning clinches the diagnosis by disclosing the bilateral perisylvyan softenings including the rolandic operculum of both sides. Secondly, the patient we describe was complete- ly speechless, but not aphasic, as revealed by neuropsychological examination. Her speech 77