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We report on the case of an elderly bilingual woman presenting with a diagnosis of primary progressive aphasia. The participant's native language was Friulian (L1), a predominantly oral Romance language, and her second language was Italian (L2), formally learned at primary school in oral and written forms. We investigated her linguistic abilities by means of the Bilingual Aphasia Test ( Paradis, M., & Libben, G. (1987). "The assessment of bilingual aphasia". Hillsdale, NJ: Lawrence Erlbaum Associates), which is specifically devised for studying language levels and skills in bilingual/polyglot individuals with aphasia. Specifically, we focused on different tasks extracted from the Bilingual Aphasia Test, targeting phonology, morphology, syntax and lexical semantics. Results show that both languages were affected to a clinically significant degree, but with different profiles in terms of linguistic levels, suggesting the presence of greater phonological, morphological, grammatical and syntactic impairments in L2. Results are discussed in terms of possible dissociations both within the language system of each language and between languages, within the Procedural/Declarative theoretical framework of language acquisition in bilinguals. (Contains 3 tables and 1 figure.)

Nine early non-demented bilingual (L1--Friulian, L2--Italian) patients with Parkinson's disease and nine normal controls matched for age, sex and years of education were studied on a spontaneous language production task. All subjects had acquired L1 from birth in a home environment and L2 at the age of six at school formally. Patients with PD evidenced more phonological, morphological and syntactic errors in L1 than in L2. The opposite pattern was observed in normal controls as far as grammar was concerned. These findings suggest that implicit language processing is more impaired than explicit language processing in Parkinson's disease. (Contains 2 tables.)

24 Italian medical students performed a task of verbal fluency. 12 students (the control group) receiving Normal Auditory Feedback and 12 students receiving Delayed Auditory Feedback (delay of 200 msec.) performed six trials in six different experimental settings: normal or increased speaking rate, and, for each condition, once with bilateral input of the auditory feedback, once to the right ear, and once to the left ear. At the normal speaking rate, the disruptive effect of delayed feedback was confirmed. As the speaking rate increased, the total number of errors increased within the control group but decreased within the group given delayed feedback, although the total number of errors was always greater for the latter. In addition, speech was more disrupted when the auditory input was returned to the right ear (left hemisphere) for all the different conditions: Normal and Delayed Auditory Feedback, normal and increased speaking rate. In particular, the left hemisphere was less resistant to the disruptive effect of the delayed feedback than the right hemisphere. From these results, we suggest that, when speaking more quickly, one uses more central mechanisms of movement programming (cortical-cerebellum-thalamus-cortical, cortical-corpus striatum-thalamus-cortical, and cortical-thalamus-cortical circuits), or attentional control (cortico-reticular-cortical circuits) than peripheral mechanisms (tactile, proprioceptive, and acoustic circuits). This may explain the decreased disruptive influence of delayed auditory feedback on speed, fluency, and quality at increased speaking rates. Hemispheric specialization processes, however, may explain the more pronounced susceptibility of the left hemisphere or the less pronounced susceptibility of the right hemisphere during the delayed feedback condition. In fact, the former processes phonemic, grammatical, and lexical features of words whilst the latter is competent in using metaphors and prosody in controlling the emotional aspects of language. Moreover, the right hemisphere is more active on attentional tasks.

Background: Habituation deficit, suggesting a deregulation of cortical excitability, represents a typical hallmark of interictal stages of migraine. We previously demonstrated that several neurophysiological markers of altered cortical excitability are significantly correlated to spontaneous clinical fluctuations of migraine. We therefore aimed at verifying whether clinical fluctuations are correlated to specific patterns of somatosensory evoked potential (SEP) habituation., Methods: We analyzed habituation after median nerve stimulation of both high-frequency oscillations (HFOs) and N20 SEP in 25 migraine patients and 18 healthy volunteers. Subjects underwent six consecutive series of 500 stimuli., Results: Migraine patients as a whole showed a significant habituation deficit of the N20 response. Moreover, spontaneously worsening patients show a clear potentiation of this wave in the last block of stimuli, whereas in spontaneously improving patients the N20 amplitude remained stable. Presynaptic HFOs were smaller in worsening patients and larger in improving ones, but they did not undergo habituation in patients as well as in healthy subjects., Conclusions: Potentiation of the N20 response in spontaneously worsening migraineurs confirms that the reduction of the thalamocortical drive plays a major role in migraine pathogenesis. Moreover, the stable pattern we observed in spontaneously improving patients suggests that compensatory mechanisms can also play an important role. The normal response to repeated stimuli of HFOs in migraineurs might indicate that, although its initial amount depends on clinical conditions, high-frequency thalamocortical drive remains stable during the stimulation and probably reflects the activity of a buffer mechanism.