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Multimodal Protocol for Assessing Metacognition and Self-Regulation in Adults with Learning Difficulties
Published on: September 27, 2020
[Communication disorders: differential diagnosis]
J Campos-Castelló1, S Briceño-Cuadros
1Hospital Clinico Universitario San Carlos, Madrid, España. jcampos@hcsc.insalud.es
Objective:
To evaluate components of clinical semiology in the differential diagnosis of communication disorders (TC) and their possible biological markers. We consider two groups, according to the communication disorders themselves and their effects on social interaction. In the first case both aspects are affected in parallel and in the second it is predominantly social interaction which is affected.
Development:
In the first groups we studied dyslalias, dyrhrythmias, acquired aphasias, TC relation to epilepsy, types of seizures and EEG discharges. The dysphasia of development and epilepsy may be associated by chance, as a result of the same cause or the epilepsy be responsible for the TC, either because of seizures or continuously (acquired epileptic aphasia, SLK). Based on personal data and the literature we studied the semiology, possible biological markers and differential diagnosis. We consider disorders of neurone migration and metabolic alterations of initial neuropsychological semiology and cerebellar anomalies involved in cognitive functions. In the second group we assessed autism, generalized disorders of development and particular syndromes with semantic pragmatic TC.
Conclusions:
The development of language cannot be separated from other aspects of neurological maturation. One cannot affirm that there is a direct relationship between epilepsy and TC, although this does occur in some cases. We accept the hypothesis that SLK, POCSL and atypical EPB are clinical forms of the same syndrome of epilepsy. Recognition of the cognitive affective cerebellar syndrome by its involvement in social executive function, language and personality characterizes certain conditions (Williams, Asperger, fragile X, autism). A progressive rational battery of complementary studies on clinical data is essential to determine biological markers in syndromes which still lack them.
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