The Edinburgh cognitive and behavioral amyotrophic lateral sclerosis screen (ECAS):Sensitivity in differentiating between ALS and Alzheimer's disease in a Greek population

International audienceObjectives: (1) Adapt the ECAS into Greek, validate it in ALS patients and compare with the ALS-CBS. (2) Determine the sensitivity and specificity of ECAS in the differentiation between AD and non-demented ALS patients as compared with the ACE-III and mini-ACE. Methods: ALS patients (n = 28) were recruited and AD patients (n = 26) were matched in age, sex, and education with ALS patients (n = 24). The normative data were derived from a random sample of controls (n = 52). Bayes correlation analysis was conducted to examine convergent validity. Bayes t-test was performed to assess between groups’ differences. Receiver operating characteristics (ROC) curve analyses and area under the curve (AUC) were implemented to appraise the sensitivity and specificity in the differentiation between the AD and non-demented ALS patients. Results: The ECAS and its sub-scores in addition to the behavior interview demonstrated robust correlations with the ALS-CBS. Impairment in language and verbal fluency were the most prominent deficits in the ALS patients. The most frequently reported change was apathy. The ROC analysis demonstrated that the ECAS-ALS nonspecific score (comprising memory and visuospatial domains) is the most sensitive and specific in differentiating the AD from ALS patients. The other measures expressed high sensitivity, yet a poor specificity. Conclusions: The ECAS is a multi-purpose screening tool. The ECAS-ALS specific appraises the whole spectrum of the highly prevalent cognitive impairments in ALS. The ECAS-ALS nonspecific (memory and visuospatial) is a sensitive score to detect AD related deficits and is able to differentiate the AD from the non-demented ALS patients better than the ACE-III and mini-ACE

Syntactic predictions and asyntactic comprehension in aphasia: Evidence from scope relations

People with aphasia (PWA) often fail to understand syntactically complex sentences. This phenomenon has been described as asyntactic comprehension and has been explored in various studies cross-linguistically in the past decades. However, until now there has been no consensus among researchers as to the nature of sentence comprehension failures in aphasia. Impaired representations accounts ascribe comprehension deficits to loss of syntactic knowledge, whereas processing/resource reduction accounts assume that PWA are unable to use syntactic knowledge in comprehension due to resource limitation resulting from the brain damage. The aim of this paper is to use independently motivated psycholinguistic models of sentence processing to test a variant of the processing/resource reduction accounts that we dub the Complexity Threshold Hypothesis. According to this hypothesis, PWA are capable of building well-formed syntactic representations, but, because their resources for language processing are limited, their syntactic parser fails when processing complexity exceeds a certain threshold. The source of complexity investigated in the experiments reported in this paper is syntactic prediction. We conducted two experiments involving comprehension of sentences with different types of syntactic dependencies, namely dependencies that do not require syntactic prediction (i.e. unpredictable dependencies in sentences that require Quantifier Raising) and dependencies whose resolution requires syntactic predictions at an early stage of processing based on syntactic cues (i.e. predictable dependencies in movement-derived sentences). In line with the predictions of the Complexity Threshold Hypothesis, the results show that the agrammatic patients that participated in this study had no difficulties comprehending sentences with the former type of dependencies, whereas their comprehension of sentences with the latter type of dependencies was impaired

Neural competition via lateral inhibition between decision processes and not a STOP signal accounts for the antisaccade performance in healthy and schizophrenia subjects

A commentary on Re-starting a neural race: anti-saccade correction by Noorani, I., and Carpenter, R. H. S. (2014). Eur. J. Neurosci. 39, 159–164. doi: 10.1111/ejn.12396 Decision making is the process of accumulating evidence about the world and the utility of possible outcomes (Cutsuridis, 2010). A paradigm often used by behavioral neuroscientists to investigate decision processes is the antisaccade paradigm (see Figure 1A; Hallett, 1978). In the antisaccade paradigm subjects are required to suppress an erroneous saccade (error prosaccade) toward a peripheral stimulus and instead make an eye movement to a position in the opposite hemifield (antisaccade). The response repertoire of a subject performing the antisaccade task has been reported to be: (1) the subject makes an erroneous response (i.e., looking toward the peripheral stimulus), (2) the subject makes the antisaccade (i.e., looking in the opposite direction of the peripheral stimulus, and (3) the subject makes an erroneous response followed by a corrected antisaccade (Evdokimidis et al., 2002)

A biophysical model of decision making in an antisaccade task through variable climbing activity

We present a biophysical model of saccade initiation based on competitive integration of planned and reactive cortical saccade decision signals in the intermediate layer of the superior colliculus. In the model, the variable slopes of the climbing activities of the input cortical decision signals are produced from variability in the conductances of Na+, K+, Ca2+ activated K+, NMDA and GABA currents. These cortical decision signals are integrated in the activities of buildup neurons in the intermediate layer of the superior colliculus, whose activities grow nonlinearly towards a preset criterion level. When the level is crossed, a movement is initiated. The resultant model reproduces the unimodal distributions of saccade reaction times (SRTs) for correct antisaccades and erroneous prosaccades as well as the variability of SRTs (ranging from 80ms to 600ms) and the overall 25% of erroneous prosaccade responses in a large sample of 2006 young men performing an antisaccade task

Clinical and Radiological Markers of Extra-Motor Deficits in Amyotrophic Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is now universally recognized as a complex multisystem disorder with considerable extra-motor involvement. The neuropsychological manifestations of frontotemporal, parietal, and basal ganglia involvement in ALS have important implications for compliance with assistive devices, survival, participation in clinical trials, caregiver burden, and the management of individual care needs. Recent advances in neuroimaging have been instrumental in characterizing the biological substrate of heterogeneous cognitive and behavioral deficits in ALS. In this review we discuss the clinical and radiological aspects of cognitive and behavioral impairment in ALS focusing on the recognition, assessment, and monitoring of these symptoms

Why is it difficult to predict language impairment and outcome in patients with aphasia after stroke?

One of the most devastating consequences of stroke is aphasia. Communication problems after stroke can severely impair the patient's quality of life and make even simple everyday tasks challenging. Despite intense research in the field of aphasiology, the type of language impairment has not yet been localized and correlated with brain damage, making it difficult to predict the language outcome for stroke patients with aphasia. Our primary objective is to present the available evidence that highlights the difficulties of predicting language impairment after stroke. The different levels of complexity involved in predicting the lesion site from language impairment and ultimately predicting the long-term outcome in stroke patients with aphasia were explored. Future directions and potential implications for research and clinical practice are highlighted

The Clinical and Radiological Spectrum of Hippocampal Pathology in Amyotrophic Lateral Sclerosis

Hippocampal pathology in Amyotrophic Lateral Sclerosis (ALS) remains surprisingly under recognized despite compelling evidence from neuropsychology, neuroimaging and neuropathology studies. Hippocampal dysfunction contributes significantly to the clinical heterogeneity of ALS and requires structure-specific cognitive and neuroimaging tools for accurate in vivo evaluation. Recent imaging studies have generated unprecedented insights into the presymptomatic and longitudinal processes affecting this structure and have contributed to the characterisation of both focal and network-level changes. Emerging neuropsychology data suggest that memory deficits in ALS may be independent from executive dysfunction. In the era of precision medicine, where the development of individualized care strategies and patient stratification for clinical trials are key priorities, the comprehensive review of hippocampal dysfunction in ALS is particularly timely