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Neuroanatomical foundations of naming impairments across different neurologic conditions.

ABSTRACT: The ability to name objects or abstract entities is an essential feature of speech and language, being commonly considered a central component of normal neurologic function. For this reason, the bedside testing of naming performance is part of the neurologic examination, especially since naming impairments can signify the early onset of a progressive disease or the occurrence of a more established problem. Modern neuroscience research suggests that naming relies on specific and distributed networks that operate in concert to support various processing stages, spanning from object recognition to spoken words. Likewise, studies evaluating the types of naming impairments in patients with neurologic conditions have contributed to the understanding of acquired forms of naming impairments and the underlying stages during normal language processing. In this article, we review the neurobiological mechanisms supporting naming, with a focus on the clinical application of these concepts. We provide an overview of the stages of cognitive processing that are hypothesized to support naming. For each stage, we explore the evidence revealing its neural basis, drawing parallels to clinical syndromes that commonly disrupt each stage. We review the patterns of naming impairment across various neurologic conditions, including classic language disorders, such as poststroke aphasia or primary progressive aphasia, as well as other diseases where language impairments may be subtle but helpful for the appropriate diagnosis. In this context, we provide a structured and practical guide for the bedside naming assessments rooted in modern neuroscience, aimed at supporting the evaluation and diagnosis of neurologic conditions that affect language.

SUBMITTER: Gleichgerrcht E

PROVIDER: S-EPMC4516297 | biostudies-literature | 2015 Jul

REPOSITORIES: biostudies-literature

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Neuroanatomical foundations of naming impairments across different neurologic conditions.

Gleichgerrcht Ezequiel E Fridriksson Julius J Bonilha Leonardo L

Neurology 20150626 3

The ability to name objects or abstract entities is an essential feature of speech and language, being commonly considered a central component of normal neurologic function. For this reason, the bedside testing of naming performance is part of the neurologic examination, especially since naming impairments can signify the early onset of a progressive disease or the occurrence of a more established problem. Modern neuroscience research suggests that naming relies on specific and distributed netwo ...[more]

PMID: 26115732

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Project description:In order to gain a better understanding of aphasia one must consider the complex combinations of language impairments along with the pattern of paraphasias. Despite the fact that both deficits and paraphasias feature in diagnostic criteria, most research has focused only on the lesion correlates of language deficits, with minimal attention on the pattern of patients' paraphasias. In this study, we used a data-driven approach (principal component analysis - PCA) to fuse patient impairments and their pattern of errors into one unified model of chronic post-stroke aphasia. This model was subsequently mapped onto the patients' lesion profiles to generate the triangulation of language-cognitive impairments, naming errors and their neural correlates. Specifically, we established the pattern of co-occurrence between fifteen error types, which avoids focussing on a subset of errors or the use of experimenter-derived methods to combine across error types. We obtained five principal components underlying the patients' errors: omission errors; semantically-related responses; phonologically-related responses; dysfluent responses; and a combination of circumlocutions with mixed errors. In the second step, we aligned these paraphasia-related principal components with the patients' performance on a detailed language and cognitive assessment battery, utilising an additional PCA. This omnibus PCA revealed seven unique fused impairment-paraphasia factors: output phonology; semantics; phonological working memory; speech quanta; executive-cognitive skill; phonological (input) discrimination; and the production of circumlocution errors. In doing so we were able to resolve the complex relationships between error types and impairments. Some are relatively straightforward: circumlocution errors formed their own independent factor; there was a one-to-one mapping for phonological errors with expressive phonological abilities and for dysfluent errors with speech fluency. In contrast, omission-type errors loaded across both semantic and phonological working memory factors, whilst semantically-related errors had the most complex relationship by loading across four factors (phonological ability, speech quanta, executive-cognitive skills and circumlocution-type errors). Three components had unique lesion correlates: phonological working memory with the primary auditory region; semantics with the anterior temporal region; and fluency with the pre-central gyrus, converging with existing literature. In conclusion, the data-driven approach allowed derivation of the triangulation of deficits, error types and lesion correlates in post-stroke aphasia.

Project description:Integrating multiple assessment parameters of motor behavior is critical for understanding neural activity dynamics during motor control in both intact and dysfunctional nervous systems. Here, we described a novel approach (termed Multifactorial Behavioral Assessment (MfBA)) to integrate, in real-time, electrophysiological and biomechanical properties of rodent spinal sensorimotor network activity with behavioral aspects of motor task performance. Specifically, the MfBA simultaneously records limb kinematics, multi-directional forces and electrophysiological metrics, such as high-fidelity chronic intramuscular electromyography synchronized in time to spinal stimulation in order to characterize spinal cord functional motor evoked potentials (fMEPs). Additionally, we designed the MfBA to incorporate a body weight support system to allow bipedal and quadrupedal stepping on a treadmill and in an open field environment to assess function in rodent models of neurologic disorders that impact motor activity. This novel approach was validated using, a neurologically intact cohort, a cohort with unilateral Parkinsonian motor deficits due to midbrain lesioning, and a cohort with complete hind limb paralysis due to T8 spinal cord transection. In the SCI cohort, lumbosacral epidural electrical stimulation (EES) was applied, with and without administration of the serotonergic agonist Quipazine, to enable hind limb motor functions following paralysis. The results presented herein demonstrate the MfBA is capable of integrating multiple metrics of motor activity in order to characterize relationships between EES inputs that modulate mono- and polysynaptic outputs from spinal circuitry which in turn, can be used to elucidate underlying electrophysiologic mechanisms of motor behavior. These results also demonstrate that proposed MfBA is an effective tool to integrate biomechanical and electrophysiology metrics, synchronized to therapeutic inputs such as EES or pharmacology, during body weight supported treadmill or open field motor activities, to target a high range of variations in motor behavior as a result of neurological deficit at the different levels of CNS.

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Neuroanatomical foundations of naming impairments across different neurologic conditions.

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Neuroanatomical foundations of naming impairments across different neurologic conditions.

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