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RESEARCH ROUNDUP: Foreign Accent Syndrome

6/16/2014

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Foreign Accent Syndrome

I was once mistaken for a native of Québec while speaking French to a native French speaker, and I couldn’t have been happier since I’d worked so hard at minimizing my American accent. Unfortunately, changes in accent are sometimes very much unwanted, unexpected, and distressing. Foreign accent syndrome is a rare condition that is characterized by changes in the fine execution of speech, giving to hearers the impression that the individual is not a native speaker of the language or that their typical accent has been altered. Because of its rare occurrence, understanding the neural underpinnings of the foreign accent syndrome is difficult and often based on case studies. 

 
ABSTRACT

Foreign accent syndrome: a multimodal evaluation in the search of neuroscience-driven treatments.

Foreign accent syndrome (FAS) is a rare condition which is placed in the mildest end of the spectrum of speech disorders. The impairment, not severe enough to elicit phonological errors, is associated with various alterations in the fine execution of speech sounds which cause the impression of foreignness. There is a growing interest in the study of linguistic and paralinguistic components, psychosocial aftermaths, and neural basis of FAS, but there are not yet neuroscience-driven treatments for this condition. A multimodal evaluation was conducted in a single patient with the aim of searching for clues which may assist to design neuroscience-driven therapies. The patient was a middle-aged bilingual woman who had chronic FAS. She had segmental deficits, abnormal production of linguistic and emotional prosody, impaired verbal communication, and reduced motivation and social engagement. Magnetic resonance imaging showed bilateral small lesions mainly affecting the left deep frontal operculum and dorsal anterior insula. Diffusion tensor tractography suggested disrupted left deep frontal operculum-anterior insula connectivity. Metabolic activity measured with positron emission tomography was primarily decreased in key components of networks implicated in planning and execution of speech production, cognitive control and emotional communication (Brodmann's areas 4/6/9/10/13/25/47, basal ganglia, and anterior cerebellar vermis). Compensatory increases of metabolic activity were found in cortical areas (left anterior cingulate gyrus, left superior temporal gyrus and right prefrontal cortex) associated with feedback and focal attention processes critical for monitoring and adjustment of verbal utterances. Moreover, bilateral structural and functional abnormalities probably interrupted the trajectory of the lateral and medial cholinergic pathways causing region-specific hypoactivity. The results from this study provide targets for further investigation and some clues to design therapeutic interventions.

[Moreno-Torres, et al. (2013). Neuropsychologia, 51(3): 520.537.]


FURTHER READING

Two French-speaking cases of foreign accent syndrome: an acoustic-phonetic analysis. [Roy, et al. (2012). Clinical Linguistics & Phonetics, 26(11-12): 934.945.]

Neural bases of the foreign accent syndrome: a functional magnetic resonance imaging case study. [Katz, et al. (2012). Neurocase, 18(3): 199.211.]Multidisciplinary assessment and diagnosis of conversion disorder in a patient with foreign accent syndrome. [Jones, et al. (2011). Behavioural Neurology, 24(3): 245-255.]Video of Australian news piece about Foreign Accent Syndrome



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RESEARCH ROUNDUP: Dementia with Lewy Bodies

6/2/2014

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Dementia with Lewy Bodies

Dementia with Lewy Bodies (DLB) is a progressive neurodegenerative condition that is construed on a spectrum between Alzheimer's disease and Parkinson's disease. Core symptoms of LBD are gradual cognitive decline, fluctuation in alertness, visual hallucinations, and parkinsonism (motor symptoms such as rigidity, gait changes, or bradykinesia). Pathophysiology of DLB consists of the build-up of Lewy bodies, which are composed of α-synuclein protein. Treatment and management usually includes acetylcholinesterase inhibitors, such as donepezil and rivastigmine, for cognitive symptoms and occasionally levodopa for parkinsonian features.

ABSTRACT:
Dementia with Lewy Bodies
The advent of new immunostains have improved our ability to detect limbic and cortical Lewy bodies, and it is now evident that Dementa with Lewy bodies (DLB) is the second most common neurodegenerative dementia, after Alzheimer’s disease (AD). Distinguishing DLB from AD has important implications for treatment, in terms of substances that may worsen symptoms (i.e., anticholinergic and certain neuroleptic medications) and those that may improve them (i.e., cholinesterase inhibitors, carbidopa-levodopa). Neurocognitive patterns, psychiatric features, extrapyramidal signs and sleep disturbance are helpful in differentiating DLB from AD early in the disease course. Differences in the severity of cholinergic depletion as well as type and distribution of neuropathology contribute to these clinical differences, though DLB patients with a high density of co-occuring AD pathology are less clinical distinguishable from AD. [Ferman, T. J. & Boeve, B. F. (2007), Neurologic Clinic, 25 (3), 741-760]

ABSTRACT: 
Neuropsychological Characteristics of Dementia with Lewy Bodies and Parkinson’s Disease with Dementia: Differentiation, Early Detection, and Implications for “Mild Cognitive Impairment” and Biomarkers
Parkinson’s disease with dementia (PDD) and dementia with Lewy bodies (DLB) are neurodegenerative conditions sharing a disorder of α-synuclein metabolism. Temporal differences in the emergence of symptoms and clinical features warrant the continued clinical distinction between DLB and PDD. While DLB and PDD groups’ neuropsychological profiles often differ from those in Alzheimer’s disease (AD), the diagnostic sensitivity, specificity, and predictive values of these profiles remain largely unknown. PDD and DLB neuropsychological profiles share sufficient similarity to resist accurate and reliable differentiation. Although heterogeneous cognitive changes (predominantly in memory and executive function) may manifest earlier and more frequently than previously appreciated in Parkinson’s disease (PD), and executive deficits may be harbingers of dementia, the enthusiasm to uncritically extend the concept of mild cognitive impairment (MCI) to PD should be tempered. Instead, future research might strive to identify the precise neuropsychological characteristics of the prodromal stages of PD, PDD, and DLB which, in conjunction with other potential biomarkers, facilitate early and accurate diagnosis, and the definition of neuroprotective, neurorestorative, and symptomatic treatment endpoints. [Tröster, A. (2008), Neuropsychology Review, 18, 103–119]

FURTHER READING:
  • Mild cognitive impairment associated with underlying Alzheimer’s disease versus Lewy body disease [Boeve, B.F. (2012),Parkinsonism and Related Disorders, 18S1, S41–S44]
  • Amyloid PET Imaging in Lewy Body Disorders. [Donaghy P, Thomas AJ, O'Brien JT. (2013),American Journal of Geriatric Psychiatry,doi: 10.1016/j.jagp.2013.03.001. [Epub ahead of print]
  • Dementia with Lewy bodies. Review of diagnosis and pharmacologic management. [Frank C. (2003),Canadian Family Physician, 49, 1304-1311]

About the Contributor:

Surabhi Patwardhan, Ph. D. is a post-doctoral resident in clinical neuropsychology at the Arizona Psychology Training Consortium.
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