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Marcelo L. Berthier – One of the best experts on this subject based on the ideXlab platform.

  • Poststroke Aphasia
    Drugs & Aging, 2005
    Co-Authors: Marcelo L. Berthier
    Abstract:

    Aphasia, the loss or impairment of language caused by brain damage, is one of the most devastating cognitive impairments of stroke. Aphasia is present in 21–38% of acute stroke patients and is associated with high short- and long-term morbidity, mortality and expenditure. Recovery from Aphasia is possible even in severe cases. While speech-language therapy remains the mainstay treatment of Aphasia, the effectiveness of conventional therapies has not been conclusively proved. This has motivated attempts to integrate knowledge from several domains in an effort to plan more rational therapies and to introduce other therapeutic strategies, including the use of intensive language therapy and pharmacological agents. Several placebo-controlled trials suggest that piracetam is effective in recovery from Aphasia when started soon after the stroke, but its efficacy vanishes in patients with chronic Aphasia. Drugs acting on catecholamine systems (bromocriptine, dexamfetamine) have shown varying degrees of efficacy in case series, open-label studies and placebo-controlled trials. Bromocriptine is useful in acute and chronic Aphasias, but its beneficial action appears restricted to nonfluent Aphasias with reduced initiation of spontaneous verbal messages. Dexamfetamine improves language function in subacute Aphasia and the beneficial effect is maintained in the long term, but its use is restricted to highly selected samples. Pharmacological agents operating on the cholinergic system (e.g. donepezil) have shown promise. Data from single-case studies, case series and an open-label study suggest that donepezil may have beneficial effects on chronic poststroke Aphasia. Preliminary evidence suggests that donepezil is well tolerated and its efficacy is maintained in the long term. Randomised controlled trials of donepezil and other cholinergic agents in poststroke Aphasia are warranted.

  • poststroke Aphasia epidemiology pathophysiology and treatment
    Drugs & Aging, 2005
    Co-Authors: Marcelo L. Berthier
    Abstract:

    Aphasia, the loss or impairment of language caused by brain damage, is one of the most devastating cognitive impairments of stroke. Aphasia is present in 21-38% of acute stroke patients and is associated with high short- and long-term morbidity, mortality and expenditure. Recovery from Aphasia is possible even in severe cases. While speech-language therapy remains the mainstay treatment of Aphasia, the effectiveness of conventional therapies has not been conclusively proved. This has motivated attempts to integrate knowledge from several domains in an effort to plan more rational therapies and to introduce other therapeutic strategies, including the use of intensive language therapy and pharmacological agents. Several placebo-controlled trials suggest that piracetam is effective in recovery from Aphasia when started soon after the stroke, but its efficacy vanishes in patients with chronic Aphasia. Drugs acting on catecholamine systems (bromocriptine, dexamfetamine) have shown varying degrees of efficacy in case series, open-label studies and placebo-controlled trials. Bromocriptine is useful in acute and chronic Aphasias, but its beneficial action appears restricted to nonfluent Aphasias with reduced initiation of spontaneous verbal messages. Dexamfetamine improves language function in subacute Aphasia and the beneficial effect is maintained in the long term, but its use is restricted to highly selected samples. Pharmacological agents operating on the cholinergic system (e.g. donepezil) have shown promise. Data from single-case studies, case series and an open-label study suggest that donepezil may have beneficial effects on chronic poststroke Aphasia. Preliminary evidence suggests that donepezil is well tolerated and its efficacy is maintained in the long term. Randomised controlled trials of donepezil and other cholinergic agents in poststroke Aphasia are warranted.

Martin N Rossor – One of the best experts on this subject based on the ideXlab platform.

  • Primary progressive Aphasia: a clinical approach
    Journal of Neurology, 2018
    Co-Authors: Charles R. Marshall, Chris J D Hardy, Anna Volkmer, Lucy L. Russell, Rebecca L. Bond, Phillip D Fletcher, Camilla N Clark, Catherine J. Mummery, Jonathan M Schott, Martin N Rossor
    Abstract:

    The primary progressive Aphasias are a heterogeneous group of focal ‘language-led’ dementias that pose substantial challenges for diagnosis and management. Here we present a clinical approach to the progressive Aphasias, based on our experience of these disorders and directed at non-specialists. We first outline a framework for assessing language, tailored to the common presentations of progressive Aphasia. We then consider the defining features of the canonical progressive nonfluent, semantic and logopenic aphasic syndromes, including ‘clinical pearls’ that we have found diagnostically useful and neuroanatomical and other key associations of each syndrome. We review potential diagnostic pitfalls and problematic presentations not well captured by conventional classifications and propose a diagnostic ‘roadmap’. After outlining principles of management, we conclude with a prospect for future progress in these diseases, emphasising generic information processing deficits and novel pathophysiological biomarkers.

Christian Denier – One of the best experts on this subject based on the ideXlab platform.

  • Borderzone Strokes and Transcortical Aphasia
    Current Neurology and Neuroscience Reports, 2011
    Co-Authors: Cécile Cauquil-michon, C. Flamand-roze, Christian Denier
    Abstract:

    Borderzone infarcts (BZIs) are anatomically defined as ischemic lesions occurring at the junction between two arterial territories, accounting for 2% to 10% of strokes. Three types of hemispheric BZIs are described according to topography (ie, superficial anterior, posterior, and deep). Although published series on related Aphasia are rare in the setting of BZI, Aphasia is of transcortical (TCA) type, characterized by the preservation of repetition. TCA can be of motor, sensory, or mixed type depending on whether expression, understanding, or both are impaired. Recent studies have reported specific aphasic patterns. BZI patients initially presented with mixed TCA. Aphasia specifically evolved according to the stroke location, toward motor or sensory TCA in patients with respectively anterior or posterior BZI. TCA was associated with good long-term prognosis. This specific aphasic pattern is interesting in clinical practice because it prompts the suspicion of a BZI before the MRI is done, and it helps in the planning of rehabilitation and in providing adapted information to the patient and family concerning the likelihood of language recovery.

  • Aphasia in border-zone infarcts has a specific initial pattern and good long-term prognosis
    European Journal of Neurology, 2011
    Co-Authors: C. Flamand-roze, Cécile Cauquil-michon, Emmanuel Roze, Raphaëlle Souillard-scemama, Lisa Maintigneux, Denis Ducreux, David H. Adams, Christian Denier
    Abstract:

    Background:  While border-zone infarcts (BZI) account for about 10% of strokes, studies on related Aphasia are infrequent. The aim of this work was to redefine specifically their early clinical pattern and evolution. Methods:  We prospectively studied consecutive patients referred to our stroke unit within a 2-year period. Cases of Aphasia in right-handed patients associated with a MRI confirmed left-sided hemispheric BZI were included. These patients had a standardized language examination in the first 48 h, at discharge from stroke unit and between 6 and 18 months later. Results:  Eight patients were included. Three had anterior (MCA/ACA), two posterior (MCA/PCA), two both anterior and posterior, and one bilateral BZI. All our patients initially presented transcortical mixed Aphasia, characterized by comprehension and naming difficulties associated with preserved repetition. In all patients, Aphasia rapidly improved. It fully recovered within a few days in three patients. Initial improvement was marked, although incomplete in the five remaining patients: their Aphasias specifically evolved according to the stroke location toward transcortical motor Aphasia for the three patients with anterior BZI and transcortical sensory Aphasia for the two patients with posterior BZI. All patients made a full language recovery within 18 months after stroke. Conclusions:  We report a specific aphasic pattern associated with hemispheric BZI, including an excellent long-term outcome. These findings appear relevant to (i) clinically suspect BZI and (ii) plan rehabilitation and inform the patient and his family of likelihood of full language recovery.

Dennis W Dickson – One of the best experts on this subject based on the ideXlab platform.

  • progressive Aphasia secondary to alzheimer disease vs ftld pathology
    Neurology, 2008
    Co-Authors: Keith A Josephs, Bradley F. Boeve, Joseph R Duffy, Jennifer L Whitwell, Wendy A Vanvoorst, Edyth A Strand, Neill R Graffradford, Joseph E Parisi, David S Knopman, Dennis W Dickson
    Abstract:

    Background: The pathology causing progressive Aphasia is typically a variant of frontotemporal lobar degeneration, especially with ubiquitin-positive inclusions (FTLD-U). Less commonly the underlying pathology is Alzheimer disease (AD). Objective: To compare clinicopathologic and MRI features of subjects with progressive Aphasia and AD pathology to subjects with Aphasia and FTLD-U pathology and subjects with typical AD. Methods: We identified 5 subjects with Aphasia and AD pathology and 5 with Aphasia and FTLD-U pathology with an MRI from a total of 216 Aphasia subjects. Ten subjects with typical AD clinical features and AD pathology were also identified. All subjects with AD pathology underwent pathologic reanalysis with TDP-43 immunohistochemistry. Voxel-based morphometry (VBM) was used to assess patterns of gray matter atrophy in the Aphasia cases with AD pathology, Aphasia cases with FTLD-U, and typical AD cases with AD pathology, compared with a normal control group. Results: All aphasic subjects had fluent speech output. However, those with AD pathology had better processing speed than those with FTLD-U pathology. Immunohistochemistry with TDP-43 antibodies was negative. VBM revealed gray matter atrophy predominantly in the temporoparietal cortices, with notable sparing of the hippocampus in the Aphasia with AD subjects. In comparison, the aphasic subjects with FTLD-U showed sparing of the parietal lobe. Typical AD subjects showed temporoparietal and hippocampal atrophy. Conclusions: A temporoparietal pattern of atrophy on MRI in patients with progressive fluent Aphasia and relatively preserved processing speed is suggestive of underlying Alzheimer disease pathology rather than frontotemporal lobar degeneration with ubiquitin-only immunoreactive changes. GLOSSARY: AD = Alzheimer disease; ADPR = Alzheimer9s Disease Patient Registry; ADRC = Alzheimer9s Disease Research Center; Aphasia–AD = subjects with progressive Aphasia and Alzheimer disease pathology; Aphasia–FTLD-U = subjects with progressive Aphasia and frontotemporal lobar degeneration with ubiquitin-only immunoreactive changes pathology; CDR = Clinical Dementia Rating; DCT = discrete cosine transformation; FTLD = frontotemporal lobar degeneration; FTLD-U = frontotemporal lobar degeneration with ubiquitin-only immunoreactive changes; FWHM = full-width at half-maximum; GM = gray matter; MMSE = Mini-Mental State Examination; MNI = Montreal Neurological Institute; NA = not applicable; NIA = National Institute on Aging; NR = not reported; NS = not significant; PPA = primary progressive Aphasia; typical AD = subjects with a clinical and pathologic diagnosis of Alzheimer disease; VBM = voxel-based morphometry; WAIS-R = Wechsler Adult Intelligence Scale–Revised; WM = white matter; WMS-R = Wechsler Memory Scale–Revised.

  • progressive nonfluent Aphasia and subsequent aphasic dementia associated with atypical progressive supranuclear palsy pathology
    European Neurology, 2003
    Co-Authors: Bradley F. Boeve, Dennis W Dickson, Joseph R Duffy, J D Bartleson, Max R Trenerry, R C Petersen
    Abstract:

    We describe a right-handed man who developed progressive nonfluent Aphasia and apraxia of speech beginning at age 71. By age 74 he had behavioral changes, aphasic dementia, as well as mild parkinsonis

Charles R. Marshall – One of the best experts on this subject based on the ideXlab platform.

  • Primary progressive Aphasia: a clinical approach
    Journal of Neurology, 2018
    Co-Authors: Charles R. Marshall, Chris J D Hardy, Anna Volkmer, Lucy L. Russell, Rebecca L. Bond, Phillip D Fletcher, Camilla N Clark, Catherine J. Mummery, Jonathan M Schott, Martin N Rossor
    Abstract:

    The primary progressive Aphasias are a heterogeneous group of focal ‘language-led’ dementias that pose substantial challenges for diagnosis and management. Here we present a clinical approach to the progressive Aphasias, based on our experience of these disorders and directed at non-specialists. We first outline a framework for assessing language, tailored to the common presentations of progressive Aphasia. We then consider the defining features of the canonical progressive nonfluent, semantic and logopenic aphasic syndromes, including ‘clinical pearls’ that we have found diagnostically useful and neuroanatomical and other key associations of each syndrome. We review potential diagnostic pitfalls and problematic presentations not well captured by conventional classifications and propose a diagnostic ‘roadmap’. After outlining principles of management, we conclude with a prospect for future progress in these diseases, emphasising generic information processing deficits and novel pathophysiological biomarkers.