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> Disorders > Mental or Behavioral Dysfunction > Broca Aphasia

Broca Aphasia

Broca Aphasia is a type of nonfluent aphasia characterized by impaired speech production, difficulties with articulation, and reduced sentence complexity.
Individuals with Broca Aphasia often struggle to find the right words and may speak in short, telegraphic phrases.
This condition is typically caused by damage to the inferior frontal gyrus, particularly the Broca's area, which is crucial for language production.
Broca Aphasia can have a significant impact on a person's ability to communicate effectively, making it an important area of study for researchers and clinicians.
Understanding the underlying mechanisms and developing effective interventions for Broca Aphasia is crucial for improving the quality of life for those affected by this disorder.

Most cited protocols related to «Broca Aphasia»

1
Multi-Cohort Study of FTD and ALS Patients
Cited 41 times

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Publication 2011
Alzheimer's Disease Aphasia Biopharmaceuticals Brain Broca Aphasia Chromosomes, Human, Pair 20 Corticobasal Degeneration Dementia Diagnosis Electromyography Family Member Frontotemporal Dementia Frontotemporal Lobar Degeneration Memory Deficits Neurodegenerative Disorders Neurologic Examination Neuropsychological Tests Parkinsonian Disorders Patients Phenotype protein TDP-43, human Schizophrenia Semantic Dementia Vision
2
Comprehensive Analysis of FTLD-U Subtypes
Cited 32 times
The following cases from the Center for Neuropathology and Prion Research (Munich, Germany), Center for Neurodegenerative Disease Research (Philadelphia, USA) and Department of Neuropathology (Aalborg, Denmark) were included in the study: i) familial FTLD-U with linkage to chrom 9p (n=4), GRN (n=5), and VCP (n= 4) mutations; ii) FTLD-U either sporadic or familial with unknown genetic defect (subtype 1 (n=14); subtype 2 (n=19); subtype 3 (n=18) according to [33 (link)]); iii) ALS (n=18); iv) Tauopathies with concomitant TDP-43 pathology (AD+TDP-43 (n=3); CBD+TDP-43 (n=2). Cases of FTLD-U had a clinical diagnosis of the FTD spectrum (behavioural variant of FTD, progressive non-fluent aphasia, semantic dementia) with or without concomitant MND. Cases of ALS had clinical signs of MND with some of them developing cognitive changes only late in disease process. In addition, healthy controls (n=5), AD without TDP-43 pathology (n=5), CBD without TDP-43 (n=4) and TDP-43 negative FTLD-U cases (n=9) [31 (link)] were included. Demographic, clinical and neuropathological data are summarized in Table 1.
Neumann M., Kwong L.K., Lee E.B., Kremmer E., Flatley A., Xu Y., Forman M., Troost D., Kretzschmar H.A., Trojanowski J.Q, & Lee V.M. (2009). Phosphorylation of S409/410 of TDP-43 is a consistent feature in all sporadic and familial forms of TDP-43 proteinopathies. Acta neuropathologica, 117(2), 137-149.
Publication 2009
Broca Aphasia Chromium Cognition Disorders Congenital Abnormality Diagnosis Frontotemporal Lobar Degeneration Mutation Neurodegenerative Disorders Prions protein TDP-43, human Semantic Dementia Tauopathies
3
Anatomical Basis of Aphasia Deficits
Cited 8 times
Participants were drawn from an ongoing project investigating the anatomical basis of psycholinguistic deficits in post-acute aphasia. Results from this project and some of these participants have been reported in several previous publications17 (link),18 (link),32 (link),34 (link),54 (link),58 (link). In particular, the original demonstration that semantic errors in naming localize to the left ATL was based on 64 patients from the current group of 9917 (link),18 (link). To be included in this study, participants had to be at least 1 month post-onset of aphasia secondary to stroke, living at home, medically stable without major psychiatric or neurological co-morbidities, and have been premorbidly right handed. Participants were also required to have English as primary language, adequate vision and hearing (with or without correction) and CT or MRI confirmed left hemisphere cortical lesion. Only participants who had completed all 17 tests were included in this study. All participants gave informed consent to take part in a multisession language assessment under protocols approved by the Institutional Review Boards at the Albert Einstein Medical Center and University of Pennsylvania School of Medicine. The sample consisted of 43 women and 56 men, 48 African-Americans and 51 Caucasians. They averaged 58 years of age (SD = 11; range = 26–79), 14 years of education (SD = 3; range = 10–21), and 53 months post onset of stroke (SD = 68; range = 1–381). 83% were in the chronic phase (> 6 mo.) The predominant subtype diagnosis was anomic aphasia (44%), followed by Broca’s aphasia (27%) and conduction aphasia (16%). The Aphasia Quotient, which rates overall severity on a scale from 1 (most severe) to 100, averaged 73 (SD = 18.4; range = 27.2–97.9).
Mirman D., Chen Q., Zhang Y., Wang Z., Faseyitan O.K., Coslett H.B, & Schwartz M.F. (2015). Neural Organization of Spoken Language Revealed by Lesion-Symptom Mapping. Nature communications, 6, 6762.
Publication 2015
African American Anomia Aphasia Associative Aphasia Broca Aphasia Caucasoid Races Cerebrovascular Accident Cortex, Cerebral Diagnosis Ethics Committees, Research Patients Vision Woman
4
Neuroimaging Study of Non-Fluent Primary Progressive Aphasia
Cited 7 times
We successfully scanned eight patients with non-fluent PPA and 24 normal controls over an 18-month period. Patients and normal control subjects were recruited through the Memory and Aging Center at the University of California, San Francisco (UCSF). All participants gave written informed consent, and the study was approved by the Committee on Human Research at UCSF. Patients and controls received a comprehensive multidisciplinary evaluation including neurological history and examination, neuropsychological testing, and neuroimaging.
A diagnosis of PPA required progressive deterioration of speech and/or language functions, and that deficits be largely restricted to speech and/or language for at least two years (Mesulam, 2001 (link)). Patients were diagnosed with the non-fluent variant of PPA based on new consensus guidelines (Gorno-Tempini et al., 2010 ). The non-fluent variant criteria require the presence of one or both of two core features: agrammatism, and/or effortful speech. Additionally, at least two of three supporting features must be present: comprehension deficits for syntactically complex sentences, spared single word comprehension, and/or spared object knowledge. Neuroimaging results were not used for diagnostic purposes, but only to rule out other causes of focal brain damage.
Additional inclusion criteria were fluency in English, and a Mini-Mental State Examination score of at least 15. Nine patients met these criteria and were scanned, but one was excluded since she performed at chance on all conditions including those that required lexical knowledge alone (see below), so all analyses were based on the remaining eight patients.
Two of the eight patients were severely agrammatic in their speech production (e.g. and uh a blanket… and… a thongs off the man… and um… uh… teenagers um… in the kite), two were moderately so (e.g. the family is have a picnic, and um, the young son is flying their kei- k- kite), one was near-mute with severely agrammatic written language (e.g. man read book girl the coffee in cup), one was near-mute with moderately agrammatic written language (e.g. the couple having a picnic, they are sitting a blanket under a tree), and two had primarily speech motor deficits, with intact syntax in production (e.g. the fellow is reading a book, the woman is pouring some l- liquids), and mild syntactic deficits evident only in comprehension of complex sentences. All patients were clinically diagnosed with apraxia of speech, with severity ranging from 2 to 7 on a 7-point scale (Wertz et al., 1984 ), and 4 of the 8 were dysarthric (including the two who were near-mute).
Demographic, clinical and neuropsychological characteristics for all participants are provided in Table 1. There were no significant differences between patients and controls in age, sex, handedness or education.
In addition to the 24 normal controls who took part in functional imaging, structural images from another group of 50 healthy age-matched controls were used to create a template for intersubject normalization and voxel-based morphometry.
Wilson S.M., Dronkers N.F., Ogar J.M., Jang J., Growdon M.E., Agosta F., Henry M.L., Miller B.L, & Gorno-Tempini M.L. (2010). Neural Correlates of Syntactic Processing in the Nonfluent Variant of Primary Progressive Aphasia. The Journal of Neuroscience, 30(50), 16845-16854.
Publication 2010
Adolescent Apraxia of Phonation Brain Injuries, Focal Broca Aphasia Coffee Homo sapiens Memory Mini Mental State Examination Patients Speech Trees Woman
5
Genetic Correlations Across Neurological and Psychiatric Disorders
Cited 6 times
GWAS summary statistics for clinically diagnosed AD86 (link), PD87 (link), FTD88 , CBD89 (link) and PSP20 (link) in individuals of European ancestry were obtained. For AD, we used the clinical diagnosis as the case definition to avoid spurious genetic correlations that could have been introduced through the by-proxy design31 (link), in which by-proxy cases are defined as having a parent with AD. Although this is a powerful design for gene discovery and the genetic correlation with clinically diagnosed AD is high90 (link), mislabeling by-proxy cases when parents suffer from other types of dementia (for example, Lewy body dementia, Parkinson’s dementia, FTD or vascular dementia) can lead to spurious genetic correlations with ALS and other neurodegenerative diseases. For FTD, we primarily used the results of the cross-subtype meta-analysis, which includes behavioral variant FTD, semantic dementia FTD, progressive non-fluent aphasia FTD and mndFTD. For CBD, allele coding was unavailable, and effect alleles were inferred by matching allele frequencies to those observed in the Haplotype Reference Consortium. SNPs with MAF > 0.4 were excluded. Because downstream methods rely on LD scores or population-specific LD patterns, the European ancestry summary statistics from the present study were used for ALS. For sample size parameters, effective sample size was calculated as described previously.
Multiple sclerosis summary statistics were obtained from the International Multiple Sclerosis Genetics Consortium91 (link). For cerebrovascular diseases, GWAS summary statistics were obtained for ischemic stroke (any ischemic stroke)92 (link), intracerebral hemorrhage93 (link) and intracranial aneurysm94 (link). For psychiatric traits, GWAS summary statistics were obtained from Psychiatric Genomics Consortium studies on anorexia nervosa95 (link), obsessive–compulsive disorder96 , anxiety disorders (anxiety score)97 (link), post-traumatic stress disorder (all European ancestries)98 (link), major depressive disorder99 (link), bipolar disorder100 (link), schizophrenia101 , Tourette’s syndrome102 (link), autism spectrum disorder103 (link) and attention-deficit hyperactivity disorder (European ancestries)104 (link).
van Rheenen W., van der Spek R.A., Bakker M.K., van Vugt J.J., Hop P.J., Zwamborn R.A., de Klein N., Westra H.J., Bakker O.B., Deelen P., Shireby G., Hannon E., Moisse M., Baird D., Restuadi R., Dolzhenko E., Dekker A.M., Gawor K., Westeneng H.J., Tazelaar G.H., van Eijk K.R., Kooyman M., Byrne R.P., Doherty M., Heverin M., Al Khleifat A., Iacoangeli A., Shatunov A., Ticozzi N., Cooper-Knock J., Smith B.N., Gromicho M., Chandran S., Pal S., Morrison K.E., Shaw P.J., Hardy J., Orrell R.W., Sendtner M., Meyer T., Başak N., van der Kooi A.J., Ratti A., Fogh I., Gellera C., Lauria G., Corti S., Cereda C., Sproviero D., D’Alfonso S., Sorarù G., Siciliano G., Filosto M., Padovani A., Chiò A., Calvo A., Moglia C., Brunetti M., Canosa A., Grassano M., Beghi E., Pupillo E., Logroscino G., Nefussy B., Osmanovic A., Nordin A., Lerner Y., Zabari M., Gotkine M., Baloh R.H., Bell S., Vourc’h P., Corcia P., Couratier P., Millecamps S., Meininger V., Salachas F., Mora Pardina J.S., Assialioui A., Rojas-García R., Dion P.A., Ross J.P., Ludolph A.C., Weishaupt J.H., Brenner D., Freischmidt A., Bensimon G., Brice A., Durr A., Payan C.A., Saker-Delye S., Wood N.W., Topp S., Rademakers R., Tittmann L., Lieb W., Franke A., Ripke S., Braun A., Kraft J., Whiteman D.C., Olsen C.M., Uitterlinden A.G., Hofman A., Rietschel M., Cichon S., Nöthen M.M., Amouyel P., Traynor B.J., Singleton A.B., Mitne Neto M., Cauchi R.J., Ophoff R.A., Wiedau-Pazos M., Lomen-Hoerth C., van Deerlin V.M., Grosskreutz J., Roediger A., Gaur N., Jörk A., Barthel T., Theele E., Ilse B., Stubendorff B., Witte O.W., Steinbach R., Hübner C.A., Graff C., Brylev L., Fominykh V., Demeshonok V., Ataulina A., Rogelj B., Koritnik B., Zidar J., Ravnik-Glavač M., Glavač D., Stević Z., Drory V., Povedano M., Blair I.P., Kiernan M.C., Benyamin B., Henderson R.D., Furlong S., Mathers S., McCombe P.A., Needham M., Ngo S.T., Nicholson G.A., Pamphlett R., Rowe D.B., Steyn F.J., Williams K.L., Mather K.A., Sachdev P.S., Henders A.K., Wallace L., de Carvalho M., Pinto S., Petri S., Weber M., Rouleau G.A., Silani V., Curtis C.J., Breen G., Glass J.D., Brown RH J.r., Landers J.E., Shaw C.E., Andersen P.M., Groen E.J., van Es M.A., Pasterkamp R.J., Fan D., Garton F.C., McRae A.F., Davey Smith G., Gaunt T.R., Eberle M.A., Mill J., McLaughlin R.L., Hardiman O., Kenna K.P., Wray N.R., Tsai E., Runz H., Franke L., Al-Chalabi A., Van Damme P., van den Berg L.H, & Veldink J.H. (2021). Common and rare variant association analyses in amyotrophic lateral sclerosis identify 15 risk loci with distinct genetic architectures and neuron-specific biology. Nature Genetics, 53(12), 1636-1648.
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Publication 2021
Alleles Anorexia Anxiety Disorders Broca Aphasia Candidate Gene Identification Cerebrovascular Disorders Dementia Dementia, Vascular Disorder, Attention Deficit-Hyperactivity Europeans Genes, vif Genome-Wide Association Study Haplotypes Lewy Body Disease Multiple Sclerosis Neurodegenerative Disorders Parent Pervasive Development Disorders Post-Traumatic Stress Disorder Reproduction Semantic Dementia Single Nucleotide Polymorphism Stroke, Ischemic

Most recents protocols related to «Broca Aphasia»

1
Histological analysis of traumatic brain injury
Authorizations for reporting these three cases were granted by the Eastern Ontario Regional Forensic Unit and the Laboratoire de Sciences Judiciaires et de Médecine Légale du Québec.
The sampling followed a relatively standardized protocol for all TBI cases: samples were collected from the cortex and underlying white matter of the pre-frontal gyrus, superior and middle frontal gyri, temporal pole, parietal and occipital lobes, deep frontal white matter, hippocampus, anterior and posterior corpus callosum with the cingula, lenticular nucleus, thalamus with the posterior limb of the internal capsule, midbrain, pons, medulla, cerebellar cortex and dentate nucleus. In some cases, gross pathology (e.g. contusions) mandated further sampling along with the dura and spinal cord if available. The number of available sections for these three cases was 26 for case1, and 24 for cases 2 and 3.
For the detection of ballooned neurons, all HE or HPS sections, including contusions, were screened at 200×.
Representative sections were stained with either hematoxylin–eosin (HE) or hematoxylin-phloxin-saffron (HPS). The following histochemical stains were used: iron, Luxol-periodic acid Schiff (Luxol-PAS) and Bielschowsky. The following antibodies were used for immunohistochemistry: glial fibrillary acidic protein (GFAP) (Leica, PA0026,ready to use), CD-68 (Leica, PA0073, ready to use), neurofilament 200 (NF200) (Leica, PA371, ready to use), beta-amyloid precursor-protein (β-APP) (Chemicon/Millipore, MAB348, 1/5000), αB-crystallin (EMD Millipore, MABN2552 1/1000), ubiquitin (Vector, 1/400), β-amyloid (Dako/Agilent, 1/100), tau protein (Thermo/Fisher, MN1020 1/2500), synaptophysin (Dako/Agilent, ready to use), TAR DNA binding protein 43 (TDP-43) ((Protein Tech, 10,782-2AP, 1/50), fused in sarcoma binding protein (FUS) (Protein tech, 60,160–1-1 g, 1/100), and p62 (BD Transduc, 1/25). In our index cases, the following were used for the evaluation of TAI: β-APP, GFAP, CD68 and NF200; for the neurodegenerative changes: αB-crystallin, NF200, ubiquitin, tau protein, synaptophysin, TDP-43, FUS were used.
For the characterization of the ballooned neurons only, two cases of fronto-temporal lobar degeneration, FTLD-Tau, were used as controls. One was a female aged 72 who presented with speech difficulties followed by neurocognitive decline and eye movement abnormalities raising the possibility of Richardson’s disorder. The other was a male aged 67 who presented with a primary non-fluent aphasia progressing to fronto-temporal demαentia. In both cases, the morphological findings were characteristic of a corticobasal degeneration.
Michaud J., Plu I., Parai J., Bourgault A., Tanguay C., Seilhean D, & Woulfe J. (2023). Ballooned neurons in semi-recent severe traumatic brain injury. Acta Neuropathologica Communications, 11, 37.
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Publication 2023
Amyloid beta-Protein Precursor Amyloid Proteins Antibodies Broca Aphasia Cloning Vectors Congenital Abnormality Contusions Corpus Callosum Cortex, Cerebellar Cortex, Cerebral Corticobasal Degeneration Crystallins Dura Mater Eosin Eye Abnormalities Eye Movements Frontotemporal Lobar Degeneration FUBP1 protein, human Glial Fibrillary Acidic Protein Hematoxylin Immunohistochemistry Internal Capsule Iron Males Medial Frontal Gyrus Medulla Oblongata Mesencephalon Movement Movement Disorders neurofilament protein H Neurons Nucleus, Dentate Nucleus, Lenticular Occipital Lobe Periodic Acid phloxine Pons Proteins protein TDP-43, human RNA-Binding Protein FUS Saffron Sarcoma Seahorses Speech Spinal Cord Staining Synaptophysin Temporal Lobe Thalamus Ubiquitin White Matter Woman
2
Bihemispheric tDCS for Stroke Motor Recovery
We conducted a double-blind, randomized, sham-controlled study to investigate the efficacy and safety of bihemispheric tDCS for motor recovery in subacute stroke patients. The ethics committee approved the study at the Taipei Veterans General Hospital (VGHIRB No. 2015-03-003C) and registered with ClinicalTrials.gov (NCT02731508). We screened 282 consecutive inpatients between September 2015 and June 2021 and validated their eligibility for the following inclusion criteria (Fig. 1): (1) age between 20 and 80 years; (2) acute first-ever unilateral infarction confirmed by diffusion-weighted MRI; (3) consciousness clear and able to sign the informed consent form. The exclusion criteria were: (1) sensorimotor cortical infarcts; (2) too mild or too severe FMA-UE scores, i.e. > 56 or < 2 (0–66, where 0 is no function and 66 is maximum) [38 (link)]; (3) sensory or motor aphasia; (4) severe medical diseases (advanced malignancy, end-stage heart, liver or kidney failure, etc.) with premorbid modified Rankin Scale (mRS) > 1; (5) major neuropsychiatric diseases (dementia, epilepsy, parkinsonism, cerebellar ataxia, major depression, etc.); (6) contraindications to transcranial magnetic stimulation (TMS) for increased risk (presence of metallic implants, pregnancy); and (7) participating in other interventional studies.

Enrollment flowchart of this randomized controlled trial. FMA-UE, Fugl-Meyer Assessment of Upper Extremity; tDCS, transcranial direct current stimulation

Hsu S.P., Lu C.F., Lin B.F., Tang C.W., Kuo I.J., Tsai Y.A., Guo C.Y., Lee P.L., Shyu K.K., Niddam D.M, & Lee I.H. (2023). Effects of bihemispheric transcranial direct current stimulation on motor recovery in subacute stroke patients: a double-blind, randomized sham-controlled trial. Journal of NeuroEngineering and Rehabilitation, 20, 27.
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Publication 2023
Broca Aphasia Cerebellar Ataxia Cerebrovascular Accident Consciousness Dementia Diffusion Magnetic Resonance Imaging Eligibility Determination Epilepsy Ethics Committees Heart Infarction Inpatient Kidney Failure Liver Major Depressive Disorder Malignant Neoplasms Metals Parkinsonian Disorders Patients Pregnancy Safety Sensorimotor Cortex Stimulation, Transcranial Magnetic Transcranial Direct Current Stimulation Upper Extremity
3
Predictors of Stroke Recovery Outcomes
This study was a secondary analysis conducted on a large database already used in some previous studies [3 (link),5 (link),12 (link),13 (link)] and further augmented with new data. The inclusion criteria were: diagnosis of ischemic stroke confirmed by brain imaging (magnetic resonance imaging or computerized tomography), subacute phase of stroke, and admission to a neurorehabilitation hospital. The exclusion criteria were: previous cerebrovascular accidents, hemorrhagic stroke, subarachnoid hemorrhage, and presence of other chronic disabling pathologies (i.e., severe Parkinson’s disease, polyneuropathy, cancer, or limb amputation).
Because our hospital is also an institute of research, at the time of admission all patients signed an informed consent for the utilization of their data in translational research. In the present study, a sample of 862 patients was extracted from the dataset according to the above inclusion/exclusion criteria and further divided into a subgroup previously treated with thrombolysis (TG) and another not treated with it (NTG).
The dataset reported for each patient consisted of 22 variables accounted for at admission to the neurorehabilitation hospital. The variables were as follows: age (continuous variable), time (days) between the stroke acute event and admission into the neurorehabilitation hospital (DAS, continuous variable), Barthel Index score (BI) at admission (ordinal variable, Barthel Index is a clinical scale assessing the independency of a patient into the activities of daily living), and binary variables such as gender, if patients received thrombolysis, damaged hemisphere, if there was a diagnosis of hypertension, heart diseases, diabetes, depression, epilepsy, dysphagia, malnutrition, obesity, Broca’s aphasia (related to deficits in speech and language production), Wernicke’s aphasia (related to deficits in language understanding), global aphasia (including both the previous types of language deficits), unilateral spatial neglect (USN, related to deficits in reporting or responding to stimuli presented from the space contralateral to the lesion, often a right hemisphere lesion), and the category of Bamford classification. This latter variable refers to the anatomical type of stroke and was further divided into four binary variables, in accordance with previous studies that dichotomized each one of these categories [3 (link),5 (link)]: TACI (total anterior circulatory infarction), PACI (partial anterior), POCI (partial posterior), and LACI (lateral anterior).
The dependent variable was the outcome: good responders were defined as subjects who were discharged from a neurorehabilitation hospital with a BI-score >75, whereas low-medium responders were those who died, were transferred to emergency hospitals, or were discharged with a BI-score ≤75.
Iosa M., Paolucci S., Antonucci G., Ciancarelli I, & Morone G. (2023). Application of an Artificial Neural Network to Identify the Factors Influencing Neurorehabilitation Outcomes of Patients with Ischemic Stroke Treated with Thrombolysis. Biomolecules, 13(2), 334.
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Publication 2023
Amputation Anterior Wall Myocardial Infarction Aphasia, Global Brain Broca Aphasia Cardiovascular System Cerebrovascular Accident Deglutition Disorders Diabetes Mellitus Diagnosis Emergencies Epilepsy Fibrinolytic Agents Gender Heart Diseases Hemorrhagic Stroke High Blood Pressures Malignant Neoplasms Malnutrition Neurological Rehabilitation Obesity Patients Polyneuropathy Speech Stroke, Ischemic Subarachnoid Hemorrhage TNFRSF13B protein, human Wernicke Aphasia X-Ray Computed Tomography
4
Lesion Mapping of Aphasia Types
We used three traditional mass univariate methods: voxel-, region-, and connectivity-based lesion symptom mapping (VLSM, RLSM, CSLM). Whole brain V- and RLSM was used to identify brain damage associated with aphasia type (anomic or Broca’s). VLSM shows the statistical likelihood that damage to a given voxel is associated with aphasia type group membership, where each voxel in each patient is binarily demarcated as either damaged or undamaged (Bates, Wilson, Saygin, & et al., 2003 (link)). RLSM differs from VLSM in that instead of using binary voxel-wise values, it uses the percent of voxels damaged within each ROI as the predictor of aphasia type. This sacrifices spatial specificity while providing the advantage of analyzing the effects of damage over an entire region without requiring overlapping damage at level of an individual voxel. We conducted RLSM using the AICHA ROIs. We then conducted CLSM (Gleichgerrcht, Fridriksson, Rorden, & Bonilha, 2017 (link)) using resting-state functional connectivity based on the AICHA atlas, including all left-to-left, left-to-right, and right-to-right connections in the analysis. Only voxels (or regions for RLSM) where at least 5 patients had damage were considered, based on the minimum overlap recommendation of 10% of the patient sample (Baldo, Ivanova, Herron, & et al., 2022 ). All tests were two-tailed, with α = 0.05, and significance was determined via permutation testing, where stability of p-value were tested in increments of 1000 permutations, ranging from 1,000 permutation to 10,000 permutations.
On top of whole-brain analysis, we also restricted the analysis to the ‘dorsal stream’ areas, i.e. frontoparietal and superior temporal areas that are involved in form-to-NBS articulation during speech (Fridriksson et al., 2016 ). These areas would be hypothesized to be especially disrupted in individuals with Broca’s aphasia who struggle with many aspects of speech production compared to the relatively mild anomic cases where the individuals just have occasional word-finding difficulties. We included the AICHA ROIs corresponding to supramarginal gyrus, primary sensory and motor cortices, inferior frontal gyrus (Broca’s area), superior temporal gyrus, and rolandic operculum. This allowed us to restrict the # of connections while also allowing us to use a one-tailed analysis since we specifically hypothesized these connections would be associated with Broca’s aphasia. It is worth noting that we also tried the alternate analysis, using a different set of language regions that might be implicated in anomic aphasia more than Broca’s, but this did not reveal any significant results. This is likely because anomic aphasia as a behavioral syndrome may be caused by deficits at various functional levels within the language production system (conceptual, lexical, semantic, phonological, for example), so that similar surface behavior may result from different patterns of neural damage. In addition, in our own sample anomic aphasia was ‘less severe’ than Broca’s aphasia, on average, which would also make the detection of areas specifically related to the anomic group more difficult.
Zhao X., Riccardi N., den Ouden D.B., Desai R.H., Fridriksson J, & Wang Y. (2023). Network-based statistics distinguish anomic and Broca aphasia. ArXiv.
Publication Preprint 2023
Anomia Aphasia Brain Brain Injuries Broca Aphasia Broca Area Inferior Frontal Gyrus Joints Motor Cortex Nervousness Opercular Cortex Patients Speech Superior Temporal Gyrus Supramarginal Gyrus Syndrome
5
Aphasia Subtypes and Neuroanatomical Profiles
Aphasia types were classified based on the Western Aphasia Battery-Revised (WAB-R) (Kertesz, 2007 ). Among the 49 participants included in the study sample, 15 were diagnosed with anomic aphasia, and 34 were diagnosed with Broca’s aphasia. Figure 1 shows a lesion overlap map of the participants in the two groups. Demographic statistics of the two groups are summarized in Table 1. The mean age in the anomic group was 62.73 y.o. (s.d. = 11.97; range = 41) and the mean age in the Broca’s group is 59.82 y.o. (s.d. = 10.35; range = 39). Respectively 60% and 68% of the participants in the anomic and Broca’s group were male. There was no significant difference in age and gender between the anomic and Broca’s group (age: p-value = 0.42 by two-sample t-test; gender: p = 0.74 by χ2-test). The mean WAB-R score for the anomic group was 85.74 (s.d. = 6.38; range = 22.1) and 46.44 (s.d. = 16.93; range = 59.1) for the Broca’s group. The WAB-R score for the anomic group is significantly higher than the Broca’s group (p-value < 0.01 by two-sample t-test), since the participants with Broca’s aphasia tend to have a lower score in the section of fluency and repetition than the participants with anomic aphasia.
Zhao X., Riccardi N., den Ouden D.B., Desai R.H., Fridriksson J, & Wang Y. (2023). Network-based statistics distinguish anomic and Broca aphasia. ArXiv.
Publication Preprint 2023
Age Groups Anomia Aphasia Broca Aphasia Gender Males

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More about "Broca Aphasia"

Broca's Aphasia, Nonfluent Aphasia, Language Production Disorder, Articulation Difficulty, Frontal Lobe Damage, Speech Impairment, Communication Challenges, Linguistic Deficits, Telegraphic Speech, MiSeq Sequencing, MagPro Magnetic Particle Processor, SPSS Statistical Software.
Broca Aphasia, a type of nonfluent aphasia, is characterized by impaired speech production, difficulties with articulation, and reduced sentence complexity.
Individuals with Broca Aphasia often struggle to find the right words and may speak in short, telegraphic phrases.
This condition is typically caused by damage to the inferior frontal gyrus, particularly the Broca's area, which is crucial for language production.
Researchers and clinicians studying Broca Aphasia can leverage advanced tools and technologies to enhance their research and improve outcomes for those affected by this disorder.
The MiSeq platform, for example, can be used for genetic analysis to understand the underlying biological mechanisms of Broca Aphasia.
The MagPro magnetic particle processor can assist with sample preparation and purification, while SPSS statistical software version 22.0 can be utilized for data analysis and interpretation.
By understanding the complex nature of Broca Aphasia and utilizing the latest research tools and technologies, researchers can work towards developing more effective interventions and improving the quality of life for those affected by this challenging condition.
PubCompare.ai, an AI-driven platform, can help optimize Broca Aphasia research by locating relevant protocols from literature, pre-prints, and patents, and providing AI-driven comparisons to identify the best approaches for your studies.
Enhancing reproducibility and accuracy in Broca Aphasia research is crucial for advancing our understanding and improving outcomes for those living with this disorder.