scholarly journals Beta modulation reflects name retrieval in the human anterior temporal lobe: an intracranial recording study

2016 ◽  
Vol 115 (6) ◽  
pp. 3052-3061 ◽  
Author(s):  
Taylor J. Abel ◽  
Ariane E. Rhone ◽  
Kirill V. Nourski ◽  
Timothy K. Ando ◽  
Hiroyuki Oya ◽  
...  
Keyword(s):  
Temporal Lobe ◽  
Beta Band ◽  
Anterior Temporal Lobe ◽  
Famous People ◽  
Human Ability ◽  
Neurosurgical Patients ◽  
Focus Localization ◽  
Left And Right ◽  
Intracranial Recording ◽  
Name Retrieval

Naming people, places, and things is a fundamental human ability that is often impaired in patients with language-dominant anterior temporal lobe (ATL) dysfunction or ATL resection as part of epilepsy treatment. Convergent lines of evidence point to the importance of the ATL in name retrieval. The physiologic mechanisms that mediate name retrieval in the ATL, however, are not well understood. The purpose of this study was to characterize the electrophysiologic responses of the human ATL during overt cued naming of famous people and objects. Eight neurosurgical patients with suspected temporal lobe epilepsy who underwent implantation of intracranial electrodes for seizure focus localization were the subjects of this study. Specialized coverage of the ATL was achieved in each subject. The subjects named pictures of U.S. presidents and images of common hand-held tools. Event-related band power was measured for each ATL recording site. Both the left and right ATL demonstrated robust and focal increases in beta-band (14–30 Hz) power during person and tool naming. The onset of this response typically occurred at 400 ms but sometimes as early as 200 ms. Visual naming of famous people and tools is associated with robust and localized modulation of the beta band in both the left and right ATL. Measurement of visual naming responses may provide the groundwork for future mapping modalities to localize eloquent cortex in the ATL.

scholarly journals Regional and hemispheric susceptibility of the temporal lobe to FTLD-TDP type C pathology

2019 ◽  
Author(s):  
V. Borghesani ◽  
G. Battistella ◽  
M.L. Mandelli ◽  
A. Welch ◽  
E. Weis ◽  
...  
Keyword(s):  
Temporal Lobe ◽  
Primary Progressive Aphasia ◽  
Semantic Knowledge ◽  
Similar Distribution ◽  
Anterior Temporal Lobe ◽  
Temporal Pole ◽  
Neuroimaging Data ◽  
Type C ◽  
Left And Right ◽  
Anterior Temporal Pole

AbstractPost-mortem studies show that focal anterior temporal lobe (ATL) neurodegeneration is most often caused by frontotemporal lobar degeneration TDP-43 type C pathology. Clinically, these patients are described with different terms, such as semantic variant primary progressive aphasia (svPPA), semantic dementia (SD), or right temporal variant frontotemporal dementia (FTD) depending on whether the predominant symptoms affect language, semantic knowledge for object or people, or socio-emotional behaviors. ATL atrophy presents with various degrees of lateralization, with right-sided cases considered rarer even though estimation of their prevalence is hampered by the paucity of studies on well-characterized, pathology-proven cohorts. Moreover, it is not clear whether left and right variants show a similar distribution of atrophy within the ATL cross-sectionally and longitudinally.Here we study the largest cohort to-date of pathology-proven TDP-43-C cases diagnosed during life as svPPA, SD or right temporal variant FTD. We analyzed clinical, cognitive, and neuroimaging data from 30 cases, a subset of which was followed longitudinally. Guided by recent structural and functional parcellation studies, we constructed four bilateral ATL regions of interest (ROIs). The computation of an atrophy lateralization index allowed the comparison of atrophy patterns between the two hemispheres. This led to an automatic, imaging-based classification of the cases as left-predominant or right-predominant. We then compared the two groups in terms of regional atrophy patterns within the ATL ROIs (cross-sectionally) and atrophy progression (longitudinally).Results showed that 40% of pathology proven cases of TDP-43-C diagnosed with a temporal variant presented with right-lateralized atrophy. Moreover, the findings of our ATL ROI analysis indicated that, irrespective of atrophy lateralization, atrophy distribution within both ATLs follows a medial-to-lateral gradient. Finally, in both left and right cases, atrophy appeared to progress to the contralateral ATL, and from the anterior temporal pole to posterior temporal and orbitofrontal regions.Taken together, our findings indicate that incipient right predominant ATL atrophy is common in TDP-43-C pathology, and that distribution of damage within the ATLs appears to be the same in left- and right- sided variants. Thus, regardless of differences in clinical phenotype and atrophy lateralization, both temporal variants of FTD should be viewed as a spectrum presentation of the same disease.Highlights⍰ Anterior temporal lobe (ATL) degeneration is most often caused by FTLD-TDP type C pathology⍰ Cases can present with predominantly left (60%) or right (40%) ATL atrophy⍰ Within ATLs, medial regions are more vulnerable than lateral ones⍰ The observed spectrum of clinical phenotypes is driven by atrophy lateralization⍰ Left and right temporal variants of FTD should be considered the same disease

scholarly journals Cerebral trauma-induced dyschromatopsia in the left hemifield: case presentation

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yoko Mase ◽  
Yoshitsugu Matsui ◽  
Eriko Uchiyama ◽  
Hisashi Matsubara ◽  
Masahiko Sugimoto ◽  
...  
Keyword(s):  
Visual Field ◽  
Color Vision ◽  
Temporal Lobe ◽  
Fusiform Gyrus ◽  
Ganglion Cell Complex ◽  
Automated Perimetry ◽  
Subjective Symptoms ◽  
Anterior Temporal Lobe ◽  
Case Presentation ◽  
Cerebral Trauma

Abstract Background Acquired color anomalies caused by cerebral trauma are classified as either achromatopsias or dyschromatopsias (Zeki, Brain 113:1721–1777, 1990). The three main brain regions stimulated by color are V1, the lingual gyrus, which was designated as human V4 (hV4), and the fusiform gyrus, designated as V4α. (Zeki, Brain 113:1721–1777, 1990). An acquired cerebral color anomaly is often accompanied by visual field loss (hemi- and quadrantanopia), facial agnosia, prosopagnosia, visual agnosia, and anosognosia depending on the underlying pathology (Bartels and Zeki, Eur J Neurosci 12:172–193, 2000), (Meadows, Brain 97:615–632, 1974), (Pearman et al., Ann Neurol 5:253–261, 1979). The purpose of this study was to determine the characteristics of a patient who developed dyschromatopsia following a traumatic injury to her brain. Case presentation The patient was a 24-year-old woman who had a contusion to her right anterior temporal lobe. After the injury, she noticed color distortion and that blue objects appeared green in the left half of the visual field. Although conventional color vision tests did not detect any color vision abnormalities, short wavelength automated perimetry (SWAP) showed a decrease in sensitivity consistent with a left hemi-dyschromatopsia. Magnetic resonance imaging (MRI) detected abnormalities in the right fusiform gyrus, a part of the anterior temporal lobe. At follow-up 14 months later, subjective symptoms had disappeared, but the SWAP abnormalities persisted and a thinning of the sectorial ganglion cell complex (GCC) was detected. Conclusion The results indicate that although the subjective symptoms resolved early, a reduced sensitivity of SWAP remained and the optical coherence tomography (OCT) showed GCC thinning. We conclude that local abnormalities in the anterior section of fusiform gyrus can cause mild cerebral dyschromatopsia without other symptoms. These findings indicate that it is important to listen to the symptoms of the patient and perform appropriate tests including the SWAP and OCT at the early stage to objectively prove the presence of acquired cerebral color anomaly.

scholarly journals M146. NEUROCHEMICAL MODULATION OF AUDITORY CORTEX FUNCTIONAL CONNECTIVITY IN PATIENTS WITH AUDITORY VERBAL HALLUCINATIONS

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S191-S191
Author(s):  
Sarah Weber ◽  
Helene Hjelmervik ◽  
Alexander R Craven ◽  
Erik Johnsen ◽  
Rune Kroken ◽  
...  
Keyword(s):  
Functional Connectivity ◽  
Temporal Lobe ◽  
Superior Temporal Gyrus ◽  
Underlying Mechanism ◽  
Auditory Hallucinations ◽  
Anterior Cingulate ◽  
Gamma Aminobutyric Acid ◽  
Auditory Verbal Hallucinations ◽  
Left And Right ◽  
Neurochemical Correlates

Abstract Background Auditory hallucinations have been linked to aberrant functioning of the left superior temporal gyrus (STG) and are associated with impaired cognitive control regulated by areas in the prefrontal cortex. However, the mechanisms behind these dysfunctions are still unclear. Methods The current study combined resting state connectivity fMRI with MR spectroscopy (MRS) in a sample of 81 psychosis patients to explore how neurochemical correlates of auditory hallucinations modulate left STG functioning. The analyses were focused on glutamate (Glu) and gamma-aminobutyric acid (GABA), two neurotransmitters with excitatory and inhibitory functions, respectively, since these have previously been implicated in psychosis. Results Glu and GABA showed differential relationships with left STG connectivity in patients with and without hallucinations. Specifically, Glu concentration in the anterior cingulate cortex (ACC) was positively related to functional connectivity between the left and right temporal lobe in hallucinating patients only. In contrast, GABA concentration in the ACC was negatively related to connectivity between the left and right temporal lobe in non-hallucinating patients only. Discussion These findings support a recently proposed model of interhemispheric temporal lobe miscommunication in auditory hallucinations and indicate prefrontal neurochemical modulation as a potential underlying mechanism. The results can further be integrated with previously suggested excitatory/inhibitory imbalances as neurochemical modulators in AVH.

scholarly journals Pre-Surgical Mood Predicts Memory Decline after Anterior Temporal Lobe Resection for Epilepsy

2011 ◽  
Vol 26 (8) ◽  
pp. 739-745 ◽  
Author(s):  
R. M. Busch ◽  
M. F. Dulay ◽  
K. H. Kim ◽  
J. S. Chapin ◽  
L. Jehi ◽  
...  
Keyword(s):  
Temporal Lobe ◽  
Anterior Temporal Lobe ◽  
Memory Decline ◽  
Temporal Lobe Resection
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