Effects to exposure of tobacco smoke and alcohol on the tongue and pharynx of rats.

AIM: To study in rats the effects of exposure to tobacco and alcohol on the mucosa of the tongue and pharynx. MATERIAL AND METHODS: Forty adult Wistar rats were allocated into four groups of 10 animals each: GI (control), food and water "ad libitum"; GII (alcohol), 30% of ethanol diluted in drinking water and food "ad libitum"; GIII (tobacco), exposure to the smoke of 10 cigarettes/day, food and water "ad libitum"; GIV (alcohol and tobacco), simultaneous exposure to both agents. After 260 days, the animals were sacrificed. Tongue and pharynx were removed for histopathological analysis. RESULTS: GI had the lowest tongue and pharynx histological scores. In GII, GIII, and GIV tongue samples revealed: apical cell hyperplasia (GII: 60%, GIII: 30%, GIV: 20%), basal cell hyperplasia (GII: 60%, GIII: 40%), hyperkeratosis (GII: 70%, GIII: 30%, GIV: 30%), dysplasia (GII: 60%, GIII: 60%, GIV: 50%), and apoptosis (GII: 60%, GIII: 40%, GIV: 60%). Pharynx samples revealed: apical cell hyperplasia (GII: 40%, GIII: 30%, GIV: 70%), basal cell hyperplasia (GII: 30%, GIII: 40%, GIV: 40%), hyperkeratosis (GII: 50%, GIII: 80%, GIV: 40%), and dysplasia (GII: 50%, GIII: 80%, GIV: 50%). Carcinoma in situ was detected in both sites. CONCLUSIONS: Alcohol and tobacco led to significant tongue and pharyngeal lesions that ranged from benign events to severe dysplasia. These findings confirm the deleterious effects of alcohol and tobacco on the airway mucosa.

Source Analysis of Triphasic Waves Using Quantitative Neuroimaging.

PURPOSE: Triphasic waves (TWs), a common EEG pattern, are considered a subtype of generalized periodic discharges. Most patients with TWs present with an altered level of consciousness, and the TW pattern is believed to represent thalamocortical dysfunction. However, the exact meaning and mechanism of TWs remain unclear. The objective of the current study was to evaluate the source of TWs using EEG source imaging and computerized tomography. METHODS: Twenty-eight patients with TWs were investigated. Source analysis was performed on the averaged TWs for each individual, and source maps were extracted. Normalization and automatic segmentation of gray matter were performed on computerized tomography scans before analysis. Finally, voxelwise correlation analyses were conducted between EEG source maps and gray matter volumes. RESULTS: Source analyses showed that the anterior cingulate cortex was mainly involved in TWs (16/28 patients, 57%). Correlation analyses showed moderate positive and negative correlations between source location and gray matter volumes for the posterior cingulate ( T = 2.85; volume = 6,533 mm 3 ; r = 0.53; P = 0.002) and the superior frontal gyrus ( T = 2.54; volume = 18,167 mm 3 ; r = -0.48; P < 0.0001), respectively. CONCLUSIONS: The results suggest that the anterior cingulate is involved in the origin of TWs. Furthermore, the volumes of posterior brain regions were positively correlated with TWs, indicating a possible preservation of these structures. Conversely, the volumes of anterior regions were negatively correlated with TWs. These findings may indicate a structural pattern necessary for the generation of the abnormal network responsible for TWs.

What are the barriers to participation in a neuromodulation pilot trial for aphasia after stroke?

PURPOSE: Aphasia is a common and debilitating manifestation of stroke. Transcranial electrical stimulation uses low-intensity electric currents to induce changes in neuronal activity. Recent evidence suggests that noninvasive techniques can be a valuable rehabilitation tool for patients with aphasia. However, it is difficult to recruit patients with aphasia for trials, and the reasons for this are not well understood. This study aimed to elucidate the main difficulties involved in patient's recruitment and inclusion in a randomized clinical study of neuromodulation in aphasia. METHODS: We evaluated the reasons for the exclusion of patients in a pilot, randomized, double-blinded clinical trial in which patients diagnosed with motor aphasia after stroke were recruited from March to November 2018. A descriptive statistical analysis was performed. RESULTS: Only 12.9% (4) of patients with ischemic stroke were included in the clinical trial. A total of 87.1% (27) of the 31 recruited patients were excluded for various reasons including: sensory aphasia (32.2%), dysarthria (25.8%), spontaneous clinical recovery (16.1%), previous stroke (6.4%), and death or mutism (3.2%). CONCLUSION: The presence of other types of aphasia, dysarthria, spontaneous recovery, deaths, and mutism were barriers to recruiting patients evidenced in this neuromodulation study.

Analysis of Interictal Epileptiform Discharges in Mesial Temporal Lobe Epilepsy Using Quantitative EEG and Neuroimaging.

Objective: Investigate areas of correlation between gray matter volumes by MRI and interictal EEG source maps in subtypes of mesial temporal lobe epilepsy (MTLE). Method: 71 patients and 36 controls underwent 3T MRI and and routine EEG was performed. Voxel-based morphometry (VBM) was used for gray matter analysis and analysis of interictal discharge sources for quantitative EEG. Voxel-wise correlation analysis was conducted between the gray matter and EEG source maps in MTLE subtypes. Results: The claustrum was the main structure involved in the individual source analysis. Twelve patients had bilateral HA, VBM showed bilateral hippocampal. Twenty-one patients had right HA, VBM showed right hippocampal and thalamic atrophy and negatively correlated involving the right inferior frontal gyrus and insula. Twenty-two patients had left HA, VBM showed left hippocampal atrophy and negatively correlated involving the left temporal lobe and insula. Sixteen patients had MTLE without HA, VBM showed middle cingulate gyrus atrophy and were negatively correlated involving extra-temporal regions, the main one located in postcentral gyrus. Conclusions: Negative correlations between gray matter volumes and EEG source imaging. Neuroanatomical generators of interictal discharges are heterogeneous and vary according to MTLE subtype. Significance: These findings suggest different pathophysiological mechanisms among patients with different subtypes of MTLE.

Analysis of patients with obstructive sleep apnea with and without pharyngeal myopathy using brain neuroimaging.

STUDY OBJECTIVES: Elements impairing upper airway anatomy or muscle function (e.g. pharyngeal neuromyopathy) contribute to obstructive sleep apnea syndrome (OSAS). Structural brain imaging may differ in patients with OSAS according to dilator muscle dysfunction. Magnetic resonance imaging (MRI) with voxel-based morphometry (VBM) and surface-based morphometry (SBM) was used to investigate this hypothesis. METHODS: Eighteen patients with OSAS and 32 controls underwent 3T brain MRI. T1 volumetric images were used for structural analysis. Pharyngeal electroneuromyography was performed; patients with OSAS were classified as with or without neuromyopathy. VBM and SBM analyses were conducted using SPM12 and CAT12 software. Image processing was standard. Cortical surface parameters and gray and white matter volumes from participants with OSAS with and without neuromyopathy were compared with those from controls. RESULTS: Eleven patients had OSAS with neuromyopathy and seven patients had OSAS without neuromyopathy (normal pharyngeal electroneuromyography). Comparing these groups to the controls, VBM revealed: four clusters (total volume 15,368 mm3) for patients with neuromyopathy, the largest cluster in the left cerebellum (9,263 mm3, p = 0.0001), and three clusters (total 8,971 mm3) for patients without neuromyopathy, the largest cluster in the left cerebellum (5,017 mm3, p = 0.002). Patients with OSAS with neuromyopathy showed increased proportion of atrophy (p < 0.0001). SBM showed abnormalities in patients without neuromyopathy (decreased cortical thickness, left precentral gyrus [672 vertices, p = 0.04]; increased cortical complexity, right middle temporal gyrus [578 vertices, p = 0.032]). CONCLUSION: Damaged areas were larger in patients with OSAS with than in those without neuromyopathy, suggesting differences in brain involvement. Patients with OSAS and neuromyopathy may be more susceptible to cerebral damage.