Incidental Transient Cortical Blindness after Lung Resection.
Ontology highlight
ABSTRACT:
SUBMITTER: Oncel M
PROVIDER: S-EPMC5553457 | biostudies-other | 2016 Mar
REPOSITORIES: biostudies-other
Similar Datasets
Project description:The prevalence of incidental nonneoplastic lung disease in patients undergoing resection for mass lesions is unknown. We determined the prevalence and characteristics of parenchymal findings in patients with lung nodules, aiming to increase awareness of findings that could potentially impact patient management. A total of 397 patients with benign or malignant mass lesions with available presurgical chest computed tomography scans resected between January 2001 and July 2015 were included. Retrospective histologic assessment of parenchymal abnormalities in at least 1 section of grossly normal lung was performed for each case by 2 pulmonary pathologists and correlated with original pathology reports, clinical history, and radiologic findings. A total of 233 women and 164 men underwent resections for carcinomas (78%) or benign nodules (22%). One hundred one (25%) patients showed parenchymal abnormalities, including 14 patients with multiple findings. The most common abnormal findings were fibrotic interstitial changes (10%), including usual interstitial pneumonia (1%), followed by granulomatous processes (8%). Other findings included aspiration (4%), intravascular thrombi (2%), Langerhans cell histiocytosis (1.5%), constrictive bronchiolitis (1%), atypical lymphoid infiltrates (1%), and amyloidosis (0.5%). Abnormalities were more likely to have been documented in the original pathology report by pulmonary pathologists (68%) than by general pathologists (15%) (P < .0001). Cases with histologic parenchymal abnormalities were more likely to show radiologic interstitial lung abnormalities than those without (16% versus 5%; P = .001). Evaluation of background lung parenchyma may yield valuable and unanticipated information in patients undergoing surgical resections for lung masses that may correlate with radiographic interstitial lung abnormalities and influence clinical management.
| S-EPMC6492265 | biostudies-literature
Project description:We report the case of a patient suffering from cortical blindness following bilateral occipital stroke, who recovered normal vision in his right visual field following injection of the local anesthetic mepivacaïne. The effect was transient but reproducible, allowing the patient to lead a normal life. Effect duration increased after adjunction of paroxetine. We provide anatomical and functional brain imaging correlates of this improvement, showing particularly how functional connectivity is restored between intact perilesional cortex and distant brain regions. This serendipitous finding may potentially benefit patients suffering from visual but also nonvisual handicap following brain lesions.
| S-EPMC6689678 | biostudies-literature
Project description: Not available
| S-EPMC4208121 | biostudies-literature
Project description:We herein report a case of life-threatening haemothorax that occurred 40 days after pulmonary segmentectomy in a 60-year-old man. The patient uneventfully underwent resection of the apical and posterior segments of the right upper lobe by video-assisted thoracic surgery for early-stage lung cancer. An emergency operation of haemostat for active bleeding from the intercostal artery was successful via a right thoracotomy. The bleeding point was in the vicinity of the staple line dividing the intersegmental plane. This case reveals that scratch by staples can cause haemothorax through incidental injury of the intercostal artery.
| S-EPMC6908458 | biostudies-literature
Project description:Fast and automatic behavioral responses are required to avoid collision with an approaching stimulus. Accordingly, looming stimuli have been found to be highly salient and efficient attractors of attention due to the implication of potential collision and potential threat. Here, we address the question of whether looming motion is processed in the absence of any functional primary visual cortex and consequently without awareness. For this, we investigated a patient (TN) suffering from complete, bilateral damage to his primary visual cortex. Using an fMRI paradigm, we measured TN's brain activation during the presentation of looming, receding, rotating, and static point lights, of which he was unaware. When contrasted with other conditions, looming was found to produce bilateral activation of the middle temporal areas, as well as the superior temporal sulcus and inferior parietal lobe (IPL). The latter are generally thought to be involved in multisensory processing of motion in extrapersonal space, as well as attentional capture and saliency. No activity was found close to the lesioned V1 area. This demonstrates that looming motion is processed in the absence of awareness through direct subcortical projections to areas involved in multisensory processing of motion and saliency that bypass V1.
| S-EPMC4614319 | biostudies-literature
Project description:Damage to the primary visual cortex typically causes cortical blindness (CB) in the hemifield contralateral to the damaged hemisphere. Recent evidence indicates that visual training can partially reverse CB at trained locations. Whereas training induces near-complete recovery of coarse direction and orientation discriminations, deficits in fine motion processing remain. Here, we systematically disentangle components of the perceptual inefficiencies present in CB fields before and after coarse direction discrimination training. In seven human CB subjects, we measured threshold versus noise functions before and after coarse direction discrimination training in the blind field and at corresponding intact field locations. Threshold versus noise functions were analyzed within the framework of the linear amplifier model and the perceptual template model. Linear amplifier model analysis identified internal noise as a key factor differentiating motion processing across the tested areas, with visual training reducing internal noise in the blind field. Differences in internal noise also explained residual perceptual deficits at retrained locations. These findings were confirmed with perceptual template model analysis, which further revealed that the major residual deficits between retrained and intact field locations could be explained by differences in internal additive noise. There were no significant differences in multiplicative noise or the ability to process external noise. Together, these results highlight the critical role of altered internal noise processing in mediating training-induced visual recovery in CB fields, and may explain residual perceptual deficits relative to intact regions of the visual field.
| S-EPMC4585331 | biostudies-literature
Project description:When the primary visual cortex (V1) is damaged, cortical blindness results. However, visual information obtained from the superior colliculus (SC) or direct thalamic afferents to higher visual cortices produces unconscious visual functions called blindsight. Alarming visual stimuli suggesting the approach of a predator are known to trigger escape behaviors via visual information mediated by the SC and amygdala in small animals, and salient and dynamic visual stimuli also produce some conscious visual experience even in patients with blindsight. Fresh cortical blindness sometimes recovers spontaneously in patients with fresh cerebral damages, and recovery can be accelerated by early rehabilitation. However, the mechanisms underlying recovery are not well-known. We analyzed a patient with cortical blindness caused by an old cerebral infarction. After repeated presentation of alarming visual stimuli, the ability to detect visual stimuli in the impaired visual field showed behavioral short-term improvement (STI) within a few minutes. Repeated behavioral STI induction was followed by behavioral long-term improvement (LTI) lasting more than several days. After behavioral LTI, the patient partially recovered the ability to read letters presented in the impaired visual field. The behavioral STI experiment, which can be performed within 10 min, may serve as a clinical screening test for anticipating recovery from cortical blindness.
| S-EPMC7020609 | biostudies-literature
Project description:Epileptic encephalopathies are increasingly thought to be of genetic origin, although the exact etiology remains uncertain in many cases. We describe here three girls from two nonconsanguineous families affected by a clinical entity characterized by dysmorphic features, early-onset intractable epilepsy, intellectual disability, and cortical blindness. In individuals from each family, brain imaging also showed specific changes, including an abnormally marked pontobulbar sulcus and abnormal signals (T2 hyperintensities) and atrophy in the occipital lobe. Exome sequencing performed in the first family did not reveal any gene with rare homozygous variants shared by both affected siblings. It did, however, show one gene, DOCK7, with two rare heterozygous variants (c.2510delA [p.Asp837Alafs(∗)48] and c.3709C>T [p.Arg1237(∗)]) found in both affected sisters. Exome sequencing performed in the proband of the second family also showed the presence of two rare heterozygous variants (c.983C>G [p.Ser328(∗)] and c.6232G>T [p.Glu2078(∗)]) in DOCK7. Sanger sequencing confirmed that all three individuals are compound heterozygotes for these truncating mutations in DOCK7. These mutations have not been observed in public SNP databases and are predicted to abolish domains critical for DOCK7 function. DOCK7 codes for a Rac guanine nucleotide exchange factor that has been implicated in the genesis and polarization of newborn pyramidal neurons and in the morphological differentiation of GABAergic interneurons in the developing cortex. All together, these observations suggest that loss of DOCK7 function causes a syndromic form of epileptic encephalopathy by affecting multiple neuronal processes.
| S-EPMC4121477 | biostudies-literature
Project description:The ability of sensory networks to transiently store information on the scale of seconds can confer many advantages in processing time-varying stimuli. How a network could store information on such intermediate time scales, between typical neurophysiological time scales and those of long-term memory, is typically attributed to persistent neural activity. An alternative mechanism which might allow for such information storage is through temporary modifications to the neural connectivity which decay on the same second-long time scale as the underlying memories. Earlier work that has explored this method has done so by emphasizing one attractor from a limited, pre-defined set. Here, we describe an alternative, a Transient Attractor network, which can learn any pattern presented to it, store several simultaneously, and robustly recall them on demand using targeted probes in a manner reminiscent of Hopfield networks. We hypothesize that such functionality could be usefully embedded within sensory cortex, and allow for a flexibly-gated short-term memory, as well as conferring the ability of the network to perform automatic de-noising, and separation of input signals into distinct perceptual objects. We demonstrate that the stored information can be refreshed to extend storage time, is not sensitive to noise in the system, and can be turned on or off by simple neuromodulation. The diverse capabilities of transient attractors, as well as their resemblance to many features observed in sensory cortex, suggest the possibility that their actions might underlie neural processing in many sensory areas.
| S-EPMC5720801 | biostudies-other
Project description:BackgroundThe epileptic encephalopathies display extensive locus and allelic heterogeneity. Biallelic truncating DOCK7 variants were recently reported in five children with early-onset epilepsy, intellectual disability, and cortical blindness, indicating that DOCK7 deficiency causes a specific type of epileptic encephalopathy.MethodsWe identified 23- and 27-year-old siblings with the clinical pattern reported for DOCK7 deficiency, and conducted genome-wide linkage analysis and WES. The consequences of a DOCK7 variant were analyzed on the transcript and protein level in patients' fibroblasts.ResultsWe identified a novel homozygous DOCK7 frameshift variant, an intragenic tandem duplication of 124-kb, previously missed by CGH array, in adult patients. Patients display atrophy in the occipital lobe and pontine hypoplasia with marked pontobulbar sulcus, and focal atrophy of occasional cerebellar folia is a novel finding. Recognizable dysmorphic features include normo-brachycephaly, narrow forehead, low anterior and posterior hairlines, prominent ears, full cheeks, and long eyelashes. Our patients function on the level of 4-year-old children, never showed signs of regression, and seizures are largely controlled with multi-pharmacotherapy. Studies of patients' fibroblasts showed nonsense-mediated RNA decay and lack of DOCK7 protein.ConclusionDOCK7 deficiency causes a definable clinical entity, a recognizable type of epileptic encephalopathy.
| S-EPMC8104163 | biostudies-literature