Impaired vision and cerebral blindness were observed in a patient who had suffered brain trauma. One year after the trauma, the impairment was characterized by low visual acuity, visual field restricted to central tunnel vision and impaired recognition of objects, line drawings, colors and faces. Vision improved six years after the brain trauma with more rapid recognition of objects and line drawings, increased visual acuity and broadening of the visual field. Reading was possible at this time. However, prosopagnosia remained very severe and was still the primary complaint of the patient. Improvement of visual function continuing for several years after a brain injury is discussed on the basis of cognitive and neurophysiological knowledge. The place of rehabilitation is discussed. Functional improvement is explained by extrastriate cortical afferences and the cortical network of visual pathways.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Adolescent mice exposed to TBI developed PD-like pathology in middle age.
Transl Psychiatry
January 2025
Department of Neurosurgery, General Hospital of Northern Theater Command, Postgraduate Training Base of General Hospital of Northern Theater Command of Jinzhou Medical University, Shenyang, Liaoning, China.
Traumatic brain injury (TBI) is identified as a risk factor for Parkinson's disease (PD), which is a neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra (SN). However, the precise mechanism by which chronic TBI initiates PD pathogenesis is not yet fully understood. In our present study, we assessed the chronic progression and pathogenesis of PD-like behavior at different intervals in TBI mice.
View Article and Find Full Text PDFUnique considerations in the assessment and management of traumatic brain injury in older adults.
Lancet Neurol
February 2025
Department of Neurology AB51, University of Groningen, University Medical Center Groningen, Groningen, Netherlands.
The age-specific incidence of traumatic brain injury in older adults is rising in high-income countries, mainly due to an increase in the incidence of falls. The severity of traumatic brain injury in older adults can be underestimated because of a delay in the development of mass effect and symptoms of intracranial haemorrhage. Management and rehabilitation in older adults must consider comorbidities and frailty, the treatment of pre-existing disorders, the reduced potential for recovery, the likelihood of cognitive decline, and the avoidance of future falls.
View Article and Find Full Text PDFEvidence for cellular and solute passage between the brain and skull bone marrow across meninges: A systematic review.
J Cereb Blood Flow Metab
January 2025
KG Jebsen Centre for Brain Fluid Research, University of Oslo, Oslo, Norway.
A potential two-way passage of cells and substances between the brain and skull bone marrow may open for new insights into neurological disease. The arachnoid membrane was traditionally considered to restrict cells and larger molecules in CSF from entering the dura and bone marrow directly. However, new data on exchange between brain and skull bone marrow have recently emerged.
View Article and Find Full Text PDFA-kinase anchor protein 12 promotes oligodendrogenesis and cognitive recovery in carbon monoxide therapy for traumatic brain injury.
J Cereb Blood Flow Metab
January 2025
Departments of Neurology and Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, USA.
Therapeutic drug development for central nervous system injuries, such as traumatic brain injury (TBI), presents significant challenges. TBI results in primary mechanical damage followed by secondary injury, leading to cognitive dysfunction and memory loss. Our recent study demonstrated the potential of carbon monoxide-releasing molecules (CORMs) to improve TBI recovery by enhancing neurogenesis.
View Article and Find Full Text PDFMitochondria as a Therapeutic Target: Focusing on Traumatic Brain Injury.
J Integr Neurosci
January 2025
Department of Hepatology, Federal University of Health Sciences of Porto Alegre (UFCSPA), 90050-170 Porto Alegre, Rio Grande do Sul (RS), Brazil.
Mitochondria are organelles of eukaryotic cells delimited by two membranes and cristae that consume oxygen to produce adenosine triphosphate (ATP), and are involved in the synthesis of vital metabolites, calcium homeostasis, and cell death mechanisms. Strikingly, normal mitochondria function as an integration center between multiple conditions that determine neural cell homeostasis, whereas lesions that lead to mitochondrial dysfunction can desynchronize cellular functions, thus contributing to the pathophysiology of traumatic brain injury (TBI). In addition, TBI leads to impaired coupling of the mitochondrial electron transport system with oxidative phosphorylation that provides most of the energy needed to maintain vital functions, ionic homeostasis, and membrane potentials.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!