Traumatic brain injury: Mechanisms, manifestations, and visual sequelae

Abstract

Traumatic brain injury (TBI) results when external physical forces impact the head with sufficient intensity to cause damage to the brain. TBI can be mild, moderate, or severe and may have long-term consequences including visual difficulties, cognitive deficits, headache, pain, sleep disturbances, and post-traumatic epilepsy. Disruption of the normal functioning of the brain leads to a cascade of effects with molecular and anatomical changes, persistent neuronal hyperexcitation, neuroinflammation, and neuronal loss. Destructive processes that occur at the cellular and molecular level lead to inflammation, oxidative stress, calcium dysregulation, and apoptosis. Vascular damage, ischemia and loss of blood brain barrier integrity contribute to destruction of brain tissue. This review focuses on the cellular damage incited during TBI and the frequently life-altering lasting effects of this destruction on vision, cognition, balance, and sleep. The wide range of visual complaints associated with TBI are addressed and repair processes where there is potential for intervention and neuronal preservation are highlighted.

Association between pediatric traumatic brain injury and epilepsy at later ages in Finland: A nationwide register‐based cohort study

“…Adult PTE is a more widely studied subject, and the estimation of PTE is between 3% and 5% after moderate TBI and between 25% and 50% after severe TBI 23 . Approximately 5% of incident cases and 20% of prevalent cases in the epilepsy population are considered to be due to previous TBI 11 .…”

Multifocal motor neuropathy as a mimic of amyotrophic lateral sclerosis: Serum neurofilament light chain as a reliable diagnostic biomarker

“…We excluded patients with clinical symptoms of other neurodegenerative diseases or recent neuro-traumatic events likely to result in axonal damage and/or neuronal loss. 22 ALS patients with generalized ALS, bulbar involvement, and/or upper motor neuron (UMN) signs (positive Babinski sign, increased muscle tone, spasticity, clonus, and/or loss of dexterity) were excluded. Brisk reflexes were not an exclusion criterion, as this can be observed in a small proportion of MMN patients as well.…”

“…Patients diagnosed with ALS according to the Gold Coast Criteria, with upper or lower extremity onset, 19 and patients with definite and probable MMN according to the criteria of the European Federation of Neurological Societies 20 or, in absence of conduction block, patients with MMN symptomatology and positive response to IVIg therapy 21 were included. We excluded patients with clinical symptoms of other neurodegenerative diseases or recent neuro‐traumatic events likely to result in axonal damage and/or neuronal loss 22 …”

Modulation of beta-hydroxybutyrate in traumatic brain injury

“…Traumatic brain injury (TBI) remains a major public health concern globally with long term consequences that reduce quality of life. Even mild TBI may lead to chronic cognitive impairment [1]. It is associated with a high mortality rate ranging from 30 to 40% across various age groups.…”