What is as mild TBI?
An injury to the head that result in one or more of the following:
- Transient confusion, disorientation, impaired consciousness
- Dysfunction of memory around the time of injury
- Loss of consciousness lasting less than 30 min (Plane of rotation of injury determines if there will be loss of consciousness in an mTBI)
-Diagnosed clinically with exclusion, no neuroimaging/blood tests can detect them (future: diffusion tensor imaging and biomarkers)
Risk factors for mTBI
Age
-65
Sex
-male
Sports
Occupation
Alcohol and drugs
Diffuse axonal injury (DAI)
- Likely the primary pathological substrate of mTBI (mechanical stretching of axons)
- Multifocal injury in which midline structures (like the corpus callosum) are especially vulnerable. The pattern of injury is dependent on the forces/angles of acceleration/contact.
- DAI occurs due to mechanical disruption of the axonal cytoskeleton. There is injury to microtubules–>transport interruption–>swelling and degeneration
Dementia Pugilistica
Renamed chronic traumatic encephalopathy (CTE), it is a dementia associated with boxers.
- Has neurofibrillary tangles
- Increased repetitive trauma leads to increased risk
Gross pathology of mTBI
- Ventricular dilation
- Cerebral atrophy
- ->alz disease looks similar
-Cavum septum pellucidum absent or with fenestrations
Microscopic pathologies
- -Tauopathy in a distribution different than other tauopathies
- -sulcal depth, superficial cortex and perivascular
- Amyloid plaques show up with repetitive TBI or an acute single TBI can cause diffuse amyloid plaques
- TDP-43 proteinopathy
Glasgow Coma Scale
- What is it
- What are the general categories
- What defines mild-severe
Grades the severity of TBI and classifies patient outcome 6-12 mo post-injury (1 is good recovery, 5 is death, not a great scale since recovery means dif things to dif ppl)
Categories: eyes, verbal responses, motor (most impt)
Mild: 13-15
Moderate: 9-12
Severe: 3-8
Glasgow Coma Scale (actual scale)
Eye: 4-eyes open spontaneously 3-eyes open to verbal command 2-eyes open to pain on supraorbital notch 1-eyes do not open
Verbal: 5-oriented, conversant, coherent 4-disoriented, conversant 3-inappropriate words 2-incoherent 1-no response
Motor: 6-follows commands 5-localizes painful stimulus 4-withdrawal from painful stimulus 3-decorticate posture (flexion) 2-decerebrate posture (extension) 1-no response
Contact loading
Direct trauma. Deforms the brain and causes contusions and hematomas
Inertial loading
Causes DAI, most significantly in brainstem, corpus callosum and subcortical white matter
What are the molecular/morphological events in the brain after TBI
- Necrosis/apoptosis of glial cells and neurons
- Inflammation
- Atrophy, especially the hippocampus and cortical tissue
How does the brain recover after TBI?
- Plasticity
- Septal fibers and the entorhinal cortex both innervate the dentate gyrus of the hippocampus
- If the entorhinal cortex is damaged, septal fibers ACh will sprout
- Plasticity can be aberrant leading to phantom limb pain and epilepsy (think seizures after brain trauma) - Neurogenesis
- Increases with exercise, decreases with stress - Physiological recovery
- Behavioral response
- Rat with cortical and hippocampal lesions take longer to find a hidden platform in the water than control rats. They need more time to learn and remember where the platform is
