Changes In Intra/extracellular Processes At Cellular Level During Neurometabolic Tbi

Front 1

Changes in intra/extracellular processes at cellular level during neurometabolic TBI

Back 1

Cascade 1: Nonspecific depolarization and initiation of action potentials (no messenger telling them to stop causing increased activity and quickens fatigue) release of excitatory amino acid (glutamate (which is made by glial cells)) this is the messenger at the synaptic cleft that allows action potentials to be processed. This causes a massive efflux (moving out) of potassium as constant action potential are occuring. Normally this excess potassium is taken up by glial cells (as they are known as scavengers) but this mechanism is overused as there are too many action potentials occuring. Excitation is always followed by a wave of neuronal suppression as repolarization and hyperpolarization need to occur. This depresses the neurons which affect areas through the brain and may be the root of many of the cognitive deficits that are observed post injury. Cascade 2: Increased activity of membrane ionic pumps due to increased nonspecific depolarization causes and increase in glucose use. This results in hyperglycolysis to generate more atp (oxidative metabolism cannot keep up with the increased glucose use so anaerobic glycolysis occurs in order to maintin energy supply=hyperglycolysis) this anaerobic glycolysis causes lactate accumulation and can possibly leave the brain more vulnerable. The mitochondria responds to the increased glutamate in the cell body by increasing calcium influx and sequestration (isolating) in mitochondria which leads to impaired oxidative metabolism. This leads to decreased energy (ATP) production and intracellular magnesium. Initiation of apoptosis (replacing of damaged cells) through a variety of potential mechanisms

Front 2

measures used to assess neurometabolic changesat the cellular level

Back 2

Various componenets of cerebral metabolism are made prior to and various times after the injury to assess the effects of the damage. Or in mice, a fluid percussion injury is induced.

Front 3

changesin axonal processes

Back 3

neurofilament compaction causes decreased permeability inthe axons and sidearm cleavage is the splitting of the neurofilamentmicrotubule disassembly cause by impact and prevent axon tobe in resting status causing a wavy axon. since these axons are not sound, theycannot create an action potentialall caused by axonal diffusion which is the shearing of theinside of the axon when a concussion occurs, it is not the impact that causesthe axons to sheer but moreso the moving around of the brain inside the head.this sheering often cause people to pass out. axonal disruption gets increased over time after theincident occurs, microglia is then released as scavengers to pick up deadtissue

Front 4

measures used to assess axonal changes

Back 4

Damage can be detected by diffusion weighted imaging -since the TBi lead to abnormalities in the pathway. shows pathways are notsound (wave like) and therefore cannot create action potentials

Front 5

correlation between symptoms/severity and cellular measures

Back 5

Fractional Anisotropy (FA) score – the higher the score, the lessdisruption there is and the more intact the white matter is. And vice versa Thisrepresent the correlation of water molecules. So in a good axon they can moveone way but if it is disrupted then the water can leave. Low fa score iscorrelated with a bigger conflict score (periphereal arrow is pointed away oftowards middle arrow) and the harder time you have deciding this, the morenegative your score is and is associated with low FA.

Front 6

animal models and human correlates

Back 6

Both get similar results in diffuse axonal injury

Front 7

neuropathological findings in neuronsand glial cells

Back 7

Microglia cells are activated as part of response to head injury and act as scavengers for damaged tissue. During a TBI they change shape, cell body expands and dendrites change shape.Greater density of microglial cells as a response of brain injury

Front 8

Attentional/cognitive deficitsfollowing concussion

Back 8

Attention is the cognitive process ofselectively concentrating on one thing while ignoring other things.

Concussion participants had slightly highererror rates

Disproportionately slower on accurate comparedto inaccurate trials. (in order for concussed people to be accurate they needto slow down a lot more) both as slow on inaccurate tasks

Orientingdeficit resolved within 1 week, conflict deficit still present 1 month after injury. (Conflict effect mirrorsreaction time – improvement overall at disentangling flanker arrows. )·

Things are mostly resolved within a week exceptfor conflict.

Alerting effect - time before target appears

learning effect still doesn't change after a month