NEUR 1203 Lecture 8-10: Concussions, Symptoms, and Brain Injury PDF

2/10/25, 12:48 PM NEUR 1203 LECTURE 8-10 NEUR 1203 LECTURE 8-10 violent jarring or shaking that results in a...

2/10/25, 12:48 PM NEUR 1203 LECTURE 8-10 NEUR 1203 LECTURE 8-10 violent jarring or shaking that results in a disturbance of brain function type of mild traumatic brain injury - a bump/blow to the head or body that causes the brain to move back and forth rapidly in the What are concussions? skull occasionally there can be bleeding when there is a mTBI it doesnt necessarily have to be a physical blow to the head if the brain moves within the skull it is a concussion can happen anywhere, anytime you hit your head majority of concussions in children due to Epidemiology of concussions sporting accidents (ie. football - most common, hockey, soccer, lacrosse) in adults or sensiors it is a slip or fall concussions are the main reasons for a TBI physical symptoms: headache, ringing in ears, nausea, vomiting, fatigue, drowsiness, blurry vision cognitive symptoms: confusion, amnesia, dizziness/seeing stars, forgetfulness, light sensitivity, emotional disturbances Symptoms of a concussion Amygdala: headache, feeling “slow” or “foggy”, irritability, sadness, nervousness, more emotional, loss of sleep anterior intra-parietal sulcus: light sensitivity, noise sensitivity, motor control, visual problems symptoms depend on the brain region affected/where they were hit what causes a concussion? rapid changes in the velocity of the head (ie. accerleration/deacceleration) = brain hitting the skull https://knowt.com/flashcards/513b057a-4fc2-4792-a4b0-2d715455e785?isNew=true 1/7  can occur front to back, side to side - brain 2/10/25, 12:48 PM NEUR 1203 LECTURE 8-10 essentially bounces off skull and hits the other side meninges and CSF work together to prevent the brain from damage but cannot stop this kind of movement followed by bruising/swelling for up to 48 hours, which leads to increased intracranial pressure, affects neurons and they dont work as well contusion: brain bruise edema: swelling our brains are floating in CSF = weightless, abrupt change in velocity, the brain keeps going in the original directional direction of the hit is what changes the severity, generally skull is not broken in concussion Coup: refers to the side of the skull that receives the hit - pressure from a coup produces a contre coup on the opposite end Coup-Contre Coup Contrecoup: the after effect where the brain hits the opposite side of the skull movement of the brain may shear nerve fibers causing microscopic kesions, especially in frontal and temporal lobes hematoma: blood trapped in the skull epidermal hematoma: physical breaking of the skull impact to the skull dont need to be direct, can still get concussed indirectly, like a blast in a warzone, 1 in 5 US military personnel have experienced a concussion type of impact does matter: Impact of a concussion 1. angular 2. rotational 3. linear usually a combination of one or more, direction of force predicts severity of concussion https://knowt.com/flashcards/513b057a-4fc2-4792-a4b0-2d715455e785?isNew=true 2/7 2/10/25, 12:48 PM NEUR 1203 LECTURE 8-10 concussions require 90-100 g-force (20mph) - severity is not associated with the magnitude of the force, there is a minium amount of force needed for a concussion after that point is reached, incresing force will not increase direction of a hit in concussions severity direction of force dictates symptom presentation & long-term consequences causes individualized symptom presentation, very hard to compare between patients magnitude of rotation related directly to severity, cayses Diffuse axonal injury (DAI) DAI: shears the white matter, when you have too much glutamate, your neurons fire too much and dont have the resources to keep up so they die, tearing is more common that shearing so the axons are able to repair themselves over a couple of weeks excitatory induced lesions due to Rotational forces and the brain indiscriminate release of glutamate 24-48Hr after concussion DAI in the midbrain and diencephalon = loss of consciousness shearing of axons can lead to subdural hematoma = clotted blood in the subdural space, which increased pressure on the brain epidural hematoma is not typically found in concussions, but results from a skull fracture severing the middle meningeal artery acute damage of neural and vascular brain tissue = distortion of cell membranes causes increase in neural activity through Acute Metabolic Cascade glutamate release - thus leads to an energy crisis because u are using more resources interrupts blood flow to the brain metabolic cascade = energy crisis what happens in acute metabolic cascade? membrane stretching opens voltage gated calcium and potassoum channels = depolarization and glutamate release https://knowt.com/flashcards/513b057a-4fc2-4792-a4b0-2d715455e785?isNew=true 3/7  more transient increase in glucose 2/10/25, 12:48 PM NEUR 1203 LECTURE 8-10 mentabolism and lactate production immediate decreased in blood flow glucose goes up blood flow goes down massive increase in depolarized cells, sodium and potassium pump need to work overtime to return to ionic balance pump requires ATP which is produced from metabolizing glucose but blood flow is reduced, less resources to affected areas main excitatory neurotransmitter in the brain, can become excitotoxic, too much can damage surrounding neurons receptors like AMPA, NMDA, Kainate are all permeable to sodium = EPSPS why is a glutamate surge bad? Necrosis: rapid lysis due to osmotic swelling (too much ionic influx forces more water into the cell causing it to bursts) Apoptosis: programmed cell death, delayed response to biochemical events that causes DNA break up and cell death activation of NMDA ( glutamate receptor) also leads to the entry of calcium neurons increased calcium causes the negative effects on the mitochondria where most energy is Glutamate & Calcium produced, too fast oroduction of anything is bad increased deman of ATP (energy) and reduction in blood flow bringing molecules in the brain and reduced energy metabolism due to impaired mitochondria steps of acute metabolic cascade 1. rotational force = shearing of neurons and vasculature, release of glutamate 2. membrane gets strecthed and potassium goes out and calcium goes into cell 3. release of more glutamate 4. glutamate continues to cause further depolarizations sodium and calcium https://knowt.com/flashcards/513b057a-4fc2-4792-a4b0-2d715455e785?isNew=true 4/7  are in 2/10/25, 12:48 PM NEUR 1203 LECTURE 8-10 5. increased glucose metabolism for ATP production 6. decreased blood flow and impairment to mitochondria leads to energy crisis - not enough blood sugar in specific areas 7. energy crisis leads to secondary injuries due to the increased energy requirements, brain switches to anaerobic glucose metabolism (glycolysis) which produces lactic acid lactic acid overproduction can lead to acidosis secondary inuries - blood brain barrier = damaging to the blood brain barrier damage to the BBB causes increased permeability and increased risk for toxins to get through to the brain if you need energy fast, you produce lactic acid, too much lactic acid creates a less strong BBB normally the brain is rather resistant to inflammations due to the BBB preventing cytokines from entering disruption to this can allow cytokines to eneter which can leads to patients deterioration in BBB & Inflammations stages, cytokines dont degrade as quickly and symptoms lasts longer primary injuries: axonal damage, membrane disruption and indlammation secondary injuries: cellular damage, apoptosis, oxidative stresss https://knowt.com/flashcards/513b057a-4fc2-4792-a4b0-2d715455e785?isNew=true 5/7 2/10/25, 12:48 PM NEUR 1203 LECTURE 8-10 signs observed: cant recall events prior to hit or fall, appears dazed or stunned, forgets intructions,moves clumisly, answers questions slowly, loss of consicousness (even briefly), Symptoms and Signs of a concussion shows mood,behaviour or personality changes Symptoms reported: headache or pressure in the head, nausea or vomitting, balance problems or dizziness, double or blurry vision, bother by light or noise, slugish,lazy, not feeling right or feeling down Concussion recognition tool 5 (CRT5): for use by non-medical professionals immediately after injury, allows coaches to make immediate call to pull a player and seek medical attention Immediate post concussions & cognitive testing (ImPACT) : computer based program, pre-screening evaluation following concussions screening SCATS: medical personnel are trained to use Concussion Detection this tool which involved these steps: 1. red flags (ie. blurry vision, dizziness) 2. observable signs (visible disorientation) 3. memory assessment questionnaire 4. glasgow coma score assessment - light in eye, pushing on hands and feet..etc. 5. cervical spine assessment 6. follow up with an office assessment Second Impact Syndrome SIS is a condition that occurs when a concussed individual sustains a second impact upon their head before fully recovering from the first blow, prior concussions greatly increase likelihood of another concussion and increase morbidity repeated concussions have a cumulative effect on the human brain ( the more you have the worse they get), energy crisis leaves the brain extremely sysceptible to further injury for up to 10 days https://knowt.com/flashcards/513b057a-4fc2-4792-a4b0-2d715455e785?isNew=true 6/7  animal models show 50% mortality rate and 2/10/25, 12:48 PM NEUR 1203 LECTURE 8-10 100% morbidity rate result of repeated head trauma, not necessarily from concussions, can occur due to repeated sub-concussive blows repeated concussions are one of the highest Chronic Traumatic Encephalopathy (CTE) risk factors for developping CTE progressive degenerative disease similar to Alzheimers, charcaterized by neurofibrillary tangles, amyloid-beta plaques and neuronal cell death typically appears years or decades after last brain trauma/end of sports participation Symptoms of CTE memory loss, confusion, impaired judement, impulse control problems, agression anxiety, suicidality, parkinsonism, dementia..etc. neurofibrillary tangles (NFT) and increased Tau protein begins to be noticeable in the cortex mild enlargement if lateral and 3rd ventricles Pathophysiology of CTE Amyloid beta plaques if > 50 yrs old frontal and temporal atrophy NFT degeneration in Hippocampus atrophy in white matter tracts, widespread myelin loss, dense tau endured 10 recorded concussions during his football career after career began to experience problems with decision making and temper control, Case Study: Dave Duerson symptoms got worse over time age 50 he shot himseld and post morterm was diagnosed with CTE, brain showed tau proteins, degenerating tissue in the frontal cortex and MTL commited suiced while in jail after being found Case Study: Aaron Hernandez not guilty of a murder, post moertem he had extremely advanced CTE (Stage IV), typically only seen in people over 46 yrs old What is a stroke? https://knowt.com/flashcards/513b057a-4fc2-4792-a4b0-2d715455e785?isNew=true 7/7