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H&I 3 final- Intracranial regulation part 1 & TBI

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H&I 3 final- Intracranial regulation part 1 & TBI

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  • 19 juin 2024
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  • 2023/2024
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  • hi 3 final intracranial regulation part 1 tbi

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H&I 3 final- Intracranial regulation part 1
& TBI
Intracranial regulation
-Maintaining a balance that promotes an environment for optimal brain functioning

*Brain doesn't store nutrients, so needs continuous supply of nutrients/o2 (cerebral
circulation)
*Brain only gets 15% of resting CO
Most important electrolyte for brain functioning
-Glucose (brain thrives)
-Needs to be balanced, cant go overboard bc after awhile sugar can cause damage
but if not getting blood needed, impacts balance & no optimal brain functioning
Defining characteristics
1. Adequate nourishment of brain cells
-Consistent flow of CSF & oxygenated blood to & from brain cells (MAP> 70 & <170.
Diabetic MAP > 70. Non-diabetic MAP > 65. Don't want MAP too high: < 170 to keep
brain vessels in good shape)
-Constant supply of glucose to brain
-CO2 homeostasis (balance, not too high or too low)
-Normal ICP (Monro-Kellie hypothesis)

Monro-kellie hypothesis
-Balance of cranial components: blood, CSF, & brain tissue (must be constant
balance)
-Bc of limited space for expansion, increase in 1 component causes change in vol of
others
-Accomplished by displacing or shifting CSF, increasing absorption or diminishing
production of CSF, or decreasing cerebral blood vol
-If swelling in brain, vol of CSF or blood flow to brain decreases so it maintains
homeostasis
-Only works for short period of time
-W/out changes, ICP begins to rise
Defining characteristics cont.
2. Adequate protection of brain
-Well fxning BBB: difficult for neurotoxic substances to pass to brain (dyes, meds,
antibiotics). Certain substances make it more permeable & allow larger molecules to
cross. Allows approp. nutrients to cross & some chemicals depending on molecular
size & bound (to protein or not). Drugs like coke, meth, PCP increase permeability
(reason for neuro problems overtime w abuse). Trauma, cerebral edema, & cerebral
hypoxemia can alter BBB fxn

,-Intact meningeal layers (dura mater, arachnoid layer, & pia mater w/ subarachnoid
space where CSF flows. Protect brain & spinal cord)
-Strong intact skull
*Protect fontanelles in children & infants

3. Optimal transmission of nerve impulses across neuronal synapses by
neurotransmitters
-Adequate amount of neurotransmitters (serotonin, dopamine, NE: not made in brain,
80% of serotonin made in gut, so neurotransmitters won't work correctly if unhealthy
gut)
-Adequate # of functioning neurons
-Responsiveness of neurons: need to work & respond (ex: If depressed d/t alc, may
not fxn correctly)
Risk factors for neurological disorders
Risk taking behaviors
-Adolescents/young adults from MVA & risk taking behaviors: TBI
-Professional athletes: TBI (get hit in head a lot)
*Drug abuse, "Hold my beer" (ETOH involved in 50% of TBI cases)

Falls (age 0-4 & > 65 yrs)
-Falls in very young & elderly: TBI

Diseases
-DM, HTN, smoking (+ vaping & weed), obesity, CVD: stroke
-Infection: meningitis, encephalitis (high ammonia, abuse alc & destroy liver leading
to chronically high ammonia, interferes w brain fxn)

Genetics
-Neurodegenerative diseases (Alzheimer's, Parkison's), seizures (genetic or
autoimmune)

Congenital
-Idiopathic cranial HTN or hydrocephalus (brain produces CSF faster than it can be
destroyed)
Interrelated concepts
-Causes of intracranial regulation (abuse, perfusion, oxygenation, clotting)
-Signs of intracranial regulation (oxygenation, perfusion, mobility, cognitive
impairment, comfort, sensory perception)
Pathophysiology of Brain Damage
-Primary injury: direct contact to head/brain during initial injury (ex: initial fall, tackle,
direct impact, rapid acceleration/deceleration, penetrating injury, blast waves. Result
from external mechanical forces transferred to intracranial contents)

, -Secondary injury: cascade of molecular injury mechanisms initiated at time of initial
trauma & continue for hrs or days (subsequent consequences of that injury:
increased swelling, ripped axons, torn vessel, bleeding into brain. Caused by
cerebral edema, ischemia, or chemical changes associated w/ trauma)

*Electrolyte balances (hyponatremia): confusion, seen in young ppl that do water
challenges. Do not go overboard when drinking water. Never more than 90 oz a day.
Dilutes sodium & causes confusion & seizure, coma, death. Important to monitor
this!
*Egg toss ex: yolk inside bounces, brain does same thing. Even w helmet on,
prevents skull fracture, but brain still moves inside
*Ex: rollar coaster, head bounces around
*Concussion: brain bounces inside head
*Nothing to protect it. Can put helmet on, wrap in bubble wrap, but doesn't stop
damage from being done
*Football players, boxers, kick boxing, continue to get those injuries
Types of Brain Injury
Epidural hematoma
- 10% of ppl w TBIs
-Bleeding btw skull & dura mater
-High pressure bleeding, so fills up cranial cavity quickly w blood. Faster bleed,
increase pressure very quickly
-As pressure increases, see unequal pupils & neuro deficits
-Common w/ falls & higher in adolescents & young adults: 20-30 yrs (50-60 yrs rare
bc w aging, dura mater more adherent to overlying bone & decreases chance of
hematoma in space btw cranium & dura). Ex: walking into door. Not lot of damage,
but if keep hitting head or taking anticoagulants, high risk

Subdural hematoma
- 25% of ppl w TBIs
-Bleeding btw dura mater & above arachnoid mater
-Low pressure bleeding, so can continue to cause problems over several days
-Wont see immediately, but overtime bleeding continues & causes problems
(continues for longer period of time bc lower pressure)
-Often caused by head injury (head moving rapidly forward & stopped) & most
common in elderly (falls), athletes in contact sports, alc abuse, babies (SBS)

Subarachnoid hemorrhage
- 75-80% involve ruptured brain aneurysms
-Bleeding in subarachnoid space (past arachnoid btw arachnoid & pia mater)
-Bleeding is high pressure & fast, large level of compression in brain
-Common sign: sudden, severe HE

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