CNS Trauma Flashcards
(40 cards)
Common concussion symptoms
Confusion, amnesia, headache, dizziness, poor attention, inability to concentrate, irritable, fatigued, depressed, intolerant of bright light/loud noise, sleep disturbance
leading cause of death up to age 45?
trauma
Grading scales
no universal scale
Colorado Concussion Grading Scale
Grade 1: confusion/no amnesia or LOC
Grade 2: Confusion + amnesia
Grade 3 - LOC
Second Impact Syndrome
Rare; consequence of second concussion while still having effects of first. loss of autoregulation of CNS vasculature that cerebral vessels lose tone and get congested with blood –>increased ICP –> reduced perfusion (ischemia, vasogenic edema); almost impossible to halt process once started
concussion
mild TBI; alteration i mental status due to biomechanical forces that may/may not cause LOC
Concussion management
Observe 24 hrs; no need to wake pt at night unless anmesia/unconsciousness; acetominophen for pain
Gradual return to activities and different therapies if needed
Peak age groups for head injuries
25-35
Males 2x as likely (4x fatality risk)
small peaks in 0-4 (abuse) and >65 (falls)
Highest incidence in economically disadvantaged populations within major cities
Principle forces of injury in cerebral trauma
- Contact (object striking head)
- Acceleration/deceleration(rapid head movement that can create shear, tensile, compressive strains; DON’T need to involve impact) – translation vs rotational
- Results in stretching/tearing of veins between brain and dura and bruising of brain as it impacts skull - Penetrating (GSW, knives, tree branches)
- Secondary Injury
Primary injury
Injury at moment of impact; little regeneration of neural tissue; largely irreversible injury
Secondary injury
Due to inadequate reuscitation (hypoxia, dysautoregulation, released of free radicals that break down BBB –> interstitial edema)
Injuries due to contact phenomena
scalp lacerations, skull fractures, cerebral contusion, epidural hematoma, subgaleal hematoma
Injuries from Acceleration/Deceleration
Diffuse axonal injury, cerebral contusion, subdural hematoma
Excitotoxicity
pathological process where neurons are damaged/killed by overactivation of receptors for glutamate. This causes increased Ca inside cell that activates enzymes that damage cell structures and BBB—> Vasogenic edema
Cytotoxic edema
due to high K outside cell that causes glutamate transporter to reverse and pump more K into cell. Leads to cell swelling and thus brain swelling.
Treating elevated ICP
minimize ICP/maximize oxygen and metabolite delivery
Emergency measures to treat ICP
IV osmotic diuretics, ventricular catheters, treat obstructive hydrocephalus, drug-induced coma with barbituates, elevate head, controlled CO2 ventilation
Monroe-Kellie doctrine
Intracranial compensation for expanding mass; allows you to compensate and retain normal ICP up to a point.
Brain in rigid container; increase volume of mass of one compartment will increase the pressure unless there is a compensatory decrease in volume of another compartment
Volume of intracranial compartment = volume FSC + blood volume in arterial/venous systems+ brain + intracranial mass lesion = constant volume. To keep pressure, maintain volume.
Increase pressure too much, have compression of compartments. Some elements more compressible than others
Intracranial compensation
Brain is essentially noncompressible. Increase in ICV decreases CSF or cranial blood volume, and CSF wlil displace into spinal subarachnoid space and venoconstriction of CNS capacitance vessels displaces blood in jugular venous system
Herniation
ICP increases not distributed equally in skull, so you have pressure gradients that cause parts of brain to herniate.
Types – subfalcine, central, uncal (transtentorial), tonsillar
Lateral/Subfalcine herniation
cingulate gyrus eing pushed by expanding mass and herniates under falx cerebri; often kinks anterior cerebral artery to potentially cause stroke in the distribution of that vessel
Central herniation
downard pressure centrally can cause bilateral uncal herniation below tentorium cerebrlli
Uncal herniation
Uncus herniates across tentorial edge, and downward into posterior fossa.
Compression of midbrain/ipsilateral cerebral peduncle–> usually produces ipsilateral third nerve palsy and contralateral hemiparesis/hemiplegia.
Rarely compresses contralateral cerebral peduncle against tentorial edge to cause hemiparesis ipsilateral to mass lesion/herniated uncus –> this is called Kernohan’s notch
Can also produce Duret hemorrhage
Kernohan’s notch
phenomenon when uncal herniation causes contralateral cerebral peduncal to compress against tentorial edge, resulting in hemiparesis ipsilateral to mass lesion/herniated uncus
