CNS I Path - CNS Trauma and Hemorrhages Flashcards
CT or MRI for path lesions?
CT! Cheaper and rapid, and can also see blood and hemorrhage far better than MRI
Admission criteria for a head injury
Neuro deficits, new onset seizures, N/V, severe headache, fever, LOC, altered mental state, unexplained injuries
Central Pontine Myelinolysis (from Robbins)
Loss of myelin (preservation of axons and cell bodies) in a roughly symmetric pattern involving the pons; extremely rare for the process to extend below the pontomedullary junction;
Most commonly associated with rapid correction of hyponatremia, though it can be associated with other severe electrolyte or osmolar imbalance, as well as orthotopic liver transplantation.
Presents clinically as RAPIDLY EVOLVING QUADRIPLEGIA; radiologic imaging usually localize the lesion to the BASIS PONTIS (basilar pons)
Myelin loss without evidence of inflammation; neurons and axons WELL PRESERVED;
Monophasic disease, all lesions appear to be at the same stage of myelin loss and rxn
Define Concussions
Totally REVERSIBLE, transient cerebral malfunction which may be associated with a brief loss of consciousness or postural tone
Can be multiple and cumulative; likely a change of consciousness, easy to spot;
Repeated concussions can lead to CTE
Other complications from head injury
Amnesia – dense retrograde (can’t remember what happened right at time of injury) or anterograde (can’t form new memories)
Primary complications (caused by initial trauma) –> scalp laceration, skill fractures, cerebral contusions, cerebral lacerations, intracranial hemorrhages, diffuse axonal injury
Secondary Complications –> show up later –> ischemia, hypoxia, cerebral swelling, infection
Fractures
Can happen along suture lines; linear fractures or comminuted fractures (multiple breaks)
Contusions of the base of the brain may lead to bleeding around the eyes without injury to the face
Contusions of scalp lead to “goose eggs” on the skull –> press on them gives CREPTIUS SIGN – displacement of fibrin and clot material around the injured area, mimicking a fracture…
Epidural Fracture
Fracture between the scalp and the dura
Common with fracture along the MIDDLE MENINGEAL ARTERY leading to hemorrhage
The largest problem with this is pooling of blood that may push the brain –> HERNIATION
Imaging studies can be used to tell if herniation is occurring by checking out compression of the ventricles
LENS SHAPED hemorrhage on CT
Gyri vs. Sulci damage
Contusions of the brain and skull causes SHRINKAGE of the GYRI
Stroke will damage the SULCI
Plaque Jaunes
Yellow plaques that may indicate an OLD CONTUSION injury
Coup and Countrecoup
Coup = injury on the same side of head as the impact
Countrecoup = Injury on the opposite side of the initial impact
Weak blows – only coup seen
Harder blows – coup primarily, but some minor countrecoup (brain sloshes around in CSF and impact is so hard that it hits the opposite side of the skull too)
What if a person is hit so hard with a baseball bat that they fall?
Initial Coup, immediate minor countrecoup, and then a larger countrecoup when the person hits the ground, and then an additional coup as a result on that impact!
Epidural Hemorrhage
Bleeding outside the outer dura; MMA rupture commonly causes this
Subdural hematoma
Bleeding beneath the outer dura
May be a slow bleed and present with a mild headache over weeks
Can be rapid, thus acute, subacute and chronic symptoms can all occur
Depends on how much volume is pushing on the brain and where the bleed is
Subarachnoid/Parenchymal
Bleeding beneath the arachnoid layer; blood leaks in between the gyri and sulci; serious bleeds can push aside parenchyma, go into ventricles; many vessels in the arachnoid which can become ruptured or occluded
What is the BIGGEST PROBLEM with cerebral hemorrhages?
HERNIATIONS!!!!!
Types of Herniations
Cingulate – hemorrhage causes the cingulate gyrus to herniate underneath the hard falx cerebri
Sideways herniation – pushing brain to one side
Downward herniation – pushing downward, causing the temporal lobe to compress the cerebellar tentorium and the uncus (hippocampus underneath it), leading to uncal herniation –> may lead to swelling of the brainstem; downward herniation causes bleeds, hypoxia, ischemia and eventually LEADS TO DEATH
Tonsillar – tonsils of the cerebellum push on the foramen magnum, compressing the brainstem!!
Diffuse Axonal Injury
Widespread damage to axons within the CNS that results from SEVERE ACCELERATION or DECELERATION of the head
Most patients are comatose immediately after the injury, no lucid interval (temporary improvement right after), remain unconscious, vegetative or severely disabled until death
Requires imaging to detect, occurs when an injury is severe enough to cause a SHEARING of axons or a TORSIONAL ROTATION strong enough the cause breakage
White matter problem – corpus callosum, walls of the third ventricle, dorsolateral surface of brainstem
Time Course of DAI (Harris said don’t worry, but who knows)
4-5 hrs –> focal axonal accumulations of BEA AMYLOID
12-24 hrs –> axonal varicosities evident on H&E
24 hours - 2 months –> axonal swellings and microglial nodules demonstrated on H&E –> microglia coming to eat dead tissue
Long Term –> Wallerian degeneration, atrophy
Diffuse Edema
Ipsilateral edema underlying a subdural hemorrhage
Bi-phasic swelling after trauma in children due to abnormal vasoregulation
This type of injury is difficult to prevent in kids
Diffuse Hypoxic Brain Damage
Occurs as a combo of one or more of the following –> brain shifts, raised ICP, systemic hypoxia, arterial spasm
Ischemic changes often seen at arterial boundary zones
Pathology of Child Abuse/Shaken Baby Syndrome
Occurs with young children, present in a coma with a low Glasgow Coma Score
Common findings –> retinal hemorrhages, intracranial and cervical injury, including subarachnoid/subdural hemorrhage, DAI, or contusion of the cervical spinal cord
Less neck musculature in infants, so the movement is dramatic
Cortical tears can be present
Inconsistent history/physical and parental risk factors (age, socioeconomic status, education, family history) need to be considered
Hypertensive Hemorrhages – Non-traumatic
Around the basal ganglia commonly
Middle cerebral artery gives rise to the LENTICULOSTRIATE arteries which come off at 90 deg angles
As we develop HTN, there are changes in the way the vessels are formed –> more hyalinized, resulting in thicker walls, which leads to decreased malleability
May lead to rupture of an artery –> hemorrhage –> parenchymal bleeds
Charcot-Bouchard Aneurysms
90% of the time this occurs in a person with UNCONTROLLED HTN
Germinal Matrix Hemorrhages
Central portion of the FETAL BRAIN from which glioblasts and microblasts emerge
This are is SUSCEPTIBLE to bleeds because of the lack of MATRIX STRUCTURAL MATERIALS and lots of activity
Bleeding may occur into the ventricle or into the germinal matrix –> minor are OK, major bleeds fatal!
Berry/Sacular Aneurysms
Form in the CIRCLE OF WILLIS
Often occur at the bifurcation of arteries, and can sometimes be OK, but can get LARGE and RUPTURE
Cause bleeds underneath arachnoid (subarachnoid hemorrhage) –> WORST HEADACHE ever
Survival determined by surgery
Aneurysms that are not causing problems can be clipped if patient wants to or if they have risk of rupture
Vascular Malformations
Telangeiectasis (small dilated vessels near the surface of the skin, commonly on the face and eyes)
Cavernous hemangiomas – consist of greatly distended, loosely organized vascular channels with thin, collagenized walls and are devoid of intervening nervous tissue; occur most often in the cerebellum, pons, and subcortical regions
AV MALFORMATIONS –> People present with headaches, seizures, hemorrhages and can be dealt with via surgery –> microscopically, there are arterio and venous formations –> may be too large (death) –> not normal vessels (incomplete elastic lamina) –> basically these are abnormal connections between arteries and veins –>
“Tortuous group of vessels that are not well organized and prone to rupture” – Younger men more likely
STROKE
- 85% = ischemic, 15% hemorrhagic
- Ischemia: 1. Thrombotic or 2. Embolic
- Thrombotic type of CVA is typically related to ATHEROSCLEROSIS in CNS, causing white infarcts
- Embolism can occur from an atherosclerotic plaque where a thrombus forms and emboli breaks off OR from the heart most commonly (vegetations or emboli from a thrombus) causing red infarcts.
Most commonly the MCA is involved and it is typically a non-convulsive event – evolves: SUDDEN ONSET (focal neurologic deficit – can’t speak, move arm, etc.), progresses for a while and then stops – patient can regain function, either over time or immediately
