TBI Flashcards
Traumatic Brain Injury (TBI)Outcome depends o?n:**
- Location of the injury
- Brain’s limited repair ability [Unlike skin or liver, brain tissue can’t fully regenerate]
- what are the **Types of damage that can occur in TBI? **
- Skull fractures
- Parenchymal injury (damage to the actual brain tissue)
- Vascular injury (damage to blood vessels)
[These often happen together because the brain, skull, and vessels are closely packed]
- Severity and spread of injury depend on?:
- Shape of the object hitting the head (sharp vs blunt)
- Force of impact
- Whether the head was moving during trauma
[Moving head + impact = worse because of more energy transfer]
- Kinds of trauma:
- Open injury (object penetrates skull)
- Closed injury (blow without penetration)
What’s Skull Fractures
- Displaced fracture:
- Definition: The broken bone is pushed inward into the cranial cavity more than the bone’s thickness.
[Imagine a dent where the skull caves inward]
- Bone thickness matters:
- Skull thickness varies, so thinner areas break easier.
- Fracture patterns and falls:
- Occipital impacts (back of head) and frontal impacts (forehead) are common fall patterns.
-what are the signs of Basal skull fracture?:
- Orbital hematomas (bruises around the eyes)RACCOON EYES
- Mastoid hematomas (bruises behind the ears)BATTLE SIGN
[These bruises form far away from the point of impact — a clue for base-of-skull fractures]
- Other signs of basal skull fracture:
- CSF leakage from nose (rhinorrhea) or ear (otorrhea)
- Risk of meningitis (infection from open CSF pathways)
what’s a Diastatic fractures:
- Definition: Fractures that cross cranial sutures.
[Normally, energy from trauma gets “stopped” at sutures (bone fusion lines). In diastatic fractures, the force is so high it breaks across sutures.]
Parenchymal Injuries
[Parenchyma = the main functional tissue of an organ; in brain, it’s neurons and glial cells]
What’s a Concussion? And it’s symptoms
- What it is:
- A clinical syndrome of temporary altered consciousness after a head injury. And can be caused by
- How it happens:
- Caused by a change in head momentum (like moving fast, then hitting a wall suddenly).
[Your brain “sloshes” inside the skull when you stop suddenly]
- Symptoms:
- Rapid onset of temporary brain dysfunction
- Loss of consciousness
- Temporary stop of breathing (respiratory arrest)
- Loss of reflexes
- Recovery:
- Consciousness and basic function usually come back fully,
- But amnesia (memory loss) for the event itself is very common.
[You wake up not remembering the injury]
** what’s the Mechanism (Pathogenesis) of concussion:**
- Not fully understood.
- Likely involves dysregulation of the reticular activating system (RAS) in the brainstem.
[RAS = area that keeps you awake and alert. If it glitches, you lose consciousness.]
- Post-concussive syndrome:
- Some people develop long-term neuropsychiatric symptoms like mood changes, headaches, or trouble concentrating.
What’s the difference between Contusions and Lacerations
- Contusion = Bruise on the brain (due to blunt trauma).
[Blood vessels break but the tissue is not torn]
- Laceration = Tear in brain tissue (due to sharp object penetrating).
[Tissue is cut or ripped]
What’s the Mechanism of Injury in contusion:
- Blunt force ⏩Rapid tissue displacement ⏩Blood vessels rupture⏩ Bleeding,Tissue damage,Swelling (edema)
- What are the Most vulnerable areas, location and less common location of T parenchymal brain injury?:
- Gyri crests (the raised parts of brain folds) get hit first because they’re closest to the skull.
- Common locations:
- Frontal lobes
- Temporal lobes
[These sit next to rough bony surfaces inside the skull — so they get injured easily]
- Less common sites:
- Occipital lobes
- Brainstem
- Cerebellum
[These get injured mainly if there’s a nearby skull fracture]
What are Coup and Contrecoup Injuries and when they can’t occur
- Coup Injury:
- At the site of impact.
[Brain slams against the skull at the hit site]
- Contrecoup Injury:
- Opposite side of impact.
[Brain “bounces” and slams into the opposite side]
- When they occur:
- If head is stationary ➡️Only coup injury.
- If head is moving ➡️ Both coup and contrecoup injuries.
- Example:
- You’re running and hit a wall ➡️ Coup at the forehead, contrecoup at the back of the head.
- Appearance:
- Looks the same under the microscope, so doctors use injury location and context to tell them apart.
What’s Severe Neck Hyperextension Injury and why does it cause sudden death?
- What can happen:
- Sudden violent bending of the neck backward or sideways can tear important brainstem parts.
[The pons or medulla can rip off from where they attach]
- Result:
- Instant death because those areas control basic life functions like breathing and heartbeat.
What’s the Morphology of Contusion
- Shape:
- On cross-section, a contusion is wedge-shaped.
[Think of a slice of cake — broad part at the surface where the hit occurred, narrow point deeper in]
What are the feature of contusion in the
Early stages
Progressive stage
Neuronal and Axon damage
And chronic contusions
- Early Appearance (First few hours):
- Edema (swelling from fluid buildup) and pericapillary hemorrhage (tiny bleeds around small blood vessels).
[Small vessels leak blood causing swelling and redness]
- Progression (Next few hours):
- Blood spreads through:
- Entire width of the cerebral cortex (outer layer of brain),
- Into the white matter (deeper brain tissue),
- And into the subarachnoid space (area with brain’s protective fluid).
- Neuronal Damage:
- Morphologic (structural) evidence appears after about 24 hours:
- Pyknosis: Shrinking and darkening of the cell nucleus.
- Eosinophilia: Cytoplasm becomes bright pink on staining.
- Cell disintegration: Breakdown of neuron structure.
> [The neurons “die” visibly, but functional damage happens earlier]
- Axonal Injury:
- Axonal swellings (bulging parts along the nerve fibers) show up near damaged neurons or far away.
[Injury can disturb long nerve fibers across the brain]
- Inflammatory Response:
- Follows the usual sequence:
- First neutrophils (fast immune responders),
- Then macrophages (cleanup cells).
Old (Chronic) Contusions:
- Gross Appearance:
- Depressed, shrunken, yellowish-brown patches seen on brain surface.
[Old injury sites look sunken and discolored due to scarring and blood pigment deposits]
Whaare tthe common sites of contusions? And old contusions are called?
- Common Sites:
- Inferior frontal cortex,
- Temporal poles,
- Occipital poles
[These are parts near bony prominences inside the skull, making them vulnerable]
- Special Name:
- These old contusions are called “plaque jaune” (French for “yellow plaque”).
- what are the Microscopic Features in Old Contusions:
- Gliosis: Scarring made by astrocytes (brain repair cells).
- Hemosiderin-laden macrophages:
- Macrophages loaded with iron pigment from old blood.
[Hemosiderin = iron-rich breakdown product of blood]
- Clinical Relevance:
- These areas can become epileptic foci.
[Scarred brain tissue can trigger seizures]
- Severe Cases:
- Larger hemorrhagic injuries can create big cavities (empty spaces),
- Resembling remote infarcts (old areas of dead tissue from stroke).
Quick Visual Analogy:
- Fresh contusion: Swollen and red (like a bruise).
- Old contusion: Sunken yellow patch (like an old scar with rust).
What part of the brain are affected by Diffuse Axonal Injury (DAI)
- Affected Areas:
- Deep white matter regions:
- Corpus callosum (connects right and left brain hemispheres),
- Paraventricular regions (around the brain’s fluid spaces),
- Hippocampus (important for memory),
- Cerebral peduncles (brainstem structures that carry motor signals),
- Brachium conjunctivum (pathway in brainstem for coordination),
- Superior colliculi (visual reflex centers),
- Deep reticular formation (brainstem area controlling consciousness).
[All these are deep parts of the brain critical for basic functions]
What are the Microscopic Features in diffuse axonal injury?:
- Axonal swelling (nerve fibers swell up due to damage),
- Focal hemorrhagic lesions (small spots of bleeding).
Clinical Importance:
- Seen in ~50% of people who become comatose after trauma,
- Even if there are no visible contusions.
[So even without bruising, brain wiring can be severely disrupted]
Traumatic Vascular Injury
- Mechanism:
- Direct trauma causes vessel wall disruption ➡️ leads to bleeding.
- Possible Bleeding Sites are? :
- Epidural space (between skull and dura),
- Subdural space (between dura and arachnoid),
- Subarachnoid space (where CSF circulates),
- Brain parenchyma (brain tissue itself).
[Location of bleeding depends on which vessel is torn]
Which vascular Injury is most associated with trauma
- Trauma Association:
- Epidural and subdural hemorrhages almost always follow trauma.
- In elderly or alcoholics (with cerebral atrophy), even minor trauma can tear veins and cause subdural hemorrhage.
[Shrunken brains pull on veins making them easier to tear]
Which blood vessel is commonly injured in Epidural Hematoma.whats it’s pathology?
- Normal Anatomy:
- Dura mater is stuck to the inside of the skull.
- Middle meningeal artery runs between them — vulnerable to injury.
- Mechanism of Injury:
- Commonly after temporal bone fractures (fracture crosses artery path).
- In children, skull can bend without fracture but still tear vessels.
[Child’s skull is soft; vessels can tear even without a crack]
- Pathology:
- Arterial blood leaks under high pressure,
- Peels the dura away from the skull,
- Forms a smooth, lens-shaped (biconvex) hematoma,
- Compresses the brain.
What are the Clinical Signs of epidural injury?:
- Lucid interval:
- Patient may seem fine for hours before brain pressure symptoms start.
[Blood slowly builds up unnoticed at first]
- Emergency:
- Rapid expansion can lead to brain herniation and death,
- Requires immediate surgical drainage.
Quick Visual Analogy:
- DAI:
> Like electrical wires are pulled and snapped all over the brain.
- Epidural hematoma:
> Like peeling wallpaper — blood lifts the dura away, forming a bulge.
What’s the pathogenesis of Subdural Hematoma (SDH)
Basic Anatomy:
- Subdural space = between dura mater and arachnoid mater.
- Bleeding into this space → Subdural hematoma.
Pathogenesis:
- Caused by rupture of bridging veins.
- These veins travel from the brain’s surface (convexities) to the venous sinuses (especially the superior sagittal sinus).
- Brain is suspended in CSF and moves freely,
- Venous sinuses are fixed to the dura.
[So, during trauma, brain shifts → veins tear where they enter dura]
What’s the risk factors for sub dural hematoma?
Risk Factors:
- Elderly:
- Brain atrophy stretches the bridging veins ➡️ more vulnerable even with minor trauma.
- Infants:
- Thin-walled veins ➡️ higher risk even without major force.
What’s the Morphology of Subdural Hematoma
- Gross Appearance:
- Freshly clotted blood layer along brain surface,
- Does NOT enter into sulci (stays on the surface),
- Brain looks flattened,
- Subarachnoid space remains clear.
- What’s the Healing of both acute and chronic sub dural hematoma:
- ~1 week: Clot starts to lyse (break down),
- ~2 weeks: Fibroblasts from dura invade the hematoma,
- 1–3 months: Formation of hyalinized connective tissue.
[Over time, the clot becomes organized fibrous tissue stuck to dura]
- Chronic Subdural Hematoma:
- Forms thin-walled, fragile vessels inside granulation tissue,
- High risk of rebleeding, especially in first few months.
Clinical Features of sub dural hematoma
- Timing:
- Symptoms usually within 48 hours of trauma.
- Symptoms:
- Headache,
- Confusion,
- Focal neurologic deficits (sometimes),
- Often non-localizing signs (not pointing to a specific brain area).
- Progression:
- Slow worsening is typical (over days to weeks),
- Sudden deterioration (acute decompensation) can also happen.
[That’s why chronic subdural hematomas can sometimes be mistaken for dementia or psychiatric disorders in elderly patients]
Quick Visual Analogy:
- Subdural hematoma =
Like a soft pancake of blood slowly spreading between the brain and its outer covering, pressing on the brain.
