TBI Flashcards
(62 cards)
1
Q
Traumatic Brain Injury (TBI)Outcome depends o?n:**
A
- Location of the injury
- Brain’s limited repair ability [Unlike skin or liver, brain tissue can’t fully regenerate]
2
Q
- what are the **Types of damage that can occur in TBI? **
A
- 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]
3
Q
- Severity and spread of injury depend on?:
A
- 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]
4
Q
- Kinds of trauma:
- Open injury (object penetrates skull)
- Closed injury (blow without penetration)
A
5
Q
What’s Skull Fractures
A
- 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.
6
Q
- Fracture patterns and falls:
- Occipital impacts (back of head) and frontal impacts (forehead) are common fall patterns.
A
7
Q
-what are the signs of Basal skull fracture?:
A
- 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)
8
Q
what’s a Diastatic fractures:
A
- 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.]
9
Q
Parenchymal Injuries
[Parenchyma = the main functional tissue of an organ; in brain, it’s neurons and glial cells]
A
10
Q
What’s a Concussion? And it’s symptoms
A
- 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
11
Q
- 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]
A
12
Q
** what’s the Mechanism (Pathogenesis) of concussion:**
A
- 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.]
13
Q
- Post-concussive syndrome:
- Some people develop long-term neuropsychiatric symptoms like mood changes, headaches, or trouble concentrating.
A
14
Q
What’s the difference between Contusions and Lacerations
A
- 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]
15
Q
What’s the Mechanism of Injury in contusion:
A
- Blunt force ⏩Rapid tissue displacement ⏩Blood vessels rupture⏩ Bleeding,Tissue damage,Swelling (edema)
16
Q
- What are the Most vulnerable areas, location and less common location of T parenchymal brain injury?:
A
- 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]
17
Q
What are Coup and Contrecoup Injuries and when they can’t occur
A
- 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.
18
Q
What’s Severe Neck Hyperextension Injury and why does it cause sudden death?
A
- 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.
19
Q
What’s the Morphology of Contusion
A
- 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]
20
Q
What are the feature of contusion in the
Early stages
Progressive stage
Neuronal and Axon damage
And chronic contusions
A
- 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]
21
Q
Whaare tthe common sites of contusions? And old contusions are called?
A
- 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”).
22
Q
- what are the Microscopic Features in Old Contusions:
A
- 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]
23
Q
- 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).
A
24
Q
Quick Visual Analogy:
- Fresh contusion: Swollen and red (like a bruise).
- Old contusion: Sunken yellow patch (like an old scar with rust).
A
25
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]
26
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).
27
**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]
28
**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]
29
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]
30
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.
31
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**.
32
**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.
33
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]
34
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.
35
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**.
36
- 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.
37
**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]
38
**Quick Visual Analogy:**
- Subdural hematoma =
Like a soft pancake of blood slowly spreading between the brain and its outer covering, pressing on the brain.
39
Which TBI often presents as a stroke?
IPH
**Intraparenchymal Hemorrhage**
---
**Definition:**
- Bleeding **directly into the brain tissue** from rupture of small intraparenchymal vessels.
- **Often presents like a stroke** (sudden neurologic symptoms).
40
The Most common BV damage in IPH is?
- **Peak incidence:** around **___ years old**.
in **middle to late adulthood**,
60
41
**Location and Terminology:**
Bleeding in - **Basal ganglia/thalamus:** is called?
In the - **Cerebral lobes is also called? :** → "**
1. Ganglionic hemorrhages**",
2. Lobar hemorrhages**".
42
**List the Causes of IPH **
Note those commonly associated with Cerebrum and thalamus/ganglions
- **Hypertension**⏩ Deep (ganglionic) hemorrhages,
- **Cerebral amyloid angiopathy (CAA)** ⏩ Lobar hemorrhages.
Other less common causes:
- Coagulation disorders,
- Neoplasms,
- Vasculitis,
- Aneurysms,
- Vascular malformations.
43
- **Hypertension** accounts for:
- ____% of clinically significant brain hemorrhages,
- ____% of deaths in people with chronic hypertension
50%
15%
44
- **list the Common sites for Hypertension-Related Hemorrhages :**
.
- **Deep white matter**,
- **Deep gray structures** (basal ganglia, thalamus),
- **Brainstem**,
- **Cerebellum** (less often).
45
**what are the Vascular Changes in Hypertension:**
- **Large arteries:** Accelerated atherosclerosis,
- **Small arteries:** Hyaline arteriolosclerosis,
- **Arterioles:** Proliferative changes and necrosis,
- **Charcot-Bouchard microaneurysms** can develop ⏩ rupture risk.
46
What's the Morphology of Intraparenchymal Hemorrhage
- **Acute Stage:**
- **Extravasated blood** compresses nearby brain tissue.
- **Early Lesions:**
- Central **clot**,
- Surrounding rim of **anoxic neuronal/glial injury**,
- Significant **edema**.
- **Chronic Stage:**
- **Cavitary destruction** (cyst-like empty spaces),
- Rim of **brownish discoloration** (from hemosiderin),
- **Hemosiderin-laden macrophages** clean up blood,
- **Reactive astrocyte proliferation** at edges (gliosis).
Or
- **Common sites of origin include the putamen (50%–60% of cases), thalamus, pons, and cerebellar hemispheres (rarely).**
→ These deep brain regions are supplied by small penetrating arteries prone to damage from hypertension.
- **Acute hemorrhages show extravasation of blood with compression of adjacent brain parenchyma.**
→ The sudden accumulation of blood exerts mass effect, squeezing surrounding tissue.
- **Old hemorrhages show cavitary destruction of brain with a rim of brownish discoloration.**
→ The blood is broken down over time, leaving a cavity and hemosiderin (iron pigment) from degraded red cells.
- **Early lesions consist of a central clotted blood core surrounded by brain tissue showing anoxic neuronal and glial changes and edema.**
→ The hemorrhage cuts off local blood supply, leading to oxygen deprivation (anoxia) and swelling.
- **As healing progresses, edema resolves and macrophages containing hemosiderin and lipids appear.**
→ Macrophages clean up debris from the hemorrhage, including iron and fat from damaged cells.
- **Reactive astrocyte proliferation occurs at the lesion's periphery.**
→ Astrocytes form a gliotic scar to wall off and stabilize the damaged area.
47
Explain how **Cerebral Amyloid Angiopathy (CAA)** can cause IPH
Explain how **Cerebral Amyloid Angiopathy (CAA)** can cause IPH
- **CAA is the most common risk factor for lobar hemorrhages.**
➡️ Lobar areas are supplied by cortical vessels, which are affected by amyloid deposition.
- **Amyloidogenic peptides (usually Aβ40, like in Alzheimer’s) deposit in small and medium meningeal and cortical vessel walls.**
➡️ These peptides cause vessel wall fragility and loss of structural integrity.
- **This amyloid deposition weakens vessel walls and leads to hemorrhage.**
➡️ Fragile vessels are more likely to rupture under normal blood pressure.
- **CAA is associated with multiple small brain hemorrhages ("microbleeds") visible on imaging.**
➡️ Repeated minor vessel leaks occur due to ongoing wall degeneration.
48
- **whats CADASIL?
It's a related hereditary condition caused by NOTCH3 gene mutations.**
➡️ This mutation affects vascular smooth muscle, leading to structural vessel changes.
- **NOTCH3 is highly expressed in vascular smooth muscle cells.**
➡️Mutations here disrupt vessel function and stability, contributing to infarcts and white matter disease.
49
- **Most subarachnoid hemorrhages are due to rupture of?
A saccular ("berry") aneurysm.**
⏩These aneurysms occur at weak arterial branch points, making rupture more likely under pressure.
- **Other causes include trauma (hematoma extension), hypertensive bleeds, vascular malformations, blood disorders, or tumors.**
⏩ All these can lead to vessel rupture and bleeding into the subarachnoid space.
50
- **____ aneurysm is the most common type of intracranial aneurysm.**
⏩It develops due to focal weakness at arterial bifurcations.
Saccular aneurysm
51
What are the other types of Saccular aneurysm?
- **Other types:**
- **Atherosclerotic (fusiform):** Related to vessel wall damage from chronic plaque buildup.
- **Mycotic:** Caused by infection-induced vessel wall weakening.
- **Traumatic or dissecting:** Result from direct injury or intramural tearing of arteries.
➡️ These types are less likely to cause subarachnoid hemorrhage and more likely to lead to infarcts.
52
- **Most aneurysms occur in the ___ circulation in the brain near arterial branch points.** and why?
Anterior circulation
⏩ Turbulent blood flow in these areas increases wall stress and risk of aneurysm formation.
53
- **Saccular aneurysms are present in ~2% of the general population (based on imaging studies).**
➡️ Many remain asymptomatic until rupture.
- **20–30% of patients may have multiple aneurysms.**
➡️ Suggests a systemic predisposition to vessel wall weakness.
54
**whats the Pathogenesis of Saccular Aneurysm
- **Saccular aneurysms lack smooth muscle and the internal elastic lamina in the vessel wall.**
⏩ These structural weaknesses make the wall prone to ballooning over time.
- **They’re not congenital (not present at birth) but develop later due to media defects.**
⏩The vessel degenerates gradually, increasing the risk of aneurysm formation.
- **Most are sporadic, but first-degree relatives of affected individuals have increased risk.**
⏩Suggests a heritable vulnerability in vessel structure.
55
- **Higher incidence Saccular aneurysm is seen in genetic disorders like? :**
Which is the most common risk factor?
- **Autosomal dominant polycystic kidney disease**
- **Ehlers-Danlos type IV**
- **Neurofibromatosis type 1 (NF1)**
- **Marfan syndrome**
➡️ These conditions weaken connective tissue, including vascular walls.
- **Other vascular abnormalities like fibromuscular dysplasia and coarctation of the aorta also increase risk.**
➡️ They disrupt normal vascular integrity and flow dynamics.
- **Smoking and hypertension are major acquired risk factors.**
➡️ They cause chronic vascular injury and pressure-related stress on vessel walls.
56
Explain the **Morphology of Saccular Aneurysm **
- **Aneurysm is a thin-walled outpouching at an arterial branch point, especially around the circle of Willis.**
➡️ These sites are prone to turbulent blood flow, which stresses weak vessel walls.
- **Size ranges from a few millimeters to 2–3 cm.**
➡️ Larger aneurysms have a higher risk of rupture.
- **Surface is bright red and shiny, and the wall is thin and translucent.**
➡️ Reflects the absence of normal vascular layers and high tension in the wall.
- **Wall or lumen may contain:**
- **Atheromatous plaques** → From chronic vascular damage.
- **Calcification** ➡️ Indicates long-standing disease.
- **Thrombi** ➡️ May form due to stasis within the sac.
- **Signs of prior bleeding may appear as brownish discoloration of nearby brain/meninges.**
➡️ Evidence of subclinical or resolved hemorrhages.
- **Neck of aneurysm may be wide or narrow.**
➡️ Wide-necked aneurysms are harder to clip surgically.
- **Rupture usually occurs at the apex of the sac.**
➡️ This is the thinnest, most fragile point, leading to blood leaking into the subarachnoid space or brain tissue.
57
What are the **Clinical Features of Subarachnoid Hemorrhage**
- **Most common in the fifth decade, with a slight female predominance.**
➡️ Hormonal or anatomical differences may contribute to vessel wall vulnerability.
- **Annual rupture risk is about 1.3% overall, but higher for large aneurysms.**
➡️ Aneurysms >10 mm have a ~50% rupture risk/year due to increased wall tension.
- **Rupture often triggered by sudden spikes in intracranial pressure (e.g., straining, orgasm).**
➡️ These transient pressure surges can rupture already weak vessel walls.
- **Blood is forced under arterial pressure into the subarachnoid space.**
➡️ Rapid bleeding leads to increased intracranial pressure and brainstem compression.
- **Classic symptom: sudden, severe headache (“worst headache of my life”), followed by loss of consciousness.**
➡️ Due to rapid meningeal irritation and increased intracranial pressure.
- **Mortality is high: 25–50% die with the first rupture.**
➡️ Sudden massive hemorrhage leaves little time for intervention.
- **Endothelins, nitric oxide, and arachidonic acid metabolites may contribute to vascular dysfunction and spasm.**
➡️ These mediators may worsen ischemia or prolong vasospasm after bleeding.
- **Healing often causes meningeal fibrosis and scarring.**
➡️ This may block CSF pathways, leading to hydrocephalus.
58
Vascular malformations of the brain are classified into four principal groups which are?
Arteriovenous malformations
Cavernous malformations,
Capillary telangiectasias, and
Venous angiomas.
59
Arteriovenous Malformations (AVMs) Involves vessels in the
subarachnoid space, brain, or both.
➡️ Explains their potential to cause both intracerebral and subarachnoid hemorrhage.
60
Whats the morphology of Arteriovenous Malformations (AVMs)**
- **Appear as tangled, wormlike vascular channels with pulsatile arteriovenous shunting.**
➡️Shunting bypasses capillaries, creating high-pressure flow that can rupture vessels.
- **Composed of enlarged vessels, separated by gliotic brain tissue, often with signs of old hemorrhage.**
➡️ Chronic damage from repeated microbleeds leads to scarring and gliosis.
- **Arteries may show duplication/fragmentation of internal elastic lamina.**
➡️Reflects chronic vascular stress and structural weakening.
- **Veins may have thickened or hyalinized walls.**
➡️ Suggests previous damage and repair attempts from high-flow stress.
61
What's the **Morphology of Cavernous Malformations**
- **Distended, back-to-back vascular channels with collagenized, variably thickened walls.**
⏩ These thin, irregular walls increase the risk of leakage or hemorrhage.
- **No intervening brain parenchyma.**
⏩Unlike AVMs, this structure makes them prone to cause focal damage.
- **Common in cerebellum, pons, and subcortical areas.**
⏩ Their location influences the type of neurologic symptoms.
- **Do not show arteriovenous shunting; they are low-flow lesions.**
⏩Less risk of rupture than AVMs but still cause microhemorrhages.
- **Surrounded by hemosiderin, infarct, and calcifications.**
⏩ Indicates chronic bleeding and poor perfusion in surrounding tissue.
**Other Malformations**
- **Capillary Telangiectasias:**
⏩ Tiny dilated vessels with normal brain in between. Usually asymptomatic.
- **Venous Angiomas:**
⏩ Dilated venous channels, usually incidental findings with minimal clinical impact.
62
What are the **Clinical Features of Vascular Malformations**?
- **Males affected twice as often.**
⏩ Cause unknown, but likely genetic or hormonal factors.
- **Presentation: seizures, intracerebral, or subarachnoid hemorrhage (usually ages 10–30).**
⏩ High-flow AVMs can rupture or irritate nearby brain, triggering symptoms.
- **Most common in the middle cerebral artery territory, especially its posterior branches.**
⏩ This region supplies a large cortical area, explaining seizure and focal neurologic signs.
