Trauma

Question 1

• What is the BBB also called?
• Where is the site of the BBB?
• Small substances & small lipophilic molecules …..
• Large substances & hydrophilic molecules require ….

Answer 1

• Also called “Blood-brain neurovascular unit”
• Site of BBB: brain capillary endothelium
  
  • Tight intercellular junctions (non-permissive compared to systemic endothelial cells)
  • Endothelium has low pinocytotic rate & basement membrane
  • Dynamic interaction of endothelium with astrocytes & pericytes
• Small substances & small lipophilic molecules freely diffuse through membrane
• Large substances & hydrophilic molecules require active transport

Question 2

• Definition of cerebral edema:
• 2 major forms:

Answer 2

• Accumulation of excess fluid in intracellular or extracellular spaces of the brain
  
  • Major consequence ⇒ ↑ intracranial pressure
  • Results from a variety of processes & associated with significant morbidity/mortality
• 2 major forms:
  
  • Vasogenic edema
  • Cytotoxic edema

Question 3

What are the gross changes of cerebral edema?

Answer 3

Widened, flattened gyri with narrowed sulci

Question 4

What is the pathophysiology of vasogenic edema (“extracellular edema”)?

Answer 4

• Disruption (increased permeability) of blood-brain barrier:
  
  • RESULTS IN SHIFT OF FLUID FROM THE INTRAVASCULAR TO THE EXTRAVASCULAR COMPARTMENT
• Predominantly involves white matter
• Mechanisms:
  
  1. Newly formed vessels (in tumors) deficient in tight junctions
  2. Production of vascular endothelial growth factor (VEGF) by tumor cells
  3. Production of inflammatory mediators, chemokines, cytokines, and other growth factors

Question 5

What are the most common causes of vasogenic edema?

Answer 5

1. primary or secondary brain tumors
2. abscesses
3. contusions
4. intracerebral hematomas

Question 6

• What are the gross changes seen in vasogenic edema?
• What is an example of a tumor that causes vasogenic edema?
• What treatment can be used?

Answer 6

• **Gross changes: **
  
  • Flattened gyri
  • Narrowed sulci
  • Compressed ventricles
  • Brain softening
• Example: Glioblastoma (1° brain tumor)
• Treatment:
  
  • corticosteroids
  • anti-VEGF antibody (bevacizumab)

Question 7

What caused this vasogenic edema?

Answer 7

Cerebral abscess

Question 8

What is the pathophysiology of cytoxic edema (“intracellular edema”)?

Answer 8

• Occurs secondary to cellular energy failure
  
  • RESULTS IN A SHIFT OF WATER FROM THE EXTRACELLULAR TO INTRACELLULAR COMPARTMENT
    
    • Intracellular swelling -large amounts of Na enter cells, H₂O follows
    • Histologically brain tissue vacuolation
• More pronounced in gray matter
• Mechanisms:
  
  • dysfunction of neuronal and astrocytic membrane pumps
    
    • caused by excess glutamate, extracellular potassium, inflammatory cytokines, etc.

Question 9

What are the most common causes of cytoxic edema?

Answer 9

1. ischemia/infarct
2. meningitis
3. trauma
4. seizures
5. hepatic encephalopathy

Question 10

What leads to decreased perfusion or herniation caused by edema?

Answer 10

↑ intracranial pressure

• The brain is in a closed rigid box
• Brain volume = Brain + blood + CSF (+ lesion)
• Increased volume = increased pressure

Question 11

What determines the type of herniation?

Answer 11

Rigid dural folds (falx, tentorium) dictate what type of herniation

Question 12

Subfalcine Herniation

• Definition:
• Cause by:
• Complication:

Answer 12

• Cingulate gyrus herniates under the falx
• Caused by asymmetric expanding hemispheric lesions
• May cause in compression of ant. cerebral art. resulting in infarction

Question 13

Trantentorial Uncal Herniation

• Definition:
• Complications:

Answer 13

• Medial temporal lobe displaced through the tentorial opening because of asymmetric expanding lesion
• Complications:
  
  • Ipsilateral CN 3 compression with pupillary dilatation
  • Compression of brainstem (midbrain peduncle containing corticospinal tracts) against the tentorial edge opposite the direction of herniation (can lead to false localization of motor deficit-ipsilateral hemiparesis) (Kernohan’s notch)
  • Posterior cerebral artery compression (ipsi-or bilateral)
  • Duret hemorrhage

Question 14

Why is there CN 3 compression with pupillary dilation in a transtentorial uncal herniation?

Answer 14

• Tentorium is firmly attached to the skull and taut
• When the midbrain is pushed down from above it is pushed against the tentorium compressing the CN 3
• Pupillary constrictor fibers are located on surface of CN 3

Question 15

1. What is Kernohan’s notch a product of?
2. What clinical signs are seen along with Kernohan’s notch?

Answer 15

1. With compression of the midbrain due to herniation from above, the opposite cerebral penduncle is pushed against the opposite free edge of the tentorium
   
   • creasing of the peduncle is called Kernohan’s notch
2. Causes weakness and a Babinski sign ipsilateral to the cerebral hemispheric lesion
   
   • corticospinal tracts cross in distal medulla

Question 16

What is duret hemorrhage?

Answer 16

• Fatal brainstem hemorrhage
• Secondary to progression of uncal herniation and resultant tearing of vessels in midbrain/pons

Question 17

Cerebellar Tonsillar Herniation

• Definition:
• Caused by:
• Complication:

Answer 17

• Definition:
  
  • Caudal cerebellar structures (“tonsils”) attempt to escape through the foramen magnum
• Caused by:
  
  • Symmetric expansion of supratentorial contents into posterior fossa
  • Expanding mass lesion in posterior fossa
• Complication:
  
  • Medullary compression results in cardiorespiratory arrest

Question 18

Define **hydrocephalus: **

• What are the 2 types?

Answer 18

Enlargement of ventricles associated with increase in CSF volume

• 2 types:
  
  1. Communicating (non-obstructive)
  2. Non-communicating

Question 19

• Define **communicating hydrocephalus: **
• What leads to an increase in ventricle size?

Answer 19

• Ventricular system is patent
• Increased size of ventricles may be due to:
  
  • Arachnoid villi obstruction due to decreased absorption at arachnoid granulations
    
    • Causes of decreased absorption: meningitis, hemorrhage in subarachnoid space, or sinus thrombosis
  • Overproduction of CSF from a choroid plexus papilloma

Question 20

# * Define **non-communicating hydrocephalus:** 
* What are examples of causes?

Answer 20

• Obstruction within ventricular system
  
  • Prevents “communication” between the ventricles proximal and distal to obstruction
• Examples of causes:
  
  • Tumor in ventricle blocking flow
    
    • Example: At foramen of Monro
  • Congenital malformation
    
    • Example: Atresia of aqueduct of Sylvius
  • Thick meninges at base of brain blocking flow
    
    • Example: fibrosis secondary to meningitis

Question 21

What is the leading cause of death of people < 45 years old, in developed countries?

Answer 21

head trauma

Question 22

What are the 2 main types of head trauma?

Answer 22

• Blunt (nonmissile) – most common
  
  • Associated with acceleration or deceleration forces to the head
  • Results in:
    
    • Skull fractures
    • Parenchymal injury
    • Vascular injury
• Penetrating (missile) – penetration by external object (bullet)

Question 23

How can head trauma be characterized?

Answer 23

• Open versus closed (referring to skull)
• Focal versus diffuse
• Primary damage versus secondary damage

Question 24

1. What are the 3 patterns of skull fractures?
2. How else can skulll fractures be characterized?

Answer 24

1. Three patterns:
   
   1. Linear: single fracture line, through entire thickness of skull
   2. Comminuted: multiple linear fractures radiate from point of impact
   3. Depressed: bone fragments displaced inward
2. Other characterizations:
   
   • Occur over convexity or base
   • Skin may be open or closed

Question 26

What does a basillar skull fracture result in?

Answer 26

Results in a “ring” fracture encircling the foramen magnum

Question 27

What are the two types of **focal parenchymal damage**?

Answer 27

1. **Concussion** – pathophysiologic process induced by traumatic biomechanical forces * also called mild traumatic brain injury 2. **Contusion** – superficial bruises of the brain

Question 28

**Concussion** * What are the causes? * What type of abnormalities occur? * How long until symptoms are seen? * What kind of sypmtoms are seen? * Duration?

Answer 28

* Caused by **direct or indirect forces to head** * Biochemical and physiologic abnormalities occur; * usually no structural abnormalities on imaging acutely * **Immediate transient neurologic impairment** * Constellation of physical, cognitive, emotional, and/or sleep-related symptoms that may or may not involve loss of consciousness * Duration is highly variable: several minutes to days, weeks, months, or longer

Question 29

**Brain Contusion** * Where is the typical location? * Where are the pathological results seen? * What type of abnormalities are seen? * Are there any clinical correlations?

Answer 29

* **Usually at crests of gyri** * **Occur overlying rough area of inner skull** (orbital, temporal regions) * Results at **point of impact** from fall or from direct blow to head * **Structural abnormalities are seen** * Small blood vessels, neurons, and glia are damaged * **Clinical correlations:** deficits correlate with size and location of injury

Question 30

What are the gross and microscopic changes seen in **acute contusions**?

Answer 30

* **Wedge-shaped** * **Superficial hemorrhage in cortex and meninges** * **Microscopically:** * _Perivascular accumulation of blood_ * After hours, _brain edema_

Question 31

What are the gross and microscopic changes seen in an **old brain contusion**?

Answer 31

* **Orbital surfaces of frontal +/or temporal lobes** * Gyri indented, cavitated, with _brown/orange discoloration_ * **Macrophages with hemosiderin, fibrillary astrocytes**

Question 32

What is a **coup contusion**?

Answer 32

* Contusion occurs **at point of impact** * Usually secondary to blow to stationary head * May occur at point of impact from fall

Question 33

What is a **countrecoupe contusion**?

Answer 33

* Contusion **directly opposite the point of impact** * Usually occur with fall * As head hits ground a sudden deceleration occurs that causes brain to “bounce” back and hit skull 180° opposite the point of impact with ground * Another theory: * brain in motion lags behind skull, and with deceleration or impact of skull, it keeps moving; * tensile strength of vessels at the site opposite of impact is exceeded producing damage

Question 34

What are the **most common locations** of contrecoup contusions?

Answer 34

Bilateral contusions of **frontal and temporal poles,** **opposite the point of impact** of head on ground

Question 35

What causes **diffuse parenchymal damage**?

Answer 35

**Diffuse axonal injury** (DAI) * Deceleration/acceleration injury and/or angular acceleration * Loss of consciousness at onset WITHOUT lucid interval * Unconscious or disabled till death * Lesser degrees may be compatible with varying severity of neurologic deficits * Widespread damage to the axons * Mechanical forces disrupt axons

Question 36

**Diffuse Axonal Injury** – Gross lesions * **White matter:** * **Acute changes:** * **Chronic changes:**

Answer 36

* **White matter:** * corpus callosum, paraventricular white matter, superior cerebellar peduncle, superior colliculi * **Acute changes:** * clusters of petechial hemorrhages and soft hemorrhagic foci * **Chronic changes:** * hydrocephalus ex vacuo, thinned corpus callosum, gray discoloration of white matter

Question 37

What must be done to confirm a diagnosis of DAI?

Answer 37

**Microscopic exam**

Question 38

**Diffuse Axonal Injury** – Microscopic Exam * **Apperance of the axons?** * Why? * **Chronology:** 1. Acute 2. Subacute 3. Chronic

Answer 38

* **Axons are disrupted** * axonal transport continues ⇒ axonal swellings * **Chronology:** 1. **Acute** –axonal swellings, positive for ß amyloid protein and silver stains 2. **Subacute** –microglia and axonal swellings 3. **Chronic** –Degeneration of involved fiber tracts

Question 39

List the diffrent types of vascular injury (4):

Answer 39

1. Epidural hematoma 2. Subdural hematoma 3. Subarachnoid space hemorrhage 4. Intracerebral hemorrhage

Question 40

**Epidural hematoma** * Associated with? * Is there lucid interval? * How fast does the blood accumulate?

Answer 40

* Associated with **skull fx & middle meningeal artery tear** * **LUCID INTERVAL** between trauma & clinical symptoms * **Slow accumulation** because of _adherence between skull & dura_

Question 41

**Acute subdural hematoma** * Clinical Signs: * What is the pathophysiology? * What population has the highest incidence?

Answer 41

* **Most often non-localizing signs:** headache, confusion * **Tear of bridging veins** extending from subarachnoid space to dura * More common in **elderly people with brain atrophy**

Question 42

**Chronic Subdural Hematoma** * When did the injury occur? * What gross change can be seen? * What is a complication?

Answer 42

* Original injury occurred **months ago** * **Well organized membrane enclosing hematoma** * **Susceptible to recurrent bleeds** from friable vessels in granulation tissue

Question 43

What causes **subarachnoid space hemorrhage**?

Answer 43

* contusions * lacerations skull base fractures * escape of blood from ventricular system

Question 44

What are the **sequela** associated with brain trauma?

Answer 44

1. **Post-traumatic hydrocephalus** * Obstruction of CSF resorption due to subarachnoid space hemorrhage 2. **Post-traumatic epilepsy** 3. **Chronic traumatic encephalopathy** * Associated with mild repetitive traumatic brain injury * Described in athletes (football, hockey) and veterans * Initially impulsivity, aggression, depression, short-term memory loss * Eventually dementia, gait, speech abn, parkinsonism * Pathology: extensive deposition of tau in form of neurofibrillary and glial tangles and TDP-43 inclusions