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Neurology > Trauma > Flashcards

Trauma Flashcards

1
Q
  • What is the BBB also called?
  • Where is the site of the BBB?
  • Small substances & small lipophilic molecules …..
  • Large substances & hydrophilic molecules require ….
A
  • 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
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2
Q
  • Definition of cerebral edema:
  • 2 major forms:
A
  • 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
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3
Q

What are the gross changes of cerebral edema?

A

Widened, flattened gyri with narrowed sulci

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4
Q

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

A
  • 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
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5
Q

What are the most common causes of vasogenic edema?

A
  1. primary or secondary brain tumors
  2. abscesses
  3. contusions
  4. intracerebral hematomas
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6
Q
  • 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?
A
  • **Gross changes: **
    • Flattened gyri
    • Narrowed sulci
    • Compressed ventricles
    • Brain softening
  • Example: Glioblastoma (1° brain tumor)
  • Treatment:
    • corticosteroids
    • anti-VEGF antibody (bevacizumab)
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7
Q

What caused this vasogenic edema?

A

Cerebral abscess

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8
Q

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

A
  • 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.
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9
Q

What are the most common causes of cytoxic edema?

A
  1. ischemia/infarct
  2. meningitis
  3. trauma
  4. seizures
  5. hepatic encephalopathy
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10
Q

What leads to decreased perfusion or herniation caused by edema?

A

↑ intracranial pressure

  • The brain is in a closed rigid box
  • Brain volume = Brain + blood + CSF (+ lesion)
  • Increased volume = increased pressure
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11
Q

What determines the type of herniation?

A

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

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12
Q

Subfalcine Herniation

  • Definition:
  • Cause by:
  • Complication:
A
  • Cingulate gyrus herniates under the falx
  • Caused by asymmetric expanding hemispheric lesions
  • May cause in compression of ant. cerebral art. resulting in infarction
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13
Q

Trantentorial Uncal Herniation

  • Definition:
  • Complications:
A
  • 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
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14
Q

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

A
  • 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
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15
Q
  1. What is Kernohan’s notch a product of?
  2. What clinical signs are seen along with Kernohan’s notch?
A
  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
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16
Q

What is duret hemorrhage?

A
  • Fatal brainstem hemorrhage
  • Secondary to progression of uncal herniation and resultant tearing of vessels in midbrain/pons
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17
Q

Cerebellar Tonsillar Herniation

  • Definition:
  • Caused by:
  • Complication:
A
  • 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
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18
Q

Define **hydrocephalus: **

  • What are the 2 types?
A

Enlargement of ventricles associated with increase in CSF volume

  • 2 types:
    1. Communicating (non-obstructive)
    2. Non-communicating
19
Q
  • Define **communicating hydrocephalus: **
  • What leads to an increase in ventricle size?
A
  • 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
20
Q 
# * Define **non-communicating hydrocephalus:** 
* What are examples of causes?
A
  • 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
21
Q

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

A

head trauma

22
Q

What are the 2 main types of head trauma?

A
  • 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)
23
Q

How can head trauma be characterized?

A
  • Open versus closed (referring to skull)
  • Focal versus diffuse
  • Primary damage versus secondary damage
24
Q
  1. What are the 3 patterns of skull fractures?
  2. How else can skulll fractures be characterized?
A
  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
25
Q
A
26
Q

What does a basillar skull fracture result in?

A

Results in a “ring” fracture encircling the foramen magnum

27
Q

What are the two types of focal parenchymal damage?

A
  1. Concussion – pathophysiologic process induced by traumatic biomechanical forces
    • also called mild traumatic brain injury
  2. Contusion – superficial bruises of the brain
28
Q

Concussion

  • What are the causes?
  • What type of abnormalities occur?
  • How long until symptoms are seen?
  • What kind of sypmtoms are seen?
    • Duration?
A
  • 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
29
Q

Brain Contusion

  • Where is the typical location?
  • Where are the pathological results seen?
  • What type of abnormalities are seen?
  • Are there any clinical correlations?
A
  • 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
30
Q

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

A
  • Wedge-shaped
  • Superficial hemorrhage in cortex and meninges
  • Microscopically:
    • Perivascular accumulation of blood
    • After hours, brain edema
31
Q

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

A
  • Orbital surfaces of frontal +/or temporal lobes
  • Gyri indented, cavitated, with brown/orange discoloration
  • Macrophages with hemosiderin, fibrillary astrocytes
32
Q

What is a coup contusion?

A
  • Contusion occurs at point of impact
  • Usually secondary to blow to stationary head
  • May occur at point of impact from fall
33
Q

What is a countrecoupe contusion?

A
  • 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
34
Q

What are the most common locations of contrecoup contusions?

A

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

35
Q

What causes diffuse parenchymal damage?

A

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
36
Q

Diffuse Axonal Injury – Gross lesions

  • White matter:
  • Acute changes:
  • Chronic changes:
A
  • 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
37
Q

What must be done to confirm a diagnosis of DAI?

A

Microscopic exam

38
Q

Diffuse Axonal Injury – Microscopic Exam

  • Apperance of the axons?
    • Why?
  • Chronology:
    1. Acute
    2. Subacute
    3. Chronic
A
  • 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
39
Q

List the diffrent types of vascular injury (4):

A
  1. Epidural hematoma
  2. Subdural hematoma
  3. Subarachnoid space hemorrhage
  4. Intracerebral hemorrhage
40
Q

Epidural hematoma

  • Associated with?
  • Is there lucid interval?
  • How fast does the blood accumulate?
A
  • Associated with skull fx & middle meningeal artery tear
  • LUCID INTERVAL between trauma & clinical symptoms
  • Slow accumulation because of adherence between skull & dura
41
Q

Acute subdural hematoma

  • Clinical Signs:
  • What is the pathophysiology?
  • What population has the highest incidence?
A
  • 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
42
Q

Chronic Subdural Hematoma

  • When did the injury occur?
  • What gross change can be seen?
  • What is a complication?
A
  • Original injury occurred months ago
  • Well organized membrane enclosing hematoma
  • Susceptible to recurrent bleeds from friable vessels in granulation tissue
43
Q

What causes subarachnoid space hemorrhage?

A
  • contusions
  • lacerations skull base fractures
  • escape of blood from ventricular system
44
Q

What are the sequela associated with brain trauma?

A
  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

Neurology (26 decks)

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