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Nervous System > P- CNS Vascular Disease and Trauma > Flashcards

P- CNS Vascular Disease and Trauma Flashcards

1
Q

Define brain edema.

What are the 2 major types?

A

Brain edema is the presence of increased water within the brain PARENCHYMA

  1. vasogenic edema
  2. cytotoxic edema
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2
Q

What are the 3 major things that can disrupt the balance between brain parenchymal mass and the fixed boundaries of the intracranial vault?

A
  1. generalized brain edema
  2. hydrocephalus
  3. localized expanding mass lesions
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3
Q

What is vasogenic edema?

A

It is when the integrity of the BBB is disrupted and fluid escapes from the vasculature into the interstitial space of the brain. Absence of lymphatic drainage in the brain –> excess ECF

  1. localized = permeable vessels near abscess or neoplasm
  2. generalized = global ischemic injury

It is most pronounced in white matter

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4
Q

What is cytotoxic edema?

A

It is when there is increased fluid in individual cells of the brain secondary to cellular injury [energy failure at the cellular level]. It usually occurs as the result of an ischemic insult.
Insult–> Na excess in cell –> H20 excess in cell

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5
Q

How does an edematous brain differ from a normal brain grossly?

A
  1. softened parenchyma
  2. flattened gyri
  3. sulci are narrow
  4. ventricular cavities are compressed
  5. grey/white matter border is blurred
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6
Q

What are common sequelae associated with brain edema?

A
  1. increased intracranial pressure [headache, altered mental status]
  2. papilledema [swelling of optic disk]
  3. parenchymal herniation
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7
Q

What is the relationship between size of brain and intracranial pressure?

A

Intracranial pressure rises slowly at first and then increases in an exponential fashion as the volume continues to increase

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8
Q

What are the 2 most common forms of herniation in the brain?

A
  1. Uncal herniation

2. cerebellar tonsil herniation - can compress the brainstem

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9
Q

Describe uncal herniation.
Where does it herniate?
What are signs/symptoms?

A

Uncal herniation occurs when the medial aspect of the temporal lobe is compressed against the free margin of the tentorium cerebelli.

  1. pupillary dilation and impaired eye movement on the side of the lesion
  2. if it compresses posterior cerebral artery it can lead to secondary ischemic injury of the primary visual cortex
  3. if it displaces the brainstem laterally, the cerebral peduncles on the OPPOSITE side to be compressed causing hemiparesis on the same side of the body as the lesion
  4. if it displaces the brainstem downward, it can cause Duret hemorrhages in the pons/medulla
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10
Q

What is the “false localizing sign” associated with uncal herniation?

A

If the herniation exerts mass effect on the brainstem it can compress the contralateral cerebral peduncle.
The cerebral peduncle carries fibers from the opposite side of the brain to the same side of the body as the lesion
Therefore, there will be hemiparesis on the same side of the body as the lesion

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11
Q

Describe cerebellar tonsillar herniation.

What are the major sequelae?

A

It is when the cerebellar tonsils get displaced through the foramen magnum.

Sequelae:

  1. compression of brainstem–> compromised respiratory centers in pons/medulla
  2. hemorrhagic lesions in the brainstem [Duret hemorrhages]
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12
Q

What is a Duret hemorrhage?
What is the physiological cause?
Which herniations can lead to this type of hemorrhage?

A

It is a secondary brainstem hemorrhage that occurs as the result of downward displacement of the brainstem due to:

  1. transtentorial [uncal]
  2. cerebellar tonsillar herniation

It is a linear hemorrhage in the midline of the brainstem most likely caused by kinking of the basilar artery penetrating branches as the brainstem is pulled down –>necrosis and hemorrhage in the parts of the brainstem supplied by the penetrating arteries

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13
Q

What percent of cardiac output goes to the brain?
What % of the bodies oxygen is used by the brain?
What is the blood flow to the brain?
How does it keep this flow despite changes in perfusion pressure?

A

15% of the CO
20% of the oxygen

Q is maintained at 50mL/100g of brain tissue/min over a wide range of perfusion pressures due to autoregulation.

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14
Q

What are the 3 major categories of cerebrovascular disease?

A
  1. generalized reduction in blood flow
    - artery “border zone” infarct
    - hippocampal injury
    - purkinje cell injury
  2. Infarct or transient ischemic attack [TIAs]
    - local vascular obstruction
  3. primary hemorrhage in the parenchyma or subarachnoid space
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15
Q

Below what systolic pressure do autoregulatory mechanisms fail to compensate for reduction in blood flow?

A

70mmHg

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16
Q

How does ischemia differ from hypoxia/hypoxemia?

Which plays a bigger role in the development of brain injury?

A

Ischemia plays a more important role than hypoxia in the development of brain injury.

Hypoxia = decreased oxygen to the brain

Ischemia =

  1. associated with decrease tissue perfusion so low oxygen AND low glucose delivery to cells
  2. stagnation of flow allows the accumulation of metabolic by-products like lactic acid
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17
Q

How does ischemia cause cell death?

A

It decreases the ability of the cell to generate ATP:

  1. low ATP –> disrupted Na/K pump, glutamate transporter
  2. Na, Ca and water build up in the cell
  3. Ca activates enzymes like ATPase, protease, lipase, endonuclease
  4. cell membrane injury, nucleic acid injury, denaturation of proteins
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18
Q

What role is played by glutamate and the glutamate receptor in cell injury?

A
  1. Low ATP leads to inhibition of glutamate transporters.
  2. Increased glutamate in the extracellular compartment
  3. Excess binds glutamate receptors [NMDA] causing cell death via excessive excitation and increased intracellular Ca
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19
Q

What is selective vulnerability? What 3 areas of the brain are most susceptible?

A

It means that certain regions and neuronal populations are more susceptible than others to ischemic injury.

  1. Arterial border zones
  2. pyramidal cells in the CA1 region of hippocampus
  3. Purkinje cells of the cerebellum

[2 and 3 have higher levels of glutamate receptors and thus are more vulnerable to excitotoxicity]

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20
Q

What are the “arterial border zones”?

What is a common location for border zone injury?

A

Areas of the brain located at the junction of arterial territories that are susceptible to ischemic injury.

A common location for border zone injury is the superior cerebral convexity near the terminal territory of the anterior cerebral and middle cerebral arteries

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21
Q

Describe the time frame of gross changes to the brain after global ischemic injury.

A
  1. immediately after, the brain is grossly normal
  2. hours = visible change to selectively vulnerable areas
  3. 24-48 hours = whole brain is soft and edematous, the cerebral cortex has linear zones of discoloration, grey/white delineation is blurred
  4. soft, necrotic cerebellar parenchyma may drift into the spinal subarachnoid space
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22
Q

Describe the microscopic changes associated with global ischemic injury.

A

Seen in 12-24 hours

  1. neuron shrinking or swelling
  2. cytoplasmic eosinophilia [red nucleus], nuclear pyknosis, features of necrosis
  3. vacuolated parenchyma with widened perivascular and pericellular spaces
  4. LITTLE TO NO INFLAMMATION because overall perfusion is decreased
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23
Q

What are common causes of global ischemic injury?

A

Anything that results in a global decrease in the amount of oxygenated blood reaching the brain:

  1. cardiac arrhythmia
  2. shock
  3. severe increases of intracranial pressure
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24
Q

What factors determine the degree of parenchymal injury associated with global ischemic injury?

A
  1. age of the patient
  2. duration of the insult
  3. temperature [hypothermia increases resistance to hypoxic injury]
  4. concomitant acidosis, hypoxemia, hyperglycemia
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25
Q

What is a cerebral infarct? What age group and sex are most likely to experience one?

A

It is localized area of parenchymal necrosis [neurons AND glia] caused by an interruption in blood flow.

It occurs most commonly in the seventh decade of life and is more common in men

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26
Q

What are risk factors that increase the chance of having a cerebral infarct?

A

Atherosclerosis is one of the most important lesions predisposing to brain infarct so:

  1. hypertension
  2. DM
  3. hypercholesterolemia
  4. smoking
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27
Q

What arteries in the brain are most likely to have atherosclerotic lesions?

A
  1. internal carotids
  2. middle cerebral arteries [proximal]
  3. basilar artery

Thrombosis is most common in the carotid bifurcation or basilar artery

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28
Q

Where do emboli to the brain most commonly originate from?

A
  1. heart
  2. atherosclerotic plaques in proximal artery segments
  3. paradoxical from right-left shunts
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29
Q

Which causes more cases of cerebral infarction: local thrombi or embolic events?

A

Embolic events- either from cardiac sources or artheromatous plaques in proximal vessels

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30
Q

Where are embolic occlusions in the brain most likely to occur?

A

branches of MCA

31
Q

What determines the location and size of a cerebral infarct?

A
  1. site of arterial occlusion
  2. time over which the occlusion develops
  3. presence or absence of collaterals
  4. systemic perfusion pressure
32
Q

What is a lacunar infarct?
Where are they most likely to occur?
What is the most common cause of a lacunar infarct?

A

collateral circulation is less well developed in more distal arterial branches like the small penetrating branches to deep areas of the brain.

Lacunar infarcts are small (15mm or less) infarcts that are most likely to occur in:

  1. basal ganglia
  2. thalamus
  3. cerebral white matter
  4. pons

Most often caused by hypertension

33
Q

Athough cell death occurs within _______ of arterial occlusion, the gross and histologic appearance of the brain is normal for the first ___________.

A

Cell death occurs within minutes, but there is no gross or histologic changes for the first 4-12 hours

34
Q

What are the earliest visible alteration in non-hemorrhagic infarcts at the microscopic level?

A
  1. coagulative necrosis of neurons, glial cells, and neuropil
  2. neutrophilic inflammatory reaction
35
Q

36 to 48 hours after a non-hemorrhagic infarct, what will the brain look like?
72 hours?
1 month?
6months?

A

36-48 hours:

  1. necrotic area is swollen and softer than adjacent parenchyma
  2. demarcation between grey/white is blurred
  3. if emboli or border zone –> hemorrhage

72hours:
1. macrophages infiltrate and engulf necrotic tissue –> progressively sharper demarcation of the infarct

1month:

  1. softening and liquifaction of the infarct
  2. development of irregular cavities

6months:

  1. completely liquified
  2. irregular cystic defects
36
Q

How do you differentiate remote infarcts from old contusions?

A

Remote infarcts will have a thin layer of subpial parenchyma that is preserved.

Contusions will not

37
Q

What factors make an infarct more likely to be hemorrhagic?

A
  1. incomplete vessel occlusion
  2. transient vessel occlusion
  3. collateral circulation
  4. anticoagulants
  5. venous obstruction
38
Q

How does the appearance of a hemorrhagic infarct differ from that of a primary parenchymal hemorrhage?

A

Infarct : blood seeps into necrotic tissue in an irregular fashion

Primary hemorrhage: well-demarcated mass of blood that tears and displaces adjacent tissue

39
Q

What is a transient ischemic attack?

How many patients with TIA will have a significant infarct within 5 years?

A

24 hours or LESS of neurologic symptoms caused by self-limited episodes of vascular obstruction by atheromatous emboli or platelet-fibrin aggregates

1/3 of patients with TIAs will progress to infarct

40
Q

What is the most common site of infarct in the brain and what is the cause?
What will the patient present with?

A

MCA infarcts are the most common and are caused by emboli.

The patient will have:

  1. contralateral hemiparesis
  2. loss of sensation contralaterally
  3. visual abnormalities
  4. speech/language aphasias if on the left
41
Q

A patient presents with contralateral hemiparesis, loss of sensation on the same side. They have aphasia. They also are experiencing monocular blindness on the opposite side from the paresis/sensory loss.
What is the likely site of the infarct?
What probably caused the infarction: emboli or thrombosis?

A

The left internal carotid was probably thrombosed

Left because of the aphasias
Internal carotid and not MCA because of the monocular blindness which shows that there was loss of flow to the opthalmic artery on the ipsilateral side

42
Q

In what spaces are you likely to see primary hemorrhages in the brain?
What is the typical cause in each area?

A

epidural/subdural space = trauma

parenchyma = cerebrovascular disease [or trauma]

43
Q

Spontaneous [non-traumatic] intraparenchymal hemorrhages are most common at what age? What causes most ?

A

Peak incidence is around age 60 due to rupture of small intraparenchymal vessels due to systemic hypertension

44
Q

What are the ways hypertension can cause brain abnormalities?

A
  1. atherosclerosis of large vessels
  2. hyaline arteriolosclerosis in small vessels
  3. proliferative change and frank necrosis of arterioles
45
Q

What is a Charcot-Bouchard microaneurysm?
What is the cause?
Where in the brain are you most likely to see it?

A

It is a minute arteriolar aneuryms that occur in vessels less than 300 microns [usually the basal ganglia].

They form as a result of chronic hypertension

46
Q

Where do parenchymal hemorrhages occur most commonly?

A
  1. Basal ganglia - putamen and external capsule

followed by:

  • thalamus
  • cerebral white matter
  • pons
  • cerebellum
47
Q

Some softening of adjacent neuropil is present with primary parenchymal hematomas, however, in contrast to hemorrhagic infarcts, ___________________ are not seen.

A

large areas of necrosis

48
Q

In pateints who survive acute hemorrhage, the hematoma gets reabsorbed over time ultimately leaving _________________________.

A

a slit-like fluid filled cavity lined by gliotic neuropil and hemosiderin laden macrophages

49
Q

A patient presents with abrupt onset increase in intracranial pressure, severe headache, vomiting and rapid loss of consciousness.
They fall into a deep coma with altered respiratory patterns, dilated non-responsive pupils, and spasticity. Is this more likely to be a brain infarct or a primary hemorrhage?

A

Hemorrhage

50
Q

What is the most common cause of spontaneous [non-traumatic] subarachnoid hemorrhage?

A

rupture of a saccular aneurysm

51
Q

What increases the incidence of saccular aneurysms?

Where in the brain vasculature are most found?

A

Acquired, degenerative lesions related to chronic hemodynamic injury to the vessel wall from:

  1. PCKD
  2. fibromuscular dysplasia
  3. coarctation of the aorta
  4. AV malformations

Most saccular aneurysms are at the arterial bifurcations in the territory of the internal carotid artery [anterior circulation]

  • MCA
  • intracranial branches of int. carotid
  • anterior cerebral and ant. communicating
52
Q

When are saccular aneurysms at greatest risk for rupture?

A

when they get to 10mm in diameter

[but less than 25mm]

53
Q

Describe the structure of a saccular aneurysm. What vessel layers are involved?

A

The wall of the aneurysm is composed of:

  • intima
  • adventitia of the parent vessel

Media ends abruptly at the neck of the aneurysm
Lumen often contains a laminated thrombus

54
Q

Why d o infarcts of the brain parenchyma develop in the setting of a subarachnoid hemorrhage?

A

arterial spasms

55
Q

A patient presents with abrupt onset severe headache, vomiting and loss of consciousness.
They have no significant PMH.
The patient has neck rigidity and a the CSF is grossly bloody.
What most likely occured?
If the patient is going to die from this, when will they do so?
If they survive, what is the sequelae?

A

Subarachnoid hemorrhage

If they die, they will do so within a week of symptoms onset.

If they live, they will have chronic hydrocephalus because of blood organizing in the leptomeninges

56
Q

What are the 2 main traumatic CNS injuries?

A
  1. blunt force trauma- MVA, falls, assault

2. penetrating missile wounds

57
Q

Blunt force trauma can be further broken down into what three presentations?

A
  1. parenchymal injury
  2. epidural hematoma
  3. subdural hematoma
58
Q

What are the 3 types of traumatic injury to the brain parenchyma?

A
  1. diffuse axonal injury
  2. contusion
  3. chronic traumatic encephalopathy
59
Q

What is the cause of traumatic axonal injury [diffuse axonal injury]?
What is it the most common cause for?

A

It is caused by sudden deceleration and or acceleration that stretches or tears nerve cell processes within the cerebral/brain stem white matter.

DAI is the most common cause of persistant vegetative state.

60
Q

Describe the gross and microscopic appearance of a brain that has DAI/traumatic axonal injury.

A

Gross: hemorrhage in the white matter, especially

  • corpus callosum
  • dorsolateral brainstem
  • internal capsules

Microscopically:
axonal swellings -SPHEROIDS w/in white matter
[immunostaining for APP can find the swellings]

61
Q

What is a brain contusion and what is the most common location for them?

A

They are hemorrhages of superficial parenchyma due to blunt force trauma.
The most common spots are parts of the brain in areas where the bones of the skull are irregular:

  1. frontal poles
  2. orbital surfaces
  3. ant/inf frontal lobes
  4. cortex around the sylvian fissure
62
Q

What are the 2 patterns of contusion?

A
  1. Coup- blunt trauma to an immobile head with a small object. The hemorrhage will be pronounced under the point of impact
  2. Contrecoup- lesions in the brain area opposite the point of impact - falling and moving head strikes an immobile object
63
Q

Brain contusions, especially of accompanied by tearing of the superficial layers of the brain can cause ________________.

A

subarachnoid hemorrhage

64
Q

You are examining a brain and are trying to decide if it is a contusion or remote infarct. How can you tell?

A

A contusion will disrupt the subpial molecular layer where an infarct will not.

65
Q

What is chronic traumatic encephalopathy?

A

progressive neurological disorder than follows repetitive episodes of head trauma

66
Q

A former NFL player presents to you with speech difficulties, personality changes, confusion, memory loss and clumsiness.
Over time, he has been having spasticity, ataxia and parkinsonism like abnormalities.

What is it likely that he has?
What will you see microscopically in his brain?

A

Chronic traumatic encephalopathy:

  1. abnormal tau in neuronal cell bodies [neurofibrillary tangles]
  2. abnormal tau in astrocytes **
  3. B- amyloid but in a different distribution than alzheimers
67
Q

Epidural hematomas are most often caused by a rupture to what artery?

A

a branch of the middle meningeal artery

[usually in association with a skull fracture of the temporal bone because the artery is firmly attacked to the periosteum of the bone]

68
Q

A man gets hit in the temporal region with a baseball. He gets up and says he is fine, but when he gets to the dugout, he feels disoriented. What is the likely issue? What are sequelae?

A

Epidural hematoma which can compress adjacent dura, flatten underlying gyri and cause uncal/cerebellar tonsiller herniation–> brainstem compression–> death

69
Q

What is the most common cause of traumatic subdural hematoma?

A

disruption of bridging veins that extend from the brain surface to the dural sinuses usually caused by:

  1. whiplash
  2. blows to the head
  3. shaking of infants
70
Q

How do you differentiate acute from chronic subdural hematoma?

A 
Acute = clotted blood 
chronic = liquified blood clots
71
Q

How do the gyri differ in epidural hematomas and acute subdural hematomas?

A

Epidural = flattened convexities

Subdural = preserved gyri because the pressure is evenly distributed within the sulci and over the gyri

72
Q

Why is the progression of symptoms in a subdural hematoma slower than that of an epidural hematoma?

A 
Epidural = artery
Subdural = torn veins
73
Q

What happens over time with nonfatal subdural hematomas?

A

The hematoma will liquify and become demarcated from the underlying brain by a reactive “neomembrane”.

74
Q

Who is likely to develop a chronic subdural hematoma?

A

Patients with atrophic brains [alcoholics, coagulation disorders]

Nervous System (32 decks)

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