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HistoPath > Histopathology 19: Cerebrovascular Disease And Trauma > Flashcards

Histopathology 19: Cerebrovascular Disease And Trauma Flashcards

1
Q

What are the 2 types of hydrocephalus ?

A

Non-communicating
Communicating

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2
Q

What is the main cause of non-communicating hydrocephalus ?

A
  • Get obstruction of flow to CSF
  • Due to the choroid plexus getting stuck in the cerebral aqueduct (between 3rd and 4th ventricle)
  • NB most common form in neonate
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3
Q

What is a common cause of communicating hydrocephalus?

A
  • NOT due to obstruction
  • Instead to do with reabsorption of CSF into venous sinuses
  • Caused by meningitis infection - causes inflammation of the meninges which blocks csf reabsorption into the venous sinuses
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4
Q

What are the 3 main types of herniation in the brain ?

A
  • Subfalcine herniation
  • Transtentorial (Uncal) herniation (medial temporal lobe down through the tentorial notch)
  • Tonsillar herniation (coning)- cerebellum is pushed through the foramen magnum
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5
Q

What features can be seen on histology suggesting AVM (atrioventricular malformation) ?

A

Complex intertwining vessels

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6
Q

What is the characteristic sign of Cavernous Angioma on MRI ?

A

Target sign on T2 weighted MRI

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7
Q

What is a non-traumatic Intra-parenchymal haemorrhage ?

A

Haemorrhage into the brain parenchyma due to rupture of a small intraparenchymal vessels

Most commonly into the basal ganglia

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8
Q

2 types of Cerebral Oedema (XS fluid accumulation in brain, causing RAISED ICP)

A
  • Vasogenic- disruption of the blood brain barrier (breakdown of tight junctions of BBB)
  • Cytotoxic- secondary to cellular injury e.g. hypoxia/ ischaemia
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9
Q

What channels can increase development of cerebral oedema?

A

aquaporin 4 channels at the end feet of the astrocytes

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10
Q

How to reverse cerebral oedema

A
  • reverse the activity of the AQP4 channels at the astrocytic end feet- so you want water going back into the vasculature
  • can also move fluid into subarachnoid space
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11
Q

What you see on MRI in cerebral oedema

A

small gaps between the gyri and sulci which are very tight (all just a smooth brain with no notches)

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12
Q

Mx of non-communicating hydrocephalus

A

ventriculo-peritoneal shunt

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13
Q

Process of CSF from the point it is made

A
  • Made: choroid plexus (mainly in the lateral horns of the lateral ventricles)
  • goes from the lateral ventricles, through the intraventricular foramina, into the 3rd ventricle (slit-like ventricle in middle of the brain)
  • then goes down the cerebral aqueduct (which is in the midbrain) into the 4th ventricle
  • floor of the 4th ventricle is the pons and the roof is the cerebellum (so the 4th ventricle sits in the posterior cranial fossa)
  • Some CSF then flows down into the medulla and further down into the central canal of the spinal cord
  • Relatively little CSF volume will go down the spinal cord because most of it exits via a number of apertures in the 4th ventricle, into the subarachnoid space
  • CSF will then circulate through the subarachnoid space and via the arachnoid granulations which pierce the superior sagittal sinus, thereby returning the CSF to the venous sinuses which allow resorption and recycling of CSF
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14
Q

Normal ICP

What happens if raised ICP?

A

7-15 mmHg

Get brain herniation

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15
Q

Herniation when cortex is pushed under the rigid falx cerebri of the dura

A

Subfalcine herniation

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16
Q

Brain herniation where there is herniation of the medial temporal lobe through the tentorial notch

A

Transtentorial (Uncal) Herniation

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17
Q

Brain herniation where the medial aspect of the cerebellum (tonsil) is pushed through the foramen magnum

A

Tonsillar Herniation

NB puts pressure on the medulla and can kill

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18
Q

When the BBB integrity is disrupted, what is the resulting oedema described as?

A

Vasogenic

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19
Q

Which of the following types of herniation does not involve the cerebral cortex?

A

Tonsillar

Since it involves cerebellum

20
Q

How long must stroke Sx last to be defined as such?

A

>24 hrs

21
Q

Which type of haemorrhage is classed as stroke?

A

Subarachnoid + Intraventricular

22
Q

Aetiology of epidural haemorrhage

Aetiology of subdural haemorrhage

A

Trauma -> skull fracture -> rupturing the middle meningeal artery

SURGICAL EMERGENCY

usually venous origin (slower onset)

23
Q

How long do Sx in most TIA’s last?

A

<5 mins

24
Q

How many with TIA will get significant infarct within 5 years?

A

1/3rd (TIA = important predictor)

25
Q

Non-Traumatic Intra-Parenchymal Haemorrhage aetiology

A
  • haemorrhage into parenchyma
  • Most common in the basal ganglia
  • HTN plays a big role
26
Q

Main cause of Subarachnoid Haemorrhage

A

rupture of a berry aneurysm

HIGHEST risk of rupture when 6-10mm in diameter

NB 80% occur at the internal carotid bifurcation (anterior part of the Circle of Willis or in the extra-cranial carotid bifurcation area)

27
Q
A
28
Q

What is the most common cause of non-traumatic intra-parenchymal haemorrhages?

A

HTN

29
Q

Main cause of death in those <45 y/o

A

Traumatic Brain Injury (TBI)

30
Q

What is a cavernous angioma?

A
  • similar to AVM but no interposed brain tissue between vascular spaces
  • can be found anywhere in the CNS
  • usually symptomatic > 50 years

NB occur at lower pressure and can cause recurrent small bleeds

31
Q

MRI sign for Cavernous Angioma

A

target sign

32
Q

Infart vs haemorrhage in terms of permanence of damage, amount of recovery

A
  • infarct = no recovery, haemorrhage = partial recovery
  • infarct = permanent, haemorrhage = less so
33
Q

What is the meaning of straw-coloured fluid coming from ear or nose?

A

rupture to the base of the skull from a fracture - increased R of infection

34
Q

Laceration development from contusion of brain

A
  • Contusion happens due to collision with internal surface of brain
  • If it is severe enough, then it is called a laceration

NB rebound of the brain after direct impact with the anterior part of the skull can cause contrecoup damage to the opposite side of the brain (happens in rapid deceleration in road traffic accidents)

35
Q

Most common cause of coma

A

Diffuse Axonal Injury

  • occurs at the moment of injury
  • build-up of proteins where there has been axonal injury
  • Midline structures are PARTIALLY affected (corpus callosum, rostral brainstem and septum pellucidum)
36
Q

MOST COMMON form of cerebrovascular disease

A

Cerebral Infarction (causes 70-80% of strokes)

37
Q
A
38
Q

Most common cause of Cerebral Infarction

A

Cerebral atherosclerosis

39
Q

2 arteries, if affected by Cerebral atherosclerosis, that have the most devastating effect

A
  • carotid bifurcation
  • basilar artery
40
Q

Focal vs global cerebral oedema

A
  • Focal cerebral ischaemia- due to lack of blood flow a defined vascular territory (usually due to thrombus or embolus)
  • Global cerebral ischaemia- when the systemic circulation fails (can be due to cardiac insufficiency whereby there is not enough blood getting to the brain)
41
Q

Main artery affected in cerebral ischaemia, and the effects of this

A

Middle Cerebral Artery

  • Contralateral hemiplegia
  • Contralateral sensory loss
  • Language difficulties (if on the left side)
42
Q

Effect of ischaemia in Broca’s area

A

Expressive aphasia: patient understands what you are saying but cannot reply properly

43
Q

Effect of ischaemia if in Wernicke’s area

A

Receptive aphasia: cannot understand

44
Q

Effect of ischaemia in posterior Cerebral Artery

A

Mostly VISUAL deficits

45
Q

Effect of ischaemia in Anterior Cerebral Artery

A

personality-based whereby there are changes in personality

  • loss of inhibition
  • Executive function problems

HistoPath (21 decks)

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