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PATH FINAL > Histo: Cerebrovascular disease and Trauma > Flashcards

Histo: Cerebrovascular disease and Trauma Flashcards

1
Q

What are the 5 common types of pathology that can cause damage to the CNS

A

Oedema
Hydrocephalus
Raised ICP
Stroke
Traumatic brain injury

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2
Q

What are the two types of cerebral oedema?

A
  • Vasogenic - due to disruption of blood-brain barrier due to endothelial tight junctions breaking down
  • Cytotoxic - secondary to cellular injury (e.g. hypoxia, ischaemia). This is usually due to damage to astrocytes (which surround the endothelial cells).
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3
Q

Which water transporting channel is found in the brain?

A

Aquaporin 4

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4
Q

What radiological appearance is characteristic of cerebral oedema?

A

Loss of gyri

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5
Q

What are the mechanisms which prevent oedema in the CNS in a healthy brain

A

Astrocytes surrounding vessels pump fluid into vasculature to reduce oedema

Movement of fluid into subarachnoid CSF or into ventricles

Fluid is pumped via AQP4 channel

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6
Q

Describe the passage of CSF through the brain.

A
  • The choroid plexus (mainly found in the lateral ventricles) pumps out CSF
  • It passes from the lateral ventricles, through the interventricular foramina and into the 3rd ventricle
  • It then goes down the cerebral aqueduct into the 4th ventricle
  • It then flows down into the medulla and down the spinal cord in the central canal of the spinal cord
  • Most of the CSF will leave the 4th ventricle and enter the subarachnoid space
  • CSF will circulate around the subarachnoid space and will drain via arachnoid granulations into the superior sagittal sinus (and hence back into the systemic circulation)
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7
Q

Define hydrocephalus

A

An increase in CSF and enlargement of the ventricular system

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8
Q

Name and describe the two types of hydrocephalus.

A
  • Non-communicating - caused by obstruction of CSF flow (usually in the cerebral aqueduct)
  • Communicating - caused by reduced reabsorption of CSF into the venous sinuses (this could be caused by infection e.g. meningitis as meninges become fibrous and have reduced absorption)
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9
Q

What is the normal range for ICP?

A

7 - 15 mmHg

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10
Q

Name and describe the three sites of brain herniation.

A
  • Subfalcine - the cortex is pushed under the falx cerebri
  • Transtentorial (uncal) - the posterior cranial fossa is covered by the tentorium cerebelli which has a rigid opening for the brainstem. Supratentorial pressure can result in herniation of the medial temporal lobe over the rigid end of the opening of the tentorium cerebelli
  • Tonsillar - herniation of the cerebellar tonsils through the foramen magnum (this can put pressure on the medulla and kill) (commonly occuring if LP is performed in cases of increased ICP)
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11
Q

Define stroke.

A

A clinical syndrome characterised by rapidly developing focal/global neurological deficit lasting >24 hours or leading to death woth no apparent cause other than that of vascular origin

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12
Q

Which diseases are encompassed by the term ‘stroke’?

A
  • Cerebral infarction
  • Primary intracerebral haemorrhage
  • Intraventricular haemorrhage
  • Subarachnoid haemorrhage (most of the time)

NOTE: subdural, epidural haemorrhage or infarction due to infection or tumour IS NOT INCLUDED in stroke definition.

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13
Q

What is a TIA?

A

Same definition as stroke but resolving within 24 hours with no permenant damage to brain.

NOTE: TIA is an important predictor of future infarct (1/3 people with TIA will have a significant infarct within 5 years)

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14
Q

what investigation must you always do following a TIA

A

Carotid US

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15
Q

What is non-traumatic intraparenchymal haemorrhage?

A

Haemorrhage into the substance of the brain (parenchyma) due to rupture of small intraparenchymal vessels

Commonly in basal ganglia.

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16
Q

Commonest cause of non-traumatic intraparenchymal haermorrhages?

A

Chronic hypertension

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17
Q

How does someone with a intraparenchymal haemorrhage present

A

Severe headache
Vomiting
Rapid loss of consciousness
Focal neurological signs

18
Q

What is an arteriovenous malformation?

A
  • A malformation where blood bypasses quickly from artery to vein without going through a normal capillary network
  • They can occur anywhere in the CNS and they can rupture
  • As they occur under high pressure, they tend to cause massive bleeds
19
Q

How are arteriovenous malformations treated?

A
  • Surgery
  • Embolisation
  • Radiosurgery
20
Q

Define cavernous angioma.

A
  • Well-defined malformative lesion composed of closely-packed vessels with no parenchyma interposed between vascular spaces
  • NOTE: it is similar to an arteriovenous malformation but there is no brain substance wrapped up amongst the vessels
  • NOTE: these tend to bleed at lower pressure causing recurrent small bleeds
21
Q

Describe the appearance of cavernous angiomas on MRI.

A

Shows target sign

22
Q

What causes subarachnoid haemorrhages?

A

Rupture of a berry aneurysm

NOTE: berry aneurysms are congenital

23
Q

Where are berry aneurysms typically found?

A
  • 80% at the internal carotid bifurcation
  • 20% within the vertebro-basillar circulation
  • NOTE: highest risk of rupture if diameter of 6-10 mm
24
Q

How does someone with a subarachnoid haemorrhage typically present

A

Thunderclap headache
Vomiting
Loss of consciousness

25
Q

Define infarction

A

Tissue death due to ischaemia (NOT hypoxia - it is due to ischaemia which is lack of blood supply!)

26
Q

What is the most common cause of cerebral infarctions?

A

Cerebral atherosclerosis

27
Q

Where is atherosclerosis most commonly found within the cerebral vasculature?

A
  • Carotid bifurcation
  • Basilar artery
28
Q

Which part of the cerebral vasculature tends to be affected by infarcts resulting from emboli?

A

Middle cerebral artery branches

29
Q

List some differences between infarctions and haemorrhagic strokes.

A

Infarction

  • Tissue necrosis
  • Rarely haemorrhagic
  • Permanent damage in the affected area
  • No recovery

Haemorrhage

  • Fewer macrophages
  • Limited tissue damage
  • Partial recovery
30
Q

What is the biggest cause of death in people < 45 years?

A

Traumatic brain injury

31
Q

Describe how traumatic brain injury can be classified.

A
  • Non-missile and missile (e.g. penetrative injury)
  • Acceleration and deceleration (e.g. RTA, includes rotational)
  • Focal or diffuse
32
Q

What are the consequences of base of skull fractures?

What are the clinical features of basal skull fracture

A
  • The fracture may pass through the middle ear or anterior cranial fossa
  • It can cause otorrhoea or rhinorrhoea of CSF fluid (straw colour fluid leaking)
  • Increased risk of infection

Clinical Features: battle sign (mastoid process bruising), raccoon eyes, straw coloured otorrhoea or rhinorrhoea

33
Q

Define a contusion

A

collision between brain and skull causing brain bruising

34
Q

Distinguish between coup and countercoup injury in contusions

A

Coup = front of brain hitting front of skull causing bruising to front of brain

Contracoup = brain richocheting from front of skull and hitting the back of the skull causing damage to back of brain (opposite to region of impact)

35
Q

With regards to brain injury, what is a laceration?

A

Bruising of the brain that causes rupture of the pia mater

36
Q

What is diffuse axonal injury?

A
  • Shear and tensile forces causes axons to break apart hence occurs at moment of injury
  • This is the most common non-bleed related cause of coma (e.g. post-trauma)
  • Midline structure are particularly affected (e.g. corpus callosum)
  • Some people suffer cognitive and behavioural changes further down the line
37
Q

Which vessel is commonly damaged in trauma and causing a extradural haemorrhage

A

Middle meningeal artery

38
Q

CT changes seen in extradural haemorrhage

What type of CT is used for suspected strokes

A

“Lemon” shaped hyperdensity

HEAD NON CONTRAST CT!

39
Q

Which vessels are damaged to cause a subdural haemorrahge

What are the risk factors for subdural haemorrahge

A

bridging veins - hence slow venous bleed (more gradual onset of sx compared to extradural haemorrhage).

Risk factors: alcoholic, elderly, on anticoagulants

40
Q

CT changes seen in subdural haemorrhage

A

Crescent (or banana) shape

PATH FINAL (36 decks)

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