Cerebrovascular disease and trauma Flashcards

1
Q

What is cerebral oedema?

A

Excess accumulation of fluid in the brain parenchyma.

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2
Q

What are the two types of cerebral oedema?

A

Vasogenic: Disruption of the blood brain barrier.

Cytotoxic: Secondary to cellular injury e.g. hypoxia/ischaemia.

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3
Q

What is the result of cerebral oedema?

A

Raised intracranial pressure

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4
Q

What are the two types of hydrocephalus?

A

Non-communicating involves obstruction of flow of CSF.

Communicating involves no obstruction but problems with reabsorption of CSF into venous sinuses.

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5
Q

What is normal ICP?

A

ICP is measured in mmHg and, at rest, is normally 7–15mmHg for a supine adult.

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6
Q

What are consequences of raised ICP?

A

Enclosed bony box: Pressure can increase because of localised (space occupying) lesions, oedema or both.

Increased pressure forces brain against unyielding bony wall of skull and inflexible dural folds. This results in herniation of brain structures where space is available.

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7
Q

What is the definition of stroke?

A

A stroke is a clinical syndrome characterised by rapidly developing clinical symptoms and/or signs of focal, and at times global loss of cerebral function, with symptoms lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin.

This definition includes stroke due to cerebral infarction, primary intracerebral haemorrhage, intraventricular haemorrhage and most cases of subarachnoid haemorrhage.

It excludes subdural haemorrhage, epidural haemorrhage, intracerebral haemorrhage (ICH) or infarction caused by infection or tumour.

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8
Q

What is a TIA?

A

TIA is a warning stroke that should be taken very seriously.

TIA is caused by a clot; the blockage is temporary.

Most TIAs last less than five minutes; the average is about a minute. Unlike a stroke, when a TIA is over, there is usually no permanent injury to the brain.

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9
Q

What is the significance of TIA?

A

1/3 of those with TIA get significant infarct within 5 years.

REMEMBER: TIA important predictor of future infarct.

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10
Q

What is a non-traumatic intra-parenchymal haemorrhage?

A

Haemorrhage into the substance of the brain - rupture of a small intraparenchymal vessel.

Most common in basal ganglia.

Hypertension > 50% of bleeds.

Presentation with severe headache, vomiting, rapid loss of consciousness, focal neurological signs.

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11
Q

What are arteriovenous malformations?

A

Occur anywhere in the CNS. Become symptomatic between 2nd and 5th decade (mean age 31.2 years). Present with haemorrhage, seizures, headache, focal neurological deficits.

High pressure – MASSIVE BLEEDING!!!

Seen on angiography.

Morbidity after rupture 53-81% - high in eloquent areas. Mortality 10-17.6%

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12
Q

What is the treatment of arteriovenous malformations?

A

Surgery, embolization, radiosurgery.

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13
Q

What is a cavernous angioma?

A

Well-defined malformative lesion composed of closely packed vessels with no parenchyma interposed between vascular spaces.

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14
Q

What is the pathogenesis/clinical presentation of cavernous angiomas?

A

Can be found anywhere in the CNS, usually symptomatic after age 50.

Pathogenesis unknown.

Present with headache, seizures, focal deficits, haemorrhage.

Low pressure – recurrent bleeds.

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15
Q

What is the treatment of cavernous angiomas?

A

Surgery

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16
Q

What is this?

A

Arteriovenous malformation

17
Q

What is this?

A

Arteriovenous malformations

18
Q

What is this?

A

Cavernous angioma

19
Q

What is this?

A

Cavernous angioma

20
Q

What are subarachnoid haemorrhages?

A

Rupture of a berry aneurysm; present in 1% of general population.

  • 80 %: Internal carotid artery bifurcation
  • 20% occur within the vertebro-basilar circulation.
21
Q

What is the clinical presentation of subarachnoid haemorrhages?

A

30% of patients have multiple aneurysms.

Greatest risk of rupture when 6-10mm diameter.

Present with sudden onset of severe headache, vomiting, loss of consciousness.

22
Q

What is this?

A

Berry aneurysm

23
Q

What is the treatment for subarachnoid haemorrhages?

A

Endovascular treatment - coils

24
Q

What are infarctions?

A

Tissue death due to ischaemia.

Commonest form of cerebrovascular disease

70-80% of strokes

25
Q

What are risk factors for infarctions?

A

Cerebral atherosclerosis most common cause.

Hypertension, diabetes, smoking are major risks factors.

26
Q

Where do the worst thrombosis occur?

A

Worst atherosclerosis in larger vessels (extracerebral arteries).

Often near carotid bifurcation or in basilar artery.

27
Q

Where do emboli occur?

A

Intracerebral arteries.

Usually from heart or atherosclerotic plaques.

Embolic occlusion usually in middle cerebral artery branches.

28
Q

What is the difference between an infarction and haemorrhagic stroke?

A

Infarction:

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

Haemorrhage:

  • Bleeding
  • Dissection of parenchyma
  • Fewer macrophages
  • Limited tissue damage (periphery)
  • Partial recovery
29
Q

What is the epidemiology of TBI?

A

Trauma single largest cause of death in people under 45.

9 deaths from head injury per 100,000.

Account for 25% of all trauma deaths.

High morbidity:

  • 19% vegetative or severely disabled
  • 31% good recovery
30
Q

What are different classifications of TBI?

A

Non-missile and missile

Non-missile:

  • Acceleration/deceleration
  • Rotation

RTA, falls and assaults.

Focal or diffuse.

31
Q

What are fractures associated with cerebrovascular disease?

A

Fissure fractures often extend into base of skull

May pass through middle ear or anterior cranial fossa

Otorrhea or rhinorrhea

Infection risk

32
Q

What is a contusion in the context of cerebrovascular trauma?

A

Brain in collision with skull.

Surface “bruising”.

If pia mater torn then becomes laceration.

Lateral surfaces of hemispheres, inferior surfaces of frontal and temporal lobes.

Coup or contrecoup.

33
Q

What is diffuse axonal injury in the context of cerebrovascular trauma?

A

Occurs at moment of injury.

Shear & tensile forces affecting axons.

Commonest cause of coma (when no bleed).

Midline structures particularly affected e.g. corpus callosum, rostral brainstem and septum pellucidum.