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Neurology > Cerebrovascular Disease > Flashcards

Cerebrovascular Disease Flashcards

1
Q

What is stroke defined as?

A

A syndrome of rapid onset of neurological deficit caused by focal, cerebral, spinal or retinal infarction (vascular in origin)

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2
Q

The underlying pathology of a stroke is either _________

A 
infarction/ ischaemia (clot blocking artery)
 or haemorrhage (bleeding in the brain)
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3
Q

What type of stroke is more common?

A

Ischaemic (make up to 85%)

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4
Q

Causes of ischaemic strokes?

A

atherosclerotic plaques causing thrombosis and vessel occlusion
cardioembolic strokes occurs when an embolism comes from the heart and a common cause of this is AF

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5
Q

Causes of haemorrhagic strokes?

A

structural abnormalities, hypertension, amyloid angiopathy or a combination

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6
Q

Presentation of a stroke?

A
  • Speech: dysarthria, dysphasia
  • (Note dysarthria is speech disorder caused by impairment of muscle control, dysphasia is impairment of language)
  • Facial weakness: stroke can affect the UMN of cranial nerve 7 which supplies the muscles of facial expression, the facial nerve receives bilateral cortical innervation to the upper part of the face (raising eyebrows) but unilateral to the lower part of the face, so someone with a stroke affecting the facial nerve may not be able to smile on the affected side but will be able to raise their eyebrows and close their eyes
  • Contralateral limb weakness and sensory loss
  • Cerebellar signs
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7
Q

1/3 of all stroke presentations are _______

A

stroke mimics

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8
Q

Give some examples of stroke mimics?

A

seizures, sepsis, toxic, metabolic, syncope, acute confusion/ delirium, vestibular dysfunction, functional, dementia

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9
Q

Describe use of imaging in strokes?

A
  • Immediate urgent investigations include a CT brain scan, blood count an glucose
  • Non contrast CT will allow someone to differentiate between an ischaemic and haemorrhagic stroke meaning it can be determined whether thrombolysis is suitable
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10
Q

Describe initial management of an ischaemic stroke?

A

Thrombolysis with alteplase should be done in ischaemic strokes up to 4.5hrs from onset of symptoms (although note that not everyone with an ischaemic stroke is eligible as there is a risk of bleeding).
Studies have also been done with end-vascular thrombectomy and this is a growing treatment option.

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11
Q

Describe treatment of haemorrhagic stroke?

A

Can’t thrombolyse.
If patients have a systolic BP > 150 mmHg they should be aggressively treated with IV GTN to lower BP as this has been shown to improve outcomes.

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12
Q

Describe use of anti platelets in management of ischaemic stroke?

A

Aspirin should be given within hours for a few weeks and then most patients go on clopidogrel for life

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13
Q

Describe other management of stroke?

A

patients who have had a stroke are at risk of DVT and PE due to immobility. Intermittent pneumatic compression reduces risk of DVT compared to control and these should be worn as long as possible.
Patients need an initial swallow screen as they may have lost their safe swallow and are at risk of aspiration. If swallow test is not passed they have a more comprehensive assessment and nil by mouth to begin with.

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14
Q

Describe what a TIA is?

A

transient ischaemic attack
TIAs cause sudden loss of function, usually lasting for minutes only, with complete recovery and no evidence of infarction on images

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15
Q

2 common symptoms of TIA?

A

Hemiparesis (weakness of one entire side of the body) and aphasia (impairment of language, cant produce or comprehend speech)

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16
Q

What do TIAs mean in terms of risk of stroke?

A

The person is at a much higher risk of stroke in days and weeks to come and should be treated for the TIA in an effort to prevent this.

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17
Q

Describe cerebral amyloid angiopathy and intracerebral haemorrhage?

A

deposition of amyloid beta in the walls of small and medium size arteries in normotensive patients, particularly those over 60 causes lobar intracerebral haemorrhage which is often recurrent
associated with some genotypes and more common in those with alzheimers

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18
Q

Patients on oral anticoagulants should be assumed

A

to have had a haemorrhage until proven otherwise

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19
Q

Describe the appearance of haemorrhage stroke/ intracerebral haemorrhage on non contrast CT?

A

Haemorrhage is demonstrated immediately on CT as a white area (acute blood appears white on non contrast CT)

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20
Q

Describe the appearance of ischaemic stroke on non contrast CT and how this develops over time?

A
  • Very early findings of an ischaemic stroke may be a hyperdense segment of a vessel (direct visualisation of thrombus)
  • Within the first few hours there is loss of grey white matter differentiation, cortical hypodensity (appears darker) with associated parenchymal swelling and effacement of gyri
  • Within time the swelling becomes more marked and there is mass effect
  • Eventually gliosis occurs and there is a low density region visible with volume loss
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21
Q

Define a subarachnoid haemorrhage?

A

to extravasation of blood in the SA space between the pia and arachnoid membrane

22
Q

Causes of SA haemorrhage?

A
  • It can be caused by head trauma or be non traumatic
  • The main cause of non traumatic SAH is rupture of a intracranial (berry) aneurysm (although there are other non traumatic causes like AVM and cavernous malformations)
23
Q

Describe how berry aneurysms form and what increases risk of rupture?

A
  • These aneurysms form due to congenital weakness of the elastic tissues in the arterial wall, incidence of haemorrhage increases with age, hypertension is an important contributing factor
  • Aneurysms often develop near arterial junctions in the Circle of Willis
  • The prevalence of berry aneurysms in the population is estimated at about 3%, so there will be many people with these aneurysms who never know and never have any problems
  • Factors that make berry aneurysms more likely to rupture include: smoking, hypertension, location of aneurysm, size of aneurysm, conditions such as polycystic kidney disease where aneurysms are both more common and likely to rupture
24
Q

Clinical features of SAH?

A
  • Sudden onset of “thunderclap headache” patients claim it is the worst headache of their life
  • Neck stiffness and photophobia due to meningeal irritation
  • Headache is often accompanied by nausea or vomiting due to increased ICP or meningeal irritation
  • If the aneurysm is of the posterior communicating artery then a third nerve palsy may occur
  • Sometimes confusion, seizures and loss of consciousness can occur
  • Sometimes can get vitreous haemorrhage associated with SAH
25
Q

Investigations for SAH?

A
  • Diagnosis is usually confirmed with an unenhanced CT scan where a large volume of acute blood which appears white is seen in the suprasellar cistern, sylvian fissures and sulci
  • When SA blood is found in the absence of a history of trauma CT cerebral angiography is performed to look for the underlying berry aneurysm
26
Q

Management of SAH?

A
  • Immediate treatment of SAH involves bed rest and supportive measures. Hypertension should be controlled. Nimodipine, a calcium-channel blocker given for 3 weeks, reduces mortality
  • Where angiography demonstrates an aneurysm (the cause of the vast majority of SAHs), endovascular treatment by placing platinum coils via a catheter in the aneurysm sac, to promote thrombosis and ablation of the aneurysm, is now the first-line treatment
  • Endovascular coiling has a lower complication rate than surgery but direct surgical clipping of the aneurysm neck is still required in some selected cases
27
Q

Prognosis of SAH?

A

• Nearly half of SAH cases are either dead or moribund before reaching hospital. Of the remainder, a further 10–20% rebleed and die within weeks. Failure to diagnose SAH – for example, mistaking SAH for migraine – contributes to this mortality

28
Q

Describe complications of SAH?

A
  • Vasospasm occurs because blood in the SA space is very irritant to vessels, there can be prolonged arterial contraction leading to delayed ischaemic neurological deficits. This usually peaks 3-14 days following the haemorrhage where patients may develop a new focal neurological deficit or present with altered state of consciousness. It can be diagnosed clinically and confirmed with an angiogram or, less invasively, with a transcranial Doppler. Treatment for vasospasm includes the use of nimodipine (to prevent spasmodic effects) and blood pressure control
  • Re-bleed: The risk of re-bleeding is highest in the first 2 weeks and is increased in elderly patients and patients with hypertension. It can be managed with surgical clipping or coiling.
  • Hydrocephalus
  • Seizures
  • Hyponatraemia
29
Q

What is a subdural haematoma?

A

This is a collection of blood between the dura and the arachnoid layer, typically caused by a traumatic event

30
Q

Describe acute SDH?

A

• Acute SDH is due to high impact head trauma which results in rupture of the bridging veins (these are the veins in the subarachnoid space which puncture the dura matter to drain into the dural venous sinuses hence if these are ruptured because they are going from the SA space to the dura they will bleed under the dura)

31
Q

Describe chronic SDH?

A

• Chronic SDH is associated with brain atrophy (due to age, chronic alcoholism or dementia), brain atrophy causes the bridging veins to be stretched meaning that even minor trauma can cause them to rupture, the leaky vessels cause blood to accumulate in the space

32
Q

Presentation of SDH?

A
  • Acute SDH forms quickly and the patient becomes almost immediately symptomatic following the head trauma
  • Chronic SDH can take longer for symptoms to develop
  • Patients with acute SDH typically present with severely decreased state of consciousness
  • Patients with chronic SDH can present with a more insidious course, common symptoms are of headache and confusion but other symptoms include urinary incontinence, weakness, seizures, cognitive dysfunction and gait abnormalities
33
Q

CT appearance of SDH?

A
  • Unenhanced CT is the imaging of choice
  • SDH appears as a semilunar shape because the blood is not bounded by the fissures like it is in extradural haemorrhage
  • Acute SDH appears as a crescent shape hyperdensity and chronic as a hypodense crescent shaped appearance
34
Q

Management of SDH?

A
  • May not need immediate treatment but it is important to involve neurosurgery
  • Even large collections can resolve on their own
  • Serial imaging is required to assess progress
  • If needed they can be drained surgically
35
Q

Define EDH?

A

• Accumulation of blood between dura and bone usually caused by separation of dura and bone following a shearing stress from head trauma with disruption of vessels

36
Q

Most common cause of EDH?

A

• The most common source of bleeding is from the middle meningeal artery from a temporoparietal fracture because this runs under the thinnest part of the skull called the pterion

37
Q

Presentation of EDH?

A
  • Typically presents in a young adult after head trauma
  • Classically presents with a brief loss of consciousness, followed by a lucid interval after that the patient further deteriorates, exhibiting symptoms such as headache, vomiting, contralateral hemiparesis (due to compression of cerebral peduncles that are stalks that attach the cerebrum to the brainstem and contain a lot of the ascending and descending tracts) and ipsilateral pupillary dilatation (due to temporal lobe herniating and compressing the oculomotor nerve)
38
Q

CT appearance of EDH?

A
  • Unenhanced CT is imaging modality of choice
  • Extradural haematoma has a lens shaped appearance (because it is bounded by the fissures as the haemorrhage is above the dura)
  • It is acute so the blood appears white
39
Q

Management of EDH?

A
  • Expanding extradural haematomas need immediate neurosurgical evacuation
  • Conservative management is sometimes considered in neurologically intact patients with small haematomas
40
Q

Describe AVMs?

A
  • A complex tangle of arteries and veins connected together with one or more fistulas creating a shunt (there is no capillary bed present)
  • They are a common cause of haemorrhage (because the walls are weak and high pressure arterial blood is flowing directly into veins)
41
Q

Presentation of AVMs?

A
  • Often they are asymptomatic and diagnosis is not made until the person presents with something serious such as haemorrhage, seizure or other neurological dysfunctions
  • Haemorrhages are the most common feature of AVM and most commonly they are intracerebral
  • Seizures are second more common complaint
  • Progressive neurological deficits can occur in some individuals due to local ischaemic effect of AVMs
  • Some patients also complain of headaches
42
Q

Investigation if suspected AVM?

A

catheter angiography

43
Q

Management of AVM?

A

• Surgery is usually treatment of choice (in some cases observation may be considered if surgery is risky)

44
Q

Describe cavernous malformations?

A
  • Well circumscribed benign vascular lesions encompassing sinusoidal spaces
  • They can be familial or sporadic (more common)
45
Q

Presentation of cavernous malformations?

A
  • Seizures are most common symptom
  • Progressive neurological deficit is also common
  • Haemorrhage can be recurrent and cause neurological signs and symptoms
46
Q

Investigations for cavernous malformations?

A
  • CT can be used if suspect acute haemorrhage
  • MRI is gold standard “popcorn like” lesion
  • Angiography is not helpful (because the lesions aren’t high flow so won’t show up) but can rule out other things e.g. AVM
47
Q

Management of cavernous malformations?

A

• Like AVM depending on size and risk of surgery there is the option for surgical excision or just observation

48
Q

Name 3 conditions associated with aneurysms?

A

polycystic kidney disease, fibromuscular dysplasia and Ehlers-Danlos

49
Q

What is an aneurysm?

A

Bulge in blood vessel caused by weakness in the blood vessel wall

50
Q

Describe locations of most aneurysms?

A
  • Most aneurysms arise in the anterior circulation
  • They are commonly found in the circle of Willis at the branching points of major arteries, most common locations are the junction of anterior communicating with anterior cerebral and junction of posterior communicating with internal carotid

Neurology (22 decks)

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