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Neurology > Cerebrovascular diseases > Flashcards

Cerebrovascular diseases Flashcards

1
Q

What causes cerebrovascular diseases and what do they include

A

Caused by cerebrovascular pathological changes due to various reasons
- includes disorders of arterial or venous criculatory systems to produce injury in the central nervous system
(arteries > veins)

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2
Q

Define: stroke

A

Generally, stroke refers to an acute evnt, in which a neurological deficit appears, and is presumed to be due to an impairment of blood supply to one part of the brain

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3
Q

Name and breiefly explain the two types of stroke

A
  1. Ishchaemic stroke:
    - cerebral infarction: cerebral thrombosis/embolism
    - transcient ishchaemic attack
  2. Haemorrhage strokes:
    - primary cerebral haemorrhage
    - subarachnoid haemorrhage
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4
Q

What is the epidemiology of stroke?

A

about 8% of stroke: cerebral infarction
10% to primary intracerebral haemorrhage
10% subarachnoid haemorrhage

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5
Q

Where is the cerebral arterial circulation derived from

A

from 4 major extracerebral (neck) arteries
* two internal carotid arteries
* two vertebral arteries

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6
Q

Describe the following:
1. Anterior intracranial circulation
2. Posterior intracranial circulation
3. Circle of Willis

A
  1. Supplies the blood to the eyeball and anterior 3/5 of the cerebral hemisphere; including: frontal lobe, temporal lobe, parietal lobe, basal ganglia
  2. VA, BA, PCA and their tributaries supply the entire brainstem, cerebellum and posterior 2/5 of the cerebral hemisphere; including: occipital lobe, thalamus, inner aspect of the temporal lobe
  3. Consists of the terminal portions of internal carotid arteries, the 2 anterior cerebral arteries united by anterior communicating artery, the terminal potion of the basilar artery, the 2 posterior cerebral arteries and the 2 posterior communcating arteries
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7
Q

Describe the concept of a “Transcient ishchaemic attack (TIA)

A

An episode of an acute focal neurological deficit, of presumed vascular origin, which lasts less than 24hrs, followed by complete functional recovery (repeated stereotyped episodes may occur)

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8
Q

Describe the focal neurological dysfunctions for TIA

A
  1. Internal carotid terriotry
    - attacks indicate the involvemnet of one cerebral hemisphere or eye
    the visaul disturbance is ipsilateral, the sensory-motor disturbance is contralateral
    - transcient ischaemia in the internal ccarotid area usually produces contralateral hemiplegia
    - dysphagia if the dominant hemisphere is affected
    - in occular attacks, transcient monocular blindness is the usual symptom
  2. Vertebrobasilar territory
    - TIA may cause weakness or numbness of part or all of one or both sides of the body (hallmarks)
    *vertigo
    *diplopia
    *dysarthria
    *bifacial numbness
    * visual blurring or loss
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9
Q

Describe the examination and diagnosis of TIA

A
  • Between attacks –> no neurological signs
    general examination is directed towards identifying associated factors such as hypertension, peripheral vascular disease and cardiac abnormailites

Exam to perform:
- full blood count
- glucose tolerance test
- fasting lipids
- chest x-ray, ECG, ESR
- urea and electrolytes

  • consider patients with TIA for CT/MRI/MRA
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10
Q

How is TIA diagnosed

A
  • history
  • clinical episodes
  • no neurological signs between attacks
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11
Q

How is TIA managed

A
  1. General treatment: identify and treat risk factors
    - treat HT and hyperlipidemia, control diabetes, stop smoking and reduce weight
  2. Anti-platelet agents:
    Aspirin to reduce platelet aggregation (50-325mg/day)
    If aspiring is poorly tolerated: Clopidogeral (75mg/day)
  3. Anti-coagulants:
    Warfarin and heparin to prevent TIA and imending stroke
  4. Surgical management:
    Arterial stenosis or ulcerating arterial plaque in the neck and thorax of patients with recurrent ischaemic attacks is amenable to surgery
    *endarterectomy or angioplasty with stenting
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12
Q

What is the conept of “Thrombotic cerebral infarction” (central thombosis)

A

Refers to the most common type of cerebral infarction
- atherosclerosis develops and forms thrombus which occludes the cerebral artery and then results in clinical symptoms

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13
Q

What are the major causes of cerebral infarction

A
  • atherosclerosis
  • hypertension
  • diabetes
  • hyperlipidemia
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14
Q

What are the 2 pathophysiological processes of cerebral infarction

A
  1. loss of oxygen supply and glucose supply; secondary to vascular occlusion
  2. array of changes in cellular metabolism consequent upon the collapse of energy producing proceses, with disintergration of cell membranes
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15
Q

List the general features for thrombotic cerebral infarction

A
  • atient is often elderly with history of artherosclerosis, HT, diabetes, TIA, heart disease
  • patient is smoker
  • onset of cerebral thrombosis is abrupt, and the occurence of thrombotic stoke is during sleep, the patient awakens paralysed
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16
Q

According to evolution of symptoms and signs, thrombotic stoke can be divided into several subtypes
List them:

A
  1. Complete stroke: when there is persistence and more severe neurologica deficit for longer than 24hr. The deficit usually reaches its peak within several hours
  2. progressive stroke (slow and worsens over hours/days)
  3. reversible ischaemic neurologic deficit (RIND)
    - in some cases, neurologic defict resolves completely within 3 week, this is caused by sustained ischaemia that is not severe enough to produce infarction
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17
Q

What are the syndromes of major cerebral artery occlusion

A
  1. Middle cerebral artery occlusion
  2. Anterior cerebral artery occlusion
  3. Infarction of posterior circulation
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18
Q

Describe posterior inferior cerebellar artery occlusion

A

Wallenberg syndrome
- the PICA occlusion syndrom eis often due to vertebral occlusion of PICA

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19
Q

List the symptoms of PICA occlusion

A
  • ipsilateral facial paraesthesia or pain and/or contralateral limb sensory impairment
  • severe vertogo, vomitting and nystagmus
  • dysathria
  • ataxia
  • ipsilateral Horner’s syndrome
20
Q

What exams are carried out for thrombotic cerebral infarction

A
  • CT/MRI
  • carotid doppler
  • angiography
  • lumbar puncture: if CT shows displacement of brain structures AVOID lumbar puncture
21
Q

How is thrombotic cerebral infarction diagnosed

A
  • 50-60y.o
  • Hx: HT, AT, DM
  • TIA befire ictus
  • onset usually occurs during sleep (early morning)
  • Main signs: hemiplegia, contraleteral homonymou hemianopia and contralateral hemisensory loss
  • CT: 24hrs after onset –> lower densit area
22
Q

How can thrombotic cerebral infarction be managed?

A
  1. control BP: inducing HT during the early stages of infarction can increase perfusion pressure through ischaemic tissue sufficiently enough for infarction to be minimised
  2. thrombolytic agent
    - tissue plasminogen factor for treatment of coronary artery occlusion
    t-PA 0.9mg/kg (10% via bolus, rest is an infusion over an hour); maxx. dose of 90mg
  3. Anticoagulant drugs
    Warfarin and heparin
  4. anti-platlet drugs
  5. treatment of cerebral edema nd raised intracranial pressure
23
Q

Explain the concept of embolic cerebral infarction (Cerebral embolism)

A

Cerebral embolism refers to verious emboli, which within the blood and following blood flow, enter the cerebral artery and occlude the vessels then resut in ishchemic necrosis of cerebral tissue of supply terriotry by the artery, and produce a focal neurological deficit

24
Q

Cerebral embolism accounts for 15-20% of stroke
What is the cardiac and non-cardiac origin

A
  1. Cardiac origin: atrial fibrillation and other arrythmias: MI with mural thrombosus; acute and subacute bacterial endocarditis; complications of cardiac surgery
  2. Non-cardiac origin: atherosclerosis of aorta and carotid arteries; vertebrobasilar arteries, thrombus in pulmonary vein, fat, tumour
25
Q

What are the clinical features of embolic cerebral infarction/cerebral embolism

A
  • embolic strokes occur suddenly, and the deficit reaches its peak almost immediately –> cerebral embolism develops most rapidly
  • neurologic picture will depend on the artery involved and the site of obstruction
  • an embolus may produce a severe deficit that is only temporary; symptoms disappear as embolus fragments
26
Q

What is one of the main investigations that should be done for cerebral embolism

A

prolonged study of heart rhythm with Holter monitoring

27
Q

How is embolic cerebral infarction/cerebral embolism diagnosed

A

presence of atrial fibrillation, history of MI, or occurance of embolism to other vascular territories

28
Q

Why should antibiotics rather than anti-coagulant therapy be used in the case of cerebral embolism assoicated wit subacte bacterial endocarditis

A

risk of intracranial bleeding

29
Q

Explain the concept of lacunar cerebral infarction

A
  • refers to small, deep infarcts in region of deep white matter of cerebral hemisphere and brain stem
  • it is caused by ischaemia, necrosis of cerebral tssue and as is the softened tissue s rmoved it leaves behind a small cavity or lacunae (3-20mm)
  • represents 20% of all strokes
30
Q

How is lacunar cerebral infarction managed?

A
  • calcium channel blockers and anti-platelet agenst
  • most patients are hypertensive so anticoagulants can be harmful
31
Q

explain the concept of promary intracerebral haemorrhage

A
  • caused by spontaenous reupture of blood vessles, usually arteires
  • 10-15% of all strokes
  • 60% originate from basal ganglia
32
Q

What are the most common causes of primary intracerebral haemorrhage

A
  • hypertesnion and arteriosclerosis
  • arteriovenous malformation, aneurysm and blood diseases
32
Q

What are the most common causes of primary intracerebral haemorrhage

A
  • hypertesnion and arteriosclerosis
  • arteriovenous malformation, aneurysm and blood diseases
33
Q

List the clinical features of primary intracerebral haemorrhage

A
  • 50+y.o
  • most patients have HT, the bleeding may occur with a suden elevation of blood pressure
  • ictus always strikes during active exercise or in a state of great emotion
  • no prodromes before onset
  • patients complain of: headachesm soon start to vomit, show hemiplegia, hemisensory or hemianopic disturbance or ataxia and then there is a rapid deterioration into stupor or coma within a few minutes
34
Q

There are several syndromes according to the different positions of bleeding for primary intracranial haemorrhage
List them

A
  1. Putamina haemorrhage
  2. Thalamic haemorrhage
  3. Cerebellar haemorrgae
  4. Pontine haemorrhage
  5. Lobar haemorrhage
35
Q

What investigations should be carried out for primary intracranial haemorrhage

A

CT scan is the most useful –> shows high density area
Lumbar puncture: only carry out if CT is unavailable or if CT results are inconclusive
Angiography to help localise

36
Q

How is primary intracranial haemorrhage diagnosed

A
  1. 50+
  2. Hx: HT
  3. Sx: appear quickly, during active exercise or state of great emotion and deteriorate quickly
  4. headache, nausea, vomiting and loss of consiousness may occur
  5. hemiplegia, dysarthria, hemi-hypesthesia
37
Q

What is the treatment plan for primary intracranial haemorrhage

A
  1. control cerebral oedema: 20% mannitol 125ml-250ml i.v infusion 6-8hrs once for 7-10days
  2. control hypertension
  3. surgical management
38
Q

Explain the concept of subaracnoid haemorrhaege

A

refers to a sponatenous arterial bleed into the subarachnoid apce. It is the 4th most frequent cerebrovascuar disorder following atherothrombosis, embolism and primary intracerebra haemorrhage

39
Q

List the causes of SAH

A
  • saccular aneurysms (70%)
  • degenerative and hypertensive aneurysms (10%)
  • arteriovenous malformation (10%)
  • not defined (10%)
40
Q

List the clinical features of SAH

A
  • can occur at any age (important cause of death for 20-40 age group)
  • rupture of aneurym occurs when patient is asleep rather than active
  • most common sx: severe headache, nausea, vomiting (patients can lose consiousness or have a seizure)
  • chief signs: meningeal irritation such as stiffness, neck pain, Kernig’s sign (+) and retinal haemorrhage
41
Q

List the complications in SAH

A
  1. rebleeding or re-rupture
  2. vasospasm
  3. hydrocephalus
42
Q

What investigations should be carried out for SAH

A
  • CT scan
  • Lumbar puncture
  • DSA
43
Q

How is SAH diagnosed

A
  1. ictus suddenly appears during active exercise
    - main sympotms: headache, nausea, vomiting, seizure, loss of consciousness
    - signs: meningeal irritation, neck stiffness. Kernings sign
    - lumbar puncture: CSF is above normal limit and bloody
    - CT shows SA blood
44
Q

How is SAH treated?

A
  • anticonvulsants
  • bed rest
  • stool softeners
  • fluid administration to maintain normal circulating volume
  • lower intracranial pressure
  • calcium channel blocker
  • anti-fibrinolytic agents
  • replacement CSF

Neurology (13 decks)

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