Cerebrovascular diseases Flashcards
What causes cerebrovascular diseases and what do they include
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)
Define: stroke
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
Name and breiefly explain the two types of stroke
- Ishchaemic stroke:
- cerebral infarction: cerebral thrombosis/embolism
- transcient ishchaemic attack - Haemorrhage strokes:
- primary cerebral haemorrhage
- subarachnoid haemorrhage
What is the epidemiology of stroke?
about 8% of stroke: cerebral infarction
10% to primary intracerebral haemorrhage
10% subarachnoid haemorrhage
Where is the cerebral arterial circulation derived from
from 4 major extracerebral (neck) arteries
* two internal carotid arteries
* two vertebral arteries
Describe the following:
1. Anterior intracranial circulation
2. Posterior intracranial circulation
3. Circle of Willis
- Supplies the blood to the eyeball and anterior 3/5 of the cerebral hemisphere; including: frontal lobe, temporal lobe, parietal lobe, basal ganglia
- 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
- 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
Describe the concept of a “Transcient ishchaemic attack (TIA)
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)
Describe the focal neurological dysfunctions for TIA
- 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 - 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
Describe the examination and diagnosis of TIA
- 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
How is TIA diagnosed
- history
- clinical episodes
- no neurological signs between attacks
How is TIA managed
- General treatment: identify and treat risk factors
- treat HT and hyperlipidemia, control diabetes, stop smoking and reduce weight - Anti-platelet agents:
Aspirin to reduce platelet aggregation (50-325mg/day)
If aspiring is poorly tolerated: Clopidogeral (75mg/day) - Anti-coagulants:
Warfarin and heparin to prevent TIA and imending stroke - 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
What is the conept of “Thrombotic cerebral infarction” (central thombosis)
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
What are the major causes of cerebral infarction
- atherosclerosis
- hypertension
- diabetes
- hyperlipidemia
What are the 2 pathophysiological processes of cerebral infarction
- loss of oxygen supply and glucose supply; secondary to vascular occlusion
- array of changes in cellular metabolism consequent upon the collapse of energy producing proceses, with disintergration of cell membranes
List the general features for thrombotic cerebral infarction
- 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
According to evolution of symptoms and signs, thrombotic stoke can be divided into several subtypes
List them:
- Complete stroke: when there is persistence and more severe neurologica deficit for longer than 24hr. The deficit usually reaches its peak within several hours
- progressive stroke (slow and worsens over hours/days)
- 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
What are the syndromes of major cerebral artery occlusion
- Middle cerebral artery occlusion
- Anterior cerebral artery occlusion
- Infarction of posterior circulation
Describe posterior inferior cerebellar artery occlusion
Wallenberg syndrome
- the PICA occlusion syndrom eis often due to vertebral occlusion of PICA
List the symptoms of PICA occlusion
- ipsilateral facial paraesthesia or pain and/or contralateral limb sensory impairment
- severe vertogo, vomitting and nystagmus
- dysathria
- ataxia
- ipsilateral Horner’s syndrome
What exams are carried out for thrombotic cerebral infarction
- CT/MRI
- carotid doppler
- angiography
- lumbar puncture: if CT shows displacement of brain structures AVOID lumbar puncture
How is thrombotic cerebral infarction diagnosed
- 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
How can thrombotic cerebral infarction be managed?
- control BP: inducing HT during the early stages of infarction can increase perfusion pressure through ischaemic tissue sufficiently enough for infarction to be minimised
- 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 - Anticoagulant drugs
Warfarin and heparin - anti-platlet drugs
- treatment of cerebral edema nd raised intracranial pressure
Explain the concept of embolic cerebral infarction (Cerebral embolism)
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
Cerebral embolism accounts for 15-20% of stroke
What is the cardiac and non-cardiac origin
- Cardiac origin: atrial fibrillation and other arrythmias: MI with mural thrombosus; acute and subacute bacterial endocarditis; complications of cardiac surgery
- Non-cardiac origin: atherosclerosis of aorta and carotid arteries; vertebrobasilar arteries, thrombus in pulmonary vein, fat, tumour
