Cerebrovascular Disease Flashcards
What is ischaemic stroke?
-Acute focal neurological dysfunction due to focal infarction at single or multiple sites of the brain or retina. Blockage in blood vessel, 85%
=Symptoms lasting >24hrs
=Imaging findings in the clinically relevant area of the brain
=Thrombotic (thrombosis from carotid)/ embolic (blood clot/ fat/ air/ bacteria/ AF)
Risk factors for ischaemic stroke
General risk factors for cardiovascular disease
age
hypertension
smoking
hyperlipidaemia
diabetes mellitus
Risk factors for cardioembolism
atrial fibrillation
What is an intracerebral haemorrhage?
Acute neurological dysfunction from haemorrhage in brain parenchyma or ventricular system
=Blood vessel bursts, 15%
=Intracerebral haemorrhage vs subarachnoid haemorrhage
Risk factors haemorrhagic stroke
age
hypertension
arteriovenous malformation
anticoagulation therapy
What is a TIA?
-Transient focal neurological symptoms due to cerebral ischaemia without evidence of infarction
=a subtype of ischaemic stroke is a transient ischaemic attack (TIA). This describes the sudden onset of a focal neurologic symptom and/or sign lasting typically less than an hour, brought on by a transient decrease in blood flow. This is sometimes referred to by patients as a ‘mini-stroke’
=The original definition of a TIA was time-based: a sudden onset of a focal neurologic symptom and/or sign lasting less than 24 hours, brought on by a transient decrease in blood flow. However, this has now changed as it is recognised that even short periods of ischaemia can result in pathological changes to the brain. Therefore, a new ‘tissue-based’ definition is now used: a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.
What is infarction
Positive imaging or symptoms at 24hr follow up
What are focal symptoms?
-Motor weakness, clumsiness, sensory alteration in limb(s) on the same side
-Speech or language disturbance (dysphasia)
-Swallowing problems
-Loss of vision in eye/part of eye/ homonymous hemianopsia
-Sensory alteration, ataxia, imbalance, unsteadiness not associated with vertigo
-2 or more diplopia, dysphagia, dysarthria, or vertigo
Cerebral hemisphere infarcts:
=contralateral hemiplegia: initially flaccid then spastic
contralateral sensory loss
homonymous hemianopia
dysphasia
Brainstem infraction
=Quadriplegia
=Locked in syndrome
Lacunar
=Pure motor/ pure sensory/ mixed motor and sensory signs or ataxia
Symptoms less likely to be TIA
-Disturbances of vision with flashes, objects, distorted-view tunnel vision or image moving
-Tiredness/ heavy sensation in limb(s)
-Sensory symptoms or gradual spread of sensory symptoms
-Isolated disorder of swallowing or articulation, double vision, dizziness, or uncoordinated movements
-Unconsciousness, limb jerking, tingling of limbs/lips, disorientation
Stroke classification system
-Oxford/ Bamford
- Unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphasia
ROSIER scoring
Exclude hypoglycaemia first, then assess the following:
-Loss of consciousness or syncope (-1)
-Seizure activity (-1)
-New acute onset of:
=Asymmetric facial weakness (+1)
=Asymmetric arm weakness (+1)
=Asymmetric leg weakness (+1)
=Speech disturbance (+1)
=Visual field defect (+1)
A stroke is likely if > 0.
Treatment of carotid stenosis
Endarterectomy
=Atheroma removal
Primary and secondary prevention of stroke
-DOAC= more convenient than warfarin (monitoring, slow onset of action, bridging, and multiple drug interactions)
=Reduce risk of stroke or systemic embolic events compared with warfarin and reduce bleeding
=Warfarin has role in renal failure and mechanical heart valves
-Antiplatelet (clopidogrel)/ aspirin 300mg
-Blood pressure lowering
-LDL-cholesterol lowering
-Look for AF
-Look for carotid stenosis
-Stopping smoking advice
-Diet advice
-Look for PFO (patent foramen Ovale)
Causes of SAH
-intracranial aneurysm (saccular ‘berry’ aneurysms)
=accounts for around 85% of cases
=conditions associated with berry aneurysms include hypertension,adult polycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta
-arteriovenous malformation
-pituitary apoplexy
-mycotic (infective) aneurysms
Presentation of subarachnoid haemorrhage
-Sudden-onset thunderclap headache, severe, occipital, peaking in intensity 1-5 minutes
=Maybe history of less-severe ‘sentinel’ headache in weeks prior
-Nausea and vomiting
-Meningism (photophobia, neck stiffness)
-Coma
-Seizures
Diagnosis of subarachnoid haemorrhage
-Non-contrast CT head= hyperdense/ bright on CT. If done within 6 hours and normal, not LP, alternative diagnosis
-If CT done more than 6 hours after symptom onset and is normal= LP (at least 12 hours following onset of symptoms to allow xanthochromia), normal or raised opening pressure
-CT angiography to identify cause
-ECG changes including ST elevation may be seen
=this may be secondary to either autonomic neural stimulation from the hypothalamus or elevated levels of circulating catecholamines
Management of subarachnoid haemorrhage
-Pain relief, bed rest, VTE prophylaxis, discontinue antithrombotic
-Enteral nimodipine for ruptured aneurysm
-Endovascular coiling, or neurosurgical clipping
Complications of SAH
-re-bleeding
=happens in around 10% of cases and most common in the first 12 hours
=if rebleeding is suspected (e.g. sudden worsening of neurological symptoms) then a repeat CT should be arranged
=associated with a high mortality (up to 70%)
-hydrocephalus
=hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculoperitoneal shunt
-vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset
=ensure euvolaemia (normal blood volume)
=consider treatment with a vasopressor if symptoms persist
-hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH))
-seizures
Important predictive factors in SAH:
conscious level on admission
age
amount of blood visible on CT head
Presentation of subdural haemorrhage
The typical presentation of a subdural haematoma (SDH) often involves a history of head trauma, which may range from minor to severe. Patients frequently exhibit a lucid interval followed by a gradual decline in consciousness. This pattern is particularly common in chronic SDH. Other hallmark features include headache, confusion, and lethargy.
-Acute/ subacute/ chronic.
-Headache, often unilateral, worsening
-Nausea and vomiting (ICP)
-Cushing’s triad: bradycardia, hypertension, respiratory irregularities (ICP)
-Diminished GCS/ fluctuations in consciousness
-Confusion, memory loss (chronic), irritability, apathy, depression, cognitive impairment
-Loss of bowel and bladder continence
-Localised weakness, aphasia, visual field defect
-Seizure.
-Papilloedema (raised ICP)
-Pupil changes: unilateral dilated pupil, ipsilateral, compression of third cranial nerve
-Gait abnormalities: ataxia or weakness in one leg
-Hemiparesis or hemiplegia: mass effect/ midline shift
-ACUTE= high impact trauma, incidental finding vs severe coma and coning due to herniation. 48 hours, rapid neurological deterioration
-SUBACUTE= days to weeks post-injury, more gradual progression
-CHRONIC= weeks to months, rupture of small bridging veins causing slow bleeding, elderly and alcoholic (brain atrophy), progressive history of confusion, reduced consciousness, neurological deficit.
Investigation of subdural haemorrhage
-Non-contrast CT imaging (crescentic collection not limited by suture lines, large= mass effect= midline shift or herniation).
-ACUTE= hyperdense
-CHRONIC= hypodense
Management of subdural haemorrhage
-Prophylactic antiepileptic
-Correction of coagulopathy
-ICP lowering.
-ACUTE= conservative/ surgical decompressive craniectomy, monitoring of ICP.
-Surgical decompression with burr holes= chronic, confusion, neurological deficit.