Stroke Flashcards
Brain MAP
50-150mmhg
TACS & PACS
Unilateral weakness (and/or sensory deficit) of the face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia, visuospatial disorder) TACS: 3/3 PACS : 2/3
POCS
Any of:Cranial nerve palsy and a contralateral motor/sensory deficit
Bilateral motor/sensory deficit
Conjugate eye movement disorder (e.g. horizontal gaze palsy)
Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
Isolated homonymous hemianopia
LACS
Pure sensory stroke
Pure motor stroke
Senori-motor stroke
Ataxic hemiparesis
Where do most silent infarcts occur
89% in the lacune and basal ganglia
Basal ganglia perfusion
Striate arteries
Anterior choroidal ( globus pallidus internae)
Imaging in stroke
CT works 48 hours after
DWI MRI at time of stroke
SPECT can determine size at stroke
leukoaraiosis
White matter changes seen on ct/mri from small vessel strokes
Cellular changes in stroke
Pyknotic neurons: death - condensation of chromatin
Peri-infarct gliosis: Proliferation and hypertrophy of astrocytes, microglia, oligodendrocytes
These changes occur days after a stroke and lead to glial scar
Differences between hypoxia and ischaemia in neurones
Ischaemia=> lost function: no protein synthesis and glutamate release
Hypoxia => changes in metabolism, synaptic function and gene activation
Sequence of events in ischaemia causing neuronal injury
Ischaemia => Energy failure => Cell depolarisation=> Ca2+ channels opening and Glutamate relsease positive loop in rise in i[Ca2+] and glutamate release => cell death
Which arteries largely supply blood to the brain?
Internal Carotids (70%)
Verterbral arteries(30%)
Clinical Presentations of stroke
- Stroke occurs when there is a reduction in blood and oxygen supply to the brain.
-
Ischemic and haemorrhagic stroke
- 80% of all strokes are Ischemic: Lack of oxygen caused by a stenosed or blocked artery
- 50% caused by atherosclerosis thromboembolism of arteries
- 20% is emboli form circulation of heart
- 25% by lacunar infarcts
- 5% by vascular disease, bacterial infection, dissections
- RF: Diabetes, AF, obesity, smoking, pregnancy, HRT/COCP, MI, RHD, prosthetic valves
- 20%= Haemorrhagic: 15% caused by inter-cerebral haemorrhage, rest is caused by subdural, sun-arachnoid and epidural haemorrhage
- RF: Hypertension, Blood thinners, angiopathy, aneurysms
- 80% of all strokes are Ischemic: Lack of oxygen caused by a stenosed or blocked artery
Oxford-Bamford Classifications
TACS-PACS
POCS
LACS
Rare forms of stroke ?
- However, on occasion we would encounter rarer strokes such as; global cerebral ischemia and silent infarcts
- Global cerebral ischemia:
- Caused by cardiac arrest, causing laminar necrosis, white matter infarcts, watershed infarcts and hippocampal sclerosis
- Silent infarcts:
- Asymptomatic and can possibly cause behavioural changes. 89% are subcortical and the lacuna region affecting the basal ganglia which gives you a 2X risk of dementia and steeper cognitive decline
- Global cerebral ischemia:
Diagnostic investiagations
- First we have to rule out a haemorrhagic stroke using a CT scan.
- You can see a haemorrhagic stroke immediately on a CT scan.
-
Pressman et al
- For a thrombotic stroke - The earliest CT sign is a hyper-dense segment of vessel which is the direct visualisation of the intravascular thrombus/ emboli. Most commonly seen in the MCA.
- CT perfusion is another way of identifying ischemic stokes, it helps to identify the penumbra
- To show the salvageable tissues post stroke
- CT angiogram identifies thrombus, guide inter-arterial thrombolysis / clot retrieval.
- MRI:
- Diffusion weighted – shows in depth resolution of the damage and can be used immediately (within minutes). Clinically, we don’t normally use MRI, as it is more time consuming and has less availability than CT, however, MRI is used in hospitals with patients who present with more complex symptoms where the extent and location of stroke are unknown
- T1: damage can be seen 16 hours later and persists
- T2: 6 hours later
- Diffusion weighted – shows in depth resolution of the damage and can be used immediately (within minutes). Clinically, we don’t normally use MRI, as it is more time consuming and has less availability than CT, however, MRI is used in hospitals with patients who present with more complex symptoms where the extent and location of stroke are unknown
Pathophysiology
-
Changhong et al describes the pathogenesis of neuronal injury in stroke
- Ischemia leads to a decrease in high energy metabolism and a decrease in synthesis of ATP, causing lactic acidosis production and leads to a few major pathways
- Without ATP, the sodium/potassium pump no longer works. Causing an increase in sodium inside the cell, followed by increase in H2O causing swelling and cytotoxic oedema.
- Acid sensing ion channels (ASIC) detect lactic acidosis and cause an influx of Ca2+, causing depolarisation in the cell and therefore Ca2+ influx by voltage gated calcium channels. Resulting in glutamate release which further depolarises the cell.
- Without ATP, the calcium and sodium co-transporter pump does not work, therefore calcium builds up inside the cell. This attributes to 2 things:
- Glutamate release
- Activates proteasomes and lysosomes that degrade the cell.
- The increase in glutamate and calcium further depolarises the cell and stimulates excessive mitochondrial oxygen radical and free radical production damaging lipids, proteins, nucleic acid, carbohydrates causing neuronal death – inflammatory response
- Pinton et al: When there is a high enough concentration of Ca2+ in the cells, the mitochondria is overloaded by Ca2+ that releases caspase co-factors 3 and 9 leading to apoptosis.
- To conclude, there is an overall rise in excite-toxicity caused by CA2+ in the cell and that leads glutamate release by positive feedback and therefore degradation of cells due to oedema, cytotoxicity, caspases and ROS
- Ischemia leads to a decrease in high energy metabolism and a decrease in synthesis of ATP, causing lactic acidosis production and leads to a few major pathways
Cellular changes post stroke
- There are some cellular changes that occur during stroke. A few are highlighted below:
- Pyknosis – Formation of pyknotic neurones: Irreversible condensation of chromatin in the nucleus of the cell undergoing necrosis or apoptosis. Followed by karyorrhexis also known as the fragmentation of the nucleus
- Peri-infarct gliosis – Proliferation and hypertrophy of astrocytes, microglia and oligodendrocytes which occurs a leaves a glial scar a few days later
Management post stroke
The key to stroke management is to act F.A.S.T. The primary, secondary and tertiary prevention methods are listed below.
- Primary prevention
- Lifestyle changes such as diet, increase physical activity, reduce smoking
- Manage other co-morbidities e.g. diabetes, CVD, AF
- Secondary prevention
- Thrombotic stroke:
- Thrombolysis by alteplase
- Donnan et al: Aspirin for penumbral salvage, 9 patients saved form death or disability per thousand treated
- Warfarin – anticoagulant
- Clopidegrol – antiplatelet
- Carotid endarterectomy
- Haemorrhagic stroke:
- Refer to surgery to drain the bleed and cranial decompression
- Thrombotic stroke:
Stroke puts you at risk of ?
Post stroke dementia
Stroke papers
Investigation:
Pressman et al: For a thrombotic stroke - The earliest CT sign is a hyper-dense segment of vessel which is the direct visualisation of the intravascular thrombus/ emboli. Most commonly seen in the MCA.
Pathophysiology
Changhong at al: describes the pathogenesis of neuronal injury in stroke
Pinton et al: during neuronal injury, the mitochondria is overloaded by Ca2+ that releases caspase co-factors 3 and 9 leading to apoptosis.
Management
Donnan et al: Aspirin for penumbral salvage, 9 patients saved form death or disability per thousand treated
White matter changes seen on ct/mri from small vessel strokes
leukoaraiosis