Stroke

Question 1

Brain MAP

Answer 1

50-150mmhg

Question 2

TACS & PACS

Answer 2

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

Question 3

POCS

Answer 3

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

Question 4

LACS

Answer 4

Pure sensory stroke

Pure motor stroke

Senori-motor stroke

Ataxic hemiparesis

Question 5

Where do most silent infarcts occur

Answer 5

89% in the lacune and basal ganglia

Question 6

Basal ganglia perfusion

Answer 6

Striate arteries

Anterior choroidal ( globus pallidus internae)

Question 7

Imaging in stroke

Answer 7

CT works 48 hours after

DWI MRI at time of stroke

SPECT can determine size at stroke

Question 8

leukoaraiosis

Answer 8

White matter changes seen on ct/mri from small vessel strokes

Question 9

Cellular changes in stroke

Answer 9

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

Question 10

Differences between hypoxia and ischaemia in neurones

Answer 10

Ischaemia=> lost function: no protein synthesis and glutamate release

Hypoxia => changes in metabolism, synaptic function and gene activation

Question 11

Sequence of events in ischaemia causing neuronal injury

Answer 11

Ischaemia => Energy failure => Cell depolarisation=> Ca2+ channels opening and Glutamate relsease positive loop in rise in i[Ca2+] and glutamate release => cell death

Question 12

Which arteries largely supply blood to the brain?

Answer 12

Internal Carotids (70%)

Verterbral arteries(30%)

Question 13

Clinical Presentations of stroke

Answer 13

• 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

Question 14

Oxford-Bamford Classifications

Answer 14

TACS-PACS

POCS

LACS

Question 15

Rare forms of stroke ?

Answer 15

• 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

Question 16

Diagnostic investiagations

Answer 16

• 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

Question 17

Pathophysiology

Answer 17

• 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

Question 18

Cellular changes post stroke

Answer 18

• 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

Question 19

Management post stroke

Answer 19

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

Question 20

Stroke puts you at risk of ?

Answer 20

Post stroke dementia

Question 21

Stroke papers

Answer 21

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

Question 22

White matter changes seen on ct/mri from small vessel strokes

Answer 22

leukoaraiosis