B6W8 - Stroke And Vascular Supply Of The Brain And Brainstem

Front 1

What part of the brainstem and brain controls 'arousal'?

Back 1

Reticular activating system.
Controlled by: hypothalamus - Ventral PosteroLateral (VPLO) and fine tuned by the orexin system. Specially in relation to orexin system.

Front 2

What is the key neurotransmitter in sleep and arousal/wakefulness?

Back 2

Orexin.

Front 3

What are the stages of sleep cycle?

Back 3

a) Slow Wave Sleep (SWS) or NREM sleep
Stages I - IV
b) Rapid Eye Movement (REM)

Front 4

What are the neural features of REM sleep?

Back 4

- Inhibited movement but commanded
- Illogical thought, bizarre
- Vivid sensation and perception. And internally generated.
- High neuronal activity in cortex and paralimbic structures (facilitate creativity and memory) and in selected REM sleep promoting networks of the hypothalamus and brainstem - similar to awake brain.

An active brain in immovable body.

Front 5

What are the characteristics of NREM sleep?

Back 5

- Dull or absent sensation and perception.
- Logical thoughts
- Episodic involuntary movement.

Low overall neuronal activity in the entire brain, most notably in the cortex and thalamus.

Front 6

What NTs are shut down during REM sleep?

Back 6

Monoamines:
- norepinephrine
- serotonin
- Histamine

Front 7

What is the epidemiology of stroke? What is the prognosis?

Back 7

Stroke is the second leading cause of death in Australia after CHD. The prognosis:
o 1/3 – die within 12 months
o 1/3 – permanently disabled
o 1/3 – progress past 12 months without permanent disability

Front 8

What are the characteristics of stroke and TIA? What is the difference?

Back 8

Both stroke and TIA are characterized by focal neurological deficit, negative symptomology and sudden onset. The difference is TIA lasts less than 24 hours (majority resolved within 1 hour) while stroke >24 hrs. TIA also characterized by acute loss of monocular function.

Front 9

What are the causes of stroke? Which one is the commonest?

Back 9

Causes of stroke:
o Thromboembolic (ischaemic stroke) – 80%
o Haemorrhagic stroke - <20%
o Low blood flow

Front 10

Describe the pathophysiology of stroke.

Back 10

Perfusion failure (thromboembolic or haemorrhagic) -> compensatory mechanism by the body to increase perfusion -> opening of anastomotic channel and BV dilatation until it reaches its maximum -> Blood flow is compensated until BV dilatation reaches its max -> brain blood flow begins to decrease -> brain oxygen extraction increases until it extracts all the oxygen contents (max) -> metabolism of the brain begins to fail -> symptoms showing (reversible initially (TIA) then irreversible)

Front 11

What are the risk factors for stroke (11)?

Back 11

1. old age (in all races)
2. hypertension
3. Diabetes mellitus
4. high cholesterol
5. cigarette
6. homocysteine
7. obesity
8. TIA
9. AF, IHD
10. haematological abnormalities
11. drugs (oral contraceptive pill)

Front 12

How is stroke diagnosed?

Back 12

Mainly clinical diagnosis. Use CT-scan to determine haemorrhagic or not BUT it is not good to see ischaemic stroke, need MRI.

Front 13

What is the immediate management of stroke?

Back 13

o Supportive measures:
• Restore O2 content, blood pressure control, temp control, corrections of high sugars
• Refer to stroke unit
o Thromboembolic stroke – thrombolysis, thrombectomy
o Haemorrhagic stroke – reverse any clotting disorder, consider recombinant factor VIIa.

Front 14

What is the immediate management for thromboembolic stroke?
o What is the rationale for thrombolysis?
o What are the potential problems with thrombolysis?

Back 14

<2 hr and meet inclusion criteria:
1. administer rt-PA over 1 hour
2. start aspirin 24 hrs later

Thrombolysis inappropriate:
1. start aspirin if not already on it
2. change to clopidogrel if already on aspirin.

Rationale for thrombolysis:
80% of strokes are thromboembolic. Lysis of clot should restore blood flow and preservation of ischaemic penumbra.

Potential problems with thrombolysis:
o Intolerance of brain cells for prolonged ischaemia, hence critical.
o Risk of bleeding
• Stroke damaged vessels are leakier than normal. Haemorrhages in confined space of skull potentially more troublematic than at other sites.
o Cochrane review shows tPA is better to use in acute ischaemic stroke; it reduces the rate of disability.

Front 15

What are the treatment options for carotid disease (occlusion)?

Back 15

o Carotid endarterectomy
o Carotid angioplasty (not as good as endarterectomy)
o Possible closure of foramen ovale

Front 16

What are the possible patterns for brain cell death following injury?
o What are the mechanisms for each pattern?

Back 16

Patterns of cellular injury:
o Immediate cell death
o Delayed cell death (days – weeks)
o Late cell death (weeks – months)

Mechanisms:
o Immediate – direct cellular trauma, anoxia, necrosis
o Delayed , 3 mechanisms of injury:
1.Peri-infarct depolarization
2. Excitotoxicity  pathological process by which nerve cells are damaged and killed by glutamate
3. Inflammation (cellular and humoral)
o Late – apoptosis

Front 17

Which of the cell death area is salvageable?
What is the time limit before this area become non salvageable?

Back 17

Delayed cell death is salvageable – penumbra region. It takes 48 hours before this area become non salvageable. Cerebral Blood Flow (CBF) needs to be restored to normal before this happens.

Front 18

Describe the 3 mechanisms of delayed cell death.

Back 18

Ischaemia leads to ↓ATP
↓
Pre-synaptically: Ion pumps fail – NCX reversed (↑Ca++ influx) & Na/K-ATPase failure (↑[K+] extracellularly & ↑[Na+] intracellularly) – since the leaky channels are not dependent on ATP and still working
↓
Depolarisation  ↑ release of NT (glutamate) to synaptic cleft.
↓
Post-synaptically: Glutamate binds to NMDA, AMPA and metabotropic receptors
↓
Increased [Ca++] intracellularly to a toxic level
↓
Release of nNOS, endonucleases, lipases
↓
Damages to membrane, protein, DNA  glial cells activation -> recruitment of neutrophils

Front 19

What are the 3 strategies to protect brain from further damage? Give examples of how they can be done.

Back 19

Focus on penumbra:
o Increase cerebral oxygen delivery
o Reduce cerebral oxygen demand
 Non pharmacological
• Hypothermia
 Pharmacological – poor evidence
o Improve cellular integrity on the presence of a corrupt supply / demand balance
 E.g. NMDA antagonists (magnesium sulphate), EPO, anti-apoptotic agents.

Front 20

Name the arteries on the diagram below.

Back 20

.

Front 21

Where are the basillar artery, circle of willis located?

Back 21

Basillar artery is at the base of the pons. Circle of willis form a circle encompassing the colliculus, pituitary stalk and optic chiasm. Internal carotid artery in the cavernous sinus.

Front 22

What structures can be found in the cavernous sinus?

Back 22

Cavernous sinus – O TOM CAT:
O TOM are the lateral wall components, in order from superior to inferior.
CA are the components within the sinus, from medial to lateral. CA ends at the level of T from TOM
o Occulomotor nerve
o Trochlear nerve
o Ophthalmic nerve
o Maxillary nerve
o Carotid artery
o Abducent nerve
o T – CA ends at the level of T.

Front 23

How do carotid artery and vertebral artery enter the cranium?

Back 23

Carotid artery through carotid canal. Vertebral artery through the foramen magnum.

Front 24

Label the diagram of interior base of skull below.

Back 24

.

Front 25

What are the arteries supplying the brain stem?

Back 25

Blood supply of the brain stem:
o Superior cerebellar artery (SCA) – from basillar artery
o Anterior Inferior Cerebellar Artery (AICA) – from basillar artery
o Posterior Inferior Cerebellar Artery (PICA) – from vertebral arteries

Front 26

What are the blood supplies of the spine?

Back 26

• Blood supply of the spine:
o Anterior 2/3 – anterior spinal artery
o Posterior 1/3 – posterior spinal artery

Front 27

Draw the blood vessels territories of the brain, medially and laterally.

Back 27

.

Front 28

What blood vessels supply the internal capsule and corpus striatum?

Back 28

Medial and lateral groups of the striate arteries supply the corpus striatum and internal capsule.

Front 29

Name the 3 sinuses of the brain and where are they located.

Back 29

Sinuses: superior sagittal sinus, transverse sinus, straight sinus.

Front 30

What is the sign of lesion of trochlear nerve (CN IV)?

Back 30

It controls the Superior rectus muscle.
Eye drops to 9 o'clock position.

Front 31

What are the signs of lesion of oculomotor nerve (CN III)?

Back 31

- Eye drops to 7 o'clock position.
- Droopy eyelids
- Loss of pupillary reflex - huge pupil.

Front 32

What is the the sign of lesion of abducens nerve (CN VI)?

Back 32

Eye droops to 3 o'clock.

Front 33

What is the relevance of arousal and awareness of brain function?

Back 33

They both assess conscious state but are not always identical. While both are high in normal and low in coma, it is possible to be aroused but not aware as in a vegetative state & in a minimally conscious state.

Front 34

Discuss what can affect the sleep homeostat.

Back 34

- biological clock (12 hours) - even if animal blind or prevented from sight.
This is impacted by our senses such as the sun and stimuli.

Front 35

Find all the CNs.

Back 35

.

Front 36

What are the 3 main sections of the brainstem and their roles in brief?

Back 36

Midbrain
- Has visual and auditory functions, controlling eye and body movements.

Pons
- Major role in consciousness, sleep, breathing, alertness and arousal.

Medulla
- Controls autonomic functions such as maintenance equilibrium, audition, deglutition, coughing, vomiting, salivation, tongue movement, respiration and circulation.

Front 37

Brainstem anatomy.

Back 37

.

Front 38

What CN nuclei can you find in the:
- Midbrain?
- Pons?
- Medulla?

Back 38

Midbrain: III & IV (posteriorly)
Pons: V, VI, VII
Medulla: VIII, IX, X, parts of XI & XII.