Podcast
Questions and Answers
What is the primary distinction between a stroke and a transient ischemic attack (TIA)?
What is the primary distinction between a stroke and a transient ischemic attack (TIA)?
- Strokes always involve haemorrhage, while TIAs do not.
- TIAs cause permanent brain damage visible on MRI, while strokes do not.
- Symptoms of a TIA resolve completely within 24 hours, while stroke symptoms persist longer. (correct)
- Strokes are caused by embolisms, while TIAs are caused by thrombosis.
Which of the following best describes the role of the Circle of Willis in cerebral blood supply?
Which of the following best describes the role of the Circle of Willis in cerebral blood supply?
- It provides collateral circulation, allowing blood to reach areas even if a major artery is blocked. (correct)
- It is the primary site for thrombus formation leading to ischaemic stroke.
- It ensures constant blood supply to the brain by preventing vasoconstriction during increased metabolic activity.
- It directly supplies blood to the internal structures of the brain, such as the basal nuclei.
Why is the brain so vulnerable to irreversible damage from even brief periods of oxygen and glucose deprivation?
Why is the brain so vulnerable to irreversible damage from even brief periods of oxygen and glucose deprivation?
- It has a very high metabolic demand and no capacity for anaerobic ATP production or fuel storage. (correct)
- The brain's extensive venous drainage system causes rapid depletion of essential nutrients.
- Brain tissue undergoes immediate liquefactive necrosis upon nutrient deprivation.
- The blood-brain barrier prevents rapid restoration of oxygen and glucose levels.
In the context of stroke, what is the 'ischaemic penumbra,' and why is it clinically significant?
In the context of stroke, what is the 'ischaemic penumbra,' and why is it clinically significant?
Which of the following is the most accurate description of liquefactive necrosis in the context of a stroke?
Which of the following is the most accurate description of liquefactive necrosis in the context of a stroke?
How do cytotoxic and vasogenic oedema contribute to secondary brain injury after a stroke?
How do cytotoxic and vasogenic oedema contribute to secondary brain injury after a stroke?
Which of the following best describes the sequence of events in ischaemic tissue that ultimately leads to cell damage?
Which of the following best describes the sequence of events in ischaemic tissue that ultimately leads to cell damage?
How does increased intracranial pressure (ICP) lead to herniation, and why is herniation a life-threatening condition?
How does increased intracranial pressure (ICP) lead to herniation, and why is herniation a life-threatening condition?
What is the primary difference between 'stroke in evolution' and a completed stroke?
What is the primary difference between 'stroke in evolution' and a completed stroke?
Why is it difficult to accurately distinguish between ischaemic and haemorrhagic stroke based solely on a patient's medical history and initial presentation?
Why is it difficult to accurately distinguish between ischaemic and haemorrhagic stroke based solely on a patient's medical history and initial presentation?
Which of the following is a common cause of intracerebral haemorrhage?
Which of the following is a common cause of intracerebral haemorrhage?
In a subarachnoid haemorrhage due to a ruptured aneurysm, what is the primary mechanism by which it causes neuronal dysfunction?
In a subarachnoid haemorrhage due to a ruptured aneurysm, what is the primary mechanism by which it causes neuronal dysfunction?
Which of the following is the most accurate clinical presentation of an acute stroke?
Which of the following is the most accurate clinical presentation of an acute stroke?
A patient presents with aphasia (incoherent speech) and right hemiparesis following a stroke. Which area of the brain is MOST LIKELY affected?
A patient presents with aphasia (incoherent speech) and right hemiparesis following a stroke. Which area of the brain is MOST LIKELY affected?
Which set of clinical signs and symptoms is most indicative of increasing intracranial pressure (ICP)?
Which set of clinical signs and symptoms is most indicative of increasing intracranial pressure (ICP)?
Which of the following is the most critical component of the Glasgow Coma Scale (GCS)?
Which of the following is the most critical component of the Glasgow Coma Scale (GCS)?
What distinguishes a 'closed' head injury from an 'open' head injury?
What distinguishes a 'closed' head injury from an 'open' head injury?
What characterizes 'primary injury' in the context of head trauma?
What characterizes 'primary injury' in the context of head trauma?
What is the significance of 'brain herniation' as a consequence of elevated intracranial pressure?
What is the significance of 'brain herniation' as a consequence of elevated intracranial pressure?
What characterizes the cerebral blood supply in patients with head injuries?
What characterizes the cerebral blood supply in patients with head injuries?
What is the role of the ascending reticular activating system (RAS) in brain injuries?
What is the role of the ascending reticular activating system (RAS) in brain injuries?
Why is 'post-traumatic amnesia' (PTA) significant in head injuries?
Why is 'post-traumatic amnesia' (PTA) significant in head injuries?
How does the brain's metabolic need contribute to stroke-induced injuries?
How does the brain's metabolic need contribute to stroke-induced injuries?
In stroke management, why would a patient receive oxygen and ventilation support?
In stroke management, why would a patient receive oxygen and ventilation support?
What effect does a space-occupying lesion, such as a haematoma, have on intracranial pressure (ICP)?
What effect does a space-occupying lesion, such as a haematoma, have on intracranial pressure (ICP)?
Identify the consequence of an expanding haematoma regarding surrounding brain tissues.
Identify the consequence of an expanding haematoma regarding surrounding brain tissues.
Classify 'Contrecoup' injury in traumatic brain injury mechanisms.
Classify 'Contrecoup' injury in traumatic brain injury mechanisms.
How should mannitol be understood regarding brain injury management?
How should mannitol be understood regarding brain injury management?
What aspect distinguishes the primary effect of subarachnoid haemorrhage from intracerebral haemorrhage?
What aspect distinguishes the primary effect of subarachnoid haemorrhage from intracerebral haemorrhage?
What is the function of the blood-brain barrier (BBB)?
What is the function of the blood-brain barrier (BBB)?
What ascending artery feeds into the basilar artery?
What ascending artery feeds into the basilar artery?
What is a common cause of subarachnoid haemorrhage?
What is a common cause of subarachnoid haemorrhage?
What can be expected with someone who has had PTA greater than 7 days?
What can be expected with someone who has had PTA greater than 7 days?
Flashcards
What is a stroke?
What is a stroke?
A stroke occurs when blood flow to the brain is interrupted.
Carotid artery function
Carotid artery function
The common carotid artery divides into internal and external carotid arteries, supplying the brain.
What forms the basilar artery?
What forms the basilar artery?
The vertebral arteries fuse to form the basilar artery, which branches into cerebellar and posterior cerebral arteries.
What is the Circle of Willis?
What is the Circle of Willis?
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How is blood drained?
How is blood drained?
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What is the blood-brain barrier?
What is the blood-brain barrier?
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Why does the brain need blood?
Why does the brain need blood?
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How is blood flow maintained?
How is blood flow maintained?
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Define stroke
Define stroke
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What is a TIA?
What is a TIA?
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Define infarcted
Define infarcted
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What is liquefactive necrosis?
What is liquefactive necrosis?
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Modifiable stroke risk factors
Modifiable stroke risk factors
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TIA symptom duration
TIA symptom duration
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What is thrombosis?
What is thrombosis?
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What is embolism?
What is embolism?
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What is the ischaemic penumbra?
What is the ischaemic penumbra?
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What is the result of severe ischaemia?
What is the result of severe ischaemia?
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Define cytotoxic oedema
Define cytotoxic oedema
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What is vasogenic oedema?
What is vasogenic oedema?
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Why is brain herniation life-threatening?
Why is brain herniation life-threatening?
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Hemorrhagic stroke symptoms
Hemorrhagic stroke symptoms
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Cause of subarachnoid haemorrhage
Cause of subarachnoid haemorrhage
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Signs of strokes
Signs of strokes
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What is aphasia?
What is aphasia?
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What is the Glasgow Coma Scale?
What is the Glasgow Coma Scale?
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Cause of closed head injury?
Cause of closed head injury?
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Cause of open head injury
Cause of open head injury
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Two causes of secondary brain injury
Two causes of secondary brain injury
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What causes tertiary brain injury?
What causes tertiary brain injury?
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What is Post traumatic amnesia?
What is Post traumatic amnesia?
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Study Notes
Brain Blood Supply and CVA
- A stroke happens when blood flow to the brain is interrupted.
- Interruption of blood flow can be due to a blockage from occlusive stroke (85% of cases) or bleeding from haemorrhagic stroke (15% of cases)
Blood Supply
- The common carotid artery (originating from the thorax) divides into internal and external carotid arteries
- The internal carotid artery goes into the skull through the temporal bone before branching into the anterior cerebral artery, middle cerebral artery, and posterior communicating artery
- The vertebral artery goes up the neck through cervical vertebrae
- The vertebral arteries go into the skull through the foramen magnum and fuse into the basilar artery, which leads to cerebellar arteries and posterior cerebral arteries
- The Circle of Willis is an arterial circle around the pituitary gland that allows blood to be distributed to the brain
- Blockage of some blood supply may be compensated as a result of the circle of willis
Venous Drainage
- Venous sinuses are located in dura mater
- Sinuses converge at the back of the skull to the sigmoid sinus on each side
- Sigmoid sinus moves to the internal jugular vein
Blood-Brain Barrier
- Most brain capillaries are "tightly sealed", preventing many substances from crossing freely from the blood into the brain's intercellular fluid
- Blood gases, water, alcohol, and anaesthetics move freely through the barrier
- Many antibiotics and drugs do not pass through
- Glucose and amino acids need proteins for their carriage
- The blood-brain barrier is less effective in newborns
- Brain inflammation reduces the effectiveness of the barrier because capillaries become "leaky"
Intracranial Pressure
- Within the skull, the brain occupies 80%, blood occupies 12%, and CSF occupies 8%
- The total volume within the skull is 1600ml
- The skull is a rigid box
- Fluid is equalized initially but the pressure will rise if the volume of the contents increases
- Intracranial Pressure (ICP) is normally 5-13 mmHg
- Intracranial pressure has limited capacity
Brains and Blood
- The brain weighs roughly 1.5 kg, about 2% of body weight
- The brain requires continuous supply of oxygen (20% of body's amount) and glucose (70% of blood glucose)
- The brain also removes H+ produced by metabolism
- The brain has no anaerobic ATP production capacity
- The brain does not store fuel like glucose
- Deprival of oxygen/glucose for a few minutes leads to irreversible damage
Cerebral Blood Flow
- The brain needs a steady blood flow of 1000mL per minute, about 20% of cardiac output
- Arterioles in the brain automatically dilate to increase brain flow if systematic blood pressue falls, and rise of blood pressue causes constriction
- Local increase in CO2 in a particular region causes vasodilation, increasing flow to carry away the CO2
Defining Stroke
- Stroke, also labelled Cerebrovascular Accident (CVA), is a sudden onset of a focal (or sometimes global) neurological impairment that lasts more than 24 hours (or leads to death) and is presumed to be of vascular origin.
- CVA is the rapidly developing loss of brain functions due to a disturbance in blood vessels supplying blood to the brain, caused by thrombosis, embolism, or hemorrhage
- Infarction is the term for tissues that have died due to failed blood supply
- Liquefactive necrosis is the process the brain undergoes when part of it dies
- When blood supply is spontaneously restored before tissue death occurs, and recovery is complete, the event is a transient ischaemic attack (TIA) (aka "mini stroke")
- Signs and symptoms of stroke or TIA depend on which areas of the CNS have been deprived of blood
Risk Factors for Stroke
- Increasing age
- Hypertension
- Heart disease
- Atherosclerosis
- High blood cholesterol
- Hypercoagulability
- Diabetes mellitus
- Smoking
- Oral contraceptives
- Pregnancy
- Cocaine use
Transient Ischaemic Attack (TIA)
- Blood flow occlusion temporarily reduces blood flow to part of the brain (like ischaemic stroke) for less than 24 hours
- Occurs in an eye, causing fleeting blindness on one side
- The occlusion clears itself before brain tissue has died
- Damage may be shown on MRI after TIA
- Is an increased risk of future stroke
Occlusive Stroke
- Thrombosis is obstruction of vessels from blood clot forming locally, arising from atherosclerosis, usually diabetes or HTN
- Embolism is obstruction from a blood clot from elsewhere, particularly the heart (atrial fibrillation, heart valve disease)
- Obstruction/failure of arterial blood flow is caused by venous thrombosis or shock
Blood Clots in the Brain
- Clots can form in large or small blood vessels
- In large vessels, clots can form in the carotid arteries, vertebral arteries, or the Circle of Willis
- In small vessels, clots can form in the arteries within the brain itself
- Most common sites of thrombotic occlusion are branch points of arteries
- Emboli commonly originate from the heart, especially in atrial fibrillation
Location and Impact of Clots
- The affected area depends on the distribution of the artery blocked
- Arterial anastomoses (direct arterial connections, as in the Circle of Willis), facilitate blood flow to some areas even when the main artery is blocked
- The cortex (outer layer) can undergo the process due to arterial anastomes, whereas the internal structures (ie basal nuclei) do not due to a lack of arterial anastomes
Impacts of Ischaemic Tissue
- ATP Depletion
- Membrane ion transport systems stop functioning
- Depolarization of neurone
- Influx of calcium
- Release of neurotransmitters, including glutamate, activates N-methyl-D-aspartate and other excitatory receptors on other neurones
- Further depolarisation of cell
- Further calcium influx
Ischaemic Penumbra
- Within the ischaemic area, there are the core ischaemic zone and the ischaemic penumbra
- The penumbra defines ischaemic yet still viable cerebral tissue
- In the core zone, severe ischemia can result in necrosis in neurones and glial cells
- Penumbra has a rim of mild to moderately ischaemic tissue
- Brain cells within the penumbra may remain viable for several hours.
- the penumbral zone is supplied with blood by collateral arteries anastomosing with branches of the occluded vessel.
- The extent of the penumbra varies directly with the number and patency of collateral arteries
- Cells will die if blood does not resume in hours due to insufficient circulation
- Pharmocologic interventions are most effective in the penumbra
Necrosis
- Severe ischaemia causes neurones and glial cells die, leading to liquefactive necrosis
- Cells breakdown by their own enzymes, causing tissue to be replaced w/ cerebralspinal fluid
- Astrocytes proliferate at the margin of the cavity to line it, and this process takes months during large infarcts
Types of Oedema
- Cytotoxic oedema is swelling of all cellular elements of affected area, occurring minutes to hours after, caused by hypoxia that leads to failure of ATP-dependent transport
- Vasogenic oedema is the increase of interstitial fluid volume, occurring hours to days after, because of increased permeability of small vessels because of inflammatory response from cell damage
More on Oedema
- Cerebral oedema peaks about 2-5 days after stroke, followed by stabilization and lessening
- Recovery of function post-stroke involves resorption of Oedema
- Oedema increase life-threatening intercranial pressure
Herniation
- Occurs whenever pressure rises inside the skull and displaces brain tissues
- Can occur through the opening at base of skull (occipital foramen)
- Can occur in compartments like the one separated by the tentorium
- Rapidly leads to death because of compression of blood vessels as those in the respiratory centre
Stroke in Evolution
- Thrombosis can take minutes, hours, or days to evolve
- Stroke is actively progressing as a result of increasing occlusion and ischaemia
- Larger blood vessels (carotid, middle cerebral, or basilar arteries) can take longer to become occluded than a smaller vessel and there may be warning signs, like transient ischemic attacks
Haemorrhagic Stroke
- 10-15% of strokes, with higher mortality than ischaemic strokes
- May occur within brain or surrounding menigeal spaces
- Cannot distinguish between ischaemic and haemorrhagic stroke based on history
- More likely when patient is generally more ill
- Presentation includes raised intracranial pressure symptoms via nausea, vomiting, and headache
Haemorrhagic Stroke, continued
- Seizures are more common compared to ischaemic strokes
- Symptoms of meningeal irritation may result from blood in the ventircles
- Haemorrhage is more acute than infarct from same sized
- When hematoma is resorbed, tissue generally retains much function
- Less severe long term disabilities compared to infarct
Haemorrhage
- Results in tissue injury
- Compression of expanding haematoma to distory and injure surrounding tissue, increasing pressure and reducing blood flow
- Increase intercranial pressure with possibility of herniation
- Blood emptys into ventricular system or the pial system from hematoma
- Blood in the ventricles is noxious and painful when in the subarachnoid space
Basal Ganglia Area and Haemorrhage
- Haemorrhages in area of basal ganglia is contributed by hypertension
- Hypertension damages and weakens the penetrating arteries
- Mass effect in midline shift
- Secondary oedema can lead to herniation
Subarachnoid Haemorrhage
- A "berry" aneurysm bursts, and blood erupts into the subarachnoid space
- This causes excruciating pain, followed by neurologic problems
- Vasospasm occur, producing additional cerebral damage
- High chance of death or rebleeding
- Subarachnoid haemorrhage from ruptured aneurysm more of irritant producing vasospasm than mass lesion
Aneurysm
- Defect in arterial wall is present from birth and considered "congenital"
- Aneurysms take years to develop and rupture in middle age, commonly in the Circle of Willis
Presentations of Acute Stroke
- Onset of focal neurological symptoms and signs, and patient was well beforehand
Altered Consciousness
- Stupor or coma
- Confusion or agitation
- Memory loss
- Seizures
- Delirium
- Usually intense or unusually severe
Headache
- Associated with decreased level of consiousness or neurological deficit
- With unusual/severe neck or facial pain
- Incoherent speech
- Difficulty understanding speech
Other Presentations
- Facial weakness or asymmetry
- Incoordination, weakness, paralysis, or sensory loss (usually one half of the body and particularly the hand)
- Ataxia, via poor balance, clumsiness, or difficulty walking
- Visual loss, monocular or binocular with partial loss of field
- Intensive vertigo, double vision, unilateral hearing loss, nausea, vomiting, photophobia
Common Stroke Patterns
- Left Hemisphere Strokes result in aphasia, rightsided issues (hemiparesis and sensory loss), right visual field defect, and poor right conjugate gaze, dysarthria and difficulty with reading and calculating
- Right Hemisphere Strokes result in a neglect of left visual field, extinction of left sided stimuli, left hemiparesis and sensory loss, left visual field defect, poor left conjugate gaze, dysarthria and difficulty with spatial orientation
- Brain Stem, Cerebellum Strokes result in loss in all 4 limbs, limb or gait ataxia, dysarthria, dysconjugate gaze, nystagmus and amnesia
- Subcortical Hemisphere Stroke results in weakness of face and limbs
Head Injury
- Classified as closed or open
- In closed head injuries, brain trauma usually occurs from blunt trauma and presents as diffuse axonal injury or focal brain injury, while the skull is still intact
- In open head injuries, penetrating trauma occurs, the dura mater in broken, causing focal brain injury and skull penetration from eg bone fragments or a foreign body
Head Injury, Continued
- Damage occurs from primary, secondary, and tertiary injury
- Primary injury occurs from acceleration/deceleration, direct impact and damage
- Can affect neurons, glia, and blood vessels
- Seconary injury factors include cerebral oedema, haematoma, increased intercranial pressure and infection
- Tertiary injury is from apnoea, hypotension, and respiratory and cardiovascular effects from primary and secondary injury
Intercranial Pressure
- Increase in content like haematoma, and inflammation causes increase in pressure
- Damage to blood vessels
- Arterial bleeding can rapidly bring on injury hours
- Venous bleeding can be delayed for days/weeks
- Signs when injury occurs
- Arterial Bleeding
- High risk of rebleed
- Venous Bleeding
- Common to occur during infanthood or at elderly stage
- Arterial Bleeding
Effects of Increasing Intracranial Pressure
- Decreating levels of consiousness by hindering pressure on RAS in Brainsteam or cerebral vortex
- Stretching wall of blood vessels can result in headache
- Pressure of vomitting can act on the emetic center in the medulla
- Increasing pulse pressure with intercranial pressure
- Cushing's reflex can systemically vasoconstrict
- Increase of CSF pressure, causes optic disc to swell
General Indicators of intercranial pressure
- The brain has compliance to a point
- Some increase of CSF will be accommodated, but not too much, otherwise intracranial pressure will rise
Increase the Intercranial pressure
- Compensation of increase in systolic, pulse, and diastolic pressure
- Resperation increases and lessens with time
Progression of injury
- Level of consiousness can vary by extent of injury, medical intervention, fever and environment.
- Deterioration will increase from the fundamental reflexes of the brainstem
Common Factors Related to Brain injuries
- Respiratory rate changes
- Important to assess severity of injury from Glasgow Coma Scale -Standard Stimuli -Score 3-15, 3 is the worst, 15 is the best
Key Clinical Management
- May require sedation, like coma patients
- Oxygen, steroids, and diuretics are the standard approach, as well as ventilation
More on Amnesia
- Loss of memory around time of trauma
- Agitation, disorientation, and decreased cognitive ability and attention are major signs
- Duration is indicative to the level of injury
- Can be rated as "very mild injury" after 5 minutes, moderate to 24 minutes, or may be greater than 7 days
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