Session 9:Strokes, Head Trauma and Acute Inflammatory Response Flashcards
What happens if there is disruption to the blood supply of the brain?
The brain makes up ~2% of body weight but receives 15% of the Cardiac Output (i.e. 750ml/min) and from this, it receives glucose and 20% of the total available oxygen.
This disproportionately high blood supply to the brain is necessary because brain tissue uses glucose as the only source of its energy, whilst being incapable of making or keeping energy stores.
So the brain is entirely reliant upon continuous perfusion for its energy.
As such, disruption of brain tissue perfusion inevitably leads to immediate loss of consciousness (syncope).
If this persists continuously for more than 3 minutes, ischaemia and consequently, irreversible brain tissue damage would occur.
How does the brain ensure a constant supply of blod?
To ensure continuous blood supply in the face of fluctuations in systemic arterial pressure, the brain has evolved an efficient cerebrovascular perfusion system that autoregulates (variable vascular resistance) to overcome these fluctuations and thereby minimise disruptions of blood delivery to the brain.
Autoregulation also ensures that highly metabolically active areas of the brain receive increased blood supply whilst less active areas receive less.
In addition to autoregulation, the circular anastomotic trunk collectively known as the Circle of Willis/Circulus Arteriosus has in-built redundancy which ensures that if blockage or critical narrowing occurs anywhere along the Circle of Willis, adequate tissue perfusion remains unaffected (through shunting).
Describe the Circle of Willis
The right and left vertebral arteries unite to give rise to the basilar artery that runs caudo-rostrally along the mid-sagittal line to meet the left and right internal carotid arteries through left and right posterior communicating arteries.
The corresponding anterior cerebral arteries take root from the internal carotid arteries and unite through the anterior communicating artery to complete the circular arterial formation.
Anterior Circulation:
- Internal Carotid Artery (ICA)
- Middle Cerebral Artery (MCA)
- Anterior Cerebral Artery (ACA)
- Posterior Communicating Artery (PCommA)
Posterior Circulation:
- Basilar Artery (BA)
- Vertebral Artery (VA)
- Posterior Cerebral Artery (PCA)
Remember the common carotid arteries have different origins: left common carotid artery is a branch of the arch of the aorta, right common carotid artery is a branch of the brachiocephalic artery.
- Carotid bifurcation (C4)
- Internal and external branches
- External carotid arteries supply face, scalp, mouth and jaw tissues
Describe the Internal Carotid Artery
4 Segments (old system)
7 Segments – Bouthiller (Cervical, Petrous, Lacerum, Carvenous, Clinoid, Ophthalmic, Communicating)
- Important branches include ophthalmic artery (supplies orbit, part of nose etc), posterior communicating artery, anterior choroidal artery (supplies the optic chiasm, internal capsule, glonus pallidus, hippocampus, substantia nigra etc).
NB: aneurysm of posterior cerebral artery could lead to oculomotor palsy
Describe the Middle Cerebral Artery
Direct continuation of ICA (60-80% of flow)
Supplies 2/3 of brain convexity – runs in the lateral sulcus, where it branches and projects to many parts of the lateral cerebral cortex
Lateral aspect of frontal/parietal/occipital lobes
Lateral striate arteries supply basal ganglia
Most strokes occur in MCA territory
Describe the Anterior Cerebral Artery
Smaller branch of ICA
Supplies medial surface and adjacent convexity (frontal and parietal lobes)
Jointed by anterior communicating artery
NB: anterior cerebral artery and middle cerebral artery do not anastomose – the middle cerebral arteries do not contribute to the circle.
Describe the Vertebral Artery and the Basilar Artery
Vertebral Artery
- Arises from the subclavian arteries
- Tortuous course
- Largest branch is posterior inferior cerebellar artery (PICA)
- Other branches include spinal arteries
Basilar Artery
- Overlies the pons
- Supplies most of the brainstem
- Superior and anterior inferior cerebellar arteries
- Bifurcates into 2 PCAs
Describe the Posterior Cerebral Artery
Bifurcation of basilar artery (but 25% get main supply from ICA)
Goes around the midbrain
Supplies the midbrain, thalamus, temporal and occipital lobes
PCA stroke involves visual agnosia (impairment in recognition of visually presented objects), homonymous hemianopsia, visual field defects
What’s the definition of a stroke? Describe the problem of stroke
Stroke is the second most common cause of death (after coronary artery disease) in developed countries, yet is uncommon before the age of 40 and is more common in males.
- 25% occur in the under-65s (more and more younger people are having a stroke).
- Commonest cause of long-term disability
- 1 million stroke survivors living in UK
- A new stroke occurs every 5 minutes. 1 in 4 of us will have a stroke
- 5% of NHS expenditure; £7 billion 1st year after stroke.
Definition of Stroke: Clinical Syndrome of abrupt loss of focal brain function (sudden onset) lasting >24 hours (or causing death).
Describe the main cerebrovascular problems that can cause a stroke
The main cerebrovascular problems are thromboembolic infarction (80-85%), cerebral and cerebellar haemorrhage (intracranial) (10-15%) and subarachnoid haemorrhage (5%).
A stroke will normally be the result of arterial embolism and subsequent brain infarction, arterial thrombosis from atheromatous artery, or from spontaneous haemorrhage into the brain; other less common causes include venous infarctions, carotid or vertebral artery dissection, or fat or air embolism.
As a result they can be divided into transient ischaemic attack, cerebral infarction and intracranial haemorrhage
What is meant by Cerebral Infarct, Intracerebral haemorrhage, Cerebrovascular disease? And what’s the name for a ‘mini-stroke’?
Cerebral Infarct (Ischaemic stroke – impairment of blood supply due to clot)
- Acute versus old
- Could be large vessel atheroma/embolism, cardiac embolism, small vessel disease/ Lacunae, non atheromatous arterial disease (arteritis), blood disorders, other known aetiologies, cryptogenic (no cause identified, perhaps undiagnosed AF in history)
Intracerebral haemorrhage
- Primary (no structural lesion – bleeding is spontaneous) vs Secondary (e.g. tumour)
- Haemorrhagic transformation of infarct (in extensive ischaemic infarct => cerebral oedema compressing fragile blood vessels => leaking of blood)
- Could be hypertensive microaneurysms / lipophyalinosis (40%), arteriovenous malformations or aneurysms (15%), amyloid angiopathy (10%), haemostatic anticoagulant/thrombolytic/thrombocytopenia (10%), other e.g. cocaine, amphetamines, tumour, venous thrombosis (associated with T1 diabetes)
- Pregnant women during the peripartum period tend to have haemorrhagic strokes more than ischaemic strokes.
Cerebrovascular disease
- Small vessel disease identified on brain imaging (associated with cardiovascular risks), more prone to having cognitive impairment, dementia
Transient Ischaemic Attack
Describe the risk factors and prevention for stroke
The main risk factors for stroke risk are hypertension and smoking, so treatment and cessation of these respectively will significantly reduce stroke incidence.
- Non-Modifiable: age, gender, genetic (family history), previous stroke / TIA
- Lifestyle: smoking, sedentary lifestyle, heavy alcohol intake, poor diet
- Medical: hypertension, hypercholesterolaemia, diabetes mellitus, arrhythmia (e.g. AF)
Location of brain injury will affect presentation:
Localisation of brain injury
- Hemisphere
- Lobe
- Vascular territory (consider anterior circulation, middle cerebral, posterior circulation)
What important structures are in the Frontal and Temporal Lobes?
Frontal Lobe:
- Motor area (pre-motor and motor cortex)
- Broca’s area (stroke could lead to expressive dysphasia => comprehension retained, but not able to read or write)
- Prefrontal cortex (personality / behaviour)
Temporal Lobe:
- Central representation
- Auditory/vestibular function
- Taste and smell
- Wernicke’s area (could lead to receptive aphasia – speak fluent but unable to understand language in its spoken or written form)
- Memory circuits
- Optic radiation (inferior) = > superior quadrantanopia
What important structures are in the Parietal and Occipital Lobes? What about in the Cerebellum and Brainstem?
Parietal Lobe:
- Primary sensory cortex
- Non-dominant lesions – visuospatial issues (e.g. right sided lesion if right-handed)
- Optic radiation (superior)
- Inferior quadrantanopia / hemianopia
Occipital Lobe:
- Visual Cortex
Cerebellum/Brainstem
- Motor and sensory tracts
- Cranial nerve nuclei
- Cerebellum – balance coordination
What are the aims of the history?
Stroke versus non-stroke (lots of stroke mimics)
Suspect a Stroke?
- Facial weakness: has their face fallen on side? Can they smile?
- Arm weakness: can they raise both arms and keep them there?
- Speech problems: is their speech slurred?
- Time to call 999
TIA versus stroke (investigation different, treatment is similar)
What type of stroke? – location/pathology.
- Symptom onset
- When exactly?
- Speed of onset?
- Progression of symptoms
Neurological symptoms: localisation and characterisation
- Body part affected
- Modalities involved
- Positive (e.g. pain, pins and needles) vs negative symptoms important – why? Stroke and TIA symptoms are always negative e.g. I lost sensation, I lost the power of my arms
What are red flag symptoms? What about atypical presentations? What else do you need to consider
Other symptoms (red flags)
- Suggesting bleeding: headache (thunderclap in subarachnoid haemorrhage + neck stiffness), seizure
- Suggesting raised ICP: headache, vomiting, drowsiness
- Suggesting aetiology: cardiac symptoms
Atypical presentations – particularly in the elderly with extensive strokes
- Delirium, confusion, collapse, incontinence
Also need to consider
- Why did the stroke occur?
- Suitable for thrombolysis????
What are the differential diagnoses for stroke?
Hypoglycaemia and other metabolic disturbance
Migrainous aura
Epilepsy
SOL (secondary vs primary tumour, others)
Demyelination e.g. multiple sclerosis
Labyrinthine disorders
Others such as retinal bleeds or infarcts (same pathology but not defined under stroke), peripheral neuropathy, myopathies, delirium, hyperventilation (usually transient), functional or psychological
Describe the General examination you would do?
Observations: BP, pulse rate and rhythm (irregular associated with worst stroke), proteinuria/haematuria
GEN: telangiectasia (spider veins), hyperlipidaemia, stigmata of vasculitis (endocarditis), neoplastic screen
CVS: cardiac source of embolus (arrhythmia, valve), vascular – carotid or renal bruits, peripheral pulses
RESP: complications (may need to give antibiotics for chest infections etc).
Describe the neurological examination you would do and possible neurological deficit pattern presentations
localises the lesion
NB: any neurological deficit on review > not TIA (always treat patient as stroke if unsure about TIA)
Questions
- Anterior vs posterior
- Dominant vs nondominant (if right handed, left cortical cortex is dominant but left cortical cortex is almost dominant in some lefties – dominant in up to to 85% of people)
- Infarct vs haemorrhage
Neurological deficit patterns
- Unilateral hemiparesis/monoparesis
- Unilateral facial palsy (upper – can still raise eyebrows- vs lower MNL (Bell’s palsy, smooth forehead))
- Unilateral sensory deficit (and modalities)
- Dominant cortical (dysphasia, dysgraphia, dyslexia)
- Nondominant cortical (visuospatial disorder, neglect)
- Hemianopia/quadrantanopia – NB: both eyes involves
- Cranial nerve signs
- Cerebellar signs
What initial investigations would you do?
BM (blood sugar) stat ?? (always check liver function before statin)
Haematological: FBC, INR
Biochemical: U&E, LFT, TFT (thyroid function), glucose, lipid
ECG (a lot of people have undiagnosed AF but AF is associated with worse stroke, greater mortality)
Radiological: CXR where indicated
What brain imaging would you do?
Urgent where thrombolysis is an option
Indications
- Look for bleeding (intracranial, subdural, subarachnoid haemorrhage, bleed into tumour)
- Screen for stroke mimics (tumours, other rarities)
- May visualise infarct
Most early CT scans (<3 hours) show no changes. Early normal CT does not rule out ischaemic stroke or infarct, only rules out bleeding.
MRI brain – consider in certain scenarios – more sensitive
First image: left MCA infarct (needs to be thrombolysed); second image: right MCA – loss of grey:white matter differentiation; third image: haemorrhagic infarction on top of a massive necrosis => midline shift
What investigations would you consider?
Carotid Ultrasound Scan
- Could consider carotid endartectomy = reduces risk of stroke recurrency
Cardiac Investigations
- FOR WHOM?
- Echocardiography
- Trans-thoracic
- Trans-oesophageal
- 24 hour cardiac monitoring (to rule out shunting or PFO or thrombosis or AF) but very expensive and does not detect episodes that do not occur every 24 hours (e.g. does not detect irregular rhythm episodes that only occur once every few months).
What investigations would you do for younger/cryptogenic strokes?
Full coagulation profile
Thrombophilia screen
- Protein C/S, AT III, FV Leiden, P20210A
Antiphospholipid antibodies
- Anticardiolipin, lupus anticoagulant
Autoimmune screen
Fasting plasma homocysteine
Blood cultures
Thyroid function test, syphilis serology, HIV serology
Describe thrombolytic therapy
Intravenous thrombolysis (alteplase)
- Within 3h (up to 4.5h) of documented onset
- CT excludes bleeding, and established infarct
- No bleeding risk (not on warfarin)
- Independent with self care/mobility
- Results – majority will benefit, small group won’t
- 1 in 3 improve
- Full recovery in 1 in 10
- 3 in 100 have a worse final outcome
- 1 in 14 ICH => 1 in 20 worsen as a result
Who should be thrombolysed?
- IST3 trial – all ages / longer time delay
- Any patient within 3 hours (no age limit)
- Consider all up to 4.5 hours (under 80 yeara)
- Between 3 and 6 hours of known stroke symptom onset, patients should be considered for treatment with alteplase on an individual basis.
Apart from thrombolysis, what other options for stroke are there?
Early aspirin therapy (where not thrombolysed) – high dose initially
Management in an acute stroke unit – associated with better recovery and less disability
Specialist rehabilitation therapists
Routine carer involvement
Education and training programs
Describe the prevention of stroke
Antithrombotic
Medical risk factor treatment
- Treat hypertension
- Treat hypercholesterolaemia
- Carotid surgery (if significant carotid stenosis)
- Treat diabetes
- Lifestyle changes
- Medication compliance
What is a transient ischaemic attack?
Focal (occasionally global) deficits (disturbance of brain function) that last less than 24 hours and will result in complete recovery. They are usually the result of microemboli and result in temporary ischaemia to the region (presumed to be of vascular origin) however autoregulation of the brain vasculature prevents any infarction developing.
However they may sometimes be caused by a small intracranial haemorrhage; as a result TIAs are not a good indicator for thromboembolism.
TIAs will cause a sudden loss of function, usually within seconds and last for <24 hours. The most common symptoms to present are hemiparesis and aphasia, yet amaurosis fugax (loss of vision in one eye) and transient global amnesia may also occur.
Individuals who have suffered a TIA have an increased risk of going on to suffer a stroke or myocardial infarction.
Describe Cerebral Infarctions?
Major thromboembolic cerebral infarctions usually cause an obvious stroke (yet some may cause TIAs whilst others are silent). The clinical picture is very dependent on infarct site and the extent of the infarct, and whilst the general site of damage can be deduced from clinical signs, clinical estimation of the precise vascular terriotroy is often inaccurate. Most commonly, an occlusion will be seen in the middle cerebral artery, affecting the internal capsule.
Whilst the specific classification of strokes can be seen in the table below, the common clinical features seen in a stroke are contralateral hemiaparesis or hemiplegia (with facial weakness) and aphasia. However, symptoms will vary depending on the site and extent of the occlusion.
Secondary prevention is very important for PACS strokes otherwise patient could have a TACS
Investigations into a suspected cerebral infarction involve CT scan to exclude any haemorrhage yet infarct may not show in CT for a while so an MRI is commonly used, which can identify infarcted areas within a few minutes.
Thrombolytics should be given to those with acute ischaemic stroke who are eligible (e.g. thromboembolic stroke, >18 years old, symptoms not improving etc).
Long-term anti-hypertensives (in those with hypertension) and anti-platelets (e.g. aspirin) and anticoagulants to those with AF, should be given following stroke.
Rehabilitation will then be required via physiotherapy and speech therapy.
Describe a brainstem infarction
Complex signs are seen with brainstem infarctions, depending on CN nuclei, long tracts and brainstem connections involved. The ones of note are:
Lateral Medullary Syndrome (or Wallenberg’s Syndrome) is caused by occlusion of the posterior inferior cerebellar artery (PICA) and causes acute vertigo with cerebellar and other signs.
- Characterized by sensory deficits affecting the trunk and extremities on the opposite side of the infarction and sensory deficits affecting the face and cranial nerves on the same side with the infarct. Specifically, there is a loss of pain and temperature sensation o nthe contralateral (opposite) side of the body and ipsilateral (same) side of the face.
Locked-in syndrome is caused by an upper brainstem infarction.
Describe Vascular Dementia
Multiple large infarcts can cause generalised intellectual loss seen with advanced cerebrovascular disease.
Condition progressed with each infarct with eventual dementia, pseudobulbar palsy (the inability to control facial muscles including the tongue, may manifest as: dysarthia, dysphagia, dysphonia and emotional lability) and shuffling gait
Describe an intracerebral haemorrhage
Intracerebral haemorrhage causes around 10% of strokes and is commonly caused by the degeneration of small deep penetrating arteries (rupture of microaneurysms called Charcot-Bouchard aneurysms), commonly leading to a massive bleed.
They are often caused by chronic hypertension and occur at well-defined sites (basal ganglia, pons, cerebellum and subcortical white matter).
In normotensive patients, normally a lobar intracranial haemorrhage will occur.
Intracerebral haemorrhage and cerebral infarctions are very hard to distinguish as both will cause a stroke, however intracerebral haemorrhage tends to be “dramatic with a severe headache”. Initially they can be detected on a CT scan, yet after a few hours, a MRI scan is more effective.
A haemorrhagic stroke may require neurosurgery to remove any clot, along with any anti-hypertensive therapy for the long-term management; anti-platelets and anti-coagulants are contraindicated. The prognosis is usually poor.
The main prevention of reoccurrence for strokes comes from anticoagulants, targeting the risk factors (i.e. treating hypertension, hypercholesterolaemia, and diabetes), changing the lifestyle and medication compliance.
Describe the blood supply to the spinal cord
The blood supply to the spinal cord comes from the anterior spinal artery, supplying the anterior 2/3rds of the spinal cord, and the paired posterior spinal cord arteries, supplying the posterior columns; the artery of Adamkiewicz starts in the thoracolumbar region and supplies the anterior spinal artery.
- 21 pairs of segmental arteries
The central area supplied by the anterior spinal artery is predominantly a motor area
The aetiologies to these conditions can be intrinsic spinal vessel disease (caused by arteritis, SLE or atherosclerosis), aortic disease (such as dissection or surgery), decompression sickness, tumours (compressing on the spinal cord), or prolonged hypertension.
Describe the decorticate and decerebrate responses
Decorticate response: severe injury to the head or following a large infarct can destroy the connections between thalamus and cortex, and effectively isolates the cortex from the lower brain and spinal cord. In this situation, the lower limbs become extended and the upper limbs become flexed, known as the decorticate response.
Decerebrate response: if damage occurs to the lower parts of the brain or brainstem, there is complete loss to descending inhibition on the descending motor tracts. The result extension of lower and upper limbs, as well as to the head, known as the decerebrate response.
Describe a Subarachnoid haemorrhage
Spontaneous arterial bleeding into the subarachnoid space, recognised clinically by a rapidly onsetting severe headache (commonly occipital), commonly known as a “thunderclap headache”. Other clinical features include vomiting and coma, as well as potential neck stiffness.
Main causes are saccular (berry) aneurysms and arteriovenous malformations.
- Berry aneurysms develop on the circle of Willis and adjacent arteries, causing symptoms by rupture or compression on surrounding structures.
- Arteriovenous malformations are collection of arteries and veins of developmental origin. Other rarer associations are found with collagen disorders (e.g. Marfan’s or Ehlers-Danloas syndrome) or polycystic kidney disease.
CT imaging will show intraventricular or subarachnoid blood. The main differential diagnosis to exclude is severe migraine, yet bacterial meningitis should also be considered.
A complication for SAHs is communicating hydrocephalus as the SAH occludes CSF reabsorption; this may be asymptomatic but can cause deterioration of consciousness after SAH. Management involves immediate bed-rest and supportive treatment and referral to specialist neurosurgery. Prognosis is poor.
Describe a subdural haematoma
The accumulation of venous blood in the subdural space following the rupture of a bridging vein, normally following a head injury yet a spontaneous SDH is common in the elderly and alcoholics (from atrophy of neural tissue).
Commonly present with initial trauma and potential temporary loss of consciousness before slow deterioration. Common clinical features are headache, drowsiness and confusion, as well as focal deficits such as hemiparesis and sensory loss. Stupor and coma may subsequently develop.
Management requires immediate imaging (where they show a lentiform-shaped appearance) and then referred for urgent neurosurgery, yet even large subdural haematomas can resolve naturally.
Describe an Extradural haematoma
Extradural or epidural haematomas is accumulation of blood rapidly outside the dura, commonly following damage to the anterior branch of the middle meningeal artery following trauma to the temporal region with subsequent fracture to the pterion.
The most characteristic clinical picture is of a patient who loses consciousness, followed by lucid interval of recovery, before developing a progressive hemiparesis and stupor, rapid tentorial or tonsillar herniation, and ipsilateral pupil dilation.
Eventual bilateral fixed pupil dilation, tetraplegia and respiratory arrest will then occur.
Imaging should be done urgently, with CT scan showing a “lemon-shaped” bleed. Management involves urgent neurosurgery to drain the blood and relieve the compression of the brain (which if performed early enough, has a very good prognosis).
How could raised intracranial pressure lead to herniation of the brain?
Raised intracranial pressure is a common outcome of severe cerebral pathology. Increasing pressure within the closed box of the skull (normal contents: brain, blood and CSF; abnormal contents: haematoma, tumour) results in the compression of the brain and herniation of key parts of the brain.
Three areas are involved: the cingulate gyrus, the uncus and the cerebellar tonsils.
Damage to these structures and compression of adjacent brain tissue and vessels lead to distinct clinical signs.
Compensation
- Blood squeezed out initially
- CSF squeezed out
- Brain squeezed out through the foramen magnum, compressing the brainstem => brainstem death
- Brain is squeezed out through Tentorial herniation and Uncal herniation (through foramen magnum) if pressure keeps increasing
What pathologies could lead to raised intracranial pressure?
Many cranial pathologies can lead to raised pressure. These include haemorrhage and tumours as well as less obviously expanding lesions such a meningitis or cerebral infarction.
Brain
- Head injury
- Infection – meningitis/encephalitis
Blood
- Coughing
- Impaired venous drainage => impaired CSF drainage, e.g. due to constriction around neck e.g. in strangulation or tumours around neck area
CSF:
- Subarachnoid blood (usually due to rupture of congenital aneurysm)
Haematoma (extra volume in rigid skull)
- Trauma: extradural, subdural, intra-cerebral
- Haemorrhagic stroke
Tumour: primary/secondary (normally symptoms are gradual and progressive, don’t normally present acute until there is sudden haemorrhage into tumour)
What are the possible complications if a patient survives the raised ICP?
Head injury is common and results in the brain being shaken inside the skull. This causes direct injury to the brain, resulting in two pathologies (diffuse axonal injury or bleeding) resulting in oedema or haemorrhage due to rupture of arteries or veins producing extradural, subdural or subarachnoid haematoma.
If the patient survives the initial raised intracranial pressure produced by a head injury, he may be at risk of neurological deficit, infection, epilepsy or chronically raised pressure if the circulation of CSF has been impaired by scarring.
How do you tell if a brain injury is serious?
Mechanism of injury
Signs of brain injury
- Changes in consciousness
- Focal neurology
- Pattern of change
- Primary v Secondary injury
- Secondary Brain Injury
- Cannot change primary injury
- Secondary injury
- Hypoxia
- Hypotension
- Blood clot causing raised ICP
Need to spot secondary injury early and stop it
What is meant by a Coup and a Contracoup injury?
Head injuries can occur due to many reasons such as vehicular accidents cycling and horse-riding.
Injury:
- Coup Injury: the result of a sudden, violent stop that causes the brain to accelerate forward and hit the side of the skull. It will present a contusion at the site of impact.
- A contracoup injury, on the other hand, occurs when the brain accelerates forward, hits the side of the skull and then bounces off the other side of the skull. It will present a contusion on the opposite site of impact
In both cases, the brain is damaged as it rubs against the inner ridges of the skull.
A brain that undergoes a particularly violent and sudden impact can experience a coup and contracoup injury simultaneously.
What is the significance of traction of axons? What could a primary insult cause? What could a secondary insult cause?
Increased traction of axons during injury => increased risk of damage. The more axonal injury, the more severe clinical signs.
Primary Insult: (doctors have no control over) can cause haematoma, contusions, haemorrhage and/or diffuse axonal injury (worse end of spectrum).
Secondary Insult: (doctors can have a bigger impact on) can cause hypoxia, hypoperfusion, oedema and raised intracranial pressure.
Differentiate between Cytotoxic and Vasogenic Cerebral Oedema
Cytotoxic cerebral oedema, most commonly seen in cerebral ischaemia, in which extracellular water passes into cell as the cells are unable to maintain ATP dependent sodium (Na+/K+) membrane pumps. The BBB is not compromised and endothelial dysfunction nor changes in capillary permeability are involved. It is an intracellular type of oedema.
Vasogenic cerebral oedema is an extracellular type of cerebral oedema- the BBB is disrupted and there is leakage of fluid out of capillaries. It is most frequently seen around brain tumorus and cerebral abscesses, although some vasogenic oedema may be seen around maturing cerebral contusion and cerebral haemorrhage.
NB: In surgery and anaesthesia, intubation may be required if GCS<9 (if not able to protect airway safely).
What is the Monro-Kellie Hypothesis?
Pressure volume relationship
Skull is a rigid box of fixed volume. Contains 3 components (blood, CSF and brain) with varying ability to alter their volume to maintain constant pressure (blood and CSF can compensate up to a point)
Compensated state: ICP normal (lower blood and CSF to accommodate for oedema)
But compensation only up to a point – increased ICP beyong that rapidly leads to decompensation and risk of herniation
How would you calculate cerebral perfusion pressure? How does cerebral autoregulation attempt to solve hypoxia?
Cerebral Perfusion Pressure = Mean Arterial Pressure – Intra-Cranial Pressure
*Interstitial osmotic pressure = ICP in this case
Cerebral Metabolic Requirement for oxygen
- Resting oxygen consumption of the brain is 50ml/min (i.e. 20% of total body oxygen requirements)
- Global blood flow is 50ml/100g brain.min
Cerebral autoregulation:
Hypoxia => vasodilation (attempt to increase perfusion) => increased ICP => decreased cerebral perfusion pressure
What is meant by the higher centres of the brain?
Higher functions of the brain: learning, memory, emotion, behaviour, awareness, consciousness.
Although certain areas crucial to these activities can be identified, proper function depends upon the brain acting as whole. Failure to perform as a unified whole gives rise to problems that may involve intellectual ability, behaviour and the ability to cope with everyday tasks. Such malfunctions may impact upon family members and work colleagues rather than presenting with symptoms and physical signs.
Some of the important structures and regions of the brain which give rise to complex behaviours include the Cortical Association Areas, the Limbic System and the Reticular Activating Regions of the Brainstem.
These higher functions such as emotion, memory, learning and consciousness involve a diversity of interconnected regions of the cerebral cortex and the subcortical structures of the limbic system. These are connected by way of the hypothalamus to the autonomic and endocrine systems through which many emotion states are manifested physically e.g. pallor and sweating in anxiety.
