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ALL YOU NEED
TO KNOW ABOUT
STROKES AND CT
HEAD
INTERPRETATION
MRama Aubeeluckeen
Reviewed by Dr Rajiv Ark Here’s what we do:
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Things! upcoming events via email and
groupchats!https://app.medall.org/c/teaching-thingsStrokes
Mohammed BinyameenContents
- Stroke Vs TIA
- Presentation + RFs
- Function and blood supply of the brain, brainstem +
cerebellum
- Different types of stroke based on location
- Treatment
- Other differentials to considerPoll - How much neurology has
everyone covered?SBA
A 68-year-old man presents with sudden-onset right-sided weakness and
slurred speech that resolved completely within 30 minutes. CT head is
unremarkable. What is the most appropriate diagnosis?
● A) Ischemic stroke
● B) Transient ischemic attack (TIA)
● C) Hemorrhagic stroke
● D) Seizure with Todd’s paresis
● E) Migraine with auraSBAS
A 68-year-old man presents with sudden-onset right-sided weakness and
slurred speech that resolved completely within 30 minutes. CT head is
unremarkable. What is the most appropriate diagnosis?
● A) Ischemic stroke
● B) Transient ischemic attack (TIA)
● C) Hemorrhagic stroke
● D) Seizure with Todd’s paresis
● E) Migraine with aura
Answer: B) Transient ischemic attack (TIA)Stroke Vs T ransient Ischaemic
Attack
Lack of blood flow = ischaemia Stroke types:
- Haemorrhage (15%) - SAH / / Thrombus
Prolonged ischaemia = Necrosis + infarction Intracerebral haemorrhage
Stroke - Ischaemia with infarction
TIA - Ischaemia without infarctionPresentation
Features:
- Unilateral weakness/sensory loss
- Aphasia/Dysarthria
- Vertigo/Ataxia
- Visual problems
- Swallowing problems
Assessment tools:
- FAST
- ROSIERRisk factors
RFs for ischaemic stroke: RFs for haemorrhagic stroke:
- Age - Age
- Hypertension - Hypertension
- Smoking - AVMs
- Hyperlipidaemia - Anticoagulation
- Diabetes - Underlying conditions (ADPKD)
- Atrial fibrillation
- Think all the general CVD risk
factorsFunction of different lobes
Lobe Major functions
Frontal Behaviour, Executive
function, Movement
Parietal Sensation, Vision,
Reading, Language
Temporal Vision, Speech,
Memory, Hearing
Occipital VisionBlood supply of the brain
Blood supply for cerebral cortex:
- Internal carotid artery -> Anterior cerebral
+ Middle cerebral
- Vertebral artery -> Basilar artery ->
Posterior cerebralHomunculus of the PMC
In an ACA stroke the leg weakness
would be more pronounced than in
a MCA strokeStroke symptoms by artery
ACA: Lacunar strokes:
- Contralateral leg weakness/sensory loss - Pure motor loss
- Pure sensory loss
MCA: - Ataxic hemiparesis
- Contralateral arm + face weakness/sensory
loss
- Aphasia (dominant, usually LHS)
- Hemispatial neglect (non-dominant)
- Contralateral homonymous hemianopia
PCA:
- Contralateral homonymous hemianopia
with macular sparing
- Visual processing difficulties (e.g. agnosia)
Learn the Bamford/Oxford stroke classificationHomonymous hemianopia with Homonymous hemianopia without
macular sparing macular sparingSBA
A 60-year-old man presents with sudden-onset weakness predominantly in his
right leg and mild slowness of speech. He denies facial weakness or significant
arm involvement. Examination reveals increased tone and brisk reflexes in the
right lower limb. Which artery is most likely affected?
● A) Middle cerebral artery
● B) Anterior cerebral artery
● C) Posterior cerebral artery
● D) Basilar artery
● E) Vertebral arterySBA
A 60-year-old man presents with sudden-onset weakness predominantly in his
right leg and mild slowness of speech. He denies facial weakness or significant
arm involvement. Examination reveals increased tone and brisk reflexes in the
right lower limb. Which artery is most likely affected?
● A) Middle cerebral artery
● B) Anterior cerebral artery
● C) Posterior cerebral artery
● D) Basilar artery
● E) Vertebral artery
Answer: B) Anterior cerebral arteryBrainstem anatomy + Blood supplyCranial nerve recap
Not going to go through these
but will leave it here as it'll
help with the next partBrainstem strokes
Weber’s syndrome (blockage of the PCA that supplies the midbrain):
- Ipsilateral CNIII palsy (dilated, down + out pupil, ptosis)
- Contralateral weakness of upper and lower limbs
Lateral pontine syndrome (blockage of the AICA):
- Facial nerve palsy + hearing loss (CN 5 and 8)
- Ataxia + nystagmus (cerebellar damage)
- CL body and IL face anaesthesia (spinothalamic damage)
- IL Horner’s (sympathetic damage)
Lateral medullary/Wallenberg syndrome (blockage of the PICA):
- Dysphagia (CN 9/10)
- Ataxia + nystagmus (cerebellar damage)
- CL body and IL face anaesthesia (spinothalamic damage)
- IL Horner’s (sympathetic damage)SBA
A 55-year-old man presents with sudden onset of right-sided weakness and
diplopia. Examination reveals right-sided hemiparesis and left-sided ptosis, with
the eye deviated down and out. Which artery is most likely affected?
● A) Posterior cerebral artery
● B) Middle cerebral artery
● C) Basilar artery
● D) Superior cerebellar artery
● E) Anterior inferior cerebellar arterySBA
A 55-year-old man presents with sudden onset of right-sided weakness and
diplopia. Examination reveals right-sided hemiparesis and left-sided ptosis, with
the eye deviated down and out. Which artery is most likely affected?
● A) Posterior cerebral artery
● B) Middle cerebral artery
● C) Basilar artery
● D) Superior cerebellar artery
● E) Anterior inferior cerebellar artery
Answer: A) Posterior cerebral arteryCerebellar strokes
Think DANISH
- Dysdiadochokinesia
- Ataxia
- Nystagmus
- Intention tremor
- Scanning speech (Slow speech)
- HypotoniaAphasias
Broca’s aphasia (MCA) - Preserved
comprehension but cannot articulate the
words.
Wernicke’s aphasia (MCA) - Fluent
language with nonsensical speech
Conduction aphasia - Normal fluency and
comprehension. Cannot repeat things backInvestigation and managementIs it a haemorrhage or ischaemia?
First line Ix = Non-contrast CT head. Covered in more detail laterManagement of TIA
- Refer to stroke specialist - 24 hour referral if TIA within last 7 days. 7 day
referral otherwise
- Antiplatelets - Aspirin 300mg immediately followed by 75mg OD for 21
days. Clopidogrel started by specialist (300mg loading dose followed by
75mg OD indefinitely)
- Control CVD RFs - Check BP, lipids, HbA1c and provide diet/exercise advice
- Imaging - May be done by stroke specialist (usually MRI). May also docarotid
US if required. Consider CT head if patient is on anticoagulantsT reatment for ischaemic stroke
Initial management:
- ABCDE - Make sure they are stable and not hypoxic
- Maintain normal blood glucose, oxygen, temperature, hydration, etc.
- Screen for unsafe swallow
- Blood pressure - Do not aim for normotensive (CPP = MAP - ICP). Should be
less than 185/110
- CT head within 1 hour
Ischaemic stroke specific management - depends on time of presentation:
- If within 4.5 hours can offer thrombolysis AND thrombectomy
- If between 4.5 and 24 hours can offer thrombectomy alone if potential to
salvage brain tissue
- If presented after 24 hours offer just antiplatelets
Antiplatelets - Aspirin 300mg for 14 days followed by Clopidogrel 75mg
indefinitelyThrombolysis vs thrombectomy
Alteplase = Tissue plasminogen activator.
Plasmin causes breakdown of clot by
degrading fibrinSBA
A 70-year-old woman presents to the Emergency Department with
sudden-onset right-sided weakness and slurred speech. Symptoms began 2
hours ago. CT head shows no evidence of hemorrhage and she is clinically
stable. She has been given 300mg Aspirin in the community. What is the most
appropriate next step in management?
● A) IV thrombolysis with alteplase
● B) IV thrombolysis with alteplase and mechanical thrombectomy
● C) Mechanical thrombectomy
● D) Clopidogrel 75 mg orally
● E) IV mannitolSBA
A 70-year-old woman presents to the Emergency Department with
sudden-onset right-sided weakness and slurred speech. Symptoms began 2
hours ago. CT head shows no evidence of hemorrhage and she is clinically
stable. She has been given 300mg Aspirin in the community. What is the most
appropriate next step in management?
● A) IV thrombolysis with alteplase
● B) IV thrombolysis with alteplase and mechanical thrombectomy
● C) Mechanical thrombectomy
● D) Clopidogrel 75 mg orally
● E) IV mannitol
Answer: B) IV thrombolysis with alteplase and mechanical thrombectomyT reatment of haemorrhagic stroke
Initial management = Same as before
Haemorrhagic stroke specific management:
- Urgent neurosurgical referral
- Reversal of any anticoagulation
- Lower BP to below 140 systolicOther differentials to think of
Transient ischaemic attack - Resolves usually within an hour
Todd's paresis - Preceding seizure + Resolves within a few hours
Migraine with aura - Usually resolve completely + Previous history of migraines
Bell’s palsy - No forehead sparing + Sx confined to one side of face
Multiple sclerosis - Symptoms disseminated in time and space + Younger
patient + History of optic neuritis
Neuropathies - Follows distribution of peripheral nerve + Lack of central
symptoms such as dysphagia Imaging
interpretation
Rama AubeeluckHow confident are you about
interpreting neurological imaging?
● Practically a neuroradiologist
● I can do spot diagnosestructure but I’m unsure on a few things
● I know nothing
● I am not sureRapid fire spot diagnosis!Spot diagnosis 1
1. Subdural haematoma
2. Brain cancer
3. HSV encephalitis
4. Extradural haematoma
5. Multiple sclerosisSpot diagnosis 1
1. Subdural haematoma
2. Brain cancer
3. HSV encephalitis
4. Extradural haematoma
5. Multiple sclerosis
● Right sided
● Biconvex (bulging outwards)
● Limited by suture linesSpot diagnosis 2
1. HSV encephalitis
2. Brain cancer: gliobastoma
multiforme
3. Subdural haematoma
4. Brain cancer: meningioma
5. Multiple sclerosisSpot diagnosis 2
1. HSV encephalitis
2. Brain cancer: gliobastoma
multiforme
3. Subdural haematoma
4. Brain cancer: meningioma
5. Multiple sclerosis
● Left sided
● In fronto temporal region
● Surrounding oedemaSpot diagnosis 3
1. Multiple sclerosis
2. Chronic subdural haematoma
3. HSV encephalitis
4. Acute subdural haematoma
5. Brain cancer: meningiomaSpot diagnosis 3
1. Multiple sclerosis
2. Chronic subdural haematoma
3. HSV encephalitis
4. Acute subdural haematoma
5. Brain cancer: meningioma
● Left sided
● Hyperdense crescent shaped
bleed
● Not limited by suture linesSpot diagnosis 4
1. Multiple sclerosis
2. Subarachnoid haemorrage
3. Meningioma (brain cancer)
4. HSV encephalitis
5. Chronic subdural haematomaSpot diagnosis 4
1. Multiple sclerosis
2. Subarachnoid haemorrage
3. Meningioma (brain cancer)
4. HSV encephalitis
5. Chronic subdural haematoma
● Hyperattenuation of
supracellar and sylvian cisterns
● Not the starfish signSpot diagnosis 5
1. Motor neurone disease
2. Acute subdural haematoma
3. Guillan-Barre syndrome
4. Multiple sclerosis
5. Chronic subdural haematomaSpot diagnosis 5
1. Motor neurone disease
2. Acute subdural haematoma
3. Guillan-Barre syndrome
4. Multiple sclerosis
5. Chronic subdural haematoma
● Left sided
● Hypodense crescent shaped
bleed
● Not limited by suture linesSpot diagnosis 6 (MRI)
1. Chronic subdural haematoma
2. HSV encephalitis
3. Temporal arteritis
4. Broca’s aphasia
5. Motor neurone diseaseSpot diagnosis 6 (MRI)
1. Chronic subdural haematoma
2. HSV encephalitis
3. Temporal arteritis
4. Broca’s aphasia
5. Motor neurone disease
● Right sided frontotemporal
discharges
● Concurrent with HSV
encephalitis if presentHow does a CT scan work?
Any ideas?CT scan: how it works?
● CT = Computed tomography
● Tomography = Imaging technique allowing you to take cross-sectional
images (slices) of the body
● CT head = Imaging technique using multiple X-rays to take multiple images
of the head
● Hounsfield Units: Some tissues allow X-rays to pass through them (lots of
penetration), whereas others have a poor penetration - so X-rays cannot
pass through them
● The brightness in an X-ray or CT image depends on how many X-rays hit the
detector!● Denser materials e.g. bone absorb MORE x-rays, so LESS x-rays pass
to the detector
● Imaging software assigns high absorption to bright pixels
● The detector "sees" less signal in those regions -> a brighter
appearanceAnatomy basicsAnatomy basics: the skullAnatomy basics: middle meningeal
artery
● Branch of the maxillary artery
● dura materion is to supply the
● Passes behind the pterion bone,
which is relatively thin, and is
more likely to be fractured in
traumatic injuries
● This can lead to extradural
haematomasAnatomy basics: layers of the scalpAnatomy basics: dural layersAnatomy basics: bridging veins
● Bridge the subarachnoid space to the
dura mater
● Help cool the brain and form an
alternative drainage route of the brain in
the case of obstruction of dural venous
sinuses
● Rupture of these causes subdural
haematomasAnatomy basics: the subarachnoid
space
● The arachnoid granulations /villi
are outpouchings of the
arachnoid mater
● These go into the subarachnoid
● CSF is drained here and goes into
the venous systemAnatomy
basics: brain
lobes and
thalamusAnatomy basics: ventricle system
● Produce CSF
● 4 ventricles: right and left lateral
ventricles (counts as 2), third
ventricle and fourth ventricle
● Lateral: have horns which project
into the frontal, occipital and
temporal lobes. Most visible on a
CT headAnatomy basics: ventricle system
● Third: Connects to lateral via foramen
of Monro. Situated in between the right
and the left thalamus
● Fourth: Connects to 3rd via cerebral
aqueduct, and lies within the
brainstem. Drains into the spinal cord
and subarachnoid cisterns (where it is
reabsorbed into the circulation)Anatomy basics - putting it togetherCT head interpretation
Why is a structured approach important?
First step: confirm patient details, compare to any previous images
Call out any obvious diagnosis you can see
Mnemonic - Blood Can Be Very Bad
● Blood: bleeding
● Can: cisterns
● Be: brain
● Very: ventricles
● Bad: boneBlood - 4 main bleeds to think about
On a CT head, bleeding appears as areas of increased
density (hyperattenuation) compared to the
surrounding brain tissue due to the higher
concentration of hemoglobin in blood.
● Acute bleeding (within hours): Appears bright
white because fresh blood has a high Hounsfield
Unit (HU).
● Chronic bleeding (after days to weeks): Becomes
darker (hypodense) as the blood is broken down
and reabsorbed, blending with the surrounding
brain tissue.What are some symptoms of raised
intracranial pressure?
List in the chat !Symptoms of raised intracranial
pressure
Common to anything increasing pressure in the brain: bleeding, infection
causing inflammation, tumours, hydrocephalus etc.
● Cushing's response (decreased HR , increased BP)
● Headache (worse on coughing, leaning forwards), vomiting
● Altered GCS: drowsiness, listlessness, irritability, coma
● Pupil constriction then dilation
● Decreased visual acuityExtradural haematoma
● Between the dura mater and
the skull
● Dura is tightly adhered to the
inner surface of the skull,
and this attachment is
particularly strong at the
suture lines.
● Blood in this space cannot
cross suture lines because
the dura is fixed at these
boundaries
● The haematoma therefore
takes on a lens-shaped or
biconvex appearance on
imaging
● Extra-axial (outside the
brain)Blood - extradural haematoma
● Cause: trauma - affects the middle meningial
artery
● Pathophysiology: blood collects between the
skull and dura (“extra-axial”)
● Clinical features: patient initially loses, briefly
regains (lucid interval) and then loses again
consciousness after a low-impact head injury.
Plus general raised ICP symptoms
● CT head findings: biconvex (or lentiform),
hyperdense collection around the surface of
the brain, limited by the suture lines of the
skull
● Definitive management: craniotomy and
evacuation of the haematomaSubdural haematoma
● Between the dura mater
and the arachnoid mater
● These layers are
continuous across the
skull, so blood can spread
freely over the brain's
surface, crossing suture
lines.
● Extra-axialBlood - subdural haematoma
● Cause: Low impact head injury
● Pathophysiology: blood collects between the dura
and arachnoid layer - can be chronic
(hypoattenuated)) or acute (hyperattenuated)
● Risk factors: Old age and alcohol make the bridging
veins weaker
● Clinical features: Fluctuating level of consciousness
(seen in 35%) ± insidious physical or intellectual
slowing, sleepiness, headache, personality change,
and unsteadiness. Plus general raised ICP symptoms.
● CT head findings: Hyper/hypo dense crescentic
collection, not limited by suture lines. Large bleeds
can shift the brain and cause midline shift or
herniation.
● Definitive management: If severe, craniotomy or burr
hole washoutBlood - subarachnoid haemorrhage
Acute blood
(hyperdense/bright on
CT) is typically
distributed in the basal
cisterns, sulci and in
severe cases the
ventricular system Blood - subarachnoid haemorrhage
● Cause: Traumatic injury most common cause. If no trauma, consider
spontaneous SAH, where berry aneurysms are the most common cause
(think ADPKD, Ehlers-Danlos, coaraction of the aorta)
● Pathophysiology: Bleeding in to the subarachnoid space, where CSF is
located, between the pia mater and the arachnoid membrane
● Clinical features: Thunderclap headache at the back of the head,
meningism, N/V
● CT Head findings: Acute blood (hyperdense/bright on CT) is typically
distributed in the basal cisterns, sulci and in severe cases the
ventricular system. Negative in 7% case.
● Definitive management: Treat underlying cause e.g. if aneurysm
suspected, consider clipping or coiling
● Complications: Re-bleeding, vasospasm (ischaemia), hyponatraemia,
seizures Blood
Other places of bleeding can be intracerebral (within the brain tissue - left
image), and intraventricular (within the ventricles themselves)Blood
Strokes
● Hypodensity (darker)
● Loss of grey white differentiationCisterns
Anatomy basics
● Recall from earlier the subarachnoid space (between the arachnoid layer
and the pia)
● Cisterns refer to any of the openings in the subarachnoid space of the
brain filled with CSF
● CSF is made in the choiroid plexus in the ventricles (lateral, third, fourth)
● CSF flows through the ventricles, and passes into the subarachnoid
space through different apertures
● This allows CSF to enter the different cisterns within the subarachnoid
spaceCisterns Cisterns
Key cisterns to assess for effacement, blood
and asymmetry:
● Ambient: surrounding the midbrain
● Suprasellar: superior to the sella turcica
(where the pituitary gland sits)
● Sylvian: across the insular surface and
within the Sylvian fissure (lateral side)
● corpora quadrigeminal: adjacent to the
By examining these cisterns on a CT head, you can
detect signs of subarachnoid haemorrhage, mass
effect, or hydrocephalus.Brain - any pathologies in the brain
tissue itself?
Things to look out for
● Midline shift - has the brain been pushed toward one side?
● Sulcal effacement (thinning)
● Grey-white matter differentiation: poor differentiation suggests hypoxia,
infarction, tumours or abscesses
● Any abnormal shifts in the brain tissue
● Masses - suggestive of tumours
● Hypodense foci: less dense, so think air (pneumocephalus) or fluid (oedema)
● Hyperdense foci: more dense, so thinkBrain - midline shift
● Subdural haematoma
● sidees the brain to the leftBrain - sulcal effacement
Not a diagnosis in
itself
Causes:
● Oedema
● Space occupying
lesions
● Hydrocephalus
● Bleeds
● InfectionsHow do I comment on a mass /
bleed / pathology?
Think about
● What side is the pathology on?
● Is there a specific anatomical landmark the pathology is predominantly
covering e.g. a lobe or ventricle?
● Is the pathology hyperdense or hypodense?
E.g. for the glioblastoma multiforme “I can see a mass in the left hemisphere,
predominantly in the front-temporal region. There is an area of hypeodensity
glioblastoma multiforme”.e of oedema. These findings are suggestive of aBrain - tumours
Meningioma has oedema around itrme - classicallyWhat is the most common cause of
brain cancer?
1. Glioblastoma multiforme
3. Metastases
4. Vestibular Schwannoma
5. Pilocytic astrocytomaWhat is the most common cause of
brain cancer?
1. Glioblastoma multiforme - most common primary tumour in adults
3. Metastases - most common overallprimary tumour in adults
4. Vestibular Schwannoma
5. Pilocytic astrocytoma - most common primary tumour in childrenBrain - tumours
form of brain cancerost common
MeningiomaVentricles - normally the lateral componentVentricles
Pathologies to look out for
● Bleeds
● Hydrocephalus: excess CSF in the ventricular wall space - normal pressure,
obstructive, non-obstructive
● Calcification: The choroid plexus produces CSF and exists within all
ventricles - this can become calcified in older individuals and is normal - do
not mistake this for a bleed!Ventricles
● Clear hyperattenuation in
● More so on the left sideVentricles
Normal pressure hydrocephalus
● Cause: secondary to reduced
absorption at arachnoid villi
● Clinical features: incontinence,
confusion, and gait disturbance (“wet,
wacky, wobbly”
● CT head findings: Hydrocephalus with
ventriculomegaly in the absence of, or
out of proportion to, sulcal enlargement
● Management: VP shuntingVentriclesBone
Can you identify any bony
abnormalities?
In a medical school exam this is
unlikely to be a pathology they’d test
you on: “I cannot see any bony
pathologies”Category Condition Imaging findings
Bleeds/Stroke Extradural haematoma (CT) Biconvex / lens-shaped hyperdensity; does
not cross sutures. May have midline shifting List of conditions
Subdural haematoma (CT) Crescent-shaped hyperdensity; can cross
sutures. May have midline shifting to learn
Subarachnoid haemorrhage Hyperdensity in the basal cisterns, Sylvian
(CT) fissures, or sulci
Intracerebral haemorrhage Localised hyperdensity within the brain
(CT) parenchyma
Ischaemic stroke (CT) Loss of grey-white differentiation,
hypodensity in vascular territory
Intracranial venous Dense dural sinus (clot), empty delta sign
thrombosis (MRI)
Infections HSV encephalitis (MRI) Hyperintensity in the fronto-temporal lobes
Cancer Glioblastoma multiforme Irregular rim-enhancing lesion with
(MRI) surrounding oedema
Meningioma (CT/MRI) Extra-axial, well-defined, enhancing lesion;
often with dural tail
Metastases (MRI) Multiple enhancing lesions with oedema
Ventricles Hydrocephalus (CT) Enlarged ventricles; possible periventricular
hypodensity (CSF leakage)
Autoimmune Multiple sclerosis (MRI) Hyperintense white matter plaques, often
periventricular (Dawson’s fingers)T est yourself!
Leandro Trossard, a 44 year old male,
presents with a severe headache. He
has a PMH of ADPKD.
In 5 minutes, please:
● Present this CT head
● Give your most likely diagnosis
● Propose a management plan for
this patient Example answer
This is a non-contrast CT head for a 54-year-old male presenting with a sudden onset severe headache
Bleeding: There is diffuse subarachnoid haemorrhage (SAH) visualised in the basal cisterns, bilateral Sylvian fissures, and
inter-hemispheric fissure.
Cisterns: All basal cisterns are hyperdense due to the presence of blood.
Brain: There is no evidence of midline shift, infarction, or mass effect. No focal parenchymal abnormalities.
Ventricles: The ventricular system appears normal in size, with no signs of hydrocephalus or calcification
Bone: No bony abnormalities identified.
The most likely diagnosis given the findings suggest a diffuse subarachnoid haemorrhage likely due to a ruptured intracranial
aneurysm given the medical history of ADPKD
Management Plan
1. Stabilise: A2E approach, monitor and control BP to prevent rebleeding
2. Neurological Support: Admit to a high-dependency unit (HDU) or intensive care unit (ICU), monitor for signs of raised
intracranial pressure (ICP) and neurological deterioration.
3. Imaging and Intervention: Urgent CT angiogram to identify bleeding source, discuss with neurosurgery for considerationof
surgical clipping or coiling.
4. Complication Prevention: Administer nimodipine to reduce the risk of vasospasm, monitor for and manage complications
such as seizures, hydrocephalus, and rebleeding. Resources I found helpful
1. https://geekymedics.com/ct-hea
d-interpretation/
2. Radiopaedia for understanding
pathologies
3. Running through OSCE cases
where I have to present a CT
head THANKS
FOR
W ATCHING!
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on Medall and see you next week!References