Neurosurgery JC030: Headache And Loss Of Consciousness: Acute Stroke, Subarachnoid Haemorrhage And Vascular Malformation

Question 1

Causes of headache

Answer 1

1. ***TMJ disease
2. Sinus disease
3. Cluster headchae
4. Tension headache
5. Cervical spine pathology
6. Migraine
7. ***↑ ICP (concern of neurosurgery)

Question 2

Consciousness

Answer 2

2 components:
1. Brainstem reticular activating system —> provide **Arousal (keep cortex awake)
2. Cerebral cortex —> provide **Awareness

LOC = Failure of either / both
- A gradation
- when GCS <=8 —> Coma
—> Unarousable
—> **Cannot protect airway
—> **Inadequate breathing

Question 3

Common causes of Coma

Answer 3

Intracranial
- **Vascular
- Trauma
- **Tumour
- ***Hydrocephalus
- Infection / Inflammation

Extracranial
- **Cardiac insufficiency
- **Respiratory insufficiency
- Metabolic
- Drug, Toxins

A sudden onset of **headache + **deterioration in consciousness is a ***Cerebrovascular event (唔係淨係指stroke) until proven otherwise

Question 4

Cerebrovascular events

Answer 4

• **Ischaemic / **Haemorrhagic
• Typically abrupt onset
• Severely disabling / fatal but potentially reversible
• Distinct types with different prognoses

Clinical features:
1. **Headache (∵ ↑ ICP / Meningeal irritation / Infarction)
2. **LOC (if brainstem / cortical failure)
3. ***Focal deficits (depending on location)

Question 5

***Types of Brain haemorrhages: Traumatic vs Spontaneous

Answer 5

Traumatic mostly:
- Epidural haemorrhage
- Subdural haemorrhage

Spontaneous mostly:
- Intraventricular haemorrhage (IVH)
- Deep intracerebral haemorrhage

Traumatic / Spontaneous:
- Subarachnoid haemorrhage (SAH)
- Lobar intracerebral haemorrhage

Question 6

1. Haemorrhagic Stroke (i.e. Intracerebral Haemorrhage)

Answer 6

• Often refers to ***Spontaneous Intraparenchymal haemorrhage (e.g. lenticulostriate arteries of MCA —> Basal ganglia)
• Primary destruction of brain tissue
• Haematoma causes ***↑ ICP —> affect other regions by compression
• ***Rebleeding occurs (aka Haemotoma expansion)

Causes:
1. **Systemic HT
2. **Cerebral amyloid angiopathy (common in elderly)
3. **Haemorrhagic transformation of infarction
4. **Bleeding tendency
5. Tumour bleeding
6. **AVM / Cavernoma
7. Venous sinus thrombosis
8. Moyamoya disease
9. Arterial dissection
10. **Vasculitis
11. ***Sympathomimetic abuse
Etc.

Question 7

***Treatment of Haemorrhagic Stroke

Answer 7

ABC + ICP control:
1. **Mannitol
2. Surgical decompression
- **CSF drainage
- **Clot evacuation
3. **NO role for steroids
4. **Tranexamic acid might help —> ↓ rate of haematoma expansion
5. **Reverse bleeding tendency (e.g. in Warfarin patients)
6. Principles of maintaining Cerebral perfusion (pressure + bloodflow) apply

Patient selection:
- Age
- Co-morbidities
- Location of haematoma
- Neurological status
- Etiology

**Clot evacuation:
- Craniotomy to take out clot
- Decompress brain, ↓ ICP, Life-saving but does **NOT affect primary injury
- Functional prognosis depends on location + extent of haemorrhage (usually poor)

Question 8

Haemorrhage location

Answer 8

Superficial lobes (Lobar / Subcortical haemorrhage)
1. Frontal lobe
2. Parietal lobe
3. Occipital lobe
4. Temporal lobe
- Involves superficial lobe
- Deep nuclei / brainstem may be compressed but **not primarily injured
- Commonly due to **HT, other pathology (e.g. **tumour, **bleeding tendency, **vasculitis, **AVM)
- Surgery has better outcome / prognosis (can operate to decompress brain) —> even may lose some functions (e.g. limb movements), usually recover well in terms of consciousness

Deep nuclei
1. Basal ganglion
2. Internal capsule
3. Thalamus
4. Intraventricular
5. Brainstem
- Damage usually **severe + Hard to reverse
- **Poor functional outcome / prognosis (tend not to treat)
- Managed conservatively unless young
- Commonly due to ***systemic HT

(Basal ganglion more prone to HT since less branching off from main artery —> sustain higher BP)

Question 9

2. Cerebellar haemorrhage

Answer 9

• ***Distinct entity
• **IVH + **Direct brainstem compression —> **Respiratory distress + **Obstructive hydrocephalus
• ***Rapidly fatal if large size
• ***Good prognosis if timely surgery (more dispensable than other regions of brain)

Treatment:
1. ***Evacuation of haematoma +/- Suboccipital craniectomy (SpC Revision)
Indications:
- Brainstem compression
- Obliteration of cistern
- Haematoma >3cm

2. ***External ventricular drainage (EVD)
   - Hydrocephalus
   - Small haematoma

Question 10

3. Acute ischaemic stroke

Answer 10

Causes:
1. **Cardioembolism
2. **Critical arterial stenosis (complicated by **hypotension) (Large + Small vessel disease)
3. **Arterial dissection

• Can be painful without ↑ ICP
• ***+/- LOC depending on location / extent
• Acute cell death + Loss of function —> cannot salvage
• Cells in ***penumbra potentially salvageable (∵ only ischaemic, injured / potentially injured) —> aim at timely **restoration of perfusion
• Act **FAST + Treat like **heart attack (2 million brain cells die every minute)
  —> Face drooping
  —> Arm weakness
  —> Speech difficulty
  —> Time to call 999

CBF:
- Ischaemic threshold ~20 ml/min/100g
- Infarction threshold ~10 ml/min/100g

Question 11

Management of Acute ischaemic stroke

Answer 11

1. **IV tPA thrombolysis
   - standard treatment (but not yet available 24/7 in HK)
   - converts plasminogen —> plasmin —> lyse clot in **small vessels
   - therapeutic window of **3-4.5 hours from **symptom onset (or ***last seen well time (SC teaching clinic)) (x admission) (UpToDate: if exact onset time unknown —> use last seen well time)
   - can completely reverse deficit (quite effective)
2. Acute Large Vessel Occlusion (LVO)
   - **Large vessel branch blocked by thrombus (e.g. circle of Willis, ICA, CCA) —> potential large infarction
   - Plain CT: appear **hyperdense elongated structure (thrombus)
   - Does **NOT respond well to IV tPA
   - Confirm LVO with urgent CT **angiography
   - Standard treatment: Endovascular mechanical thrombectomy (EMT) within ***6 hours of symptom onset
3. Established infarction (beyond 4.5 / 6 hour window)
   **Decompressive Craniectomy
   - large infarct can swell with mass effect + ↑ ICP
   —> maybe initially conscious but deteriorate in next 24-48 hours
   —> may die ∵ brainstem compression / brain herniation
   - dead brain does not respond well to medical therapy
   - surgical decompression saves lives but does **not reverse deficits
   - for young + fit patient
   - ethical issues

Question 12

Haemorrhagic Transformation: Complications of Ischaemic stroke

Answer 12

• Ischaemic brain has **disturbed BBB + **vascular reactivity
• Reperfusion of dead brain —> ***Haemorrhagic transformation (aka Reperfusion haemorrhage) —> worsens outcome
• Particularly delayed perfusion hence limit EMT within ***6 hours

Pathophysiology:
- preserved collateral perfusion (from adjacent vessels/territories)
- reperfusion of infarcted tissues which have weakened vessels (i.e. from extravasation or diapedesis)

However, reperfusion of penumbra —> ↓ risk of haemorrhagic transformation
- size of salvageable penumbra varies with collateral vascular supply
- routine CT / MRI cannot tell
- advanced imaging can delineate a “mismatch” between truly dead brain and salvageable penumbra tissue
- identify who may benefit from treatment >6 hours post-onset

Question 13

4. Subarachnoid haemorrhage (+ SpC Revision)

Answer 13

Causes:
1. **Trauma (commonest)
2. Spontaneous (i.e. Non-traumatic)
- **Saccular / Dissecting aneurysm
- “Mycotic” aneurysm (due to infection but not necessarily fungus, usually infective embolus lodged in distal artery —> forming aneurysm)
- ***Vascular malformation
- Cocaine

Risk factors:
1. Smoking
2. Hypertension (Haemodynamic stress)
3. Genetic predisposition
4. Connective tissue diseases

Clinical features:
- Amount of SAH varies (can be very minor (25-50%))
- High index of suspicion

If no history of trauma —> SAH is **aneurysmal until proven otherwise
- beware spontaneous SAH —> LOC —> fall and head injury
- need to ask patient headache **before / after LOC (before: SAH)

WFNS subarachnoid hemorrhage grading system:
- Grade 1: GCS 15, No neurological deficit
- Grade 2: GCS 13-14, No neurological deficit
- Grade 3: GCS 13-14, Have neurological deficit
- Grade 4: GCS 7-12, +/- neurological deficit
- Grade 5: GCS 3-6, +/- neurological deficit
—> Grade 1-3: Good prognosis —> Early surgery
—> Grade 4-5: Poor prognosis —> Control ICP by CSF drainage

Question 14

Cerebral aneurysm

Answer 14

• Outpouches of arterial tree in brain
• Commonly in ***Circle of Willis
  —> AComA
  —> ICA
  —> PComA
  —> MCA

Predisposing factors:
- **Smoking
- **HT
- **Age >40
- Family history
- Female
- **Connective tissue disease: Ehlers-Danlos syndrome, ***AD polycystic kidney disease, Marfan syndrome, Fibromuscular dysplasia

• Can be forever asymptomatic
• ***Unpredictable spontaneous rupture
• ↑ Size —> ↑ Risk of rupture
• Unstable aneurysms: **Pseudoaneurysm due to arterial dissection (∵ outer wall is thin), **Mycotic aneurysm (∵ thin wall made up of inflammatory tissue)
• Large aneurysms: cause **Mass effect (e.g. CN palsy) / **Thromboembolism (∵ stagnant bloodflow)

Question 15

Impending aneurysmal rupture

Answer 15

Can have symptoms before a rupture
- e.g. an enlarging **PComA aneurysm compresses on CN3 (run below PComA)
—> “Surgical” CN3 palsy
—> **Peripheral parasympathetic fibres affected (run peripheral of CN3) —> **Dilated pupils + **Ptosis
—> Central motor fibres intact (preserved eye movement)

• ***Urgent angiogram before rupture!

Medical vs Surgical CN3 palsy
Medical:
- Ophthalmoplegia with Pupillary sparing

Surgical:
- Pupillary involvement with EOM sparing

Question 16

Aneurysmal rupture and SAH

Answer 16

Clinical features
1. **Sudden severe headache
- worst headache in life
- like being clubbed on head
2. **Signs of Meningism (Kernig’s sign, Brudzinski’s neck sign)
3. **Photophobia
4. **+/- LOC
5. ***Focal neurological deficit
6. Cardiac arrest and out-of-hospital death
7. Fundi: Subhyaloid haemorrhage

DDx: Meningitis (difference: SAH usually sudden onset)

Question 17

***Diagnosis of SAH (+ SpC Revision)

Answer 17

1. Clinical suspicion
   - History
   - P/E
2. **CT
   - can be subtle / even normal
   - **“Star” sign on brain base
3. **Lumbar puncture
   - **ONLY if CT negative
   - blood-stained CSF
   - SAH vs Traumatic tap
   —> **3-bottle test (genuine SAH: **uniform cell count / redness in all 3 bottles, traumatic: less red in last bottle)
   —> **Xanthochromia after **several hours (breakdown of blood products —> redness turn ***yellow (haemosiderin) —> yellowish CSF tapped out)
4. MRI
   - can be ***false-negative at acute stage
5. CT angiogram / DSA

Potential pitfalls in diagnosis:
1. No / Substandard History + P/E + poor documentation
- Onset, Severity, Meningism, Photophobia

2. Head injury + SAH on CT
   - maybe SAH first —> LOC —> TBI
   - maybe LOC / TBI first —> Traumatic SAH
3. Dismiss headache as
   - migraine, stress, psychological etc.
   - part of other conditions e.g. URTI
4. Leave till tomorrow / grand round
5. Radiologist refuses angiogram

Question 18

Principles of management of SAH (+ SpC Revision)

Answer 18

Cannot undo injury caused by initial haemorrhage
1. ABC
2. Optimise ICP + CBF
3. ***Prevent secondary injury
4. Angiogram

Once diagnosed SAH:
1. **Tranexamic acid (Stop bleeding)
2. **Anticonvulsant
3. Call neurosurgeon

Complications:
1. **Rebleeding of aneurysm (Day 14: **20%) —> Need to identify + obliterate aneurysm
2. **Vasospasm
3. **Hydrocephalus

Angiography to identify Cerebral aneurysm:
1. CT Angiogram
- non-invasive but can be false-negative
- ***proceed to DSA if CTA negative

2. ***Digital Subtraction Angiogram (DSA, gold standard)
   - direct injection of contrast into ICA / Vertebral artery
   - invasive
   - 1% stroke risk
3. MR angiogram
   - hard to get one acutely

Question 19

Obliteration of Cerebral aneurysm

Answer 19

1. ***Microsurgical clipping (open surgery)
   - apply small aneurysm clip at neck of aneurysm without obstructing parent artery
   - risk of intra-operative rupture / occlusion of parent artery
2. ***Endovascular embolisation (endovascular surgery)
   - Guglielmi detachable coil —> induce thrombosis —> close off aneurysm
3. ***Flow diverter (endovascular surgery)
   - stenting at base of aneurysm —> cut off bloodflow into aneurysm

Aim:
- Complete obliteration to prevent re-rupture “as soon as is feasible”

Method, Patient selection, Timing depends on:
- age
- premorbid status
- neurological prognosis
- technical feasibility

Question 20

Post-SAH Vasospasm (+ SpC Revision)

Answer 20

• Delayed complication of SAH
• Delayed cerebral ischaemia (aka Delayed ischaemic neurological deficit (DIND))
• Starts ***~day 4, peaks day 7-10
• High mortality / morbidity

Pathophysiology (web):
- Breakdown products of blood —> Ca-dependent and Ca-independent vasoconstriction

Investigation:
- Transcranial cranial doppler (TCD)

Treatment:
1. **Maintain good perfusion
2. **Nimodipine (act selectively to dilate cerebral vessel, do NOT give Nifedipine —> ∵ ↓ systemic BP)
3. ***Chemical / Mechanical angioplasty

SpC Revision:
1. Triple H therapy
- Hypertensive (Inotrope)
- Haemodilution
- Hypervolaemia (Give fluid)
2. Endovascular intervention: Mechanical angioplasty / Chemical (e.g. Verapamil)

Question 21

Post-SAH Hydrocephalus

Answer 21

• ∵ Blockage of CSF flow + absorption
• Acute ↑ in ICP
• CSF drainage helps but might ***provoke re-bleeding if aneurysm not yet secured
• Delayed: Poor absorption and usually communicating
• Beware of new symptoms several months post-SAH

Treatment:
- ***CSF shunting

Question 22

***Summary of management of Aneurysmal SAH

Answer 22

Clinical suspicion
—> **CT scan (Star sign) / **LP (Blood-stained)
—> **Diagnosis of SAH
—> Identify Aneurysm by **DSA / CTA / MRA
—> Secure aneurysm by **Clip / Coil / Flow diverter
—> ICU Care + **Angioplasty / **Nimodipine for Vasospasm + **CSF shunting for Hydrocephalus

Question 23

5. Cerebral Vascular Malformation

Answer 23

4 types:
1. Arteriovenous (AVM)
2. Cavernous angioma (CA)
3. Venous angioma (VA)
4. Capillary telangiectasia (CT)

• most likely ***congenital
• different bleeding risk: ***AVM highest
• AVM, CA: whether to treat depend on balance between treatment / harm
• VA, CT: Conservative management

Question 24

Cerebral AVM (+ SpC Revision)

Answer 24

Abnormal development of arteries and vein
—> Direct connection between artery and vein (i.e. no intervening capillary)
—> AV shunting and arterialisation of cerebral veins (under high pressure)
—> ***Unstable high-pressure system
—> Prone to rupture + Associated with aneurysm (esp. on feeding artery)
—> Disturbs normal cerebral perfusion

Spetzler and Martin classification (1986):
- Based on Size, Eloquence (Location), Venous drainage
- Higher score —> Higher risk of surgery

Clinical features:
1. **Haemorrhage (3% / year)
- Deep, IVH, Lobar
2. **Seizure (if microbleed)
3. **Ischaemia (“vascular steal”: shunt blood away from adjacent normal brain)
4. **Headache (∵ high pressure)
5. Others
- Bruit
- Hydrocephalus
- Heart failure (∵ high haemodynamic stress)

Treatment:
- Mainly to prevent bleeding
- Risk-Benefit balance
1. ***Surgical excision
- cure is immediate if a total resection is achieved
- recommended for grade 1, 2, and 3 lesions

2. ***Endovascular embolisation
   - less invasive than surgery and can reach lesions that are inaccessible surgically
   - risk of embolic stroke
   - rarely achieves complete eradication
3. ***Stereotactic Radiosurgery
   - non-invasive
   - access all anatomic locations of brain
   - only small lesions
   - may require 2 years for a full destructive effect
4. ***Combination
   - total eradication of lesion often requires >1 modality

Question 25

6. Moyamoya disease

Answer 25

• Common in Asia
• ***Congenital ICA stenosis —> Brain ischaemia —> Compensatory proliferation of vascular collaterals “puff of smoke”

Clinical features:
- Young: **Ischaemic symptoms (∵ collaterals still not well formed)
—> develop symptoms when hyperventilate (PaCO2 ↓ —> vasoconstriction)
- Older: **Bleeding (dense + fragile collaterals)

Treatment:
- ***Revascularisation surgery of ICA might help (during young age)

Question 26

7. Cervical Arterial Dissection

Answer 26

Causes
1. ***Spontaneous
- Connective tissue disorder

2. ***Traumatic
   - Fall
   - Sports
   - Chiropractic

Clinical features:
1. **ICA: Retroorbital pain, **Horner’s syndrome (∵ ICA carries sympathetic fibres to eyes)
2. **VA: Occipital pain, **Vertebrobasilar symptoms (i.e. ischaemia)
3. **Ischaemia from arterial occlusion / **embolism
4. **Rupture of Dissecting aneurysm —> cause **SAH intracranially

Treatment:
1. ***Anticoagulation if no bleeding
- ↓ rate of haematoma formation within false lumen —> allow time for artery to heal
- CI if bleeding already

2. Endovascular / Bypass surgery

Question 27

Summary of lecture

Answer 27

Sudden headache + LOC is ***cerebrovascular in origin until proven otherwise

1. Haemorrhagic stroke:
   - Deep vs Superficial —> surgery in selected patients
   - ***NO role of steroid

(2. Cerebellar haemorrhage
- **IVH + **Direct brainstem compression —> **Respiratory distress + **Obstructive hydrocephalus
- Evacuation of haematoma / EVD)

3. Acute ischaemic stroke (“Brain attack”):
   - Small vessel: IV tPA thrombolysis within 3-4.5 hours
   - Large vessel: Endovascular mechanical thrombectomy within 6 hours
4. Aneurysmal SAH:
   - Surgical clipping / Endovascular treatment
   - Complications: Rebleeding, Hydrocephalus, Vasospasm
5. Cerebral AVM:
   - Headache, Bleeding, Seizure, Vascular steal
6. Moyamoya disease:
   - Ischaemia when young
   - Haemorrhage when older
7. Cervical artery dissection:
   - Ischaemia / Dissecting aneurysm rupture causing SAH

Question 28

SpC Interactive tutorial: Cerebrovascular disease
General principles of management in Cerebrovascular disease

Answer 28

ICH:
1. Control HT
- No need aggressive

2. Control ICP
   - Elevate head
   - IV mannitol
3. ***Monitor
   - GCS
   - BP, Pulse
   - Limb power
   - Pupil size
4. ***Stress ulcer prevention
   - IV PPI
5. ***DVT prophylaxis
   - Mechanical (Stocking) / Pharmacological (Anticoagulant)
6. Definitive treatment
   - Only prevent secondary complications (∵ primary damage already made)

(7. Tranexamic acid
- Potentially useful

8. Factor 7 concentrate
   - proven to reduce re-bleeding but not widely used and associated with MI)

Question 29

Last seen well time vs Symptom onset time (web)

Answer 29

Last seen well time:
- Date and time at which the patient was last known to be ***without the signs and symptoms of the current stroke or at their prior baseline.

Symptom onset time:
- Date and time of discovery of **patient’s symptoms (i.e. when the patient was found with symptoms). This should be the **earliest time that patient was known to have symptoms.

If the event was witnessed, then the last known well date and time and the discovery date and time will be identical. Record both, even if identical.