JC M WCS 3
HEADACHE & LOC
Dr. Fan Yiu-wah
Neurosurgery
Wed 23-10-02
CONSCIOUSNESS - state of awareness of self + surr
- Intact cerebral hemispheres
- Intact reticular activating system BS - midbrain, hypothalamus, thalamus
- GCS - see WCS 2
- COMA
- no speech/ eye opening/ motor response
- Intracranial
- trauma, vascular, infective, neoplastic
- Extra-cranial
- metabolic, drugs & toxin, vascular occlusion, endocrine, respiratory insufficiency, cardiac insufficiency, psychiatric
- trauma history ® shearing injury
- DM ® hypoglycaemia
- sudden collapse ® stroke
- gradual onset ® tumour
- alcoholics ® drug overdose
- Bruised ® head inj
- neck stiffness ® SAH, meningitis
- hepatomegaly ® liver failure
- decerebrate posture ® intracranial lesion
- Investigation
- Intracranial ® CT brain « metabolic screening ¬ extracranial
HEADACHE
Causes
- Functional
- tension headache (bilat temporal + suboccipital regions; subconscious contraction of m; HK - rel to wk)
- Structural
intracranial lesion - related to
ICP (most imp to exclude)
Referred pain - ear, sinuses, eye; neuralgia (eg. trigeminal)
Note: Morning headache
ICP: headache wakes Pt up
Tension: Pt wakes up fine, thinks about work, develops headache
Headache - specific causes
- Tension
headache - 95%
- Migraine
- one-sided, preceded by aura/ vomiting, pulsatile
- Raised ICP
- Generalised
w/ coughing & straining ( thoracic press transmit to head)
morning headache
vomiting
progressing severity
- Intracranial haemorrhage
(sudden
ICP)
- Sudden onset + severe pain
- vomiting:
ICP
focal deficit: hemiplegia, speech deficit
meningism: neck stiffness, Kernig sign (subarachnoid haemorrhage = irritant)
Note: sudden = vascular event
Pain sensitive structures
- Intracranial
- venous sinuses, cortical veins, basal arteries, dura mater
- Extracranial
- scalp vessels & muscles, orbital content, mucous membranes, external & middle ear, teeth & gum
STROKE
Types of Stroke
Ischaemic (HK 70%, West 85%)
- vessel occlusion: carotid, IC BV
- embolism: atrial fib, arrhythmia
- arteritis
- blood disorder
- Haemorrhagic
(HK 30%, West 15%)
- intracerebral haemorrhage
- subarachnoid haemorrhage
Stroke Management
- Prevention
- becoming more imp
- Acute
treatment for brain attack
- Rehabilitation
Acute Treatment for Stroke
- Concept of Brain Attack
- Therapeutic window of 3-6 hours (lyse clot, recanalise BV, reperfuse brain)
- Stroke thrombolysis - eg. TPA
Carotid Endarterectomy
- Open neck, remove atheroma, enlarge conduit
- Justified if occlusion > 70%
- Risk: peri-operative stroke (b/c clamp BV to brain)
Management of established cerebral Infarction
- Most Pt outside therapeutic window
- ICP treatment: neurones die - swell - ICP
- Decompressive procedure: craniectomy - young, non-dominant hemisphere, potential for neuro recovery
Note
- Is it worth saving a Pt who will be severely disabled afterwards?
- What will QOL be like after Tx?
Cerebellar infarct
- hydrocephalus: cerebellum in post fossa (all post fossa path require drainage of CSF)
- brain stem compression
- surgical options
- ventriculostomy
- suboccipital craniectomy, infarctectomy (remove infarct)
- More aggressive Tx b/c if lesion, Pt trouble walking/ balancing (not as severe as cerebral hemispheres)
Causes of Haemorrhagic Stroke
- Hypertension - 40%
- Vascular: AVM, Cavernoma, Aneurysm
- Haemorrhagic infarct
- Amyloid angiopathy
- Tumour
- Bleeding tendency
- Sympathomimetic abuse
- Venous sinus thrombosis
- Moya Moya
Note: DO NOT open BV beyond therapeutic window - bleed
- Eg. atrial fib - embolus - ischaemic stroke - clot lyse - brain tissue dead but then reperfused \ haemorrhagic phenomenon
Subarachnoid Haemorrhage
Aggressive Tx, treatable, brain not diseased (cf. HT haemorrhagic stroke) \ Px
Spontaneous subarachnoid haemorrhage
- Aneurysm 75%
- AVM 5%
- tumour, bleeding tendency 5%
- idiopathic 15% (even after angiogram, MRI) - Note: most idiopathic are very small aneurysms + AVM that cannot be seen in Ix
Cerebral aneurysm
- Dilatation of part of BV
- Usually rupture at fundus (direction of blood jet)
- Within BV/ aneurysm 80 mmHg; ICP 10 mmHg
® rupture: blood jets out until ICP pressure 80 mmHg ® CPP becomes 0 (global low perfusion) ® LOC
Once aneurysm + ICP both 80 mmHg, clot forms
Venous + CSF drain to compensate for ICP, so ICP drops to 10 mmHg ® reperfusion ® regain consciousness (H&N pain, meningism)
Not like aortic aneurysm (continuous bleeding) - cerebral aneurysm clots but has high chance of re-bleed
Aetiology
- Haemodynamic stress on arterial bifurcation
- congenital weakness of arterial wall
- abnormal circle of Willis
- incidence of cerebral aneurysm
- incidence increase with age
- 2-5% of adult population
- mean age of SAH 50
- rupture
- subarachnoid haemorrhage
- mass effect
- cranial nerve palsy
- oculomotor (PCoA, basilar)
- optic (ophthalmic artery)
Subarachnoid haemorrhage
- sudden onset of severe headache ("most severe headache ever experienced")
- LOC
- P/E neck rigidity
- Fundi - subhyaloid ocular haemorrhage
Problems after SAH
- Rebleeding
: highest chance as soon as clot forms (later: stronger clot) - exponential curve, highest immediately after clot formation (day 1 = 4%, say 2 = 2%, 2w = 20%)
- Vasospasm
: blood bathing structures at skull vase
® lyse ® toxic substance (NK) ® irritate BV ® vasospasm ® ischaemia/ infarct
- Delayed cerebral ischaemia
- starts on Day 4
- maximum on Day 7-Day 10
- resolves within 2-3 week
- cause: blood in CSF, SAH
- Tx: 3H therapy (empirical, want to
BF into brain)
- Hypertensive: increase inflow pressure (
effective circulation ® CO ® BP)
Haemodilution: improve rheology of blood (help blood go through stenotic BV more easily; if too thin - ¯ haematocrit ® hypoxic brain)
Hypervolaemia: enhance hypertension and haemodilution
Mx Protocol for Aneurysmal SAH
Aneursmal SAH
¯
CT scan
95% +ve 5% -ve
¯
v sug LP RBC xanthochromia
Hx
¯
Clinical grading SAH
¯ ¯
Grade 1,2,3 Grade 4,5
¯ ¯
4 vessels angiogram conservative
¯ Tx hydrocephalus
clipping ICH
endovascular coiling
Clinical grading:
1 = very good condition
5 = moribund
"3 bottle test" to distinguish between epidural vein puncture (traumatic tap 1>2>3) and subarachnoid haemorrhage (1=2=3)
WFNS grading of Subarachnoid Haemorrhage (World Federation of Neurological Surgeons Scale)
GCS Motor deficit
Grade 1 15 -
Grade 2 13-14 -
Grade 3 13-14 +
Grade 4 7-12 +/-
Grade 5 3-6 +/-
Management of SAH
- Nimodipine (Ca++-channel blocker)
- does not improve angiographic narrowing
- improve clinical outcome
- work at cellular level
® cerebral protection (cf. specific VD)
S/E: hT \ do not prescribe with ¯ CPP
- Epsilon aminocaproic acid
- Tranexamic acid
- decrease rebleeding
- increase vasospasm (clot remains in CSL
\ S/E)
no difference in management mortality
Management of Vasospasm
- Early clipping of aneurysm, nimodipine
- Baseline haemodilution Hct 30-34
- Hypertensive Px, SBP to 200 mmHg or deficits resolve
- Endovascular intervention, Angioplasty, Intra-arterial papaverine
Management of SAH
- Hydrocephalus
- obstructing CSF flow in subarachnoid space
- CSF drainage provokes rebleeding
Management of ruptured aneurysm
- Microsurgical clipping - clip neck (classical Tx)
- Endovascular coiling - "regrowth of aneurysm after coiling - blood pushes out coil) - eg. GDC coiling of aneurysm - Guglielmi Detachable Coils (coil = embolic material)
VASCULAR MALFORMATION
Vascular malformation of CNS
Capillary telangiectasia
Cavernous malformation - pool of blood in brain
Venous malformation - not eruptive rupture
AVM - rupture pressure
Cerebral AVM - no resistance (capillary) between a + v, vein not designed for press
- Rupture
- "Steal phenomenon" - ischaemic around AVM
- Epilepsy - 50%
AVM
- abnormally developed arteries and vein without intervening capillary
- AV shunting, Venous varix is common
- aneurysm on feeding artery 15%
- Presentation
- haemorrhage(50%)
- seizure, ischaemia (steal), mass effect
- headache, bruit, ICP, heart failure
- hydrocephalus (Vein of Galen aneurysm)
- 10% mortality; 30-50% morbidity
- Small AVMs bleed > large AVMs
- Risk of bleeding 2-4% per year
Risk of bleeding 3% per year
Expected years of remaining life
Risk of bleeding (at least once) = 1- [annual risk of not bleeding]
Age 25 at diagnosis - expected to live up to 80
55
Risk of bleeding = 1- (0.97) = 1 - 0.18 = 82% (lifetime risk)
-
Age Pt ® conservative Tx
- Need to balance risk of bleeding vs. risk of Tx
Treatment of AVM
- surgical excision, embolisation, radiosurgery
Spetzler -Martin Grading of AVM
Points
Size <3 cm 1
3-6 cm 2
>6 cm 3
Eloquence area non-eloquent 0
Eloquent 1
Venous drainage superficial only 0
Deep 1
Grade = sum of points
AVM treatment
Surgery
Deficit - + ++
Grade 1 100%
Grade 2 95% 5%
Grade 3 84% 12% 4%
Grade 4 73% 20% 7%
Grade 5 69% 19% 12%
Embolisation of AVM - catheter injected into cerebral BV, embolic material injected
- Death 1-2%
- Severe deficit 1-5%
- Minor deficit 9%
- Transient deficit 11%
- Haemorrhage 10%
- Seizure 3%
Radiosurgery for AVM
- X-knife Tx - single dose high radiation (S/E radiation: endarteritis obliterans - BV constriction - shut-down AVM) - NOT for AVM > 3cm Æ
- Radiosurgery planning
MANAGEMENT
Acute Mx cerebral haemorrhage
location of haematoma - ¯ surgical trauma with superficial haemorrhage
neurological status - QOL after removing haematoma (family support, $)
aetiology - 95% haemorrhage due to HT (BV hyaline degeneration) - control HT B4 surg
Cerebellar Haemorrhage - aggressive,
QOL
Cerebellar haemorrhage
- 4th ventricular obstruction, BS compression
- brain stem compression
- surg: ventricular drainage, suboccipital craniectomy, clot evacuation
Lobar Haemorrhage - haematoma on surface of brain, usually struc cause (eg. AVM)
- Operative intervention provide diagnosis
- Need to exclude vascular abnormality
- Surgery better than medical Tx
Ganglionic Haemorrhage - occurs at BG, aka internal capsule haemorrhage, deep tissue, caused by HT
- Ganglionic haemorrhage
- No difference in outcome + mortality of med vs. surg
- GCS 7-10: surgery lower mortality;
vegetative states
GCS 11-15: surgery worse than medical Tx \ DO NOT operate on Pt in good condition
Thalamic Haemorrhage - spill into ventricle - hydrocephalus
Thalamic, brainstem haemorrhage
- conservative treatment
- CSF diversion for hydrocephalus