JC M WCS 3

HEADACHE & LOC

Dr. Fan Yiu-wah

Neurosurgery

Wed 23-10-02

  1. Intact cerebral hemispheres
  2. Intact reticular activating system BS - midbrain, hypothalamus, thalamus
  3. GCS - see WCS 2
    1. Intracranial - trauma, vascular, infective, neoplastic
    2. Extra-cranial - metabolic, drugs & toxin, vascular occlusion, endocrine, respiratory insufficiency, cardiac insufficiency, psychiatric
    1. trauma history ® shearing injury
    2. DM ® hypoglycaemia
    3. sudden collapse ® stroke
    4. gradual onset ® tumour
    5. alcoholics ® drug overdose
    1. Bruised ® head inj
    2. neck stiffness ® SAH, meningitis
    3. hepatomegaly ® liver failure
    4. decerebrate posture ® intracranial lesion

HEADACHE

Causes

  1. Functional - tension headache (bilat temporal + suboccipital regions; subconscious contraction of m; HK - rel to wk)
  2. Structural intracranial lesion - related to ­ ICP (most imp to exclude)
  3. Referred pain - ear, sinuses, eye; neuralgia (eg. trigeminal)

Note: Morning headache

  1. ­ ICP: headache wakes Pt up
  2. Tension: Pt wakes up fine, thinks about work, develops headache

Headache - specific causes

    1. Generalised
    2. ­ w/ coughing & straining (­ thoracic press transmit to head)
    3. morning headache
    4. vomiting
    5. progressing severity
    1. Sudden onset + severe pain
    2. vomiting: ­ ICP
    3. focal deficit: hemiplegia, speech deficit
    4. meningism: neck stiffness, Kernig sign (subarachnoid haemorrhage = irritant)

Note: sudden = vascular event

Pain sensitive structures

STROKE

Types of Stroke

    1. vessel occlusion: carotid, IC BV
    2. embolism: atrial fib, arrhythmia
    3. arteritis
    4. blood disorder
    1. intracerebral haemorrhage
    2. subarachnoid haemorrhage

Stroke Management

  1. Prevention - becoming more imp
  2. Acute treatment for brain attack
  3. Rehabilitation

Acute Treatment for Stroke

Carotid Endarterectomy

Management of established cerebral Infarction

Note

Cerebellar infarct

    1. ventriculostomy
    2. suboccipital craniectomy, infarctectomy (remove infarct)
    3. More aggressive Tx b/c if lesion, Pt trouble walking/ balancing (not as severe as cerebral hemispheres)

Causes of Haemorrhagic Stroke

Note: DO NOT open BV beyond therapeutic window - ­ bleed

Subarachnoid Haemorrhage

Spontaneous subarachnoid haemorrhage

Cerebral aneurysm

    1. Haemodynamic stress on arterial bifurcation
    2. congenital weakness of arterial wall
    3. abnormal circle of Willis
    1. incidence increase with age
    2. 2-5% of adult population
    3. mean age of SAH 50
    1. rupture
    2. subarachnoid haemorrhage
    3. mass effect
    4. cranial nerve palsy
    5. oculomotor (PCoA, basilar)
    6. optic (ophthalmic artery)

Subarachnoid haemorrhage

Problems after SAH

    1. Delayed cerebral ischaemia
    2. starts on Day 4
    3. maximum on Day 7-Day 10
    4. resolves within 2-3 week
    5. cause: blood in CSF, SAH
    1. Hypertensive: increase inflow pressure (­ effective circulation ® ­ CO ® ­ BP)
    2. Haemodilution: improve rheology of blood (help blood go through stenotic BV more easily; if too thin - ¯ haematocrit ® hypoxic brain)
    3. 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

      1. does not improve angiographic narrowing
      2. improve clinical outcome
      3. work at cellular level ® cerebral protection (cf. specific VD)
      4. S/E: hT \ do not prescribe with ¯ CPP
      1. Epsilon aminocaproic acid
      2. Tranexamic acid
      3. decrease rebleeding
      4. increase vasospasm (clot remains in CSL \ S/E)
      5. no difference in management mortality

Management of Vasospasm

Management of SAH

Management of ruptured aneurysm

VASCULAR MALFORMATION

Vascular malformation of CNS

Cerebral AVM - no resistance (capillary) between a + v, vein not designed for ­ press

  1. Rupture
  2. "Steal phenomenon" - ischaemic around AVM
  3. Epilepsy - 50%

AVM

    1. haemorrhage(50%)
    2. seizure, ischaemia (steal), mass effect
    3. headache, bruit, ­ ICP, heart failure
    4. hydrocephalus (Vein of Galen aneurysm)
    1. 10% mortality; 30-50% morbidity
    2. Small AVMs bleed > large AVMs
    3. 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)

Treatment of AVM

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

Radiosurgery for AVM

MANAGEMENT

Acute Mx cerebral haemorrhage

Cerebellar Haemorrhage - aggressive, ­ QOL

Cerebellar haemorrhage

Lobar Haemorrhage - haematoma on surface of brain, usually struc cause (eg. AVM)

Ganglionic Haemorrhage - occurs at BG, aka internal capsule haemorrhage, deep tissue, caused by HT

Thalamic Haemorrhage - spill into ventricle - hydrocephalus

Thalamic, brainstem haemorrhage