Subarachnoid Haemorrhage When to screen? Whom to treat?

1. Subarachnoid Haemorrhage When to screen? Whom to treat? ASHIS PATHAK LEAD CONSULTANT for VASCULAR NEUROSURGERY HULL ROYAL INFIRMARY

2. SAH • 9% of all strokes • 75% caused by ruptured aneurysms • 6% by AVMs • 6% due to bleeding diathesis • 13% no cause

3. Ruptured Intra-Cranial AneurysmsClassical presentation First described in Bible Probably first mentioned in scientific literature by Bonet 1679 Devastating headache, collapse, abrupt in onset, incapacitating in severity Diffuse, often radiates posteriorly & down to neck Accompanied by blunting of consciousness, vomiting, stiff neck, sometimes subhyaloid hges Headache remains for hours, more commonly days then clears off in few weeks, survival permitting

4. Pathogenesis of Headache in SAH • Initial pain Stretching & tearing of distended vessel and adjacent arachnoid Sudden transmission of intra arterial pressure to the rigid intracranial compartment • Post-ictal pain Chemical irritation of pain sensitive meninges by blood • Delayed pain Chemical meningitis Vasospasm Hydrocephalus Infarction

5. Sentinel bleed • Less dramatic symptom - unusual sudden headaches, vomiting, dizziness • Up to 10% cases • Indicate small bleeds

6. CT negative SAH CT positivity depends on Grade of SAH Time after Hge Quality of scan After few days SA blood becomes isodense Minor leak Blood localised around the aneurysm

7. CT negative SAH Lumbar Puncture Contraindications: Abnormal clotting, Raised ICP, Spinal AVM CSF Pressure normal to raised RBC 10,000 to 50,0000 ?mm3 WBC increased in proportion to red cells Glucose N Proteins high (for 1000 RBC 1.5 Gm /dl proteins)

8. CT negative SAH CSF to be kept at 4 0 C & centrifuged immediately Xanthochromia - Spectrophotometry appears within Hrs universal after 12 hours Spectrophotometry – No haemoglobin or bilirubin after few hours further investigations not necessary unless strong history After 3 weeks - History is most important angiography decisive

10. Warning leak / Bleed

11. Prerupture Manifestations • III N palsy 7% -12% of aneurysm pts III N palsy prior to rupture 20-30% of isolated IIIN palsy are due to aneurysm Mean time from onset of palsy to rupture - 29.6 days • Patient with oculomotor palsy with headaches is an emergency, ideally needs CT & angiogram • Other features Hemiparesis Dysphasia Visual loss Field defect Seizures

12. Atypical presentation of aneurysmal SAH D/D Migraine Systemic infection Viral illness, Hypertensive crisis Cervical spinal disorders / arthritis Herniated disc Aseptic meningitis Brain tumours Sinusitis Alcohol intoxication

13. Migraine Vs Aneurysmal SAH

14. Migraine Vs Aneurysmal SAH

15. Head Injury & Aneurysmal SAH

16. Head Injury & Aneurysmal SAH

17. Non Aneurysmal SAH 10% of SAH No vascular cause detected on angiogram Course usually benign Outcome good in 90% pts

18. Non –aneurysmal SAH

19. Non –aneurysmal SAH

20. Exertional activity & Aneurysmal SAH • First co-operative study on 2288 ruptured aneurysms One third ruptured in sleep One third ruptured in unspecified circumstances One third ruptured during exertional activity e.g. Lifting, emotional strain, defaecation, coitus, coughing, parturition

21. Post coital cephalgia or SAH

22. SAH Or Post-coital Headaches Duration of headache Vomiting Disturbance of consciousness Meningeal signs Demonstraion of blood in CSF Absence of prior sexually associated headaches

23. Paediatric SAH Pre -op Post-op

24. Moya Moya disease PRE - OP POST- OP

26. Drug Abuse & Stroke

27. THREE WEEKS LATER

28. Headaches with Incidental Aneurysms

29. Patient undecided - wants to think

30. Patient decides for image surveillance

31. Patient not concerned

32. Needs Intervention

33. Conclusion Awareness History is of paramount importance Neurological examination gives the clue Good investigative tools are a must Whenever in doubt – DO NOT HESITATE Remember - There are always exceptions

35. Sensitivity of Cerebral Blood vessels to pain Common, internal & external carotid vessels are sensitive to pain Main trunk of dural arteries & veinous sinuses are sensitive to pain Myelinated & unmyelinated nerve fibres project from dural arteries & veins to trigeminal nerve Larger areteies at Circle of Willis and upto first CM sensitive to pain. But substance P has been demonstrated in distal blood vessels also

36. Pattern of pain referral Pain from ICA is referred to ipsilateral sid eof head Pain from supratentorial structures is referred to the front of head Pain from infratentorial structures id referred to posterior aspect of head due to innervation of C2

37. Headaches of genereal physical exertion Primary ICH Embolism Thrombo-occlusive disease

38. Reversible cerebral vasoconstriction syndrome (RCVS) Orgasmic headache (OH) is an "explosive" headache that occurs at orgasm. Historically, it was considered benign with no treatment needed. Reversible cerebral vasoconstriction syndrome (RCVS) refers to a group of disorders characterized by recurrent thunderclap headache (TCH) and multifocal vasoconstriction.

39. Sudden catastrophic headache during sexual intercourse SAH due to rupture or expansion of intracranial aneurysm or AVM may need to be excluded Lundberg & Osterman (1974)reviewed 50 patents of SAH – 6 cases 12% SAH occured during coitus All cases residual pain lasted 24 hrs. 2 Pts became unconscious & 5 had vomiting

40. Physiology of sexual activity Increase in heart rate & BP Values reach maximum during orgasm Erratic respiratory pattern Valsalva with paroxysmal Increased intrathoracic pressure due to closed glottis Phenomenon similar to any severe exertional efforts with compartmental pressure changes

41. Physiology of sexual activityBenign Coital Cephalgia Raised intrathoracic pressure Transmitted intracranially Increased tension in dural matrix Tear in dural matrix leading to leakage of CSF

42. Physiology of sexual activity As sexual tension is elevated individual frowns, scowls, grimaces and facial muscles contract involuntarily in semispasm Jaw is clenched spastically, neck muscles contract rigidly as orgasm is imminent There is local and general vasodialtion during orgasm This mechanism can be cause of pre-orgasmal headaches. Primary migraine can be triggered with coitus but occurs following coitus but Benign Coital Cephalgia occurs during the act of intercourse

43. Physiology of sexual activity Gross vascular & autonomic changes during orgasm can be causes of vascular headaches. During orgasm there is abrupt increase in parasympathetic outflow. Sudden vasodiltion superadded with maximum cardiac output& extreme elevation of BP Unique intracranial context leading to sudden increase in intracranial blood volume or acute failure in intracranial autoregulation