The subarachnoid space is located between the arachnoid membrane and pia mater in the brain. It contains cerebrospinal fluid and spongy connective tissue. Bleeding into this space is called a subarachnoid hemorrhage (SAH), which is often caused by the rupture of an intracranial aneurysm. CT and MRI are used to detect SAH. Treatment involves relieving vasospasm, removing blood, and clipping or coiling the aneurysm to prevent rebleeding. Complications include hydrocephalus, infarction, and herniation. The mortality rate of SAH is 30-60% even after reaching the hospital.

2. Anatomy of Subarachnoid
space
 In the central nervous system, the
subarachnoid cavity (subarachnoid space) is
the interval between the arachnoid
membrane and pia mater.

3.  It is occupied by spongy tissue consisting of
trabeculae (delicate connective tissue
filaments that extend from the arachnoid
mater and blend into the pia mater) and
intercommunicating channels in which the
cerebrospinal fluid is contained.

4.  This cavity is small on the surface of the
hemispheres of the brain. On the summit of
each gyrus the pia mater and the arachnoid
are in close contact, but in the sulci between
the gyri, triangular spaces are left, in which
the subarachnoid trabecular tissue is found.

5.  Whilst the pia mater closely follows the
surface of the brain and dips into the sulci,
the arachnoid bridges across them from
gyrus to gyrus.

6.  At certain parts of the base of the brain, the
arachnoid is separated from the pia mater by
wide intervals, which communicate freely
with each other and are named subarachnoid
cisternae; in these the subarachnoid tissue is
less abundant.

7.  The subarachnoid space is the location of the
interface between the vascular tissue and the
cerebrospinal fluid and is active in the blood
brain barrier.

9. Subarachnoid Hemorrhage
 Bleeding into the subarachnoid space,
between the pia mater and the arachnoid
 Most commonly occurs between ages of 25 to
65, increasing in frequency with age

11. Causes
 Intracranial aneurysms
 Cause of approximately 80% of non traumatic
subarachnoid hemorrhage
 Most occur around the circle of Willis (berry
aneurysm) at
 Middle cerebral artery bifurcation
 Anterior communicating artery
 Posterior communicating artery
 Also
 Ophthalmic arteries
 Vertebral and basilar arteries

12.  Head trauma
 Benign perimesencephalic hemorrhage
 Blood limited to midbrain

13.  Less frequent causes of SAH
 Arteriovenous malformation (AVM)
 Extension from intracerebral hemorrhage
 Arteriovenous fistulae
 Meningitis
 Neoplasm

14. Risk Factors
 Vasculitis
 Fibromuscular dysplasia (FMD)
 Hypertension
 History of polycystic kidney disease
 Smoking

15. Clinical Findings
 Headache is most common symptom
 Frequently reported as severe (“worst
headache of life"), of abrupt onset, reaches
maximum intensity within seconds
(“thunderclap headache”)

16.  Nausea
 Vomiting
 Change in mental status -- confusion
 Decreased level of consciousness including
coma
 Spinal fluid may be bloody

17. CT Scan
 Unenhanced CT of the brain is the study of
choice for establishing presence of SAH
 Acute hemorrhage is most evident 2-3 days
after the acute bleed

18.  Acute hemorrhage appears as high-
attenuation material that fills the normally
black subarachnoid spaces, which include
 The basilar cisterns
 Especially the suprasellar cistern
 The sulci
 Especially the Sylvian fissures
 Over the convexities of the brain, SAH produces
white, branching densities representing the
normally black sulci filled with blood

19.  Cortical vein sign = visualization of cortical
veins passing through extra axial fluid
collection

20.  False positives may occur by mistaking
normal visualization of the falx cerebri and
tentorium cerebelli for SAH

21. A, Axial brain CT scan shows an isolated slight right frontal
subarachnoid hyperattenuation. B, Because of clinical
aggravation the next day, another brain CT was performed and
demonstrated a larger right Sylvian SAH.

22. There is high-attenuation blood in the Sylvian fissures
(blue arrows) and the inter hemispheric fissure (red arrow)
seen on this non-contrast enhanced CT of the brain. Do not
confuse normal, physiologic calcifications (white and black
arrows) for blood.

23. Non-enhanced CT scan demonstrates increased density at the
convexity consistent with a small amount of subarachnoid
hemorrhage in the right frontal lobe.

24. CT scan reveals subarachnoid hemorrhage in the right sylvian
fissure; no evidence of hydrocephalus is apparent.

25. Axial NECT section shows hyperattenuating acute SAH in the Sylvian
fissures (yellow ovals) and interhemispheric fissures (yellow arrows).
Third ventricle and atria of the lateral ventricles are mildly dilated.
Small amount of intraventricular hemorrhage is seen in the dependent
occipital horn of left lateral ventricle (red arrow).

26. (A)Noncontrast CT demonstrates subarachnoid hemorrhage
(arrows). (B)3-D reconstruction image from a CT angiogram
demonstrates an aneurysm (arrow) from the anterior
communicating artery as the cause of the bleed.

27. Non-contrast CT scan brain demonstrating a subarachnoid hemorrhage in
the right Sylvian fissure and a hypodense filling defect due to the
cysticercal cyst within the fissure B. Craniocaudal view of the
reconstructed CT angiogram showing an aneurysm (arrow) at a branch of
the middle cerebral artery.

28. MRI
 MR is relatively insensitive within first 48
hours
 Hyperintense sulci and cisterns on FLAIR (more
sensitive than CT for small amounts of blood)
 ‘’Dirty’’ CSF isointense to brain on T1WI + T2WI
 Low-signal intensity on brain surfaces in recurrent
subarachnoid hemorrhages (hemosiderin
deposition)

29. 41-year-old man 3 days after traumatic subarachnoid hemorrhage. Axial
FLAIR MR image shows posttraumatic subarachnoid hemorrhage
(arrows) overlying temporal lobes.

30. MR imaging shows subarachnoid hemorrhage (SAH). SAH appears
hyperintense on the T2-weighted and fluid-attenuated inversion
recovery (FLAIR) images

31. MRI images show an extensive subarachnoid hemorrhage along the right
cerebral convexity, most prominently in the frontal region. Also
depicted are edema in the underlying cerebral parenchyma, mass
effect, and compression of the right lateral ventricle. The
hemorrhage appears hyperintense on T1-weighted images, with low
signal on T2-weighted images

32.  CT angiography and MRA have replaced
conventional angiography in most
institutions for the identification and location
of the aneurysm itself

33.  Cerebral angiography is used for the
detection of intracranial aneurysms
 Such features as aneurysm size and shape can
help determine which aneurysm has bled
 Still considered the “gold” standard for diagnosis
of intracranial aneurysm

34. Management
 Relief of associated vasospasm (occurs in as
many as 50% of patients with SAH) may be
accomplished medically with calcium channel
blockers
 Urgent surgical removal of blood may be
indicated

35.  Early surgical clipping is used to prevent
rebleeding
 Endovascular management is also now widely
used
 Coiling

36. Complications
 Acute obstructive hydrocephalus (in <1 week)
secondary to intraventricular hemorrhage /
ependymitis obstructing aqueduct of Sylvius or
outlet of 4th ventricle

37.  Delayed communicating hydrocephalus (after 1
week) secondary to fibroblastic proliferation in
subarachnoid space and arachnoid villi interfering
with CSF resorption

38.  Cerebral vasospasm + infarction (develops after 72
hours, at maximum between 5-17 days, amount of
blood is prognostic parameter)
 Transtentorial herniation (cerebral hematoma,
hydrocephalus, infarction, brain edema)

39. Prognosis
 About 10 to 30% die before reaching medical
help with first bleed
 Nontraumatic subarachnoid hemorrhage in
patients who reach the hospital still has a
mortality rate of 30 to 60%
 SAH from an arteriovenous malformation has
a better prognosis than SAH from a ruptured
aneurysm