Anatomy of Subarachnoid space In the central nervous system, the

subarachnoid cavity (subarachnoid space) is the interval between the arachnoid membrane and pia mater.

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.

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.

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.

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.

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.

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

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

Head trauma

Benign perimesencephalic hemorrhage Blood limited to midbrain

Less frequent causes of SAH Arteriovenous malformation (AVM) Extension from intracerebral

hemorrhage Arteriovenous fistulae Meningitis Neoplasm

Risk Factors

Vasculitis Fibromuscular dysplasia (FMD) Hypertension History of polycystic kidney

disease Smoking

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”)

Nausea Vomiting Change in mental status -- confusion Decreased level of consciousness

including coma Spinal fluid may be bloody

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

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

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

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

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.

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.

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

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

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).

(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.

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.

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)

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

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

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

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

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

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

Early surgical clipping is used to prevent rebleeding

Endovascular management is also now widely used Coiling

Complications

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

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

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)

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