Hyperintensity along cortical sulci

Case : A 40 yo male with severe recent onset headache. On admission Plain CT study show hardly any obvious abnormality, except marginal fullness of lateral ventricles - a subjective finding.

MR Axial FLAIR study of brain performed immediately after that shows abnormal hyperintensities in the region of hemispheric cortical sulci. 

T2*GRE and Diffusion normal. MR Angiography and Venography of Brain normal.
So the final Impression was "Diffuse sulcal hyperintensity on FLAIR" as the only important positive finding in the study. Possible DDs suggested were SAH and Exudates of Meningitis. 

Csf evaluation strongly supported SAH. 

DSA performed 4 days after also could not reveal any obvious cause of SAH. 

FLAIR 

• Stands for 'Fluid Attenuated Inversion Recovery' Sequence sequence has become a routine part of MRI studies of the brain; rather it has become the most commonly used sequence in MRI brain studies. In some institution like ours it is performed as a screening study for brain in cases of emergencies and non affordable patient.

• An inversion recovery pulse to null the signal from CSF and a long echo time to produce a heavily T2-weighted sequence. Produces images highly sensitive to T2-weighted prolongation in tissue but minus the Csf. Improves detection of lesions within the subarachnoid space and brain parenchyma, particularly the lesions located near the brain–CSF interface.

• When disease occurs within the subarachnoid space, the relaxation time of CSF is altered, result in hyperintensity of the CSF or subarachnoid space during the FLAIR sequence. Commonly seen in dependent portions of brain in parieto occipital region with effacement of cortical sulci, an alternative term cerebral odema can be used to describe this associated finding. 

•Common causes of such non specific diffuse hyperintensity along sulcal space is Meningitis and Subarachnoid hemorrhage. 

• In meningitis and SAH both the  higher protein content and cellular concentrations causes an offset in the null point of CSF inversion times, resulting in increased T2-weighted prolongation.

• In massive SAH or obvious Meningitis with exudates and hydrocephalus diagnosis may not be a problem but in subtle cases, results of both in vivo and in vitro studies have suggested that FLAIR imaging is more sensitive than CT in the evaluation of these milder and subtle form of acute SAH and meningeal inflammation in which cases where CT may show only mild effacement of cortical sulci. T2*GRE has not role in cases of milder forms of sub arachnoid hemorrhages, may be normal as in above case. Differentiation between the two is difficult most of time and is out of imaging consecus. Contrast enhanced T1 or Flair may help out by demonstrating leptomeningeal enhancement in meningitis.

• Always keep in mind other, less common cause of subarachnoid space FLAIR hyperintensity is artifact. In my institution one patient was advised brain axial FLAIR and sagittal T2 cervical spine screening. First brain screening was performed, which was showing similar abnormal diffuse non specific hyperintensity along sulci spaces and basal cisterns. Cervical spine screening performed and axial Flair repeated again. It is strange to mention that this time axial flair screening was absolutely normal. I had two such incidences. After discussion with my technician i came to conclusion that this was artifactual as some changes were done by him in hurry in TR TE during the study.
Patient intubated and on inhaled O2 can show similarPatient intubated and on inhaled O2 can show similar abnormal diffuse hyper intensity in the region of cortical sulci and basal cisterns due to para magnetic effect of dissolved oxygen. 

Conclusion: Most of the time an associated finding may suggest the cause of the subarachnoid space hyperintensity on FLAIR. But in cases of milder form, diffuse distribution and a lack of ancillary findings often make this finding nonspecific and may require clinical correlation and CSF analysis. It’s better to mention the finding and suggest csf analysis. Commonest causes of diffuse sulcal hyperintensity on FLAIR include Meningitis and SAH. 

Intubated patient on inhaled O2 can show similar picture due to para magnetic effect of dissolved oxygen.
To read more about effect of inhaled oxygen on FLAIR Click here 

Imaging in Sub Arachnoid H'rhage

SAH, An extravasation of blood into the subarachnoid space between pia and arachnoid.

Divided as Spontaneous and Post traumatic. 
Spontaneous SAH include Aneurysmal and Non-aneurysmal causes SAH. 
- Aneurysmal SAH 
The most common cause of Spontaneous SAH.
Rupture of a saccular (berry) aneurysm (80%)
Rupture of an arteriovenous malformation (AVM) (10%).
Rarely in the setting of mycotic aneurysms and congenital disorders, including coarctation of the aorta, Marfan's syndrome, Ehlers-Danlos syndrome, fibromuscular dysplasia and polycystic kidney disease.
- Non Aneurysmal SAH: include CVT, amyloid angiopathy, blood dyscrasias, fibromuscular dysplasia, Moyamoya disease, and vasculitis (10%).


Rupture is related to the tension on the aneurysm wall. Tension on the wall is proportional to the diameter. Thus, the rate of rupture is directly related to the size of the aneurysm.

Symptoms and signs:
A sudden onset of severe headache ("thunderclap headache"), often described as the “worst headache of my life" .... most common.
Nuchal pain and rigidity
A sudden loss of consciousness (occurs in half of patients at bleeding onset; it is usually transient)

Location: 
The most common and specific locations of intracranial aneurysms are at the middle cerebral artery bifurcation and along the anterior communicating artery. These 2 locations account for approximately 70% of all intracranial aneurysms.
Other common sites are at the origins of the posterior communicating and ophthalmic arteries.
Approximately 10-20% of aneurysms arise from the vertebral and basilar arteries. The tip of the basilar artery is the most common location of aneurysm formation in the posterior circulation.

Preferred examinations:
Non contrast CT
MRI with MRA (Non contrast 3 D TOF)
DSA

Non contrast CT
A preferred initial diagnostic study.

On CT, subarachnoid haemorrhage appears as a high-attenuating, amorphous substance that fills the normally dark, CSF-filled subarachnoid spaces around the brain, appear white in acute haemorrhage, most evident in the largest subarachnoid spaces, such as the supra sellar cistern and Sylvian fissures.
Prediction of site of bleed on CT, is possible. If bleed is marked in anterior inter hemispheric fissure, an Acom aneurysm is possible and if marked only in one side sylvian fissure corresponding MCA aneurysm is possible.

Magnetic Resonance Imaging
Fluid Attenuated Inversion Recovery (FLAIR) is the most sensitive sequence.

On FLAIR images, SAH appears as high signal-intensity (white) in normally low signal-intensity (black) CSF spaces.
MRA for evaluating aneurysms and other vascular lesions that cause SAH. The  sensitivity is low for aneurysms smaller than 5 mm.

DSA (Digital Substraction Angiography)
Considered the standard imaging technique for the detection of intracranial aneurysms.

Detected as focal areas of out pouching or dilatation of the arterial wall, frequently occur at arterial branching points in characteristic locations within or near the circle of Willis.
Gives valuable information about aneurysm location, shape, neck size, and neck-to-maximal diameter ratio  which are crucial in determining whether the aneurysm is better treated with open craniotomy or with an endovascular technique.

Sentinel bleed

Sentinel or "warning" leaks that produce minor blood leakage, reported to occur in 30-50% of cases, precedes the aneurysm rupture and major episode of SAH by a few hours to a few months, so should not be overlooked. MRI FLAIR is the best sequence. Lumbar puncture is confirmatory.

Complications of Subarachnoid Haemorrhage

Hydrocephalus, Communicating and Non-Communicating Hydrocephalus.

Vasospasm.

Communicating Hydrocephalus

SAH with dilatation of the anterior and temporal horns, as well as the third and fourth ventricles. Flow is most likely blocked at the arachnoid granulations resulting in communicating hydrocephalus. 

Requires emergency ventricular shunting.

Non-Communicating Hydrocephalus

Non-communicating (obstructive) hydrocephalus occurs when the ventricular system is not in continuity with the subarachnoid space due to blood clots. Most often, the site of the blockage in non-communicating hydrocephalus is at the cerebral aqueduct, but rarely can occur at the foramen of Monro, the third ventricle, or the outlet of the fourth ventricle.

Important to recognize as it is potentially treatable by shunting.

Vasospasm following Subarachnoid Hemorrhage. 

A known delayed complication of subarachnoid hemorrhage.

Reported to occur in as many as 70% of patients with SAH.

Most commonly occurs 4-14 days after the onset of bleeding.

If severe enough, may lead to progressive ischemia and stroke.
Imp to recognize as typically treated with the calcium channel blocker nimodipine, volume expansion, mild elevation of blood pressure.