Brain stem hemorrhage may cause additional symptoms such as shortness of breath, dysphagia (difficulty swallowing), chewing problems, abnormal heart rate, and irregular heartbeat.

Other advantages of CT over MRI scan are ability to detect bony fractures, vascular injury, and cerebrospinal fluid (CSF) leak.

[4] Moreover, CT scans have also been used to train deep learning models to automatically perform intracranial hemorrhage detection.

If CT scan shows normal findings, but the subject has persistent neurological symptoms, MRI is also indicated.

[4] Swirl sign on CT scan (areas of low densities with surrounding areas of high densities) is indicative of active intracranial bleeding, high chance of death within one month, and poor subject's function in three months if the subject is still alive.

MRI is more sensitive than CT scan in detecting such small hemorrhagic contusions, with the use of gradient echo sequence.

[3] Cerebral microhemorrhages is a smaller form of hemorrhagic parenchymal contusion and are typically found in white matter.

Such EDH is limited and does not require surgery because its extension is confined within the sphenosquamosal suture and the superior or inferior orbital fissures.

[9] When the epidural hematoma is large enough, it will cause mass effect on contralateral brain which lead to midline, subfalcine (below the falx cerebri), and trans-tentorial (crossing tentorium cerebelli) herniations.

Those with SDH that have same density with brain parenchyma may represent acute bleed such as those with anemia, arachnoid tear, and the mixing of hemorrhage and CSF.

Membranes with granulation tissue can rupture within SDH, and give high density appearance on CT scan.

SDH can be treated with burr hole drainage, craniotomy or port system placement for blood clot evacuation, or middle meningeal artery embolisation.

It is usually located at the cerebral sulci near the vertex of the head and spare the basal cisterns on CT scan.

When the SAH volume is large, rarely it can cause cerebral infarction a few days after trauma due to arterial vasospasm.

SAH shows hyperintense signal of Fluid-attenuated inversion recovery (FLAIR) sequence and blooming artifact on susceptibility weighted imaging (SWI).

An image during the delayed phase of the CTA may be taken to look for pooling of contrast that signifies active bleeding (known as "Spot sign").

SAH in CAA usually occurs in those who age more than 60 years, temporary motor and sensory deficits, and intracranial bleed in white matter adjacent to cerebral cortex.

Definitive diagnosis of CAA is by performing brain biopsy[3] CT scan may show hyperdense intra-axial hemorrhage in the subcortical region.

On MRI these lesions will be presented as blooming artifact on gradient echo and susceptibility weighted imaging.

[3] Those who has infarction should be monitored frequently with CT brains to access hemorrhagic conversions or worsening vasogenic oedema that may require neurosurgical decompression.

[3] Dual energy CT scan maybe useful to differentiate the high densities caused by reperfusion hemorrhage (bleeding after endovascular stroke treatment) and high density due to iodinated contrast administered during cerebral angiography.

If CT scan is normal but SAH is still strongly suspected, lumbar puncture can be done at six to twelfth hours after the onset of headache.

[10] SAH is generally located within basal cisterns, extends diffusely to all subarachnoid spaces (cerebral sulci) or into the ventricular system, or brain parenchyma.

Since the 1990s, many aneurysms are treated by a minimal invasive procedure known as endovascular coiling, which is carried out by instrumentation through large blood vessels.

Signs and symptoms of DAVF are: headache, tinnitus, neurological deficits involving cranial nerves, and increased intracranial pressure.

DVST are frequently caused by infections in the skull base, dehydration, thrombophilia, meningioma, and other dural tumours.

[3] On CT scans, brain parenchymal hemorrhage that does not confined to specific arterial territory along with hyperdense appearance on dural venous sinuses raises the suspicion of DVST.

These are pseudoaneurysm, caused by thrombus clogging the distal arteries, which results in inflammation and small tears at the site of occlusion.

Similar to vasculitis, rupture of mycotic aneurysm also causes SAH in cerebral sulci, mostly located in the vertex.

[3] For those who is already on blood thinners such as aspirin or clopidogrel for prevention of myocardial infarction or stroke, traumatic intracranial hemorrhage should prompt the use of platelet function assays (PFA-100) to assess the effect of these antiplalelet agents.